Supraventricular arrhythmias: Pathology review

Definitions & Key takeaways

An arrhythmia is any disturbance in the rate, rhythm, site of origin, or conduction of the cardiac electrical impulse. Supraventricular arrhythmias are a group of cardiac arrhythmias that originate at or above the atrioventricular node and have a narrow QRS complex (<120 ms). Supraventricular arrhythmias include atrial fibrillation, atrial flutter, and supraventricular tachycardia.

Supraventricular arrhythmias can cause a patient's heart rate to become too fast (tachycardia) or too slow (bradycardia). They can also cause stasis of blood flow in the atrial compartment and increase the risk of clot formation, especially in the left atrial appendage. These clots can dislodge, and travel into the systemic circulation, causing potentially life-threatening pathologies like embolic strokes, acute limb ischemia, central retinal artery occlusion, or acute mesenteric ischemia.

Common symptoms seen in supraventricular arrhythmias include palpitations, dizziness, shortness of breath, and chest pain. Treatment for these arrhythmias usually involves medications like beta-blockers, calcium channel blockers, digoxin, and other antiarrhythmic drugs; or procedures like electrical cardioversion and catheter ablation. In some cases, lifestyle modifications may be recommended to reduce the risk of developing arrhythmias.

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Case study0:00–1:01

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.

Physiology1:01–3:38

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.

Arrhythmias3:38–4:35

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.

Supraventricular arrhythmias4:35–5:11

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.

Arrhythmias of sinus origin5:11–8:15

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.

Reentrant arrhythmias8:15–9:24

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.

Paroxysmal supraventricular tachycardia9:24–11:17

PSVT can happen in people with totally normal hearts and no history of cardiac disease. A clue to this can be recent consumption of things like alcohol and coffee .
On the ECG, PSVT appears as a regular rhythm with a rate ranging between 150 to 250 beats per minute, and a narrow QRS complex.
The key is the absence of normal P waves, which tells us that the SA node is no longer in control. Now the reentrant circuit is within the AV node, meaning it can go from the AV node up towards the atria.
Since it’s going in the opposite direction, you may be able to see retrograde P waves. However, because the PSVT is super fast, these retrograde P waves are usually buried in the QRS complex, so you may or may not see them.
PSVTs are classically treated with vagal maneuvers like carotid massage. When the carotid artery is massaged, the carotid sinus is stimulated, which stimulates the vagus nerve to fire.
This slows conduction through the AV node, which interrupts the reentrant circuit, effectively slowing the heart rate, and terminating the arrhythmia.
Now, if vagal maneuvers don’t work, the next step for treatment is adenosine, and this is commonly tested. Adenosine rapidly acts in about 15 seconds, causing a decrease in AV node conduction.
Keep in mind that its effect is blunted by theophylline and caffeine. Another important thing to remember are its side effects, which include facial flushing, hypotension, bronchospasm, and chest pain.
Moving on, atrial flutter is usually caused by a reentrant circuit that runs around the annulus of the tricuspid valve. On ECG, this usually appears as a regular rhythm with an atrial heart rate ranging between 250 to 350 beats per minute.

Atrial flutter11:17–12:39

Now, because of this super fast atrial heart rate, the AV node cannot handle all this impulses coming at it. So, some impulses get through, and some don’t.
This generates what’s called an atrial-ventricular conduction ratio, which is usually 2:1, meaning one impulse gets through to the ventricles, and the next does not, and so on.
So let’s say the atrial heart rate is 300, the ventricular heart rate would then be 150. The AV-conduction ratio can be 3:1 ore even 4:1.
Ok, on the ECG, the giveaway will be flutter waves, which are P waves that give off a “saw-tooth appearance”. Now, because the reentrant circuit is not within the AV node like in PSVT, vagal maneuvers will not work here, simply because the vagus nerve isn’t innervating where the arrhythmia started.
Instead medications or electrical cardioversion is required to keep atrial flutter under control, while definitive treatment can be done with catheter ablation.All right, in atrial flutter, there was a single reentrant circuit causing the problem.

