Electrocardiography; Types, Indications/Uses, Procedures

Electrocardiography (ECG or EKG) is the process of recording the electrical activity of the heart over a period of time using electrodes placed on the skin. These electrodes detect the tiny electrical changes on the skin that arise from the heart muscle’s electrophysiologic pattern of depolarizing and repolarizing during each heartbeat. It is a very commonly performed cardiology test.

In a conventional 12-lead ECG, ten electrodes are placed on the patient’s limbs and on the surface of the chest. The overall magnitude of the heart’s electrical potential is then measured from twelve different angles (“leads”) and is recorded over a period of time (usually ten seconds). In this way, the overall magnitude and direction of the heart’s electrical depolarization is captured at each moment throughout the cardiac cycle. The graph of voltage versus time produced by this noninvasive medical procedure is an electrocardiogram.

Medical Uses

A 12-lead ECG of a 26-year-old male with an incomplete RBBB

The overall goal of performing electrocardiography is to obtain information about the structure and function of the heart. Medical uses for this information are varied and generally relate to having a need for knowledge of the structure and/or function. Some indications for performing electrocardiography include:

Suspected myocardial infarction (heart attack) or new chest pain
Suspected pulmonary embolism or new shortness of breath
A third heart sound, fourth heart sound, a cardiac murmur or other findings to suggest structural heart disease
Perceived cardiac dysrhythmias either by pulse or palpitations
Monitoring of known cardiac dysrhythmias
Chest pain
Atypical chest pain
Epigastric pain
Back, neck, jaw or arm pain without chest pain
Palpitations
Syncope or near syncope
Pulmonary edema
Exertional dyspnea
Weakness
Diaphoresis unexplained by ambient temperature
Feel of anxiety or impending doom
Suspected diabetic ketoacidosis
Fainting or collapse
Seizures
Monitoring the effects of a heart medication (e.g. drug-induced QT prolongation)
Assessing severity of electrolyte abnormalities, such as hyperkalemia
Hypertrophic cardiomyopathy screening in adolescents as part of a sports physical out of concern for sudden cardiac death (varies by country)
Perioperative monitoring in which any form of anesthesia is involved (e.g. monitored anesthesia care, general anesthesia); typically both intraoperative and postoperative
As a part of a pre-operative assessment some time before a surgical procedure (especially for those with known cardiovascular disease or who are undergoing invasive or cardiac, vascular or pulmonary procedures, or who will receive general anesthesia)
Cardiac stress testing
Computed tomography angiography (CTA) and Magnetic resonance angiography (MRA) of the heart (ECG is used to “gate” the scanning so that the anatomical position of the heart is steady)
Biotelemetry of patients for any of the above reasons and such monitoring can include internal and external defibrillators and pacemakers

Diagnosis

Numerous diagnoses and findings can be made based upon electrocardiography, and many are discussed above. Overall, the diagnoses are made based on the patterns. For example, an “irregularly irregular” QRS complex without P waves is the hallmark of atrial fibrillation; however, other findings can be present as well, such as a bundle branch block that alters the shape of the QRS complexes. ECGs can be interpreted in isolation but should be applied – like all diagnostic tests – in the context of the patient. For example, an observation of peaked T waves is not sufficient to diagnose hyperkalemia; such a diagnosis should be verified by measuring the blood potassium level. Conversely, a discovery of hyperkalemia should be followed by an ECG for manifestations such as peaked T waves, widened QRS complexes, and loss of P waves. The following is an organized list of possible ECG-based diagnoses.

Rhythm disturbances/arrhythmias:

Atrial fibrillation & atrial flutter without rapid ventricular response
Premature atrial contraction (PACs) & Premature ventricular contraction (PVCs)
Sinus arrhythmia
Sinus bradycardia & sinus tachycardia
Sinus pause & sinoatrial arrest
Sick sinus syndrome: bradycardia-tachycardia syndrome
Supraventricular tachycardia
- Atrial fibrillation (afib) with rapid ventricular response
- Atrial flutter with rapid ventricular response
- AV nodal reentrant tachycardia
- Atrioventricular reentrant tachycardia
- Junctional ectopic tachycardia
- Atrial tachycardia
  - Ectopic atrial tachycardia (unicentric)
  - Multifocal atrial tachycardia
  - Paroxysmal atrial tachycardia
- Sinoatrial nodal reentrant tachycardia
Torsades de pointes (polymorphic ventricular tachycardia)
Wide complex tachycardia
- Ventricular flutter
- Ventricular fibrillation
- Ventricular tachycardia (monomorphic ventricular tachycardia)
Pre-excitation syndrome
- Lown–Ganong–Levine syndrome
- Wolff–Parkinson–White syndrome
J wave/Osborn wave

