Back to Book/course

Clinical ECG Interpretation

0% Complete
0/91 Steps
  1. Introduction to ECG Interpretation
    6 Chapters
  2. Arrhythmias and arrhythmology
    24 Chapters
  3. Myocardial Ischemia & Infarction
    21 Chapters
  4. Conduction Defects
    11 Chapters
  5. Cardiac Hypertrophy & Enlargement
    5 Chapters
  6. Drugs & Electrolyte Imbalance
    3 Chapters
  7. Genetics, Syndromes & Miscellaneous
    7 Chapters
  8. Exercise Stress Testing (Exercise ECG)
    6 Chapters
Section Progress
0% Complete

Ventricular tachycardia (VT): types, causes, ECG features and management

This chapter deals with ventricular tachycardia from a clinical perspective, with emphasis on ECG diagnosis, definitions, management and clinical characteristics. Ventricular tachycardia is a highly nuanced arrhythmia which originates in the ventricles. A wide range of conditions may cause ventricular tachycardia and the ECG is as nuanced as are those conditions. Regardless of etiology and ECG, ventricular tachycardia is always a potentially life-threatening arrhythmia which requires immediate attention. The ventricular rate is typically very high (100–250 beats per minute) and cardiac output is affected (i.e reduced) in virtually all cases. Ventricular tachycardia cause immense strain on the ventricular myocardium, simultaneously as the cause of the arrhythmia already affects cellular function. This results in electrical instability which explains why ventricular tachycardia may progress to ventricular fibrillation. Left untreated, ventricular fibrillation leads to asystole and cardiac arrest. All health care providers, regardless of profession, must be able to diagnose ventricular tachycardia.

Causes of ventricular tachycardia

Patients with ventricular tachycardia almost invariably have significant underlying heart disease. The most common causes are coronary heart disease (acute coronary syndromes or ischemic heart disease), heart failure, cardiomyopathy (dilated cardiomyopathy, hypertrophic obstructive cardiomyopathy), valvular disease. Less common causes are arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/ARVD), Brugada syndrome, long QT syndrome, sarcoidosis, Prinzmetal’s angina (coronary vasospasm), electrolyte disorders, congenital heart disease and catecholamine induced ventricular tachycardia.

The vast majority of patients with ventricular tachycardia either have coronary artery disease (ischemic heart disease), heart failure, cardiomyopathy or valvular heart disease. In these populations one of the strongest predictors of sudden cardiac death is left ventricular function. Individuals with reduced left ventricular function (e.g defined as ejection fraction <40 %) are at high risk of sudden cardiac arrest.

Idiopathic ventricular tachycardia (IVT)

Ventricular tachycardia may be classified as idiopathic if no cause can be identified. Idiopathic ventricular tachycardia has a more favorable prognosis, as compared with other forms of ventricular tachycardia.

Mechanisms of ventricular tachycardia

Ventricular tachycardia (VT) may emerge due to increased/abnormal automaticity, re-entry or triggered activity. All types of myocardial cells may be engaged in initiation and maintenance of this arrhythmia. As mentioned above VT causes hemodynamic compromise. The rapid ventricular rate, which may be accompanied by already impaired ventricular function, does not allow for adequate filling of the ventricles, which results in reduced stroke volume and reduced cardiac output.

Most patients experience presyncope or syncope if the arrhythmia is sustained. In its fulminant course, VT degenerates to ventricular fibrillation, which then degenerates into asystole and cardiac arrest. Importantly, the progress from VT to cardiac arrest may be aborted either spontaneously or by means of treatment. Interestingly, treatment of VT is considered one of the greatest advances in cardiology. Until 1961, patients with acute myocardial infarction were placed in beds located far away from physicians’ and nurses’ stations in order to not disturb the patients’ rest. It was believed that the mere presence of physicians and nurses caused harmful stress. Approximately 30% of patients died in the hospital and fatal tachyarrhythmias was presumably the leading cause. Animal studies conducted in the late 1950s, 1960 and 1961 showed that VT could be terminated by delivering an electrical shock. This prompted physicians to construct coronary care units, in which all patients with acute myocardial infarction were monitored with continuous ECG and ventricular tachyarrhythmias were handled by means of immediate resuscitation and defibrillation.