Atrial fibrillation12:39–14:50

On the other hand, in atrial fibrillation there are hundreds of reentrant circuits scattered around the atria. The most common risk factors are hypertension and coronary artery disease.
Another interesting cause is the “holiday heart syndrome” where atrial fibrillation occurs after binge drinking. Now, for your exams, remember that here, the atrial heart rate is really fast, going above 500 beats per minute, so on the ECG, no P waves are seen.
The poor AV node is seriously overwhelmed now, so we don’t even get an AV conduction ratio. Instead the AV node allows impulses to pass in a random and unpredictable fashion.
On the ECG, this typically appears as an irregularly irregular rhythm, which means the QRS complexes will have no pattern at all, with a ventricular rate usually ranging between 120 and 180 beats per minute.
The name “fibrillation” implies that the atrial muscles are shaking uncontrollably, meaning there is no actual atrial contraction.
Now atrial contraction only contributes to about 10 to 20% of the cardiac output, but in an individual with a history of cardiac disease, that 20% might be crucial.
Another high- yield fact is that the absence of a true contraction causes stasis of blood flow in the atrial compartment, and this increases the risk of clot formation, especially in the left atrial appendage.
This clot can dislodge, and travel into the systemic circulation, causing multiple potentially life-threatening pathologies like embolic strokes, acute limb ischemia, central retinal artery occlusion, or acute mesenteric ischemia.
Therefore, individuals often need treatment with anticoagulants, in addition to treating the arrhythmia itself with medications like beta-blockers and calcium channel blockers.
Finally, some individuals can be treated with cardioversion.A third type of supraventricular arrhythmia are ectopic rhythms, in which electrical activity may originate from a place other than the sinus node.

Ectopic rhythms14:50–15:13

Fastest one to fire gets to be the pacemaker of the heart! If any myocardial cell gets a bit ambitious, and starts firing faster than the SA node, then it can overtake the SA node as the pacemaker of the heart.
A type of supraventricular arrhythmia with ectopic origin is multifocal atrial tachycardia or MAT, which usually results from multiple ectopic foci firing from the atrium.

Multifocal atrial tachycardia15:13–16:01

MAT is classically associated with lung disease like asthma or COPD, so be sure to look for that in the question stem. On ECG, this also appears as an irregularly irregular rhythm at a rate of around 100 to 200 beats per minute.
However, unlike atrial fibrillation, P waves are present in MAT. Because the P waves are originating from multiple sites in the atrium, they often vary in shape, and so will the PR intervals.
In order to diagnose MAT, you need to identify at least 3 different P wave morphologies on ECG. Now, before we wrap things up, we should talk about preexcitation syndromes, which may ultimately lead to supraventricular arrhythmias, especially PSVT.

Preexcitation syndromes16:01–17:27

In preexcitation syndromes, there’s an accessory pathway that acts as a shortcut to the normal electrical circuit, causing the ventricles to be excited earlier than usual.
The most important preexcitation syndrome is Wolff-Parkinson White syndrome or WPW. People with WPW are born with an additional conduction pathway between the atria and the ventricles called the Bundle of Kent.
The cause of WPW is most often unknown, whereas a few cases are inherited through an autosomal dominant mutation of the P R K A G 2 gene, which helps regulate ion channels specific to cardiac tissue.
The three major changes on ECG in WPW are shortening of the PR interval, widening of the QRS complex, and presence of a delta wave, which is an upward slurring of the initial portion of the QRS complex.
The delta wave indicates that the ventricle is being activated earlier than it normally should. Now, most people remain asymptomatic despite having this classic ECG pattern, whereas a small number can develop arrhythmias that can manifest as palpitations, dizziness, syncope, and even sudden cardiac death.
All right, as a quick recap... An arrhythmia is any disturbance in the rate, rhythm, site of origin or conduction of the cardiac electrical impulse.

Review17:27–18:55

Arrhythmias can be classified based on their origin into supraventricular arrhythmias, which have a narrow QRS complex, or ventricular arrhythmias, which have a wide QRS complex.
Supraventricular arrhythmias can be of sinus origin. This includes sinus tachycardia, which is a heart rate above 100, with a regular rhythm and normal P waves before each QRS complex; and sinus arrhythmia, which is a normal phenomenon that reflects the changes in heart rate during inspiration and expiration.
Supraventricular arrhythmias can also have a reentrant origin. This includes PSVT, a regular rhythm with a narrow QRS complex and absence of normal P waves; atrial flutter, a regular rhythm with P waves that give off a saw-tooth appearance; and atrial fibrillation, an irregularly irregular rhythm with no P waves.
Finally, supraventricular arrhythmias can have an ectopic origin like multifocal atrial tachycardia, which is an irregularly irregular rhythm with present P waves.
An important cause of supraventricular arrhythmias are preexcitation syndromes like Wolff-Parkinson-White syndrome, in which an accessory pathway acts as a shortcut to that causes the ventricles to be excited earlier than usual.

Summary18:55–19:36

Okay, back to our cases. Both Melissa and Taylor’s presentations describe syncope and palpitations, suggesting something is going on with their hearts.
Based on Melissa’s ECG, this is likely a paroxysmal supraventricular tachycardia, or PSVT. In her case, it was likely triggered by consumption of alcohol and caffeine.
After a carotid massage is performed, her ECG converts back to a normal sinus rhythm. On the other hand, Taylor’s ECG shows a short PR interval, and a wide QRS complex with an initial delta wave, which is the classic ECG pattern of Wolff-Parkinson-White syndrome.
Supraventricular arrhythmias: Video and Causes | Osmosis