Renovascular hypertension is one of the most common causes of secondary hypertension. It is mostly due to the narrowing of blood vessels in the kidney. This activity reviews the evaluation and management of renovascular hypertension and highlights the role of the healthcare team in evaluating and treating patients with this condition.

High blood pressure affects 75 million adults in the United States[rx] and accounts for 8.6% of all primary care visits.[rx] Renovascular hypertension is one of the most common causes of secondary hypertension and often leads to resistant hypertension. It is defined as systemic hypertension that manifests secondary to the compromised blood supply to the kidneys, usually due to an occlusive lesion in the main renal artery.

Causes of Renovascular Hypertension

The cause of renovascular hypertension is consistent with any narrowing/blockage of blood supply to the renal organ (renal artery stenosis). As a consequence of this action the renal organs release hormones that indicate to the body to maintain a higher amount of sodium and water, which in turn causes blood pressure to rise. Factors that may contribute are: diabetes, high cholesterol and advanced age,^[rx] also of importance is that a unilateral condition is sufficient to cause renovascular hypertension.^[rx]

It is important to realize that any condition that compromises blood flow to the kidneys can contribute to renovascular hypertension.[rx] The most common causes of renovascular hypertension include:

• Renal artery stenosis (RAS), mostly secondary to atherosclerosis
• Fibromuscular dysplasia (FMD)
• Arteritides such as Takayasu’s, Antiphospholipid Antibody (APLA) or Mid aortic syndrome[rx][rx]
• Extrinsic compression of a renal artery
• Renal artery dissection or infarction[rx]
• Radiation fibrosis
• Obstruction from aortic endovascular grafts[rx]

The underlying mechanism in renovascular hypertension involves decreased perfusion to the kidney and activation of the Renin-Angiotensin-Aldosterone (RAAS) pathway. This was first explained by Goldblatt et al. in the 1930s. His model studied the effect of decreased blood supply to the kidneys in dogs and found that ischemic kidneys contribute to persistent hypertension. He also proposed the presence of a substance that “may affect a pressor action like that of a hormone.” This hormone he was referring to was ‘renin,’ which is secreted by juxtaglomerular cells of the kidney. Renin secretion by the kidneys is stimulated by three main pathways,

• 1) renal baroreceptors that sense decrease perfusion to the kidney,
• 2) low sodium chloride levels detected by the macula densa and
• 3) beta-adrenergic stimulation. Prolonged ischemia also increases the number of renin expressing cells in the kidney in a process called ‘JG recruitment.’[rx] When renin is secreted into the blood, it acts on angiotensinogen (produced by the liver). Renin cleaves angiotensinogen to angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme (ACE) that is primarily found in the vascular endothelium of lungs and kidney. Angiotensin II raises blood pressure by multiple mechanisms, which include:
• Vasoconstriction, mostly in the heart, kidney, and vascular smooth muscle[rx]
• Sympathetic nervous stimulation causing a presynaptic release of norepinephrine
• Stimulates secretion of aldosterone by the adrenal cortex, which in turn causes sodium and water retention, thereby raising blood pressure.
• It also causes the increased synthesis of collagen type I and III in fibroblasts, leading to thickening of the vascular wall and myocardium, and fibrosis
• It has been shown to have a growth effect on renal cells, which has been implicated in the development of glomerulosclerosis and tubulointerstitial fibrosis

Though atherosclerotic renal artery stenosis (ARAS) and FMD are the two most common conditions causing this cascade, any pathology leading to decreased blood flow to the kidneys can essentially trigger this and lead to high blood pressure.

Symptoms Of Renovascular Hypertension

The main symptoms of renovascular hypertension are rapidly increasing blood pressure of 180/120 or higher and signs of organ damage. Usually, the damage happens to the kidneys or the eyes.

Other symptoms depend on how the rise in blood pressure affects your organs. A common symptom is bleeding and swelling in the tiny blood vessels in the retina. The retina is the layer of nerves that line the back of the eye. It senses light and sends signals to the brain through the optic nerve, which can also be affected by renovascular hypertension. When the eye is involved, can renovascular hypertension cause changes in vision.

Other symptoms of malignant hypertension include

• Pheochromocytoma – Sweating, increased frequency or force of heartbeats, headache, anxiety
• Cushing’s syndrome – Weight gain, weakness, abnormal growth of body hair or loss of menstrual periods (in women), purple striations (lines) on the skin of the abdomen
• Thyroid problems – Fatigue (tiredness), weight gain or weight loss, intolerance to heat or cold
• Conn’s syndrome or primary aldosteronism – Weakness due to low levels of potassium in the body
• Obstructive sleep apnea – excessive fatigue or sleepiness during daytime, snoring, pauses in breathing during sleep
• High blood pressure at a young age
• High blood pressure that suddenly gets worse or is hard to control
• Kidneys that are not working well (this can start suddenly)
• Narrowing of other arteries in the body, such as to the legs, the brain, the eyes and elsewhere
• Sudden buildup of fluid in the air sacs of the lungs (pulmonary edema)
• High blood pressure (early age)
• Kidney dysfunction
• Narrowing of arteries elsewhere in the body
• Pulmonary edema
• Change in mental status, such as anxiety, confusion, decreased alertness, decreased ability to concentrate, fatigue, restlessness, sleepiness, or stupor
• Chest pain (feeling of crushing or pressure)
• Cough
• Headache
• Nausea or vomiting
• Numbness of the arms, legs, face, or other areas
• Reduced urine output
• Seizure
• Shortness of breath
• Weakness of the arms, legs, face, or other areas
• Blurred vision
• Chest pain (angina)
• Difficulty breathing
• Dizziness
• Numbness in the arms, legs, and face
• Severe headache
• Shortness of breath

In rare cases, renovascular hypertension can cause brain swelling, which leads to a dangerous condition called hypertensive encephalopathy. Symptoms include:

• Changes in mental status
• Coma
• Confusion
• Drowsiness
• Headache that continues to get worse
• Nausea and vomiting
• Seizures

Diagnosis of Renovascular Hypertension

History and Physical

Salient points in history that suggest the presence of renovascular hypertension include:

• Resistant hypertension –  Uncontrolled blood pressure necessitating the use of 2 or 3 antihypertensive agents of different classes, one of which is a diuretic
• Trial of multiple medications to control blood pressure
• History of multiple hospital admissions for hypertensive crisis
• Elevation in creatinine of more than 30% after starting an angiotensin-converting enzyme (ACE) inhibitor (ACEI)
• Patients with renal artery stenosis secondary to atherosclerosis are usually older and might have the presence of other atherosclerotic diseases such as carotid artery stenosis, peripheral artery stenosis or coronary artery disease
• A premenopausal female (15-50 years) with hypertension is most likely to have FMD[rx]
• Long term history of smoking
• Patients with systemic vasculitis can develop vasculitis of renal arteries and present with renovascular hypertension
• Recurrent episodes of flash pulmonary edema and/or unexplained congestive heart failure
• Unexplained Azotemia
• Elevation in serum creatinine on starting ACE-I, which occurs due to interference with autoregulation and post glomerular arterial tone
• Unexplained hypokalemia and metabolic alkalosis
• Unilateral small or atrophic kidney.

Physical examination may reveal an abdominal bruit, indicating the presence of renal artery stenosis.

Lab Test

Patients with renovascular hypertension often undergo an extensive evaluation to find a cause for uncontrolled hypertension.

Laboratory tests

• Urine analysis – to check for proteinuria, hematuria, and casts. The presence of proteinuria indicates the presence of renal parenchymal disorder, whereas the presence of hematuria or RBC casts indicates the presence of glomerulonephritis.
• Blood urea nitrogen and serum creatinine – to assess baseline kidney function.
• Basal metabolic profile: to assess for electrolyte disturbances and acid-base balance.
• Complement levels and autoimmune profile – in suspected cases of autoimmune diseases affecting the renal vasculature.
• Plasma free metanephrines or 24-hour urinary fractionated metanephrines and normetanephrine to rule out pheochromocytoma
• Plasma renin-aldosterone ratio to rule out hyperaldosteronism
• 24 hr urinary free cortisol or low dose dexamethasone suppression test to rule out Cushing’s syndrome

Imaging

• Catheter angiography  – There are multiple imaging modalities available to evaluate renovascular hypertension. Since the most common cause of renovascular hypertension is renal artery stenosis, renal arteriography remains the gold standard diagnostic test.[rx] However, catheter angiography is invasive, costly, time-consuming, and can lead to complications such as renal artery dissection or cholesterol embolization. Other imaging tests that can be done to evaluate the renal vessels include duplex ultrasonography, computed tomography with angiography (CTA), and magnetic resonance angiography (MRA). The type of imaging test used often depends on the suspicion for high-grade lesions, and the need for intervention.[rx]
• Duplex ultrasonography – is the initial imaging test of choice to evaluate the renal arteries. It is relatively cheap, non-invasive, and does not involve the administration of contrast or exposure to radiation. A duplex scan has been shown to have an excellent correlation with contrast-enhanced angiography.[rx] Though there are several criteria to assess the presence of renal artery stenosis, the most important sign is peak systolic velocity (PSV). A PSV higher than 180 cm/s suggests the presence of stenosis of greater than 60%.[rx]
• Ultrasonography – can also measure the resistive index (RI), which is calculated as ((PSV-End diastolic velocity)/PSV)). A value of more than 0.7 indicates the presence of pathological resistance to flow, and studies have shown that a value >0.8 predicts poor response to revascularization treatments.[rx] The most significant setbacks for duplex ultrasonography are its reduced sensitivity in obese patients, hindrance by overlying bowel gas and operator dependence.
• CT angiography – involves the administration of intravenous contrast and acquiring detailed images of blood vessels or tissues by moving the beam in a helical manner across the area being studied. In a study by Wittenberg et al, the sensitivity and specificity for hemodynamically significant RAS (>50%) by CTA was found to be 96% and 99%. CTA also has a comparable negative predictive value to MRA in ruling out renal artery stenosis.[rx] It can also diagnose extrinsic compression of renal arteries, FMD, arterial dissection, and help in evaluating surrounding structures. However, CTA can only provide an anatomical assessment of the lesion and is not able to evaluate the degree of obstruction to renal blood flow. Exposure to radiation, allergy to contrast, and acute kidney injury are other downfalls of CTA.
• MRA  – uses a powerful magnetic field, pulses of radio waves, and intravenous gadolinium to evaluate the renal blood vessels and surrounding structures. Several studies have shown the sensitivity and specificity of MRA to be around 97% and 92%[rx] in diagnosing renal artery. MRA does not involve radiation, and gadolinium contrast is less likely to cause an allergic reaction as compared to the iodine contrast used in CTA. However, MRA has been shown to overestimate the grade of stenosis and is often affected by motion artifacts or opacification of renal veins, leading to difficulty visualizing the renal arteries.[15] Also, gadolinium has been shown to induce a rare, progressively fatal disease called nephrogenic systemic fibrosis (NSF).  NSF can affect the skin, joints, and multiple organs leading to progressive, irreversible fibrosis and eventual death. This occurs due to a transmetalation reaction that displaces gadolinium ion from its chelate, resulting in the deposition of gadolinium in the skin and soft tissues. The 1-year incidence of NSF has been reported to be around 4.6%[rx] and almost all cases occurred in patients with a glomerular filtration rate < 30 mL/min/1.73 m.
• Nuclear medicine ACE-Inhibitor (ACE-I) renography – is another non-invasive, relatively safe imaging method that uses radioactive material, a special camera, and a computer to evaluate for renovascular hypertension. It involves the administration of an ACE-I to determine if the cause of hypertension is due to the narrowing of the renal arteries. The sensitivity and specificity of this test have shown to be variable, with values between 74% – 94% for sensitivity and 59% – 95% for specificity.[rx] It is a time-consuming procedure, and there is a risk of radiation exposure and irritation or pain from the injection of the radiotracer. The sensitivity of ultrasound has shown to be higher than captopril renography[rx] which makes it a better choice for an initial diagnostic test.
• Magnetic resonance angiogram, or MRA – Images from this test show blood flow and organ function without using x-rays. Contrast medium may be injected into a vein in your arm to better see the structure of your arteries. You remain awake, although a muscle relaxer may be used, if necessary. You lie still on a table that slides into a tunnel-shaped device. There is no radiation exposure with this study. Claustrophobia can be an issue with MRAs as the tube is quite narrow.
• Catheter angiogram – A special kind of x-ray in which a catheter, or a thin, flexible tube, is threaded through your large arteries into your renal artery. This often is from a small slit in the groin. The patient is usually awake, although a muscle relaxer may be given to lessen anxiety during the procedure. A contrast medium, or a colored dye, is injected through the catheter, so the renal artery shows up more clearly on the x-ray. The benefits of this study are that it is more accurate than the other tests and if a significant narrowing is seen, it can be dilated with a balloon (angioplasty) or stented (a tube-like cage that keeps the vessels open) at the same time. A catheter angiogram is an invasive procedure so this is usually reserved for patients who have a positive result of one of the other tests and plans are made to dilate the blood vessel.

Catheter arteriography – is the gold standard test to evaluate for renovascular hypertension and provides the best temporal and spatial resolution. Catheter angiography has the added advantage of measuring translesional pressure gradients to assess the hemodynamic significance of anatomically severe lesions.[rx] It is most useful in:

• Patients with a disparity between imaging modalities
• Patients with a high index of suspicion and negative imaging findings
• Patients anticipated having an intervention

It can also evaluate anatomical abnormalities of the kidney, renal arteries, aorta, and can be followed by endovascular intervention for the treatment of significant lesions. Also, the surrounding tissues and bones can be removed or subtracted from the final image revealing only the arterial framework. This method is known as digital subtraction angiography (DSA). However, the radiation doses are higher than CTA, and because it is an invasive procedure, there are risks of complications such as arterial dissection, tear, rupture, or thromboembolic phenomenon.[rx]

Treatment of Renovascular Hypertension

The management of renovascular hypertension aims to treat the underlying cause. Several options are available, which include pharmacological and invasive therapy.

Pharmacological therapy entails the use of antihypertensive medications to control blood pressure. The American College of Cardiology and the American Heart Association (ACC/AHA) advocates pharmacological therapy as the first-line treatment for renal artery stenosis.[rx] Since RAAS is the most prominent pathway contributing to hypertension in these disorders,

• ACEI and angiotensin receptor blockers (ARBs) form the cornerstone of managing renovascular hypertension (Class 1a indication). Often more than one medication will be needed to control the blood pressure.
• Calcium channel blockers, thiazides, beta-blockers, and hydralazine have been shown to be effective to control blood pressure in patients with RAS.[rx] Direct renin inhibitors such as aliskiren have been studied as monotherapy or in combination with ACEIs/ARBs to treat hypertension. Though it has been shown to be effective for the treatment of hypertension[rx][rx][rx][rx][rx] there is not enough data to prove its efficacy in treating renovascular hypertension.
• ACEIs and ARBs inhibit the action of angiotensin II, thereby causing vasodilation and promote sodium and water excretion. However, these medications are contraindicated in patients with a single functioning kidney or bilateral lesions as they can cause efferent arteriolar vasodilatation leading to interruption in autoregulation and thereby decreasing glomerular filtration. While these medications are effective in controlling blood pressure, they can also lead to worsening renal function.
• Percutaneous angioplasty is the treatment of choice for renovascular hypertension due to FMD and for patients with atherosclerotic renal artery stenosis that is not controlled with medications.[rx] The ACC/AHA guidelines recommend revascularization for renal artery disease in the following scenarios:[rx]
• Patients with hemodynamically significant RAS and recurrent, unexplained congestive heart failure or sudden, unexplained pulmonary edema (class Ia)
• Hemodynamically significant RAS and accelerated hypertension, resistant hypertension, malignant hypertension or hypertension with an unexplained unilateral small kidney, and hypertension with intolerance to medication (Class IIa)
• Patients with bilateral RAS and progressive chronic kidney disease or a RAS to a solitary functioning kidney (Class IIa)
• Patients with hemodynamically significant RAS and unstable angina (class IIa)
• Asymptomatic bilateral or solitary viable kidney with hemodynamically significant RAS (Class IIb)
• Patients with RAS and chronic renal insufficiency with unilateral RAS (class IIb)
• In addition to angioplasty, renal stent placement is indicated for patients with ostial atherosclerotic lesions (Class I).
• Patients with FMD and renovascular hypertension are also treated with percutaneous intervention with or without a stent.[rx] Multiple studies have shown a decrease in baseline blood pressure after intervention for FMD.[rx][rx] However, there remains an ongoing debate about the benefit of revascularization when compared to medical management in patients with atherosclerotic renal artery stenosis (ARAS). Several studies have failed to show a significant decrease in blood pressure or the number of antihypertensive agents between angioplasty and medical treatment groups.

A meta-analysis of 7 trials by Zhu et al. revealed that medical management is as effective as percutaneous revascularization in the treatment of RAS.[rx] Three recent trials ASTRAL, CORAL, and STAR found no difference between stenting and medical therapy in patients with atherosclerotic renal artery stenosis.[rx] [rx][rx] Thus it can be established that revascularization does not reverse renal damage or decrease blood pressure in patients with atherosclerotic renal artery stenosis.

In the case of recurrent renal artery stenosis or blood pressure not controlled with medication and or/angioplasty, renal bypass surgery may be an option. In this procedure, the surgeon uses a vein or synthetic tube to connect the kidney to the aorta, to create an alternate route for blood to flow around the blocked artery into the kidney. This is a complex procedure and rarely used. The ACC/AHA guidelines recommend surgery for RAS in[rx]

• Patients with RAS secondary to FMD, especially those with complex disease and/or those having microaneurysms
• Patients with atherosclerotic RAS involving multiple vessels or involvement of early primary branch of the main renal artery
• Patients with atherosclerotic RAS who require pararenal aortic reconstructions (such as with aortic aneurysms or severe aortoiliac obstruction).

Several studies have also evaluated the role of unilateral nephrectomy in patients with renovascular hypertension and have shown improvement in blood pressure control, renal function, and decrease in the use of anti-hypertensives.[rx][rx] However, this is an invasive procedure with inherent risks and long term consequences of such a procedure are unclear.

Surgery

• In terms of treatment for renovascular hypertension surgical revascularization versus medical therapy for atherosclerosis, it is not clear if one option is better than the other according to a 2014 Cochrane review; balloon angioplasty did show a small improvement in blood pressure .^[rx]
• Surgery can include percutaneous surgical revascularization, and also nephrectomy or autotransplantation, and the individual may be given beta-adrenergic blockers.^[rx] Early therapeutic intervention is important if ischemic nephropathy is to be prevented. Inpatient care is necessary for the management of hypertensive urgencies, quick intervention is required to prevent further damage to the kidneys.^[rx]

References

A hypertensive emergency is a life-threatening condition where ongoing target-organ damage occurs due to markedly elevated blood pressure. Pulmonary edema, cardiac ischemic events, acute renal failure, aortic dissection, eclampsia, retinopathy, and encephalopathy may present as a result of organ injury due to hypertension.

Hypertensive encephalopathy is a less commonly encountered type of hypertensive emergency. It is characterized by signs of cerebral edema that occur after a severe episode of hypertension. This condition is usually diagnosed retrospectively after symptoms dramatically resolve by lowering the patient’s blood pressure, and other causes of the neurologic disease have been ruled out. Symptoms of hypertensive encephalopathy include the gradual onset of headache, nausea, and vomiting, followed by neurologic symptoms such as restlessness, confusion, seizures, and potentially coma. If hypertension is treated promptly, the symptoms of encephalopathy are usually reversible.[rx]

Causes of Hypertensive Encephalopathy

Hypertensive encephalopathy is triggered most commonly by inadequately controlled primary hypertension. Secondary causes of hypertension can also predispose patients to this condition.