Ventricular tachycardia in acute coronary syndromes (myocardial infarction)

Acute coronary syndromes are subdivided into unstable angina (UA), ST elevation myocardial infarction (STEMI) and non ST elevation myocardial infarction (NSTEMI). The risk of VT is high in these conditions. Moreover, the risk is highly time-dependent, being highest in the hyperacute phase (the first minutes to hours after symptom onset). The vast majority of individuals who die in the acute phase of myocardial infarction actually die from ventricular tachyarrhythmias. Death due to pumping failure (i.e cardiogenic shock) is less common. Because the risk is highest in the first minutes to hours, most deaths occur outside of the hospital. The risk of VT (and thus ventricular fibrillation) diminishes gradually as time elapses. In addition to time, the major determinant of VT is the extent of the ischemia/infarction. The larger the ischemic are the greater the risk of arrhythmias.

ECG criteria for ventricular tachycardia

ECG features of ventricular tachycardia

  • ≥3 consecutive ventricular beats with rate 100–250 beats per minute (in most cases >120 beats per minute). Ventricular tachycardia with rate 100 to 120 beats per minute is referred to as slow ventricular tachycardia.  Ventricular tachycardia with rate >250 beats per minute is referred to as ventricular flutter.
  • Wide QRS complexes (QRS duration ≥0,12 s).

Types of ventricular tachycardia

The ECG allows for subclassification of ventricular tachycardia. The discussion below may be perceived as advanced, but the reader should know that it is not required th-at all clinicians be able to classify ventricular tachycardias; merely being able to recognize it is sufficient. Therefore, the purpose of the discussion below is to present the reader with several types of ventricular tachycardia just for reference.

Sustained vs. Non-sustained ventricular tachycardia

Ventricular tachycardia with duration <30 seconds is classified as non-sustained ventricular tachycardia. Sustained ventricular tachycardia has duration >30 seconds.

Monomorphic ventricular tachycardia

In monomorphic ventricular tachycardia all QRS complexes display the same morphology (minor differences are allowed). This indicates that the impulses originate in the same ectopic focus. In structural heart disease (coronary heart disease, heart failure, cardiomyopathy, valvular disease etc) monomorphic ventricular tachycardia is typically caused by re-entry. Refer to Figure 1.

Figure 1. Monomorphic ventricular tachycardia (VT, VTach). P-waves are visible but they do not have any relation to the QRS complexes. This situation is referred to as “AV dissociation” and indicates that atrial and ventricular activity and independent. AV dissociation confirms that the arrhythmia is ventricular tachycardia. However, AV dissociation is frequently difficult to spot.

The Purkinje fibers in the interventricular septum appear to have an important role in ventricular tachycardia among patients with coronary heart disease. These Purkinje fibers appear to be highly arrhythmogenic in the setting of myocardial ischemia, particularly re-ischemia. Because any impulse arising in the interventricular septum will enter the Purkinje network (to some degree) the QRS complexes tend to be shorter than arrhythmias originating in the free ventricular walls. QRS duration is generally 120 to 145 ms in ventricular tachycardias arising in the septum.

Fascicular ventricular tachycardia is an idiopathic form of VT. It is caused by re-entry in the fascicles of the left bundle branch (i.e in the Purkinje fibers). Fascicular ventricular tachycardia occurs in people aged less than 50 years of age, and predominantly in males. The QRS complexes display morphology similar to right bundle branch block and there is left axis deviation.

Right ventricular outflow tract (RVOT) ventricular tachycardia is a monomorphic VT originating in the outflow tract of the right ventricle. The arrhythmia is mostly idiopathic but some patients may have ARVC (arrhythmogenic right ventricular cardiomyopathy). Because the impulses originate in the right ventricle, the QRS complexes have left bundle branch appearance and the electrical axis is around 90°. Refer to Figure 2.

Figure 2. Ventricular tachycardia (VT) originating in the right ventricular outflow tract (RVOT).

Polymorphic ventricular tachycardia

A ventricular tachycardia with varying QRS morphology or varying electrical axis is classified as polymorphic. The rhythm may be irregular. Polymorphic ventricular tachycardia is typically very fast (100–320 beats per minute) and unstable. There are several types of polymorphic ventricular tachycardia. The most common cause is myocardial ischemia. The second most common cause is prolonged QTc interval (Long QT syndrome).

