Now it’s time to learn about EKGs and arrhythmias. I’ll try to keep it simple.
This diagram roughly illustrates the anatomical pathways of the arrhythmias.
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AV NODE
Dysfunction of the AV Node commonly results in two different blocks. They’re both asymptomatic and benign. They’re usually found incidentally, and don’t require treatment. You can slow down the AV node with beta blockers and calcium channel blockers. Now let's jump into AV blocks, and how to recognize them on an EKG. But first, take a look at the AV block poem!
The AV Block Poem
If the R is far from P, then you have a first degree.
If some Ps don’t get through, then you have a Mobitz II.
Longer, longer, longer, drop! Then you have a Wenkebach.
If Ps and Qs don’t agree, then you have a third degree.
Here's a normal looking PR interval.
Type 1 AV Block
normal PR interval is 0.120 to 0.200 ms
Type 2 AV Block, Mobitz I (Wenckebach)
HIS-PURKINJE SYSTEM
The remaining AV Blocks usually originate from shitiness in the HIS system. These are more symptomatic than the AV disorders above. Patients can experience lightheadedness and palpitations. You don’t have to know the underlying pathophysiological difference between these two disorders, just understand what they look like on EKG. Type 3 blocks are especially high yield.
Type 2 AV Block, Mobitz II
Looks very similar to Mobitz I, but the PR interval doesn’t change. May degenerate into Type 3, so a pacemaker is a solid idea.
Type 3 AV Block
(a.k.a. Complete Heart Block)
MEDICAL URGENCY -- they need a pacemaker pretty soon.
The atria can’t speak to the ventricles. So the ventricles pace themselves (this is called an escape rhythm). The (ventricular) rate will be really slow, like in the 30’s, because that’s the inherent rate of the ventricular pacemakers.
⚡️VENTRICULAR TACHYCARDIA⚡️
V-tach
V-tach is another example of an AV dissociation (the beat doesn’t start in the atria). It occurs whenever the ventricles (which normally generate a beat at a rate of 30bpm) generate a faster beat than the SA node (which normally runs at 60 - 100bpm). It usually occurs because there is an electrical loop within the ventricles, which serves as a sort of pacemaker. It usually occurs because there is an anatomical lesion within the heart, and the most common cause of that is a heart attack. Here’s what the EKG looks like.
The QRS is wide. This is your proof that something is wrong in the ventricles.
It’s really fast (around 200).
It’s regular. If it were irregular, suspect WPW with afib.
No discernable P waves (if you look meticulously, you may notice occasional P waves going at 60 to 100 bpms. Like in the Type 3 AV block, there is no relationship between the QRS and these P waves).
To me, V-tach looks like big scary fangs.
V-tach is a MEDICAL EMERGENCY. Use a defibrillator to SHOCK them. Do it quickly. Technically, some of the arrhythmic drugs can be used to address V-tach with a normal blood pressure. But who cares, just shock them.
⚡️ VENTRICULAR FIBRILLATION ⚡️
V-fib
If you don’t shock it, V-tach can devolve into V-fib. V-fib is due to multiple ectopic pacemaker cells firing within the ventricles (similar to afib in the atria). This only occurs in very sick hearts. A heart with v-fib isn’t even pumping, it’s just quivering. CO drops to zero. No pulses. This is the worst possible rhythm, a true MEDICAL EMERGENCY. SHOCK them with a defibrillator.
You can’t identify any organized heart beats. It looks like white noise.
It looks like a low-amplitude V-tach
TORSADES DES POINTES
“Twisting of the points”
Torsades is a special kind of V-tach. It occurs when a PVC starts in the middle of a T wave (R on T phenomenon). That only occurs when the QT interval is too long. QT prolongation is usually due to drugs, genetics or electrolyte abnormalities. Drawn out repolarization allows Early-After Depolarizations to arise (EADs are frustratingly complicated, save yourself the headache and don’t sweat it). It’s often short-lived and self-terminating, but it can devolve into V-fib. Instead of shocking, treat with Magnesium.