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Heart block and conduction problems:

Aberration
Sinoatrial block: first, second, and third-degree
AV node
- First-degree AV block
- Second-degree AV block (Mobitz I & II; Mobitz I aka Wenckebach)
- Third-degree AV block/complete AV block
Right bundle
- Incomplete right bundle branch block
- Complete right bundle branch block (RBBB)
Left bundle
- Complete left bundle branch block (LBBB)
- Incomplete left bundle branch block
- Left anterior fascicular block (LAFB)
- Left posterior fascicular block (LPFB)
- Bifascicular block (LAFB plus LPFB)
- Trifascicular block (LAFP plus FPFB plus RBBB)
QT syndromes
- Brugada syndrome
- Short QT syndrome
- Long QT syndromes, genetic and drug-induced
Right and left atrial abnormality

Electrolytes disturbances & intoxication:

Digitalis intoxication
Calcium: hypocalcemia and hypercalcemia
Potassium: hypokalemia and hyperkalemia

Ischemia and infarction:

Wellens’ syndrome (LAD occlusion)
de Winter T waves (LAD occlusion)
ST elevation and ST depression
High Frequency QRS changes
Myocardial infarction (heart attack)
- Non-Q wave myocardial infarction
- NSTEMI
- STEMI
- Sgarbossa’s criteria for ischemia with a LBBB

Structural

Acute pericarditis
Right and left ventricular hypertrophy
Right ventricular strain/S1Q3T3 (can be seen in pulmonary embolism)

Grid and Leads

The ECG grid

Axis

Atrial Enlargement

Normal:: First portion of deflection is RA, second is LA
Right Atrial Enlargement:: P-wave amplitude > 2.5mm in inferior leads; Normal duration P-wave
Left Atrial Enlargement:: P-wave duration increased (terminal negative portion >0.04s); Amplitude of terminal negative component >1mm below isoelectric line in V1

Ventricular Hypertrophy

Right Ventricular Hypertrophy:

Right axis deviation

Abnormal R-wave progression

Increased R-wave amplitude in leads overlying the right ventricle (V1)
Increased S-wave amplitude in leads overlying the left ventricle (V6)

Criteria

V1: R>S
V6: S>R

Left Ventricular Hypertrophy:

Left axis deviation

Increased R-wave amplitude in leads overlying the LV (I, aVL, V5, V6)

Increased S-wave amplitude in leads overlying the RV (V1)

Criteria:

Precordial Leads
- R-wave in V5/V6 + S-wave in V1/V2 > 35mm
- R-wave in V5 > 26mm
- R-wave in V6 > 20mm
Limb Leads
- R-wave in aVL > 11mm
- R-wave in aVF > 20mm
Combined
- R-wave in aVL + S-wave in V3 > 20mm (F), 28mm (M)

Secondary Repolarization Abnormalities

Downsloping ST-segment depression
Asymmetric T-wave inversion

Bundle Branch Blocks

Left Bundle Branch Block

QRS duration > 0.12s (3 boxes)
Broad or notched R-wave with prolonged upstroke in I, aVL, V5, V6
Associated ST-segment depression and T-wave inversion
Reciprocal changes in V1, V2 (deep S-wave)
Possible LAD

Right Bundle Branch Block

QRS duration > 0.12s (3 boxes)
RSR’ in V1, V2
Reciprocal changes in I, aVL, V5, V6 (deep S-wave)

Hemiblocks

Other Blocks

Non-specific intraventricular conduction delay: QRS >0.10s without BBB
Incomplete BBB: LBBB/RBBB pattern with non-prolonged QRS
Bifascicular block: RBBB + LAFB/LPFB (by axis deviation)

Ischemia and Infarction

Hyperacute T-waves
T-wave inversion: Symmetric, compared to TWI associated with repolarization abnormalities
ST-elevation: Unlike J-point elevation, ST-segment merges with T-wave
Q-waves
1. Duration > 0.04s
2. Amplitude > 1/3 R-wave
3. Normal in aVR