Familial catecholaminergic polymorphic ventricular tachycardia (CPVT) is an hereditary ventricular tachycardia in which emotional or physical stress induce the arrhythmia, which may lead to circulatory colapse and cardiac arrest. This type of ventricular tachycardia may be bidirectional (see below). The diagnosis is established by means of exercise stress testing since the sympathetic activity induces the tachycardia.

Brugada syndrome causes polymorphic VT (mostly during sleep or fever).

Early repolarization and hypertrophic obstructive cardiomyopathy also causes polymorphic VT.

Bidirectional ventricular tachycardia means that the QRS morphology alternates from one ebat to another. In most cases it alternates between two variants of the QRS complex.  Bidirectional ventricular tachycardia is seen in familial CPVT, digoxin overdoes and long QT syndrome. Refer to Figure 3.

Figure 3. Bidirectional ventricular tachycardia.

Ventricular tachycardia in ischemic heart disease

Coronary artery disease (ischemic heart disease) is by far the most common cause of ventricular tachycardia and the mechanism is mostly re-entry. As mentioned earlier in this chapter, re-entry occurs when there is a central block ahead of the depolarizing impulse and the cells surrounding the block has varying conductivity. In ischemic heart disease, the central block is typically ischemic/necrotic myocardium (which do not conduct any impulses) while the surrounding cells have dysfunctional conduction due to ischemia. Ventricular tachycardia due to ischemia poses a high risk of degenerating into ventricular fibrillation and cardiac arrest.

Hence, ventricular tachycardia in coronary artery disease is mostly monomorphic. It may be polymorphic, if there are several ectopic foci or if the impulse from one foci spreads varyingly.

Locating the ectopic foci causing ventricular tachycardia

The ECG provides valuable information regarding the location of the ectopic foci causing the tachycardia. This is done by classifying ventricular tachycardias broadly as either “left bundle branch appearance” or “right bundle branch appearance”. Ventricular tachycardias with ECG waveforms reminding of a left bundle branch block (dominant S-wave in V1) originate in the right ventricle. The opposite is also true, namely that ventricular tachycardias reminding of right bundle branch block (dominant R-wave in V1) originates in the left ventricle. This might be useful in trying to decipher what the cause of the ventricular tachycardia may be. Figure 4 and Figure 5 below shows examples.

Figure 4. Ventricular tachycardia with right bundle branch block (RBBB) morphology. However, the first R-wave is larger than the second R-wave, which is not the case in RBBB. This suggests that the rhythm is not a supraventricular tachycardia conducted with RBBB, but rather ventricular tachycardia (VT).
Figure 5. Ventricular tachycardia with left bundle branch block morphology.

Distinguishing ventricular tachycardia from supraventricular tachycardias with wide QRS complexes

Occasionally supraventricular tachycardias (which mostly have normal QRS complexes, i.e QRS duration <0.12 seconds) may display wide QRS complexes. This might be due to concomitant bundle branch block, aberration, hyperkalemia, pre-excitation or side effect of drugs (tricyclic antidepressants, antiarrhythmic drugs class I). It is fundamental to be able to differentiate supraventricular tachycardias with wide QRS from VT and the reason for this is simple: VT is potentially life-threatening, whereas supraventricular arrhythmias rarely are. Hence, wide QRS complexes do not guarantee that the rhythm is ventricular in origin.

Fortunately, there are several characteristics that separate ventricular tachycardia from supraventricular tachycardias (SVT). These characteristics can be used separately or in algorithms (Which are easy to use) to determine whether a tachycardia with wide QRS complexes (often called wide complex tachycardia) is a ventricular tachycardia or an SVT. Before dwelling into these characteristics and algorithm it should be noted that 90% of all wide complex tachycardias are ventricular tachycardias! If the patient suffers from any of the conditions stated above as risk factors for ventricular tachycardia, one should be very prone to assume that it is ventricular tachycardia.

Characteristics of ventricular tachycardia are now discussed.

Atrioventricular (AV) dissociation

AV dissociation means that atria and ventricles function independently of each other. On the ECG this manifests as P-waves having no relation to QRS complexes (P-P intervals are different from R-R intervals, PR intervals vary and there is no relation between P and QRS). Note that it is often difficult to discern P-waves during VT (esophagus ECG may be very helpful). If AV dissociation can be verified, VT is very likely to be the cause of the arrhythmia. However, occasionally the ventricular impulses may be conducted retrogradely through the His bundle and AV node to the atria and depolarize the atria synchronously with the ventricles; thus VT may actually display synchronized P-waves.  The following ECG shows VT with AV dissociation (the arrows point at P-waves).