***************draw it***********************
The amplitude oscillates in a smooth wavy pattern
Drugs that prolong the QT
AntiArrhythmics (Class 1a, 3)
AntiBiotics (Macrolides, Fluoroquinolones)
Anti”C”ychotics (Haloperidol)
AntiDepressants (TCAs)
AntiEmetics (Ondansetron)
Fun times (Methadone)
BUNDLE BRANCH BLOCKS
BBBBBBBs
If one BB is blocked (or slowed), then the QRS elongates and the QRS changes shape (if both BBs are blocked, then you get a Type 3 AV Block). BBBs are usually due to progressive fibrosis and sclerosis in older patients. They sometimes appear after an MI or cardiomyopathy. These are pretty low yield, but maybe learn the two patterns if you feel like it.
BBB’s don’t cause symptoms. There may be an underlying structural deformity, and it may progress to one of the more serious AV blocks. But in and of themselves BBBs are not dangerous. (Note that LBBBs can interfere with the diagnosis of STEMIs. Try and find an old EKG if you see a new LBBB).
V1 is the most helpful lead to distinguish RBBB from LBBB.
RBBB Rises, and LBBB gets Low.
ATRIAL FIBRILLATION
Ectopic firing of atrial pacemakers
EKG Criteria
1. Irregularly irregular QRS rhythm (random timing)
2. No P waves (sometimes see white-noise instead)
Afib occurs when the SA node gets too tired. So the other cells in your atria (especially the ones close to the pulmonary veins) begin to compete to replace the SA node. They all generate a blip of electricity, but there are too many cooks in the kitchen, and it ends up becoming a chaotic electrical flurry. So the atria simply quivers. Every once in a while, one of the atrial blips build up enough steam to get through the AV node, allowing the ventricle to contract. That results in a QRS spike, but this occurs a bit randomly because it can’t be generated consistently.
The most common cause of Afib is old age. Afib is really common. Other important causes are hyperthyroidism, alcohol and atrial dilation (mitral regurge anyone?). The biggest problem with Afib is that blood stands still when the atrial kick is lost. Thrombi can then form in the left atrial appendage and embolize to the brain (stroke). Blood thinners mitigate that risk. The moment you have a run of Afib, you’re going to get blasted with anticoagulants for months/years. Use the CHADS score to pick the right drug (high score = high risk of stroke). Warfarin / DOAC for CHADS score ≥ 2. Aspirin for CHADS score of 0 or 1
Afib with RVR (Rapid Ventricular Rate) is tachycardic Afib. It often causes uncomfortable palpitations. Left untreated for months, it can lead to systolic CHF. There are two treatment strategies, both of them are probably equally efficacious (although the literature is evolving):
Rate Control - slow their heart rate, and put them into regular afib (which is asymptomatic and doesn’t permanently damage the heart). Beta blockers (Metoprolol) or cardiac CCBs (Verapamil / Diltiazem) are good options.
Rhythm Control - fixes the irregular rhythm, which should also lower the rate.
Electric Cardioversion - anesthetize the patient, then electrocute them with a special synchronized defibrillator. All the myocytes depolarize. The SA node is usually the first pacemaker cell to repolarize and fire again. About 80% effective in the short term, but the results don’t last forever. Sounds great right? The problem is that you should only perform this if the afib started less than 48 hours ago (that’s the time it takes to form a thrombus). Late cardioversion can (supposedly) cause thrombi to eject.
Chemical Cardioversion - antiarrhythmics are messy, complicated drugs and require a lot of cardiology surveillance. For that reason, rate control is a lot more popular. Ibutilide is one that pops up a lot on Step 1 questions, so you could do that.
Ablation - ok I lied there’s a third treatment option. And this one’s permanent -- surgical ablation (cauterizing) of the ectopic sites. It’s not super effective (70% cure rate) because the ectopic sites are usually within the fragile pulmonary veins. But this is the best option for young people.
ATRIAL FLUTTER
A single ectopic loop in the atria
Aflutter occurs when there is a single mischievous electrical loop in the aria. You don’t have to know a ton about this, just focus on recognizing the EKG, which has a sawtooth pattern of P waves. In afib there are a million new pacemaker cells. In aflutter there are one or two well organized new pacer tracks (usually in the RA) that circle around and generate lots of P waves. Once the AV node has cooled down, one of those P waves will pass through and initiate ventricular contraction. Responds extremely well to ablation (cure rate over 90%).