Hypertensive encephalopathy shares multiple characteristics with other syndromes causing cerebral edema, such as posterior reversible encephalopathy syndrome (PRES), hypertensive brainstem encephalopathy, and eclampsia.

Evaluation for chronic or acute renal disease, sympathomimetic ingestion (amphetamines, cocaine), side effects from drugs such as immunosuppressive agents, preeclampsia, and eclampsia should be considered if primary hypertension has not been previously diagnosed.

Normally, the brain sustains blood flow within a narrow perfusion pressure range without being affected by fluctuations in systemic arterial pressure. For healthy individuals, the pressure ranges are 50-150 mm Hg cerebral perfusion pressure (CPP) or 60 to 160 mm Hg mean arterial pressure (MAP).The CPP = MAP – intracranial pressure (ICP).[rx]

With increased MAP, cerebral arteriolar vasoconstriction occurs, and conversely, with decreased MAP, arteriolar dilation occurs to keep the CPP constant. This adaptive process maintains brain perfusion at a constant level despite systemic blood pressure changes. However, a sudden and severe increase in arterial pressure can exceed this autoregulatory mechanism because the arterioles are limited in their ability to constrict. The then intracerebral elevated blood pressure causes a breach in the blood-brain barrier, and vascular fluid diffuses across the capillary membranes into the brain parenchyma. This leads to the development of cerebral edema, increased intracranial pressure, and neurologic deficits such as altered mentation, visual deficits, and seizures.

In patients with chronic hypertension, the cerebral vasculature undergoes adaptations, such as arteriolar hypertrophy, to allow for a higher autoregulatory range. Lowering the blood pressure too quickly in these patients can produce cerebral ischemia at a higher MAP compared to normotensive patients.

In previously normotensive patients, acute episodes of hypertension may induce hypertensive encephalopathy at diastolic blood pressures as low as 100 mm Hg. This scenario may be seen with patients that develop eclampsia or in patients receiving cytotoxic and immunosuppressive therapies.[rx][rx] It is hypothesized that these conditions directly elicit a toxic effect on the vascular endothelium and lead to dysfunction of the blood-brain barrier.

Symptoms Of Hypertensive Encephalopathy

The main symptoms of hypertensive encephalopathyare rapidly increasing blood pressure of 180/120 or higher and signs of organ damage. Usually, the damage happens to the kidneys or the eyes.

Other symptoms depend on how the rise in blood pressure affects your organs. A common symptom is bleeding and swelling in the tiny blood vessels in the retina. The retina is the layer of nerves that line the back of the eye. It senses light and sends signals to the brain through the optic nerve, which can also be affected by hypertensive encephalopathy. When the eye is involved,  can hypertensive encephalopathy cause changes in vision.

Other symptoms of malignant hypertension include

• Pheochromocytoma – Sweating, increased frequency or force of heartbeats, headache, anxiety
• Cushing’s syndrome – Weight gain, weakness, abnormal growth of body hair or loss of menstrual periods (in women), purple striations (lines) on the skin of the abdomen
• Thyroid problems – Fatigue (tiredness), weight gain or weight loss, intolerance to heat or cold
• Conn’s syndrome or primary aldosteronism – Weakness due to low levels of potassium in the body
• Obstructive sleep apnea – excessive fatigue or sleepiness during daytime, snoring, pauses in breathing during sleep
• Change in mental status, such as anxiety, confusion, decreased alertness, decreased ability to concentrate, fatigue, restlessness, sleepiness, or stupor
• Chest pain (feeling of crushing or pressure)
• Cough
• Headache
• Nausea or vomiting
• Numbness of the arms, legs, face, or other areas
• Reduced urine output
• Seizure
• Shortness of breath
• Weakness of the arms, legs, face, or other areas
• Blurred vision
• Chest pain (angina)
• Difficulty breathing
• Dizziness
• Numbness in the arms, legs, and face
• Severe headache
• Shortness of breath

In rare cases, hypertensive encephalopathy can cause brain swelling, which leads to a dangerous condition called hypertensive encephalopathy. Symptoms include:

• Blindness
• Changes in mental status
• Coma
• Confusion
• Drowsiness
• Headache that continues to get worse
• Nausea and vomiting
• Seizures

Diagnosis of Hypertensive Encephalopathy

A thorough physical exam and history are primarily used to diagnose hypertensive encephalopathy in patients presenting with elevated blood pressure in addition to altered mental status, visual abnormalities, headache, or seizures. Eliciting a thorough drug history is essential for identifying any previously used antihypertensive drugs. Typically, patients who develop hypertensive encephalopathy have chronic uncontrolled hypertension and may have recently discontinued their antihypertensive medication.[rx] Individuals that have rapidly developing and/or intermittent episodes of hypertension are also more at risk for developing hypertensive encephalopathy.

The majority of patients with this diagnosis have blood pressures in excess of 220/120 mm Hg.[rx] These patients should be evaluated for signs of organ damage that can be found during a hypertensive emergency. In particular, thoracic auscultation may reveal signs reflective of cardiac dysfunction, such as extra heart sounds or pulmonary edema, with rales heard on lung auscultation.[rx] Fundoscopy may show retinal hemorrhages and papilledema, which is a sign of severe hypertensive retinopathy. A complete neurologic exam can identify whether focal or non-focal deficits are present and may warrant other differential diagnoses for conditions that cause similar symptoms to be considered.

Lab Test and Imaging

A diagnosis of hypertensive encephalopathy is made in patients with severely elevated blood pressure plus neurologic symptoms by ruling out other conditions that may cause similar symptoms. Ischemic stroke and the intracerebral hemorrhage must be excluded in these patients because these conditions are treated differently and are not managed primarily or exclusively by lowering blood pressure.

Neuroimaging, such as computerized tomography (CT) or magnetic resonance imaging (MRI), should be performed to aid in identifying brain lesions responsible for neurologic signs or to exclude conditions such as ischemic stroke or intracerebral hemorrhage. CT may not be as sensitive as MRI in identifying regions of brain edema, but it is usually more readily available, and takes less time to perform, and is essential in ruling out some intracranial lesions. T2-weighted MRI can localize regions of cerebral edema found with hypertensive encephalopathy, which can then be characterized further as posterior reversible encephalopathy syndrome (PRES) or hypertensive brainstem encephalopathy. Bilateral white matter edema in the posterior cerebral hemispheres is characteristic of PRES.[11] The distribution of cerebral edema is localized, particularly to the parieto-occipital regions in PRES and the pontine region in cases of hypertensive brainstem encephalopathy. Although PRES can be associated with hypertensive encephalopathy, it can be found in normotensive individuals with conditions that cause vascular injuries, such as autoimmune disease, use of immunosuppressive drugs, and preeclampsia.

Lumbar puncture is not required for the diagnosis of hypertensive encephalopathy but may be performed when a patient is being evaluated for encephalopathy to determine etiology. In PRES, there may be a modestly elevated protein level without pleocytosis, i.e., an albuminocytologic dissociation.[12]

Other end-organ injuries in a hypertensive emergency may be present in addition to hypertensive encephalopathy. Heart failure, acute kidney injury, or retinopathy can be seen with this condition. Diagnostics such as ECG, thoracic radiography, urinalysis, cardiac enzymes, and a metabolic panel with electrolytes and creatinine should be pursued to evaluate for end-organ damage and potential causes of secondary hypertension. In female patients of childbearing age, urine pregnancy testing or serum human chorionic gonadotropin level can be measured to evaluate for eclampsia-related conditions. Toxicologic screening assays can be considered if there is clinical suspicion for the ingestion of sympathomimetic agents.

Treatment of Hypertensive Encephalopathy

Parenteral Antihypertensives

• Nicardipine: The initial dose is 5 mg/hour, and the usual maximum dose is 15 mg/hour.
• Labetalol: A 20 mg bolus is given initially, followed by subsequent boluses of 20 to 80 mg intravenously every 10 minutes to a maximum total dose of 300 mg in a day. Labetalol can also be given as a continuous infusion at 0.5 to 2 mg/min. Labetalol should not be used without prior adequate alpha blockade in patients with hyperadrenergic states (e.g., cocaine-induced hypertension)
• Fendolopam: The initial dose of infusion is 0.1 mcg/kg per min, and the dose is titrated at 15-minute intervals, depending upon the response. Especially beneficial in patients with kidney disease.
• Clevidipine: The initial dose is 1 mg/hour, and the usual maximum dose is 21 mg/hour.
• Sodium nitroprusside: The initial dose is 0.25 to 0.5 mcg/kg/min and the usual maximum dose is 8 to 10 mcg/kg/min. Not a first-line drug as it may cause cyanide toxicity. Use with caution in patients with kidney disease.

While the initial diagnosis and treatment of a hypertensive emergency may occur in the emergency department, definitive treatment for this condition is usually performed in an intensive care unit. The primary treatment for this condition involves administering antihypertensive drug therapy to lower the MAP by 10% to 15% during the first hour. The MAP should not be lowered by more than 25% of the original baseline MAP within the first day of treatment. This cautious reduction of blood pressure decreases the risk of ischemic events and allows for the healing of brain vasculature. If the MAP falls below the hypertensive-adapted autoregulatory range in the brain, as would occur with overaggressive hypertensive therapy, there is an increased risk of stroke as well as ischemic complications in other organs.[rx][rx] Exceptions to this conservative lowering of blood pressure include ischemic stroke, intracerebral hemorrhage, and aortic dissection.

Parenteral antihypertensive agents should be used initially. Oral antihypertensive agents should be avoided in this initial treatment phase because of the inability to titrate to effect, as well as a potentially slower onset of action. Parenteral antihypertensive drugs commonly used for this condition include nicardipine (5 mg/hour to the usual maximum dose 15 mg/hour), labetalol, fenoldopam, and clevidipine. Fenoldopam, a dopamine receptor agonist, may be preferential in patients with renal impairment as it has demonstrated a renal-protective effect.[rx]

Oral antihypertensives may be started as the initial intravenous therapy is tapered and discontinued after a suitable period (often 8 to 24 hours) of reaching the target blood pressure.

In pregnant patients with eclampsia, antihypertensive therapies are chosen based on concerns for the health of the placenta and fetus. Delivery of the infant and placental tissues may be instituted.

Antiseizure medication may be prescribed and continued until symptoms and neuroimaging findings begin to improve. The antiseizure medication can be tapered usually after one to two weeks, as continued seizure recurrence after resolution of encephalopathy is rare.[rx] Drug selection for seizure treatment may depend on other comorbidities the patient has, such as pregnancy or renal function impairment.

Patients with PRES that concurrently have hypertension are treated with antihypertensive drugs similarly as those with hypertensive encephalopathy.[rx] Immunosuppressive drug dosages may be reduced or discontinued in patients that develop symptoms of PRES. If a patient is changed to a different immunosuppressive drug, it is recommended that neuroimaging be performed if symptoms of PRES recur and to avoid using prior drugs that were associated with an encephalopathic episode. It has been reported that fluid therapy overload, MAP greater than 25% of baseline, and creatinine values greater than 1.8 mg/dL are risk factors for developing this condition in patients receiving cytotoxic and immunosuppressive drugs.[rx]

Blood Pressure Goals

• SHEP and HYVET trials have shown significant benefits of antihypertensive treatment in patients with the goal of SBP <150 mmHg[rx].
• The VALsartan in Elderly Isolated Systolic Hypertension (VALISH) trial showed no significant difference in the primary outcome of sudden death, fatal or nonfatal myocardial infarction and stroke, heart failure death, or other cardiovascular death among patients with strict (< 140 mmHg) and moderate (140 to 150 mmHg) SBP control[rx].
• However, the VALISH trial was underpowered due to the low number of events.
• Hence, the optimal SBP in patients with hypertensive disorder remained a controversial topic.
• The most recent Systolic Blood Pressure Intervention Trial (SPRINT) has shown that intensive SBP target of < 120 mmHg improved the cardiovascular outcomes and the overall survival compared to the standard SBP target of 135 to 139 mmHg[rx].
• However, aggressive SBP lowering may be harmful in the elderly and incite more adverse effects such as hypotension, end-organ hypoperfusion (causing acute kidney injury, and intracranial hypoperfusion which may link to cognitive decline), and polypharmacy.
• It is suggested that a goal blood pressure of < 130/80 mmHg is appropriate as long as the patient tolerates it.
• Otherwise, < 140/90 mmHg is considered reasonable in patients who are in the elderly population and patients with labile blood pressure or polypharmacy.
• Management strategies should always be patient-centered, with the aim of optimizing blood pressure control and avoiding polypharmacy, especially in the elderly.

J-curve Phenomenon

• Various studies have shown a J-curve association between blood pressure with risk of myocardial infarction and death.
• Patients with isolated systolic hypertension who receive antihypertensive treatment may precipitously drop their DBP as well.[rx][rx]
• As myocardial perfusion occurs mainly during diastole, an excessive drop in DBP may increase the risk of cardiovascular disease and death.

Lifestyle changes

You may also need to make some lifestyle changes as part of your ISH treatment plan. These can include:

• Losing weight. This can help lower your blood pressure. In fact, for every two pounds you lose, you could lower your blood pressure by about 1 mm Hg.
• Eating a heart-healthy diet. You should also aim to reduce the amount of sodium in your diet. Consider the DASH diet, which emphasizes eating:
  • vegetables
  •  whole grains
  •  low-fat dairy products
  •  fruits
• Exercising. Not only can exercise help you lower your blood pressure, but it can help you control your weight and stress levels. Aim to perform some sort of aerobic exercise for at least 30 minutes most days of the week.
• Decreasing alcohol consumption. Healthy alcohol intake is one drink per day for women and two per day for men.
• Quitting smoking. Smoking can raise your blood pressure and also contribute to a variety of other health problems.
• Managing stress. Stress can raise your blood pressure, so finding ways to relieve it are important. Examples of techniques to help lower stress are meditation and deep breathing exercises.

• https://www.ncbi.nlm.nih.gov/books/NBK268/
• https://www.ncbi.nlm.nih.gov/books/NBK279239/
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• https://www.ncbi.nlm.nih.gov/books/NBK482189/
• https://www.ncbi.nlm.nih.gov/books/NBK482408/
• https://www.ncbi.nlm.nih.gov/books/NBK538226/
• https://www.ncbi.nlm.nih.gov/books/NBK538313/
• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6477925/
• https://www.ncbi.nlm.nih.gov/books/NBK513351/
• https://www.ncbi.nlm.nih.gov/books/NBK279027/
• https://www.ncbi.nlm.nih.gov/books/NBK431051/
• https://www.ncbi.nlm.nih.gov/books/NBK430839/
• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1120075/
• https://www.ncbi.nlm.nih.gov/books/NBK9630/
• https://www.ncbi.nlm.nih.gov/books/NBK539859/
• https://www.ncbi.nlm.nih.gov/books/NBK482472/
• https://www.ncbi.nlm.nih.gov/books/NBK499961/
• https://www.ncbi.nlm.nih.gov/books/NBK554579/
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• https://www.ncbi.nlm.nih.gov/books/NBK537297/
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• https://www.ncbi.nlm.nih.gov/books/NBK507701/
• https://www.ncbi.nlm.nih.gov/books/NBK544305/
• https://www.ncbi.nlm.nih.gov/books/NBK554499/
• https://www.ncbi.nlm.nih.gov/books/NBK525980/
• https://en.wikipedia.org/wiki/Essential_hypertension
• https://en.wikipedia.org/wiki/Systolic_hypertension
• https://www.sciencedirect.com/topics/medicine-and-dentistry/essential-hypertension
• https://www.mayoclinic.org/diseases-conditions/high-blood-pressure/diagnosis-treatment/drc-20373417

Secondary hypertension is elevated blood pressure (BP), which is secondary to an identifiable cause. This activity outlines the causes, history, and physical examination findings, diagnostic tests, and management of secondary hypertension, giving particular importance to the role of interprofessional teamwork in managing such patients. It highlights all the clinical clues that can point towards a secondary cause of hypertension.

Secondary hypertension (or, less commonly, inessential hypertension) is a type of hypertension which by definition is caused by an identifiable underlying primary cause. It is much less common than the other type, called essential hypertension, affecting only 5-10% of hypertensive patients. It has many different causes including endocrine diseases, kidney diseases, and tumors. It also can be a side effect of many medications.

Hypertension affects about 30% of adults in the United States. Most cases are due to essential hypertension, i.e., hypertension without an identifiable cause. But, about 5 to 10% of cases of hypertension are due to secondary hypertension.[rx]

Types

Renovascular hypertension – Renovascular hypertension is a condition in which high blood pressure is caused by the kidneys’ hormonal response to the narrowing of the arteries supplying the kidneys.^[rx] When functioning properly this hormonal axis regulates blood pressure. Due to low local blood flow, the kidneys mistakenly increase the blood pressure of the entire circulatory system. It is a form of secondary hypertension – a form of hypertension whose cause is identifiable

Kidney

Other well-known causes include diseases of the kidney. This includes diseases such as polycystic kidney disease which is a cystic genetic disorder of the kidneys, PKD, which is characterized by the presence of multiple cysts (hence, “polycystic”) in both kidneys, can also damage the liver, pancreas, and rarely, the heart and brain.^{[rx][rx][rx][rx]} It can be autosomal dominant or autosomal recessive, with the autosomal dominant form being more common and characterized by progressive cyst development and bilaterally enlarged kidneys with multiple cysts, with concurrent development of hypertension, chronic kidney disease and kidney pain.^[rx] Or chronic glomerulonephritis which is a disease characterized by inflammation of the glomeruli, or small blood vessels in the kidneys.^[rx][rx][rx]

Hypertension can also be produced by diseases of the renal arteries supplying the kidney. This is known as renovascular hypertension; it is thought that decreased perfusion of renal tissue due to stenosis of a main or branch renal artery activates the renin-angiotensin system.^[rx][rx][rx]

Also, some renal tumors can cause hypertension. The differential diagnosis of a renal tumor in a young patient with hypertension includes Juxtaglomerular cell tumor, Wilms’ tumor, and renal cell carcinoma, all of which may produce renin.^[rx]

Hypertension secondary to other renal disorders

• Chronic kidney disease
• Kidney disease / renal artery stenosis – the normal physiological response to low blood pressure in the renal arteries is to increase cardiac output (CO) to maintain the pressure needed for glomerular filtration. Here, however, increased CO cannot solve the structural problems causing renal artery hypotension, with the result that CO remains chronically elevated.
• Renal segmental hypoplasia (Ask-Upmark kidney)

Hypertension secondary to endocrine disorders

• Neurogenic hypertension – excessive secretion of norepinephrine and epinephrine which promotes vasoconstriction resulting from the chronic high activity of the sympathoadrenal system, the sympathetic nervous system, and the adrenal gland. The specific mechanism involved is increased release of the “stress hormones”, epinephrine (adrenaline), and norepinephrine which increase blood output from the heart and constrict arteries. People with neurogenic hypertension respond poorly to treatment with diuretics as the underlying cause of their hypertension is not addressed.^[rx]
  • Pheochromocytoma – a tumor that results in an excessive secretion of norepinephrine and epinephrine which promotes vasoconstriction
• Hyperaldosteronism (Conn’s syndrome) – idiopathic hyperaldosteronism, Liddle’s syndrome (also called pseudoaldosteronism), glucocorticoid remediable aldosteronism
• Cushing’s syndrome – excessive secretion of glucocorticoids causes the hypertension
• Hyperparathyroidism
• Acromegaly
• Hyperthyroidism
• Hypothyroidism

Adrenal

A variety of adrenal cortical abnormalities can cause hypertension, In primary aldosteronism, there is a clear relationship between aldosterone-induced sodium retention and hypertension.^[rx]

Congenital adrenal hyperplasia, a group of autosomal recessive disorders of the enzymes responsible for steroid hormone production, can lead to secondary hypertension by creating atypically high levels of mineralocorticoid steroid hormones. These mineralocorticoids cross-react with the aldosterone receptor, activating it and raising blood pressure.

