Category Archive Science

Trophoblast Development – Anatomy, Mechanism

Trophoblast Development/Week 2 is often referred to as the week of twos. It’s the week when the embryoblast, extraembryonic mesoderm and trophoblast each separate into two distinct .

Trophoblast Development

Trophoblasts are the outer layer of cells that provide nutrients to the embryo and form part of the placenta.

Key Points

The trophoblast is subdivided into two layers, the inner cytotrophoblast, which proliferates upon implantation, and the outer syncytiotrophoblast, which supports cytotrophoblast proliferation through contact with the maternal blood.

The cytotrophoblast, at the edges of the villi in the placenta, further differentiates into extravillous trophoblasts, which penetrate into the uterus and attach to the placenta and the mother to promote placental vasculature.

Some trophoblasts replace endothelial cells in the uterine spiral arteries and remodel them into wide-bore conduits that are independent of maternal vasoconstriction. This ensures the fetus receives a steady supply of blood, and that the placenta is not sensitive to damaging fluctuations in oxygen.

Key Terms

  • decidualization: The changes in the endometrial lining after ovulation, characterized by its transformation into a secretory lining in preparation to accept an embryo.
  • extravillous trophoblast: These grow out from the placenta and penetrate into the decidualized uterus.
  • trophoblast: The membrane of cells that forms the wall of a blastocyst during early pregnancy, and also provides nutrients to the embryo and later develops into part of the placenta.

Trophoblasts

Trophoblasts (from the Greek words trephein, to feed, and blastos, germinator) are cells that form the outer layer of a blastocyst. These cells provide nutrients to the embryo and develop into a large part of the placenta.

They are formed during the first stage of pregnancy and are the first cells to differentiate from the fertilized egg. This layer of trophoblasts is also collectively referred to as the trophoblast, or, after gastrulation, the trophectoderm, as it is then contiguous with the ectoderm of the embryo.

Trophoblast Function

Trophoblasts play an important role in embryo implantation and interaction with the endometrium of the maternal uterus following decidualization. The trophoblast is composed of two layers: an inner cytotrophoblast and an outer syncytiotrophoblast.

The syncytiotrophoblast is non-proliferative and thus relies on fusion of the underlying cytotrophoblast cells to expand. The syncytiotrophoblast are the cells in direct contact with the maternal blood that reaches the placental surface, and thus facilitates the exchange of nutrients, wastes, and gases between the maternal and fetal systems.

Cytotrophoblast in the tips of villi can differentiate into another type of trophoblast called the extravillous trophoblast. Extravillous trophoblasts grow out from the placenta and penetrate into the decidualized uterus.

This process is essential not only for physically attaching the placenta to the mother, but also for altering the vasculature in the uterus to allow it to provide an adequate blood supply to the growing fetus as pregnancy progresses.

Some of the trophoblast even replaces the endothelial cells in the uterine spiral arteries as they remodel these vessels into wide bore conduits that are independent of maternal vasoconstriction. This ensures the fetus receives a steady supply of blood, and the placenta is not sensitive to fluctuations in oxygen that could cause it damage.

This is a drawing of the extraembryonic coelom or chorionic cavitiy It depicts a blastocyst embedded in the uterine decidua. Also identified are the amniotic cavity, blood clot, body stalk, embryonic ectoderm, entoderm, mesoderm, maternal vessels, trophoblast, uterine epithelium, uterine glands, and yolk-sac.

Extraembryonic coelom or chorionic cavitiy: A blastocyst embedded in the uterine decidua. (am. Amniotic cavity, b.c. Blood clot., b.s. Body stalk., etc Embryonic ectoderm, ent. Entoderm., mes. Mesoderm, m.v. Maternal vessels., tr. Trophoblast., u.e. Uterine epithelium, u.g. Uterine glands., y.s. Yolk-sac.)

Clinical Example

Intrauterine growth restriction (IUGR) can result in an undersized fetus with poor organ development or even death. The primary factor in IUGR is placental dysfunction caused by a failure of the extravillous trophoblasts to penetrate and modify the uterine spiral arteries. The result is a poorly-oxygenated environment and reduced fetal growth.

Bilaminar Embryonic Disc Development

The floor of the amniotic cavity is formed by the embryonic disc.

Key Points

In humans, the formation of the embryonic disc occurs after implantation and prior to embryonic folding (between about day 14 to day 21 post-fertilization).

The embryonic disc is derived from the epiblast layer, which lies between the hypoblast layer and the amnion. The epiblast layer is derived from the inner cell mass.

The formation of the bilaminar embryonic disc precedes gastrulation.

Key Terms

  • optic disc: The location where ganglion cell axons exit the eye to form the optic nerve.
  • bilaminar: Formed of, or having, two laminae, or thin plates.

The floor of the amniotic cavity is formed by the embryonic disc, which is composed of a layer of prismatic cells and the embryonic ectoderm. It is derived from the inner cell mass and lies adjacent to the endoderm.

In humans, the formation of the embryonic disc occurs after implantation and prior to embryonic folding (between about day 14 to day 21 post-fertilization). The embryonic disc is derived from the epiblast layer, which lies between the hypoblast layer and the amnion. The epiblast layer is derived from the inner cell mass.

Embryonic Disc Development

A drawing of a rabbit embryo that identifies the embryonic disc and the primitive streak on it.

Surface view of a rabbit embryo: A drawing of a rabbit embryo that identifies the embryonic disc and the primitive streak (arg—embryonic disc; pr—primitive streak).

The embryonic disc forms during early development. By the blastocyst stage, the embryo is a hollow ball of cells with the inner cell mass (embryoblast) off to one side, and the blastocystic cavity fills the remainder of the sphere.

As the embryo progresses in implantation, a small space appears in the embryoblast and forms the amniotic cavity. Simultaneously, morphological changes occur in the embryoblast that result in the formation of a flat, almost circular bilaminar plate of cells that include the epiblast and the hypoblast—the embryonic disk.

The epiblast forms the floor of the amniotic cavity and is continuous with the amnion. The hypoblast forms the roof of the exocoelomic cavity and is continuous with the thin exocoelomic membrane.

The formation of the bilaminar embryonic disc precedes gastrulation. As gastrulation progresses, the embryonic disc becomes trilaminar and the notochord is formed. Through the process of neurulation, the notochord induces the formation of the central nervous system in the embryonic disc.

Amnion Development

The amnion contains the fluid that cushions and protects the fetus.

Key Points

In humans, the amnion is present in the earliest observed embryonic stage, appearing as a cavity within a mass of cells.

The amniotic cavity is roofed in by a single stratum of flattened, ectodermal cells, called the amniotic ectoderm, while the floor is composed of the prismatic ectoderm of the embryonic disk.

Outside the amniotic ectoderm, a thin layer of mesoderm is connected by the body stalk with the mesodermal lining of the chorion.

By approximately the fourth to fifth week, amniotic fluid (liquor amnii) begins to accumulate in the amnion, which increases in quantity and expands to contact the chorion.

During the later stages of pregnancy, the amniotic fluid allows easier and more fluid movements of the fetus and diminishes the risk of injury.

Key Terms

  • amniotic fluid: In placental mammals, a fluid contained within the amnion membrane that surrounds a developing embryo or fetus (also called liquor amnii).
  • embryonic disk: The floor of the amniotic cavity is formed by the embryonic disk (or disc), which is composed of a layer of prismatic cells.
  • amnion: The innermost membrane of the fetal membranes of reptiles, birds, and mammals; the sac in which the embryo is suspended.
  • chorion: One of the membranes that exist during pregnancy between the developing fetus and mother.

This is a cutaway drawing showing a human fetus in a womb. The fetus is seen enclosed within the amnion.

Amnion: The human fetus is enclosed within the amnion.

The amnion is a closed sac appearing in the inner cell mass as a cavity. This cavity is roofed in by a single stratum of flattened, ectodermal cells called the amniotic ectoderm. Its floor consists of the prismatic ectoderm of the embryonic disk.

The continuity between the roof and the floor is established at the margin of the embryonic disk. Outside the amniotic ectoderm is a thin layer of mesoderm (continuous with that of the somatopleure), which is connected by the body stalk with the mesodermal lining of the chorion.

When first formed, the amnion is in contact with the body of the embryo, but by about the fourth or fifth week, amniotic fluid (liquor amnii) begins to accumulate within it. This fluid increases in quantity, causing the amnion to expand and ultimately to adhere to the inner surface of the chorion so that the extra-embryonic part of the coelom is obliterated.

This increase continues up to the sixth or seventh month of pregnancy, after which it diminishes somewhat. At the end of pregnancy, it amounts to about one liter.

The amniotic fluid allows some free movement for the fetus during the later stages of pregnancy and also diminishes the risk of injury. It contains less than two percent solids, and consists mainly of urea and other extractives, inorganic salts, a small amount of protein, and, frequently, a trace of sugar.

Note: That some of the liquor amnii is swallowed by the fetus is proved by the fact that epidermal debris and hairs have been found among the contents of the fetal alimentary canal.

Yolk Sac Development

The yolk sac is vascularized and contributes nutrients to the embryo.

Key Points

The yolk sac is the earliest visible portion of the gestational sac and is situated on the ventral portion of the embryo, arising from extra-embryonic endoderm.

The blood to and from the yolk sac is conveyed via the primitive aorta and vitelline circulation.

At approximately the end of the fourth week, the yolk sac is connected to the primitive digestive system, which allows the yolk sac to contribute nutrients to the embryo.

Key Terms

  • yolk sac: A membranous sac attached to an embryo that provides early nourishment in the form of yolk in bony fishes, sharks, reptiles, birds, and mammals. It functions as the developmental circulatory system of the human embryo before internal circulation begins.
  • vitelline circulation: The system of blood flowing from the embryo to the yolk sac and back again.
  • gestational sac: The gestational sac (or gestation sac) is the only available intrauterine structure that can be used to determine if an intrauterine pregnancy (IUP) exists until the embryo is identified.
  • Heuser’s membrane: Also called the exocoelomic membrane, it is a short lived combination of hypoblast cells and extracellular matrix.
  • mesenchyme: A type of tissue characterized by loosely associated cells that lack polarity and are surrounded by a large extracellular matrix.

The yolk sac is the first element seen in the gestational sac during pregnancy. In humans, it is usually visible at five weeks of gestation. Identifying a true gestation sac is a critical landmark, and is reliably seen in early pregnancy through ultrasound. The yolk sac, situated on the ventral aspect of the embryo, is lined by extra-embryonic endoderm, outside of which is a layer of extra-embryonic mesenchyme derived from the mesoderm.

Blood is conveyed to the wall of the sac by the primitive aorta. After circulating through a wide-meshed capillary plexus, it is returned by the vitelline veins to the tubular heart of the embryo. This vitelline circulation absorbs nutritive material from the yolk sac that is conveyed to the embryo.

The yolk sac is a membranous sac attached to the embryo that provides nourishment in the form of yolk. In this drawing the yolk sac is off to the right side of the amnion, heart, and body stalk.

Yolk sac: The yolk sac is a membranous sac attached to the embryo that provides nourishment in the form of yolk.

At the end of the fourth week, the yolk sac has the appearance of a small, pear-shaped vesicle (umbilical vesicle) opening into the digestive tube by a long, narrow tube, the vitelline duct. The vesicle can be seen in the afterbirth as a small, somewhat oval-shaped body whose diameter varies from 1 mm to 5 mm. It is situated between the amnion and the chorion and may lie on or at a varying distance from the placenta.

As a rule, the vitelline duct undergoes complete obliteration during the seventh week. In about 2% of the cases, its proximal portion persists as a diverticulum from the small intestine (Meckel’s diverticulum), which is situated about 60 cm proximal to the ileocecal valve. It may be attached by a fibrous cord to the abdominal wall at the umbilicus. Sometimes, a narrowing of the lumen of the ileum is seen opposite the site of attachment of the duct.

The yolk sac starts forming during the second week of embryonic development, at the same time of the shaping of the amniotic sac. The hypoblast starts proliferating laterally and descending. In the meantime Heuser’s membrane, located on the opposite pole of the developing vesicle, starts its upward proliferation and meets the hypoblast.

Sinusoid Development

The sinusoids are capillaries that develop after implantation to allow the exchange of gas and nutrients with the mother.

Key Points

The vitelline veins drain blood from the yolk sac. Portions of the veins above the upper ring become interrupted by the developing liver and broken up by it into a plexus of small capillary -like vessels termed sinusoids.

Sinusoids are found in the liver, lymphoid tissue, endocrine organs, and hematopoietic organs such as the bone marrow and the spleen. Sinusoids found within the terminal villi of the placenta are not comparable to these because they possess a continuous endothelium and complete basal lamina.

The invasion of endometrial sinusoids by the trophoblast
allows maternal blood flow into the trophoblastic lacunae; this forms
uteroplacental blood circulation.

Key Terms

  • sinusoid: Any of several channels through which venous blood passes in various organs.
  • trophoblastic lacunae: Spaces in the early syncytiotrophoblastic layer of the chorion present prior to the development of the villi.
  • vitelline veins: Veins that drain blood from the yolk sac.

The vitelline veins drain blood from the yolk sac. At first, they run upward in front on either side of the intestinal canal and, subsequently, unite on the ventral aspect of the canal. Beyond this, they are connected to one another by two anastomotic branches, one on the dorsal and the other on the ventral aspect of the duodenal portion of the intestine.

Thus, it is encircled by two venous rings. The superior mesenteric vein opens into the middle or dorsal anastomosis. The portions of the veins above the upper ring become interrupted by the developing liver and broken up by it into a plexus of small, capillary-like vessels termed sinusoids.

This is a drawing of the liver and veins of a human embryo, 24 or 25 days old, as seen from the ventral surface. The drawing shows the vitelline veins surrounding the stomach and the connection points of the vitelline veins to the left and right umbilical veins.

Vitelline veins: The liver and veins of a human embryo, 24 or 25 days old, as seen from the ventral surface. (The vitelline veins are visible at the center bottom.)

A sinusoid is a small blood vessel that is a type of capillary similar to a fenestrated endothelium. Sinusoids are actually classified as a type of open pore capillary (that is, discontinuous) as opposed to fenestrated.

Fenestrated capillaries have diaphragms that cover the pores, whereas open pore capillaries lack a diaphragm, having just an open pore. The open pore endothelial cells greatly increase their permeability.

Permeability is also increased by large intercellular clefts and fewer tight junctions. The level of permeability can allow small and medium-sized proteins, such as albumin, to readily enter and leave the blood stream.

Sinusoids are found in the liver, lymphoid tissue, endocrine organs, and hematopoietic organs, such as the bone marrow and the spleen. Sinusoids found within the terminal villi of the placenta are not comparable to these because they possess a continuous endothelium and complete basal lamina.

The invasion of endometrial sinusoids by the trophoblast allows maternal blood flow into the trophoblastic lacunae; this forms the uteroplacental blood circulation.

Development of the Extraembryonic Coelom

The extra-embryonic coelom is a cavity that contains the chorion. It is located between Heuser’s membrane and the trophoblast.

Key Points

The extra-embryonic coelom develops at the same time as the primitive yolk sac through the proliferation and differentiation of hypoblast cells into mesenchymal cells that fill the area between Heuser’s membrane and the trophoblast. The entire structure is enclosed by the chorionic plate.

The extra-embryonic mesoderm is subdivided into two layers: the extra-embryonic splanchnopleuric mesoderm, which is outside the primitive yolk sac; and the extra-embryonic somatopleuric mesoderm, which is adjacent to the cytotrophoblast.

The chorion is one of the membranes that exist during pregnancy between the developing fetus and mother.

Key Terms

  • chorion: The protective and nutritive membrane that attaches higher vertebrate fetuses to the uterus.
  • Heuser’s membrane: Heuser’s membrane (or the exocoelomic membrane) is a short-lived combination of hypoblast cells and extracellular matrix.
  • coelum: Also called the chorionic cavity, this is a portion of the conceptus that consists of a cavity between Heuser’s membrane and the trophoblast.

Development of the Extra-Embryonic Coelom

This is an artificially colored image of the contents in the cavity of the uterus seen at approximately 5 weeks of gestational age by obstetric ultrasonography. It shows the gestational sac, yolk sac, and embryo.

Gestational sac: An artificially colored image of the contents in the cavity of the uterus seen at approximately 5 weeks of gestational age by obstetric ultrasonography.

The extra-embryonic coelom (or chorionic cavity) is a portion of the conceptus consisting of a cavity between Heuser’s membrane and the trophoblast. During the formation of the primitive yolk sac, some of the migrating hypoblast cells transdifferentiate into mesenchymal cells that fill the space between Heuser’s membrane and the trophoblast to form the extra-embryonic mesoderm.

As development progresses, small lacunae begin to form within the extra-embryonic mesoderm that become larger and form the extra-embryonic coelom.

The extra-embryonic mesoderm is divided into two layers: the extra-embryonic splanchnopleuric mesoderm, which lies adjacent to Heuser’s membrane around the outside of the primitive yolk sac; and the extra-embryonic somatopleuric mesoderm, which lies adjacent to the cytotrophoblast layer of the embryo.

The extra-embryonic coelomic cavity is also called the chorionic cavity—it is enclosed by the chorionic plate. The chorionic plate is composed of an inner layer of somatopleuric mesoderm and an outer layer of trophoblast cells. It is the fetal
aspect of the placenta that gives rise to chorionic villi.

Chorion Development

The chorion is one of the membranes that exist during pregnancy between the developing fetus and the mother. It consists of an extra-embryonic mesoderm and two layers of trophoblast and surrounds the embryo and other membranes.

Villi emerge from the chorion, which invade the endometrium, destroy the uterine decidua, and allow the transfer of nutrients from maternal blood to fetal blood.

Chorionic villi are at first small and nonvascular, and consist of only trophoblast, but they increase in size and branch. Blood is carried to the villi by the paired umbilical arteries, which branch into chorionic arteries and enter the chorionic villi as cotyledon arteries.

After circulating through the capillaries of the villi, the blood is returned to the embryo by the umbilical veins. Until about the end of the second month of pregnancy, the villi cover the entire chorion, and are almost uniform in size; but, after this stage, they develop unequally.

2nd weeks

Following all the excitement associated with the first gestational week, the newly formed blastocyst is ready to settle into a supportive environment and continue the growth process. Week 2 is often referred to as the week of twos. It’s the week when the embryoblast, extraembryonic mesoderm and trophoblast each separate into two distinct layers. Additionally, there are two cavities that develop within the embryonic unit at this time as well.

While every step is integral for adequate foetal development, one of the most important features of the second week is the completion of implantation and establishment of fetomaternal interactions. This article will follow the developing embryo through the completion of implantation and development of the non-embryonic components of the conceptus. It will also discuss some complications associated with implantation.

Implantation of the blastocyst

Implantation is a complex biochemical and mechanical process that begins in the first week of gestation and extends into the second week. There are many influencing factors that affect the process. These can be grouped into maternal and embryonal factors. However, both entities work synchronously in order to effectively achieve implantation. The process of implantation can be subdivided into three phases:

  • There is a period of apposition where the blastocyst establishes weak interactions with the uterine wall.
  • The attachment phase occurs when definitive binding of the blastocyst to the uterine epithelium is more established, such that the blastocyst cannot be flushed from the uterine cavity.
  • Finally invasion occurs when the blastocyst begins to burrow into the endometrium.

This period usually occurs between the 19th and 24th day of the menstrual cycle. This coincides roughly with the 6th to 10th day following ovulation.

Maternal factors affecting implantation

In anticipation for successful fertilization each month, the inner uterine wall (endometrium) undergoes a series of changes in order to facilitate the blastocyst. Recall that there are three layers of the endometrium – the strata basalis, spongiosum and compactum.

The deepest layer is the stratum basalis, which functions as the regenerative layer and proliferates to form the stratum spongiosum and stratum compactum. Stratum compactum is the most superficial and the stratum spongiosum resides between the two. Together, the strata compactum and spongiosum form the stratum functionalis; which is the functional layer of the endometrium that facilitates implantation.

The development of the stratum functionalis is mitigated by surges in estrogen (which are released from the maturing ovarian follicle, under the influence of follicle stimulating hormone). If fertilization did not occur during the previous menstrual cycle, the fall in reproductive hormones result in the degeneration of the stratum functionalis. The shedding of this layer during the menstrual phase of the cycle accounts for the vaginal bleeding known as menstruation.

In the subsequent cycle, as follicle stimulating hormone levels rise and stimulate maturation of another ovarian follicle, the resultant increase in estrogen levels leads to proliferation of the stratum basalis. This is known as the proliferative phase, during which time there is thickening of the endometrium. Following an increase in luteinizing hormone and the release of a secondary oocyte, the remaining corpus luteum continues to release estrogen and progesterone to maintain the stratum functionalis. The spiral arteries of the uterus become longer and more tortuous under the influence of the sex hormones.

Endometrium - dorsal view
Endometrium (posterior view)

Following successful fertilization the uterine epithelia, which is characterized by ciliated columnar cells with microvilli, undergoes morphological changes to accommodate the growing embryo. The expression of these cilia (extended processes located at the apical aspect of the cells) is regulated by both progesterone and estrogen. The underlying motile microtubules allow the cilia to move the developing embryo toward a favourable site on the uterine wall. This process usually starts around the end of the first gestational week, when the conceptus is classified as a blastocyst.

The process of bringing the conceptus close to the uterine wall is referred to as adplantation (apposition). As the blastocyst rolls along the surface of the uterus, the pole of the blastocyst with the inner cell mass is adjacent to the uterine wall. Early attachments to the microvilli (short, non-motile, apical epithelial processes) also facilitate the initiation of implantation.

Once the uterine lining is receptive for implantation, the endometrium is said to be in the implantation window. However, this is a complex process that depends on the presence of numerous cytokines, immunomodulators, and increased binding capacity of the epithelium in order for implantation to work. Recall from the first week of gestation that the resulting conceptus is genetically unique when compared with its parents. Therefore, the mother’s immune system should identify the blastocyst as a parasitic entity that should be destroyed.

A key element in the implantation phase that is thought to modify this anticipated immune response (and other parts of implantation) is known as leukaemia inhibitory factor (LIF). This is a member of the interleukin – 6 (IL-6) family that has the ability to influence several unrelated gene expressions (i.e. it’s a pleiotropic entity). Within the reproductive system, it is produced by both the endometrial epithelium as well as the developing blastocyst. Leukaemia inhibitory factor has the following functions with regards to endometrial receptivity:

  • The decidualization of the stromal cells (discussed below) is by LIF. This response is generated by way of a cyclic adenosine monophosphate (cAMP) pathway that activates a biochemical cascade involving estrogen and progesterone, IL-5, IL-6, prostaglandins, and cyclooxygenase 2 (COX-2). The resultant cellular morphological change creates a more favourable implantation environment. This particular reaction is important because it plays a significant role in immunomodulation. It is particularly difficult for thymocytes (T-cells) to invade decidual tissue; similarly, decidual cells have a hard time recruiting T-cells from the percolating blood. Therefore, the probability of the maternal immune system mounting a cytotoxic T-lymphocyte (CTL) response against the allogeneic conceptus is markedly reduced.
  • In addition, LIF upregulates numerous epidermal growth factors such as heparin – binding epidermal growth factor like protein (HB-EGF), epiregulin (EPR), and amphiregulin (AREG). These proteins act as ligands for the epidermal growth factor receptors and subsequently stimulate the proliferation of the endometrial epidermis.
  • LIF also stimulates the activity of implantation genes, including members of the Wnt family (Wnt 4, 5a, and others) and MutS homolog homebox 1 gene (MSX 1). These and other implantation genes result in differentiation of the luminal and glandular epithelia (decidualization), proliferation of the stromal cells, and decrease in the polarity of the epithelium to foster adhesion.
  • Uterodomes (also known as pinopods) are micro-protrusions of the luminal surface of the uterine epithelium that interdigitate with the blastocyst during adplantation and attachment. While they are present throughout the luteal phase of the menstrual cycle, they increase in number under the influence of LIF. In lower other mammals, pinopods are thought to play a significant role in pinocytosis (cell drinking). However, this is not its primary role in humans. As a result, they are referred to as uterodomes based on their appearance.
  • Under normal circumstances, the luminal surface of the uterus is coated with a thick layer of glycocalyx. This is a carbohydrate, glycoprotein rich layer that promotes repulsion of foreign entities from the cell membranes. It also has a large quantity of mucins (MUC-1 and MUC-4). LIF mediates significant local downregulation of MUC-1 in the area of the epithelium adjacent to the hatched blastocyst, which reduces repulsion of the blastocyst. However, relatively high levels of mucins are normally present in unfavourable implantation sites to prevent attachment.
  • Finally, the presence and activity of a member of the junctional adhesion molecule family (JAM-2) is also noted to be increased within the uterus during the 1st to 2nd gestational weeks. Junctional adhesion molecules have the ability to interact within the family (i.e. JAM-JAM binding) as well as with other integrins on non-uterine cells. They therefore promote cellular attachment to the epithelial membrane. Both LIF and progesterone have been shown to upregulate the expression of these adhesion molecules.

As mentioned earlier, the luminal uterine stroma undergoes morphological transformation under the influence of LIF, estrogen and progesterone. This process – known as decidualization – involves accumulation of lipids and glycogen at a cellular level. The cells (i.e. decidual cells) subsequently acquire a polyhedral shape (as opposed to their previous columnar appearance). The process begins locally at the site of fetomaternal attachment, but gradually radiates until the entire endometrium has been transformed. On a molecular level, bone morphogenetic protein 2 (BMP-2) is needed for this transformation to occur; its deficiency is a known cause of infertility. The decidua provides an immunologically safe space for the embryo, in addition to providing nutrition for its development.

Fetal factors affecting implantation

As the blastocyst is hatched from the zona pellucida, it comes into contact with the endometrium. Surface proteins on the trophoblast known as trophinin interact with similar trophinin molecules on the endometrial surface. This plays a role in the differentiation of the trophoblast into two distinct layers:

  • In the periphery, there are multinucleated cells that have no discernible cell walls. This area is referred to as the syncytiotrophoblast. There is no mitotic activity in this area.
  • Deep to the syncytiotrophoblast is a cluster of mitotically active cells known as the cytotrophoblast. This cluster of cells rapidly replicates and migrates to the periphery in order to support the growing syncytiotrophoblast.

Of note, by the end of week 2, the bilaminar disc develops a localized region of thickened cells in the hypoblast. This area is referred to as the prechordal plate. Not only does the prechordal plate help with the organization of the head region during development, but it also indicates the future head region and the location of the mouth.

The syncytiotrophoblast is a highly invasive structure that penetrates the endometrium in order for the blastocyst to become embedded. The trophinin-trophinin binding also induces endometrial epithelial apoptosis in the mother in order to accommodate the invading cell mass. The blastocyst then utilizes the nutrients from the recently destroyed maternal cells as it continues to grow. Furthermore, the syncytiotrophoblast (under the influence of LIF) begins to produce human chorionic gonadotropin hormone (β-hCG). The presence of β-hCG prevents corpus luteum degeneration, resulting in the continued release of estrogen and progesterone. The detection of the glycoprotein in maternal circulation and urine also forms the basis of the pregnancy test.