Coronary Artery Territories

DISTRIBUTION	CORONARY ARTERY	LEADS	RECIPROCAL CHANGES
1. Inferior	RCA, PDA	II, III, aVF	Anterior, Lateral
2. Lateral	LCx	I, aVL, V5, V6	Inferior
3. Anterior	LAD	V1-V6	Inferior
4. Posterior	RCA	Posterior	Anterior (esp. V1)

ECG Guide: Pediatrics

ECG Standard

Full standard: no adjustment
Half-standard: commensurate reduction in amplitude (usually 50%)
Mixed: reduction in amplitude of precordial leads

Atrial Abnormalities

Right Atrial Abnormality (P pulmonale): Peaked P-wave in II (>3mm from 0-6mo or >2.5mm >6mo); Causes: right atrial volume overload, ASD, Ebstein, Fontan
Left Atrial Abnormality (P mitrale): Wide, notched P-wave in II or biphasic in V1; Causes: MS, MR

Axis

Anatomical dominance of right ventricle until approximately 6mo
RAD normal
eRAD suggests AV canal defect

T-waves

1st week of life: Upright
Adolescent: Inverted
Adult: Upright

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Ventricular Hypertrophy

Right Ventricular Hypertrophy: R-wave height >98% for age in lead V1; S-wave depth >98% for age in lead V6; T-wave abnormality (ex. upright in childhood); Causes: pHTN, PS, ToF

Left Ventricular Hypertrophy: R-wave height >98% for age in lead V6; S-wave depth >98% for age in lead V1; Adult-pattern R-wave progression in newborn (no large R-waves and small S-waves in right precordial leads); Left-axis deviation; Causes: AS, coarctation, VSD, PDA

Examples

Normal Neonatal ECG

2mo old
RAD
Inverted T-waves (normal)
Tall R-waves in V1-V3

Extreme Axis Deviation

Neonate with Down syndrome
Isoelectric in I, Negative in aVF negative in II  mean QRS vector -87°
Extreme RAD suggestive of AV canal defect

LVH:

Unrepaired Coarctation
Deep S-wave in V1 (>98%)
Tall R-wave in V6 (>98%)

RVH:

10 year-old boy with pulmonary Hypertension
RAD after expected age for normal RAD
Tall R-waves in V1 (>98%)
Deep S-wave in V6 (>98%)

STEMI

ALCAPA (anomalous origin of the left coronary artery from the pulmonary artery): coronary artery arises anomalously from the pulmonary artery; as pulmonary arterial pressure falls during the first 6 months of infancy, prograde flow through the left coronary artery ceases and may even reverse.
HLHS (hypoplastic left heart syndrome): coronary arteries are perfused from a hypoplastic, narrow aorta that is susceptible to flow disruption
Orthotopic heart transplant with allograft vasculopathy
Kawasaki: coronary artery aneurysm with subsequent thrombosis

Benign early repolarization

14 year-old male
Concave ST-segment elevation

Left Atrial Abnormality:

9mo female with mitral insufficiency
Broad biphasic P-wave in V1
Tall, notched P-wave in II

Prolonged QT interval

18-year-old female
Familial long QT syndrome and a history of cardiac arrest

WPW:

Delta wave, shortened PR interval

ECG Guide: Part II

STEMI

ST-segment elevation ≥ 1mm in two contiguous leads
: ≥ 2mm V2-V3
: ≥ 1.5mm V2-V3

Posterior STEMI

ST-segment depression V1-V3 Posterior ECG
ST-segment elevation ≥ 0.5mm in V7-V9

Sgarbossa Criteria

Evaluation for STEMI in LBBB or paced rhythm
Normal: ST-segment discordant with QRS
- QRS associated with ST-segment depression
- QRS associated with (commensurate) ST-segment elevation
Score ≥ 3 98% specific for MI

Elevation

Concordant ST-segment elevation ≥ 1mm in any lead (5 points)

Depression

Concordant ST-segment depression ≥ 1mm in V1-V3 (3 points)

Discordant Elevation

Discordant ST-segment elevation ≥ 5mm in any lead (2 points)

Modified Sgarbossa Criteria

ST:S ratio ≥ 0.25 in any lead
Presence of any criterion is positive

Other Causes of ST-segment Elevation

Benign Early Repolarization

Concave ST-segment elevation
Notch at J-point
Asymmetric T-waves (steeper descent)