• 17 alpha-hydroxylase deficiency causes an inability to produce cortisol. Instead, extremely high levels of the precursor hormone corticosterone are produced, some of which is converted to 11-Deoxycorticosterone (DOC), a potent mineralocorticoid not normally clinically important in humans. DOC has blood-pressure raising effects similar to aldosterone, and abnormally high levels result in hypokalemic hypertension.^[rx]
• 11β-hydroxylase deficiency, aka apparent mineralocorticoid excess syndrome, involves a defect in the gene for 11β-hydroxysteroid dehydrogenase, an enzyme that normally inactivates circulating cortisol to the less-active metabolite cortisone.^[16] At high concentrations cortisol can cross-react and activate the mineralocorticoid receptor, leading to aldosterone-like effects in the kidney, causing hypertension.^[17] This effect can also be produced by prolonged ingestion of licorice (which can be of potent strength in licorice candy), by causing inhibition of the 11β-hydroxysteroid dehydrogenase enzyme and likewise leading to secondary apparent mineralocorticoid excess syndrome.^[rx][rx][rx] Frequently, if licorice is the cause of the high blood pressure, a low blood level of potassium will also be present.^[rx] Cortisol-induced hypertension cannot be completely explained by the activity of Cortisol on Aldosterone receptors. Experiments show that treatment with Spironolactone (an inhibitor of the aldosterone receptor), does not prevent hypertension with excess cortisol. It seems that inhibition of nitric oxide synthesis may also play a role in cortisol-induced hypertension.^[rx]

Yet another related disorder causing hypertension is glucocorticoid remediable aldosteronism, which is an autosomal dominant disorder in which the increase in aldosterone secretion produced by ACTH is no longer transient, causing of primary hyperaldosteronism, the Gene mutated will result in an aldosterone synthase that is ACTH-sensitive, which is normally not.^{[rx]rx][rx][rx][rx]} GRA appears to be the most common monogenic form of human hypertension.^[rx]

Compare these effects to those seen in Conn’s disease, an adrenocortical tumor that causes excess release of aldosterone,^[rx] that leads to hypertension.^[rx][rx][rx]

Another adrenal-related cause is Cushing’s syndrome which is a disorder caused by high levels of cortisol. Cortisol is a hormone secreted by the cortex of the adrenal glands. Cushing’s syndrome can be caused by taking glucocorticoid drugs, or by tumors that produce cortisol or adrenocorticotropic hormone (ACTH).^[rx] More than 80% of patients with Cushing’s syndrome develop hypertension.,^[rx] which is accompanied by distinct symptoms of the syndrome, such as central obesity, lipodystrophy, moon face, sweating, hirsutism, and anxiety.^[rx]

Neuroendocrine tumors are also a well-known cause of secondary hypertension. Pheochromocytoma^[rx] (most often located in the adrenal medulla) increases secretion of catecholamines such as epinephrine and norepinephrine, causing excessive stimulation of adrenergic receptors, which results in peripheral vasoconstriction and cardiac stimulation. This diagnosis is confirmed by demonstrating increased urinary excretion of epinephrine and norepinephrine and/or their metabolites (vanillylmandelic acid).

Other secondary hypertension

• Hormonal contraceptives
• Neurologic disorders
• Obstructive sleep apnea
• Licorice (when consumed in excessive amounts)
• Scleroderma
• Neurofibromatosis
• Pregnancy: unclear cause.
• Cancers: tumors in the kidney can operate in the same way as kidney disease. More commonly, however, tumors cause inessential hypertension by ectopic secretion of hormones involved in the normal physiological control of blood pressure.
• Drugs: In particular, alcohol, nasal decongestants with adrenergic effects, NSAIDs, MAOIs, adrenoceptor stimulants, and combined methods of hormonal contraception (those containing ethinylestradiol) can cause hypertension while in use.
  • Heavy alcohol use
  • Steroid use
  • Nicotine use.^[rx]
• Malformed aorta, slow pulse, ischemia: these cause reduced blood flow to the renal arteries, with physiological responses as already outlined.
  • Coarctation of the aorta
  • Atherosclerosis
• Anemia: unclear cause.
• Fever: unclear cause.
• Whitecoat hypertension, that is, elevated blood pressure in a clinical setting but not in other settings, probably due to the anxiety some people experience during a clinic visit.
• Perioperative hypertension is the development of hypertension just before, during or after surgery. It may occur before surgery during the induction of anesthesia; intraoperatively e.g. by pain-induced sympathetic nervous system stimulation; in the early postanesthesia period, e.g. by pain-induced sympathetic stimulation, hypothermia, hypoxia, or hypervolemia from excessive intraoperative fluid therapy; and in the 24 to 48 hours after the postoperative period as fluid is mobilized from the extravascular space. In addition, hypertension may develop perioperatively because of the discontinuation of long-term antihypertensive medication.^[rx]

Causes of Secondary Hypertension

Secondary hypertension is elevated blood pressure (BP), which is secondary to an identifiable cause. Since its prevalence is relatively low, performing routine evaluations in every case of hypertension is not cost-effective and is also time-consuming. However, one must be aware of clinical clues that could suggest a secondary cause of hypertension. The clinical clues to look out for that could be suggestive of a secondary cause of hypertension are as follows[rx]

• Diabetes complications (diabetic nephropathy) – Diabetes can damage your kidneys’ filtering system, which can lead to high blood pressure.
• Polycystic kidney disease – In this inherited condition, cysts in your kidneys prevent the kidneys from working normally and can raise blood pressure.
• Glomerular disease – Your kidneys filter waste and sodium using microscopic filters called glomeruli that can sometimes become swollen. If the swollen glomeruli can’t work normally, you may develop high blood pressure.
• Renovascular hypertension – This type of high blood pressure is caused by narrowing (stenosis) of one or both arteries leading to your kidneys.
• Resistant hypertension, i.e., persistent blood pressure greater than 140/90 mm Hg despite using three anti-hypertensives from different classes, that includes a diuretic, all at adequate doses.
• Increased lability or acute rise in blood pressure in a patient who had previously stable pressures.
• Hypertension that develops in non-black patients less than 30 years of age, who do not have any other risk factors for hypertension, e.g., obesity, family history, etc.
• Patients with severe hypertension (BP greater than 180/110 mm Hg) and patients with end-organ damage like acute kidney injury, neurological manifestations, flash pulmonary edema, hypertensive retinopathy, left ventricular hypertrophy, etc.
• Hypertension is associated with electrolyte disorders like hypokalemia or metabolic alkalosis
• Age of onset of hypertension before puberty.
• Non-dipping or reverse dipping presents while monitoring 24-hour ambulatory blood pressure. (Normally, the blood pressure at night is lower than the blood pressure during the day, i.e., there is a ‘dip’ in blood pressure at night. The absence of this ‘dip’ or ‘reverse dipping,’ i.e., ‘dip’ present during the day instead of at night can be suggestive of a secondary cause of hypertension).

The etiology of secondary hypertension is varied. The causes subdivide into the following four categories: 

• A. Renal causes: Among these, the major categories are renal parenchymal disease (which includes chronic kidney disease and polycystic kidney disease) and reno-vascular disease (which includes renal artery stenosis and fibromuscular dysplasia).
• B. Endocrine causes –  Primary aldosteronism, Cushing syndrome/disease, hyperthyroidism, hypothyroidism, hyperparathyroidism, pheochromocytoma including drug-mediated pheochromocytoma crisis,[rx] acromegaly, congenital adrenal hyperplasia.
• C. Vascular: Coarctation of the aorta.
• D. Other: Obstructive sleep apnea, drug-induced hypertension, pregnancy, scleroderma.

Drug-induced hypertension is a significant cause of secondary hypertension. Hence, it is essential to look at the patient’s medication list. Following are the drugs that can cause hypertension[rx]:

• Non-steroidal anti-inflammatory drugs, acetaminophen, and aspirin are the commonest implicated drugs in the worsening of blood pressure control due to their widespread use
• Sodium-containing antacids
• Drugs used to treat attention-deficit/hyperactivity disorder(ADHD):  Methylphenidate, amphetamine, dexmethylphenidate, and dextroamphetamine
• Anti-depressants: Monoamine oxidase inhibitors, tricyclic antidepressants, and serotonin-norepinephrine reuptake inhibitors
• Atypical antipsychotics like clozapine and olanzapine
• Decongestants that have phenylephrine or pseudoephedrine
• Appetite suppressants
• Herbal supplements like St John wort, ephedra, and yohimbine
• Systemic corticosteroids like  dexamethasone, methylprednisolone, prednisone, prednisolone, and fludrocortisone
• Mineralocorticoids like carbenoxolone, licorice, 9-alpha fludrocortisone and ketoconazole
• Estrogens, androgens, and oral contraceptives
• Immunosuppressants like cyclosporine
• Chronic recombinant human erythropoietin
• Recreational drugs: cocaine, methamphetamine, MDMA, bath salts
• Nicotine, alcohol
• Chemotherapeutic agents like gemcitabine (which causes microvascular injury)

Symptoms Of Secondary Hypertension 

The main symptoms of Secondary hypertension are rapidly increasing blood pressure of 180/120 or higher and signs of organ damage. Usually, the damage happens to the kidneys or the eyes.

Other symptoms depend on how the rise in blood pressure affects your organs. A common symptom is bleeding and swelling in the tiny blood vessels in the retina. The retina is the layer of nerves that line the back of the eye. It senses light and sends signals to the brain through the optic nerve, which can also be affected by malignant hypertension. When the eye is involved,  can secondary hypertension cause changes in vision.

Other symptoms of malignant hypertension include

• Pheochromocytoma – Sweating, increased frequency or force of heartbeats, headache, anxiety
• Cushing’s syndrome – Weight gain, weakness, abnormal growth of body hair or loss of menstrual periods (in women), purple striations (lines) on the skin of the abdomen
• Thyroid problems – Fatigue (tiredness), weight gain or weight loss, intolerance to heat or cold
• Conn’s syndrome or primary aldosteronism – Weakness due to low levels of potassium in the body
• Obstructive sleep apnea – excessive fatigue or sleepiness during daytime, snoring, pauses in breathing during sleep
• Change in mental status, such as anxiety, confusion, decreased alertness, decreased ability to concentrate, fatigue, restlessness, sleepiness, or stupor
• Chest pain (feeling of crushing or pressure)
• Cough
• Headache
• Nausea or vomiting
• Numbness of the arms, legs, face, or other areas
• Reduced urine output
• Seizure
• Shortness of breath
• Weakness of the arms, legs, face, or other areas
• Blurred vision
• Chest pain (angina)
• Difficulty breathing
• Dizziness
• Numbness in the arms, legs, and face
• Severe headache
• Shortness of breath

In rare cases, secondary hypertension can cause brain swelling, which leads to a dangerous condition called hypertensive encephalopathy. Symptoms include:

• Blindness
• Changes in mental status
• Coma
• Confusion
• Drowsiness
• Headache that continues to get worse
• Nausea and vomiting
• Seizures

Diagnosis of Secondary Hypertension

Obtaining a complete history and performing a good physical exam is very important when trying to find the underlying cause of hypertension. The following history and physical exam findings point towards a specific cause of secondary hypertension:

• Snoring, obesity, and daytime sleepiness could be indicative of obstructive sleep apnea.
• History of renal insufficiency, atherosclerotic cardiovascular disease, edema may warrant further evaluation of chronic kidney disease (renal parenchymal disease).
• History of recurrent urinary tract infections, kidney stones, acute/chronic abdominal/flank pain, hematuria, progressive renal failure may point towards autosomal dominant polycystic kidney disease (renal parenchymal disease).
• A systolic/ diastolic abdominal bruit is audible in reno-vascular disease.
• Use of sympathomimetics, acute stress, perioperative setting, tachycardia could all be in the context of excess catecholamines.
• Decreased or delayed femoral pulses are seen in coarctation of the aorta.
• Weight gain, fatigue, weakness, hirsutism, amenorrhea, moon facies, dorsal hump, purple striae, and truncal obesity present in Cushing syndrome/disease.
• Paroxysmal hypertension, headaches, diaphoresis, palpitations, and tachycardia are features in pheochromocytoma.
• Fatigue, weight loss, hair loss, diastolic hypertension, and muscle weakness are seen in hypothyroidism.
• Heat intolerance, weight loss, palpitations, systolic hypertension, exophthalmos, tremor, and tachycardia will occur in hyperthyroidism.
• Kidney stones, osteoporosis, depression, lethargy, and muscle weakness present in hyperparathyroidism.
• Headaches, fatigue, visual problems, enlargement of the hands, feet, and tongue are features in acromegaly.
• Heartburn, Raynaud phenomenon, nail pitting on the exam may be suggestive of scleroderma.

Lab Test and Imaging

Laboratory tests and imaging modalities also help in diagnosing secondary hypertension. Some of the findings on common tests that can create suspicion for an underlying cause of hypertension are as follows:

• Basic Metabolic Panel (BMP) – Hypokalemia presents in primary hyperaldosteronism and Cushing syndrome/disease. Also seen on the BMP in primary hyperaldosteronism, is metabolic alkalosis and hypernatremia. Blood urea nitrogen (BUN) and creatinine become elevated in renal parenchymal disease.
• Complete blood count (CBC)  – Polycythemia can be present in obstructive sleep apnea.
• Urine analysis – Proteinuria can be a feature in renal parenchymal disease.
• Chest X-Ray in coarctation of aorta shows inferior rib notching and a figure of 3 sign (abnormality of the contour of the aorta).

Upon establishing suspicion for a particular cause based on history, physical exam findings, and common laboratory tests, certain tests can be used to specifically rule out or rule in a cause of secondary hypertension. They are as follows:

• Obstructive sleep apnea (OSA) – Polysomnography (preferably in-laboratory polysomnography) is the diagnostic study of choice when there is a suspicion of obstructive sleep apnea.
• Primary hyperaldosteronism – A plasma aldosterone to renin ratio greater than 30, points towards a diagnosis of primary aldosteronism. A CT scan of the abdomen is also done to look for the presence of adenomas or hyperplasia of the adrenal glands.
• Renal parenchymal disease – A decreased creatinine clearance occurs in renal parenchymal disease. Renal ultrasonography can be further used to determine the cause for the decreased creatinine clearance. Multiple cysts demonstrate in polycystic kidney disease, and a small contracted kidney is a feature in chronic kidney disease. Genetic testing can also be useful in ADPKD.
• Reno-vascular disease – Magnetic resonance angiography/CT angiography/doppler of renal arteries can all be used to look for the presence of stenosis of the renal arteries. Other tests that can be useful are captopril-augmented radioisotopic renography and renal arteriography.
• Excess catecholamine use – If the patient is normotensive in the absence of high catecholamines, it rules out excess catecholamines as the cause.
• Coarctation of the aorta – Doppler or CT imaging of the aorta will show a narrowing of the aorta. Echocardiography is another modality of choice.
• Cushing syndrome/disease – Overnight 1 mg dexamethasone-suppression test and adrenocorticotropic hormone can help diagnose Cushing’s disease and syndrome.
• Pheochromocytoma – Urinary catecholamine metabolites (vanillylmandelic acid, metanephrines, normetanephrine) become elevated in pheochromocytoma.
• Hyper/hypothyroidism – Serum thyroid-stimulating hormone, thyroxine, and triiodothyronine levels help to diagnose hyperthyroidism and hypothyroidism.
• Hyperparathyroidism – Serum calcium and parathyroid hormone levels help in the diagnosis of hyperparathyroidism.
• Acromegaly – Elevated growth hormone level can point towards acromegaly.
• Scleroderma/ scleroderma renal crisis – Thrombotic microangiopathy, autoantibodies against RNA polymerase III, positive antinuclear antibody (ANA) will present in scleroderma.
• Electrocardiogram (ECG or EKG) – This painless noninvasive test records the electrical signals in your heart. You might have this test if your doctor thinks a heart problem might be causing your secondary hypertension.
• Ultrasound of your kidneys – Many kidney conditions are linked to secondary hypertension. In this noninvasive test, a technician moves a small, hand-held device called a transducer over the area to be tested. The transducer sends sound waves into your body, collects the ones that bounce back and sends them to a computer, which creates images of your kidneys.

Treatment of Secondary Hypertension

Management of secondary hypertension comprises of adequate control of blood pressure with antihypertensive drugs and addressing the secondary causes mentioned above. This section briefly discusses the management of the more common causes of secondary hypertension, viz: renal parenchymal disease, renovascular hypertension, primary hyperaldosteronism, obstructive sleep apnea, drug-induced hypertension, and pregnancy.

A. Renal parenchymal disease

• Renal parenchymal disease-causing hypertension mainly involves chronic kidney disease (CKD) and autosomal dominant polycystic kidney disease (ADPKD).
• i. Management of chronic kidney disease comprises of treating the reversible causes responsible for causing CKD (e.g., treating hypovolemia with fluids, avoid nephrotoxin use, relieve urinary tract obstruction) and slowing the rate of progression of the disease. To slow the rate of progression, adequate blood pressure control, decreasing urine protein, glycemic control, lifestyle changes like dietary protein restriction, and smoking cessation help. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) are the best anti-hypertensives to use in proteinuric CKD. Bicarbonate use in patients with chronic metabolic acidosis slows progression to end-stage renal disease.[rx]
• ii. Patients with ADPKD eventually require renal replacement therapy. Before that stage reached, hypertension management is with anti-hypertensives: ACE inhibitors or ARBs and sodium restriction. Tolvaptan is an option in patients who are at high risk for progression to CKD. It decreases the rate of estimated glomerular filtration rate decline.[rx]

B. Renovascular hypertension

• Management of renovascular hypertension (i.e., renal artery stenosis from either atherosclerotic disease or fibromuscular dysplasia) divides into medical therapy and revascularization. Medical therapy involves the use of anti-hypertensives to control blood pressure and in the case of atherosclerotic disease, the use of antiplatelets, statins, diet, and lifestyle changes. ACE inhibitors and ARBs are the anti-hypertensives of choice. Other anti-hypertensives that are treatment options are calcium channel blockers and thiazide diuretics.
• Revascularization is usually done by percutaneous angioplasty with stenting of the renal artery.  Surgery (which frequently includes aorto-renal bypass or sometimes removal of the ‘pressor’ kidney) is only for patients with complex anatomy.