Another recently discovered element that contributes to implantation is the protein preimplantation factor. It is derived from the embryo and has been shown to aid in maternal immunomodulation, embryo-endometrial adhesion, and endometrial apoptosis.

Review of the initial sequence of implantation

Let’s recap the initial implantation sequence:

  • Endometrial development occurs each month in anticipation of successful fertilization.
  • Successful fertilization occurs and the zygote develops into a blastocyst.
  • The blastocyst roles along the endometrium towards a favourable implantation site.
  • Concurrently, there is maternal immunomodulation, downregulation of repelling entities and upregulation of adhesion moieties.
  • The blastocyst hatches from the zona pellucida.
  • Adplantation occurs when weak carbohydrate binding occurs between the embryo and the glycocalyx.
  • As the embryo gets closer to the endometrium, stronger bonds are formed. These involve interactions with integrins, L-selectin, osteopontin, cadherins, trophinin, as well as CD44 and CD98.
  • Attachment stimulates maternal decidualization and embryonal trophoblast differentiation.
  • Trophoblastic invasion coincides with desmosomal detachment of maternal cells, as well as apoptosis of adjacent decidua.
Blastocyst implantation
Blastocyst implantation

Amniotic cavity

While implantation ensues, the embryoblast also undergoes differentiation to form a bilaminar disc. The flat, circular disc is comprised of a thicker epiblast with high columnar cells and a thinner hypoblast with small cuboidal cells. A small space develops relative to the epiblast; it is the precursor of the amniotic cavity.

Epiblastic cells forming the floor of the cavity subsequently separate to form amnioblasts that will form the amnion (surrounding the amniotic cavity). The sac and cavity will eventually become filled with amniotic fluid later on in the pregnancy. They provide shock absorption and facilitate movement of the foetus during development.

Umbilical vesicle

Peripherally, the hypoblast is continuous with another structure known as the exocoelomic (Heuser’s) membrane. It also forms the roof of the enclosed exocoelomic cavity. Combined, the membrane and the hypoblast form the visceral lining of the yolk sac. However, since the human embryo does not possess a yolk, it is more appropriate to refer to it as the primary umbilical vesicle.

Endodermal cells arising from the exocoelomic membrane extends circumferentially to enclose the embryonic disc and both cavities. It is subsequently referred to as the extraembryonic mesoderm. Both cavities facilitate embryonic folding as growth and morphological changes occur. The umbilical vesicle may play a role in nutrient transfer to the embryo. Furthermore, it is an important source of primordial germ cells.

Early fetomaternal circulation

While the aforementioned cavities and bilaminar disc develop, the syncytiotrophoblast began to lacunate (I.e. form lacunae). The lacunae are filled with an amalgam of cellular debris and maternal blood, known as the embryotroph. This fluid gains access to the embryonic disc via diffusion and delivers nutrients as well as oxygen to the embryo. The lacunae subsequently become confluent, forming lacunar networks, which serves as the primordial uteroplacental circulation. As the networks continue to fuse, the syncytiotrophoblast has a sieve-like appearance, particularly around the embryonic pole of the conceptus. This will subsequently give rise to the intervillous spaces of the placenta.

The capillaries around the implanted embryo become engorged, dilated and their walls become thin. From here onwards, they are known as sinusoids. The syncytiotrophoblast continues to erode the walls of the sinusoids, resulting in more maternal blood flowing freely into the lacunar networks. Much of the derived nutrients is conveyed to the embryo by the trophoblast. However, the trophoblast grows a lot faster than the embryo in the early phases. As such, it is likely to have a higher nutritional requirement than the embryo.

Chorionic sac

As time progresses, the extraembryonic mesoderm increases in size. Numerous cavities known as the extraembryonic coelomic spaces begin to appear deep to the cytotrophoblast and superficial to the exocoelomic membrane. These spaces coalesce to form the extraembryonic coelom. This coincides with a decrease in the volume of the primary umbilical vesicle; which is then referred to as the secondary umbilical vesicle. The cells of the secondary umbilical vesicle arise from migratory extraembryonic endodermal cells of the hypoblast. There is a remnant of the primary umbilical vesicle within the extraembryonic coelom that is referred to as an exocoelomic cyst.

Cellular columns, lined with syncytial coverings, extending into the syncytiotrophoblast indicate the ending of the second gestational week. This phenomenon marks the formation of the primary chorionic villi. Splanchnic and somatic derivatives of the extraembryonic mesoderm line the umbilical vesicles, and the trophoblast and amnion, respectively. The somatic extraembryonic mesoderm, along with both trophoblastic layers, gives rise to the chorion. The space enclosed by the chorion is the chorionic sac; it contains the embryo, as well as the amniotic sac and umbilical vesicle. The latter three structures are attached to the chorion by the connecting stalk. The former extraembryonic coelom is now referred to as the chorionic cavity.

Implantation completed

By the 10th day following fertilization, the embryo is completely embedded in the endometrium. There is a small defect in the epithelium that is sealed by a fibrin-based blood clot known as the closing plug. By day 12, the area is completely healed. The 14 day embryo maintains the form of a flat bilaminar embryonic disc at the end of second week. The thickened prechordal plate develops as a localized thickening of hypoblast and indicates the future site of mouth and organizer of the head region.

Summary of 2nd Week

Here is a simplified summary of the events of the second week:

  • The hatched blastocyst moves along the endometrium towards a favourable point of implantation.
  • The endometrium is converted into an immunologically privileged site with optimum blood supply
  • Weak attachments are strengthened.
  • Differentiation of the trophoblast and endometrial stroma facilitate invasion of the endometrium.
  • Several cavities and membranes are formed.
  • β-hCG production is stimulated.
  • Complete implantation with endometrial scarring is achieved by day 10.
  • Complete regeneration around the scar results around day 12.
  • At the end of week 2, the chorionic cavity is formed.

References

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Blood Gas Analysis – Symptoms, Diagnosis, Treatment

Blood gas analysis is a commonly used diagnostic tool to evaluate the partial pressures of gas in blood and acid-base content. Understanding and use of blood gas analysis enable providers to interpret respiratory, circulatory, and metabolic disorders. 

A “blood gas analysis” can be performed on blood obtained from anywhere in the circulatory system (artery, vein, or capillary).  An arterial blood gas (ABG) tests explicitly blood taken from an artery. ABG analysis assesses a patient’s partial pressure of oxygen (PaO2) and carbon dioxide (PaCO2). PaO2 provides information on the oxygenation status, and PaCO2 offers information on the ventilation status (chronic or acute respiratory failure). PaCO2 is affected by hyperventilation (rapid or deep breathing), hypoventilation (slow or shallow breathing), and acid-base status. Although oxygenation and ventilation can be assessed non-invasively via pulse oximetry and end-tidal carbon dioxide monitoring, respectively, ABG analysis is the standard.

When assessing the acid-base balance, most ABG analyzers measure the pH and PaCO2 directly. A derivative of the Hasselbach equation calculates the serum bicarbonate (HCO3) and base deficit or excess. This calculation frequently results in a discrepancy from the measured due to the blood CO2 unaccounted for by the equation. The measured HCO3 uses a strong alkali that liberates all CO2 in serum, including dissolved CO2, carbamino compounds, and carbonic acid. The calculation only accounts for dissolved CO2; this measurement using a standard chemistry analysis will likely be called a “total CO2”. For that reason, the difference will amount to around 1.2 mmol/L. However, a larger difference may be seen on the ABG, compared to the measured value, especially in critically ill patients. 

The calculation has been disputed as both accurate and inaccurate based on the study, machine, or calibration used and must be interpreted appropriately based on your institutional standards.

Arterial blood gases are frequently ordered by emergency medicine,  intensivist, anesthesiology, and pulmonology clinicians but may also be needed in other clinical settings. Many diseases are evaluated using an ABG, including acute respiratory distress syndrome (ARDS), severe sepsis, septic shock, hypovolemic shock, diabetic ketoacidosis, renal tubular acidosis, acute respiratory failure, heart failure, cardiac arrest, asthma, and inborn errors of metabolism.

Specimen Requirements and Procedure

Whole blood is the required specimen for an arterial blood gas sample. The specimen is obtained through an arterial puncture or acquired from an indwelling arterial catheter. A description of these procedures is beyond the scope of this article; please refer to the StatPearls article “arterial lines” and other references for more information. Once obtained, the arterial blood sample should be placed on ice and analyzed as soon as possible to reduce the possibility of erroneous results. Automated blood gas analyzers are commonly used to analyze blood gas samples, and results are obtained within 10 to 15 minutes. Automated blood gas analyzers, directly and indirectly, measure specific components of the arterial blood gas sample (see above).

ABG Components:

  • pH = measured acid-base balance of the blood
  • PaO2 = measured the partial pressure of oxygen in arterial blood
  • PaCO2 = measured the partial pressure of carbon dioxide in arterial blood
  • HCO3 = calculated concentration of bicarbonate in arterial blood
  • Base excess/deficit = calculated relative excess or deficit of base in arterial blood
  • SaO2 = calculated arterial oxygen saturation unless a co-oximetry is obtained, in which case it is measured

Testing Procedures

A modified Allen test is a must before an ABG is drawn from either of the upper extremities to check for adequate collateral flow. Alternatively, pulse oximetry and duplex ultrasound can be used too. The arterial site commonly used is the radial artery, as it is superficial and easily palpable over the radial styloid process. The next most common site is the femoral artery. The test is performed on the unilateral upper extremity chosen for the procedure (Please look at the attached image for graphical illustration). The selected upper extremity is flexed at the elbow, and the patient requested to clench the raised fist for 30 seconds. Then pressure is applied over the ulnar and radial arteries with the intent to occlude the blood flow. After five seconds, unclench the raised fist. The palm will now appear pale, white, or blanched. Then pressure over the ulnar artery is released while the radial artery compression is maintained. In 10 to 15 seconds, the palm returns to its original color, indicating adequate Ulnar collateral blood flow. If the palm does not return to its actual color, it is an abnormal test and unsafe to puncture the radial artery. Similarly, the radial collateral blood flow is assessed by maintaining ulnar artery pressure and releasing the radial artery pressure. 

Results, Reporting, Critical Findings

An acceptable normal range of ABG values of ABG components are the following, noting that the range of normal values may vary among laboratories and in different age groups from neonates to geriatrics:

  • pH (7.35-7.45)
  • PaO2 (75-100 mmHg)
  • PaCO2 (35-45 mmHg)
  • HCO3 (22-26 meq/L)
  • Base excess/deficit (-4 to +2)
  • SaO2 (95-100%)

Arterial blood gas interpretation is best approached systematically.  Interpretation leads to an understanding of the degree or severity of abnormalities, whether the abnormalities are acute or chronic, and if the primary disorder is metabolic or respiratory in origin. Several articles have described simplistic ways to interpret ABG results. However, the Romanski method of analysis is most simplistic for all levels of providers. This method helps determine the presence of an acid-base disorder, its primary cause, and whether compensation is present.

The first step is to look at the pH and assess for the presence of acidemia (pH < 7.35) or alkalemia (pH > 7.45). If the pH is in the normal range (7.35-7.45), use a pH of 7.40 as a cutoff point.  In other words, a pH of 7.37 would be categorized as acidosis, and a pH of 7.42 would be categorized as alkalemia. Next, evaluate the respiratory and metabolic components of the ABG results, the PaCO2 and HCO3, respectively. The PaCO2 indicates whether the acidosis or alkalemia is primarily from a respiratory or metabolic acidosis/alkalosis. PaCO2 > 40 with a pH < 7.4 indicates a respiratory acidosis, while PaCO2 < 40 and pH < 7.4 indicates a respiratory alkalosis (but is often from hyperventilation from anxiety or compensation for a metabolic acidosis). Next, assess for evidence of compensation for the primary acidosis or alkalosis by looking for the value (PaCO2 or HCO3) that is not consistent with the pH.  Lastly, assess the PaO2 for any abnormalities in oxygenation.

Example 1:  ABG : pH = 7.39, PaCO2 = 51 mm Hg, PaO2 = 59 mm Hg, HCO3 = 30 mEq/L and SaO2 = 90%, on room air.

  • pH is in the normal range, so use 7.40 as a cutoff point, in which case it is <7.40, acidosis is present.
  • The PaCO2 is elevated, indicating respiratory acidosis, and the HCO3 is elevated, indicating a metabolic alkalosis.
  • The value consistent with the pH is the PaCO2. Therefore, this is a primary respiratory acidosis.  The acid-base that is inconsistent with the pH is the HCO3, as it is elevated, indicating a metabolic alkalosis, so there is compensation signifying a non-acute primary disorder because it takes days for metabolic compensation to be effective.
  • Last, the PaO2 is decreased, indicating an abnormality with oxygenation. However, a history and physical will help delineate the severity and urgency of required interventions, if any.

Example 2:  ABG : pH = 7.45, PaCO2 = 32 mm Hg, PaO2 = 138 mm Hg, HCO3 = 23 mEq/L, the base deficit = 1 mEq/L, and SaO2 is 92%, on room air.

  • pH is in the normal range. Using 7.40 as a cutoff point, it is >7.40, so alkalemia is present.
  • The PaCO2 is decreased, indicating a respiratory alkalosis, and the HCO3 is normal but on the low end of normal.
  • The value consistent with the pH is the PaCO2. Therefore, this is a primary respiratory alkalosis.  The HCO3 is in the range of normal and, thus, not inconsistent with the pH, so there is a lack of compensation.
  • Last, the PaO2 is within the normal range, so there is no abnormality in oxygenation.

When evaluating a patient’s acid-base status, it is important to include an electrolyte imbalance or anion gap in your synthesis of the information.   For example: In a patient who presents with Diabetic Ketoacidosis, they will eliminate ketones, close the anion gap but have persistent metabolic acidosis due to hyperchloremia. This is due to the strong ionic effect, which is beyond the scope of this article.

Clinical Significance

Arterial blood gas monitoring is the standard for assessing a patient’s oxygenation, ventilation, and acid-base status. Although ABG monitoring has been replaced mainly by non-invasive monitoring, it is still useful in confirming and calibrating non-invasive monitoring techniques.

In the intensive care unit (ICU) and emergency room settings, evaluation of oxygenation is frequently done in the context of severe sepsis, acute respiratory failure, and ARDS. Calculating an alveolar-arterial (A-a) oxygen gradient can aid in narrowing down the hypoxemia cause. For example, a gradient’s presence or absence can help determine whether the abnormality in oxygenation is potentially due to hypoventilation, a shunt, V/Q mismatch, or impaired diffusion. The equation for the expected A-a gradient assumes the patient is breathing room air; therefore, the A-a gradient is less accurate at higher percentages of inspired oxygen. Determining the intrapulmonary shunt fraction, the fraction of cardiac output flowing through pulmonary units that do not contribute to gas exchange is the best estimate of oxygenation status. Calculating the shunt fraction is traditionally done at a delivered FiO2 of 1.0, but if performed at a FiO2 lower than 1.0, then venous admixture would be the more appropriate term. For simplicity, assessing oxygenation is more commonly performed by computing the ratio of PaO2 and the fraction of inspired oxygen (PaO2/FiO2 or P/F ratio). However, there are limitations in using the P/F ratio in assessing oxygenation, as the discrepancy between venous admixture and the P/F ratio at a given shunt fraction depends on the delivered FiO2. For research purposes, the P/F ratio has also been used to categorize disease severity in ARDS.

Another parameter commonly used in ICUs to assess oxygenation is the oxygenation index (OI). This index is considered a better indicator of lung injury, particularly in the neonatal and pediatric population, compared to the P/F ratio. It includes the level of invasive ventilatory support required to maintain oxygenation. The OI is the product of the mean airway pressure (Paw) in cm H2O, as measured by the ventilator, and the FiO2 as the percentage divided by the PaO2. The OI is commonly used to guide management, such as initiating inhaled nitric oxide, administering surfactant, and defining the potential need for extracorporeal membrane oxygenation.

The presence of a normal PaO2 value does not rule out respiratory failure, particularly in the presence of supplemental oxygen. The PaCO2 reflects pulmonary ventilation and cellular CO2 production. It is a more sensitive marker of ventilatory failure than PaO2, particularly in the presence of supplemental oxygen, as it has a close relationship with the depth and rate of breathing. Calculation of the pulmonary dead space is a good indicator of overall lung function. Pulmonary dead space is the difference between the PaCO2 and mixed expired PCO2 (physiological dead space) or the end-tidal PCO2 divided by the PaCO2. Pulmonary dead space increases when the pulmonary units’ ventilation increases relative to their perfusion and when shunting increases. Hence, pulmonary dead space is an excellent bedside indicator of lung function and one of the best prognostic factors in ARDS patients. The pulmonary dead space fraction may also help diagnose other conditions such as pulmonary embolism.

Acid-base balance can be affected by the aforementioned respiratory system abnormalities. For instance, acute respiratory acidosis and alkalemia result in acidemia and alkalemia, respectively. Additionally, hypoxemic hypoxia leads to anaerobic metabolism, which causes metabolic acidosis that results in academia. Metabolic system abnormalities also affect acid balance as acute metabolic acidosis and alkalosis result in acidemia and alkalemia, respectively. Metabolic acidosis is seen in patients with diabetic ketoacidosis, septic shock, renal failure, drug or toxin ingestion, and gastrointestinal or renal HCO3 loss. Metabolic alkalosis is caused by conditions such as kidney disease, electrolyte imbalances, prolonged vomiting, hypovolemia, diuretic use, and hypokalemia.

Quality control and Lab Safety

An arterial blood gas can be analyzed as a point-of-care test, along with electrolytes (often called a Shock panel). It is essential that these machines are calibrated/standardized appropriately to ensure accurate and precise readings for clinical decisions. Please refer to the appropriate user manuals to ensure the appropriate device calibration at all times in discussion with the clinical laboratory team.

Enhancing Healthcare Team Outcomes

ABG is recommended for evaluating a patient’s ventilatory, acid-base, and oxygenation status. [Level 1A] Blood gas analysis is also recommended to evaluate a patient’s response to therapeutic interventions. [Level 2B] and for monitoring the severity and progression of documented cardiopulmonary disease processes. [Level 1A] Despite its clinical value, erroneous or discrepant values represent a potential drawback of blood gas analysis, so eliminating potential sources of error is paramount. Therefore, attention to detail in the sampling technique and processing is essential.

Rigorous quality control of the automated blood gas analyzers is also necessary for accurate results. However, advances in machine performance and quality assurance have now made most errors, in point of care analysis, of ABG’s attributable to clinical providers. Several necessary pre-analytic steps must be followed to obtain a valid, interpretable ABG. In most hospital settings, ABG analysis is a process that involves multiple healthcare providers (e.g., physicians, respiratory therapists, and nurses). Hence, interprofessional coordination, cooperation, and communication are vitally important.

The American Association for Respiratory Care has published Clinical Care Guidelines for Blood Gas Analysis and Hemoximetry that provides current best practices for sampling, handling, and analyzing ABG’s. Notable sources of erroneous values at the time of blood draw include abnormal or misstated FiO2, barometric pressures, or temperatures. Temperature is a significant variable as it leads to PaO2 and O2 saturation discrepancies, as do acid-base disturbances. Several physiological and clinical conditions, such as hyperleukocytosis and dyshemoglobinemias, can also lead to PaO2 and O2 saturation discrepancies. Sample dilution can be an additional error source, with both liquid heparin and saline as potential culprits. The mode of sample transportation is also of significance as discrepant values can result from air contamination after pneumatic tube system transport, compared with manual transport of the specimen, especially in the presence of inadvertent air bubbles. Therefore, procuring samples using suitable syringes filled with adequate amounts of blood without air bubbles, maintaining them at correct temperatures, and transporting them appropriately and promptly for rapid analysis can minimize erroneous values.

References

 

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Respiratory Acidosis – Causes, Symptoms, Treatment

Respiratory acidosis typically occurs due to failure of ventilation and accumulation of carbon dioxide. The primary disturbance is an elevated arterial partial pressure of carbon dioxide (pCO2) and a decreased ratio of arterial bicarbonate to arterial pCO2, which results in a decrease in the pH of the blood. This activity reviews the presentation, evaluation, and management of respiratory acidosis and stresses the role of an interprofessional team approach in the care of affected patients.

Respiratory acidosis is a state in which there is usually a failure of ventilation and an accumulation of carbon dioxide. The primary disturbance of elevated arterial PCO2 is the decreased ratio of arterial bicarbonate to arterial PCO2, which leads to a lowering of the pH. In the presence of alveolar hypoventilation, 2 features commonly are seen are respiratory acidosis and hypercapnia. To compensate for the disturbance in the balance between carbon dioxide and bicarbonate (HCO3-), the kidneys begin to excrete more acid in the forms of hydrogen and ammonium and reabsorb more base in the form of bicarbonate. This compensation helps to normalize the pH.

Causes of

The respiratory centers in the pons and medulla control alveolar ventilation. Chemoreceptors for PCO2, PO2, and pH regulate ventilation. Central chemoreceptors in the medulla are sensitive to changes in the pH level. A decreased pH level influences the mechanics of ventilation and maintains proper levels of carbon dioxide and oxygen. When ventilation is disrupted, arterial PCO2 increases, and an acid-base disorder develop. Another pathophysiological mechanism may be due to ventilation/perfusion mismatch of dead space.

Respiratory acidosis can be subcategorized as acute, chronic, or acute and chronic. In acute respiratory acidosis, there is a sudden elevation of PCO2 because of failure of ventilation. This may be due to cerebrovascular accidents, use of central nervous systems (CNS) depressants such as opioids, or inability to use muscles of respiration because of disorders like myasthenia gravis, muscular dystrophy, or Guillain-Barre Syndrome. Because of its acute nature, there is a slight compensation occurring minutes after the incidence. On the contrary, chronic respiratory acidosis may be caused by COPD where there is a decreased responsiveness of the reflexes to states of hypoxia and hypercapnia. Other individuals who develop chronic respiratory acidosis may have the fatigue of the diaphragm resulting from a muscular disorder. Chronic respiratory acidosis can also be seen in obesity hypoventilation syndrome, also known as Pickwickian syndrome, amyotrophic lateral sclerosis, and in patients with severe thoracic skeletal defects. In patients with chronic compensated respiratory disease and acidosis, an acute insult such as pneumonia or disease exacerbation can lead to ventilation/perfusion mismatch.

Respiratory acidosis may cause slight elevations in ionized calcium and an extracellular shift of potassium. However, hyperkalemia is usually mild. In chronic respiratory acidosis, renal compensation occurs gradually over the course of days.

Carbon dioxide plays a remarkable role in the human body mainly through pH regulation of the blood. The pH is the primary stimulus to initiate ventilation. In its normal state, the body maintains CO2 in a well-controlled range from 38 to 42 mm Hg by balancing its production and elimination. In a state of hypoventilation, the body produces more CO2 than it can eliminate, causing a net retention of CO2. The increased CO2 is what leads to an increase in hydrogen ions and a slight increase in bicarbonate, as seen by a right shift in the following equilibrium reaction of carbon dioxide:

  • CO2 + H2O -> H2CO3- -> HCO3- + H+

The buffer system created by carbon dioxide consists of the following three molecules in equilibrium: CO2, H2CO3-, and HCO3-. When H+ is high, HCO3- buffers the low pH. When OH- is high, H2CO3 buffers the high pH. In respiratory acidosis, the slight increase in bicarbonate serves as a buffer for the increase in H+ ions, which helps minimize the drop in pH. The increase in hydrogen ions inevitably causes a decrease in pH, which is the mechanism behind respiratory acidosis.

Symptoms of Alkalosis

Alkalosis may cause

  • Irritability
  • Muscle twitching and cramps
  • Tingling in the fingers and toes and around the lips

 

Tingling (paresthesia) is a common complaint in hyperventilation due to anxiety. Sometimes alkalosis causes no symptoms at all. If the alkalosis is severe, painful muscle spasms (tetany) can develop.

Diagnosis of

The clinical presentation of respiratory acidosis is usually a manifestation of its underlying cause. Signs and symptoms vary based on the length, severity, and progression of the disorder. Patients can present with dyspnea, anxiety, wheezing, and sleep disturbances. In some cases, patients may present with cyanosis due to hypoxemia. If the respiratory acidosis is severe and accompanied by prolonged hypoventilation, the patient may have additional symptoms such as altered mental status, myoclonus, and possibly even seizures. Respiratory acidosis leads to hypercapnia, which induces cerebral vasodilation. If severe enough, increased intracranial pressure and papilledema may ensue, increasing the risk of herniation and possibly even death. Cases of chronic respiratory acidosis may cause memory loss, impaired coordination, polycythemia, pulmonary hypertension, and heart failure. The persistence of apnea during sleep can lead to daytime somnolence and headaches. In patients with an obvious source of respiratory acidosis, the offending agent needs to be removed or reversed.

Lab Test And Imaging

An arterial blood gas (ABG) and serum bicarbonate level are necessary to evaluate patients with suspected respiratory acidosis. Other tests can be conducted to evaluate the underlying causes. In respiratory acidosis, the ABG will show an elevated PCO2 (>45 mmHg), elevated HCO3- (>30 mmHg), and decreased pH (<7.35). The respiratory acidosis can be further classified as acute or chronic based on the relative increase in HCO3- with respect to PCO2. In cases of acute respiratory acidosis, HCO3- will have increased by one mEq/L for every ten mmHg increase in PCO2 over a few minutes. In cases of chronic respiratory acidosis, HCO3- will have increased by four mEq/L for every ten mmHg increase in PCO2 over a time course of days. If the compensation does not occur in this pattern, a mixed respiratory-metabolic disorder may be present. In a patient who presents with unexplained respiratory acidosis, a drug screen may also be warranted.

Treatment / Management

Once the diagnosis has been made, the underlying cause of respiratory acidosis has to be treated. The hypercapnia should be corrected gradually because rapid alkalization of the cerebrospinal fluid (CSF) may lead to seizures. Pharmacologic therapy can also be used to help improve ventilation. Bronchodilators like beta-agonists, anticholinergic drugs, and methylxanthines can be used in treating patients with obstructive airway diseases. Naloxone can be used in patients who overdose on opioid use.

References

 

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Electrolyte Balance – Anatomy, Mechanism, Functions

Electrolyte balance is one of the key issues in maintaining homeostasis in the body, and it also plays important roles in protecting cellular function, tissue perfusion, and acid-base balance. Fluid and electrolyte balance must also be maintained for the management of many clinical conditions. Electrolyte imbalances are common findings in many diseases.[,] Imbalances in every electrolyte must be considered in a combined and associated fashion, and examinations must aim to clarify the clinical scenario for an effective and successful treatment. Most of the important and prevailing electrolyte imbalances are hypo- and hyper-states of sodium, potassium, calcium, and magnesium.

Electrolytes are essential for basic life functioning, such as maintaining electrical neutrality in cells, generating and conducting action potentials in the nerves and muscles. Sodium, potassium, and chloride are significant electrolytes along with magnesium, calcium, phosphate, and bicarbonates. Electrolytes come from our food and fluids.

These electrolytes can have an imbalance, leading to either high or low levels. High or low levels of electrolytes disrupt normal bodily functions and can lead to even life-threatening complications. This article reviews the basic physiology of electrolytes and their abnormalities, and the consequences of electrolyte imbalance.