The P waves make a sawtooth pattern. Each time the ectopic loop completes a lap, one ‘sawtooth’ is generated.
SUPRAVENTRICULAR TACHYCARDIA
Tachycardia with a narrow QRS
Supraventricular tachycardia simply means that the heart is beating fast, and that the heart beat originates in the atria. It seems like a pretty broad term, but by convention, sinus tachycardia usually isn't considered to fall into this category. By definition, these all have narrow QRS intervals. There are four causes of SVT: Afib, Aflutter, Paroxysmal Supraventricular Tachycardia (PSVT) and WPW. The nomenclature can be a bit tricky to beginners, because one of the causes, PSVT, is commonly just called “SVT.”
PSVT is the condition defined by the sudden onset/offset of SVT and strong palpitations. AV Nodal Reentrant Tachycardia (AVNRT) is the most common cause of PSVT. The mechanism is similar to aflutter, but instead of there being an ectopic loop in the atria there is a loop within the AV node. This loop is sometimes referred to as a dual AV nodal pathway. The key to treating AVNRT is to slow down the AV node. You can do this with medications like Adenosine, Procainamide, CCBs or BBs. A cooler way is to trick the body into slowing down the AV node. You can do this by upping the parasympathetic tone, with a Valsalva maneuver or Carotid massage (both of which trick the body into thinking the BP is super high). These are collectively called Vagal maneuvers.
The EKG simply looks like a very fast tachycardia, but importantly, the QRS width is narrow.
Treatment with Adenosine. This drug causes your heart to stop. Literally. But the half life is only about 6 seconds. Notice how the EKG flatlines for a few seconds! But once the Adenosine wears off, the heart will resume working. And by shutting the heart down for a moment, you’ve hopefully killed the ectopic loop. Kind of like restarting your computer!
WOLFF-PARKINSON-WHITE
A gap in the insulation between atria and ventricles
In the normal heart, there is a layer of insulation in between the atria and the ventricles. The AV node is normally the only hole in that insulation. The AV node conducts electricity really slowly, which gives the atria time to fully squeeze before the ventricles start contracting.
In WPW, there is a break in the AV insulation. In fancy cardiology terms, this is called an abnormal fast accessory pathway, or just the Bundle of Kent (it’s “fast” because the signal isn’t slowed down by the AV node).
Now let's look at the various arrhythmias seen in WPW. One of the fundamental issues with WPW is that its arrhythmias can mimic other arrhythmias; HOWEVER, the usual treatments can actually make the WPW ones worse! Procainamide can be used to treat all of these. If you’re feeling overwhelmed by EKGs, then skip the next page. Recognizing the delta wave is going to get you 90% of WPW questions.
AV Reentry Tachycardia (AVRT) is a fast arrhythmia (not to be confused with AVNRT, the common cause of SVT) seen in WPW. It occurs when the WPW-loop goes too fast, and becomes self-propagating -- effectively dethroning the SA node as the pacemaker. There are two flavors. Both of them produce a fast, regular tachycardia and palpitations.
Orthodromic - The signal leaks up the Bundle of Kent, and reaches the AV node before the SA’s signal can. The loop goes “with the normal grain.” On EKG, it looks like SVT.
Antidromic - The signal leaks down the Bundle of Kent, then races (backwards) through the bundle branches, HIS bundle and AV node. The loop goes “against the normal grain.” On EKG, it looks like Vtach. Avoid giving any antiarrhythmics that slow down the AV node (Class 2 / 3 / 4, Digoxin and Adenosine). That worsens their condition.
Afib with WPW is dangerous. The SA and AV nodes become irrelevant, because signals pour from the ectopic foci down the Bundle of Kent. On EKG, it looks like an irregular Vtach. Avoid giving any antiarrhythmics that slow down the AV node (Class 2 / 3 / 4, Digoxin and Adenosine). That worsens their condition.
BRUGADA SYNDROME
Genetic sudden death in Asians
Brugada is actually a pretty new disease - it was discovered in the 90’s! The mechanism is an autosomal dominant mutation of a sodium transporter in the heart. It classically occurs in Asian males in their teens or twenties.