In the following patients, revascularization may be more beneficial than medical therapy alone

• Patients with recurrent flash pulmonary edema
• Failure or intolerance to optimal medical treatment
• Refractory hypertension
• Unexplained, progressive, a decline in renal function,
• Recent initiation of dialysis in a patient with suspected renal artery stenosis
• An acute increase in creatinine after medical therapy and in patients with a renal resistive index of less than 80 mmHg on Doppler

C. Primary hyperaldosteronism

• Unilateral primary hyperaldosteronism (e.g., unilateral adrenal hyperplasia or aldosterone-producing adenoma) gets treated with unilateral laparoscopic adrenalectomy. If the patient is not a surgical candidate or a patient has bilateral adrenal disease, then medical management with a mineralocorticoid receptor antagonist is recommended- with spironolactone being the primary agent and eplerenone being the alternative.[rx]

D. Obstructive Sleep Apnea

• Continuous positive airway pressure (CPAP) therapy is the mainstay of treatment for OSA. To note, however, lifestyle modifications like weight loss, along with usage of CPAP have a synergistic effect on lowering blood pressure and are better than either intervention alone.[rx]
• An alternative to CPAP is oral appliances, used in mild to moderate OSA, which are non-inferior to CPAP in the reduction of blood pressure and may even help with better compliance in patients. In patients refractory to the above treatment, few upper airway surgeries can be performed to help with symptoms and reduction in blood pressure, like uvulopalatopharyngoplasty (UPPP) in adults and tonsillectomy and adenoidectomy in children.  Along with these, anti-hypertensive drugs also help, particularly the ones that modulate the renin-angiotensin system (ACE inhibitors, ARBs, aldosterone antagonists, and beta-blockers are the best options).[rx]

E. Drug-induced hypertension

• In drug-induced hypertension, upon identification of the culprit drug, the management is to withhold it and look for improvement.

F. Pregnancy

• Hypertension in pregnancy comprises chronic hypertension, gestational hypertension, pre-eclampsia, and eclampsia. Chronic hypertension is when hypertension occurs before pregnancy or before 20 weeks of gestation, whereas the other three occur after 20 weeks. Pre-eclampsia is associated with proteinuria, and eclampsia is associated with seizures.
• Interventions for hypertension in pregnancy are lifestyle modifications and anti-hypertensives. The anti-hypertensives commonly used in pregnancy are labetalol, nifedipine, and methyldopa.
• In cases of severe hypertension (severe preeclampsia, eclampsia, and HELLP syndrome), the standard of care is delivered, especially after 37 weeks of gestation. If an acute decrease in blood pressure is required, intravenous labetalol or intravenous hydralazine are options. Magnesium sulfate prevents seizures.[rx][rx]

Blood Pressure Goals

• SHEP and HYVET trials have shown significant benefits of antihypertensive treatment in patients with the goal of SBP <150 mmHg[rx].
• The VALsartan in Elderly Isolated Systolic Hypertension (VALISH) trial showed no significant difference in the primary outcome of sudden death, fatal or nonfatal myocardial infarction and stroke, heart failure death, or other cardiovascular death among patients with strict (< 140 mmHg) and moderate (140 to 150 mmHg) SBP control[rx].
• However, the VALISH trial was underpowered due to the low number of events.
• Hence, the optimal SBP in patients with hypertensive disorder remained a controversial topic.
• The most recent Systolic Blood Pressure Intervention Trial (SPRINT) has shown that intensive SBP target of < 120 mmHg improved the cardiovascular outcomes and the overall survival compared to the standard SBP target of 135 to 139 mmHg[rx].
• However, aggressive SBP lowering may be harmful in the elderly and incite more adverse effects such as hypotension, end-organ hypoperfusion (causing acute kidney injury, and intracranial hypoperfusion which may link to cognitive decline), and polypharmacy.
• It is suggested that a goal blood pressure of < 130/80 mmHg is appropriate as long as the patient tolerates it.
• Otherwise, < 140/90 mmHg is considered reasonable in patients who are in the elderly population and patients with labile blood pressure or polypharmacy.
• Management strategies should always be patient-centered, with the aim of optimizing blood pressure control and avoiding polypharmacy, especially in the elderly.

J-curve Phenomenon

• Various studies have shown a J-curve association between blood pressure with risk of myocardial infarction and death.
• Patients with isolated systolic hypertension who receive antihypertensive treatment may precipitously drop their DBP as well.[rx][rx]
• As myocardial perfusion occurs mainly during diastole, an excessive drop in DBP may increase the risk of cardiovascular disease and death.

Lifestyle changes

You may also need to make some lifestyle changes as part of your ISH treatment plan. These can include:

• Losing weight. This can help lower your blood pressure. In fact, for every two pounds you lose, you could lower your blood pressure by about 1 mm Hg.
• Eating a heart-healthy diet. You should also aim to reduce the amount of sodium in your diet. Consider the DASH diet, which emphasizes eating:
  • vegetables
  •  whole grains
  •  low-fat dairy products
  •  fruits
• Exercising. Not only can exercise help you lower your blood pressure, but it can help you control your weight and stress levels. Aim to perform some sort of aerobic exercise for at least 30 minutes most days of the week.
• Decreasing alcohol consumption. Healthy alcohol intake is one drink per day for women and two per day for men.
• Quitting smoking. Smoking can raise your blood pressure and also contribute to a variety of other health problems.
• Managing stress. Stress can raise your blood pressure, so finding ways to relieve it are important. Examples of techniques to help lower stress are meditation and deep breathing exercises.

Complications

Secondary hypertension can worsen the underlying medical condition you have that’s causing your high blood pressure. If you don’t receive treatment, secondary hypertension can lead to other health problems, such as:

• Damage to your arteries. This can result in hardening and thickening of the arteries (atherosclerosis), which can lead to a heart attack, stroke, or other complications.
• Aneurysm. Increased blood pressure can cause your blood vessels to weaken and bulge, forming an aneurysm. If an aneurysm ruptures, it can be life-threatening.
• Heart failure. To pump blood against the higher pressure in your vessels, your heart muscle thickens. Eventually, the thickened muscle may have a harder time pumping enough blood to meet your body’s needs, which can lead to heart failure.
• Weakened and narrowed blood vessels in your kidneys. This can prevent these organs from working properly.
• Thickened, narrowed, or torn blood vessels in the eyes. This can result in vision loss.
• Metabolic syndrome. This syndrome is a cluster of disorders of your body’s metabolism — including increased waist circumference, high triglycerides, low high-density lipoprotein (HDL) cholesterol (the “good” cholesterol), high blood pressure, and high insulin levels. If you have high blood pressure, you’re more likely to have other components of metabolic syndrome. The more components you have, the greater your risk of developing diabetes, heart disease, or stroke.
• Trouble with memory or understanding. Uncontrolled high blood pressure also may affect your ability to think, remember and learn. Trouble with memory or understanding concepts is more common in people who have high blood pressure.

• https://www.ncbi.nlm.nih.gov/books/NBK268/
• https://www.ncbi.nlm.nih.gov/books/NBK279239/
• https://www.ncbi.nlm.nih.gov/books/NBK2217/
• https://www.ncbi.nlm.nih.gov/books/NBK482189/
• https://www.ncbi.nlm.nih.gov/books/NBK482408/
• https://www.ncbi.nlm.nih.gov/books/NBK538226/
• https://www.ncbi.nlm.nih.gov/books/NBK538313/
• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6477925/
• https://www.ncbi.nlm.nih.gov/books/NBK513351/
• https://www.ncbi.nlm.nih.gov/books/NBK279027/
• https://www.ncbi.nlm.nih.gov/books/NBK431051/
• https://www.ncbi.nlm.nih.gov/books/NBK430839/
• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1120075/
• https://www.ncbi.nlm.nih.gov/books/NBK9630/
• https://www.ncbi.nlm.nih.gov/books/NBK539859/
• https://www.ncbi.nlm.nih.gov/books/NBK482472/
• https://www.ncbi.nlm.nih.gov/books/NBK499961/
• https://www.ncbi.nlm.nih.gov/books/NBK554579/
• https://www.ncbi.nlm.nih.gov/books/NBK538226/
• https://www.ncbi.nlm.nih.gov/books/NBK537297/
• https://www.ncbi.nlm.nih.gov/books/NBK482514/
• https://www.ncbi.nlm.nih.gov/books/NBK507701/
• https://www.ncbi.nlm.nih.gov/books/NBK544305/
• https://www.ncbi.nlm.nih.gov/books/NBK554499/
• https://www.ncbi.nlm.nih.gov/books/NBK525980/
• https://en.wikipedia.org/wiki/Essential_hypertension
• https://en.wikipedia.org/wiki/Systolic_hypertension
• https://www.sciencedirect.com/topics/medicine-and-dentistry/essential-hypertension
• https://www.mayoclinic.org/diseases-conditions/high-blood-pressure/diagnosis-treatment/drc-20373417

Malignant hypertension is a term that has been used to describe patients with elevated blood pressure (BP) and multiple complications (End organ damage) with a poor prognosis. Today, the term hypertensive crisis is used to describe patients who present with severe BP elevations as follow:

• Systolic blood pressure (SBP) greater than 180 mm Hg
• Diastolic blood pressure (DBP) greater than 120 mm Hg)

The diagnosis can be further classified as a hypertensive emergency when severe elevation in BP is associated with end-organ damage, or hypertensive urgency when severe hypertension occurs without it. Prompt treatment of BP can prevent a hypertensive emergency and consequently, serious life-threatening complications.[rx][rx][rx][rx]

In order to make a diagnosis of malignant hypertension, papilledema has to be present. In malignant hypertension, the key is to lower the blood pressure within a few hours.

Causes of Malignant Hypertension

There are multiple causes of malignant hypertension (hypertensive crisis) including the following:

• Medication noncompliance
• Renovascular diseases, such as renal artery stenosis, polyarteritis nodosa, and Takayasu arteritis
• Renal parenchymal disease including glomerulonephritis, tubulointerstitial nephritis, systemic sclerosis, hemolytic-uremic syndrome, systemic lupus erythematosus
• Endocrine dysfunction, such as pheochromocytoma, Cushing disease, primary hyperaldosteronism, renin-secreting tumor
• Coarctation of aorta; drugs or other exposures, including cocaine, phencyclidine, sympathomimetics, erythropoietin, cyclosporine
• Antihypertensive medication withdrawal
• Amphetamines
• Central nervous system disorders, such as head injury, cerebral infarction, and cerebral hemorrhage
• Hypertensive emergencies occur when a relatively rapid elevation of BP develops in a short period.
• An increase in systemic vascular resistance by an increase in vasoconstriction mechanisms through renin-angiotensin activation, pressure natriuresis, hypoperfusion, and ischemia are the most common culprits of end-organ damage.
• The classic vascular feature is fibrinoid necrosis of the small vessels. In addition, red cell destruction is common as they pass through these obstructed vessels leading to microangiopathic hemolytic anemia. Another feature of a hypertensive emergency is the loss of autoregulation in the brain, which can present as hypertensive encephalopathy.

Symptoms of Malignant Hypertension

The main symptoms of malignant hypertension are rapidly increasing blood pressure of 180/120 or higher and signs of organ damage. Usually, the damage happens to the kidneys or the eyes.

Other symptoms depend on how the rise in blood pressure affects your organs. A common symptom is bleeding and swelling in the tiny blood vessels in the retina. The retina is the layer of nerves that line the back of the eye. It senses light and sends signals to the brain through the optic nerve, which can also be affected by malignant hypertension. When the eye is involved, malignant hypertension can cause changes in vision.

Other symptoms of malignant hypertension include:

• Change in mental status, such as anxiety, confusion, decreased alertness, decreased ability to concentrate, fatigue, restlessness, sleepiness, or stupor
• Chest pain (feeling of crushing or pressure)
• Cough
• Headache
• Nausea or vomiting
• Numbness of the arms, legs, face, or other areas
• Reduced urine output
• Seizure
• Shortness of breath
• Weakness of the arms, legs, face, or other areas
• Blurred vision
• Chest pain (angina)
• Difficulty breathing
• Dizziness
• Numbness in the arms, legs, and face
• Severe headache
• Shortness of breath

In rare cases, malignant hypertension can cause brain swelling, which leads to a dangerous condition called hypertensive encephalopathy. Symptoms include:

• Blindness
• Changes in mental status
• Coma
• Confusion
• Drowsiness
• Headache that continues to get worse
• Nausea and vomiting
• Seizures

High blood pressure, in general, makes it difficult for kidneys to filter wastes and toxins from the blood. It is a leading cause of kidney failure. Malignant hypertension can cause your kidneys to suddenly stop working properly.

Diagnosis of Malignant Hypertension

Most patients have persistently elevated BP for years before presenting with a hypertensive emergency. Initial questioning should focus on finding indicators related to end-organ damage including a headache, nausea or vomiting, visual disturbances, chest or back pain, dyspnea, orthopnea, or visual disturbances. Review all prescription and nonprescription medications, adherence, and time from the last dose. Ask about recreational drug use, such as amphetamines, cocaine, phencyclidine.

Physical Examination

On physical exam, confirm BP on both arms using an appropriately-sized blood pressure cuff. Funduscopic exam findings may include hemorrhages, exudates or papilledema. Assess for murmurs and gallops or other signs of heart failure. Look for evidence of pulmonary edema, abdominal bruits. Neurological findings can include stupor, seizures, delirium, agitation.[rx][rx][rx]

Accurate Blood Pressure Measurement

• Reassess normal blood pressure yearly.
• Take blood pressure after the patient rests for 5 minutes.
• The patient should sit in a chair with both feet flat on the ground and the back straight.
• The patient’s arm should be placed on a flat surface at the level of the chest or heart.
• Choosing the right cuff size is important.
• SBP is the first Korotkoff sound.
• DBP is the fifth Korotkoff sound.
• Obtain an average of 2 to 3 blood pressure measurements on 2 or 3 separate occasions to confirm a hypertension diagnosis.

General Appearance

• Body mass index calculation
• Signs of Cushing syndrome such as buffalo hump, moon face, thinning of the skin, and red or purple striae.
• Restlessness
• Sweating
• Flushing
• Neurofibromatosis

Neck

• Thyroid enlargement
• Carotid bruits

Fundoscopy

• Papilledema
• Cotton wool spots
• Arteriolar narrowing
• Arteriovenous nicking
• Hemorrhage

Heart

• Gallop rhythm, S4
• Heave
• Jugular venous distension

Lungs

• Rales
• Rhonchi

Abdomen

• Enlarged kidneys
• Aorta or renal bruits

Neurologic

• Visual changes
• Confusion
• focal weakness

Extremities

• Peripheral pulses
• Pedal edema
• Cold peripheral limbs

An eye exam will reveal changes that indicate high blood pressure, including

• Bleeding of the retina (back part of the eye)
• Narrowing of the blood vessels in the retina
• Swelling of the optic nerve
• Other problems with the retina

Lab Test And Imaging

The history and physical examination are really important in patients presenting with a very elevated BP, or an acute rise over a previously normal baseline, even if the presenting BP is less than 180/120 mm Hg. Furthermore, the following evaluation should be performed to find the presence of end-organ damage in association with targeted clinical symptoms or signs:

• Electrocardiography
• Chest x-Ray
• Urinalysis
• Electrolytes and creatinine
• Cardiac biomarkers, when the acute coronary syndrome is suspected
• Toxicology screen
• CT/MRI of the brain, when head injury, neurologic symptoms, hypertensive retinopathy, nausea, or vomiting are present
• Contrast CT/MRI of the chest or TEE, if aortic dissection is suspected

It is often easiest to categorize hypertensive emergencies by the organ that is being damaged. The evaluation above can usually identify the at-risk target organ and can direct both, the target BP and the promptness with which the target is achieved.

The cardiac exam may reveal the presence of an MI, CHF or pulmonary edema. Concentric left ventricular hypertrophy is often present, including the 4th heart sound. Always check the blood pressure in both arms to rule out aortic dissection. Patients may also have bruit in the neck and groin

CNS exam may reveal a headache, visual changes, vomiting, confusion, and seizures. The eye exam may reveal soft exudates, flame-shaped hemorrhages, and papilledema

The renal exam may present with oliguria and the GI symptoms may include nausea, vomiting and vague abdominal pain.

Treatment of Malignant Hypertension

Adequate therapy, including the choice of the medication and the BP target, changes depending on the specific hypertensive emergency and the affected organ.[rx][rx][rx][rx]

It is not recommended to decrease the BP too fast or too much, as ischemic damage can occur in vascular territories that have become habituated with the elevated level of BP. For the majority of hypertensive emergencies, mean arterial pressure (MAP) should be reduced by approximately 10 to 20% within the first hour and by another 5% to 15% over the next 24 hours. This often results in a target BP of less than 180/120 mm Hg for the first hour and less than 160/110 mm Hg for the next 24 hours, but rarely less than 130/80 mm Hg during that time frame.

Nonpharmacologic Therapy

• Recommended for all patients, regardless of the reading of the blood pressure.
• Restrict dietary salt (aim for 1.5 g or less per day). Randomized controlled trials have shown that moderate sodium reduction can result in an average blood pressure reduction of 4.8/2.5 mmHg).
• Weight loss (every 1 pound of weight loss will result in a reduction of 1 mmHg blood pressure).
• Start a Dietary Approaches to Stop Hypertension (DASH) diet (rich in fruits, vegetables, whole grains, fish, and low-fat dairy products). A clinical trial has shown that the DASH diet helps to reduce blood pressure by an average of 6/4 mmHg.
• Increase physical activity. Aerobic and resistance training can reduce blood pressure by an average of 4/3 to 6/3 mmHg, irrespective of body weight.
• Limit alcohol intake to no more than one alcoholic drink per day for women and two for men.
• Take a potassium supplement (unless contraindicated in chronic kidney disease patients).
• Quit smoking.
• Use stress management.

Pharmacologic Therapy

Common intravenous (IV) medications and doses used to treat hypertensive emergencies include

• Nicardipine, initial infusion rate 5 mg per hour, increasing by 2.5 mg per hour every 5 minutes to a maximum of 15 mg per hour
• Sodium nitroprusside, 0.3 to 0.5 mcg/kg/minute, increase by 0.5 mcg/kg per minute every few minutes as needed to a maximum dose of 10 mcg/kg per minute
• Labetalol 10 to 20 mg IV followed by bolus doses of 20 to 80 mg at 10-minute intervals until a target blood pressure is reached to a maximum 300-mg cumulative dose
• Esmolol, initial loading dose 500 mcg/kg/minute over 1 minute, then 50 to 100 mcg/kg/minute to a maximum dose of 300 mcg/kg per minute.

If there is any possibility of over or underestimation of BP using frequent noninvasive cuff measurements or if the end-organ damage is life-threatening, consider arterial catheterization for precise, second-to-second measurements allowing for more careful medication titration.

• In general, start off with a single-agent oral antihypertensive drug therapy, especially in the elderly because of the risk of orthostatic hypotension.
• An exception to the above is when the initial SBP is above 160 or blood pressure is > 20/10 mmHg above the goal of blood pressure, which often needs the initiation of two oral antihypertensive agents.
• The four major classes of oral antihypertensive agents include thiazide-like diuretics (chlorthalidone and indapamide), dihydropyridine calcium channel blockers (CCBs: amlodipine, nifedipine, nitrendipine), angiotensin-converting enzyme inhibitors (ACEi: lisinopril, ramipril), and angiotensin receptor blockers (ARBs: losartan, valsartan).
• Randomized controlled trials have shown that thiazide-like diuretics and CCBs are the preferred first-line agents in reducing the risk of stroke and other morbidities in patients with isolated systolic hypertension.
• The dose of the single oral antihypertensive agent should be titrated to the maximum before initiating a second oral antihypertensive agent.
• In patients who require two oral antihypertensive agents, a combination of thiazide-like diuretic and CCB is the preferred strategy.
• ACEi or ARB is often used in the patient with compelling indications such as heart failure reduced ejection, post-myocardial infarction, diabetes, or chronic kidney disease.
• A combination of either ACEi or ARB with CCB or a thiazide-like diuretic can be considered.
• It is important to note that ACEi should never be used concomitantly with ARB under any circumstances.
• Patients with secondary causes of hypertension should have their respective diseases addressed concurrently.
• Studies have shown that the use of beta-blockers in the management of hypertension is inferior compared with ARB, ACEi or CCB for cardiovascular and stroke risk reduction.