Pericarditis

Diffuse ST-segment elevation (except aVR)
PR-segment depression
Ratio: ST-elevation to T-wave amplitude ≥ 0.25 in V6 suggests pericarditis

LVH Strain

ST-segment elevation in V1-V3 in the setting of LVH

LV Aneurysm

Q-waves with ST-segment elevation in precordial leads

Ischemia and Prior Infarcts

Wellens: Type A

Suggestive of proximal LAD lesion

Wellens: Type B

Q-waves

≥ 40ms duration
Depth ≥ 25% of R-wave height

Syncope

ARVD

Epsilon wave

Brugada Syndrome: Type 1

Type 1: Coved ST-segment elevation

Brugada Syndrome: Type 2

Type 2: Saddle-back ST-segment elevation

HCM

Deep, narrow Q-waves

Wolff-Parkinson-White

Shortened PR-interval
Delta-wave

Other

Atrial Abnormalities

Normal
RAA: P-wave amplitude > 2.5mm in inferior leads
LAA: P-wave duration increased (terminal negative portion >0.04s), amplitude of terminal negative component >1mm below isoelectric line in V1

Left Bundle Branch Block

QRS duration > 0.12s (3 boxes)
Broad or notched R-wave with prolonged upstroke in I, aVL, V5, V6
Associated ST-segment depression and T-wave inversion
Reciprocal changes in V1, V2 (deep S-wave)
Possible LAD

Right Bundle Branch Block

QRS duration > 0.12s (3 boxes)
RSR’ in V1, V2
Reciprocal changes in I, aVL, V5, V6 (deep S-wave)

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Axes

All ECG tracings are available for free, licensed (along with all content on this site) under Creative Commons Attribution-ShareAlike 4.0 International Public License.

Bradycardia

Brief H&P

A 38 year-old male with no medical history presents to the emergency department with abdominal pain. He had one episode each of non-bloody emesis followed by watery, non-bloody diarrhea and cited several sick contacts at home with similar symptoms. Vital signs were notable for bradycardia with a heart rate ranging from 38-46bpm though he was normotensive. The examination including abdominal examination was benign. A 12-lead electrocardiogram was obtained which demonstrated sinus bradycardia. The patient was asymptomatic during episodes of bradycardia and his heart rate responded appropriately during activity and on further history reported that he was an endurance athlete and runs multiple marathons each year. He was discharged after symptomatic improvement with anti-emetics.

Bradycardia

Definition: heart rate <60bpm
Sinus rhythm: upright P-wave in I, II, aV; inverted P-wave in aVR

Electrocardiographic Findings

Sinus bradycardia
- Potentially asymptomatic and present in healthy individuals
Sinoatrial node dysfunction (sick sinus syndrome, SSS)
- Sinus bradycardia
- Sinus arrest
- Tachy-brady syndrome (sinus bradycardia/arrest interspersed with SVT)
Atrioventricular block
- 1^st degree: PR prolongation, rarely symptomatic
- 2^nd degree: Intermittent interruption of conduction of atrial impulses to ventricles
  - Type 1: progressive PR prolongation leading to interrupted conduction
  - Type 2: fixed PR interval with interrupted conduction
- 3^rd degree: atrioventricular dissociation
Slow atrial fibrillation
- Irregular RR interval without recognizable P-wave

Epidemiology

Analysis of 277 patients presenting to the emergency department with “compromising” bradycardia.
Symptoms
- Syncope (33%)
- Dizziness (22%)
- Angina (17%)
- Dyspnea/Heart Failure (11%)
ECG
- High-grade AV block (48%)
- Sinus bradycardia (17%)
- Sinus arrest (15%)
- Slow atrial fibrillation (14%)
Cause
- Primary (49%)
- Drug (21%)
- Ischemia/Infarction (14%)
- Pacemaker failure (6%)
- Intoxication (6%)
- Electrolyte disorder (4%)

Important Historical Features

Fever/travel
Chest pain
Cold intolerance, weight gain
Headache, AMS, trauma
Abdominal pain/distension
Medication changes

Important Examination Findings

Perfusion (temperature, capillary refill)
Presence of fistula or hemodialysis catheter
Existing device (malfunction)

Workup

ECG
Continuous telemetry monitoring
Labs
- Potassium
- Digoxin level
- TFT
- Infection titers (RPR, Lyme)
- Cardiac enzymes

