Ventricular tachycardia: Clinical sciences

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Introduction0:00–1:20

Ventricular tachycardia, also known as VT or V-tach, is a wide-complex tachycardia originating from an ectopic ventricular pacemaker, often in the setting of myocardial ischemia or structural heart disease.
Ventricular tachycardia is a poorly perfusing rhythm, so patients may present with or without a pulse. It often presents with hemodynamic instability, which requires emergent intervention to restore a perfusing rhythm.
Bear in mind that some patients with VT might be hemodynamically stable upon presentation, but they’re at risk of becoming unstable quickly and with no warning, potentially even deteriorating to ventricular fibrillation, so they’re still managed emergently.
Now, based on duration, VT can be classified as non-sustained, which lasts less than 30 seconds, or sustained, which lasts more than 30 seconds.
Additionally, based on the pattern of QRS complexes, VT can be described as monomorphic or polymorphic. Now, if an individual presents with signs or symptoms of VT, you should first perform an ABCDE assessment.

Unstable patient1:20–3:13

These patients will generally be unstable, so begin acute management. Stabilize their airway, breathing, and circulation.
Next, obtain IV access, attach a cardiac rhythm monitor, and provide supplemental oxygen if they’re hypoxemic. Here’s a high-yield fact!
While providing acute management, it’s also important to look for reversible causes, which can be remembered as the 5 H's and T's.
The H’s include Hypoxia, Hypothermia, Hypovolemia, Hydrogen ions for acidosis, and Hyper- or Hypokalemia; while the T’s include Toxins, cardiac Tamponade, Thrombosis for myocardial infarction, Thrombosis again for pulmonary embolism, and Tension pneumothorax.
Next, assess for signs of VT on the cardiac rhythm monitor. Signs of VT include a heart rate above 150 beats per minute, QRS complex width of 140 milliseconds or greater, and the presence of AV dissociation, which means there’s no clear relationship between the P waves and QRS complexes.
If there are no signs of VT, consider an alternative diagnosis. On the other hand, if all signs are present, diagnose ventricular tachycardia.
Now, after diagnosing VT, you need to assess the duration.Now a clinical pearl! All patients with pulseless VT must be treated with immediate defibrillation, while patients with a pulse can be treated with antiarrhythmics like amiodarone or procainamide.

Non-sustained VT3:13–5:17

If the episode lasts less than 30 seconds, it’s called non-sustained VT. In this case, the VT terminates spontaneously and a perfusing rhythm is restored, which generally means your patient is now stable.
The next step is to perform a focused history and physical exam; obtain a 12-lead ECG; order labs, including a BMP and cardiac enzymes; and finally, obtain a transthoracic echocardiogram or TTE.If your patient reports anginal chest pain, ECG shows ST or T changes, and labs reveal elevated cardiac enzymes, diagnose Acute Coronary Syndrome.
Management typically requires reperfusion therapy, which can be either pharmacological, or mechanical, which involves percutaneous coronary intervention.
On the other hand, if your patient reports exertional dyspnea, exam reveals peripheral edema, and TTE shows systolic or diastolic dysfunction, diagnose structural heart disease.
In this case, treat the underlying cause, and consider placing an implantable cardioverter defibrillator if the left ventricular ejection fraction is under 35%.Alternatively, if your patient reports palpitations, the ECG shows U waves, and labs reveal low potassium, diagnose hypokalemia and administer intravenous potassium.Finally, if history reveals no chest pain or exertional dyspnea, ECG shows no changes, labs are normal, and TTE shows no evidence of structural heart disease, diagnose idiopathic VT.
This doesn’t require treatment unless it becomes recurrent, in which case beta-blockers are the preferred treatment.Alright, now let’s take a look at patients with VT that lasts more than 30 seconds, called sustained VT.

Sustained VT and Monomorphic VT5:17–7:33

In these individuals, first, you need to assess the QRS morphology.If the QRS complexes look similar from beat to beat, diagnose monomorphic VT.
Follow ACLS guidelines to terminate the dangerous rhythm. These might include the Pulseless Arrest guideline if no pulse is detectable, or the Tachycardia with a Pulse guideline if a pulse is present.
Once the VT terminates and a perfusing rhythm is restored, your patient will generally become more stable, so perform a focused H&P, and obtain a 12-lead ECG and TTE.
If your patient has a history of previous myocardial infarction, ECG reveals pathologic Q waves, and TTE shows an area of myocardial scar, diagnose ischemic cardiomyopathy.
These patients are at high risk of recurrent VT, so consider placing an implantable cardioverter defibrillator.On the other hand, if your patient has no history of ischemic heart disease but reports exertional dyspnea; exam reveals peripheral edema; and TTE shows systolic or diastolic dysfunction, diagnose nonischemic cardiomyopathy.
These patients are also at high risk of recurrent VT, so consider placing an implantable cardioverter defibrillator as well.Finally, if your patient has no history of chest pain or exertional dyspnea, ECG shows no ST changes, and TTE shows no evidence of structural heart disease, diagnose idiopathic monomorphic VT.
This doesn’t require treatment unless it becomes recurrent. In this case, beta-blockers are the preferred treatment, but if needed, catheter ablation of the ectopic ventricular focus can also be performed.Alright, let’s go back to an ECG showing QRS morphology changes from beat to beat.