The major exceptions to gradual BP lowering over the first day are

• Acute Phase of an Ischemic CVA – The BP is usually not treated unless it is greater than 185/110 mmHg in patients whose reperfusion therapy could be an option or greater than 220/120 mm Hg in patients who might not qualify for it. Consider labetalol or nicardipine infusion.
• Acute Aortic Dissection – The SBP should be lowered to 120 mm Hg within 20 minutes, and a target heart rate around 60 beats per minute, to reduce aortic shearing forces. Treatment usually requires a beta-blocker and a vasodilator. Options include esmolol, nicardipine, or nitroprusside.
• An Intracerebral Hemorrhage – The goals of therapy are different and depend on the location and surgical approach.
• Acute Myocardial Ischemia – Nitroglycerin is the drug of choice; do not use if the patient has taken phosphodiesterase inhibitors, including sildenafil or tadalafil, within the past 48 hours.

After a suitable period, often 8 to 24 hours, of BP control at a target, oral medications are usually given, and the initial intravenous therapy is tapered and discontinued.

References

Systolic hypertension is the predominant form of hypertension in the elderly population. Traditionally it has been defined as systolic blood pressure (SBP) above 140 mmHg with diastolic blood pressure (DBP) of less than 90 mmHg. It is estimated that 15 percent of people 60 years old and above have isolated systolic hypertension. Per the 2017 American College of Cardiology/American Heart Association Blood Pressure Guideline, however, an SBP of 130 mm Hg is now considered hypertensive at all ages. The new definition of hypertension will lead to an increased number of elderly being diagnosed with high blood pressure. Isolated systolic hypertension remains an important public health concern as chronically untreated high SBP patients carry significant mortality and morbidity

Types of Isolated Systolic Hypertension

It is important to identify white coat hypertension and masked hypertension correctly as over- or under-treatment of hypertension can have significant morbidity and mortality.

Whitecoat Hypertension

• Consistently elevated office blood pressure but normal out-of-office blood pressure

Masked Hypertension

• Consistently elevated out-of-office blood pressure but normal office blood pressure

Psuedo-hypertension[rx]

• Result of calcified blood vessels that cause incompressible of the peripheral arteries
• Blood pressure cuff unable to measure the intraluminal blood pressure accurately
• This causes a false elevation of blood pressure reading
• Use of standing blood pressure measurement can help to differentiate pseudo-hypertension from true hypertension
• Patients with poorly controlled blood pressure should be evaluated for pseudo-hypertension prior to being labeled as resistant hypertension.

Understanding readings

Blood pressure is measured in millimeters of mercury (mm Hg).

There are several different blood pressure categories, which are currently defined as the following:

ISH is when you have a systolic blood pressure reading of 140 mm Hg or higher, and a diastolic blood pressure reading of less than 90 mm Hg.

Organ Systems Involved

An abrupt rise in blood pressure or a prolonged elevation of blood pressure may cause end-organ damage in the heart, kidneys, brain, vascular tree, and more.

• Vascular System

  • Endothelial dysfunction/injury
  • Remodeling
  • Atherosclerosis
  • Aortic aneurysm
  • Aortic dissection
• Kidney

  • Albuminuria
  • Proteinuria
  • Chronic renal insufficiency
  • Renal failure
• Cerebrovascular System

  • Stroke
  • Hemorrhage
  • Lacunar infarcts
  • Vascular dementia
  • Retinopathy
• Heart

  • Left ventricular hypertrophy
  • Myocardial infarction
  • Heart failure
  • Atrial fibrillation

Causes of Isolated Systolic Hypertension

Most patients with hypertension have primary hypertension, which is also known as essential hypertension. Rarely, isolated systolic hypertension is attributed to other causes of secondary hypertension such as hypothyroidism/hyperthyroidism, chronic kidney disease, peripheral vascular disease, diabetes mellitus, aortic insufficiency, arteriovenous fistula, anemia, Paget disease, and atherosclerotic renal artery stenosis[rx].

Isolated systolic hypertension, in most cases, develops as a result of the reduced elasticity of the arterial system. This is commonly seen among the elderly as there is increased deposition of calcium and collagen to the arterial wall[rx]. Hence, this may result in reduced compliance of the arterial vessels, decreased lumen-to-wall ratio, and increased thickening and fibrotic remodeling of the vascular intima and media. As a result, these stiffened conduit arteries lead to an increase in pulse pressure and pulse wave velocity, causing an elevation in SBP and a further decline in DBP. Similarly, chronic diseases such as the above causes of secondary hypertension may contribute to the same pathological process by accelerating the deposition of calcium and collagen to the arterial system and the fibrotic remodeling of the vascular walls[rx][rx].

Systolic hypertension may be due to reduced compliance of the aorta with increasing age.^[rx] This increases the load on the ventricle and compromises coronary blood flow, eventually resulting in left ventricular hypertrophy, coronary ischemia, and heart failure.^[rx]

Contemporary science shows an immersed boundary method of computational illustration of a single heartbeat. Applied to physiologic models, immersed boundary theory sees the heart as a great folded semisolid sail fielding and retrieving a vicious blood mass. The sail likened to Windkessel affects physiology, gives and received.

Diagnosis of Isolated Systolic Hypertension

Isolated systolic hypertension, like any other hypertensive disorder, often results in end-organ damage when untreated. Hence, early diagnosis, addressing modifiable risk factors, and initiating appropriate treatment are prudent to decrease morbidity and mortality. The important aspects of the history in the hypertensive patient include the following[rx][rx]:

• Intake of precipitating agents such as nonsteroidal anti-inflammatory drugs, steroids, sympathomimetics, cocaine, steroids, estrogen
• Risk factors such as smoking, diabetes, dyslipidemia, obesity, sedentary lifestyle, unhealthy diet
• Diet, including high salt, processed food, high fat, and alcohol intake
• Family history of hypertension, renal disease, diabetes, or cardiovascular disease
• Symptoms of secondary causes such as spells of tremor, sweating or tachycardia, muscle weakness, thinning of the skin, depression, hematuria, loud snoring, and daytime somnolence
• Symptoms of end-organ damage such as headaches, loss of visual acuity, dyspnea, chest pain, and claudication

Physical Examination

Accurate Blood Pressure Measurement

• Reassess normal blood pressure yearly.
• Take blood pressure after the patient rests for 5 minutes.
• The patient should sit in a chair with both feet flat on the ground and the back straight.
• The patient’s arm should be placed on a flat surface at the level of the chest or heart.
• Choosing the right cuff size is important.
• SBP is the first Korotkoff sound.
• DBP is the fifth Korotkoff sound.
• Obtain an average of 2 to 3 blood pressure measurements on 2 or 3 separate occasions to confirm a hypertension diagnosis.

General Appearance

• Body mass index calculation
• Signs of Cushing syndrome such as buffalo hump, moon face, thinning of the skin, and red or purple striae.
• Restlessness
• Sweating
• Flushing
• Neurofibromatosis

Neck

• Thyroid enlargement
• Carotid bruits

Fundoscopy

• Papilledema
• Cotton wool spots
• Arteriolar narrowing
• Arteriovenous nicking
• Hemorrhage

Heart

• Gallop rhythm, S4
• Heave
• Jugular venous distension

Lungs

• Rales
• Rhonchi

Abdomen

• Enlarged kidneys
• Aorta or renal bruits

Neurologic

• Visual changes
• Confusion
• focal weakness

Extremities

• Peripheral pulses
• Pedal edema
• Cold peripheral limbs

Lab Test And Imaging

Further Evaluation 

When systolic hypertension is suspected based on the reliable measurements, perform a further evaluation to determine the following[rx][rx].

• Presence or absence of cardiovascular risk factors
• The extent of the end-organ damage
• Identifiable causes of hypertension
• Concomitant clinical conditions affecting prognosis and treatment

Routine Laboratory and Clinical Investigation

These tests should be performed to evaluate cardiovascular risk and concomitant diseases.

• 12-lead electrocardiographic (left ventricular hypertrophy features, atrial dilation, and arrhythmias)
• Lipid panels (calculate 10-year atherosclerotic cardiovascular disease (ASCVD) risk)
• Serum creatinine (with an estimation of GFR)
• Serum electrolytes (sodium and potassium)
• Thyroid-stimulating hormone
• Urine analysis (proteinuria)
• Urine microalbuminuria

Additional Tests

Perform the following tests based on the relevant history, physical examination, and routine laboratory findings.

• Hemoglobin A1c
• Serum uric acid
• Ankle-brachial index
• Renal ultrasound and renal duplex Doppler ultrasonography
• Quantitative proteinuria (urine protein to creatinine ratio, 24-hour urine protein)
• Echocardiogram (patient with heart failure)
• Specific tests to search for secondary causes of hypertension (plasma free metanephrines, 24-hour urinary cortisol, aldosterone-renin ratio)

Treatment of Isolated Systolic Hypertension

Goal

Based on these studies, treating to a systolic blood pressure of 140, as long as the diastolic blood pressure is 68 or more, seems safe. Corroborating this, a reanalysis of the SHEP data suggests allowing the diastolic to go below 70 may increase adverse effects.^[rx]

A meta-analysis of individual patient data from randomized controlled trials found the lowest diastolic blood pressure for which cardiovascular outcomes improve is 85 mm Hg for untreated hypertensives and 80 mm Hg for treated hypertensives.^[rx] The authors concluded “poor health conditions leading to low blood pressure and an increased risk for death probably explain the J-shaped curve”.^[rx] Interpreting the meta-analysis is difficult, but avoiding a diastolic blood pressure below 68–70 mm Hg seems reasonable because:

• The low value of 85 mm Hg for treated hypertensives in the meta-analysis is higher than the value of 68–70 mm Hg that is suggested by the two major randomized controlled trials of isolated systolic hypertension
• The two largest trials in the meta-analysis, Hypertension Detection and Follow-up Program (HDFP)^[rx] and Medical Research Council trial in mild hypertension (MRC1)^[rx] were predominantly middle-aged subjects, all of whom had diastolic hypertension before treatment.
• The independent contributions of diseases and factors other than hypertension versus effects of treatment are not clear in the meta-analysis.

A more contemporary meta-analysis by the Cochrane Hypertension group found no benefits in terms of reduced mortality or morbidity from treating patients to lower diastolic targets than 90–100 mmHg.^[rx]

New classifications of blood pressure according to the 2017 ACC/AHA guidelines[rx]

Normal Blood Pressure 

• SBP < 120 mmHg and DBP < 80 mmHg
• Promote lifestyle modification.

Elevated Blood Pressure

• SBP 120 to 129 mmHg and DBP < 80 mmHg
• Initiate nonpharmacologic therapy and reassess in three to six months.

Hypertension Stage 1

• SBP 130 to 139 mmHg or DBP 80 to 89 mmHg
• Patient without ASCVD or 10-year ASCVD risk < 10%: initiate nonpharmacologic therapy for all patients and reassess in three to six months.
• Patient with ASCVD or 10-year ASCVD risk >/= 10%: initiate nonpharmacologic therapy and single oral antihypertensive agent and reassess patient in one month.

Hypertension Stage 2

• : SBP > 139 mmHg or DBP > 89 mmHg
• Initiate nonpharmacologic therapy and single oral antihypertensive agent and reassess patient in one month.

*If the blood pressure goal is not met, assess and optimize adherence to therapy or consider intensification of therapy.

*If the blood pressure goal is met, reassess in three to six months.

Several clinical trials such as HYpertension in the Very Elderly (HYVET) and Systolic Hypertension in the Elderly Program (SHEP) have shown that active treatment of isolated systolic hypertension in older adults resulted in significant reductions in the all-cause mortality (13%), cardiovascular mortality (18%), and stroke (30%) and coronary (23%) events as compared with placebo.

Treatment of hypertension can be divided into nonpharmacologic and pharmacologic therapy[rx][rx].

Nonpharmacologic Therapy

• Recommended for all patients, regardless of the reading of the blood pressure.
• Restrict dietary salt (aim for 1.5 g or less per day). Randomized controlled trials have shown that moderate sodium reduction can result in an average blood pressure reduction of 4.8/2.5 mmHg).
• Weight loss (every 1 pound of weight loss will result in a reduction of 1 mmHg blood pressure).
• Start a Dietary Approaches to Stop Hypertension (DASH) diet (rich in fruits, vegetables, whole grains, fish, and low-fat dairy products). A clinical trial has shown that the DASH diet helps to reduce blood pressure by an average of 6/4 mmHg.
• Increase physical activity. Aerobic and resistance training can reduce blood pressure by an average of 4/3 to 6/3 mmHg, irrespective of body weight.
• Limit alcohol intake to no more than one alcoholic drink per day for women and two for men.
• Take a potassium supplement (unless contraindicated in chronic kidney disease patients).
• Quit smoking.
• Use stress management.

Pharmacologic Therapy

• In general, start off with a single-agent oral antihypertensive drug therapy, especially in the elderly because of the risk of orthostatic hypotension.
• An exception to the above is when the initial SBP is above 160 or blood pressure is > 20/10 mmHg above the goal of blood pressure, which often needs the initiation of two oral antihypertensive agents.
• The four major classes of oral antihypertensive agents include thiazide-like diuretics (chlorthalidone and indapamide), dihydropyridine calcium channel blockers (CCBs: amlodipine, nifedipine, nitrendipine), angiotensin-converting enzyme inhibitors (ACEi: lisinopril, ramipril), and angiotensin receptor blockers (ARBs: losartan, valsartan).
• Randomized controlled trials have shown that thiazide-like diuretics and CCBs are the preferred first-line agents in reducing the risk of stroke and other morbidities in patients with isolated systolic hypertension.
• The dose of the single oral antihypertensive agent should be titrated to the maximum before initiating a second oral antihypertensive agent.
• In patients who require two oral antihypertensive agents, a combination of thiazide-like diuretic and CCB is the preferred strategy.
• ACEi or ARB is often used in the patient with compelling indications such as heart failure reduced ejection, post-myocardial infarction, diabetes, or chronic kidney disease.
• A combination of either ACEi or ARB with CCB or a thiazide-like diuretic can be considered.
• It is important to note that ACEi should never be used concomitantly with ARB under any circumstances.
• Patients with secondary causes of hypertension should have their respective diseases addressed concurrently.
• Studies have shown that the use of beta-blockers in the management of hypertension is inferior compared with ARB, ACEi or CCB for cardiovascular and stroke risk reduction.

Blood Pressure Goals

• SHEP and HYVET trials have shown significant benefits of antihypertensive treatment in patients with the goal of SBP <150 mmHg[rx].
• The VALsartan in Elderly Isolated Systolic Hypertension (VALISH) trial showed no significant difference in the primary outcome of sudden death, fatal or nonfatal myocardial infarction and stroke, heart failure death, or other cardiovascular death among patients with strict (< 140 mmHg) and moderate (140 to 150 mmHg) SBP control[rx].
• However, the VALISH trial was underpowered due to the low number of events.
• Hence, the optimal SBP in patients with hypertensive disorder remained a controversial topic.
• The most recent Systolic Blood Pressure Intervention Trial (SPRINT) has shown that intensive SBP target of < 120 mmHg improved the cardiovascular outcomes and the overall survival compared to the standard SBP target of 135 to 139 mmHg[rx].
• However, aggressive SBP lowering may be harmful in the elderly and incite more adverse effects such as hypotension, end-organ hypoperfusion (causing acute kidney injury, and intracranial hypoperfusion which may link to cognitive decline), and polypharmacy.
• It is suggested that a goal blood pressure of < 130/80 mmHg is appropriate as long as the patient tolerates it.
• Otherwise, < 140/90 mmHg is considered reasonable in patients who are in the elderly population and patients with labile blood pressure or polypharmacy.
• Management strategies should always be patient-centered, with the aim of optimizing blood pressure control and avoiding polypharmacy, especially in the elderly.

J-curve Phenomenon

• Various studies have shown a J-curve association between blood pressure with risk of myocardial infarction and death.
• Patients with isolated systolic hypertension who receive antihypertensive treatment may precipitously drop their DBP as well.[rx][rx]
• As myocardial perfusion occurs mainly during diastole, an excessive drop in DBP may increase the risk of cardiovascular disease and death.

Lifestyle changes

You may also need to make some lifestyle changes as part of your ISH treatment plan. These can include:

• Losing weight. This can help lower your blood pressure. In fact, for every two pounds you lose, you could lower your blood pressure by about 1 mm Hg.
• Eating a heart-healthy diet. You should also aim to reduce the amount of sodium in your diet. Consider the DASH diet, which emphasizes eating:
  • vegetables
  •  whole grains
  •  low-fat dairy products
  •  fruits
• Exercising. Not only can exercise help you lower your blood pressure, but it can help you control your weight and stress levels. Aim to perform some sort of aerobic exercise for at least 30 minutes most days of the week.
• Decreasing alcohol consumption. Healthy alcohol intake is one drink per day for women and two per day for men.
• Quitting smoking. Smoking can raise your blood pressure and also contribute to a variety of other health problems.
• Managing stress. Stress can raise your blood pressure, so finding ways to relieve it are important. Examples of techniques to help lower stress are meditation and deep breathing exercises.

• https://www.ncbi.nlm.nih.gov/books/NBK268/
• https://www.ncbi.nlm.nih.gov/books/NBK279239/
• https://www.ncbi.nlm.nih.gov/books/NBK2217/
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• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1120075/
• https://www.ncbi.nlm.nih.gov/books/NBK9630/
• https://www.ncbi.nlm.nih.gov/books/NBK539859/
• https://www.ncbi.nlm.nih.gov/books/NBK482472/
• https://www.ncbi.nlm.nih.gov/books/NBK499961/
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• https://www.ncbi.nlm.nih.gov/books/NBK554499/
• https://www.ncbi.nlm.nih.gov/books/NBK525980/
• https://en.wikipedia.org/wiki/Essential_hypertension
• https://en.wikipedia.org/wiki/Systolic_hypertension
• https://www.sciencedirect.com/topics/medicine-and-dentistry/essential-hypertension
• https://www.mayoclinic.org/diseases-conditions/high-blood-pressure/diagnosis-treatment/drc-20373417

• https://www.ncbi.nlm.nih.gov/books/NBK268/
• https://www.ncbi.nlm.nih.gov/books/NBK279239/
• https://www.ncbi.nlm.nih.gov/books/NBK2217/
• https://www.ncbi.nlm.nih.gov/books/NBK482189/
• https://www.ncbi.nlm.nih.gov/books/NBK482408/
• https://www.ncbi.nlm.nih.gov/books/NBK538226/
• https://www.ncbi.nlm.nih.gov/books/NBK538313/
• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6477925/
• https://www.ncbi.nlm.nih.gov/books/NBK513351/
• https://www.ncbi.nlm.nih.gov/books/NBK279027/
• https://www.ncbi.nlm.nih.gov/books/NBK431051/
• https://www.ncbi.nlm.nih.gov/books/NBK430839/
• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1120075/
• https://www.ncbi.nlm.nih.gov/books/NBK9630/
• https://www.ncbi.nlm.nih.gov/books/NBK539859/
• https://www.ncbi.nlm.nih.gov/books/NBK482472/
• https://www.ncbi.nlm.nih.gov/books/NBK499961/
• https://www.ncbi.nlm.nih.gov/books/NBK554579/
• https://www.ncbi.nlm.nih.gov/books/NBK538226/
• https://www.ncbi.nlm.nih.gov/books/NBK537297/
• https://www.ncbi.nlm.nih.gov/books/NBK482514/
• https://www.ncbi.nlm.nih.gov/books/NBK507701/
• https://www.ncbi.nlm.nih.gov/books/NBK544305/
• https://www.ncbi.nlm.nih.gov/books/NBK554499/
• https://www.ncbi.nlm.nih.gov/books/NBK525980/
• https://en.wikipedia.org/wiki/Essential_hypertension
• https://www.sciencedirect.com/topics/medicine-and-dentistry/essential-hypertension
• https://www.mayoclinic.org/diseases-conditions/high-blood-pressure/diagnosis-treatment/drc-20373417

Idiopathic Hypertension/Essential hypertension is high blood pressure that doesn’t have a known secondary cause. It’s also referred to as primary hypertension. Blood pressure is the force of blood against your artery walls as your heart pumps blood through your body.