Electricity and your body

Electrolytes take on a positive or negative charge when they dissolve in your body fluid. This enables them to conduct electricity and move electrical charges or signals throughout your body. These charges are crucial to many functions that keep you alive, including the operation of your brain, nerves, and muscles, and the creation of new tissue.

Each electrolyte plays a specific role in your body. The following are some of the most important electrolytes and their primary functions:

Sodium

  • helps control fluids in the body, impacting blood pressure
  • necessary for muscle and nerve function

Chloride

  • helps balance electrolytes
  • helps balance electrolytes
  • balances acidity and alkalinity, which helps maintain a healthy pH
  • essential to digestion

Potassium

  • regulates your heart and blood pressure
  • helps balance electrolytes
  • aids in transmitting nerve impulses
  • contributes to bone health
  • necessary for muscle contraction

Magnesium

  • important to the production of DNA and RNA
  • contributes to nerve and muscle function
  • helps maintain heart rhythm
  • helps regulate blood glucose levels
  • enhances your immune system

Calcium

  • key component of bones and teeth
  • important to the movement of nerve impulses and muscle movement
  • contributes to blood clotting

Phosphate

  • strengthens bones and teeth
  • helps cells produce the energy needed for tissue growth and repair

Bicarbonate

  • helps your body maintain a healthy pH
  • regulates heart function

Sodium, Electrolytes, and Fluid Balance

Electrolytes play a vital role in maintaining homeostasis within the body.

Key Points

Electrolytes help to regulate myocardial and neurological functions, fluid balance, oxygen delivery, acid-base balance, and much more.

The most serious electrolyte disturbances involve abnormalities in the levels of sodium, potassium, and/or calcium.

Kidneys work to keep the electrolyte concentrations in the blood constant despite changes in the body.

Key Terms

  • homeostasis: The ability of a system or living organism to adjust its internal environment to maintain a stable equilibrium; such as the ability of warm-blooded animals to maintain a constant temperature.
  • electrolyte: Any of the various ions (such as sodium or chloride) that regulate the electric charge on cells and the flow of water across their membranes.
  • sodium: A chemical element with the symbol Na (from Latin: natrium) and atomic number 11. It is a soft, silvery-white, highly reactive metal and is a member of the alkali metals.

Importance of Electrolyte Balance

Electrolytes play a vital role in maintaining homeostasis within the body. They help regulate myocardial and neurological function, fluid balance, oxygen delivery, acid-base balance, and other biological processes.

Electrolytes are important because they are what cells (especially those of the nerve, heart, and muscle ) use to maintain voltages across their cell membranes and to carry electrical impulses (nerve impulses, muscle contractions) across themselves and to other cells.

Electrolyte imbalances can develop from excessive or diminished ingestion and from the excessive or diminished elimination of an electrolyte. The most common cause of electrolyte disturbances is renal failure. The most serious electrolyte disturbances involve abnormalities in the levels of sodium, potassium, and/or calcium.

Other electrolyte imbalances are less common and often occur in conjunction with major electrolyte changes. Chronic laxative abuse or severe diarrhea or vomiting (gastroenteritis) can lead to electrolyte disturbances combined with dehydration. People suffering from bulimia or anorexia nervosa are especially at high risk for an electrolyte imbalance.

Kidneys work to keep the electrolyte concentrations in blood constant despite changes in your body. For example, during heavy exercise electrolytes are lost through sweating, particularly sodium and potassium, and sweating can increase the need for electrolyte (salt) replacement. It is necessary to replace these electrolytes to keep their concentrations in the body fluids constant.

Dehydration

There are three types of dehydration:

  • Hypotonic or hyponatremic (primarily a loss of electrolytes, sodium in particular).
  • Hypertonic or hypernatremic (primarily a loss of water).
  • Isotonic or hyponatremic (an equal loss of water and electrolytes).

In humans, the most common type of dehydration by far is isotonic (isonatraemic) dehydration; which effectively equates with hypovolemia; but the distinction of isotonic from hypotonic or hypertonic dehydration may be important when treating people with dehydration.

Physiologically, and despite the name, dehydration does not simply mean loss of water, as both water and solutes (main sodium) are usually lost in roughly equal quantities as to how they exist in blood plasma. In hypotonic dehydration, intravascular water shifts to the extravascular space and exaggerates the intravascular volume depletion for a given amount of total body water loss.

Neurological complications can occur in hypotonic and hypertonic states. The former can lead to seizures, while the latter can lead to osmotic cerebral edema upon rapid rehydration.

In more severe cases, the correction of a dehydrated state is accomplished by the replenishment of necessary water and electrolytes (through oral rehydration therapy or fluid replacement by intravenous therapy). As oral rehydration is less painful, less invasive, less expensive, and easier to provide, it is the treatment of choice for mild dehydration. Solutions used for intravenous rehydration must be isotonic or hypotonic.

This diagram illustrates the mechanism for the transportation of water and electrolytes across the epithelial cells of the secretory glands.

Cell electrolytes: This diagram illustrates the mechanism for the transportation of water and electrolytes across the epithelial cells in the secretory glands.

Sodium Balance Regulation

Sodium is an important cation that is distributed primarily outside the cell.

Key Points

The body has a potent sodium-retaining mechanism: the renin-angiotensin system.

In states of sodium depletion, aldosterone levels increase; in states of sodium excess, aldosterone levels decrease.

The major physiological controller of aldosterone secretion is the plasma angiotensin II level that increases aldosterone secretion.

Key Terms

  • sodium: A chemical element with the symbol Na (from Latin: natrium) and atomic number 11. It is a soft, silvery-white, highly reactive metal and is a member of the alkali metals.
  • aldosterone: A mineralocorticoid hormone that is secreted by the adrenal cortex and regulates the balance of sodium and potassium in the body.
  • angiotensin: Any of several polypeptides that narrow the blood vessels and regulate arterial pressure.

Sodium Regulation

Sodium is an important cation that is distributed primarily outside the cell. The cell sodium concentration is about 15 mmol/l, but it varies in different organs; it has an intracellular volume of 30 liters and about 400 mmol are inside the cell.

The plasma and interstitial sodium is about 140 mmol/l with an extracellular volume of about 13 liters, 1,800 mmol are in the extracellular space. The total body sodium, however, is about 3,700 mmol as there is about 1,500 mmol stored in bones.

The body has potent sodium-retaining mechanisms and even if a person is on five mmol Na+/day they can maintain sodium balance. Extra sodium is lost from the body by reducing the activity of the renin –angiotensin system that leads to increased sodium loss from the body. Sodium is lost through the kidneys, sweat, and feces.

In states of sodium depletion, the aldosterone levels increase. In states of sodium excess, aldosterone levels decrease. The major physiological controller of aldosterone secretion is the plasma angiotensin II level that increases aldosterone secretion.

A high plasma potassium level also increases aldosterone secretion because, besides retaining Na+, high plasma aldosterone causes K+ loss by the kidney. Plasma Na+ levels have little effect on aldosterone secretion.

This is a diagram of the regulation of sodium via the hormones renin, angiotensin, and aldosterone. In states of sodium depletion, the aldosterone levels increase, and in states of sodium excess, the aldosterone levels decrease.

Renin-angiotensin system: The regulation of sodium via the hormones renin, angiotensin, and aldosterone. In states of sodium depletion, the aldosterone levels increase, and in states of sodium excess, the aldosterone levels decrease.

A low renal perfusion pressure stimulates the release of renin, which forms angiotensin I that is converted to angiotensin II. Angiotensin II will correct the low perfusion pressure by causing the blood vessels to constrict, and increase sodium retention by its direct effect on the proximal renal tubule and by an effect operated through aldosterone. The perfusion pressure to the adrenal gland has a little direct effect on aldosterone secretion and the low blood pressure operates to control aldosterone via the renin-angiotensin system.

Aldosterone also acts on the sweat ducts and colonic epithelium to conserve sodium. When aldosterone is activated to retain sodium the plasma sodium tends to rise. This immediately causes the release of ADH, which causes water to be retained, thus balancing Na+ and H2O in the right proportion to restore plasma volume.

In addition to aldosterone and angiotensin II, other factors influence sodium excretion.

  • Atrial peptide causes the loss of sodium by the kidneys: it is secreted from the heart in high sodium states due to excess intake or cardiac disease.
  • Elevated blood pressure will also cause Na+ loss, and low blood pressure usually leads to sodium retention.

Potassium Balance Regulation

Potassium is mainly an intracellular ion.

Key Points

Most of the total body potassium is inside the cells and the next largest proportion is in the bones.

In an unprocessed diet, potassium is much more plentiful than sodium and it is present as an organic salt, while sodium is added as NaCl.

High potassium intake can potentially increase the extracellular K+ level two times before the kidney can excrete the extra potassium.

High plasma potassium increases aldosterone secretion and this increases the potassium loss from the body to restore balance.

Key Terms

  • alkalotic: A condition that reduces the hydrogen ion concentration of arterial blood plasma (alkalemia). Generally, alkalosis is said to occur when the blood pH exceeds 7.45.
  • Potassium: A chemical element with the symbol K and the atomic number 19. Elemental potassium is a soft, silvery-white, alkali metal that oxidizes rapidly in the air and is very reactive with water—it can generate sufficient heat to ignite the hydrogen emitted in the reaction.
  • acidosis: An increase in acidity of the blood and other body tissue (i.e., an increased hydrogen ion concentration). If not further qualified, it usually refers to the acidity of the blood plasma.

Potassium Balance

Potassium is predominantly an intracellular ion. Most of the total body potassium of about 4,000 mmol is inside the cells, and the next largest proportion (300–500 mmol) is in the bones. Cell K+ concentration is about 150 mmol/l but varies in different organs. Extracellular potassium is about 4.0 mmol/l, with an extracellular value of about 13 liters, 52 mmol (i.e., less than 1.5%) is present here and only 12 mmol is in the plasma.

In an unprocessed diet, potassium is much more plentiful than sodium. It is present as an organic salt, while sodium is added as NaCl. In a hunter-gatherer, K+ intake may be as much as 400 mmol/d while in the Western diet it is 70 mmol/d or less if a person has a minimal amount of fresh fruit and vegetables.

The processing of foods replaces K+ with NaCl. While the body can excrete a large K+ load, it is unable to conserve K+. On a zero K+ intake, or in a person with K+ depletion, there will still be a loss of K+ of 30–50 mmol/d in the urine and feces.

Acid-Base Status Control

If there is a high potassium intake, for example, 100 mmol, this would potentially increase the extracellular K+ level two times before the kidney could excrete the extra potassium. The body buffers the extra potassium by equilibrating it within the cells.

The acid-base status controls the distribution between plasma and cells. A high pH (i.e., alkalosis >7.4) favors the movement of K+ into the cells, and a low pH (i.e., acidosis ) causes movement out of the cell. A high plasma potassium level increases aldosterone secretion and this increases the potassium loss from the body to restore balance.

This change of distribution with the acid-base status means that the plasma K+ may not reflect the total body content. Therefore, a person with acidosis (pH 7.1) and a plasma K+ of 6.5 mmol/l could be depleted of total body potassium. This occurs in diabetic acidosis. Conversely, a person who is alkalotic with a plasma K+ of 3.4 mmol/l may have a normal level of total body potassium.

Calcium and Phosphate Balance Regulation

Calcium is a key electrolyte: 99% is deposited in the bones and the remainder is associated with hormone release and cell signaling.

Key Points

Calcium absorption is controlled by vitamin D, and calcium excretion is controlled by the parathyroid hormones.

There is a constant loss of calcium by the kidney even if there is none in the diet.

Calcium in plasma exists in three forms: ionized, nonionized and protein-bound.

Key Terms

  • calcium: A chemical element, atomic number 20, that is an alkaline earth metal and occurs naturally as carbonate in limestone and as silicate in many rocks.
  • parathyroid hormone: A polypeptide hormone that is released by the chief cells of the parathyroid glands and is involved in raising the levels of calcium ions in the blood.
  • vitamin D: A fat-soluble vitamin that is required for normal bone development and that prevents rickets; it can be manufactured in the skin on exposure to sunlight.

Calcium is a very important electrolyte. Ninety-nine percent or more is deposited in the bones and the remainder plays a vital role in nerve conduction, muscle contraction, hormone release, and cell signaling.

The plasma concentration of Ca++ is 2.2 mmol/l, and phosphate is 1.0 mmol/l. The solubility product of Ca and P is close to saturation in plasma. The concentration of Ca++ in the cytoplasm is < 10–6 mmol/l but the concentration of Ca++ in the cell is much higher as calcium is taken up (and is able to be released from) cell organelles.

In the typical Australian diet, there is about 1200 mg/d of calcium. Even if it was all soluble it is not all absorbed as it combines with phosphates in the intestinal secretions. In addition, absorption is regulated by the active vitamin D; increased amounts of vitamin D increase Ca++ absorption.

Absorption is controlled by vitamin D while excretion is controlled by parathyroid hormones. However, the distribution from bone to plasma is controlled by both the parathyroid hormones and vitamin D.

There is also a constant loss of calcium via the kidneys even if there is none in the diet. This excretion of calcium by the kidneys and its distribution between bone and the rest of the body is primarily controlled by the parathyroid hormone.

The calcium in plasma exists in three forms:

  1. Ionized.
  2. Nonionized.
  3. Protein-bound.

It is the ionized calcium concentration that is monitored by the parathyroid gland —if it is low, parathyroid hormone secretion is increased. This increases the ionized calcium levels by increasing bone re-absorption, decreasing renal excretion, and acting on the kidney to increase the rate of formation of active vitamin D, thereby increasing the gut’s absorption of calcium.

The usual amount of phosphate in the diet is about 1 g/d but not all of it is absorbed. Any excess is excreted by the kidney and this excretion is increased by the parathyroid hormone.

This hormone also causes phosphate to leach out of the bones. Plasma phosphate has no direct effect on parathyroid hormone secretion; however, if it is elevated it combines with Ca++ to decrease ionized Ca++ in plasma, and thereby increase parathyroid hormone secretion.

This is an illustration of how parathyroid hormone regulates the levels of calcium in the blood. The parathyroid glands release parathyroid hormone that causes calcium reabsorption and vitamin D hydroxylation in the kidneys, calcium absorption from the intestines, calcium reabsorption from the bones, and an increase of calcium in the blood.

Calcium regulation: This is an illustration of how the parathyroid hormone regulates the levels of calcium in the blood.

Anion Regulation

The anions chloride, bicarbonate, and phosphate have important roles in maintaining the balance and neutrality of vital body mechanisms.

Key Points

Chloride is needed to maintain proper hydration, as well as to balance cations, and maintain the electrical neutrality of the extracellular fluid.

Bicarbonate‘s main role is to maintain the body’s acid-base balance through a buffer system.

Phosphate is a major constituent of the intracellular fluid, and it is important in the regulation of metabolic processes and as a buffering agent in animal cells.

The kidneys regulate the salt balance in the blood by controlling the excretion and the reabsorption of various ions.

Key Terms

  • anion: An negatively charged ion.
  • hyperphosphatemia: An elevated amount of phosphate in the blood.
  • hypochloremia: An electrolyte disturbance caused by an abnormally depleted level of chloride ions in the blood.
  • hypophosphatemia: An electrolyte disturbance caused by an abnormally low level of phosphate in the blood.

Anion Regulation

The excretion of ions occurs mainly through the kidneys, with lesser amounts of ions being lost in sweat and in feces. In addition, excessive sweating may cause a significant loss, especially of the anion chloride. Severe vomiting or diarrhea will also cause a loss of chloride and bicarbonate ions.

Adjustments in the respiratory and renal functions allow the body to regulate the levels of these ions in the extracellular fluid (ECF).

Chloride

Chloride is the predominant extracellular anion and it is a major contributor to the osmotic pressure gradient between the intracellular fluid (ICF) and extracellular fluid (ECF). Chloride maintains proper hydration and functions to balance the cations in the ECF to keep the electrical neutrality of this fluid. The paths of secretion and reabsorption of chloride ions in the renal system follow the paths of sodium ions.

Hypochloremia, or lower-than-normal blood chloride levels, can occur because of defective renal tubular absorption. Vomiting, diarrhea, and metabolic acidosis can also lead to hypochloremia.

In contrast, hyperchloremia, or higher-than-normal blood chloride levels, can occur due to dehydration, excessive intake of dietary salt (NaCl) or the swallowing of sea water, aspirin intoxication, congestive heart failure, and the hereditary, chronic lung disease cystic fibrosis. In people who have cystic fibrosis, the chloride levels in their sweat are two to five times those of normal levels; therefore, analysis of their sweat is often used to diagnose the disease.

Bicarbonate

Bicarbonate is the second-most abundant anion in the blood. Its principal function is to maintain your body’s acid–base balance by being part of buffer systems.

Bicarbonate ions result from a chemical reaction that starts with the carbon dioxide (CO2) and water (H2O) molecules that are produced at the end of aerobic metabolism. Only a small amount of CO2 can be dissolved in body fluids; thus, over 90 percent of the CO2 is converted into bicarbonate ions, HCO3-, through the following reactions:

CO2 + H2O ↔ H2CO↔ H2CO3– + H+

The bidirectional arrows indicate that the reactions can go in either direction depending on the concentrations of the reactants and products. Carbon dioxide is produced in large amounts in tissues that have a high metabolic rate, and is converted into bicarbonate in the cytoplasm of the red blood cells through the action of an enzyme called carbonic anhydrase.

Bicarbonate is transported in the blood and once in the lungs, the reactions reverse direction, and CO2 is regenerated from the bicarbonate to be exhaled as metabolic waste.

This diagram shows how carbonate acts as a buffering system. In the lungs, CO2 is produced from bicarbonate and removed as metabolic waste through the reverse reaction of the bicarbonate bidirectional equation.

Bicarbonate as a buffering system: In the lungs, CO2 is produced from bicarbonate and removed as metabolic waste through the reverse reaction of the bicarbonate bidirectional equation.

Phosphate

Phosphate is present in the body in three ionic forms:

  1. H2PO4
  2. HPO42−
  3. PO43−

The addition and removal of phosphate from the proteins in all cells is a pivotal strategy in the regulation of metabolic processes. Phosphate is useful in animal cells as a buffering agent, and the most common form is HPO2−4. Bone and teeth bind up 85 percent of the body’s phosphate as part of calcium phosphate salts. In addition, phosphate is found in phospholipids, such as those that make up the cell membrane, and in ATP, nucleotides, and buffers.

Hypophosphatemia, or abnormally low phosphate blood levels, occurs with the heavy use of antacids, during alcohol withdrawal, and during malnourishment. In the face of phosphate depletion, the kidneys usually conserve phosphate, but during starvation, this conservation is impaired greatly.

Hyperphosphatemia, or abnormally increased levels of phosphates in the blood, occurs if there is decreased renal function or in cases of acute lymphocytic leukemia. Additionally, because phosphate is a major constituent of the ICF, any significant destruction of cells can result in the dumping of phosphate into the ECF.

Normal and Critical Findings

Laboratory Values: 

Serum Sodium: 

  • Normal Range: 135 to 145 mmol/L
  • Mild-moderate Hyponatremia: 125 to 135 mmol/L, Severe: less than 125 mmol/L
  • Hypernatremia: Mild-moderate: 145 to 160 mmol/L, Severe: over 160 mmol/L

Serum Potassium:

  • Normal Range: 3.6 to 5.5 mmol/L
  • Hypokalemia: Mild Hypokalemia under 3.6 mmol/L, Moderate: 2.5 mmol/L, Severe : greater than 2.5 mmol/L
  • Hyperkalemia: Mild hyperkalemia: 5 to 5.5 mmol/L, Moderate- 5.5 to 6.5, Severe: 6.5 to 7 mmol/L

Serum Calcium: 

  • Normal Range: 8.8 to 10.7 mg/dl
  • Hypercalcemia: greater than 10.7 mg/dl , Severe: over 11.5 mg/dl
  • Hypocalcemia: less than 8.8 mg/dl

Serum Magnesium: 

  • Normal Range: 1.46 to 2.68 mg/dl
  • Hypomagnesemia: under 1.46 mg/dl
  • Hypermagenesemia: over 2.68

Bicarbonate:

  • Normal Range: 23 to 30 mmol/L\
  • It increases or decreases depending on the acid-base status.

Phosphorus:

  • Normal Range: 3.4 to 4.5 mg/dl
  • Hypophosphatemia: less than 2.5 mg/dl
  • Hyperphosphatemia: greater than 4.5 mg/dl

Complications

Both hyponatremia and hypernatremia, as well as hypomagnesemia, can lead to neurological consequences such as seizure disorders.

Hypokalemia and hyperkalemia, as well as hypocalcemia, are more responsible for arrhythmias.

Bicarbonate imbalance can lead to metabolic acidosis or alkalosis.

Patient Safety and Education

A piece of valuable advice to the patients would be to take the medications exactly as prescribed by the clinicians to avoid electrolyte imbalance as a consequence of not taking the prescribed dose.

One should call for immediate medical help when the patient feels weak, has muscle ache, or has altered consciousness.

Clinical Significance

Some of the common causes of electrolyte disorders seen in clinical practices are:

  • Hyponatremia: low dietary sodium intake, primary polydipsia, SIADH, congestive heart failure, hepatic cirrhosis, failure of adrenal glands, hyperglycemia, dyslipidemia
  • Hypernatremia: unreplaced fluid loss through the skin and gastrointestinal tract, osmotic diuresis, hypertonic saline administration
  • Hypokalemia: hyperaldosteronism, loop diuretics
  • Hyperkalemia: increase release from cells as in metabolic acidosis, insulin deficiency, beta-blocker or decreased potassium excretion as in acute or chronic kidney disease, aldosterone deficiency or resistance
  • Hypercalcemia: malignancy, hyperparathyroidism, chronic granulomatous disease
  • Hypocalcemia: acute pancreatitis, parathyroid hormone deficiency after thyroidectomy, neck dissection, resistance to parathormone, hypomagnesemia, sepsis
  • Hypermagnesemia: increase oral magnesium intake
  • Hypomagnesemia: renal losses as in diuretics, alcohol use disorder or GI losses as in diarrhea
  • Bicarbonate level: increases in primary metabolic alkalosis or compensation to primary respiratory acidosis – decreases in primary metabolic acidosis or compensation to primary respiratory alkalosis.
  • Hyperchloremia: normal saline infusion
  • Hypochloremia: GI loss as in diarrhea, renal losses with diuretics
  • Hypophosphatemia: refeeding syndrome, vitamin D deficiency, hyperparathyroidism
  • Hyperphosphatemia: hypoparathyroidism, chronic kidney disease

References

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Electrolyte Balance – Pathophysiology, Mechanism, Importance

Electrolyte Balance/Fluid and electrolyte balance is one of the key issues in maintaining homeostasis in the body, and it also plays important roles in protecting cellular function, tissue perfusion, and acid-base balance. Fluid and electrolyte balance must also be maintained for the management of many clinical conditions. Electrolyte imbalances are common findings in many diseases.[,] Imbalances in every electrolyte must be considered in a combined and associated fashion, and examinations must aim to clarify the clinical scenario for an effective and successful treatment. Most of the important and prevailing electrolyte imbalances are hypo- and hyper-states of sodium, potassium, calcium, and magnesium.

Electrolytes are essential for basic life functioning, such as maintaining electrical neutrality in cells, generating and conducting action potentials in the nerves and muscles. Sodium, potassium, and chloride are significant electrolytes along with magnesium, calcium, phosphate, and bicarbonates. Electrolytes come from our food and fluids.

These electrolytes can have an imbalance, leading to either high or low levels. High or low levels of electrolytes disrupt normal bodily functions and can lead to even life-threatening complications. This article reviews the basic physiology of electrolytes and their abnormalities, and the consequences of electrolyte imbalance.

Electricity and your body

Electrolytes take on a positive or negative charge when they dissolve in your body fluid. This enables them to conduct electricity and move electrical charges or signals throughout your body. These charges are crucial to many functions that keep you alive, including the operation of your brain, nerves, and muscles, and the creation of new tissue.

Each electrolyte plays a specific role in your body. The following are some of the most important electrolytes and their primary functions:

Sodium

  • helps control fluids in the body, impacting blood pressure
  • necessary for muscle and nerve function

Chloride

  • helps balance electrolytes
  • helps balance electrolytes
  • balances acidity and alkalinity, which helps maintain a healthy pH
  • essential to digestion

Potassium

  • regulates your heart and blood pressure
  • helps balance electrolytes
  • aids in transmitting nerve impulses
  • contributes to bone health
  • necessary for muscle contraction

Magnesium

  • important to the production of DNA and RNA
  • contributes to nerve and muscle function
  • helps maintain heart rhythm
  • helps regulate blood glucose levels
  • enhances your immune system

Calcium

  • key component of bones and teeth
  • important to the movement of nerve impulses and muscle movement
  • contributes to blood clotting

Phosphate

  • strengthens bones and teeth
  • helps cells produce the energy needed for tissue growth and repair

Bicarbonate

  • helps your body maintain a healthy pH
  • regulates heart function

Sodium, Electrolytes, and Fluid Balance

Electrolytes play a vital role in maintaining homeostasis within the body.

Key Points

Electrolytes help to regulate myocardial and neurological functions, fluid balance, oxygen delivery, acid-base balance, and much more.

The most serious electrolyte disturbances involve abnormalities in the levels of sodium, potassium, and/or calcium.

Kidneys work to keep the electrolyte concentrations in the blood constant despite changes in the body.

Key Terms

  • homeostasis: The ability of a system or living organism to adjust its internal environment to maintain a stable equilibrium; such as the ability of warm-blooded animals to maintain a constant temperature.
  • electrolyte: Any of the various ions (such as sodium or chloride) that regulate the electric charge on cells and the flow of water across their membranes.
  • sodium: A chemical element with the symbol Na (from Latin: natrium) and atomic number 11. It is a soft, silvery-white, highly reactive metal and is a member of the alkali metals.

Importance of Electrolyte Balance

Electrolytes play a vital role in maintaining homeostasis within the body. They help regulate myocardial and neurological function, fluid balance, oxygen delivery, acid-base balance, and other biological processes.

Electrolytes are important because they are what cells (especially those of the nerve, heart, and muscle ) use to maintain voltages across their cell membranes and to carry electrical impulses (nerve impulses, muscle contractions) across themselves and to other cells.

Electrolyte imbalances can develop from excessive or diminished ingestion and from the excessive or diminished elimination of an electrolyte. The most common cause of electrolyte disturbances is renal failure. The most serious electrolyte disturbances involve abnormalities in the levels of sodium, potassium, and/or calcium.

Other electrolyte imbalances are less common and often occur in conjunction with major electrolyte changes. Chronic laxative abuse or severe diarrhea or vomiting (gastroenteritis) can lead to electrolyte disturbances combined with dehydration. People suffering from bulimia or anorexia nervosa are especially at high risk for an electrolyte imbalance.

Kidneys work to keep the electrolyte concentrations in blood constant despite changes in your body. For example, during heavy exercise electrolytes are lost through sweating, particularly sodium and potassium, and sweating can increase the need for electrolyte (salt) replacement. It is necessary to replace these electrolytes to keep their concentrations in the body fluids constant.