Figure 1 (repeated). Monomorphic ventricular tachycardia (VT, VTach). P-waves are visible but they do not have any relation to the QRS complexes. This situation is referred to as “AV dissociation” and indicates that atrial and ventricular activity and independent. AV dissociation confirms that the arrhythmia is ventricular tachycardia. However, AV dissociation is frequently difficult to spot.

Initiation of the tachyarrhythmia

If the start of the tachycardia is recorded it is valuable to assess the initial beats. If the R-R intervals during the start of the tachycardia were irregular, it suggests ventricular tachycardia. This is called warp-up phenomenon and is characteristic of ventricular tachycardia. Supraventricular tachycardias do not display warm-up phenomenon (with the exception of atrial tachycardia).

Initiation by premature atrial beats

Ventricular tachycardia is not induced by premature atrial beats, but supraventricular tachycardias typically do. If the start of the tachycardia is recorded, one must examine whether it was preceded by a premature atrial beat.

Fusion beats & capture beats

If a ventricular impulse is discharged simultaneously as the atrial impulse enters the His-Purkinje system, the ventricles will be depolarized by both. The resulting QRS complex will have an appearance resembling both a normal QRS and a wide QRS. Such beats are called fusion beats, and such beats are diagnostic of ventricular tachycardia. Figure 6 shows an example.

Occasionally during a ventricular tachycardia, the atrial impulse will break through and manage to depolarize the ventricles. This is seen as the occurrence of a normal beat in the midst of the tachycardia. Such beats are called capture beats and they are also diagnostic of ventricular tachycardia.

Figure 6. Capture beats and fusion beats seen during ventricular tachycardia.


Ventricular tachycardia is mostly regular, although the R-R intervals may vary somewhat. Discrete variability in R-R intervals actually suggest ventricular tachycardia. However, polymorphic ventricular tachycardia may be irregular. Supraventricular tachycardias may also be irregular; the most common being atrial fibrillation. Note that pre-excitation during atrial fibrillation causes an irregular wide complex tachcyardia, with heart rate >190 beats per minute in most cases.

Previously existing bundle branch block

Individuals with previously existing conduction defects (right or left bundle branch block) or other causes of wide QRS complexes (pre-excitation, drugs, hyperkalemia) should have their ECGs during tachyarrhythmia compared with the ECG during sinus rhythm (or any earlier ECG). If the QRS morphology during the tachyarrhythmia is similar to the QRS complex in sinus rhythm, it is likely to be an SVT. Moreover, if the patient has recently had premature ventricular complexes, and the QRS during tachyarrhythmia resembles that of the premature ventricular complexes, then it is likely to be ventricular tachycardia.

Electrical axis

Electrical axis between –90° and –180° strongly suggest ventricular tachycardia (although antidromic AVRT is a differential diagnosis). If the electrical axis during tachycardia differs >40° from the electrical axis durign sinus rhtyhm, it also suggest ventricular tachycardia. If the tachyarrhythmia has a right bundle branch block pattern but the electrical axis is more negative than –30° it suggests ventricular tachycardia. If the tachyarrhythmia has a left bundle branch block pattern but the electrical axis is more positive than 90° it suggests ventricular tachycardia. In general, left axis deviation suggests ventricular tachycardia.

QRS duration

QRS duration >0.14 s suggest ventricular tachycardia. QRS duration >0.16 s strongly suggest ventricular tachycardia. Note that ventricular tachycardia originating in the interventricular septum may have a relatively narrow QRS complex (0.120–0.145 s). Antidromic AVRT may also have >0.16 s. Class I antiarrhythmic drugs, tricyclic antidepressants and hyperkalemia may also cause very wide QRS complexes.

Concordance in V1–V6

Concordance means that all QRS complexes from lead V1 to lead V6 head in the same direction; all are either positive or negative. If any lead displays biphasic QRS complexes (e.g qR complex or RS complex) there cannot be concordance. Negative concordance (all QRS complexes being negative) strongly suggest ventricular tachycardia). Positive concordance (all QRS complexes being positive) are mostly due to ventricular tachycardia but may be caused by antidromic AVRT. The following figure presents concordance. To conclude, concordance is strongly suggestive of ventricular tachycardia.