Essential hypertension (also called primary hypertension, or idiopathic hypertension) is the form of hypertension that by definition has no identifiable secondary cause.^[rx][rx] It is the most common type affecting 85% of those with high blood pressure.^[rx][rx] The remaining 15% is accounted for by various causes of secondary hypertension.^[rx] Primary hypertension tends to be familial and is likely to be the consequence of an interaction between environmental and genetic factors.

The current definition of hypertension (HTN) is systolic blood pressure (SBP) values of 130mmHg or more and/or diastolic blood pressure (DBP) more than 80 mmHg. Hypertension ranks among the most common chronic medical condition characterized by a persistent elevation in arterial pressure.

Hypertension has been among the most studied topics of the previous century and has been one of the most significant comorbidities contributing to the development of stroke, myocardial infarction, heart failure, and renal failure.

The definition and categories of hypertension have been evolving over years, but there is a consensus that persistent BP readings of 140/90mmHg or more should undergo treatment with the usual therapeutic target of 130/80mmHg or less.

This article will attempt to review the available knowledge derived from RCTs and the recent updates and guidelines on hypertension put forward by major societies including those from the 8th report of Joint National Committee (JNC-8), American College of Cardiology (ACC), American Society of Hypertension (ASH), European Society of Cardiology (ESC) and European Society of Hypertension (ESH).

Other names for Idiopathic Hypertension

• High blood pressure
• Arterial hypertension
• Hypertension
• Primary hypertension

Causes of Idiopathic Hypertension

Most cases of hypertension are idiopathic which is also known as essential hypertension.  It has long been suggested that an increase in salt intake increases the risk of developing hypertension.[rx] One of the described factors for the development of essential hypertension is the patient genetic ability to the salt response.[rx][rx] About 50 to 60% of the patients are salt sensitive and therefore tend to develop hypertension.[rx]

• Obesity – Data from the Nurses’ Health Study showed that a gain of 5 kg above weight at 18 years of age was associated with 60% higher risk of development of hypertension in middle age.[rx] A 4.5 mmHg increase in blood pressure has been associated with each 10 lb (4.5 kg) gain in weight.[rx] One systematic review found that risk of hypertension increased continuously with increasing body mass index (BMI), waist circumference, weight gain, and waist-to-hip and waist-to-height ratio.[rx] It has been postulated that the link between obesity and hypertension is driven by increased circulating volume, leading to increased cardiac output and persistently elevated peripheral vascular resistance.[rx] Obesity is associated with the metabolic syndrome, insulin resistance, and type 2 diabetes. Bariatric treatment of class III obesity (BMI 40 or above) can reduce or eliminate risk factors for cardiovascular disease, with an effect on hypertension, diabetes, and dyslipidemia.[rx][rx]
• Aerobic exercise <3 times/week – Patients with low level of fitness had a 52% greater relative risk of hypertension at 12-year follow-up compared with those with high levels of fitness.[rx]
• Moderate/high alcohol intake – Chronic alcohol consumption of more than 1 drink per day in women and more than 2 drinks per day in men has been shown to be associated with an increased risk of blood pressure (BP) elevation.[rx][rx] One Cochrane review of the effect of alcohol on BP found that high-dose alcohol (>30 g) has a biphasic effect, decreasing BP up to 12 hours after consumption and increasing BP after 13 hours.[rx]
• Metabolic syndrome – Abdominal obesity has been specifically associated with an increased risk of hypertension, as compared with generalized obesity.[rx] Insulin resistance and hyperinsulinemia are thought to contribute to the development of hypertension through a variety of inflammatory mechanisms.[rx]
• Diabetes mellitus – Hyperglycemia, hyperinsulinemia, and insulin resistance lead to endothelial damage and oxidative stress, and are independently associated with the development of hypertension.[rx]
• Black ancestry – Highest incidence of hypertension is seen in black non-Hispanic people, at all age levels.[rx]
• Age >60 years – Incidence of hypertension increases with age in people of all ancestries and both sexes.[rx] family history of hypertension or coronary artery disease – Patient may have family history of hypertension or coronary artery disease risk factors.[rx]
• Sleep apnea – Obstructive sleep apnea is a risk factor for several cardiovascular diseases, including hypertension.[rx] In addition, there is a possible dose-response relationship between the severity of obstructive sleep apnea and the risk of essential hypertension.[rx] Obstructive sleep apnea is also associated with an increased risk of resistant hypertension.[rx]
• Sodium intake >1.5 g/day – Individuals show a varied tolerance for sodium intake, and reduced sodium intake has modest effect on blood pressure (BP) lowering.[rx][rx] One meta-analysis has shown the amount of BP lowering achieved with sodium reduction has a dose-response relation and is greater for older populations, nonwhite populations, and those with higher baseline systolic BP.[rx]
• Low fruit and vegetable intake – Modest reduction in blood pressure with 4 to 6 servings of fruits and vegetables coupled with lower sodium and fat intake (Dietary Approaches to Stop Hypertension [DASH] diet).[rx]
• Dyslipidemia – The risk of hypertension is increased in the setting of the metabolic syndrome. There are various mechanisms described for the development of hypertension which include increased salt absorption resulting in volume expansion, an impaired response of the renin-angiotensin-aldosterone system (RAAS), increased activation of the sympathetic nervous system.  These changes lead to the development of increased total peripheral resistance and increased afterload which in turn leads to the development of hypertension.

Symptoms of Idiopathic Hypertension

In most cases, there will be no apparent symptoms of essential hypertension, and it will only be discovered during a regular medical examination. If essential hypertension is not diagnosed, the condition has the potential to worsen and create heart or kidney problems.

Sometimes, people with essential hypertension may experience headaches, dizziness, and blurred vision, but these symptoms are unlikely to occur until blood pressure reaches very high levels. Some people report that their heartbeat seems louder than usual and feels as if it is inside the ear; this may be more prominent the higher the blood pressure is. People experiencing symptoms that may be linked to hypertension can use it for a symptom assessment.

If a person experiences vomiting or nausea, severe headaches, vision changes, or nosebleeds, it may be a sign of malignant hypertension – a much more dangerous type of high blood pressure. If these symptoms appear, urgent medical attention should be sought.

Diagnosis of Idiopathic Hypertension

Most cases of hypertension are asymptomatic and are diagnosed incidentally on blood pressures recording or measurement.

Some cases present directly with symptoms of end-organ damage as stroke-like symptoms or hypertensive encephalopathy, chest pain, shortness of breath and acute pulmonary edema.

Physical examination may be unyielding other than occasional pedal edema or raised blood pressure, but one needs to look for signs of:

• Coarctation of the aorta (radio-radial delay, radio-femoral delay, differences in left and right arm BP or upper and lower limb BP more than 20mmHg)
• Aortic valve disease (systolic ejection murmur, 4th heart sound)
• Renovascular disease or fibromuscular dysplasia (FMD) – (renal bruit, carotid bruit)
• Polycystic kidneys (enlarged kidneys bilaterally)
• Endocrine disorders [hypercortisolism(thin skin, easy bruising,  hyperglycemia)
• Thyroid disorders(palpable/ painful or enlarged thyroid] which make up the common treatable causes for secondary hypertension

The presence of a 4th heart sound, which represents a stiff and non-compliant left ventricle, hints towards left ventricular hypertrophy and diastolic dysfunction.

The presence of lung rales and/or peripheral edema suggests cardiac dysfunction and gives a clue to the chronicity of hypertension.

Blood pressure measurements fall into several categories

• Normal blood pressure. Your blood pressure is normal if it’s below 120/80 mm Hg.
• Elevated blood pressure. Elevated blood pressure is a systolic pressure ranging from 120 to 129 mm Hg and a diastolic pressure below (not above) 80 mm Hg. Elevated blood pressure tends to get worse over time unless steps are taken to control blood pressure. Elevated blood pressure may also be called prehypertension.
• Stage 1 hypertension. Stage 1 hypertension is a systolic pressure ranging from 130 to 139 mm Hg or a diastolic pressure ranging from 80 to 89 mm Hg.
• Stage 2 hypertension. More severe hypertension, stage 2 hypertension is a systolic pressure of 140 mm Hg or higher or a diastolic pressure of 90 mm Hg or higher.
• Hypertensive crisis. A blood pressure measurement higher than 180/120 mm Hg is an emergency situation that requires urgent medical care. If you get this result when you take your blood pressure at home, wait five minutes and retest. If your blood pressure is still this high, contact your doctor immediately. If you also have chest pain, vision problems, numbness or weakness, breathing difficulty, or any other signs and symptoms of a stroke or heart attack, call 911 or your local emergency medical number.

Lab Test And Imaging

The ACC recommends at least two office measurements on at least two separate occasions to diagnose hypertension.

• The ESC/ESH recommends three office BP measurements at least 1 to 2 minutes apart, and additional measurements only if the initial two readings differ by greater than or equal to 10mmHg. BP is then recorded as the average of the last two readings.
• Both societies endorse the use of higher BP readings and putting patients into a higher stage/grades for adequate medical therapy.
• The patient should remain seated quietly for at least 5 minutes before taking the blood pressure, and proper technique is necessary. The blood pressure cuff should cover 80% of the arm circumference because larger or smaller pressure cuffs can falsely under-estimate or over-estimate blood pressure readings.

Ambulatory blood pressure measurement is the most accurate method to diagnose hypertension and also aids in identifying individuals with masked hypertension as well as the white coat effect.

The evaluation consists of looking for signs of end-organ damage and consists of the following,

• 12 lead ECG (to document left ventricular hypertrophy, cardiac rate, and rhythm)
• Fundoscopy to look for retinopathy/ maculopathy
• Blood workup including complete blood count, ESR, creatinine, eGFR, electrolytes, HbA1c, thyroid profile, blood cholesterol levels, and serum uric acid
• Urine albumin to creatinine ratio
• Ankle-brachial pressure index – ABI (if symptoms suggestive of peripheral arterial disease)
• Carotid doppler ultrasound – echocardiography, and brain imaging (where clinically deemed feasible)
• Cholesterol test. Also called a lipid profile, this will test your blood for your cholesterol levels.
• Echocardiogram. This test uses sound waves to make a picture of your heart.
• Electrocardiogram (EKG or ECG). An EKG records the electrical activity of your heart.
• Kidney and other organ function tests. These can include blood tests, urine tests, or ultrasounds to check how your kidneys and other organs are functioning.

Treatment of Idiopathic Hypertension

The management of hypertension subdivides into pharmacological and nonpharmacological management.

Non-pharmacological and lifestyle management are recommended for all individuals with raised BPs regardless of age, gender, comorbidities or cardiovascular risk status.

Patient education is paramount to effective management and should always include detailed instructions regarding weight management, salt restriction, smoking management, adequate management of obstructive sleep apnea, and exercise. Patients need to be informed and revised at every encounter that these changes are to be continued lifelong for effective disease treatment.

Weight reduction is advisable if obesity is present although optimum BMI and optimal weight range are still unknown. Weight reduction alone can result in decreases of up to 5 to 20mmHg in systolic blood pressure.

Smoking may not have a direct effect on blood pressure but will help in reducing long-term sequelae if the patient quits smoking.

Lifestyle changes alone can account for up to a 15% reduction in all cardiovascular-related events.

Pharmacological therapy consists of angiotensin-converting enzyme inhibitors (ACEi), angiotensin receptor blockers (ARBs), diuretics (usual thiazides), calcium channel blockers (CCBs), and beta-blockers (BBs), which are instituted taking into account age, race, and comorbidities such as the presence of renal dysfunction, LV dysfunction, heart failure, and cerebrovascular disease. JNC-8, ACC, and ESC/ ESH have their separate recommendations for pharmacological management.

JNC-8 recommends the following

• Starting pharmacological therapy for individuals with DM and CKD with BP greater than or equal to 140/90mmHg to therapeutic target BP less than 140/90mmHg
• Starting pharmacological therapy for individuals 60 years of age and over with BP greater than or equal to 150/90mmHg to therapeutic target BP less than 150/90mmHg
• Starting pharmacological therapy for individuals 18 to 59years of age with SBP greater than or equal to 140mmHg to therapeutic target SBP less than 140mmHg
• individuals with DM and non-black population, treatment should include a thiazide diuretic, CCB, and an ACEi/ARB
• individuals in the black population, including those with DM, treatment should include a thiazide diuretic and CCB
• individuals with CKD, treatment should be started with or include ACEi/ARB, and this applies to all CKD patients irrespective of race or DM status

ACC recommends the following

• Ten-year atherosclerotic cardiovascular disease (ASCVD) risk should be estimated
• Anti-hypertensive medications are usually initiated when BP readings are persistently greater than or equal to 140/90mmHg
• High-risk populations (diabetics, CKD, individuals with ASCVD) or in those individuals with 10-year ASCVD risk greater than or equal to 10%, therapy can be initiated at lower BP cutoffs
• The goal of treatment is to keep blood pressures in as close to the normal range as possible, i.e., BP less than or equal to 130/80mmHg. [rx][rx][rx][rx]

ESC/ ESH recommends the following

• Starting pharmacological therapy for grade 2 or 3 hypertension regardless of the level of risk
• Starting pharmacological therapy for grade 1 hypertension when there is hypertension mediated end-organ damage (HMOD)
• Grade 1 hypertension in the absence of HMOD requires either high risk for CVD or failure of lifestyle interventions, for initiating pharmacological therapy
• Starting pharmacological therapy for individuals greater than or equal to 80 years of age with BP greater than or equal to 160/90mmHg to therapeutic target less than 160/90mmHg regardless of DM, CKD, CAD or TIA/ CVA
• Starting pharmacological therapy for individuals 18 to 79 years of age with BP greater than or equal to 140/90mmHg to therapeutic target less than 140/90mmHg regardless of DM, CKD, CAD or TIA/ CVA

Researchers have also studied renal denervation is a form of interventional treatment where renal sympathetic supply is ablated, via specialized catheter equipment, as a potential treatment for resistant hypertension (where adequate blood pressure control is not achieved despite adequate compliance to two or three anti-hypertensive drugs and lifestyle measures). Multiple randomized trials including SPYRAL, RADIANCE, and SIMPLICITY-HTN trials have shown equivocal results, so this remains an investigational therapy.

Medications for Idiopathic Hypertension

• Diuretics. Diuretics, sometimes called water pills, are medications that help your kidneys eliminate sodium and water from the body. These drugs are often the first medications tried to treat high blood pressure. There are different classes of diuretics, including thiazide, loop, and potassium-sparing. Which one your doctor recommends depends on your blood pressure measurements and other health conditions, such a kidney disease or heart failure. Diuretics commonly used to treat blood pressure include chlorthalidone, hydrochlorothiazide (Microzide), and others. A common side effect of diuretics is increased urination, which could reduce potassium levels. If you have a low potassium level, your doctor may add a potassium-sparing diuretic — such as triamterene (Dyazide, Maxine) or spironolactone (Aldactone) — to your treatment.
• Angiotensin-converting enzyme (ACE) inhibitors. These medications — such as lisinopril (Prinivil, Zestril), benazepril (Lotensin), captopril, and others — help relax blood vessels by blocking the formation of a natural chemical that narrows blood vessels.
• Angiotensin II receptor blockers (ARBs). These medications relax blood vessels by blocking the action, not the formation, of a natural chemical that narrows blood vessels. ARBs include candesartan (Atacand), losartan (Cozaar) and others.
• Calcium channel blockers. These medications — including amlodipine (Norvasc), diltiazem (Cardizem, Tiazac, others), and others — help relax the muscles of your blood vessels. Some slow your heart rate. Calcium channel blockers may work better for older people and people of African heritage than do ACE inhibitors alone. Don’t eat or drink grapefruit products when taking calcium channel blockers. Grapefruit increases blood levels of certain calcium channel blockers, which can be dangerous. Talk to your doctor or pharmacist if you’re concerned about interactions.

Additional medications sometimes used to treat high blood pressure

If you’re having trouble reaching your blood pressure goal with combinations of the above medications, your doctor may prescribe:

• Alpha-blockers. These medications reduce nerve signals to blood vessels, lowering the effects of natural chemicals that narrow blood vessels. Alpha blockers include doxazosin (Cardura), prazosin (Minipress) and others.
• Alpha-beta blockers. Alpha-beta blockers block nerve signals to blood vessels and slow the heartbeat to reduce the amount of blood that must be pumped through the vessels. Alpha-beta blockers include carvedilol (Coreg) and labetalol (Trandate).
• Beta-blockers. These medications reduce the workload on your heart and widen your blood vessels, causing your heart to beat slower and with less force. Beta-blockers include acebutolol, atenolol (Tenormin), and others. Beta-blockers aren’t usually recommended as the only medication you’re prescribed, but they may be effective when combined with other blood pressure medications.
• Aldosterone antagonists. These drugs also are considered diuretics. Examples are spironolactone and eplerenone (Inspra). These drugs block the effect of a natural chemical that can lead to salt and fluid buildup, which can contribute to high blood pressure. They may be used to treat resistant hypertension.
• Renin-inhibitors. Aliskiren (Tekturna) slows the production of renin, an enzyme produced by your kidneys that starts a chain of chemical steps that increases blood pressure. Due to a risk of serious complications, including stroke, you shouldn’t take aliskiren with ACE inhibitors or ARBs.
• Vasodilators. These medications include hydralazine and minoxidil. They work directly on the muscles in the walls of your arteries, preventing the muscles from tightening and your arteries from narrowing.
• Central-acting agents. These medications prevent your brain from telling your nervous system to increase your heart rate and narrow your blood vessels. Examples include clonidine (Catapres, Kapvay), guanfacine (Intuniv), and methyldopa.