Dehydration

There are three types of dehydration:

  • Hypotonic or hyponatremic (primarily a loss of electrolytes, sodium in particular).
  • Hypertonic or hypernatremic (primarily a loss of water).
  • Isotonic or hyponatremic (an equal loss of water and electrolytes).

In humans, the most common type of dehydration by far is isotonic (isonatraemic) dehydration; which effectively equates with hypovolemia; but the distinction of isotonic from hypotonic or hypertonic dehydration may be important when treating people with dehydration.

Physiologically, and despite the name, dehydration does not simply mean loss of water, as both water and solutes (main sodium) are usually lost in roughly equal quantities as to how they exist in blood plasma. In hypotonic dehydration, intravascular water shifts to the extravascular space and exaggerates the intravascular volume depletion for a given amount of total body water loss.

Neurological complications can occur in hypotonic and hypertonic states. The former can lead to seizures, while the latter can lead to osmotic cerebral edema upon rapid rehydration.

In more severe cases, the correction of a dehydrated state is accomplished by the replenishment of necessary water and electrolytes (through oral rehydration therapy or fluid replacement by intravenous therapy). As oral rehydration is less painful, less invasive, less expensive, and easier to provide, it is the treatment of choice for mild dehydration. Solutions used for intravenous rehydration must be isotonic or hypotonic.

This diagram illustrates the mechanism for the transportation of water and electrolytes across the epithelial cells of the secretory glands.

Cell electrolytes: This diagram illustrates the mechanism for the transportation of water and electrolytes across the epithelial cells in the secretory glands.

Sodium Balance Regulation

Sodium is an important cation that is distributed primarily outside the cell.

Key Points

The body has a potent sodium-retaining mechanism: the renin-angiotensin system.

In states of sodium depletion, aldosterone levels increase; in states of sodium excess, aldosterone levels decrease.

The major physiological controller of aldosterone secretion is the plasma angiotensin II level that increases aldosterone secretion.

Key Terms

  • sodium: A chemical element with the symbol Na (from Latin: natrium) and atomic number 11. It is a soft, silvery-white, highly reactive metal and is a member of the alkali metals.
  • aldosterone: A mineralocorticoid hormone that is secreted by the adrenal cortex and regulates the balance of sodium and potassium in the body.
  • angiotensin: Any of several polypeptides that narrow the blood vessels and regulate arterial pressure.

Sodium Regulation

Sodium is an important cation that is distributed primarily outside the cell. The cell sodium concentration is about 15 mmol/l, but it varies in different organs; it has an intracellular volume of 30 liters and about 400 mmol are inside the cell.

The plasma and interstitial sodium is about 140 mmol/l with an extracellular volume of about 13 liters, 1,800 mmol are in the extracellular space. The total body sodium, however, is about 3,700 mmol as there is about 1,500 mmol stored in bones.

The body has potent sodium-retaining mechanisms and even if a person is on five mmol Na+/day they can maintain sodium balance. Extra sodium is lost from the body by reducing the activity of the renin –angiotensin system that leads to increased sodium loss from the body. Sodium is lost through the kidneys, sweat, and feces.

In states of sodium depletion, the aldosterone levels increase. In states of sodium excess, aldosterone levels decrease. The major physiological controller of aldosterone secretion is the plasma angiotensin II level that increases aldosterone secretion.

A high plasma potassium level also increases aldosterone secretion because, besides retaining Na+, high plasma aldosterone causes K+ loss by the kidney. Plasma Na+ levels have little effect on aldosterone secretion.

This is a diagram of the regulation of sodium via the hormones renin, angiotensin, and aldosterone. In states of sodium depletion, the aldosterone levels increase, and in states of sodium excess, the aldosterone levels decrease.

Renin-angiotensin system: The regulation of sodium via the hormones renin, angiotensin, and aldosterone. In states of sodium depletion, the aldosterone levels increase, and in states of sodium excess, the aldosterone levels decrease.

A low renal perfusion pressure stimulates the release of renin, which forms angiotensin I that is converted to angiotensin II. Angiotensin II will correct the low perfusion pressure by causing the blood vessels to constrict, and increase sodium retention by its direct effect on the proximal renal tubule and by an effect operated through aldosterone. The perfusion pressure to the adrenal gland has a little direct effect on aldosterone secretion and the low blood pressure operates to control aldosterone via the renin-angiotensin system.

Aldosterone also acts on the sweat ducts and colonic epithelium to conserve sodium. When aldosterone is activated to retain sodium the plasma sodium tends to rise. This immediately causes the release of ADH, which causes water to be retained, thus balancing Na+ and H2O in the right proportion to restore plasma volume.

In addition to aldosterone and angiotensin II, other factors influence sodium excretion.

  • Atrial peptide causes the loss of sodium by the kidneys: it is secreted from the heart in high sodium states due to excess intake or cardiac disease.
  • Elevated blood pressure will also cause Na+ loss, and low blood pressure usually leads to sodium retention.

Potassium Balance Regulation

Potassium is mainly an intracellular ion.

Key Points

Most of the total body potassium is inside the cells and the next largest proportion is in the bones.

In an unprocessed diet, potassium is much more plentiful than sodium and it is present as an organic salt, while sodium is added as NaCl.

High potassium intake can potentially increase the extracellular K+ level two times before the kidney can excrete the extra potassium.

High plasma potassium increases aldosterone secretion and this increases the potassium loss from the body to restore balance.

Key Terms

  • alkalotic: A condition that reduces the hydrogen ion concentration of arterial blood plasma (alkalemia). Generally, alkalosis is said to occur when the blood pH exceeds 7.45.
  • Potassium: A chemical element with the symbol K and the atomic number 19. Elemental potassium is a soft, silvery-white, alkali metal that oxidizes rapidly in the air and is very reactive with water—it can generate sufficient heat to ignite the hydrogen emitted in the reaction.
  • acidosis: An increase in acidity of the blood and other body tissue (i.e., an increased hydrogen ion concentration). If not further qualified, it usually refers to the acidity of the blood plasma.

Potassium Balance

Potassium is predominantly an intracellular ion. Most of the total body potassium of about 4,000 mmol is inside the cells, and the next largest proportion (300–500 mmol) is in the bones. Cell K+ concentration is about 150 mmol/l but varies in different organs. Extracellular potassium is about 4.0 mmol/l, with an extracellular value of about 13 liters, 52 mmol (i.e., less than 1.5%) is present here and only 12 mmol is in the plasma.

In an unprocessed diet, potassium is much more plentiful than sodium. It is present as an organic salt, while sodium is added as NaCl. In a hunter-gatherer, K+ intake may be as much as 400 mmol/d while in the Western diet it is 70 mmol/d or less if a person has a minimal amount of fresh fruit and vegetables.

The processing of foods replaces K+ with NaCl. While the body can excrete a large K+ load, it is unable to conserve K+. On a zero K+ intake, or in a person with K+ depletion, there will still be a loss of K+ of 30–50 mmol/d in the urine and feces.

Acid-Base Status Control

If there is a high potassium intake, for example, 100 mmol, this would potentially increase the extracellular K+ level two times before the kidney could excrete the extra potassium. The body buffers the extra potassium by equilibrating it within the cells.

The acid-base status controls the distribution between plasma and cells. A high pH (i.e., alkalosis >7.4) favors the movement of K+ into the cells, and a low pH (i.e., acidosis ) causes movement out of the cell. A high plasma potassium level increases aldosterone secretion and this increases the potassium loss from the body to restore balance.

This change of distribution with the acid-base status means that the plasma K+ may not reflect the total body content. Therefore, a person with acidosis (pH 7.1) and a plasma K+ of 6.5 mmol/l could be depleted of total body potassium. This occurs in diabetic acidosis. Conversely, a person who is alkalotic with a plasma K+ of 3.4 mmol/l may have a normal level of total body potassium.

Calcium and Phosphate Balance Regulation

Calcium is a key electrolyte: 99% is deposited in the bones and the remainder is associated with hormone release and cell signaling.

Key Points

Calcium absorption is controlled by vitamin D, and calcium excretion is controlled by the parathyroid hormones.

There is a constant loss of calcium by the kidney even if there is none in the diet.

Calcium in plasma exists in three forms: ionized, nonionized and protein-bound.

Key Terms

  • calcium: A chemical element, atomic number 20, that is an alkaline earth metal and occurs naturally as carbonate in limestone and as silicate in many rocks.
  • parathyroid hormone: A polypeptide hormone that is released by the chief cells of the parathyroid glands and is involved in raising the levels of calcium ions in the blood.
  • vitamin D: A fat-soluble vitamin that is required for normal bone development and that prevents rickets; it can be manufactured in the skin on exposure to sunlight.

Calcium is a very important electrolyte. Ninety-nine percent or more is deposited in the bones and the remainder plays a vital role in nerve conduction, muscle contraction, hormone release, and cell signaling.

The plasma concentration of Ca++ is 2.2 mmol/l, and phosphate is 1.0 mmol/l. The solubility product of Ca and P is close to saturation in plasma. The concentration of Ca++ in the cytoplasm is < 10–6 mmol/l but the concentration of Ca++ in the cell is much higher as calcium is taken up (and is able to be released from) cell organelles.

In the typical Australian diet, there is about 1200 mg/d of calcium. Even if it was all soluble it is not all absorbed as it combines with phosphates in the intestinal secretions. In addition, absorption is regulated by the active vitamin D; increased amounts of vitamin D increase Ca++ absorption.

Absorption is controlled by vitamin D while excretion is controlled by parathyroid hormones. However, the distribution from bone to plasma is controlled by both the parathyroid hormones and vitamin D.

There is also a constant loss of calcium via the kidneys even if there is none in the diet. This excretion of calcium by the kidneys and its distribution between bone and the rest of the body is primarily controlled by the parathyroid hormone.

The calcium in plasma exists in three forms:

  1. Ionized.
  2. Nonionized.
  3. Protein-bound.

It is the ionized calcium concentration that is monitored by the parathyroid gland —if it is low, parathyroid hormone secretion is increased. This increases the ionized calcium levels by increasing bone re-absorption, decreasing renal excretion, and acting on the kidney to increase the rate of formation of active vitamin D, thereby increasing the gut’s absorption of calcium.

The usual amount of phosphate in the diet is about 1 g/d but not all of it is absorbed. Any excess is excreted by the kidney and this excretion is increased by the parathyroid hormone.

This hormone also causes phosphate to leach out of the bones. Plasma phosphate has no direct effect on parathyroid hormone secretion; however, if it is elevated it combines with Ca++ to decrease ionized Ca++ in plasma, and thereby increase parathyroid hormone secretion.

This is an illustration of how parathyroid hormone regulates the levels of calcium in the blood. The parathyroid glands release parathyroid hormone that causes calcium reabsorption and vitamin D hydroxylation in the kidneys, calcium absorption from the intestines, calcium reabsorption from the bones, and an increase of calcium in the blood.

Calcium regulation: This is an illustration of how the parathyroid hormone regulates the levels of calcium in the blood.

Anion Regulation

The anions chloride, bicarbonate, and phosphate have important roles in maintaining the balance and neutrality of vital body mechanisms.

Key Points

Chloride is needed to maintain proper hydration, as well as to balance cations, and maintain the electrical neutrality of the extracellular fluid.

Bicarbonate‘s main role is to maintain the body’s acid-base balance through a buffer system.

Phosphate is a major constituent of the intracellular fluid, and it is important in the regulation of metabolic processes and as a buffering agent in animal cells.

The kidneys regulate the salt balance in the blood by controlling the excretion and the reabsorption of various ions.

Key Terms

  • anion: An negatively charged ion.
  • hyperphosphatemia: An elevated amount of phosphate in the blood.
  • hypochloremia: An electrolyte disturbance caused by an abnormally depleted level of chloride ions in the blood.
  • hypophosphatemia: An electrolyte disturbance caused by an abnormally low level of phosphate in the blood.

Anion Regulation

The excretion of ions occurs mainly through the kidneys, with lesser amounts of ions being lost in sweat and in feces. In addition, excessive sweating may cause a significant loss, especially of the anion chloride. Severe vomiting or diarrhea will also cause a loss of chloride and bicarbonate ions.

Adjustments in the respiratory and renal functions allow the body to regulate the levels of these ions in the extracellular fluid (ECF).

Chloride

Chloride is the predominant extracellular anion and it is a major contributor to the osmotic pressure gradient between the intracellular fluid (ICF) and extracellular fluid (ECF). Chloride maintains proper hydration and functions to balance the cations in the ECF to keep the electrical neutrality of this fluid. The paths of secretion and reabsorption of chloride ions in the renal system follow the paths of sodium ions.

Hypochloremia, or lower-than-normal blood chloride levels, can occur because of defective renal tubular absorption. Vomiting, diarrhea, and metabolic acidosis can also lead to hypochloremia.

In contrast, hyperchloremia, or higher-than-normal blood chloride levels, can occur due to dehydration, excessive intake of dietary salt (NaCl) or the swallowing of sea water, aspirin intoxication, congestive heart failure, and the hereditary, chronic lung disease cystic fibrosis. In people who have cystic fibrosis, the chloride levels in their sweat are two to five times those of normal levels; therefore, analysis of their sweat is often used to diagnose the disease.

Bicarbonate

Bicarbonate is the second-most abundant anion in the blood. Its principal function is to maintain your body’s acid–base balance by being part of buffer systems.

Bicarbonate ions result from a chemical reaction that starts with the carbon dioxide (CO2) and water (H2O) molecules that are produced at the end of aerobic metabolism. Only a small amount of CO2 can be dissolved in body fluids; thus, over 90 percent of the CO2 is converted into bicarbonate ions, HCO3-, through the following reactions:

CO2 + H2O ↔ H2CO↔ H2CO3– + H+

The bidirectional arrows indicate that the reactions can go in either direction depending on the concentrations of the reactants and products. Carbon dioxide is produced in large amounts in tissues that have a high metabolic rate, and is converted into bicarbonate in the cytoplasm of the red blood cells through the action of an enzyme called carbonic anhydrase.

Bicarbonate is transported in the blood and once in the lungs, the reactions reverse direction, and CO2 is regenerated from the bicarbonate to be exhaled as metabolic waste.

This diagram shows how carbonate acts as a buffering system. In the lungs, CO2 is produced from bicarbonate and removed as metabolic waste through the reverse reaction of the bicarbonate bidirectional equation.

Bicarbonate as a buffering system: In the lungs, CO2 is produced from bicarbonate and removed as metabolic waste through the reverse reaction of the bicarbonate bidirectional equation.

Phosphate

Phosphate is present in the body in three ionic forms:

  1. H2PO4
  2. HPO42−
  3. PO43−

The addition and removal of phosphate from the proteins in all cells is a pivotal strategy in the regulation of metabolic processes. Phosphate is useful in animal cells as a buffering agent, and the most common form is HPO2−4. Bone and teeth bind up 85 percent of the body’s phosphate as part of calcium phosphate salts. In addition, phosphate is found in phospholipids, such as those that make up the cell membrane, and in ATP, nucleotides, and buffers.

Hypophosphatemia, or abnormally low phosphate blood levels, occurs with the heavy use of antacids, during alcohol withdrawal, and during malnourishment. In the face of phosphate depletion, the kidneys usually conserve phosphate, but during starvation, this conservation is impaired greatly.

Hyperphosphatemia, or abnormally increased levels of phosphates in the blood, occurs if there is decreased renal function or in cases of acute lymphocytic leukemia. Additionally, because phosphate is a major constituent of the ICF, any significant destruction of cells can result in the dumping of phosphate into the ECF.

Normal and Critical Findings

Laboratory Values: 

Serum Sodium: 

  • Normal Range: 135 to 145 mmol/L
  • Mild-moderate Hyponatremia: 125 to 135 mmol/L, Severe: less than 125 mmol/L
  • Hypernatremia: Mild-moderate: 145 to 160 mmol/L, Severe: over 160 mmol/L

Serum Potassium:

  • Normal Range: 3.6 to 5.5 mmol/L
  • Hypokalemia: Mild Hypokalemia under 3.6 mmol/L, Moderate: 2.5 mmol/L, Severe : greater than 2.5 mmol/L
  • Hyperkalemia: Mild hyperkalemia: 5 to 5.5 mmol/L, Moderate- 5.5 to 6.5, Severe: 6.5 to 7 mmol/L

Serum Calcium: 

  • Normal Range: 8.8 to 10.7 mg/dl
  • Hypercalcemia: greater than 10.7 mg/dl , Severe: over 11.5 mg/dl
  • Hypocalcemia: less than 8.8 mg/dl

Serum Magnesium: 

  • Normal Range: 1.46 to 2.68 mg/dl
  • Hypomagnesemia: under 1.46 mg/dl
  • Hypermagenesemia: over 2.68

Bicarbonate:

  • Normal Range: 23 to 30 mmol/L\
  • It increases or decreases depending on the acid-base status.

Phosphorus:

  • Normal Range: 3.4 to 4.5 mg/dl
  • Hypophosphatemia: less than 2.5 mg/dl
  • Hyperphosphatemia: greater than 4.5 mg/dl

Complications

Both hyponatremia and hypernatremia, as well as hypomagnesemia, can lead to neurological consequences such as seizure disorders.

Hypokalemia and hyperkalemia, as well as hypocalcemia, are more responsible for arrhythmias.

Bicarbonate imbalance can lead to metabolic acidosis or alkalosis.

Patient Safety and Education

A piece of valuable advice to the patients would be to take the medications exactly as prescribed by the clinicians to avoid electrolyte imbalance as a consequence of not taking the prescribed dose.

One should call for immediate medical help when the patient feels weak, has muscle ache, or has altered consciousness.

Clinical Significance

Some of the common causes of electrolyte disorders seen in clinical practices are:

  • Hyponatremia: low dietary sodium intake, primary polydipsia, SIADH, congestive heart failure, hepatic cirrhosis, failure of adrenal glands, hyperglycemia, dyslipidemia
  • Hypernatremia: unreplaced fluid loss through the skin and gastrointestinal tract, osmotic diuresis, hypertonic saline administration
  • Hypokalemia: hyperaldosteronism, loop diuretics
  • Hyperkalemia: increase release from cells as in metabolic acidosis, insulin deficiency, beta-blocker or decreased potassium excretion as in acute or chronic kidney disease, aldosterone deficiency or resistance
  • Hypercalcemia: malignancy, hyperparathyroidism, chronic granulomatous disease
  • Hypocalcemia: acute pancreatitis, parathyroid hormone deficiency after thyroidectomy, neck dissection, resistance to parathormone, hypomagnesemia, sepsis
  • Hypermagnesemia: increase oral magnesium intake
  • Hypomagnesemia: renal losses as in diuretics, alcohol use disorder or GI losses as in diarrhea
  • Bicarbonate level: increases in primary metabolic alkalosis or compensation to primary respiratory acidosis – decreases in primary metabolic acidosis or compensation to primary respiratory alkalosis.
  • Hyperchloremia: normal saline infusion
  • Hypochloremia: GI loss as in diarrhea, renal losses with diuretics
  • Hypophosphatemia: refeeding syndrome, vitamin D deficiency, hyperparathyroidism
  • Hyperphosphatemia: hypoparathyroidism, chronic kidney disease

References

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Body Fluids – Physiology, Mechanism, Functions

Body fluidsbodily fluids, or biofluids are liquids within the human body. In lean healthy adult men, the total body water is about 60% (60–67%) of the total body weight; it is usually slightly lower in women (52-55%).[rx][rx] The exact percentage of fluid relative to body weight is inversely proportional to the percentage of body fat. A lean 70 kg (160 pound) man, for example, has about 42 (42–47) liters of water in his body.

The total body of water is divided into fluid compartments,[rx] between the intracellular fluid (ICF) compartment (also called space, or volume) and the extracellular fluid (ECF) compartment (space, volume) in a two-to-one ratio: 28 (28–32) liters are inside cells and 14 (14–15) liters are outside cells.

The ECF compartment is divided into the interstitial fluid volume – the fluid outside both the cells and the blood vessels – and the intravascular volume (also called the vascular volume and blood plasma volume) – the fluid inside the blood vessels – in a three-to-one ratio: the interstitial fluid volume is about 12 liters, the vascular volume is about 4 liters.

Water Content in the Body

A significant percentage of the human body is water, which includes intracellular and extracellular fluids.

Key Points

On average, body water can account for 50% of the total human body weight and it is significantly higher in newborns. Obesity decreases the percentage of water in the body.

Body water is regulated by hormones, including anti-diuretic hormone (ADH), aldosterone, and atrial natriuretic peptide.

Water content in the body can be evaluated using bioelectrical impedance and mass spectrometry.

Important functions of water in the body including supporting the cellular metabolism, molecular transport, biochemical reactions, and the physical properties of water, such as surface tension.

Key Terms

  • hydrolysis: A biochemical reaction in which water molecules are used to break down a molecule into smaller molecules.
  • bioelectrical impedance analysis: A commonly used method for estimating body composition, by measuring resistance to the flow of electricity in the body, which is associated with hydration levels.

Water Content

In physiology, body water is the water content of the human body. It makes up a significant percentage of the total composition of a body. Water is a necessary component to support life for many reasons. All cells in the human body are made mostly of water content in their cytoplasm.

This is a 3-dimensional model of hydrogen bonds (labeled 1 on the model) between molecules of water.

Water molecule: A 3-dimensional model of hydrogen bonds (labeled 1) between molecules of water.

Water also provides a fluid environment for extracellular communication and molecular transport throughout the body. Water itself is also a key component of biochemical reactions involved in physiology, such as hydrolysis. Many organ systems depend on the physical properties of water, such as the surface tension of water in the alveoli of the lungs.

Overall Water Content

The total amount of water in a human of average weight (70 kilograms) is approximately 40 liters, averaging 57 percent of his total body weight. In a newborn infant, this may be as high as 79 percent of the body weight, but it progressively decreases from birth to old age, with most of the decrease occurring during the first 10 years of life.

Also, obesity decreases the percentage of water in the body, sometimes to as low as 45 percent. The water in the body is distributed among various fluid compartments that are interspersed in the various cavities of the body through different tissue types. In diseased states where body water is affected, the fluid compartments that have changed can give clues to the nature of the problem.

Water Content Regulation and Measurement

Body water is regulated largely by the renal and neuroendocrine systems. Water content regulation is one of the most important parts of homeostasis due to its influence on blood pressure and cardiac output. Much of this regulation is mediated by hormones, including anti-diuretic hormone (ADH), renin, angiotensin II, aldosterone, and atrial natriuretic peptide (ANP).

These hormones act as messengers between the kidneys and the hypothalamus; however, the lungs and heart are also involved in the secretion of some of these hormones, such as an angiotensin-converting enzyme (ACE) and ANP respectively.

There are many clinical methods to determine body water. One way to get an uncertain estimate is by calculation based on body weight and urine output. Another way to measure body water is through dilution and equilibration using mass spectrometry, which measures the abundance of water in breath samples from an individual.

In bioelectrical impedance analysis, a person’s hydration level is calculated from high-precision measurements of the opposition to the flow of an electric current through body tissues. Since water conducts electricity, a lower hydration level will cause a greater amount of resistance to electrical flow through the body.

Fluid Compartments

The major body-fluid compartments include intracellular fluid and extracellular fluid (plasma, interstitial fluid, and transcellular fluid).

Key Points

The intracellular fluid of the cytosol or intracellular fluid (or cytoplasmic matrix) is the liquid found inside cells.

The cytosol is a complex mixture of substances that include proteins, ions, and organelles dissolved in water.

Extracellular fluid (ECF) or extracellular fluid volume (ECFV) usually denotes all body fluid outside of cells, and consists of plasma, interstitial, and transcellular fluid.

An extracellular matrix is an extracellular fluid space containing cell-excreted molecules, and they vary in their type and function.

Plasma also serves as an extracellular matrix (ECM) for the cells and molecules of the blood.

Interstitial fluid (or tissue fluid) is a solution that bathes and surrounds the cells of multicellular animals.

Transcellular fluid is the portion of total body water contained within epithelial-lined spaces.

Key Terms

  • intracellular fluid: The liquid found inside cells, between the endomembrane and the membrane-bound organelles.
  • interstitial fluid: A solution that bathes and surrounds the cells of multicellular animals; also called tissue fluid.
  • plasma: The straw-colored/pale-yellow, liquid component of blood that normally holds the blood cells of whole blood in suspension.

Fluid Compartments

The fluids of the various tissues of the human body are divided into fluid compartments. Fluid compartments are generally used to compare the position and characteristics of fluid in relation to the fluid within other compartments.

While fluid compartments may share some characteristics with the divisions defined by the anatomical compartments of the body, these terms are not one in the same. Fluid compartments are defined by their position relative to the cellular membrane of the cells that make up the body’s tissues.

Intracellular Fluid

The intracellular fluid of the cytosol or intracellular fluid (or cytoplasm ) is the fluid found inside cells. It is separated into compartments by membranes that encircle the various organelles of the cell. For example, the mitochondrial matrix separates the mitochondrion into compartments.

The contents of a eukaryotic cell within the cell membrane, excluding the cell nucleus and other membrane-bound organelles (e.g., mitochondria, plastides, lumen of endoplasmic reticulum, etc.), is referred to as the cytoplasm.

This is an illustration of a cytosol encompassing a variety of molecules in its fluid. The cytosol is the fluid within the plasma membrane of a cell and contains the organelles. The cytosol includes dissolved molecules and water.

The cytosol: The cytosol (11) is the fluid within the plasma membrane of a cell and contains the organelles. The cytosol includes dissolved molecules and water.

The cytosol is a complex mixture of substances dissolved in water. Although water forms the large majority of the cytosol, it mainly functions as a fluid medium for intracellular signaling (signal transduction ) within the cell, and plays a role in determining cell size and shape.

The concentrations of ions, such as sodium and potassium, are generally lower in the cytosol compared to the extracellular fluid; these differences in ion levels are important in processes such as osmoregulation and signal transduction. The cytosol also contains large amounts of macromolecules that can alter how molecules behave, through macromolecular crowding.

Extracellular Fluid

Extracellular fluid (ECF) or extracellular fluid volume (ECFV) usually denotes all the body fluid that is outside of the cells. The extracellular fluid can be divided into two major subcompartments: interstitial fluid and blood plasma.

The extracellular fluid also includes the transcellular fluid; this makes up only about 2.5% of the ECF. In humans, the normal glucose concentration of extracellular fluid that is regulated by homeostasis is approximately 5 mm. The pH of extracellular fluid is tightly regulated by buffers and maintained around 7.4.

The volume of ECF is typically 15L (of which 12L is interstitial fluid and 3L is plasma). The ECF contains extracellular matrices (ECMs) that act as fluids of suspension for cells and molecules inside the ECF.

This is a diagram of the extracellular matrix. It shows the spatial relationship between the blood vessels, basement membranes, and interstitial space between structures.

Extracellular matrix: Spatial relationship between the blood vessels, basement membranes, and interstitial space between structures.

Blood Plasma

Blood plasma is the straw-colored/pale-yellow, liquid component of blood that normally holds the blood cells in whole blood in suspension, making it a type of ECM for blood cells and a diverse group of molecules. It makes up about 55% of total blood volume.