It causes syncope (if you’re lucky) and / or Vfib (if you aren’t). This is one of the more common causes of sudden death in youths. So the treatment is aimed at rapidly fixing the Vfib every time that it pops up. This can be accomplished with an implantable defibrillator inside the chest wall, which constantly records an EKG, interprets it, and shocks the patient if it sees Vfib or Vtach.
You can identify it on an EKG. There are characteristically-weird-looking QRS spikes in V1 - V3. They have the RBBB-like bunny ears, and “coved” ST elevation that turns into an upside down T-wave. Pretty low yield if you ask me, but since it causes sudden death, I figured it couldn’t hurt to include it.
ANTIARRHYTHMICS
Electrical pills
Antiarrhythmics are drugs that can fix electrical problems in the heart. And frankly, they’re the worst. Why, you ask? They’re incredibly complicated, poorly classified, rarely used and highly toxic. My advice is to focus on the side effects, and then worry about the messy physiology. Don’t get bogged down in which drug treats which condition, because the indications are so complicated that only cardiologists are usually allowed to give a lot of these drugs. Many of these antiarrhythmics can actually cause arrhythmias if not used properly, which is pretty terrifying.
Here are the normal cardiac action potentials.
When you add up all of the heart's action potentials, an EKG is produced.
The “Slow” potentials are continuously being generated by pacemaker cells all over the heart, but the fastest pacemaker cells are found in the SA node. The “Fast” potentials represent a current racing down the electrical wires of the heart.
Classes 1 and 3 act on fast action potentials.
Class 1s work by blocking Sodium channels. These are highly complicated drugs, only to be used by a cardiologist. You’re expected to know side effects of the bolded drugs, particularly Procainamide and Quinidine.
Class 3s are a mixture of all the other classes. I want to draw attention to Amiodarone, arguably the most important pure antiarrhythmic. Amiodarone is the most effective all-purpose antiarrhythmic, and it has the fewest electrical side effects. Unfortunately, it has a lot of extra-cardiac side effects listed above, and these are no joking matter. Most patients cannot tolerate Amiodarone longer than about 5 or 10 years. I also want to draw attention to Sotalol because although it’s spelled like a beta-blocker it actually is not one.
Classes 2 and 4 work on the slow action potentials. They essentially slow down the pace of heart beats, and also slow down the AV node. These work great for treating SVTs.
Other Antiarrhythmics
Adenosine is a treatment for SVT. I addressed it on the SVT page, but here’s some extra info if you’re into that. It binds to receptors in the AV node, activates K+ efflux channels, and this hyperpolarizes cells. Also blocks Ca++ influx. This slows conduction through the AV node. Can be blocked by caffeine.
Magnesium is used in the acute management of Torsades de Pointes. For those curious, Mg++ blocks influx of Ca++ into cells. It’s believed that Torsades works by multiple repetitive early afterdepolarizations during phase 3.
Atropine is a muscarinic blocker that raises your heart rate. It treats bradycardia. The MOA is by blocking PNS signals to the heart.
Digoxin is super toxic. That’s the most important thing you need to know. If “Digoxin toxicity” is an answer choice, it’s assumed correct until proven otherwise. In the past, a ton of people had to be on Digoxin, making it a huge deal. But in the past decades, it has completely fallen out of favor, and is only used in select complicated cardiac patients. It works by not only increasing contractility, but also slows AV node conduction (similar to Class 2 and 4). Theoretically used in afib with RVR to slow the rate. MOA is by increasing vagal tone. Here is a list of some Digoxin side effects.
By blocking Na/K pumps, it actually competes with K. If K is low (common with diuretics), then digoxin is suddenly more powerful and toxic.
Digoxin can also CAUSE hyperkalemia, by outcompeting K to such a degree that K builds up in serum.
Also renally cleared, which is a common issue in CHF
Digoxin toxicity = yellow vision, scotomas, confusion, N/V/D and arrhythmias. Some historians suspect that Van Gogh was exposed to high levels of Digoxin through the toxins in his paint. Hence his penchant for sunflowers and acting crazy af.
By increasing the Na inside cells, it makes them more + which can lead to spontaneous firing (automaticity). This can be seen on EKGs as PVCs, PACs or PJCs. Can also cause AV node block
Digoxin's antidote is Digibind, which is made of anti-Digoxin Fab fragments that bind to dig. It’s made by sheep!
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