Lifestyle Modification for Idiopathic Hypertension

Lifestyle modification is a very important aspect of the treatment of diabetes and hypertension. It is generally agreed that lifestyle modification has a modest antihypertensive effect resulting in an effective blood pressure reduction of 5-10 mmHg. Changes to lifestyle which appear to have health benefits include:

• Maintain a healthy weight – Strive for a body mass index (BMI) between 18.5 and 24.9.
• Eat healthier – Eat lots of fruit, veggies and low-fat dairy, and less saturated and total fat.
• Reduce sodium – Ideally, stay under 1,500 mg a day, but aim for at least a 1,000 mg per day reduction.
• Get active – Aim for at least 90 to 150 minutes of aerobic and/or dynamic resistance exercise per week and/or three sessions of isometric resistance exercises per week.
• Limit alcohol – Drink no more than 1-2 drinks a day. (One for most women, two for most men.)
• Reducing salt intake to less than 1.5 g/day
• Increasing consumption of fruits and vegetables (8-10 servings per day)
• Increasing consumption of low-fat dairy products (2-3 servings per day)
• Increasing activity levels/ engaging in regular aerobic physical activity (e.g. brisk walking 30 min/day)
• Losing excess weight
• Avoiding excessive alcohol consumption (less than 2 drinks (30 ml ethanol)/day for men and less than 1 drink/day for women)
• Lifestyle modification may be used as a sole treatment modality in patients with blood pressure <140/80, but ideally should be combined with pharmacotherapy in patients with systolic blood pressure (SBP) ≥ 140 and or diastolic blood pressure (DBP) ≥ 80

Home Remedies for Idiopathic Hypertension

Lifestyle changes can help you control and prevent high blood pressure, even if you’re taking blood pressure medication. Here’s what you can do:

• Eat healthy foods. Eat a heart-healthy diet. Try the Dietary Approaches to Stop Hypertension (DASH) diet, which emphasizes fruits, vegetables, whole grains, poultry, fish and low-fat dairy foods. Get plenty of potassium, which can help prevent and control high blood pressure. Eat less saturated fat and trans fat.
• Decrease the salt in your diet. Aim to limit sodium to less than 2,300 milligrams (mg) a day or less. However, a lower sodium intake — 1,500 mg a day or less — is ideal for most adults. While you can reduce the amount of salt you eat by putting down the saltshaker, you generally should also pay attention to the amount of salt that’s in the processed foods you eat, such as canned soups or frozen dinners.
• Maintain a healthy weight. Keeping a healthy weight, or losing weight if you’re overweight or obese, can help you control your high blood pressure and lower your risk of related health problems. In general, you may reduce your blood pressure by about 1 mm Hg with each kilogram (about 2.2 pounds) of weight you lose.
• Increase physical activity. Regular physical activity can help lower your blood pressure, manage stress, keep your weight under control and reduce your risk of many health conditions. If you have high blood pressure, consistent moderate- to high-intensity workouts can lower your top blood pressure reading by about 11 mm Hg and the bottom number by about 5 mm Hg. Aim for at least 150 minutes a week of moderate aerobic activity or 75 minutes a week of vigorous aerobic activity, or a combination of moderate and vigorous activity. For example, try brisk walking for about 30 minutes most days of the week. Or try interval training, in which you alternate short bursts of intense activity with short recovery periods of lighter activity. Aim to do muscle-strengthening exercises at least two days a week.
• Limit alcohol. Even if you’re healthy, alcohol can raise your blood pressure. If you choose to drink alcohol, do so in moderation. For healthy adults, that means up to one drink a day for women, and up to two drinks a day for men. One drink equals 12 ounces of beer, 5 ounces of wine or 1.5 ounces of 80-proof liquor.
• Don’t smoke. Tobacco can injure blood vessel walls and speed up the process of buildup of plaque in the arteries. If you smoke, ask your doctor to help you quit.
• Manage stress. Reduce stress as much as possible. Practice healthy coping techniques, such as muscle relaxation, deep breathing or mindfulness. Getting regular physical activity and plenty of sleep can help, too.
• Monitor your blood pressure at home. Home blood pressure monitoring allows you to keep a daily log of blood pressure measurements. Your doctor can review the information to determine if your medication is working or if you’re having complications. Home blood pressure monitoring isn’t a substitute for visits to your doctor. Even if you get normal readings, don’t stop or change your medications or alter your diet without talking to your doctor first. If your blood pressure is under control, ask your doctor about how often you need to check it.
• Practice relaxation or slow, deep breathing. Practice taking deep, slow breaths to help relax. Some research shows that slow, paced breathing (five to seven deep breaths per minute) combined with mindfulness techniques can reduce blood pressure. There also are some devices available that promote slow, deep breathing. According to the American Heart Association, device-guided breathing may be a reasonable nondrug option for lowering blood pressure, especially if you have anxiety with high blood pressure or can’t tolerate standard treatments well.
• Control blood pressure during pregnancy. Women with high blood pressure should discuss with their doctors how to control their blood pressure during pregnancy.

Risk factors

High blood pressure has many risk factors, including:

• Age. The risk of high blood pressure increases as you age. Until about age 64, high blood pressure is more common in men. Women are more likely to develop high blood pressure after age 65.
• Race. High blood pressure is particularly common among people of African heritage, often developing at an earlier age than it does in whites. Serious complications, such as stroke, heart attack and kidney failure, also are more common in people of African heritage.
• Family history. High blood pressure tends to run in families.
• Being overweight or obese. The more you weigh, the more blood you need to supply oxygen and nutrients to your tissues. As the amount of blood flow through your blood vessels increases, so does the pressure on your artery walls.
• Not being physically active. People who are inactive tend to have higher heart rates. The higher your heart rate, the harder your heart must work with each contraction and the stronger the force on your arteries. Lack of physical activity also increases the risk of being overweight.
• Using tobacco. Not only does smoking or chewing tobacco immediately raise your blood pressure temporarily, but the chemicals in tobacco can damage the lining of your artery walls. This can cause your arteries to narrow and increase your risk of heart disease. Secondhand smoke also can increase your heart disease risk.
• Too much salt (sodium) in your diet. Too much sodium in your diet can cause your body to retain fluid, which increases blood pressure.
• Too little potassium in your diet. Potassium helps balance the amount of sodium in your cells. A proper balance of potassium is critical for good heart health. If you don’t get enough potassium in your diet, or you lose too much potassium due to dehydration or other health conditions, sodium can build up in your blood.
• Drinking too much alcohol. Over time, heavy drinking can damage your heart. Having more than one drink a day for women and more than two drinks a day for men may affect your blood pressure. If you drink alcohol, do so in moderation. For healthy adults, that means up to one drink a day for women and two drinks a day for men. One drink equals 12 ounces of beer, 5 ounces of wine or 1.5 ounces of 80-proof liquor.
• Stress. High levels of stress can lead to a temporary increase in blood pressure. Stress-related habits such as eating more, using tobacco or drinking alcohol can lead to further increases in blood pressure.
• Certain chronic conditions. Certain chronic conditions also may increase your risk of high blood pressure, including kidney disease, diabetes and sleep apnea.

Sometimes pregnancy contributes to high blood pressure as well.

Although high blood pressure is most common in adults, children may be at risk, too. For some children, high blood pressure is caused by problems with the kidneys or heart. But for a growing number of kids, poor lifestyle habits — such as an unhealthy diet and lack of exercise — contribute to high blood pressure.

Complications

The excessive pressure on your artery walls caused by high blood pressure can damage your blood vessels as well as your organs. The higher your blood pressure and the longer it goes uncontrolled, the greater the damage.

Uncontrolled high blood pressure can lead to complications including:

• Heart attack or stroke. High blood pressure can cause hardening and thickening of the arteries (atherosclerosis), which can lead to a heart attack, stroke or other complications.
• Aneurysm. Increased blood pressure can cause your blood vessels to weaken and bulge, forming an aneurysm. If an aneurysm ruptures, it can be life-threatening.
• Heart failure. To pump blood against the higher pressure in your vessels, the heart has to work harder. This causes the walls of the heart’s pumping chamber to thicken (left ventricular hypertrophy). Eventually, the thickened muscle may have a hard time pumping enough blood to meet your body’s needs, which can lead to heart failure.
• Weakened and narrowed blood vessels in your kidneys. This can prevent these organs from functioning normally.
• Thickened, narrowed or torn blood vessels in the eyes. This can result in vision loss.
• Metabolic syndrome. This syndrome is a group of disorders of your body’s metabolism, including increased waist size, high triglycerides, decreased high-density lipoprotein (HDL) cholesterol (the “good” cholesterol), high blood pressure and high insulin levels. These conditions make you more likely to develop diabetes, heart disease and stroke.
• Trouble with memory or understanding. Uncontrolled high blood pressure may also affect your ability to think, remember and learn. Trouble with memory or understanding concepts is more common in people with high blood pressure.
• Dementia. Narrowed or blocked arteries can limit blood flow to the brain, leading to a certain type of dementia (vascular dementia). A stroke that interrupts blood flow to the brain also can cause vascular dementia.

Essential hypertension FAQs

Q: Can essential hypertension be treated successfully?
A: Yes, in many cases, there is a good chance that blood pressure can be lowered if the appropriate treatment methods are followed. To ensure blood pressure remains at a healthy level, most people will be required to maintain lifestyle changes and, if required, take medication, possibly for the rest of their lives.

Q: What is malignant essential hypertension?
A: Malignant essential hypertension, sometimes called accelerated hypertension, is a form of hypertensive emergency. It involves high blood pressure that develops very quickly, causing serious complications. The malignant variety is extremely rare, affecting roughly one percent of those with high blood pressure, but if it is suspected, it should be treated as a medical emergency.

Q: What is benign essential hypertension?
A: When essential hypertension remains in its early stages for a prolonged period of time and without a specific known cause, it is known as benign essential hypertension. In this state, the condition will generally be symptomless and develop very slowly. It is still important to seek treatment after a diagnosis of benign essential hypertension.

What is non-essential hypertension?
A: Non-essential hypertension is an alternative name for secondary hypertension. Essential hypertension is characterized by a lack of clearly attributable causes, whereas secondary hypertension is directly linked to a variety of vascular, endocrine, heart and kidney conditions.

Q: Can pregnancy cause essential hypertension?
A: Essential hypertension is defined by its lack of a clearly attributable cause, meaning that pregnancy cannot be said to cause the condition. However, pregnancy can cause a form of hypertension known as gestational hypertension. By definition, this form of hypertension must occur after 20 weeks of pregnancy in a previously not hypertensive person and disappear after the delivery of the baby Longer lasting hypertension, detected either before pregnancy or before the 20th week of pregnancy, and which remains after delivery of the baby, is defined as chronic hypertension and can be a kind of essential hypertension. Both gestational and chronic hypertension can lead to preeclampsia, a potentially serious but treatable complication of pregnancy. For more information, take a look at this resource on preeclampsia.

Q: What is hypertensive heart disease?
A: Hypertensive heart disease is an umbrella term for various heart conditions that are caused by chronically or prolonged high blood pressure levels. High blood pressure puts extra strain on the heart and the vessels surrounding and supplying the heart, something which can lead to the development of a variety of heart disorders. These include heart failure, coronary artery disease and the thickening of the heart muscle, among others. People at risk of hypertensive heart disease should talk to their doctor about methods of preventing potential complications, e.g. attending regular check-ups and taking medication regularly as required by their prescription. This will typically also include getting plenty of exercise, eating a balanced, nutritious diet and losing weight, if the person in question is considerably overweight or obese.

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Essential hypertension is high blood pressure that doesn’t have a known secondary cause. It’s also referred to as primary hypertension. Blood pressure is the force of blood against your artery walls as your heart pumps blood through your body.

Essential hypertension (also called primary hypertension, or idiopathic hypertension) is the form of hypertension that by definition has no identifiable secondary cause.^[rx][rx] It is the most common type affecting 85% of those with high blood pressure.^[rx][rx] The remaining 15% is accounted for by various causes of secondary hypertension.^[rx] Primary hypertension tends to be familial and is likely to be the consequence of an interaction between environmental and genetic factors.

The current definition of hypertension (HTN) is systolic blood pressure (SBP) values of 130mmHg or more and/or diastolic blood pressure (DBP) more than 80 mmHg. Hypertension ranks among the most common chronic medical condition characterized by a persistent elevation in arterial pressure.

Hypertension has been among the most studied topics of the previous century and has been one of the most significant comorbidities contributing to the development of stroke, myocardial infarction, heart failure, and renal failure.

The definition and categories of hypertension have been evolving over years, but there is a consensus that persistent BP readings of 140/90mmHg or more should undergo treatment with the usual therapeutic target of 130/80mmHg or less.

This article will attempt to review the available knowledge derived from RCTs and the recent updates and guidelines on hypertension put forward by major societies including those from the 8th report of Joint National Committee (JNC-8), American College of Cardiology (ACC), American Society of Hypertension (ASH), European Society of Cardiology (ESC) and European Society of Hypertension (ESH).

Other names for Essential Hypertension

• High blood pressure
• Arterial hypertension
• Hypertension
• Primary hypertension

Causes of Essential Hypertension

Most cases of hypertension are idiopathic which is also known as essential hypertension.  It has long been suggested that an increase in salt intake increases the risk of developing hypertension.[rx] One of the described factors for the development of essential hypertension is the patient genetic ability to the salt response.[rx][rx] About 50 to 60% of the patients are salt sensitive and therefore tend to develop hypertension.[rx]

• Obesity – Data from the Nurses’ Health Study showed that a gain of 5 kg above weight at 18 years of age was associated with 60% higher risk of development of hypertension in middle age.[rx] A 4.5 mmHg increase in blood pressure has been associated with each 10 lb (4.5 kg) gain in weight.[rx] One systematic review found that risk of hypertension increased continuously with increasing body mass index (BMI), waist circumference, weight gain, and waist-to-hip and waist-to-height ratio.[rx] It has been postulated that the link between obesity and hypertension is driven by increased circulating volume, leading to increased cardiac output and persistently elevated peripheral vascular resistance.[rx] Obesity is associated with the metabolic syndrome, insulin resistance, and type 2 diabetes. Bariatric treatment of class III obesity (BMI 40 or above) can reduce or eliminate risk factors for cardiovascular disease, with an effect on hypertension, diabetes, and dyslipidemia.[rx][rx]
• Aerobic exercise <3 times/week – Patients with low level of fitness had a 52% greater relative risk of hypertension at 12-year follow-up compared with those with high levels of fitness.[rx]
• Moderate/high alcohol intake – Chronic alcohol consumption of more than 1 drink per day in women and more than 2 drinks per day in men has been shown to be associated with an increased risk of blood pressure (BP) elevation.[rx][rx] One Cochrane review of the effect of alcohol on BP found that high-dose alcohol (>30 g) has a biphasic effect, decreasing BP up to 12 hours after consumption and increasing BP after 13 hours.[rx]
• Metabolic syndrome – Abdominal obesity has been specifically associated with an increased risk of hypertension, as compared with generalized obesity.[rx] Insulin resistance and hyperinsulinemia are thought to contribute to the development of hypertension through a variety of inflammatory mechanisms.[rx]
• Diabetes mellitus – Hyperglycemia, hyperinsulinemia, and insulin resistance lead to endothelial damage and oxidative stress, and are independently associated with the development of hypertension.[rx]
• Black ancestry – Highest incidence of hypertension is seen in black non-Hispanic people, at all age levels.[rx]
• Age >60 years – Incidence of hypertension increases with age in people of all ancestries and both sexes.[rx] family history of hypertension or coronary artery disease – Patient may have family history of hypertension or coronary artery disease risk factors.[rx]
• Sleep apnea – Obstructive sleep apnea is a risk factor for several cardiovascular diseases, including hypertension.[rx] In addition, there is a possible dose-response relationship between the severity of obstructive sleep apnea and the risk of essential hypertension.[rx] Obstructive sleep apnea is also associated with an increased risk of resistant hypertension.[rx]
• Sodium intake >1.5 g/day – Individuals show a varied tolerance for sodium intake, and reduced sodium intake has modest effect on blood pressure (BP) lowering.[rx][rx] One meta-analysis has shown the amount of BP lowering achieved with sodium reduction has a dose-response relation and is greater for older populations, nonwhite populations, and those with higher baseline systolic BP.[rx]
• Low fruit and vegetable intake – Modest reduction in blood pressure with 4 to 6 servings of fruits and vegetables coupled with lower sodium and fat intake (Dietary Approaches to Stop Hypertension [DASH] diet).[rx]
• Dyslipidemia – Risk of hypertension is increased in the setting of the metabolic syndrome. There are various mechanisms described for the development of hypertension which include increased salt absorption resulting in volume expansion, an impaired response of the renin-angiotensin-aldosterone system (RAAS), increased activation of the sympathetic nervous system.  These changes lead to the development of increased total peripheral resistance and increased afterload which in turn leads to the development of hypertension.

Symptoms of Essential Hypertension

In most cases, there will be no apparent symptoms of essential hypertension, and it will only be discovered during a regular medical examination. If essential hypertension is not diagnosed, the condition has the potential to worsen and create heart or kidney problems.

Sometimes, people with essential hypertension may experience headaches, dizziness and blurred vision, but these symptoms are unlikely to occur until blood pressure reaches very high levels. Some people report that their heartbeat seems louder than usual and feels as if it is inside the ear; this may be more prominent the higher the blood pressure is. People experiencing symptoms that may be linked to hypertension can use for a symptom assessment.

If a person experiences vomiting or nausea, severe headaches, vision changes or nosebleeds, it may be a sign of malignant hypertension – a much more dangerous type of high blood pressure. If these symptoms appear, urgent medical attention should be sought.

Diagnosis of Essential Hypertension

Most cases of hypertension are asymptomatic and are diagnosed incidentally on blood pressures recording or measurement.

Some cases present directly with symptoms of end-organ damage as stroke-like symptoms or hypertensive encephalopathy, chest pain, shortness of breath and acute pulmonary edema.

Physical examination may be unyielding other than occasional pedal edema or raised blood pressure, but one needs to look for signs of:

• Coarctation of the aorta (radio-radial delay, radio-femoral delay, differences in left and right arm BP or upper and lower limb BP more than 20mmHg)
• Aortic valve disease (systolic ejection murmur, 4th heart sound)
• Renovascular disease or fibromuscular dysplasia (FMD) – (renal bruit, carotid bruit)
• Polycystic kidneys (enlarged kidneys bilaterally)
• Endocrine disorders [hypercortisolism(thin skin, easy bruising,  hyperglycemia)
• Thyroid disorders(palpable/ painful or enlarged thyroid] which make up the common treatable causes for secondary hypertension

The presence of a 4th heart sound, which represents a stiff and non-compliant left ventricle, hints towards left ventricular hypertrophy and diastolic dysfunction.

The presence of lung rales and/or peripheral edema suggests cardiac dysfunction and gives a clue to the chronicity of hypertension.

Blood pressure measurements fall into several categories

• Normal blood pressure. Your blood pressure is normal if it’s below 120/80 mm Hg.
• Elevated blood pressure. Elevated blood pressure is a systolic pressure ranging from 120 to 129 mm Hg and a diastolic pressure below (not above) 80 mm Hg. Elevated blood pressure tends to get worse over time unless steps are taken to control blood pressure. Elevated blood pressure may also be called prehypertension.
• Stage 1 hypertension. Stage 1 hypertension is a systolic pressure ranging from 130 to 139 mm Hg or a diastolic pressure ranging from 80 to 89 mm Hg.
• Stage 2 hypertension. More-severe hypertension, stage 2 hypertension is a systolic pressure of 140 mm Hg or higher or a diastolic pressure of 90 mm Hg or higher.
• Hypertensive crisis. A blood pressure measurement higher than 180/120 mm Hg is an emergency situation that requires urgent medical care. If you get this result when you take your blood pressure at home, wait five minutes and retest. If your blood pressure is still this high, contact your doctor immediately. If you also have chest pain, vision problems, numbness or weakness, breathing difficulty, or any other signs and symptoms of a stroke or heart attack, call 911 or your local emergency medical number.

Lab Test And Imaging

The ACC recommends at least two office measurements on at least two separate occasions to diagnose hypertension.

• The ESC/ESH recommends three office BP measurements at least 1 to 2 minutes apart, and additional measurements only if the initial two readings differ by greater than or equal to 10mmHg. BP is then recorded as the average of the last two readings.
• Both societies endorse the use of higher BP readings and putting patients into a higher stage/grades for adequate medical therapy.
• The patient should remain seated quietly for at least 5 minutes before taking the blood pressure, and proper technique is necessary. The blood pressure cuff should cover 80% of the arm circumference because larger or smaller pressure cuffs can falsely under-estimate or over-estimate blood pressure readings.

Ambulatory blood pressure measurement is the most accurate method to diagnose hypertension and also aids in identifying individuals with masked hypertension as well as the white coat effect.