Management

Unstable
- Airway
- Atropine 0.5mg IV q3-5min (maximum 3mg)
- Dopamine/epinephrine infusion
- Temporary pacemaker (transcutaneous, transvenous) with blood-pressure preserving sedation
- Admission and evaluation for permanent pacemaker placement
Stable (outpatient evaluation)
- Event monitor
- Stress test (chronotropic incompetence)

Algorithm for the Evaluation and Management of Bradycardia

Wellens Syndrome

Case Presentation

49M with a history of hypertension who presented to his primary physician for routine follow-up and was referred to the ED for an abnormal ECG. He denied chest pain, shortness of breath, or any limitation to baseline exercise tolerance. His vital signs were notable for systolic hypertension and his examination was unremarkable. A chest x-ray showed no acute cardiopulmonary findings. His initial ECG demonstrated a biphasic T-wave in V2 and deep, symmetric T-wave inversions in V3-V6. His initial serum troponin was markedly elevated at 3.499. He was admitted and urgent coronary angiography revealed proximal LAD stenosis (70%), mid-LAD stenosis (85%) and 1^st right posterolateral stenosis (85%) which were stented. He was discharged on post-procedure day one and has remained asymptomatic at outpatient follow-up.

Presentation ECG

Biphasic T-wave in V2, deep and symmetric T-wave inversions in V3-V4

Post-Catheterization ECG

Resolution of biphasic T-wave and T-wave inversions

Presentation ECG

Post-Catheterization ECG

History

Initially described in 1982 where a subset of patients who did poorly with medical management of “impending myocardial infarction” (essentialy unstable angina) were found to have characteristic ECG changes. These patients were noted to be at increased risk for extensive anterior wall myocardial infarctions due to proximal LAD stenosis.

Criteria

History of chest pain
Normal or slightly-elevated cardiac enzymes
No precordial Q-waves
Isoelectric or <1mm ST-segment elevation
Pattern present in pain-free state
Type A (25%): Biphasic T-wave in V₂/V₃
Type B (75%): Deep, symmetrically inverted T-waves in V₂/V₃

Clinical Significance

Wellens Syndrome (or LAD coronary T-wave syndrome) represents a “pre-infarction” stage of coronary artery disease manifested by critical LAD stenosis. The natural history includes progression to extensive anterior wall myocardial infarction, often associated with severe left ventricular systolic dysfunction, cardiogenic shock and death. These changes may be mistaken for “non-specific” T-wave changes (which in the presence of a non-concerning history and typically non-elevated cardiac markers) may lead providers to inappropriate dispositions such a stress testing which is contraindicated. Recognition of this pattern and its appropriate management (urgent coronary angiography) is critical.

Case Summary

The case presented above is atypical. The patient had no history of chest pain and cardiac enzymes were significantly elevated – two features which are uncommon in Wellens Syndrome. However, the patient’s elevated cardiac biomarkers led to admission and angiography with identification of the characteristic proximal LAD stenosis (and other disease).

Nonsustained Ventricular Tachycardia

Case 1

64M with a history of HFrEF (LVEF 20-25%), CAD, AICD (unknown indication), COPD, CKD III presenting with gradual onset shortness of breath, progressive bilateral lower extremity edema.
Examination consistent with severe acute decompensated heart failure presumed secondary to left ventricular dysfunction.
Telemetry monitoring with multiple episodes of nonsustained ventricular tachycardia.

In the ED, the patient developed worsening respiratory failure despite initiation of therapy, requiring endotracheal intubation. Continuous cardiac monitoring revealed persistent salvos of NSVT, progressing to slow ventricular tachycardia without device intervention.
Device interrogation revealed multiple events, 3 shocks, several ATP’s over the recorded period.

Evaluation and Management:

NSVT with known (severe) ischemic heart disease
For repetitive monomorphic ventricular tachycardia: amiodarone, beta-blockade (if tolerated), procainamide (IIA, C)

ECG’s

ECG 1

Non-specific IVCD, LAA, VPC

ECG 2

VT initiated by fusion complex

ECG 1

ECG 2

Case 2

31F with the autoimmune polyglandular syndrome (adrenal, thyroid and endocrine pancreatic insufficiency), presenting with fever and cough.
Evaluation consistent with sepsis presumed secondary to the pulmonary source.
Telemetry monitoring initially with ventricular bigeminy, then nonsustained ventricular tachycardia.

