Heart blocks: Pathology review
Case Study0:00–0:54
Mikey is a 22 year old male college student from Vermont who was sent to the emergency department after passing out. His vital signs show a heart rate of 40 beats per minute and a blood pressure of 90/50.
On examination, there is an erythematous circular rash with central clearing. His friends mention they recently went on a hiking trip.
His ECG is as follows. Natasha is a 60 year old female with chronic hypertension, diabetes, and peripheral vascular disease who comes to the emergency room complaining of sudden-onset, squeezing retrosternal chest pain accompanied by shortness of breath and sweating.
Her ECG is as follows. On laboratory evaluation, her troponin levels are significantly elevated.
Alright, so the normal electrical activity of the heart starts in the sinoatrial or SA node located near the opening of the superior vena cava into the right atrium.
Pathophysiology 0:54–1:52
Electrical activity is then conducted through the atrium 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.
Now, normally there is delay in conduction at the AV node and the Bundle of His, which gives some time for ventricular filling before the ventricle contracts.
A “heart block”, or AV block, occurs when conduction is delayed for too long at the AV node or the bundle of His. Also, electrical activity may be blocked at the level of the bundle branches, which are called bundle branch blocks.
Okay, on the ECG, the normal delay in the AV node is represented by the PR interval, which is normally less than 5 small boxes, or 200 milliseconds.
Atrioventricular Block1:52–6:25
There are three main types of AV block. 1st degree AV block is technically not really a block, it’s more of a delay.
Every single atrial impulse eventually makes it to the ventricles. The high yield concept here is that the only abnormality is a prolonged PR interval, and it’s usually asymptomatic, so it does not require treatment.
2nd degree AV block has two subtypes: Mobitz 1, and Mobitz 2. In Mobitz 1, each atrial impulse encounters a longer and longer delay until one of them does not make it through to the ventricles.
The high yield concept here is that on the ECG, this is reflected as the PR interval getting progressively longer and longer until all of a sudden, the heart drops a beat.
Like Mobitz 1, the heart also drops a beat in Mobitz 2, except this time, conduction through the AV node is all-or-nothing.
Either the atrial impulse goes through with no delay, or it doesn’t at all. There is no progressive prolongation of the PR interval in Mobitz 2.
On the ECG, Mobitz 2 shows a couple of normal PR intervals followed by a dropped beat. Also, like 1st degree AV block, Mobitz 1 is usually benign and doesn’t require treatment unless it’s causing symptoms.
On the other hand, Mobitz 2 can be dangerous and may result in severe bradycardia and decreased cardiac output. Therefore it requires treatment with a pacemaker.
Now, Mobitz 2 blocks can sometimes progress to our next type, the dangerous 3rd degree AV block. In this type, none of the electrical impulses are conducted through the AV node, and that’s why it’s also called complete heart block.
Now remember that all cardiomyocytes are capable of starting their own electrical activity, a property called automaticity.
So in 3rd degree AV block, the ventricles recognize that they’re not getting any impulses, and respond by generating their own electrical rhythm called a ventricular escape rhythm, just to hang on to dear life.
Because the atria and the ventricles each have their own pacemakers, they now contract independent of one another, which is called AV dissociation.
This desynchronization of the heart chambers can reduce cardiac output dramatically, leading to syncope or even sudden cardiac death.
On the ECG, the P-waves and QRS complexes have nothing to do with each other, each appearing at their own rates. The atrial rate is 60 to 100 beats per minute, whereas the ventricular rate usually ranges between 30 to 45 beats per minute.
Because of how dangerous 3rd degree blocks are, anyone diagnosed with it needs a pacemaker. Alright, a lot of things can cause the 3 types of AV block.
A myocardial infarction may involve the conduction pathway, causing a delay in electrical conduction. This is especially common in right coronary artery occlusion because it gives off a small branch that supplies the AV node.
On the exam, a clue towards right coronary artery occlusion would be a case of inferior wall myocardial infarction, indicated by elevation of the ST segments in leads II, III and aVF.
Also, electrolyte disturbances like hyperkalemia can alter the membrane potential. Then there are external causes like Lyme disease, medications such as beta-blockers, calcium channel blockers, adenosine, amiodarone and digoxin.
For your exams, remember that Lyme disease is typically associated with 3rd degree AV block. Interestingly, congenital heart block is a complication of neonatal lupus, which could also show up on your exam.