It is the intravascular fluid part of the extracellular fluid. It is mostly water (93% by volume) and contains dissolved proteins (the major proteins are fibrinogens, globulins, and albumins), glucose, clotting factors, mineral ions (Na+, Ca++, Mg++, HCO3- Cl-, etc.), hormones, and carbon dioxide (plasma is the main medium for excretory product transportation). It plays a vital role in intravascular osmotic effects that keep electrolyte levels balanced and protects the body from infection and other blood disorders.

Interstitial Fluid

Interstitial fluid (or tissue fluid) is a solution that bathes and surrounds the cells of multicellular animals. The interstitial fluid is found in the interstitial spaces, also known as the tissue spaces.

On average, a person has about 11 liters (2.4 imperial gallons or about 2.9 U.S. gal) of interstitial fluid that provide the cells of the body with nutrients and a means of waste removal. The majority of the interstitial space functions as an ECM, a fluid space consisting of cell-excreted molecules that lies between the basement membranes of the interstitial spaces. The interstitial ECM contains a great deal of connective tissue and proteins (such as collagen) that are involved in blood clotting and wound healing.

Transcellular Fluid

Transcellular fluid is the portion of total body water contained within the epithelial-lined spaces. It is the smallest component of extracellular fluid, which also includes interstitial fluid and plasma. It is often not calculated as a fraction of the extracellular fluid, but it is about 2.5% of the total body water.

Examples of this fluid are cerebrospinal fluid, ocular fluid, joint fluid, and the pleaural cavity that contains fluid that is only found in their respective epithelium-lined spaces.

The function of the transcellular fluid is mainly lubrication of these cavities, and sometimes electrolyte transport.

Body Fluid Composition

The composition of tissue fluid depends upon the exchanges between the cells in the biological tissue and the blood.

Key Points

The cytosol or intracellular fluid consists mostly of water, dissolved ions, small molecules, and large, water-soluble molecules (such as proteins).

Enzymes in the cytosol are important for cellular metabolism.

The extracellular fluid is mainly cations and anions.

Plasma is mostly water and dissolved proteins, but also contains metabolic blood gasses, hormones, and glucose.

The composition of transcellular fluid varies, but some of its main electrolytes include sodium ions, chloride ions, and bicarbonate ions.

Key Terms

  • electrolyte: Any of the various ions (such as sodium or chloride) that regulate the electric charge on cells and the flow of water across their membranes.
  • transcellular fluid: The portion of total body water contained within epithelial-lined spaces, such as the cerebrospinal fluid, and the fluid of the eyes and joints.
  • ion: An atom or molecule in which the total number of electrons is not equal to the total number of protons, giving it a net positive or negative electrical charge.

Body Fluid Composition

The composition of tissue fluid depends upon the exchanges between the cells in the biological tissue and the blood. This means that fluid composition varies between body compartments.

Intracellular Fluid Composition

The cytosol or intracellular fluid consists mostly of water, dissolved ions, small molecules, and large, water-soluble molecules (such as proteins). This mixture of small molecules is extraordinarily complex, as the variety of enzymes that are involved in cellular metabolism is immense.

This is a diagram of ions in a solution.

Ions: Ions in solution.

These enzymes are involved in the biochemical processes that sustain cells and activate or deactivate toxins. Most of the cytosol is water, which makes up about 70% of the total volume of a typical cell. The pH of the intracellular fluid is 7.4. The cell membrane separates cytosol from extracellular fluid but can pass through the membrane via specialized channels and pumps during passive and active transport.

The concentrations of the other ions in the cytosol or intracellular fluid are quite different from those in extracellular fluid. The cytosol also contains much higher amounts of charged macromolecules, such as proteins and nucleic acids, than the outside of the cell.

In contrast to extracellular fluid, cytosol has a high concentration of potassium ions and a low concentration of sodium ions. The reason for this specific sodium and potassium ion concentrations are Na+/K ATPase pumps that facilitate the active transport of these ions. These pumps to transport ions against their concentration gradients to maintain the cytosol fluid composition of the ions.

Extracellular Fluid Composition

The extracellular fluid is mainly cations and anions. The cations include: sodium (Na+ = 136-145 mEq/L), potassium (K+ = 3.5-5.5 mEq/L) and calcium (Ca2+ = 8.4-10.5 mEq/L). Anions include: chloride ( mEq/L) and hydrogen carbonate (HCO3- 22-26 mM). These ions are important for water transport throughout the body.

Plasma is mostly water (93% by volume) and contains dissolved proteins (the major proteins are fibrinogens, globulins, and albumins), glucose, clotting factors, mineral ions (Na+, Ca++, Mg++, HCO3- Cl- etc.), hormones and carbon dioxide (plasma being the main medium for excretory product transportation). These dissolved substances are involved in many varied physiological processes, such as gas exchange, immune system function, and drug distribution throughout the body.

Transcellular Fluid Composition

Due to the varying locations of transcellular fluid, the composition changes dramatically. Some of the electrolytes present in the transcellular fluid are sodium ions, chloride ions, and bicarbonate ions.

Cerebrospinal fluid is similar in composition to blood plasma but lacks most proteins, such as albumins, because they are too large to pass through the blood-brain barrier. Ocular fluid in the eyes contrasts with cerebrospinal fluid by containing high concentrations of proteins, including antibodies.

Movement of Fluid Among Compartments

How fluid moves through compartments depends on several variables described by Starling’s equation.

Key Points

Interstitial fluid is formed when hydrostatic pressure generated by the heart pushes the water out of the capillaries. The water passes from a high concentration outside of the vessels to a low concentration inside of the vessels, but equilibrium is never reached because of the constant blood flow.

Osmotic pressure works opposite to hydrostatic pressure to hold water and substances in the capillaries.

Hydrostatic pressure is stronger in the arterial ends of the capillaries, while osmotic pressure is stronger at the venous ends of the capillaries.

Interstitial fluid is removed through the surrounding lymph vessels and eventually ends up rejoining the blood. Sometimes the removal of tissue fluid does not function correctly and there is a buildup, called edema.

The Starling equation describes the pressure gradients that drive the movement of water across fluid compartments.

Key Terms

  • Starling equation: An equation that illustrates the role of hydrostatic and oncotic forces in the movement of fluid across capillary membranes.
  • interstitial fluid: A solution that bathes and surrounds the cells of multicellular animals.

Fluid Movement

Extracellular fluid is separated among the various compartments of the body by membranes. These membranes are hydrophobic and repel water; however, there a few ways that fluids can move between body compartments. There are small gaps in membranes, such as the tight junctions, that allow fluids and some of their contents to pass through membranes by way of pressure gradients.

Formation of Interstitial Fluid

Hydrostatic pressure is generated by the contractions of the heart during systole. It pushes water out of the small tight junctions in the capillaries. The water potential is created due to the ability of the small solutes to pass through the walls of capillaries.

This buildup of solutes induces osmosis. The water passes from a high concentration (of water) outside of the vessels to a low concentration inside of the vessels, in an attempt to reach an equilibrium. The osmotic pressure drives water back into the vessels. Because the blood in the capillaries is constantly flowing, equilibrium is never reached.

The balance between the two forces differs at different points on the capillaries. At the arterial end of a vessel, the hydrostatic pressure is greater than the osmotic pressure, so the net movement favors water and other solutes being passed into the tissue fluid.

At the venous end, the osmotic pressure is greater, so the net movement favors substances being passed back into the capillary. This difference is created by the direction of the flow of blood and the imbalance in solutes created by the net movement of water that favors the tissue fluid.

Removal of Interstitial Fluid

The lymphatic system plays a part in the transport of tissue fluid by preventing the buildup of tissue fluid that surrounds the cells in the tissue. Tissue fluid passes into the surrounding lymph vessels and eventually rejoins the blood.

Sometimes the removal of tissue fluid does not function correctly and there is a buildup, which is called edema. Edema is responsible for the swelling that occurs during inflammation, and in certain diseases where the lymphatic drainage pathways are obstructed.

Starling Equation

Capillary permeability can be increased by the release of certain cytokines, anaphylatoxins, or other mediators (such as leukotrienes, prostaglandins, histamine, bradykinin, etc.) that are released by cells during inflammation. The Starling equation defines the forces across a semipermeable membrane to calculate the net flux.

The solution to the equation is known as the net filtration or net fluid movement. If positive, fluid will tend to leave the capillary (filtration). If negative, fluid will tend to enter the capillary (absorption). This equation has a number of important physiologic implications, especially when disease processes grossly alter one or more of the variables.

This is a diagram of capillary dynamics. The oncotic pressure exerted by the proteins in blood plasma tends to pull water into the circulatory system. The illustration shows a capillary with blood flow in it. As the blood moves to the venous end of the capillary, hydrostatic pressure removes fluid from the blood, and osmotic pressure puts fluid into the blood flow.

Capillary dynamics: Oncotic pressure exerted by the proteins in blood plasma tends to pull water into the circulatory system.

This is a diagram of the Starling model. Note how the concentration of interstitial solutes increases proportionally to the distance from the arteriole.

According to Starling’s equation, the movement of fluid depends on six variables:

  • Capillary hydrostatic pressure (Pc)
  • Interstitial hydrostatic pressure (Pi)
  • Capillary oncotic pressure (πz)
  • Interstitial oncotic pressure (πi)
  • Filtration coefficient (Kf)
  • Reflection coefficient (σ)

The Starling Equation is mathematically described as Flux=Kf[(Pc-Pi)-σ (πz-πi)

Clinical Significance

A variety of pathological conditions induce abnormalities in fluid balance. Fluid balance abnormalities are either an overload of fluid or a decrease in effective fluid. Fluid overload is clinically known as edema. Edema occurs most commonly in soft tissues of the extremities; however, it is possible to occur in any tissue. Decreases in fluid load are commonly referred to as dehydration.

Edema manifests as swelling in the soft tissues of the limbs and face with a subsequent increase in size and tightness of the skin. Peripheral edema is reducible by increasing the pressure in the interstitial space and is measured by pressing a finger into the tissue, creating a dimple in the edematous skin temporarily. Likewise, wearing compression stockings can reduce peripheral edema by increasing interstitial hydrostatic pressure, forcing fluid back into the capillaries.

Pulmonary edema is a condition when excess fluid swells into interstitial tissues of the lung. Symptoms include shortness of breath and chest pain. Orthopnea, or impaired respiration while lying flat, may also be present as the excess fluid is distributed across the entire lung. Pulmonary edema is life-threatening as it compromises gas exchange in the lungs and conditions can quickly decompensate. Pulmonary edema is associated with cardiac failure and renal failure. Classically, cardiac failure causes pulmonary edema through decreased pumping efficiency and capacity of the left atrium and left ventricle. This creates a back pressure in the pulmonary veins, increasing pressure in the vessels. Subsequently, hydrostatic pressures in the pulmonary capillaries are increased, “pushing” fluid into the interstitial lung space following the Starling equation. Renal failure causes edema through a failure to remove fluids and osmotic components from the body. The net result is increased osmotic pull into tissues and increased hydrostatic push out of capillaries.[5]

Liver disease is also capable of inducing edema. This is due to a failure to produce osmotically active proteins. Specifically, a failure to produce albumin. Albumin is found physiologically primarily in the plasma of the extracellular blood. It is typically not found in the interstitial space. As such, a decrease in body albumen directly decreases the “pull” of osmotic pressure into the capillaries. According to Starling forces, this results in the fluid moving into the interstitial spaces.[rx]

Additionally, fluid overload can be iatrogenically induced by excessive fluid replacement via intravenous (IV) access.

Edema is treated for symptomatic relief using a variety of medications including diuretics to remove fluid from the body via the renal system. Diuretics are closely associated with inducing contraction metabolic alkalosis. Albumin may be supplemented in cases of low plasma albumin. Lifestyle changes can include reducing sodium intake, restricting fluid intake, and wearing compression stockings. However, targeting the underlying pathology to improve cardiac, hepatic, or renal function offers better results than symptomatic treatment by simply removing fluid, replacing osmotic components, or other lifestyle changes.

Dehydration is largely due to inadequate water intake to meet the body’s metabolic needs. The average adult has an obligatory intake requirement of 1600 mL per day. This value increases depending on activity and metabolism. Primary sources of normal fluid loss include urine, sweat, respiration, and stool. Pathological causes include diarrhea, vomiting, infection, and increased urination secondary to SIADH, diabetes mellitus, or diabetes insipidus. Dehydration manifests clinically as decreased urine output, dizziness, fatigue, tachycardia, increased skin turgidity, and fatigue or confusion in severe cases. Whenever possible, oral fluid replacement should be attempted. In more urgent situations, IV fluid replenishment should be based on bolus supplementation of the deficit of fluids and a maintenance replenishment of obligatory intake requirements. The fluid deficit can be calculated when the pre-dehydration weight and post-dehydration weight are known. The equation in males is:

  • Deficit = 0.6 X weight in kilograms X [1-(140/measured Na)]

In females, the equation is:

  • Deficit = 0.5 X weight in kilograms X [1-(140/measured Na)]

This equation is highly useful in determining the initial fluid deficit. However, it has limitations in accuracy and can underestimate total fluid loss by more than 40%. While the above equation can be useful in initial fluid resuscitation, a more accurate approach uses plasma osmolarity instead of sodium, using 290 mmol/kg as the standard value. In pediatric patients, the fluid deficit is directly correlated to bodyweight loss from pre-illness compared to post-illness. One liter of free water weighs 1 kg. Therefore, a 10-kg pre-illness child that weighs 9 kg in illness has a fluid deficit of 1 L. In emergency scenarios, a bolus volume of 30 mL/kg is used to replace the loss. In obese patients, however, this leads to over-repletion of free water. Therefore, it is recommended to base bolus fluid resuscitation on adjusted ideal body weight (AIBW) in obese patients. This is derived from the ideal body weight (IBW) and the actual body weight (ABW).

  • AIBW = IBW + 0.4 (ABW – IBW)

Where ideal body weight is calculated as:

  • Males: IBW = 50 kg + 2.3 kg for each inch over 5 feet females: IBW = 45.5 kg + 2.3 kg for each inch over 5 feet

Maintenance fluid is also determined using a formula based on weight.  Fluid should be replaced at a rate of:

  • 4 mL/kg/hr for kg 1-10 + 2 mL/kg/hr for kg 10-20 + 1 mL/kg/hr above 20 kg

In other words, a patient who weighs 55 kilograms would require:

  • 40 mL/hr + 20 mL/hr + 35 mL = 95 mL/hr of free water

IV fluid replacement options include normal saline (0.9% NaCl), one-half normal saline (0.45% NaCl), Dextrose 5% in either normal saline or one-half normal saline, and lactated Ringer’s solution. The choice of replacement fluids is patient scenario-specific and dependent on the electrolyte status of laboratory evaluation.[rx]

Burn patients require specialized increases in fluid replacement secondary to the immense loss of free water through their wounds. The needed fluid resuscitation in adults is calculated using Parkland’s formula and Brooke’s formula. The modified Brooke formula is:

  • 2 mL/kg/% body surface area burned

The modified Parkland formula is:

  • 4 mL/kg/% body surface area burned

Both formulas estimate the first 24-hour fluid requirements from the time of the burn, with half the amount to be given in the first 8 hours. While both formulas give widely different values, they give equivalent outcomes. Final fluid needs should be based on the urine output rate.[rx]

Diabetic ketoacidosis is a complication of diabetes mellitus that results when the body fails to utilize glucose for energy production. Glucose is an osmotically active substance that is excreted in the urine at high concentrations. This leads to extreme fluid loss through the urine and dehydration. This necessitates large volume resuscitation of 6 to 9 L of normal saline on average.

Hyperosmolar hyperglycemic non-ketotic acidosis is a similar illness to diabetic ketoacidosis, except it lacks ketone production. It requires a similar fluid resuscitation.

In hypernatremic patients who undergo fluid replacement with rapid subsequent correction of hypernatremia are at an increased risk for developing cerebral edema. This develops due to increased intracellular and extracellular fluid loads and increased pressure within the brain space. This leads to neurological deficits and ultimately death. This condition can be avoided by slowly infusing fluids such that sodium levels are reduced at an initial rate of 2 to 3 mEq/L per hour for a maximum total change of 12 mEq/L per day until sodium is in a normal range.

Conversely, rapid correction of hyponatremia may lead to central pontine myelinolysis syndrome. Brain cells adapt to chronic states of hyponatremia by shifting organic osmoles, such as amino acids, from the intracellular compartment to the extracellular compartment. This allows the cells to maintain their original volume. When hyponatremia is rapidly corrected, brain cells shrink and the tight junctions of the blood-brain barrier are disrupted, leading to cell damage and demyelination of neurons.[rx] This can lead to what is known as “locked-in syndrome,” which is characterized by paralysis, dysphagia, and dysarthria. The serum sodium should be increased by approximately 1 to 2 mEq/L per hour until the neurologic symptoms of hyponatremia subside or until plasma sodium concentration is over 120 mEq/L.

Crystalloid fluid resuscitation offers complications as they alter the ionic load of the serum. Specifically, normal saline replacement may lead to non-gap hyperchloremic metabolic acidosis. One-half normal saline, if not monitored closely, may dilute ionic components, leading to hyponatremia or, less often, hypokalemia. Abdominal compartment syndrome in septic shock patients is possibly secondary to fluid overload with the subsequent leak of fluid from capillaries into extravascular spaces.

Colloid fluid resuscitation has its risks as well. The two major colloids used are albumen and hydroxyethyl starch. In the SAFE trial, which compared 4% albumin fluid with 0.9% normal saline, it was determined that outcomes are equivalent. However, in specific cases involving neurological injury, 4% albumin has an increased mortality rate compared to normal saline. As such, albumin should be avoided in this situation. Hydroxyethyl starch was studied in comparison and found to carry an increased risk of death or end-stage renal failure when compared to lactated Ringer’s solution when used in sepsis patients.[rx][rx][rx]

References

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Competition Pools – All About You Need To Know

Competition Pools/A swimming poolswimming bathwading poolpaddling pool, or simply pool is a structure designed to hold water to enable swimming or other leisure activities. Pools can be built into the ground (in-ground pools) or built above ground (as a freestanding construction or as part of a building or other larger structure), and maybe found as a feature aboard ocean-liners and cruise ships. In-ground pools are most commonly constructed from materials such as concrete, natural stone, metal, plastic, or fiberglass, and can be of a custom size and shape or built to a standardized size, the largest of which is the Olympic-size swimming pool.

Many health clubs, fitness centers, and private clubs have pools used mostly for exercise or recreation. It is common for municipalities of every size to provide pools for public use. Many of these municipal pools are outdoor pools but indoor pools can also be found in buildings such as leisure centers. Hotels may have pools available for their guests to use at their own leisure. Pools as a feature in hotels are more common in tourist areas or near convention centers. Educational facilities such as high schools and universities sometimes have pools for physical education classes, recreational activities, leisure, and competitive athletics such as swimming teams. Hot tubs and spas are pools filled with water that is heated and then used for relaxation or hydrotherapy. Specially designed swimming pools are also used for diving, water sports, and physical therapy, as well as for the training of lifeguards and astronauts. Swimming pools most commonly use chlorinated water or saltwater and may be heated or unheated.

10 Best College Competition Pools in the US

IU Natatorium at IUPUI

It takes a lot more than a pool of water to host a competitive swimming event. Today’s college competition pools are getting more and more impressive. Not only are the swimming competitions heating up, but the battle to have one of the best competition pools is also getting fiercer.

Our Picks for the 10 Best College Competition Pools

Here are ten of our favorite competition pools across the United States.

10. Student Rec Center Natatorium – Texas A&M

Student Rec Center Natatorium – Texas A&M

This is one of only five pools in the United States to host a stop on the FINA World Series Circuit. A 50-meter pool with eight lanes, it has a 17-feet-deep diving well. Since it opened in 1995, this pool has hosted many competitions, including the 1990 U.S. Open and the 2018 SEC Championships.

9. Burt Flickinger Center – Erie Community College

Burt Flickinger Center – Erie Community College

This state-of-the-art athletic center at Erie Community College in Buffalo, New York was built in 1993 to serve as the swimming venue for the 1993 World University Games. It features two pools, an Olympic-sized competition pool and a 25-meter warm-up pool, and two diving boards, 1 meter and 3 meters. The center now serves as the home swimming venue for the Canisius men’s and women’s swimming and diving meets. It has also hosted the Metro Atlantic Athletic Conference (MAAC) Swimming and Diving Championships every year since 2011. The facility has capacity for 1,500 spectators.

8. Gabrielsen Natatorium – University of Georgia

Gabrielsen Natatorium – University of Georgia

The 50-meter competition pool in this natatorium can be configured into four completely different layouts with its two movable bulkheads. In addition to the competition pool, this natatorium has two other pools and enough seating for 2,000 spectators.

7. Avery Aquatic Center -Stanford University

Avery Aquatic Center -Stanford University

There are four completely separate pools in this facility, including the Avery Competition Pool, which can host as many as 2,539 spectators at a time.

6. DeNunzio Pool– Princeton University

DeNunzio Pool– Princeton University

The DeNunzio Pool has a minimum depth of nine feet and a maximum depth of 17 feet. Measuring 50 meters by 35 yards, it has two movable bulkheads for various pool configurations. This pool has seating for up to 1,700 fans, which comes in useful for the numerous competitions since it has hosted since opening its doors in 1990.

5. Freeman Aquatic Center – University of Minnesota

Freeman Aquatic Center – University of Minnesota

Since it first opened in 1990, Freeman Aquatic Center has hosted more than five million participants. Minnesota’s top aquatic facility, it is one of the best competition pools in the nation. With its 50-meter pool, double eight-lane short course pool, diving well, bubble machine and extra amenities – it’s easy to see why people love this aquatic center.

4. McCorkle Aquatic Pavilion – The Ohio State University

McCorkle Aquatic Pavilion – The Ohio State University

Many people say this is one of the best diving facilities in the U.S. It has hosted many events, including Big Ten Championships, NCAA Championships, USA Swimming invitational meets and more. This pool isn’t just for diving, though. It’s known for its speed as well, thanks to its deep gutters, lane width, depth and water inlets at the pool’s bottom.

3. Lee and Joe Jamil Texas Swimming Center – University of Texas Austin

Lee and Joe Jamil Texas Swimming Center – University of Texas Austin

This Texas-based pool has hosted Grand Prix competitions, Olympic Trials, NCAA Championships and more. It’s considered one of the fastest pools in the world thanks to its gutter system, depth, lane width and high filtration rate. Fun Fact: Michael Phelps broke his first world record in this pool at the World Championship Trials. It was the 200-meter butterfly race when he was just 15 years old.

2. Herb McAuley Aquatic Center – Georgia Tech

Herb McAuley Aquatic Center – Georgia Tech

This competition pool is 50 meters long and 10 lanes wide, with stadium seating for up to 1,950 people. This facility was built specifically for the 1996 Olympic Games, so it isn’t surprising that it’s a top pick for swimmers. This pool also has a movable floor to set the pool depth from zero to seven feet, eight inches. (As a bonus, the aquatic center also has a smaller leisure pool inside the facility).

1. IU Natatorium at IUPUI

IU Natatorium at IUPUI

This pool has hosted hundreds of events, including state, regional, national and international events—and several Olympic and World Championship trials. Since its opening in 1982, “The Nat” has been home to 19 world records and holds the title of the biggest permanent swimming facility in the United States.

Competition Pools Across the U.S.

These ten pools are just a few of the best competition pools across the United States. Every year, new facilities pop up with impressive additions and features, keeping the competition between competition pools going strong.

References

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What is the importance of water balance?

What is the importance of water balance?/Water balance means the inflows to any water system or area are equal to its outflows plus the change in storage during a time interval. In hydrology, a water balance equation can be used to describe the flow of water in and out of a system. A system can be one of several hydrological or water domains, such as a column of soil, a drainage basin, an irrigation area, or a city. Water balance can also refer to the ways in which an organism maintains water in dry or hot conditions. It is often discussed in reference to plants or arthropods, which have a variety of water retention mechanisms, including a lipid waxy coating that has limited permeability.

Regulation of Water Intake

Fluid can enter the body as preformed water, ingested food and drink, and, to a lesser extent, as metabolic water.

Key Points

A constant supply of water is needed to replenish the fluids lost through normal physiological activities, such as respiration, sweating, and urination.

Thirst is a sensation created by the hypothalamus that drives organisms to ingest water.

Increased osmolarity in the blood acts on osmoreceptors that either stimulate the hypothalamus directly or cause the release of angiotensin II to stimulate the hypothalamus to cause thirst.

The renin-angiotensin system increases thirst as a way to increase blood volume. It is activated by high plasma osmolarity, low blood volume, low blood pressure, and stimulation of the sympathetic nervous system.

Key Terms

  • thirst: The sensation that drives organisms to ingest water. It is considered a basic survival instinct.
  • osmoreceptors: Sensory receptors that are primarily found in the hypothalamus or macula densa that detect changes in the solute concentration of blood.

Water Intake

Fluid can enter the body as preformed water, ingested food and drink, and, to a lesser extent, as metabolic water that is produced as a by-product of aerobic respiration and dehydration synthesis. A constant supply is needed to replenish the fluids lost through normal physiological activities, such as respiration, sweating, and urination.

Water generated from the biochemical metabolism of nutrients provides a significant proportion of the daily water requirements for some arthropods and desert animals, but it provides only a small fraction of a human’s necessary intake. In the normal resting state, the input of water through ingested fluids is approximately 2500 ml/day.

Body water homeostasis is regulated mainly through ingested fluids, which, in turn, depends on thirst. Thirst is the basic instinct or urge that drives an organism to ingest water.

Thirst is a sensation created by the hypothalamus, the thirst center of the human body. Thirst is an important component of blood volume regulation, which is slowly regulated by homeostasis.

Hypothalamus-Mediated Thirst

An osmoreceptor is a sensory receptor that detects changes in osmotic pressure and is primarily found in the hypothalamus of most homeothermic organisms. Osmoreceptors detect changes in plasma osmolarity (that is, the concentration of solutes dissolved in the blood).

When the osmolarity of blood changes (it is more or less dilute), water diffusion into and out of the osmoreceptor cells changes. That is, the cells expand when the blood plasma is more dilute and contract with a higher concentration.

When the osmoreceptors detect high plasma osmolarity (often a sign of a low blood volume), they send signals to the hypothalamus, which creates the biological sensation of thirst. Osmoreceptors also stimulate vasopressin (ADH) secretion, which starts the events that will reduce plasma osmolality to normal levels.

The illustration shows the location of the hypothalamus in the brain. It is between the thalamus and the infundibulum. The anterior and posterior pituitary glands are seen under the infundibulum.

The hypothalamus: The hypothalamus is the thirst center of the human body.

Renin-Angiotensin System-Mediated Thirst

Another way through which thirst is induced is through angiotensin II, one of the hormones involved in the renin-angiotensin system. The renin-angiotensin system is a complex homeostatic pathway that deals with blood volume as a whole, as well as plasma osmolality and blood pressure.