The evaluation consists of looking for signs of end-organ damage and consists of the following,

• 12 lead ECG (to document left ventricular hypertrophy, cardiac rate, and rhythm)
• Fundoscopy to look for retinopathy/ maculopathy
• Blood workup including complete blood count, ESR, creatinine, eGFR, electrolytes, HbA1c, thyroid profile, blood cholesterol levels, and serum uric acid
• Urine albumin to creatinine ratio
• Ankle-brachial pressure index – ABI (if symptoms suggestive of peripheral arterial disease)
• Carotid doppler ultrasound – echocardiography, and brain imaging (where clinically deemed feasible)
• Cholesterol test. Also called a lipid profile, this will test your blood for your cholesterol levels.
• Echocardiogram. This test uses sound waves to make a picture of your heart.
• Electrocardiogram (EKG or ECG). An EKG records the electrical activity of your heart.
• Kidney and other organ function tests. These can include blood tests, urine tests, or ultrasounds to check how your kidneys and other organs are functioning.

Treatment of Essential Hypertension

The management of hypertension subdivides into pharmacological and nonpharmacological management.

Non-pharmacological and lifestyle management are recommended for all individuals with raised BPs regardless of age, gender, comorbidities or cardiovascular risk status.

Patient education is paramount to effective management and should always include detailed instructions regarding weight management, salt restriction, smoking management, adequate management of obstructive sleep apnea, and exercise. Patients need to be informed and revised at every encounter that these changes are to be continued lifelong for effective disease treatment.

Weight reduction is advisable if obesity is present although optimum BMI and optimal weight range are still unknown. Weight reduction alone can result in decreases of up to 5 to 20mmHg in systolic blood pressure.

Smoking may not have a direct effect on blood pressure but will help in reducing long-term sequelae if the patient quits smoking.

Lifestyle changes alone can account for up to a 15% reduction in all cardiovascular-related events.

Pharmacological therapy consists of angiotensin-converting enzyme inhibitors (ACEi), angiotensin receptor blockers (ARBs), diuretics (usual thiazides), calcium channel blockers (CCBs), and beta-blockers (BBs), which are instituted taking into account age, race, and comorbidities such as the presence of renal dysfunction, LV dysfunction, heart failure, and cerebrovascular disease. JNC-8, ACC, and ESC/ ESH have their separate recommendations for pharmacological management.

JNC-8 recommends the following

• Starting pharmacological therapy for individuals with DM and CKD with BP greater than or equal to 140/90mmHg to therapeutic target BP less than 140/90mmHg
• Starting pharmacological therapy for individuals 60 years of age and over with BP greater than or equal to 150/90mmHg to therapeutic target BP less than 150/90mmHg
• Starting pharmacological therapy for individuals 18 to 59years of age with SBP greater than or equal to 140mmHg to therapeutic target SBP less than 140mmHg
• individuals with DM and non-black population, treatment should include a thiazide diuretic, CCB, and an ACEi/ARB
• individuals in the black population, including those with DM, treatment should include a thiazide diuretic and CCB
• individuals with CKD, treatment should be started with or include ACEi/ARB, and this applies to all CKD patients irrespective of race or DM status

ACC recommends the following

• Ten-year atherosclerotic cardiovascular disease (ASCVD) risk should be estimated
• Anti-hypertensive medications are usually initiated when BP readings are persistently greater than or equal to 140/90mmHg
• High-risk populations (diabetics, CKD, individuals with ASCVD) or in those individuals with 10-year ASCVD risk greater than or equal to 10%, therapy can be initiated at lower BP cutoffs
• The goal of treatment is to keep blood pressures in as close to the normal range as possible, i.e., BP less than or equal to 130/80mmHg. [rx][rx][rx][rx]

ESC/ ESH recommends the following

• Starting pharmacological therapy for grade 2 or 3 hypertension regardless of the level of risk
• Starting pharmacological therapy for grade 1 hypertension when there is hypertension mediated end-organ damage (HMOD)
• Grade 1 hypertension in the absence of HMOD requires either high risk for CVD or failure of lifestyle interventions, for initiating pharmacological therapy
• Starting pharmacological therapy for individuals greater than or equal to 80 years of age with BP greater than or equal to 160/90mmHg to therapeutic target less than 160/90mmHg regardless of DM, CKD, CAD or TIA/ CVA
• Starting pharmacological therapy for individuals 18 to 79 years of age with BP greater than or equal to 140/90mmHg to therapeutic target less than 140/90mmHg regardless of DM, CKD, CAD or TIA/ CVA

Researchers have also studied renal denervation is a form of interventional treatment where renal sympathetic supply is ablated, via specialized catheter equipment, as a potential treatment for resistant hypertension (where adequate blood pressure control is not achieved despite adequate compliance to two or three anti-hypertensive drugs and lifestyle measures). Multiple randomized trials including SPYRAL, RADIANCE, and SIMPLICITY-HTN trials have shown equivocal results, so this remains an investigational therapy.

Medications for Essential Hypertension

• Diuretics. Diuretics, sometimes called water pills, are medications that help your kidneys eliminate sodium and water from the body. These drugs are often the first medications tried to treat high blood pressure. There are different classes of diuretics, including thiazide, loop and potassium sparing. Which one your doctor recommends depends on your blood pressure measurements and other health conditions, such a kidney disease or heart failure. Diuretics commonly used to treat blood pressure include chlorthalidone, hydrochlorothiazide (Microzide) and others. A common side effect of diuretics is increased urination, which could reduce potassium levels. If you have a low potassium level, your doctor may add a potassium-sparing diuretic — such as triamterene (Dyazide, Maxide) or spironolactone (Aldactone) — to your treatment.
• Angiotensin-converting enzyme (ACE) inhibitors. These medications — such as lisinopril (Prinivil, Zestril), benazepril (Lotensin), captopril and others — help relax blood vessels by blocking the formation of a natural chemical that narrows blood vessels.
• Angiotensin II receptor blockers (ARBs). These medications relax blood vessels by blocking the action, not the formation, of a natural chemical that narrows blood vessels. ARBs include candesartan (Atacand), losartan (Cozaar) and others.
• Calcium channel blockers. These medications — including amlodipine (Norvasc), diltiazem (Cardizem, Tiazac, others) and others — help relax the muscles of your blood vessels. Some slow your heart rate. Calcium channel blockers may work better for older people and people of African heritage than do ACE inhibitors alone. Don’t eat or drink grapefruit products when taking calcium channel blockers. Grapefruit increases blood levels of certain calcium channel blockers, which can be dangerous. Talk to your doctor or pharmacist if you’re concerned about interactions.

Additional medications sometimes used to treat high blood pressure

If you’re having trouble reaching your blood pressure goal with combinations of the above medications, your doctor may prescribe:

• Alpha blockers. These medications reduce nerve signals to blood vessels, lowering the effects of natural chemicals that narrow blood vessels. Alpha blockers include doxazosin (Cardura), prazosin (Minipress) and others.
• Alpha-beta blockers. Alpha-beta blockers block nerve signals to blood vessels and slow the heartbeat to reduce the amount of blood that must be pumped through the vessels. Alpha-beta blockers include carvedilol (Coreg) and labetalol (Trandate).
• Beta blockers. These medications reduce the workload on your heart and widen your blood vessels, causing your heart to beat slower and with less force. Beta blockers include acebutolol, atenolol (Tenormin) and others. Beta blockers aren’t usually recommended as the only medication you’re prescribed, but they may be effective when combined with other blood pressure medications.
• Aldosterone antagonists. These drugs also are considered diuretics. Examples are spironolactone and eplerenone (Inspra). These drugs block the effect of a natural chemical that can lead to salt and fluid buildup, which can contribute to high blood pressure. They may be used to treat resistant hypertension.
• Renin inhibitors. Aliskiren (Tekturna) slows the production of renin, an enzyme produced by your kidneys that starts a chain of chemical steps that increases blood pressure. Due to a risk of serious complications, including stroke, you shouldn’t take aliskiren with ACE inhibitors or ARBs.
• Vasodilators. These medications include hydralazine and minoxidil. They work directly on the muscles in the walls of your arteries, preventing the muscles from tightening and your arteries from narrowing.
• Central-acting agents. These medications prevent your brain from telling your nervous system to increase your heart rate and narrow your blood vessels. Examples include clonidine (Catapres, Kapvay), guanfacine (Intuniv) and methyldopa.

Lifestyle Modification

Lifestyle modification is a very important aspect of the treatment of diabetes and hypertension. It is generally agreed that lifestyle modification has a modest antihypertensive effect resulting in an effective blood pressure reduction of 5-10 mmHg. Changes to lifestyle which appear to have health benefits include:

• Maintain a healthy weight – Strive for a body mass index (BMI) between 18.5 and 24.9.
• Eat healthier – Eat lots of fruit, veggies and low-fat dairy, and less saturated and total fat.
• Reduce sodium – Ideally, stay under 1,500 mg a day, but aim for at least a 1,000 mg per day reduction.
• Get active – Aim for at least 90 to 150 minutes of aerobic and/or dynamic resistance exercise per week and/or three sessions of isometric resistance exercises per week.
• Limit alcohol – Drink no more than 1-2 drinks a day. (One for most women, two for most men.)
• Reducing salt intake to less than 1.5 g/day
• Increasing consumption of fruits and vegetables (8-10 servings per day)
• Increasing consumption of low-fat dairy products (2-3 servings per day)
• Increasing activity levels/ engaging in regular aerobic physical activity (e.g. brisk walking 30 min/day)
• Losing excess weight
• Avoiding excessive alcohol consumption (less than 2 drinks (30 ml ethanol)/day for men and less than 1 drink/day for women)
• Lifestyle modification may be used as a sole treatment modality in patients with blood pressure <140/80, but ideally should be combined with pharmacotherapy in patients with systolic blood pressure (SBP) ≥ 140 and or diastolic blood pressure (DBP) ≥ 80

Home Remedies for Essential Hypertension

Lifestyle changes can help you control and prevent high blood pressure, even if you’re taking blood pressure medication. Here’s what you can do:

• Eat healthy foods. Eat a heart-healthy diet. Try the Dietary Approaches to Stop Hypertension (DASH) diet, which emphasizes fruits, vegetables, whole grains, poultry, fish and low-fat dairy foods. Get plenty of potassium, which can help prevent and control high blood pressure. Eat less saturated fat and trans fat.
• Decrease the salt in your diet. Aim to limit sodium to less than 2,300 milligrams (mg) a day or less. However, a lower sodium intake — 1,500 mg a day or less — is ideal for most adults. While you can reduce the amount of salt you eat by putting down the saltshaker, you generally should also pay attention to the amount of salt that’s in the processed foods you eat, such as canned soups or frozen dinners.
• Maintain a healthy weight. Keeping a healthy weight, or losing weight if you’re overweight or obese, can help you control your high blood pressure and lower your risk of related health problems. In general, you may reduce your blood pressure by about 1 mm Hg with each kilogram (about 2.2 pounds) of weight you lose.
• Increase physical activity. Regular physical activity can help lower your blood pressure, manage stress, keep your weight under control and reduce your risk of many health conditions. If you have high blood pressure, consistent moderate- to high-intensity workouts can lower your top blood pressure reading by about 11 mm Hg and the bottom number by about 5 mm Hg. Aim for at least 150 minutes a week of moderate aerobic activity or 75 minutes a week of vigorous aerobic activity, or a combination of moderate and vigorous activity. For example, try brisk walking for about 30 minutes most days of the week. Or try interval training, in which you alternate short bursts of intense activity with short recovery periods of lighter activity. Aim to do muscle-strengthening exercises at least two days a week.
• Limit alcohol. Even if you’re healthy, alcohol can raise your blood pressure. If you choose to drink alcohol, do so in moderation. For healthy adults, that means up to one drink a day for women, and up to two drinks a day for men. One drink equals 12 ounces of beer, 5 ounces of wine or 1.5 ounces of 80-proof liquor.
• Don’t smoke. Tobacco can injure blood vessel walls and speed up the process of buildup of plaque in the arteries. If you smoke, ask your doctor to help you quit.
• Manage stress. Reduce stress as much as possible. Practice healthy coping techniques, such as muscle relaxation, deep breathing or mindfulness. Getting regular physical activity and plenty of sleep can help, too.
• Monitor your blood pressure at home. Home blood pressure monitoring allows you to keep a daily log of blood pressure measurements. Your doctor can review the information to determine if your medication is working or if you’re having complications. Home blood pressure monitoring isn’t a substitute for visits to your doctor. Even if you get normal readings, don’t stop or change your medications or alter your diet without talking to your doctor first. If your blood pressure is under control, ask your doctor about how often you need to check it.
• Practice relaxation or slow, deep breathing. Practice taking deep, slow breaths to help relax. Some research shows that slow, paced breathing (five to seven deep breaths per minute) combined with mindfulness techniques can reduce blood pressure. There also are some devices available that promote slow, deep breathing. According to the American Heart Association, device-guided breathing may be a reasonable nondrug option for lowering blood pressure, especially if you have anxiety with high blood pressure or can’t tolerate standard treatments well.
• Control blood pressure during pregnancy. Women with high blood pressure should discuss with their doctors how to control their blood pressure during pregnancy.

Risk factors

High blood pressure has many risk factors, including:

• Age. The risk of high blood pressure increases as you age. Until about age 64, high blood pressure is more common in men. Women are more likely to develop high blood pressure after age 65.
• Race. High blood pressure is particularly common among people of African heritage, often developing at an earlier age than it does in whites. Serious complications, such as stroke, heart attack and kidney failure, also are more common in people of African heritage.
• Family history. High blood pressure tends to run in families.
• Being overweight or obese. The more you weigh, the more blood you need to supply oxygen and nutrients to your tissues. As the amount of blood flow through your blood vessels increases, so does the pressure on your artery walls.
• Not being physically active. People who are inactive tend to have higher heart rates. The higher your heart rate, the harder your heart must work with each contraction and the stronger the force on your arteries. Lack of physical activity also increases the risk of being overweight.
• Using tobacco. Not only does smoking or chewing tobacco immediately raise your blood pressure temporarily, but the chemicals in tobacco can damage the lining of your artery walls. This can cause your arteries to narrow and increase your risk of heart disease. Secondhand smoke also can increase your heart disease risk.
• Too much salt (sodium) in your diet. Too much sodium in your diet can cause your body to retain fluid, which increases blood pressure.
• Too little potassium in your diet. Potassium helps balance the amount of sodium in your cells. A proper balance of potassium is critical for good heart health. If you don’t get enough potassium in your diet, or you lose too much potassium due to dehydration or other health conditions, sodium can build up in your blood.
• Drinking too much alcohol. Over time, heavy drinking can damage your heart. Having more than one drink a day for women and more than two drinks a day for men may affect your blood pressure. If you drink alcohol, do so in moderation. For healthy adults, that means up to one drink a day for women and two drinks a day for men. One drink equals 12 ounces of beer, 5 ounces of wine or 1.5 ounces of 80-proof liquor.
• Stress. High levels of stress can lead to a temporary increase in blood pressure. Stress-related habits such as eating more, using tobacco or drinking alcohol can lead to further increases in blood pressure.
• Certain chronic conditions. Certain chronic conditions also may increase your risk of high blood pressure, including kidney disease, diabetes and sleep apnea.

Sometimes pregnancy contributes to high blood pressure as well.

Although high blood pressure is most common in adults, children may be at risk, too. For some children, high blood pressure is caused by problems with the kidneys or heart. But for a growing number of kids, poor lifestyle habits — such as an unhealthy diet and lack of exercise — contribute to high blood pressure.

Complications

The excessive pressure on your artery walls caused by high blood pressure can damage your blood vessels as well as your organs. The higher your blood pressure and the longer it goes uncontrolled, the greater the damage.

Uncontrolled high blood pressure can lead to complications including:

• Heart attack or stroke. High blood pressure can cause hardening and thickening of the arteries (atherosclerosis), which can lead to a heart attack, stroke or other complications.
• Aneurysm. Increased blood pressure can cause your blood vessels to weaken and bulge, forming an aneurysm. If an aneurysm ruptures, it can be life-threatening.
• Heart failure. To pump blood against the higher pressure in your vessels, the heart has to work harder. This causes the walls of the heart’s pumping chamber to thicken (left ventricular hypertrophy). Eventually, the thickened muscle may have a hard time pumping enough blood to meet your body’s needs, which can lead to heart failure.
• Weakened and narrowed blood vessels in your kidneys. This can prevent these organs from functioning normally.
• Thickened, narrowed or torn blood vessels in the eyes. This can result in vision loss.
• Metabolic syndrome. This syndrome is a group of disorders of your body’s metabolism, including increased waist size, high triglycerides, decreased high-density lipoprotein (HDL) cholesterol (the “good” cholesterol), high blood pressure and high insulin levels. These conditions make you more likely to develop diabetes, heart disease and stroke.
• Trouble with memory or understanding. Uncontrolled high blood pressure may also affect your ability to think, remember and learn. Trouble with memory or understanding concepts is more common in people with high blood pressure.
• Dementia. Narrowed or blocked arteries can limit blood flow to the brain, leading to a certain type of dementia (vascular dementia). A stroke that interrupts blood flow to the brain also can cause vascular dementia.

Essential hypertension FAQs

Q: Can essential hypertension be treated successfully?
A: Yes, in many cases, there is a good chance that blood pressure can be lowered if the appropriate treatment methods are followed. To ensure blood pressure remains at a healthy level, most people will be required to maintain lifestyle changes and, if required, take medication, possibly for the rest of their lives.

Q: What is malignant essential hypertension?
A: Malignant essential hypertension, sometimes called accelerated hypertension, is a form of hypertensive emergency. It involves high blood pressure that develops very quickly, causing serious complications. The malignant variety is extremely rare, affecting roughly one percent of those with high blood pressure, but if it is suspected, it should be treated as a medical emergency.

Q: What is benign essential hypertension?
A: When essential hypertension remains in its early stages for a prolonged period of time and without a specific known cause, it is known as benign essential hypertension. In this state, the condition will generally be symptomless and develop very slowly. It is still important to seek treatment after a diagnosis of benign essential hypertension.

What is non-essential hypertension?
A: Non-essential hypertension is an alternative name for secondary hypertension. Essential hypertension is characterized by a lack of clearly attributable causes, whereas secondary hypertension is directly linked to a variety of vascular, endocrine, heart and kidney conditions.

Q: Can pregnancy cause essential hypertension?
A: Essential hypertension is defined by its lack of a clearly attributable cause, meaning that pregnancy cannot be said to cause the condition. However, pregnancy can cause a form of hypertension known as gestational hypertension. By definition, this form of hypertension must occur after 20 weeks of pregnancy in a previously not hypertensive person and disappear after the delivery of the baby Longer lasting hypertension, detected either before pregnancy or before the 20th week of pregnancy, and which remains after delivery of the baby, is defined as chronic hypertension and can be a kind of essential hypertension. Both gestational and chronic hypertension can lead to preeclampsia, a potentially serious but treatable complication of pregnancy. For more information, take a look at this resource on preeclampsia.

Q: What is hypertensive heart disease?
A: Hypertensive heart disease is an umbrella term for various heart conditions that are caused by chronically or prolonged high blood pressure levels. High blood pressure puts extra strain on the heart and the vessels surrounding and supplying the heart, something which can lead to the development of a variety of heart disorders. These include heart failure, coronary artery disease and the thickening of the heart muscle, among others. People at risk of hypertensive heart disease should talk to their doctor about methods of preventing potential complications, e.g. attending regular check-ups and taking medication regularly as required by their prescription. This will typically also include getting plenty of exercise, eating a balanced, nutritious diet and losing weight, if the person in question is considerably overweight or obese.

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