In the ED, the patient developed pulseless ventricular tachycardia – apparently polymorphic. Chest compressions and epinephrine produced the return of spontaneous circulation with recovery to baseline neurologic function.
ECG revealed prolonged QTc and chemistry panel notable for critical hypokalemia/hypomagnesemia.

Evaluation and Management:

NSVT progressing to VT
Initially attributed to electrolyte disturbances. However, serial ECG’s continued to show prolonged QTc (possibly acquired, home medications included metoclopramide and erythromycin). Early echocardiography demonstrated global hypokinesis with EF 30-35% attributed to severe sepsis and recurrent defibrillation. Cardiac CT after resolution of acute illness showed persistently depressed ejection fraction without coronary atherosclerosis. The presence of NICM associated with malignant dysrhythmias warranted ICD placement.
Cardioversion for hemodynamic compromise (I, B), B-blockade (I, B), amiodarone if no LQTS (I, C), urgent angiography if ischemia not excluded (I, C)¹
Correction of electrolyte abnormalities (specifically hypokalemia) may decrease progression to VF.

ECG’s

ECG 1

Ventricular bigeminy

ECG 2

Long-QT

VT on Telemetry

Non-sustained ventricular tachycardia noted on telemetry monitoring

ECG 1

ECG 2

VT on Telemetry

> 3-5 consecutive beats originating below the AV node
Rate > 100bpm
Duration <30s

Epidemiology

- Occurs in 0-4% of ambulatory patients
- Increased frequency in males and with increasing age

In some patients, NSVT is associated with an increased risk of sustained tachyarrhythmias and sudden cardiac death. In others, it is of little prognostic significance.

Evaluation

In all patients:History: including arrhythmogenic medications/substances, pertinent family historyPhysical examinationECG/CXRTTEIn selected patients exercise-testing advanced imaging (CT/C-MR)Electrophysiologic studies genetic testing

NSVT in the absence of structural heart disease

NSVT in Idiopathic Ventricular Tachycardia

Ventricular outflow arrhythmias:: RVOT: 70-80%, LBBB pattern; LVOT: 20-30%, RBBB pattern
Mechanism:: Adrenergically mediated; Occur during exercise, resolve as heart-rate increases, recur during recovery
Management:: Exclude arrhythmogenic right ventricular cardiomyopathy (imaging, myocardial biopsy); If symptomatic, beta-blockade, ± IC anti-arrhythmic, CCB (verapamil) for ILVT
Prognosis:: Good, rare tachycardia-induced cardiomyopathy, rare SCD

NSVT in Polymorphic Ventricular Tachycardia

Mechanism: LQTS (acquired or inherited); Familial catecholaminergic polymorphic VT
Management: Symptomatic (ex. syncope, cardiac arrest): ICD; Asymptomatic QTc > 550ms: consider ICD
Prognosis: Increased risk SCD

Arrhythmogenic Right Ventricular Cardiomyopathy

Mechanism: Fibrosis, fibro-fatty replacement of myocardium in RVIT/RVOT/RV apex; May occur with only subtle structural abnormalities of the right ventricle; LBBB morphology
Management: Anti-arrhythmias of limited utility; Catheter ablation, ICD backup
Prognosis: Increased risk SCD

NSVT with apparent structural heart disease1

Hypertension and LVH

Mechanism: Stretch-induced abnormal automaticity; Fibrotic tissue; Presence of NSVT correlates with the degree of hypertrophy and subendocardial fibrosis
Management: Evaluation for ischemic heart disease; Aggressive medical management of hypertension (including beta-blockade)
Prognosis: Unclear

Valvular Disease

Mechanism: High incidence in AS, severe MR (25%); Mechanical stress from dysfunctional valvular apparatus
Management: Beta-blockade if symptomatic
Prognosis: No evidence that NSVT is an independent predictor of SCD.

Ischemic Heart Disease^9-14

Mechanism: Monomorphic VT associated with re-entry at the borders of ventricular scars; Ischemia induces polymorphic NSVT/VF
Management: Revascularization, beta-blockade, statin, ACE/ARB; MADIT I, MUSTT: ICD for ICM LVEF <40%, NSVT, EPS inducible VT; MADIT II, SCD-HeFT: ICD for moderate-to-severe LV dysfunction irrespective of NSVT or EPS findings
Prognosis: NSTEMI with NSVT >48h after admission 2x risk SCD (MERLIN-TIMI 36); STEMI with NSVT common, not as predictive of ACM or SCD as LVEF (CARISMA); NSVT <24h after admission for NSTEMI/STEMI not of prognostic significance.