The macula densa cells in the walls of the ascending loop of Henle of the nephron is another type of osmoreceptor; however, it stimulates the juxtaglomerular apparatus (JGA) instead of the hypothalamus. When the macula densa is stimulated by high osmolarity, The JGA releases renin into the bloodstream, which cleaves angiotensinogen into angiotensin I. Angiotensin I is converted into angiotensin II by ACE in the lungs. ACE is a hormone that has many functions.

Angiotensin II acts on the hypothalamus to cause the sensation of thirst. It also causes vasoconstriction, and the release of aldosterone to cause increased water reabsorption in a mechanism that is very similar to that of ADH.

Note that the renin-angiotensin system, and thus thirst, can be caused by other stimuli besides increased plasma osmolarity or a decrease in blood volume. For example, stimulation of the sympathetic nervous system and low blood pressure in the kidneys (decreased GFR) will stimulate the renin-angiotensin system and cause an increase in thirst.

Regulation of Water Output

Fluid can leave the body in three ways: urination, excretion (feces), and perspiration (sweating).

Key Points

The majority of fluid output occurs from urination. Some fluid is lost through perspiration (part of the body’s temperature control mechanism) and as water vapor in expired air.

The body’s homeostatic control mechanisms ensure that a balance between fluid gain and fluid loss is maintained. The hormones ADH (antidiuretic hormone, also known as vasopressin ) and aldosterone play a major role in this.

If the body is becoming fluid deficient, increased plasma osmolarity is sensed by the osmoreceptors. This results in an increase in the secretion of ADH that causes fluid to be retained by the kidneys and urine output to be reduced.

Aldosterone is the major end-product of the renin-angiotensin system and increases the expression of ATPase pumps in the nephron that causes an increase in water reabsorption through sodium cotransport.

ADH increases water reabsorption by increasing the nephron’s permeability to water, while aldosterone works by increasing the reabsorption of both sodium and water.

Key Terms

  • osmoreceptors: Sensory receptors, primarily found in the hypothalamus, that detect changes in plasma osmolarity and contribute to the fluid-balance regulation in the body.
  • anti-diuretic hormone: A neurohypophysial hormone found in most mammals that is responsible for increasing water absorption in the collecting ducts of the kidney nephrons.
  • aldosterone: A corticoid hormone that is secreted by the adrenal cortex that regulates the balance of sodium and potassium and thus the water-balance levels in the body.

Water Output

Fluid can leave the body in three ways:

  • Urination
  • Excretion (feces)
  • Perspiration (sweating)

The majority of fluid output occurs from urination, at approximately 1500 ml/day (approximately 1.59 qt/day) in a normal adult at resting state. Some fluid is lost through perspiration (part of the body’s temperature control mechanism) and as water vapor in expired air; however, these fluid losses are considered to be very minor.

The body’s homeostatic control mechanisms maintain a constant internal environment to ensure that a balance between fluid gain and fluid loss is maintained. The hormones ADH (anti-diuretic hormone, also known as vasopressin) and aldosterone, a hormone created by the renin-angiotensin system, play a major role in this balance.

If the body is becoming fluid deficient, there will be an increase in the secretion of these hormones that causes water to be retained by the kidneys through increased tubular reabsorption and urine output to be reduced. Conversely, if fluid levels are excessive, the secretion of these hormones is suppressed and results in less retention of fluid by the kidneys and a subsequent increase in the volume of urine produced, due to reduced fluid retention.

ADH Feedback

When blood volume becomes too low, plasma osmolarity will increase due to a higher concentration of solutes per volume of water. Osmoreceptors in the hypothalamus detect the increased plasma osmolarity and stimulate the posterior pituitary gland to secrete ADH.

ADH causes the walls of the distal convoluted tubule and collecting duct to become permeable to water—this drastically increases the amount of water that is reabsorbed during tubular reabsorption. ADH also has a vasoconstrictive effect in the cardiovascular system, which makes it one of the most important compensatory mechanisms during hypovolemic shock (shock from excessive fluid loss or bleeding).

Aldosterone Feedback

Aldosterone is a steroid hormone (corticoid) produced at the end of the renin-angiotensin system. To review the renin-angiotensin system, low blood volume activates the juxtaglomerular apparatus in a variety of ways to make it secrete renin. Renin cleaves angiotensin I from the liver-produced angiotensinogen. Angiotensin converting enzyme (ACE) in the lungs converts angiotensin I into angiotensin II. Angiotensin II has a variety of effects (such as increased thirst) but it also causes the release of aldosterone from the adrenal cortex.

Aldosterone has a number of effects that are involved in the regulation of water output. It acts on mineral corticoid receptors in the epithelial cells of the distal convoluted tubule and collecting duct to increase their expression of Na+/K+ ATPase pumps and to activate those pumps. This causes greatly increased reabsorption of sodium and water (which follows sodium osmotically by cotransport), while causing the secretion of potassium into the urine.

Aldosterone increases water reabsorption; however, it involves an exchange of sodium and potassium that ADH absorption regulation does not involve. Aldosterone will also cause a similar ion-balancing effect in the colon and salivary glands as well.

This is a diagram overview of the renin–angiotensin system that regulates blood pressure and plasma osmolarity. The hypothalamus of the brain releases a corticotropin-releasing hormone that makes the pituitary gland release ACTH to the liver which, in turn, releases angiotensinogen. Renin cleaves angiotensin I from the liver-produced angiotensinogen. Angiotensin converting enzyme (ACE) in the lungs converts angiotensin I into angiotensin II. Angiotensin II has a variety of effects (such as increasing thirst) but it also causes release of aldosterone from the adrenal cortex.

A schematic diagram of the renin-angiotensin system: Overview of the renin-angiotensin system that regulates blood pressure and plasma osmolality.

Nitrogenous Waste in Terrestrial Animals: The Urea Cycle

Water balance in a basin

A general water balance equation is:[rx]

P = R + ET + ΔS

where

P is precipitation is streamflow is evapotranspiration
ΔS is the change in storage (in soil or the bedrock/groundwater)

This equation uses the principles of conservation of mass in a closed system, whereby any water entering a system (via precipitation), must be transferred into either evaporation, transpiration, surface runoff (eventually reaching the channel and leaving in the form of river discharge), or stored in the ground. This equation requires the system to be closed, and where it isn’t (for example when surface runoff contributes to a different basin), this must be taken into account.

Extensive water balances are discussed in agricultural hydrology.

A water balance can be used to help manage water supply and predict where there may be water shortages. It is also used in irrigation, runoff assessment (e.g. through the RainOff model [rx]), flood control, and pollution control. Further, it is used in the design of subsurface drainage systems which may be horizontal (i.e. using pipes, tile drains, or ditches) or vertical (drainage by wells).[rx] To estimate the drainage requirement, the use of a hydrogeological water balance and a groundwater model (e.g. SahysMod[rx]) may be instrumental.

The water balance can be illustrated using a water balance graph which plots levels of precipitation and evapotranspiration often on a monthly scale.

Several monthly water balance models had been developed for several conditions and purposes. Monthly water balance models had been studied since the 1940s.[rx]

Water Balance of a System

“Making water available for its many uses and users requires tools and institutions to transform it from a natural resource to one providing services”.[rx] This means that there are two types of water systems: Water Resource System (WRS) and Water Use System (WUS).

A WRS, such as a river, an aquifer, or a lake, must obey water balance. For example, the volume of water that goes into an aquifer must be equal to the amount that leaves it plus its change in storage. Under various drivers, such as climate change, population increase, and bad management, water storage of many WRS is decreasing, say per decade. This means that the volume of water in a WRS decreased after a decade, i.e., the inflow was less than outflow during that time interval.[rx]

In general, a WUS is a water construct of a user, such as a city, an industry, an irrigation zone, or a region, and not a geographic area. The schematic of a WUS shows the inflows and the outflows. For a WUS, change in storage is negligible (relative to its inflow) under a proper time interval, hence water balance becomes inflow equal to outflow with nine Water Path Types (WPT):[rx]

A typical schematic of a Water Use System (WUS) with its fixed nine Water Path Types

{\displaystyle VA+OS+PP=ET+NR+RF+RP}

Of course, instead of a river, it could be an aquifer that supplies water to a WUS as the main source. Let us briefly examine an urban water supply on an annual basis as a simplified example. It has negligible ET and PP (WUS is a piped network), has some limited amount of water from groundwater (OS), has return flow to the main source (RF) after passing through a Wastewater Treatment Plant, and RP type has various Water Path Instances (WPI), such as leakage, and water is taken to irrigate green zones. Considering that the annual change in storage of an urban area is negligible, the water balance equation becomes

{\displaystyle VA_{riv}+OS_{gw}=NR+RF_{wwtp}+RP_{leak}+RP_{irr}}

Urea, a nitrogenous waste material, is the end product excreted in urine when ammonia is metabolized by animals, such as mammals.

Key Points

Ureotelic animals, which includes mammals, produce urea as the main nitrogenous waste material.

2 NH+ CO2 + 3 ATP + H2O → H2N-CO-NH2 + 2 ADP + 4 Pi + AMP is the chemical reaction by which toxic ammonia is converted to urea.

The urea cycle involves the multi-step conversion (carried out by five different enzymes ) of the amino acid L- ornithine into different intermediates before being regenerated.

Key Terms

  • ureotelic: animals that secrete urea as the primary nitrogenous waste material
  • ornithine: an amino acid, which acts as an intermediate in the biosynthesis of urea
  • urea: a water-soluble organic compound, CO(NH2)2, formed by the metabolism of proteins and excreted in the urine

Nitrogenous Waste in Terrestrial Animals: The Urea Cycle

Mammals, including humans, are the primary producers of urea. Because they secrete urea as the primary nitrogenous waste product, they are called ureotelic animals. Urea serves an important role in the metabolism of nitrogen-containing compounds by animals. It is the main nitrogen-containing substance in the urine of mammals. Urea is a colorless, odorless solid, highly soluble in water, and practically non-toxic. Dissolved in water, it is neither acidic nor alkaline. The body uses it in many processes, the most notable one being nitrogen excretion. Urea is widely used in fertilizers as a convenient source of nitrogen. It is also an important raw material for the chemical industry.

Apart from mammals, urea is also found in the urine of amphibians, as well as some fish. Interestingly, tadpoles excrete ammonia but shift to urea production during metamorphosis. In humans, apart from being a carrier of waste nitrogen, urea also plays a role in the countercurrent exchange system of the nephrons, which allows for the re-absorption of water and critical ions from the excreted urine. This mechanism, controlled by an antidiuretic hormone, allows the body to create hyperosmotic urine, which has a higher concentration of dissolved substances than the blood plasma. This mechanism is important to prevent the loss of water, maintain blood pressure, and maintain a suitable concentration of sodium ions in the blood plasmas.

The urea cycle is the primary mechanism by which mammals convert ammonia to urea. Urea is made in the liver and excreted in the urine. The overall chemical reaction by which ammonia is converted to urea is 2 NH3 (ammonia) + CO2 + 3 ATP + H2O → H2N-CO-NH2 (urea) + 2 ADP + 4 Pi + AMP.

The urea cycle utilizes five intermediate steps, catalyzed by five different enzymes, to convert ammonia to urea. The amino acid L-ornithine is converted into different intermediates before being regenerated at the end of the urea cycle. Hence, the urea cycle is also referred to as the ornithine cycle. The enzyme ornithine transcarbamylase catalyzes a key step in the urea cycle. Its deficiency can lead to the accumulation of toxic levels of ammonia in the body. The first two reactions occur in the mitochondria, while the last three reactions occur in the cytosol.

image

Urea Cycle: The urea cycle converts ammonia to urea in five steps that include the catalyzation of five different enzymes.

Water Balance Disorders

Dehydration is the excessive loss of body fluid.

Key Points

There are three types of dehydration: hypotonic or hyponatremic, hypertonic or hypernatremic, and isotonic or hyponatremic.

Hypotonic dehydration is primarily a loss of electrolytes, sodium in particular.

Hypertonic dehydration is primarily a loss of water.

Isotonic dehydration is an equal loss of water and electrolytes.

Hypovolemia is a loss of blood volume and may cause hypovolemic shock. In humans, the most common type of dehydration by far is isotonic (isonatraemic) dehydration.

Water balance disorders are generally treated by increasing water intake and reducing or stopping fluid loss.

Key Terms

  • isotonic: When comparing solutions, an isotonic solution has the same osmolarity (ion concentration) as the solution it is being compared to.
  • plasma: The straw-colored/pale-yellow, liquid component of blood that normally holds the blood cells of whole blood in suspension.
  • electrolyte: Any of the various ions (such as sodium or chloride) that regulate the electric charge on cells and the flow of water across their membranes.

Water Balance Disorders

In physiology and medicine, dehydration (hypohydration) is defined as the excessive loss of body fluid. It is literally the removal of water from an object. However, in physiological terms, it entails a deficiency of fluid within an organism.

Much of the physiological effects of dehydration is due to the changes in ion concentration that may occur as a result of the dehydration. Alternatively, hypovolemia may occur due to loss of blood volume itself.

Dehydration

There are three types of dehydration that differ based on the type of change in ion concentrations:

  • Hypotonic – primarily a loss of electrolytes, sodium in particular. Hypotonic dehydration causes decreased plasma osmolality.
  • Hypertonic – primarily a loss of water. Hypertonic dehydration causes increased plasma osmolality.
  • Isotonic – an equal loss of water and electrolytes. Isotonic dehydration will not change plasma osmolarity, but it will reduce overall plasma volume. Isotonic dehydration is the most common type of dehydration.

Further complications may also occur. In hypotonic dehydration, intravascular water shifts to the extravascular space and exaggerates intravascular volume depletion for a given amount of total body water loss.

Neurological complications can occur in hypotonic and hypertonic states. The former can lead to seizures, while the latter can lead to osmotic cerebral edema upon rapid rehydration.

Hypovolemia

Hypovolemia is specifically a decrease in the volume of blood plasma. Furthermore, hypovolemia defines water deficiency in terms of blood volume rather than the overall water content of the body.

This is a color photograph of IV fluid and electrolyte administration. Intravenous administration of fluid is one effective treatment of dehydration in humans.

IV fluid and electrolyte administration: Intravenous administration of fluid is one effective treatment of dehydration in humans.

Hypovolemia is a cause of hypovolemic shock. Shock is any condition in which the body’s fluids are unable to properly circulate and oxygenate the major organs of the human body; this causes compensatory mechanisms to activate that cause further bodily harm as the body’s metabolism is maintained for a while longer.

In the case of hypovolemic shock, the tissue metabolism is impaired due to a lack of blood volume and makes it difficult for red blood cells to reach all of the tissues of the body. It is most often caused by severe vomiting, diarrhea, blood loss, or hemorrhage. Other forms of shock with similar symptoms may be due to problems in the heart (cardiogenic) or bacterial infection (septic).

Treatment Options

To treat minor dehydration water intake must be increased, while the source of fluid loss must be reduced or stopped altogether. Plain water restores only the volume of the blood plasma and inhibits the thirst mechanism before solute levels can be replenished.

Solid foods can contribute to fluid loss from vomiting and diarrhea. In more severe cases, correction of a dehydrated state is accomplished by the replenishment of necessary water and electrolytes through oral rehydration therapy or fluid replacement by intravenous therapy (an IV drip).

As oral rehydration is easier to provide, it is the treatment of choice for mild dehydration. Solutions used for intravenous rehydration must be isotonic or hypotonic. Pure water injected into the veins will cause the breakdown (lysis) of red blood cells that could cause other problems.

Keep Your Pool Chemicals Working

Maintaining the pH balance in your water will ensure you get the most out of your sanitizing chemicals. For instance, in water with low pH, your water is more acidic and will eat up the sanitizer faster. This doesn’t give your sanitizer enough time to do its job properly.

Fight Against Cloudy Water and Algae Growth

If your water is acidic, and your sanitizing chemical, such as chlorine or bromine, isnt’ working as well as it should, then you are opening yourself up to water issues. Your sanitizer’s job is to keep these issues at bay by constantly killing off the bacteria and debris that causes them.

Protect Your Equipment

Low pH causes your water to be acidic. In this case, your water will do whatever it takes to increase its pH level. Your water wants to be balanced. It’ll start to take what it needs from PVC, vinyl, concrete, and other parts of the pool, thus corroding and deteriorating your pool and equipment.

In fact, most equipment manufacturer’s warranties do not cover damage due to low pH.

On the other side, if your pH is high, this can cause scaling. Your water tries to get rid of everything that’s making it alkaline, so it leaves a film around PVC pipes, heater elements, concrete, and liners. For instance, extra scaling in your pool’s heater will cause it to use more energy to heat your pool. It’s like clogging your pool’s arteries from ingesting too much unhealthy food.

How To Balance Your Pool Water

The first step to achieving perfect water balance is testing. If it’s the start of the pool season, take a sample of your water to your nearest pool store to have it professionally analyzed. You should do this at least once a month and you should test your water at home, with a test kit or test strips, at least once a week.

Pool Water pH

A figure expressing the acidity or alkalinity of a solution. Your pool water should be between 7.4 and 7.6 on the pH scale, which would properly balance your pool’s water. If your pool is properly balanced, when you open your eyes underwater, they will not burn. The water will be as balanced as your tears.

Pool Water Alkalinity

This is a pH stabilizer. It helps to keep the pH from moving up and down the scale rapidly. The problem with pH is that EVERYTHING can affect it, including:

  • Animals
  • Humans
  • Plants
  • Weather

By keeping your alkalinity levels between 100 and 150 ppm (parts per million) you will help to maintain your pool’s pH balance.

But remember, these numbers can change quickly, especially after rain. So, make sure you keep an eye on your water balance. By maintaining balance and harmony in your pool water, you will increase the life of it and avoid major water issues.

References

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How do you calculate water balance?

How do you calculate water balance?/Water balance means the inflows to any water system or area are equal to its outflows plus the change in storage during a time interval. In hydrology, a water balance equation can be used to describe the flow of water in and out of a system. A system can be one of several hydrological or water domains, such as a column of soil, a drainage basin, an irrigation area or a city. Water balance can also refer to the ways in which an organism maintains water in dry or hot conditions. It is often discussed in reference to plants or arthropods, which have a variety of water retention mechanisms, including a lipid waxy coating that has limited permeability.

Regulation of Water Intake

Fluid can enter the body as preformed water, ingested food and drink, and, to a lesser extent, as metabolic water.

Key Points

A constant supply of water is needed to replenish the fluids lost through normal physiological activities, such as respiration, sweating, and urination.

Thirst is a sensation created by the hypothalamus that drives organisms to ingest water.

Increased osmolarity in the blood acts on osmoreceptors that either stimulate the hypothalamus directly or cause the release of angiotensin II to stimulate the hypothalamus to cause thirst.

The renin-angiotensin system increases thirst as a way to increase blood volume. It is activated by high plasma osmolarity, low blood volume, low blood pressure, and stimulation of the sympathetic nervous system.

Key Terms

  • thirst: The sensation that drives organisms to ingest water. It is considered a basic survival instinct.
  • osmoreceptors: Sensory receptors that are primarily found in the hypothalamus or macula densa that detect changes in the solute concentration of blood.

Water Intake

Fluid can enter the body as preformed water, ingested food and drink, and, to a lesser extent, as metabolic water that is produced as a by-product of aerobic respiration and dehydration synthesis. A constant supply is needed to replenish the fluids lost through normal physiological activities, such as respiration, sweating, and urination.

Water generated from the biochemical metabolism of nutrients provides a significant proportion of the daily water requirements for some arthropods and desert animals, but it provides only a small fraction of a human’s necessary intake. In the normal resting state, the input of water through ingested fluids is approximately 2500 ml/day.

Body water homeostasis is regulated mainly through ingested fluids, which, in turn, depends on thirst. Thirst is the basic instinct or urge that drives an organism to ingest water.

Thirst is a sensation created by the hypothalamus, the thirst center of the human body. Thirst is an important component of blood volume regulation, which is slowly regulated by homeostasis.

Hypothalamus-Mediated Thirst

An osmoreceptor is a sensory receptor that detects changes in osmotic pressure and is primarily found in the hypothalamus of most homeothermic organisms. Osmoreceptors detect changes in plasma osmolarity (that is, the concentration of solutes dissolved in the blood).

When the osmolarity of blood changes (it is more or less dilute), water diffusion into and out of the osmoreceptor cells changes. That is, the cells expand when the blood plasma is more dilute and contract with a higher concentration.

When the osmoreceptors detect high plasma osmolarity (often a sign of a low blood volume), they send signals to the hypothalamus, which creates the biological sensation of thirst. Osmoreceptors also stimulate vasopressin (ADH) secretion, which starts the events that will reduce plasma osmolality to normal levels.

The illustration shows the location of the hypothalamus in the brain. It is between the thalamus and the infundibulum. The anterior and posterior pituitary glands are seen under the infundibulum.

The hypothalamus: The hypothalamus is the thirst center of the human body.

Renin-Angiotensin System-Mediated Thirst

Another way through which thirst is induced is through angiotensin II, one of the hormones involved in the renin-angiotensin system. The renin-angiotensin system is a complex homeostatic pathway that deals with blood volume as a whole, as well as plasma osmolality and blood pressure.

The macula densa cells in the walls of the ascending loop of Henle of the nephron is another type of osmoreceptor; however, it stimulates the juxtaglomerular apparatus (JGA) instead of the hypothalamus. When the macula densa is stimulated by high osmolarity, The JGA releases renin into the bloodstream, which cleaves angiotensinogen into angiotensin I. Angiotensin I is converted into angiotensin II by ACE in the lungs. ACE is a hormone that has many functions.

Angiotensin II acts on the hypothalamus to cause the sensation of thirst. It also causes vasoconstriction, and the release of aldosterone to cause increased water reabsorption in a mechanism that is very similar to that of ADH.

Note that the renin-angiotensin system, and thus thirst, can be caused by other stimuli besides increased plasma osmolarity or a decrease in blood volume. For example, stimulation of the sympathetic nervous system and low blood pressure in the kidneys (decreased GFR) will stimulate the renin-angiotensin system and cause an increase in thirst.

Regulation of Water Output

Fluid can leave the body in three ways: urination, excretion (feces), and perspiration (sweating).

Key Points

The majority of fluid output occurs from urination. Some fluid is lost through perspiration (part of the body’s temperature control mechanism) and as water vapor in expired air.

The body’s homeostatic control mechanisms ensure that a balance between fluid gain and fluid loss is maintained. The hormones ADH (antidiuretic hormone, also known as vasopressin ) and aldosterone play a major role in this.

If the body is becoming fluid deficient, increased plasma osmolarity is sensed by the osmoreceptors. This results in an increase in the secretion of ADH that causes fluid to be retained by the kidneys and urine output to be reduced.

Aldosterone is the major end-product of the renin-angiotensin system and increases the expression of ATPase pumps in the nephron that causes an increase in water reabsorption through sodium cotransport.

ADH increases water reabsorption by increasing the nephron’s permeability to water, while aldosterone works by increasing the reabsorption of both sodium and water.

Key Terms

  • osmoreceptors: Sensory receptors, primarily found in the hypothalamus, that detect changes in plasma osmolarity and contribute to the fluid-balance regulation in the body.
  • anti-diuretic hormone: A neurohypophysial hormone found in most mammals that is responsible for increasing water absorption in the collecting ducts of the kidney nephrons.
  • aldosterone: A corticoid hormone that is secreted by the adrenal cortex that regulates the balance of sodium and potassium and thus the water-balance levels in the body.

Water Output

Fluid can leave the body in three ways:

  • Urination
  • Excretion (feces)
  • Perspiration (sweating)

The majority of fluid output occurs from urination, at approximately 1500 ml/day (approximately 1.59 qt/day) in a normal adult at resting state. Some fluid is lost through perspiration (part of the body’s temperature control mechanism) and as water vapor in expired air; however, these fluid losses are considered to be very minor.

The body’s homeostatic control mechanisms maintain a constant internal environment to ensure that a balance between fluid gain and fluid loss is maintained. The hormones ADH (anti-diuretic hormone, also known as vasopressin) and aldosterone, a hormone created by the renin-angiotensin system, play a major role in this balance.

If the body is becoming fluid deficient, there will be an increase in the secretion of these hormones that causes water to be retained by the kidneys through increased tubular reabsorption and urine output to be reduced. Conversely, if fluid levels are excessive, the secretion of these hormones is suppressed and results in less retention of fluid by the kidneys and a subsequent increase in the volume of urine produced, due to reduced fluid retention.

ADH Feedback

When blood volume becomes too low, plasma osmolarity will increase due to a higher concentration of solutes per volume of water. Osmoreceptors in the hypothalamus detect the increased plasma osmolarity and stimulate the posterior pituitary gland to secrete ADH.

ADH causes the walls of the distal convoluted tubule and collecting duct to become permeable to water—this drastically increases the amount of water that is reabsorbed during tubular reabsorption. ADH also has a vasoconstrictive effect in the cardiovascular system, which makes it one of the most important compensatory mechanisms during hypovolemic shock (shock from excessive fluid loss or bleeding).

Aldosterone Feedback

Aldosterone is a steroid hormone (corticoid) produced at the end of the renin-angiotensin system. To review the renin-angiotensin system, low blood volume activates the juxtaglomerular apparatus in a variety of ways to make it secrete renin. Renin cleaves angiotensin I from the liver-produced angiotensinogen. Angiotensin converting enzyme (ACE) in the lungs converts angiotensin I into angiotensin II. Angiotensin II has a variety of effects (such as increased thirst) but it also causes the release of aldosterone from the adrenal cortex.

Aldosterone has a number of effects that are involved in the regulation of water output. It acts on mineral corticoid receptors in the epithelial cells of the distal convoluted tubule and collecting duct to increase their expression of Na+/K+ ATPase pumps and to activate those pumps. This causes greatly increased reabsorption of sodium and water (which follows sodium osmotically by cotransport), while causing the secretion of potassium into the urine.

Aldosterone increases water reabsorption; however, it involves an exchange of sodium and potassium that ADH absorption regulation does not involve. Aldosterone will also cause a similar ion-balancing effect in the colon and salivary glands as well.

This is a diagram overview of the renin–angiotensin system that regulates blood pressure and plasma osmolarity. The hypothalamus of the brain releases a corticotropin-releasing hormone that makes the pituitary gland release ACTH to the liver which, in turn, releases angiotensinogen. Renin cleaves angiotensin I from the liver-produced angiotensinogen. Angiotensin converting enzyme (ACE) in the lungs converts angiotensin I into angiotensin II. Angiotensin II has a variety of effects (such as increasing thirst) but it also causes release of aldosterone from the adrenal cortex.

A schematic diagram of the renin-angiotensin system: Overview of the renin-angiotensin system that regulates blood pressure and plasma osmolality.

Nitrogenous Waste in Terrestrial Animals: The Urea Cycle

Water balance in a basin

A general water balance equation is:[rx]

P = R + ET + ΔS

where

P is precipitation is streamflow is evapotranspiration
ΔS is the change in storage (in soil or the bedrock/groundwater)

This equation uses the principles of conservation of mass in a closed system, whereby any water entering a system (via precipitation), must be transferred into either evaporation, transpiration, surface runoff (eventually reaching the channel and leaving in the form of river discharge), or stored in the ground. This equation requires the system to be closed, and where it isn’t (for example when surface runoff contributes to a different basin), this must be taken into account.