Figure 7. Concordance in QRS complexes from V1 to V6 in ventricular tachycardia.
Figure 8. Lead I, II, III, V1 aVR, aVL and aVF. As seen in the beginning of the recording, the patient has an underlying rhythm of atrial fibrillation. The atrial fibrillation is interrupted by a rapid and regular tachycardia with wide QRS complex. The 4th beat from the end is a premature ventricular beat and its QRS morphology is identical to the QRS seen during the tachycardia. Hence, the tachycardia also originates from the ventricles, which implies that it is ventricular tachycardia (VT). Source | License

Absence of RS complexes

If there is no QRS complex from lead V1 to lead V6 which is an RS complex (i.e consists of an R wave and an S wave), then ventricular tachycardia is very likely.


It is not recommended that adenosine be administered when ventricular tachycardia is suspected, because adenosine may accelerate the frequency and aggravate the arrhythmia. Occasionally adenosine is still administered (when suspecting that the arrhythmia is actually a SVT with wide QRS complexes). If adenosine do not have any effect or if it accelerates the tachycardia, it is likely to be ventricular tachycardia.

In addition to these characteristics, researchers have developed several algorithms to differentiate ventricular tachycardia from SVTs. These algorithms are briefly outlined below (refer to Management and Diagnosis of Tachyarrhythmias for details)

Brugada’s algorithm

This is the most used algorithm. If any of the five criteria below are fulfilled, a diagnosis of ventricular tachycardia can be made.

Brugada’s algorithm

  1. If there is no RS complex in any chest lead (V1–V6) a diagnosis of ventricular tachycardia can be made. Otherwise, continue to next criteria.
  2. Assess the RS interval (interval from start of the R-wave to the nadir of the S-wave). If any RS interval is >100 ms and the R-wave is wider than the S-wave, a diagnosis of ventricular tachycardia can be made. Otherwise, continue to next criteria.
  3. If there is AV dissociation, a diagnosis of ventricular tachycardia can be made. Otherwise, continue to next criteria.
  4. Assess the QRS morphology in V1, V2, V5 and V6 (see below). If the QRS morphology is compatible with ventricular tachycardia, then the diagnosis is ventricular tachycardia.
  5. If no criteria have been fulfilled, a diagnosis of supraventricular tachycardia can be made.

Judging the QRS morphology (criteria #4 in Brugada’s algorithm)

If the QRS complex in V1–V2 resembles a right bundle branch block (i.e positive QRS)
  • V1:
    • Monophasic R complex suggests ventricular tachycardia.
    • qR complex suggests ventricular tachycardia.
    • if R is taller than R’, ventricular tachycardia is suggested.
    • Triphasic complexes (rSr’, rsr’, rSR’, rsR’) suggests SVT
  • V6:
    • rS, QS, R or Rs complex suggests VT.
If the QRS complex in V1–V2 resembles a left bundle branch block (i.e negative QRS)
  • V1:
    • The initial portion of the QRS complex is smooth in ventricular tachycardia. SVT has a sharp start of the QRS complex.
    • R-wave duration ≥40 ms suggest ventricular tachycardia.
    • Duration from start of QRS complex to nadir of S-wave ≥60 ms suggests ventricular tachycardia.
  • V6:
    • QR or QS complex suggest ventricular tachycardia.
    • R or RR complex without initial q-wave suggests SVT.

All in all, Brugada’s criteria have very high sensitivity (90%) and specificity (60–90%) for diagnosing ventricular tachycardia.

Brugada’s algorithm for differentiating ventricular tachycardia from antidromic AVRT

The algorithm above frequently fails to differentiate ventricular tachycardia from antidromic AVRT. Although antidromic AVRT is an uncommon cause of ventricular tachycardia, it is important to be able to differentiate these entities. The older the patient and the more significant the heart disease, the more likely is ventricular tachycardia. The Brugada group has also developed an algorithm to differentiate antidromic AVRT from ventricular tachycardia. The algorithm follows:

Brugada’s algorithm for differentiating ventricular tachycardia and antidromic AVRT

  1. If the QRS complex is net negative in V4–V6, ventricular tachycardia is more likely.
  2. If the QRS complex is net positive in V4–V6 and any of the leads V2–V6 display a qR complex, ventricular tachycardia is very likely.
  3. If there is AV dissociation, ventricular tachycardia is very likely.
  4. If there are no signs of ventricular tachycardia, antidromic AVRT should be strongly considered.