Hypertrophic Cardiomyopathy

Mechanism: Genetic myocardial disease; Myocyte disarray, fibrosis, ischemia result in arrhythmogenic substrate
Management: (NSVT, LV thickness, FH SCD, syncope, abnormal BP response to exercise); Beta-blockade, anti-arrhythmic for symptoms
Prognosis: Increased risk SCD (1% annual)

Other Conditions

Non-ischemic dilated cardiomyopathy
Giant-cell myocarditis
Repaired TOF
Amyloidosis
Sarcoidosis
Chagas cardiomyopathy

Algorithm for the Evaluation of NSVT

Low Voltage ECG

Definition

QRS in limb leads <5mm
QRS in precordial leads <10mm

General Causes

Fluid, fat or air attenuating signal
Myocardial infiltration
Loss of viable myocardium

Example

Low Voltage ECG

ECG of patient with pericardial effusion

Baseline ECG

Old ECG from same patient

Low Voltage ECG

Baseline ECG

Differential Diagnosis of Low Voltage ECG

ECG Guide

The format of this article is atypical for the structure and concept of the website – but it’s always been about learning. Here is a simplified guide to ECG interpretation with a focus on the aspects I find more challenging to understand or recall.

Grid and Leads

The ECG grid

Axis

Atrial Enlargement

Normal:: First portion of deflection is RA, second is LA
Right Atrial Enlargement:: P-wave amplitude > 2.5mm in inferior leads; Normal duration P-wave
Left Atrial Enlargement:: P-wave duration increased (terminal negative portion >0.04s); Amplitude of terminal negative component >1mm below isoelectric line in V1

Ventricular Hypertrophy

Right Ventricular Hypertrophy:

Right axis deviation

Abnormal R-wave progression

Increased R-wave amplitude in leads overlying the right ventricle (V1)
Increased S-wave amplitude in leads overlying the left ventricle (V6)

Criteria

V1: R>S
V6: S>R

Left Ventricular Hypertrophy:

Left axis deviation

Increased R-wave amplitude in leads overlying the LV (I, aVL, V5, V6)

Increased S-wave amplitude in leads overlying the RV (V1)

Criteria:

Precordial Leads
- R-wave in V5/V6 + S-wave in V1/V2 > 35mm
- R-wave in V5 > 26mm
- R-wave in V6 > 20mm
Limb Leads
- R-wave in aVL > 11mm
- R-wave in aVF > 20mm
Combined
- R-wave in aVL + S-wave in V3 > 20mm (F), 28mm (M)

Secondary Repolarization Abnormalities

Downsloping ST-segment depression
Asymmetric T-wave inversion

Bundle Branch Blocks

Left Bundle Branch Block

QRS duration > 0.12s (3 boxes)
Broad or notched R-wave with prolonged upstroke in I, aVL, V5, V6
Associated ST-segment depression and T-wave inversion
Reciprocal changes in V1, V2 (deep S-wave)
Possible LAD

Right Bundle Branch Block

QRS duration > 0.12s (3 boxes)
RSR’ in V1, V2
Reciprocal changes in I, aVL, V5, V6 (deep S-wave)

Hemiblocks

Other Blocks

Non-specific intraventricular conduction delay: QRS >0.10s without BBB
Incomplete BBB: LBBB/RBBB pattern with non-prolonged QRS
Bifascicular block: RBBB + LAFB/LPFB (by axis deviation)

Ischemia and Infarction

Hyperacute T-waves
T-wave inversion: Symmetric, compared to TWI associated with repolarization abnormalities
ST-elevation: Unlike J-point elevation, ST-segment merges with T-wave
Q-waves
1. Duration > 0.04s
2. Amplitude > 1/3 R-wave
3. Normal in aVR

Coronary Artery Territories

DISTRIBUTION	CORONARY ARTERY	LEADS	RECIPROCAL CHANGES
1. Inferior	RCA, PDA	II, III, aVF	Anterior, Lateral
2. Lateral	LCx	I, aVL, V5, V6	Inferior
3. Anterior	LAD	V1-V6	Inferior
4. Posterior	RCA	Posterior	Anterior (esp. V1)

References

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