Extensive water balances are discussed in agricultural hydrology.

A water balance can be used to help manage water supply and predict where there may be water shortages. It is also used in irrigation, runoff assessment (e.g. through the RainOff model [rx]), flood control, and pollution control. Further, it is used in the design of subsurface drainage systems which may be horizontal (i.e. using pipes, tile drains, or ditches) or vertical (drainage by wells).[rx] To estimate the drainage requirement, the use of a hydrogeological water balance and a groundwater model (e.g. SahysMod[rx]) may be instrumental.

The water balance can be illustrated using a water balance graph which plots levels of precipitation and evapotranspiration often on a monthly scale.

Several monthly water balance models had been developed for several conditions and purposes. Monthly water balance models had been studied since the 1940s.[rx]

Water Balance of a System

“Making water available for its many uses and users requires tools and institutions to transform it from a natural resource to one providing services”.[rx] This means that there are two types of water systems: Water Resource System (WRS) and Water Use System (WUS).

A WRS, such as a river, an aquifer, or a lake, must obey water balance. For example, the volume of water that goes into an aquifer must be equal to the amount that leaves it plus its change in storage. Under various drivers, such as climate change, population increase, and bad management, water storage of many WRS is decreasing, say per decade. This means that the volume of water in a WRS decreased after a decade, i.e., the inflow was less than outflow during that time interval.[rx]

In general, a WUS is a water construct of a user, such as a city, an industry, an irrigation zone, or a region, and not a geographic area. The schematic of a WUS shows the inflows and the outflows. For a WUS, change in storage is negligible (relative to its inflow) under a proper time interval, hence water balance becomes inflow equal to outflow with nine Water Path Types (WPT):[rx]

A typical schematic of a Water Use System (WUS) with its fixed nine Water Path Types

{\displaystyle VA+OS+PP=ET+NR+RF+RP}

Of course, instead of a river, it could be an aquifer that supplies water to a WUS as the main source. Let us briefly examine an urban water supply on an annual basis as a simplified example. It has negligible ET and PP (WUS is a piped network), has some limited amount of water from groundwater (OS), has return flow to the main source (RF) after passing through a Wastewater Treatment Plant, and RP type has various Water Path Instances (WPI), such as leakage, and water is taken to irrigate green zones. Considering that the annual change in storage of an urban area is negligible, the water balance equation becomes

{\displaystyle VA_{riv}+OS_{gw}=NR+RF_{wwtp}+RP_{leak}+RP_{irr}}

Urea, a nitrogenous waste material, is the end product excreted in urine when ammonia is metabolized by animals, such as mammals.

Key Points

Ureotelic animals, which includes mammals, produce urea as the main nitrogenous waste material.

2 NH+ CO2 + 3 ATP + H2O → H2N-CO-NH2 + 2 ADP + 4 Pi + AMP is the chemical reaction by which toxic ammonia is converted to urea.

The urea cycle involves the multi-step conversion (carried out by five different enzymes ) of the amino acid L- ornithine into different intermediates before being regenerated.

Key Terms

  • ureotelic: animals that secrete urea as the primary nitrogenous waste material
  • ornithine: an amino acid, which acts as an intermediate in the biosynthesis of urea
  • urea: a water-soluble organic compound, CO(NH2)2, formed by the metabolism of proteins and excreted in the urine

Nitrogenous Waste in Terrestrial Animals: The Urea Cycle

Mammals, including humans, are the primary producers of urea. Because they secrete urea as the primary nitrogenous waste product, they are called ureotelic animals. Urea serves an important role in the metabolism of nitrogen-containing compounds by animals. It is the main nitrogen-containing substance in the urine of mammals. Urea is a colorless, odorless solid, highly soluble in water, and practically non-toxic. Dissolved in water, it is neither acidic nor alkaline. The body uses it in many processes, the most notable one being nitrogen excretion. Urea is widely used in fertilizers as a convenient source of nitrogen. It is also an important raw material for the chemical industry.

Apart from mammals, urea is also found in the urine of amphibians, as well as some fish. Interestingly, tadpoles excrete ammonia but shift to urea production during metamorphosis. In humans, apart from being a carrier of waste nitrogen, urea also plays a role in the countercurrent exchange system of the nephrons, which allows for the re-absorption of water and critical ions from the excreted urine. This mechanism, controlled by an antidiuretic hormone, allows the body to create hyperosmotic urine, which has a higher concentration of dissolved substances than the blood plasma. This mechanism is important to prevent the loss of water, maintain blood pressure, and maintain a suitable concentration of sodium ions in the blood plasmas.

The urea cycle is the primary mechanism by which mammals convert ammonia to urea. Urea is made in the liver and excreted in the urine. The overall chemical reaction by which ammonia is converted to urea is 2 NH3 (ammonia) + CO2 + 3 ATP + H2O → H2N-CO-NH2 (urea) + 2 ADP + 4 Pi + AMP.

The urea cycle utilizes five intermediate steps, catalyzed by five different enzymes, to convert ammonia to urea. The amino acid L-ornithine is converted into different intermediates before being regenerated at the end of the urea cycle. Hence, the urea cycle is also referred to as the ornithine cycle. The enzyme ornithine transcarbamylase catalyzes a key step in the urea cycle. Its deficiency can lead to the accumulation of toxic levels of ammonia in the body. The first two reactions occur in the mitochondria, while the last three reactions occur in the cytosol.

image

Urea Cycle: The urea cycle converts ammonia to urea in five steps that include the catalyzation of five different enzymes.

Water Balance Disorders

Dehydration is the excessive loss of body fluid.

Key Points

There are three types of dehydration: hypotonic or hyponatremic, hypertonic or hypernatremic, and isotonic or hyponatremic.

Hypotonic dehydration is primarily a loss of electrolytes, sodium in particular.

Hypertonic dehydration is primarily a loss of water.

Isotonic dehydration is an equal loss of water and electrolytes.

Hypovolemia is a loss of blood volume and may cause hypovolemic shock. In humans, the most common type of dehydration by far is isotonic (isonatraemic) dehydration.

Water balance disorders are generally treated by increasing water intake and reducing or stopping fluid loss.

Key Terms

  • isotonic: When comparing solutions, an isotonic solution has the same osmolarity (ion concentration) as the solution it is being compared to.
  • plasma: The straw-colored/pale-yellow, liquid component of blood that normally holds the blood cells of whole blood in suspension.
  • electrolyte: Any of the various ions (such as sodium or chloride) that regulate the electric charge on cells and the flow of water across their membranes.

Water Balance Disorders

In physiology and medicine, dehydration (hypohydration) is defined as the excessive loss of body fluid. It is literally the removal of water from an object. However, in physiological terms, it entails a deficiency of fluid within an organism.

Much of the physiological effects of dehydration is due to the changes in ion concentration that may occur as a result of the dehydration. Alternatively, hypovolemia may occur due to loss of blood volume itself.

Dehydration

There are three types of dehydration that differ based on the type of change in ion concentrations:

  • Hypotonic – primarily a loss of electrolytes, sodium in particular. Hypotonic dehydration causes decreased plasma osmolality.
  • Hypertonic – primarily a loss of water. Hypertonic dehydration causes increased plasma osmolality.
  • Isotonic – an equal loss of water and electrolytes. Isotonic dehydration will not change plasma osmolarity, but it will reduce overall plasma volume. Isotonic dehydration is the most common type of dehydration.

Further complications may also occur. In hypotonic dehydration, intravascular water shifts to the extravascular space and exaggerates intravascular volume depletion for a given amount of total body water loss.

Neurological complications can occur in hypotonic and hypertonic states. The former can lead to seizures, while the latter can lead to osmotic cerebral edema upon rapid rehydration.

Hypovolemia

Hypovolemia is specifically a decrease in the volume of blood plasma. Furthermore, hypovolemia defines water deficiency in terms of blood volume rather than the overall water content of the body.

This is a color photograph of IV fluid and electrolyte administration. Intravenous administration of fluid is one effective treatment of dehydration in humans.

IV fluid and electrolyte administration: Intravenous administration of fluid is one effective treatment of dehydration in humans.

Hypovolemia is a cause of hypovolemic shock. Shock is any condition in which the body’s fluids are unable to properly circulate and oxygenate the major organs of the human body; this causes compensatory mechanisms to activate that cause further bodily harm as the body’s metabolism is maintained for a while longer.

In the case of hypovolemic shock, the tissue metabolism is impaired due to a lack of blood volume and makes it difficult for red blood cells to reach all of the tissues of the body. It is most often caused by severe vomiting, diarrhea, blood loss, or hemorrhage. Other forms of shock with similar symptoms may be due to problems in the heart (cardiogenic) or bacterial infection (septic).

Treatment Options

To treat minor dehydration water intake must be increased, while the source of fluid loss must be reduced or stopped altogether. Plain water restores only the volume of the blood plasma and inhibits the thirst mechanism before solute levels can be replenished.

Solid foods can contribute to fluid loss from vomiting and diarrhea. In more severe cases, correction of a dehydrated state is accomplished by the replenishment of necessary water and electrolytes through oral rehydration therapy or fluid replacement by intravenous therapy (an IV drip).

As oral rehydration is easier to provide, it is the treatment of choice for mild dehydration. Solutions used for intravenous rehydration must be isotonic or hypotonic. Pure water injected into the veins will cause the breakdown (lysis) of red blood cells that could cause other problems.

References

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Water Balance – Procedure, Mechanism, Functions

Water balance means the inflows to any water system or area are equal to its outflows plus the change in storage during a time interval. In hydrology, a water balance equation can be used to describe the flow of water in and out of a system. A system can be one of several hydrological or water domains, such as a column of soil, a drainage basin, an irrigation area or a city. Water balance can also refer to the ways in which an organism maintains water in dry or hot conditions. It is often discussed in reference to plants or arthropods, which have a variety of water retention mechanisms, including a lipid waxy coating that has limited permeability.

Regulation of Water Intake

Fluid can enter the body as preformed water, ingested food and drink, and, to a lesser extent, as metabolic water.

Key Points

A constant supply of water is needed to replenish the fluids lost through normal physiological activities, such as respiration, sweating, and urination.

Thirst is a sensation created by the hypothalamus that drives organisms to ingest water.

Increased osmolarity in the blood acts on osmoreceptors that either stimulate the hypothalamus directly or cause the release of angiotensin II to stimulate the hypothalamus to cause thirst.

The renin-angiotensin system increases thirst as a way to increase blood volume. It is activated by high plasma osmolarity, low blood volume, low blood pressure, and stimulation of the sympathetic nervous system.

Key Terms

  • thirst: The sensation that drives organisms to ingest water. It is considered a basic survival instinct.
  • osmoreceptors: Sensory receptors that are primarily found in the hypothalamus or macula densa that detect changes in the solute concentration of blood.

Water Intake

Fluid can enter the body as preformed water, ingested food and drink, and, to a lesser extent, as metabolic water that is produced as a by-product of aerobic respiration and dehydration synthesis. A constant supply is needed to replenish the fluids lost through normal physiological activities, such as respiration, sweating, and urination.

Water generated from the biochemical metabolism of nutrients provides a significant proportion of the daily water requirements for some arthropods and desert animals, but it provides only a small fraction of a human’s necessary intake. In the normal resting state, the input of water through ingested fluids is approximately 2500 ml/day.

Body water homeostasis is regulated mainly through ingested fluids, which, in turn, depends on thirst. Thirst is the basic instinct or urge that drives an organism to ingest water.

Thirst is a sensation created by the hypothalamus, the thirst center of the human body. Thirst is an important component of blood volume regulation, which is slowly regulated by homeostasis.

Hypothalamus-Mediated Thirst

An osmoreceptor is a sensory receptor that detects changes in osmotic pressure and is primarily found in the hypothalamus of most homeothermic organisms. Osmoreceptors detect changes in plasma osmolarity (that is, the concentration of solutes dissolved in the blood).

When the osmolarity of blood changes (it is more or less dilute), water diffusion into and out of the osmoreceptor cells changes. That is, the cells expand when the blood plasma is more dilute and contract with a higher concentration.

When the osmoreceptors detect high plasma osmolarity (often a sign of a low blood volume), they send signals to the hypothalamus, which creates the biological sensation of thirst. Osmoreceptors also stimulate vasopressin (ADH) secretion, which starts the events that will reduce plasma osmolality to normal levels.

The illustration shows the location of the hypothalamus in the brain. It is between the thalamus and the infundibulum. The anterior and posterior pituitary glands are seen under the infundibulum. 

The hypothalamus: The hypothalamus is the thirst center of the human body.

Renin-Angiotensin System-Mediated Thirst

Another way through which thirst is induced is through angiotensin II, one of the hormones involved in the renin-angiotensin system. The renin-angiotensin system is a complex homeostatic pathway that deals with blood volume as a whole, as well as plasma osmolality and blood pressure.

The macula densa cells in the walls of the ascending loop of Henle of the nephron is another type of osmoreceptor; however, it stimulates the juxtaglomerular apparatus (JGA) instead of the hypothalamus. When the macula densa is stimulated by high osmolarity, The JGA releases renin into the bloodstream, which cleaves angiotensinogen into angiotensin I. Angiotensin I is converted into angiotensin II by ACE in the lungs. ACE is a hormone that has many functions.

Angiotensin II acts on the hypothalamus to cause the sensation of thirst. It also causes vasoconstriction, and the release of aldosterone to cause increased water reabsorption in a mechanism that is very similar to that of ADH.

Note that the renin-angiotensin system, and thus thirst, can be caused by other stimuli besides increased plasma osmolarity or a decrease in blood volume. For example, stimulation of the sympathetic nervous system and low blood pressure in the kidneys (decreased GFR) will stimulate the renin-angiotensin system and cause an increase in thirst.

Regulation of Water Output

Fluid can leave the body in three ways: urination, excretion (feces), and perspiration (sweating).

Key Points

The majority of fluid output occurs from urination. Some fluid is lost through perspiration (part of the body’s temperature control mechanism) and as water vapor in expired air.

The body’s homeostatic control mechanisms ensure that a balance between fluid gain and fluid loss is maintained. The hormones ADH (antidiuretic hormone, also known as vasopressin ) and aldosterone play a major role in this.

If the body is becoming fluid deficient, increased plasma osmolarity is sensed by the osmoreceptors. This results in an increase in the secretion of ADH that causes fluid to be retained by the kidneys and urine output to be reduced.

Aldosterone is the major end-product of the renin-angiotensin system and increases the expression of ATPase pumps in the nephron that causes an increase in water reabsorption through sodium cotransport.

ADH increases water reabsorption by increasing the nephron’s permeability to water, while aldosterone works by increasing the reabsorption of both sodium and water.

Key Terms

  • osmoreceptors: Sensory receptors, primarily found in the hypothalamus, that detect changes in plasma osmolarity and contribute to the fluid-balance regulation in the body.
  • anti-diuretic hormone: A neurohypophysial hormone found in most mammals that is responsible for increasing water absorption in the collecting ducts of the kidney nephrons.
  • aldosterone: A corticoid hormone that is secreted by the adrenal cortex that regulates the balance of sodium and potassium and thus the water-balance levels in the body.

Water Output

Fluid can leave the body in three ways:

  • Urination
  • Excretion (feces)
  • Perspiration (sweating)

The majority of fluid output occurs from urination, at approximately 1500 ml/day (approximately 1.59 qt/day) in a normal adult at resting state. Some fluid is lost through perspiration (part of the body’s temperature control mechanism) and as water vapor in expired air; however, these fluid losses are considered to be very minor.

The body’s homeostatic control mechanisms maintain a constant internal environment to ensure that a balance between fluid gain and fluid loss is maintained. The hormones ADH (anti-diuretic hormone, also known as vasopressin) and aldosterone, a hormone created by the renin-angiotensin system, play a major role in this balance.

If the body is becoming fluid deficient, there will be an increase in the secretion of these hormones that causes water to be retained by the kidneys through increased tubular reabsorption and urine output to be reduced. Conversely, if fluid levels are excessive, the secretion of these hormones is suppressed and results in less retention of fluid by the kidneys and a subsequent increase in the volume of urine produced, due to reduced fluid retention.

ADH Feedback

When blood volume becomes too low, plasma osmolarity will increase due to a higher concentration of solutes per volume of water. Osmoreceptors in the hypothalamus detect the increased plasma osmolarity and stimulate the posterior pituitary gland to secrete ADH.

ADH causes the walls of the distal convoluted tubule and collecting duct to become permeable to water—this drastically increases the amount of water that is reabsorbed during tubular reabsorption. ADH also has a vasoconstrictive effect in the cardiovascular system, which makes it one of the most important compensatory mechanisms during hypovolemic shock (shock from excessive fluid loss or bleeding).

Aldosterone Feedback

Aldosterone is a steroid hormone (corticoid) produced at the end of the renin-angiotensin system. To review the renin-angiotensin system, low blood volume activates the juxtaglomerular apparatus in a variety of ways to make it secrete renin. Renin cleaves angiotensin I from the liver-produced angiotensinogen. Angiotensin converting enzyme (ACE) in the lungs converts angiotensin I into angiotensin II. Angiotensin II has a variety of effects (such as increased thirst) but it also causes the release of aldosterone from the adrenal cortex.

Aldosterone has a number of effects that are involved in the regulation of water output. It acts on mineral corticoid receptors in the epithelial cells of the distal convoluted tubule and collecting duct to increase their expression of Na+/K+ ATPase pumps and to activate those pumps. This causes greatly increased reabsorption of sodium and water (which follows sodium osmotically by cotransport), while causing the secretion of potassium into the urine.

Aldosterone increases water reabsorption; however, it involves an exchange of sodium and potassium that ADH absorption regulation does not involve. Aldosterone will also cause a similar ion-balancing effect in the colon and salivary glands as well.

This is a diagram overview of the renin–angiotensin system that regulates blood pressure and plasma osmolarity. The hypothalamus of the brain releases a corticotropin-releasing hormone that makes the pituitary gland release ACTH to the liver which, in turn, releases angiotensinogen. Renin cleaves angiotensin I from the liver-produced angiotensinogen. Angiotensin converting enzyme (ACE) in the lungs converts angiotensin I into angiotensin II. Angiotensin II has a variety of effects (such as increasing thirst) but it also causes release of aldosterone from the adrenal cortex.

A schematic diagram of the renin-angiotensin system: Overview of the renin-angiotensin system that regulates blood pressure and plasma osmolality.

Nitrogenous Waste in Terrestrial Animals: The Urea Cycle

Water balance in a basin

A general water balance equation is:[rx]

P = R + ET + ΔS

where

P is precipitation is streamflow is evapotranspiration
ΔS is the change in storage (in soil or the bedrock/groundwater)

This equation uses the principles of conservation of mass in a closed system, whereby any water entering a system (via precipitation), must be transferred into either evaporation, transpiration, surface runoff (eventually reaching the channel and leaving in the form of river discharge), or stored in the ground. This equation requires the system to be closed, and where it isn’t (for example when surface runoff contributes to a different basin), this must be taken into account.

Extensive water balances are discussed in agricultural hydrology.

A water balance can be used to help manage water supply and predict where there may be water shortages. It is also used in irrigation, runoff assessment (e.g. through the RainOff model [rx]), flood control, and pollution control. Further, it is used in the design of subsurface drainage systems which may be horizontal (i.e. using pipes, tile drains, or ditches) or vertical (drainage by wells).[rx] To estimate the drainage requirement, the use of a hydrogeological water balance and a groundwater model (e.g. SahysMod[rx]) may be instrumental.

The water balance can be illustrated using a water balance graph which plots levels of precipitation and evapotranspiration often on a monthly scale.

Several monthly water balance models had been developed for several conditions and purposes. Monthly water balance models had been studied since the 1940s.[rx]

Water Balance of a System

“Making water available for its many uses and users requires tools and institutions to transform it from a natural resource to one providing services”.[rx] This means that there are two types of water systems: Water Resource System (WRS) and Water Use System (WUS).

A WRS, such as a river, an aquifer, or a lake, must obey water balance. For example, the volume of water that goes into an aquifer must be equal to the amount that leaves it plus its change in storage. Under various drivers, such as climate change, population increase, and bad management, water storage of many WRS is decreasing, say per decade. This means that the volume of water in a WRS decreased after a decade, i.e., the inflow was less than outflow during that time interval.[rx]

In general, a WUS is a water construct of a user, such as a city, an industry, an irrigation zone, or a region, and not a geographic area. The schematic of a WUS shows the inflows and the outflows. For a WUS, change in storage is negligible (relative to its inflow) under a proper time interval, hence water balance becomes inflow equal to outflow with nine Water Path Types (WPT):[rx]

A typical schematic of a Water Use System (WUS) with its fixed nine Water Path Types

{\displaystyle VA+OS+PP=ET+NR+RF+RP}

Of course, instead of a river, it could be an aquifer that supplies water to a WUS as the main source. Let us briefly examine an urban water supply on an annual basis as a simplified example. It has negligible ET and PP (WUS is a piped network), has some limited amount of water from groundwater (OS), has return flow to the main source (RF) after passing through a Wastewater Treatment Plant, and RP type has various Water Path Instances (WPI), such as leakage, and water is taken to irrigate green zones. Considering that the annual change in storage of an urban area is negligible, the water balance equation becomes

{\displaystyle VA_{riv}+OS_{gw}=NR+RF_{wwtp}+RP_{leak}+RP_{irr}}

Urea, a nitrogenous waste material, is the end product excreted in urine when ammonia is metabolized by animals, such as mammals.

Key Points

Ureotelic animals, which includes mammals, produce urea as the main nitrogenous waste material.

2 NH+ CO2 + 3 ATP + H2O → H2N-CO-NH2 + 2 ADP + 4 Pi + AMP is the chemical reaction by which toxic ammonia is converted to urea.

The urea cycle involves the multi-step conversion (carried out by five different enzymes ) of the amino acid L- ornithine into different intermediates before being regenerated.

Key Terms

  • ureotelic: animals that secrete urea as the primary nitrogenous waste material
  • ornithine: an amino acid, which acts as an intermediate in the biosynthesis of urea
  • urea: a water-soluble organic compound, CO(NH2)2, formed by the metabolism of proteins and excreted in the urine

Nitrogenous Waste in Terrestrial Animals: The Urea Cycle

Mammals, including humans, are the primary producers of urea. Because they secrete urea as the primary nitrogenous waste product, they are called ureotelic animals. Urea serves an important role in the metabolism of nitrogen-containing compounds by animals. It is the main nitrogen-containing substance in the urine of mammals. Urea is a colorless, odorless solid, highly soluble in water, and practically non-toxic. Dissolved in water, it is neither acidic nor alkaline. The body uses it in many processes, the most notable one being nitrogen excretion. Urea is widely used in fertilizers as a convenient source of nitrogen. It is also an important raw material for the chemical industry.

Apart from mammals, urea is also found in the urine of amphibians, as well as some fish. Interestingly, tadpoles excrete ammonia but shift to urea production during metamorphosis. In humans, apart from being a carrier of waste nitrogen, urea also plays a role in the countercurrent exchange system of the nephrons, which allows for the re-absorption of water and critical ions from the excreted urine. This mechanism, controlled by an antidiuretic hormone, allows the body to create hyperosmotic urine, which has a higher concentration of dissolved substances than the blood plasma. This mechanism is important to prevent the loss of water, maintain blood pressure, and maintain a suitable concentration of sodium ions in the blood plasmas.

The urea cycle is the primary mechanism by which mammals convert ammonia to urea. Urea is made in the liver and excreted in the urine. The overall chemical reaction by which ammonia is converted to urea is 2 NH3 (ammonia) + CO2 + 3 ATP + H2O → H2N-CO-NH2 (urea) + 2 ADP + 4 Pi + AMP.

The urea cycle utilizes five intermediate steps, catalyzed by five different enzymes, to convert ammonia to urea. The amino acid L-ornithine is converted into different intermediates before being regenerated at the end of the urea cycle. Hence, the urea cycle is also referred to as the ornithine cycle. The enzyme ornithine transcarbamylase catalyzes a key step in the urea cycle. Its deficiency can lead to the accumulation of toxic levels of ammonia in the body. The first two reactions occur in the mitochondria, while the last three reactions occur in the cytosol.

image 

Urea Cycle: The urea cycle converts ammonia to urea in five steps that include the catalyzation of five different enzymes.

Water Balance Disorders

Dehydration is the excessive loss of body fluid.

Key Points

There are three types of dehydration: hypotonic or hyponatremic, hypertonic or hypernatremic, and isotonic or hyponatremic.

Hypotonic dehydration is primarily a loss of electrolytes, sodium in particular.

Hypertonic dehydration is primarily a loss of water.

Isotonic dehydration is an equal loss of water and electrolytes.

Hypovolemia is a loss of blood volume and may cause hypovolemic shock. In humans, the most common type of dehydration by far is isotonic (isonatraemic) dehydration.

Water balance disorders are generally treated by increasing water intake and reducing or stopping fluid loss.

Key Terms

  • isotonic: When comparing solutions, an isotonic solution has the same osmolarity (ion concentration) as the solution it is being compared to.
  • plasma: The straw-colored/pale-yellow, liquid component of blood that normally holds the blood cells of whole blood in suspension.
  • electrolyte: Any of the various ions (such as sodium or chloride) that regulate the electric charge on cells and the flow of water across their membranes.

Water Balance Disorders

In physiology and medicine, dehydration (hypohydration) is defined as the excessive loss of body fluid. It is literally the removal of water from an object. However, in physiological terms, it entails a deficiency of fluid within an organism.

Much of the physiological effects of dehydration is due to the changes in ion concentration that may occur as a result of the dehydration. Alternatively, hypovolemia may occur due to loss of blood volume itself.

Dehydration

There are three types of dehydration that differ based on the type of change in ion concentrations:

  • Hypotonic – primarily a loss of electrolytes, sodium in particular. Hypotonic dehydration causes decreased plasma osmolality.
  • Hypertonic – primarily a loss of water. Hypertonic dehydration causes increased plasma osmolality.
  • Isotonic – an equal loss of water and electrolytes. Isotonic dehydration will not change plasma osmolarity, but it will reduce overall plasma volume. Isotonic dehydration is the most common type of dehydration.

Further complications may also occur. In hypotonic dehydration, intravascular water shifts to the extravascular space and exaggerates intravascular volume depletion for a given amount of total body water loss.

Neurological complications can occur in hypotonic and hypertonic states. The former can lead to seizures, while the latter can lead to osmotic cerebral edema upon rapid rehydration.

Hypovolemia

Hypovolemia is specifically a decrease in the volume of blood plasma. Furthermore, hypovolemia defines water deficiency in terms of blood volume rather than the overall water content of the body.

This is a color photograph of IV fluid and electrolyte administration. Intravenous administration of fluid is one effective treatment of dehydration in humans.

IV fluid and electrolyte administration: Intravenous administration of fluid is one effective treatment of dehydration in humans.

Hypovolemia is a cause of hypovolemic shock. Shock is any condition in which the body’s fluids are unable to properly circulate and oxygenate the major organs of the human body; this causes compensatory mechanisms to activate that cause further bodily harm as the body’s metabolism is maintained for a while longer.