Polymorphic VT7:33–11:46

If you see this, diagnose polymorphic VT. Next follow ACLS guidelines to try and terminate the dangerous rhythm, such as the Pulseless Arrest guideline or the Tachycardia with a Pulse guideline.
Once the VT terminates and a perfusing rhythm is restored, your patient will generally become more stable, so perform a focused H&P; order labs including a CMP and cardiac enzymes; and obtain a 12-lead ECG and TTE.Now, if your patient reports anginal chest pain, ECG shows ST or T changes, and labs reveal elevated cardiac enzymes, diagnose Acute Coronary Syndrome.
These patients require urgent reperfusion therapy.Now here’s a high-yield fact! If the cardiac rhythm monitor or ECG shows polymorphic VT with QRS complexes that wax and wane in amplitude in a sinusoidal pattern, diagnose Torsades de pointes.
First-line treatment is IV magnesium sulfate. Once the episode resolves, look for an underlying cause of the QT prolongation.
Common causes include acquired conditions, like electrolyte disturbances; and certain medications that can be remembered as ABCDE for antiArrhythmics like amiodarone or procainamide, antiBiotics like fluoroquinolones or macrolides, anti”C”ychotics like haloperidol, antiDepressants like TCAs, and antiEmetics like ondansetron.
Lastly, there’s congenital long QT syndrome caused by a mutation of potassium channels, impairing repolarization.Now, let's consider a scenario where your patient is a young adult with a history of syncope during exertion, and exercise intolerance.
On physical exam, you find a heart murmur; ECG shows left axis deviation; and the TTE reveals left ventricular wall thickness of 15 mm or more.
All these findings are highly suggestive of hypertrophic cardiomyopathy. This condition puts individuals at a high risk of sudden death, so consider an implantable cardioverter defibrillator.Finally, let’s consider an individual with unexplained syncope or sudden cardiac arrest.
If their ECG shows over 0.2 millivolts of ST elevation, with a coved ST segment and negative or biphasic T wave in leads V1, V2 and V3, diagnose Brugada syndrome.
This genetic condition is caused by a mutation of sodium channels, impairing depolarization. For treatment, ICD placement is recommended to prevent sudden cardiac death.One last clinical pearl!
If an individual has an episode of VT triggered by exercise or emotional stress, examine the QRS morphology for bi-directionality, meaning a beat-to-beat alternation in the QRS frontal plane axis.
If you see this pattern, suspect catecholaminergic polymorphic VT, which is triggered by circulating catecholamines and commonly converts back to sinus rhythm as the stress subsides.
The rhythm can often be reproduced with an exercise stress test, which confirms the diagnosis. Finally, the preferred treatment includes beta-blockers, but if episodes persist despite treatment, consider an implantable cardioverter defibrillator.Alright, as a quick recap… Ventricular tachycardia, or VT, is a wide-complex tachycardia originating from an ectopic ventricular pacemaker.
These patients are generally unstable, so first perform the acute management and assess for signs of VT on a cardiac rhythm monitor, which includes a rate above 150 beats per minute, QRS complex width of 140 milliseconds or over, and AV dissociation.

Review11:46–13:51

At this point, you can diagnose VT and assess the duration. Episodes that last less than 30 seconds are called non-sustained VT, and are typically associated with conditions like acute coronary syndrome, structural heart disease, hypokalemia, or idiopathic.
On the other hand, episodes lasting more than 30 seconds are called sustained VT. In these individuals, your next step is to assess QRS morphology.
If QRS complexes are similar beat to beat, that’s monomorphic VT, so follow ACLS guidelines to terminate the rhythm. The most common conditions associated with monomorphic VT include ischemic cardiomyopathy, nonischemic cardiomyopathy, or idiopathic.
However, if QRS complexes change from beat to beat, that’s polymorphic VT, so again, follow ACLS guidelines to terminate the rhythm.
The most common conditions associated with polymorphic VT include acute coronary syndrome, hypertrophic cardiomyopathy, or Brugada syndrome.
The treatment of VT is based on the presentation, ECG findings, and potentially reversible causes. Treatment options include reperfusion therapy, implantable cardioverter defibrillator, IV potassium, beta-blockers, and catheter ablation.
causes Treatment options include reperfusion therapy implantable cardioverter defibrillator IV
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