Supraventricular arrhythmias: Pathology review



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Supraventricular arrhythmias: Pathology review


1 / 11 complete

USMLE® Step 1 style questions USMLE

11 questions

A 73-year-old female presents to the emergency department with shortness of breath. She is concerned her “COPD is flaring up.” Past medical history is notable for hypertension, chronic obstructive pulmonary disease, and type II diabetes mellitus. She has been smoking one pack of cigarettes per day for twenty years. Temperature is 37.0°C (98.6°F), pulse is 136/min, respirations are 22/min, blood pressure is 104/72 mmHg, and oxygen saturation is 92% on room air. The patient is currently speaking in three to four word sentences and demonstrates increased work of breathing. There are bilateral rales throughout the lung fields, and the electrocardiogram from triage is shown below:  

Based on this patient's electrocardiogram, which of the following is the most likely diagnosis?  


Content Reviewers:

Antonia Syrnioti, MD

Melissa is a 21 year old college student who is having the time of her life at a party.

It’s late, and unfortunately she has class the next morning, so she drinks a ton of coffee to sober up.

On her way out, Melissa collapses to the floor, but wakes up after a couple of seconds.

On her way to the emergency room, she tells the paramedics that she’s “aware of her heartbeat”.

Then comes Taylor, a 32 year old female who is brought to the emergency room by her partner because she suddenly collapsed for a couple of minutes while cooking dinner.

Taylor is now awake, and she tells you that right before collapsing she was feeling dizzy and like her heart was racing, but now she’s fine.

They are both placed on different monitors. Melissa’s heart rate is 200 beats per minute and regular, and this is Melissa’s ECG.

On the other hand, Taylor’s heart rate is 80 beats per minute and regular, so everything seems fine.

However, her ECG shows this.

All right, so both Melissa and Taylor experienced palpitations and syncope, and their ECGs reveal they both have some form of arrhythmia.

The best way to approach arrhythmias is to first: know what a normal ECG looks like, and second: have a good classification system to narrow down the diagnosis.

First, let’s review the normal electrical conduction pathway in the heart, and how it looks like on an ECG.

An ECG tracing specifically shows how the depolarization wave flows through the heart during each heartbeat.

The normal electrical activity of the heart starts in the sinoatrial or SA node and is then conducted through the atrium, creating the P wave on ECG.

From the atrium, electrical activity goes to the atrioventricular, or AV node, after which it goes through the Bundle of His, then the right and left branches of the Bundle, and finally through the Purkinje fibers, which deliver the current to the right and left ventricles.

On an ECG, this will create the QRS complex, which represents the depolarization of the ventricles; and finally the T wave, which represents the repolarization of the ventricles.

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.

For your exams, you should be able to figure out the heart rate on an ECG.

To do that, you can count the number of boxes between R waves.

Each small box represents 0.04 seconds, and each big box is five small boxes, so each big box is 0.2 seconds.

One quick way to estimate the heart rate on an ECG, is to remember that the heart rate is 300, 150, 100, 75, 60, 50 depending on whether there’s 1, 2, 3, 4, 5, or 6 boxes between R waves.

It's also important to know that there is normally a delay in 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 can be completely asymptomatic, and be picked up incidentally on an ECG.

Arrhythmias can also present with palpitations, which is an awareness of one’s heartbeat.

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 now demands 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 even 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 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.

The first type of supraventricular arrhythmia includes those with sinus origin.

All right, so first there’s sinus tachycardia, which is a heart rate above 100, with a regular rhythm and normal P waves before each QRS complex.

It can be physiological, like during exercise, or pathological.

Pathological sinus tachycardia happens when the heart needs to compensate for an acute decrease in stroke volume, like in acute heart failure, acute myocardial infarction or pulmonary embolism.

It can also result from any overwhelming activation of the sympathetic nervous system, like in hyperthyroidism, or cocaine and amphetamine use.

Now, the thing is that a fast heart rate decreases diastolic filling time, which actually further decreases the stroke volume.

Additionally, over time, catecholamines are actually toxic to the myocytes, which results in a form of cardiomyopathy called tachycardia-induced cardiomyopathy.

Very creative name.

Okay, on the other hand of the spectrum we have sinus bradycardia.

Keep in mind that this can be completely physiological in athletes, who can have a resting heart rate between 40 and 60, and it’s also normal during sleep.

Pathological causes of sinus bradycardia include hypothyroidism, anorexia nervosa and inferior wall myocardial infarctions.

Another high-yield cause of bradycardia is the Cushing reflex, which includes the characteristic triad of bradycardia, hypertension and an irregular respiratory pattern.

This reflex occurs as a consequence of increased intracranial pressure, which can manifest from a variety of pathologies like head trauma, strokes, and brain tumors.

For your exams, note that Cushing triad may indicate impending brain herniation, and thus, it is a medical emergency.

Other causes of sinus bradycardia include a bunch of medications like beta blockers, calcium channel blockers, and opiates, in which case the solution is discontinuing the medication if possible.

Acute sinus bradycardia can be treated with IV atropine, while chronic or severe cases might need a pacemaker.

Another arrhythmia of sinus origin is... well... Sinus arrhythmia.

This arrhythmia can occur naturally during inspiration and expiration.

See, during inspiration, the heart rate increases, and during expiration it decreases.

So on an ECG, the rhythm may appear irregular, but it’s in fact a totally normal variant.

Finally, sinus arrest or sinus exit block occur when the sinus node fails to fire.

What you need to know is that on an ECG, there is simply a flatline pause.

Fortunately, if the sinus node can’t press that reset button, somebody else like the AV node or virtually any other myocardial cell can take over.

All right, now the second type of supraventricular arrhythmia are reentrant arrhythmias.

In this type, electrical activity is literally trapped in a circular electric racetrack, altering normal conduction.

To understand this, let’s picture a single myocyte with two branches, triggering two adjoining pathways; 1 and 2.

Under normal circumstances, electrical activity starts on the SA node, and then travels from one myocyte to the other.

Now, the wave of depolarization should go through both 1 and 2 at the same speed.

But let’s say pathway 2 was damaged during a myocardial infarction.

Now that pathway 2 is slowed down, the wave of depolarization rushes through pathway 1 and then returns backwards through pathway 2.

This creates an electrical loop that is now independent of the SA node, meaning it can pretty much run itself now.

There are 3 “must-know” subtypes of reentrant supraventricular arrhythmias: paroxysmal supraventricular tachycardia or PSVT, atrial flutter, and atrial fibrillation.

PSVT is usually caused by a reentrant circuit that loops within the AV node, which is why it’s also referred to as AV nodal reentrant tachycardia.

PSVT can happen in people with totally normal hearts and no history of cardiac disease.