In the case of hypovolemic shock, the tissue metabolism is impaired due to a lack of blood volume and makes it difficult for red blood cells to reach all of the tissues of the body. It is most often caused by severe vomiting, diarrhea, blood loss, or hemorrhage. Other forms of shock with similar symptoms may be due to problems in the heart (cardiogenic) or bacterial infection (septic).

Treatment Options

To treat minor dehydration water intake must be increased, while the source of fluid loss must be reduced or stopped altogether. Plain water restores only the volume of the blood plasma and inhibits the thirst mechanism before solute levels can be replenished.

Solid foods can contribute to fluid loss from vomiting and diarrhea. In more severe cases, correction of a dehydrated state is accomplished by the replenishment of necessary water and electrolytes through oral rehydration therapy or fluid replacement by intravenous therapy (an IV drip).

As oral rehydration is easier to provide, it is the treatment of choice for mild dehydration. Solutions used for intravenous rehydration must be isotonic or hypotonic. Pure water injected into the veins will cause the breakdown (lysis) of red blood cells that could cause other problems.

References

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Hormonal Responses To Food – All About You Need To Know

Hormonal responses to food (cephalic responses) are proactive physiological processes, that allow animals to prepare for food ingestion by modulating their hormonal levels in response to food cues. This process is important for digesting food, metabolizing nutrients, and maintaining glucose levels within homeostasis. In this systematic review, we summarize the evidence from animal and human research on cephalic responses. Thirty-six animal and fifty-three human studies were included. The majority (88 %) of studies demonstrated that hormonal levels are changed in response to cues previously associated with food intakes, such as feeding time, smell, and sight of food. Most evidence comes from studies on insulin, ghrelin, pancreatic polypeptide, glucagon, and c-peptide. Moreover, impaired cephalic responses were found in disorders related to metabolism and food intakes such as diabetes, pancreatic insufficiency, obesity, and eating disorders, which opens discussions about the etiological mechanisms of these disorders as well as on potential therapeutic opportunities.

Hormonal Responses to Food

The endocrine system controls the release of hormones responsible for starting, stopping, slowing, and quickening digestive processes.

Key Points

The presence and absence of hormones that are released into the bloodstream generate specific digestive responses; they either stimulate or discontinue digestive processes.

In hormone control, a negative feedback mechanism takes place when the stomach is empty and its acidic environment does not need to be maintained; as a result, a hormone is released to stop the release of hydrochloric acid, which was previously activated to aid digestion.

In some cases, hormones work in tandem and sequentially to achieve important digestive functions, such as in the breakdown of acidic chyme, where hormones act in releasing the appropriate secretions in the appropriate stages of digestion.

When digesting certain types of foods, such as ones high in fat, hormones can control the speed of food digestion and, therefore, absorption.

Key Terms

  • endocrine system: a control system of ductless glands that secrete hormones that circulate via the bloodstream to affect cells within specific organs
  • chyme: the thick semifluid mass of partly digested food that is passed from the stomach to the duodenum
  • secretin: a peptide hormone, secreted by the duodenum, that serves to regulate its acidity
  • cholecystokinin: any of several peptide hormones that stimulate the digestion of fat and protein
  • somatostatin: a polypeptide hormone, secreted by the pancreas, that inhibits the production of certain other hormones
  • gastrin: a hormone that stimulates the production of gastric acid in the stomach

Hormonal Responses to Food

The endocrine system controls the response of the various glands in the body and the release of hormones at the appropriate times. The endocrine system’s effects are slow to initiate but prolonged in their response, lasting from a few hours up to weeks. The system is made of a series of glands that produce chemicals called hormones. These hormones are chemical mediators released from endocrine tissue into the bloodstream where they travel to the target tissue and generate a response.

One of the important factors under hormonal control is the stomach acid environment. During the gastric phase, the hormone gastrin is secreted by G cells in the stomach in response to the presence of proteins. Gastrin stimulates the release of stomach acid, or hydrochloric acid (HCl), which aids in the digestion of the majority of proteins. However, when the stomach is emptied, the acidic environment need not be maintained and a hormone called somatostatin stops the release of hydrochloric acid. This is controlled by a negative feedback mechanism.

In the duodenum, digestive secretions from the liver, pancreas, and gallbladder play an important role in digesting chyme during the intestinal phase. In order to neutralize the acidic chyme, a hormone called secretin stimulates the pancreas to produce an alkaline bicarbonate solution and deliver it to the duodenum. Secretin acts in tandem with another hormone called cholecystokinin (CCK). Not only does CCK stimulate the pancreas to produce the requisite pancreatic juices, it also stimulates the gallbladder to release bile into the duodenum.

Digestive endocrine system: Hormones, such as secretin and cholecystokinin, play important roles in digestive processes. These hormones are released from endocrine tissue to generate specific controls in the digestion of chyme. As seen in the image, hormones are vital players in several bodily functions and processes.

Another level of hormonal control occurs in response to the composition of food. Foods high in lipids (fatty foods) take a long time to digest. A hormone called gastric inhibitory peptide is secreted by the small intestine to slow down the peristaltic movements of the intestine to allow fatty foods more time to be digested and absorbed.

Understanding the hormonal control of the digestive system is an important area of ongoing research. Scientists are exploring the role of each hormone in the digestive process and developing ways to target these hormones. Advances could lead to knowledge that may help to battle the obesity epidemic.

Neural Responses to Food

All three phases of digestive responses to food (the cephalic, gastric, and intestinal stages) are managed through enzymatic neural control.

Key Points

The cephalic phase is controlled by sight, sense, and smell, which trigger neural responses, including salivation and hydrochloric acid production, before food has even reached the mouth.

Once food reaches the stomach, gastric acids and enzymes process the ingested materials in the gastric phase, which involves local, hormonal, and neural responses.

The intestinal phase controls the rate of gastric emptying and the release of hormones needed to digest chyme in the small intestine.

Key Terms

  • neural: of, or relating to the nerves, neurons or the nervous system
  • salivary gland: any of several exocrine glands that produce saliva to break down carbohydrates in food enzymatically
  • peristaltic: of, or pertaining to the rhythmic, wave-like contraction of the digestive tract that forces food through it

Neural Responses to Food

In reaction to the smell, sight, or thought of food, the first hormonal response is that of salivation. The salivary glands secrete more saliva in response to the stimulus presented by food in preparation for digestion. Simultaneously, the stomach begins to produce hydrochloric acid to digest the food. Recall that the peristaltic movements of the esophagus and other organs of the digestive tract are under the control of the brain. The brain prepares these muscles for movement as well. When the stomach is full, the part of the brain that detects satiety signals fullness. There are three overlapping phases of gastric control: the cephalic phase, the gastric phase, and the intestinal phase. Each requires many enzymes and is under neural control as well.

image 

Salivation: Seeing a plate of food triggers the secretion of saliva in the mouth and the production of hydrochloric acid in the stomach.

Digestive Phases

The response to food begins even before food enters the mouth. The first phase of ingestion, called the cephalic phase, is controlled by the neural response to the stimulus provided by food. All aspects, such as sight, sense, and smell, trigger the neural responses resulting in salivation and secretion of gastric juices. The gastric and salivary secretion in the cephalic phase can also take place at the thought of food. Right now, if you think about a piece of chocolate or a crispy potato chip, the increase in salivation is a cephalic phase response to the thought. The central nervous system prepares the stomach to receive food.

The gastric phase begins once the food arrives in the stomach. It builds on the stimulation provided during the cephalic phase. Gastric acids and enzymes process the ingested materials. The gastric phase is stimulated by (1) distension of the stomach, (2) a decrease in the pH of the gastric contents, and (3) the presence of undigested material. This phase consists of local, hormonal, and neural responses. These responses stimulate secretions and powerful contractions.

The intestinal phase begins when chyme enters the small intestine, triggering digestive secretions. This phase controls the rate of gastric emptying. In addition to gastric emptying, when chyme enters the small intestine, it triggers other hormonal and neural events that coordinate the activities of the intestinal tract, pancreas, liver, and gallbladder.

Food Energy and ATP

Animals use energy for metabolism, obtaining that energy from the breakdown of food through the process of cellular respiration.

Key Points

Animals obtain energy from the food they consume, using that energy to maintain body temperature and perform other metabolic functions.

Glucose, found in the food animals eat, is broken down during the process of cellular respiration into an energy source called ATP.

When excess ATP and glucose are present, the liver converts them into a molecule called glycogen, which is stored for later use.

Key Terms

  • glucose: a simple monosaccharide (sugar) with a molecular formula of C6H12O6; it is a principal source of energy for cellular metabolism
  • adenosine triphosphate: a multifunctional nucleoside triphosphate used in cells as a coenzyme, often called the “molecular unit of energy currency” in intracellular energy transfer
  • phosphodiester: any of many biologically active compounds in which two alcohols form ester bonds with phosphate

Food Energy and ATP

Animals need food to obtain energy and maintain homeostasis. Homeostasis is the ability of a system to maintain a stable internal environment even in the face of external changes to the environment. For example, the normal body temperature of humans is 37°C (98.6°F). Humans maintain this temperature even when the external temperature is hot or cold. The energy it takes to maintain this body temperature is obtained from food.

The primary source of energy for animals is carbohydrates, primarily glucose: the body’s fuel. The digestible carbohydrates in an animal’s diet are converted to glucose molecules and into energy through a series of catabolic chemical reactions.

Adenosine triphosphate, or ATP, is the primary energy currency in cells. ATP stores energy in phosphate ester bonds, releasing energy when the phosphodiester bonds are broken: ATP is converted to ADP and a phosphate group. ATP is produced by the oxidative reactions in the cytoplasm and mitochondrion of the cell, where carbohydrates, proteins, and fats undergo a series of metabolic reactions collectively called cellular respiration.

image 

ATP production pathways: ATP is the energy molecule of the cell. It is produced through various pathways during the cellular respiration process, with each making different amounts of energy.

ATP is required for all cellular functions. It is used to build the organic molecules that are required for cells and tissues. It also provides energy for muscle contraction and for the transmission of electrical signals in the nervous system. When the amount of ATP available is in excess of the body’s requirements, the liver uses the excess ATP and excess glucose to produce molecules called glycogen (a polymeric form of glucose) that is stored in the liver and skeletal muscle cells. When blood sugar drops, the liver releases glucose from stores of glycogen. Skeletal muscle converts glycogen to glucose during intense exercise. The process of converting glucose and excess ATP to glycogen and the storage of excess energy is an evolutionarily important step in helping animals deal with mobility, food shortages, and famine.

References

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Temperature Regulation – Mechanism, Types, Functions

Temperature Regulation/Thermoregulation is a mechanism by which mammals maintain body temperature with tightly controlled self-regulation independent of external temperatures. Temperature regulation is a type of homeostasis and a means of preserving a stable internal temperature in order to survive. Ectotherms are animals that depend on their external environment for body heat, while endotherms are animals that use thermoregulation to maintain a somewhat consistent internal body temperature even when their external environment changes. Humans and other mammals and birds are endotherms. Human beings have a normal core internal temperature of around 37 degrees Celsius (98.6 degrees Fahrenheit) measured most accurately via a rectal probe thermometer. This is the optimal temperature at which the human body’s systems function. Thermoregulation is crucial to human life; without thermoregulation, the human body would cease to function. Thermoregulation also plays an adaptive role in the body’s response to infectious pathogens. 

Mechanism

Thermoregulation has three mechanisms: afferent sensing, central control, and efferent responses. There are receptors for both heat and cold throughout the human body. Afferent sensing works through these receptors to determine if the body core temperature is too hold or cold. The hypothalamus is the central controller of thermoregulation. There is also an efferent behavioral component that responds to fluctuations in body temperature. For example, if a person is feeling too warm, the normal response is to remove an outer article of clothing. If a person is feeling too cold, they choose to wear more layers of clothing. Efferent responses also consist of automatic responses by the body to protect itself from extreme changes in temperature, such as sweating, vasodilation, vasoconstriction, and shivering.

Pathophysiology

When external environments are exceedingly warm, or a person is engaging in strenuous physical activity, the heat that is produced inside his or her body is typically transported to the blood. The blood then carries the heat through numerous capillaries that are located directly under the skin. Near the surface, the blood can lose heat. This cooled blood can then be transported back through the body to prevent the body temperature from becoming too high. Sweat is also a means by which the body cools itself down. Sweat is produced by glands and evaporation at the topmost skin layer (the epidermis) can release heat. This describes vaporization, one of the four mechanisms used to maintain core body temperature. Radiation occurs when the heat that is released from the body’s surface is moved into the surrounding air; convection occurs when cooler air surrounds the body’s surface, and conduction is when heat is transferred by direct contact with a cooler object (such as an ice pack). Hydration is paramount while exposed to environmental heat or during physical activity—not only to maintain adequate circulating intravascular fluid volume but also, to aid in conduction processes that cool the body down. When cold fluids are ingested, the heat is released into the fluid and excreted out of the body as sweat or urine.

While the infection is a central mechanism for raising the core body temperature, several peripheral mechanisms can also result in elevated body temperature. As previously discussed, multiple diseases with dysfunctional thermoregulatory mechanisms including small fiber and autonomic neuropathies, radiculopathies, and central autonomic disorders such as multiple system atrophy, Parkinson’s disease with autonomic dysfunction, and pure autonomic failure. Decreased cardiac function is also a notable risk factor for dysfunctional thermoregulation as the body depends on the heart to efficiently pump blood to the surface as a cooling mechanism. Without this mechanism, patients with impaired cardiac function are at risk of having heat-related illnesses, including those whose medications exert therapeutic effects through negative inotropic and chronotropic properties.

Volume depletion in conditions such as dehydration is another risk factor for dysfunctional thermoregulation. Without sufficient intravascular fluid, the body loses a mechanism for cooling as well as increased blood viscosity and the resultant strain on the cardiovascular system.

In contrast, hypothermia is defined as low internal body temperature, or a temperature less than 35 degrees Celsius (95 degrees Fahrenheit). It is usually caused by too much heat loss from cold weather exposure or cold water immersion. During cold water immersion, the diving reflex causes vasoconstriction in the visceral muscles as a mechanism to keep a person’s essential organs, like their heart and brain, supplied with blood and protected from hypoxia and ischemia.

There are two different types of hypothermia: primary and secondary. Primary hypothermia is when the cold environment is the direct cause and secondary hypothermia is when a patient’s illness causes hypothermia. Conduction, convection, and radiation also come into play with hypothermia; this is how the rate of heat loss is determined. Hypothermia decelerates all physiologic roles include metabolic rate, mental awareness, nerve conduction, neuromuscular reaction times, and both the cardiovascular and respiratory systems. As previously mentioned, the vasoconstriction caused by hypothermia induces renal dysfunction and cold diuresis due to the decreased levels of ADH. These decreased levels of antidiuretic hormone result in dilute urine. The vasoconstriction during hypothermia can mask concomitant hypovolemia. During rewarming, the subsequent vasodilation results in a redistribution of fluid which can cause cardiac arrest or abrupt shock, known as rewarming collapse. 

Homeostatic Process

Homeostatic processes ensure a constant internal environment by various mechanisms working in combination to maintain setpoints.

Key Points

Homeostasis is the body’s attempt to maintain a constant and balanced internal environment, which requires persistent monitoring and adjustments as conditions change.

Homeostatic regulation is monitored and adjusted by the receptor, the command center, and the effector.

The receptor receives information based on the internal environment; the command center receives and processes the information; and the effector responds to the command center, opposing or enhancing the stimulus.

Key Terms

  • homeostasis: the ability of a system or living organism to adjust its internal environment to maintain a stable equilibrium
  • effector: any muscle, organ, etc. that can respond to a stimulus from a nerve

Homeostatic Process

The human organism consists of trillions of cells working together for the maintenance of the entire organism. While cells may perform very different functions, the cells are quite similar in their metabolic requirements. Maintaining a constant internal environment with everything that the cells need to survive (oxygen, glucose, mineral ions, waste removal, etc.) is necessary for the well-being of individual cells and the well-being of the entire body. The varied processes by which the body regulates its internal environment are collectively referred to as homeostasis.

Homeostasis

Homeostasis, in a general sense, refers to stability, balance, or equilibrium. Physiologically, it is the body’s attempt to maintain a constant and balanced internal environment, which requires persistent monitoring and adjustments as conditions change. Adjustment of physiological systems within the body is called homeostatic regulation, which involves three parts or mechanisms: (1) the receptor, (2) the control center, and (3) the effector.

The receptor receives information that something in the environment is changing. The control center or integration center receives and processes information from the receptor. The effector responds to the commands of the control center by either opposing or enhancing the stimulus. This ongoing process continually works to restore and maintain homeostasis. For example, during body temperature regulation, temperature receptors in the skin communicate information to the brain (the control center) which signals the effectors: blood vessels and sweat glands in the skin. As the internal and external environment of the body is constantly changing, adjustments must be made continuously to stay at or near a specific value: the set point.

Purpose of Homeostasis

The ultimate goal of homeostasis is the maintenance of equilibrium around the set point. While there are normal fluctuations from the setpoint, the body’s systems will usually attempt to revert to it. A change in the internal or external environment (a stimulus) is detected by a receptor; the response of the system is to adjust the deviation parameter toward the set point. For instance, if the body becomes too warm, adjustments are made to cool the animal. If the blood glucose rises after a meal, adjustments are made to lower the blood glucose level by moving the nutrient into tissues in the command center that require it, or storing it for later use.

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Blood glucose homeostasis: An example of how homeostasis is achieved by controlling blood sugar levels after a meal.

Homeostasis: Thermoregulation

Animals use different modes of thermoregulation processes to maintain homeostatic internal body temperatures.

Key Points

In response to varying body temperatures, processes such as enzyme production can be modified to acclimate to changes in the temperature.

Endotherms regulate their own internal body temperature, regardless of fluctuating external temperatures, while ectotherms rely on the external environment to regulate their internal body temperature.

Homeotherms maintain their body temperature within a narrow range, while poikilotherms can tolerate a wide variation in internal body temperature, usually because of environmental variation.

Heat can be exchanged between the environment and animals via radiation, evaporation, convection, or conduction processes.

Key Terms

  • ectotherm: An animal that relies on the external environment to regulate its internal body temperature.
  • endotherm: An animal that regulates its own internal body temperature through metabolic processes.
  • homeotherm: An animal that maintains a constant internal body temperature, usually within a narrow range of temperatures.
  • poikilotherm: An animal that varies its internal body temperature within a wide range of temperatures, usually as a result of variation in the environmental temperature.

Thermoregulation to Maintain Homeostasis

Internal thermoregulation contributes to an animal’s ability to maintain homeostasis within a certain range of temperatures. As internal body temperature rises, physiological processes are affected, such as enzyme activity. Although enzyme activity initially increases with temperature, enzymes begin to denature and lose their function at higher temperatures (around 40-50 C for mammals). As internal body temperature decreases below normal levels, hypothermia occurs and other physiological processes are affected. There are various thermoregulation mechanisms that animals use to regulate their internal body temperature.

Types of Thermoregulation (Ectothermy vs. Endothermy)

Thermoregulation in organisms runs along a spectrum from endothermy to ectothermy. Endotherms create most of their heat via metabolic processes, and are colloquially referred to as “warm-blooded.” Ectotherms use external sources of temperature to regulate their body temperatures. Ectotherms are colloquially referred to as “cold-blooded” even though their body temperatures often stay within the same temperature ranges as warm-blooded animals.

Ectotherm

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Ectotherm: The Common frog is an exotherm and regulates its body based on the temperature of the external environment.

An ectotherm, from the Greek (ektós) “outside” and (thermós) “hot,” is an organism in which internal physiological sources of heat are of relatively small or quite negligible importance in controlling body temperature. Since ectotherms rely on environmental heat sources, they can operate at economical metabolic rates. Ectotherms usually live in environments in which temperatures are constant, such as the tropics or the ocean. Ectotherms have developed several behavioral thermoregulation mechanisms, such as basking in the sun to increase body temperature or seeking shade to decrease body temperature.

Endotherms

In contrast to ectotherms, endotherms regulate their own body temperature through internal metabolic processes and usually maintain a narrow range of internal temperatures. Heat is usually generated from the animal’s normal metabolism, but under conditions of excessive cold or low activity, an endotherm generates additional heat by shivering. Many endotherms have a larger number of mitochondria per cell than ectotherms. These mitochondria enable them to generate heat by increasing the rate at which they metabolize fats and sugars. However, endothermic animals must sustain their higher metabolism by eating more food more often. For example, a mouse (endotherm) must consume food every day to sustain high its metabolism, while a snake (ectotherm) may only eat once a month because its metabolism is much lower.

Homeothermy vs. Poikilothermy

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Homeotherm vs. Poikilotherm: Sustained energy output of an endothermic animal (mammal) and an ectothermic animal (reptile) as a function of core temperature. In this scenario, the mammal is also a homeotherm because it maintains its internal body temperature in a very narrow range. The reptile is also a poikilotherm because it can withstand a large range of temperatures.

A poikilotherm is an organism whose internal temperature varies considerably. It is the opposite of a homeotherm, an organism that maintains thermal homeostasis. Poikilotherm’s internal temperature usually varies with the ambient environmental temperature, and many terrestrial ectotherms are poikilothermic. Poikilothermic animals include many species of fish, amphibians, and reptiles, as well as birds and mammals that lower their metabolism and body temperature as part of hibernation or torpor. Some ectotherms can also be homeotherms. For example, some species of tropical fish inhabit coral reefs that have such stable ambient temperatures that their internal temperature remains constant.

Means of Heat Transfer

Heat can be exchanged between an animal and its environment through four mechanisms: radiation, evaporation, convection, and conduction. Radiation is the emission of electromagnetic “heat” waves. Heat radiates from the sun and from dry skin the same manner. When a mammal sweats, evaporation removes heat from a surface with a liquid. Convection currents of air remove heat from the surface of dry skin as the air passes over it. Heat can be conducted from one surface to another during direct contact with the surfaces, such as an animal resting on a warm rock.

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Mechanisms for heat exchange: Heat can be exchanged by four mechanisms: (a) radiation, (b) evaporation, (c) convection, or (d) conduction.

Heat Conservation and Dissipation

Animals have processes that allow for heat conservation and dissipation in order to maintain a homeostatic internal body temperature.

Key Points

Heat conservation is characterized by the ability to ensure blood remains in the core by undergoing vasoconstriction, reducing blood flow to the periphery (also known as peripheral vasoconstriction).

Heat dissipation is characterized by the ability to undergo vasodilation which increases blood flow to the periphery, resulting in evaporative heat loss.

Endothermic animals are defined by their ability to utilize both vasoconstriction and vasodilation to maintain internal body temperature.

Ectothermic animals are defined by their change in behavior (lying in sunlight to warm up, hiding in shade to cool down) to regulate body temperature.

Key Terms

  • endotherm: a warm-blooded animal that maintains a constant body temperature
  • ectotherm: a cold-blooded animal that regulates its body temperature by exchanging heat with its surroundings

Heat Conservation and Dissipation

Animals conserve or dissipate heat in a variety of ways. In certain climates, endothermic animals have some form of insulation, such as fur, fat, feathers, or some combination thereof. Animals with thick fur or feathers create an insulating layer of air between their skin and internal organs. Polar bears and seals live and swim in a subfreezing environment, yet they maintain a constant, warm, body temperature. The arctic fox uses its fluffy tail as extra insulation when it curls up to sleep in cold weather. Mammals have a residual effect from shivering and increased muscle activity: arrector pili muscles create “goosebumps,” causing small hairs to stand up when the individual is cold; this has the intended effect of increasing body temperature. Mammals use layers of fat to achieve the same end; the loss of significant amounts of body fat will compromise an individual’s ability to conserve heat.

Endotherms use their circulatory systems to help maintain body temperature. For example, vasodilation brings more blood and heat to the body’s surface, facilitating radiation and evaporative heat loss, which helps to cool the body. However, vasoconstriction reduces blood flow in peripheral blood vessels, forcing blood toward the core and the vital organs found there, conserving heat. Some animals have adaptions to their circulatory system that enable them to transfer heat from arteries to veins, thus, warming blood that returns to the heart. This is called a countercurrent heat exchange; it prevents cold venous blood from cooling the heart and other internal organs. This adaption, which can be shut down in some animals to prevent overheating the internal organs, is found in many animals, including dolphins, sharks, bony fish, bees, and hummingbirds. In contrast, similar adaptations (as in dolphin flukes and elephant ears) can help cool endotherms when needed.

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Control of body temperature: In endotherms, the circulatory system is used to help maintain body temperature, either by vasodilation or vasoconstriction.

Many animals, especially mammals, use metabolic waste heat as a heat source. When muscles are contracted, most of the energy from the ATP used in muscle actions is wasted energy that translates into heat. In cases of severe cold, a shivering reflex is activated that generates heat for the body. Many species also have a type of adipose tissue called brown fat that specializes in generating heat.

Exothermic animals use changes in their behavior to help regulate body temperature. For example, a desert ectothermic animal may simply seek cooler areas during the hottest part of the day in the desert to keep from becoming too warm. The same animals may climb onto rocks to capture heat during a cold desert night. Some animals seek water to aid evaporation in cooling them, as seen with reptiles. Other ectotherms use group activity, such as the activity of bees to warm a hive to survive winter.

Organ Systems Involved

Multiple organs and body systems are affected when thermoregulation is impaired. During a heat-related illness, insufficient thermoregulation can result in multiple organ and system impairments. (Notice that many of these issues are interconnected.)

  • The heart experiences increased work as it increases both heart rate and cardiac output.
  • The circulatory system can experience intravascular volume depletion.
  • The brain can experience ischemia and/or edema.
  • The gastrointestinal tract is vulnerable to hemorrhage and infection as the intestinal mucosa becomes increasingly permeable.
  • The lungs become impaired if sustained hyperventilation, hyperpnea, and pulmonary vasodilation lead to ARDS.
  • Acute renal failure is an effect of intravascular volume depletion and impaired circulation.
  • Liver cells suffer because of fever, ischemia, and cytokine increase in the intestinal tract.
  • Various organs can become ischemic from microthrombi or DIC.
  • Electrolyte abnormalities are likely as well as hypoglycemia, metabolic acidosis, and respiratory alkalosis.

When body temperatures are severely decreased in hypothermia, the body’s systems are also adversely affected. The cardiovascular system is susceptible to dysrhythmias such as ventricular fibrillation. The central nervous system’s (CNS) electrical activity is noticeably diminished. Noncardiogenic pulmonary edema can occur as well as cold diuresis. Additionally, hypothermia causes preglomerular vasoconstriction which leads to decreased glomerular filtration rate (GFR) and decreased renal blood flow (RBF). 

The Function of Temperature Regulation

The core body temperature is tightly controlled in a narrow range although slight changes in core body temperature occur every day, depending upon variables such as circadian rhythm and menses. When a person is unable to regulate his or her body temperature, various pathologies ensue. The human body has four different methods for maintaining core temperature: vaporization, radiation, convection, and conduction. To keep the body functioning, it must be at its ideal temperature. This requires sufficient intravascular volume and cardiovascular function as the body must be able to transport the rising internal heat to its surface for release. Elderly people are at increased risk for disorders of thermoregulation due to a generally decreased intravascular volume and decreased cardiac function.

References

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