Here, the maternal autoantibodies called anti-Ro and Anti-La antibodies cross the placenta and attack the conduction system.
AV block may also be a normal variant in some circumstances, like in athletes. The next type of conduction block occurs in either the left or right branches of the Bundle of His, and are called bundle branch blocks.
Bundle Branch Block6:25–8:58
In normal ventricular depolarization, the QRS complexes are narrow, that is less than 3 small boxes or 120 milliseconds.
As a general rule of thumb, all bundle branch blocks cause the QRS complexes to appear wide. This is because we’re delaying the time for complete depolarization of both ventricles.
In right bundle branch block, or RBBB, the high yield fact to remember is that the QRS complexes in the right sided chest leads V1, V2 and V3, show an RSR’ configuration.
This means a pronounced R-wave, followed by a deep S-wave and then another R-wave.This gives the QRS complex the appearance of rabbit ears, or the capital letter “M”.
To remember this, think RBBB equals rabbit ears in the right sided chest leads. Causes of RBBB include right ventricular hypertrophy, right heart failure and pulmonary embolism.
These causes are due to the right heart not functioning normally, so there is delayed conduction through the heart tissue.
Also, for unknown reasons, RBBB can be present in normal hearts, possibly due to deposition of fibrous tissue that interrupts the conduction pathway.
Now let’s look at left bundle branch block LBBB. Similar to RBBB, the QRS complexes will be wide, because of the delay in ventricular depolarization.
In leads I, aVL, V5 and V6, tall R waves are present, and in lead V1, broad, deep S-waves are characteristic. Additionally, there may be ST segment depression and T-wave inversion.
Now when it causes, unlike RBBB, LBBB never occur in normal hearts, so there’s always something wrong. Examples include hypertension, ischemia, dilated cardiomyopathy,, and aortic stenosis.
Similar to the causes of RBBB, these disorders affect the left ventricle, causing a delay in conduction through the cardiac tissue.
Importantly, a new LBBB in an individual presenting with chest pain may be a sign of myocardial infarction. Okay, to review.
Review8:58–9:55
AV node block is divided into 3 major subtypes. 1st degree AV block is simply a prolonged PR interval.
2nd degree AV block has 2 subtypes, Mobitz I and Mobitz II. Mobitz I is characterized by a progressively prolonging PR interval followed by a dropped beat.
Mobitz II has a normal PR interval followed by a sudden dropped beat. In 3rd degree AV block, there is no relationship between the P-waves and QRS complexes, a phenomenon known as AV dissociation.
Bundle branch blocks all have a widened QRS complex. In RBBB, an RSR’-complex, or rabbit ears appear in the right sided precordial leads.
In LBBB, there are tall R-waves in leads I, aVL, V5 and V6, as well as deep S-waves in lead V1. Alright, back to our cases.
Summary9:55–11:04
Mikey is presenting with syncope, now let’s take a look at his ECG . We see that there is no relationship between the P-waves and the QRS complexes.
Each one is appearing at their own rate. This indicates a 3rd degree AV block.
Considering he recently went on a hiking trip in Vermont, and he’s got a bullseye rash, it’s likely that the cause of his AV block is Lyme disease.
Mikey was treated with intravenous antibiotics and is now planning his next hike. Okay, onto Natasha’s ECG.
First, we see that the QRS complexes are wide in all the leads. But that’s not really specific for anything.
Looking closer at leads I, aVL and V6, we see those characteristic tall R waves. Also, lead V1 shows a broad S wave.
These characteristics are indicative of left bundle branch block. Considering Natasha is presenting with chest pain and her troponin levels are elevated, this new LBBB may be indicative of an acute myocardial infarction.
.... And that’s heart block pathology in a nutshell!
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- "Chou's Electrocardiography in Clinical Practice" Saunders (2008)
- "Clinical electrophysiology of atrioventricular block" Cardiol Clin (1983)
- "Left Bundle Branch Block: Current and Future Perspectives" Circ Arrhythm Electrophysiol (2020)
- "2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society" J Am Coll Cardiol (2019)
- "Bradycardias and atrioventricular conduction block" BMJ. 2002 (2002)
- "Observations on second degree atrioventricular block, including new criteria for the differential diagnosis between type I and type II block" The American Journal of Cardiology (1972)
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