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Ventricular arrhythmias: Pathology review



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Ventricular arrhythmias: Pathology review


0 / 6 complete

USMLE® Step 1 style questions USMLE

6 questions

A 67-year-old male presents to the emergency department after a confirmed cardiac arrest in the field. Per EMS, the patient was found down by several bystanders without a pulse, and CPR was initiated immediately. The patient has no past medical history and is not on any medications. He is currently without a pulse, and CPR is ongoing. His 12 lead electrocardiogram is demonstrated below:  

Image reproduced from Wikimedia Commons   

The patient is shocked multiple times and dies despite resuscitation efforts. Post-mortem analysis is most likely to demonstrate which of the following as the etiology of this patient’s clinical presentation?  


Content Reviewers:

Antonia Syrnioti, MD

Clint is a 19 year old male that’s brought to the emergency department for acute chest pain. Upon examination, you notice that his heart rate is really fast, about 170 beats per minute. He has a history of depression, and is currently being treated with TCAs. He is otherwise healthy. A few minutes after arriving, Clint loses consciousness. His ECG shows this.

All right, so based on his presentation and ECG, Clint has some form of arrhythmia. The best way to approach arrhythmias is to one: know what a normal ECG looks like, and two: have a good classification system to narrow down the diagnosis. To help identify an irregular rhythm, you can look at the morphology of the waveform and make sure that there is a P wave before every QRS complex, and a QRS complex after every P wave.

Now let’s take a look at the heart rate. The resting heart beats at a rate between 60 to 100 times per minute, and each of those beats starts off with depolarization of the sinoatrial node, and so we call it a normal sinus rhythm. It's also important to know that there is typically a delay in the conduction at the AV node and the Bundle of His, which gives some time for ventricular filling before the ventricle contracts. On the ECG, this is represented by the PR interval, which should be less than 5 small boxes, or 200 milliseconds.

Now, any disturbance in the rate, rhythm, site of origin, or conduction of the cardiac electrical activity is called an arrhythmia. Arrhythmias could be completely asymptomatic, and be picked up incidentally on an ECG. Arrhythmias can also present with palpitations, which is a sensation of your heart beating too hard or fast, fluttering, or skipping a beat. Additionally, they may alter cardiac output, causing individuals to present with signs of hypotension and decreased brain perfusion, like dizziness, altered mental status, or syncope.

If an arrhythmia is really fast, the heart muscles now demand more oxygen, and if oxygen supply is not met, then the myocardium suffers from ischemia, which presents as angina. In people with underlying heart disease, the sudden onset of an arrhythmia can precipitate acute heart failure. Finally, some arrhythmias may also cause sudden cardiac death.

Now, arrhythmias can be classified into those originating from above the ventricles, so supraventricular arrhythmias, and those originating in the ventricles, so ventricular arrhythmias. In general, what's important to remember for your exams is that supraventricular arrhythmias have a narrow QRS complex because there’s a rapid excitation of the ventricles, which means the arrhythmia is originating above or within the bundle of His. On the other hand, ventricular arrhythmias have a wide QRS complex because there’s a slower spread of ventricular depolarization.

Okay, now the two types of ventricular arrhythmias are ventricular tachycardia and ventricular fibrillation. Ventricular tachycardia or VT for short originates from an ectopic focus located in the ventricle. The two main subtypes are monomorphic and polymorphic ventricular tachycardia. On ECG, both appear as wide QRS complexes at a rate ranging between 120 and 200 beats per minute.

“Monomorphic” means that all the QRS complexes look the same, and it’s classically a complication of myocardial scarring due to acute myocardial infarction. On the other hand, “polymorphic” means the QRS complexes have different shapes in each beat, as they come from different areas of the ventricle. This may occur due to acute myocardial ischemia causing the pacemaker cells to be stressed, and it’s not associated with myocardial scarring.

Another cause of polymorphic VT that is frequently tested in the exams is Brugada syndrome. This is a rare autosomal dominant condition characterized by genetic mutations hitting cardiac sodium channels. Now, the test question will typically describe a male of Asian descent, whose ECG pattern in V1 to V3 shows pseudo- right bundle branch block with the widened QRS presenting an RSR’ configuration, as well as ST elevations.

Now, some individuals affected may present this ECG pattern and yet be asymptomatic, while others may present symptoms like syncope. Regardless, they’re all at risk of developing polymorphic VT and sudden cardiac death, so treatment is primarily focused around prevention with implantable cardioverter-defibrillators.


An arrhythmia is any disturbance in the rate, rhythm, site of origin, or conduction of the cardiac electrical impulse. Ventricular arrhythmias are those that originate within the ventricles and have a wide QRS complex on ECG. These two types of ventricular arrhythmias are ventricular tachycardia and ventricular fibrillation.

Ventricular tachycardia can be monomorphic meaning that all the QRS complexes look the same, or polymorphic meaning the QRS complexes are different in each beat. A specific and very dangerous type of polymorphic ventricular tachycardia is Torsades de Pointes, which presents a twisting pattern of QRS complexes. This can rapidly progress to ventricular fibrillation, in which the whole PQRST ECG pattern breaks down completely, leaving just some random undulating waves. This is the most common cause of sudden cardiac death.

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  2. "Monomorphic ventricular tachycardia as the primary presentation of an anterior STEMI" Clinical Case Reports (2019)
  3. "Drug induced QT prolongation and torsades de pointes" Heart (2003)
  4. "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
  5. "Pathophysiology of Heart Disease" Wolters Kluwer Health (2015)
  6. "Brugada syndrome: A general cardiologist's perspective" European Journal of Internal Medicine (2017)