Management of ventricular tachycardia

Treatment in the emergency setting

Unconscious patients: start cardiopulmonary resuscitation.

Hemodynamically unstable patients (hypotension, angina, heart failure, shock, pre-syncope/syncope): the patient should be treated immediately with electrical cardioversion (during anesthesia). Ventricular tachycardia can be terminated already at 20–50 J biphasic shock. Beta-blockers are administered intravenously, unless the patient has bradycardia induced ventricular tachycardia. In that scenario, amiodarone is to be preferred after cardioversion (amiodarone 50 mg/ml, 6 ml with 14 ml glucose 50 mg/ml, i.v during 2 min). Hypokalemia and hypomagnesaemia should be corrected rapidly. Causes underlying the ventricular tachycardia must be targeted; heart failure, ischemia, hypotension, hypokalemia etc can all be treated rapidly. Thumpversion (hitting the patient’s chest with a fist) is no longer recommended although it might terminate the tachcyardia in some cases.

Hemodynamically stable patients may be treated pharmacologically (amiodarone, lidocaine, sotalol, procainamide). Only one of these drugs are administered and a loading dose is followed by infusion. Amiodarone is the primary choice with a loading dose of 150 mg i.v bolus given during 10 minutes. An infusion at 1 mg/min during 6 hours, followed by 0.5 mg/min during 18 hours is also started. The loading dose may be repeated with 15 minute intervals. Maximum dose amiodarone is 2.2 g/day. If amiodarone fails, one should consider electrical cardioversion before considering pharmacological alternatives. Lidocaine is given as iv bolus of 0.75 mg/kg which can be repeated after 5–10 minutes. Infusion lidocaine 1–4 mg/min (maximum dose 3 mg/kg/h) is started simultaneously.

Digoxin induced ventricular tachycardia may be treated as a hemodynamically stable patients above. Note that there are antibodies against digoxin.

Transcutaneous or transvenous pacing: Pacing at higher frequency than the ventricular tachycardia may terminate it (but there is a risk of degeneration into ventricular fibrillation).

Intermittent ventricular tachycardia with frequent capture beats should be treated pharmacologically.

Polymorphic ventricular tachycardia should be considered unstable and treated immediately with electrical cardioversion. Beta-blockers may be administered if the ECG does not show long QT interval. If the ECG does show long QT interval, the condition is classified as torsade de pointes; refer to this article for treatment recommendations. Amiodarone may also be administered if there is no evidence of long QT interval.

Bradycardia induced ventricular tachycardia (sinus bradycardia, AV-block etc): Bradycardia may induce premature ventricular complexes and ventricular arrhythmias. These are treated with atropine, isoproterenol (isoprenaline) or transvenous pacing.

Long-term treatment of ventricular tachycardia

Patients with preserved left ventricular function and asymptomatic non-sustained ventricular tachycardias may be adequately treated with beta-blockers. Sotalol (may cause QT prolongation) and amiodarone may also be considered. Verapamil is contraindicated. If the individual has suffered a myocardial infarction, an ICD should be considered.

Patients with high risk of sudden cardiact arrest (reduced left ventricular function, previous myocardial infarction, structural heart disease) should be considered for an ICD which offers effective protection. Otherwise, amiodarone appears to be the most effective drug in preventing new episodes of ventricular tachycardia.


Next chapter

Long QT Syndrome (LQTS) & Torsade de Pointes (TdP)

Related chapters

Mechanisms of cardiac arrhythmias

Management and diagnosis of tachycardias (narrow complex tachycardia and wide complex tachycardia)

Premature ventricular beats (premature ventricular contractions / complex)

Ventricular Rhythm, Accelerated Ventricular Rhythm (Idioventricular Rhythm)

Pacemaker Mediated Tachycardia (PMT)

Ventricular Fibrillation (VF), Pulseless Electrical Activity (PEA) & Sudden Cardiac Arrest (SCA)

Introduction to Coronary Artery Disease

STEMI – ST Elevation Myocardial Infarction

NSTEMI – Non-ST Elevation Myocardial Infarction & Unstable Angina

View all chapters in Cardiac Arrhythmias.

4.4/5 (10 Reviews)
error: Contact us for permission to use contents. Permission will be granted for non-profit sites.

Join our newsletter and get our free ECG Pocket Guide!

Start learning ECG & echo now!