Dysrhythmias

Every normal beat follows the same route: the impulse is generated in the SA node, conducted through and deliberately slowed in the AV node, then races down the bundle of His, the left and right bundle branches, and the Purkinje fibers to contract the ventricles. A dysrhythmia is a failure somewhere along this route — the pacemaker fires too fast or too slow, an abnormal circuit hijacks the rhythm, or a block stops the impulse from getting through. The rate cutoffs are the first sorting tool: normal adult resting rate is 60–100 bpm, a bradyarrhythmia is < 60, a tachyarrhythmia is > 100.

The second sorting tool is QRS width, because it tells you where the rhythm is coming from. A narrow QRS (< 120 ms) means the ventricles were activated from above the His bundle — a supraventricular rhythm. A wide QRS (≥ 120 ms) suggests the impulse originated in the ventricles themselves; ventricular tachycardia accounts for roughly 70–80% of wide-complex tachycardias. Mechanistically, most SVTs are reentry — a self-sustaining circuit involving the AV node or an accessory pathway — and atrial flutter is a macro-reentrant circuit looping around the right atrium.

Blocks are graded by how much gets through the AV junction. First-degree: every impulse conducts, just slowly — a constant PR interval > 200 ms, usually asymptomatic. Mobitz I (Wenckebach): the PR stretches progressively until one beat drops — block at the AV-node level, often a vagal normal variant. Mobitz II: the PR is constant but beats drop without warning — infranodal disease that often deteriorates into complete heart block. Third-degree: nothing crosses; the atria and ventricles beat independently and the ventricles survive on an escape focus typically running below 45–50 bpm — too slow to sustain output for long.

Dysrhythmias span the whole spectrum from entirely asymptomatic to sudden cardiac arrest, so the first question is never “what is the rhythm?” — it is “does this patient have a pulse, and are they stable?” Four rhythms are pulseless, non-perfusing arrest rhythms: VF and pulseless VT are shockable; asystole and PEA are non-shockable — no attempt at defibrillation should be made, and treatment is high-quality CPR with epinephrine 1 mg IV every 3–5 minutes while hunting the reversible H’s and T’s (hypovolemia, hypoxia, hydrogen ion, hypo-/hyperkalemia, hypothermia; tension pneumothorax, tamponade, toxins, thrombosis). PEA is the trap on a monitor: organized electrical activity without a palpable pulse — the screen looks alive while the patient is arresting, which is why you treat the patient, never the monitor.

For rhythms with a pulse, the AHA ACLS guidelines split the electricity by timing. Defibrillation is an unsynchronized shock for pulseless VF/pVT. Synchronized cardioversion times the shock to avoid the vulnerable period — a shock landing in the latter part of the T wave can itself induce VF (the R-on-T phenomenon) — and uses less energy; it is the treatment for any unstable tachyarrhythmia with a pulse, wide or narrow. The unstable criteria are worth memorizing: chest pain, dyspnea, altered mental status, hypotension, pulmonary edema, or ischemic ECG changes. Symptomatic bradycardias and blocks take the third path: atropine first, then pacing — transcutaneous, then transvenous, with a permanent pacemaker as the definitive fix.

Time is the whole game in VF: prompt defibrillation carries 39.3% survival versus 22.2% when the shock is delayed two minutes or more, and witnessed out-of-hospital VF survival approaches 30% against roughly 10% for out-of-hospital arrest overall. During any code, CPR interruptions stay under 5 seconds — resuscitation follows the published BLS/ACLS algorithms of the 2025 American Heart Association Guidelines for CPR and Emergency Cardiovascular Care.

Afib is the most common cardiac arrhythmia. Ectopic foci — most commonly around the pulmonary veins — bombard the atria until organized atrial contraction is lost entirely. On the ECG that reads as an “irregularly irregular” narrow-complex rhythm with no distinguishable P waves; at the bedside the ventricular rate usually runs 80–180/min. Because the atria quiver instead of contracting, blood flow inside them turns turbulent and stagnant — especially in the left atrial appendage — and thrombus forms. When a piece embolizes, the result is a stroke: risk is 5× higher with known afib, which is why afib is the leading cardiac cause of stroke.

That clot mechanism drives the two management clocks. The anticoagulation clock: the CHA₂DS₂-VASc score (CHF 1 · hypertension 1 · age ≥ 75 = 2 · diabetes 1 · stroke/TIA 2 · vascular disease 1 · age 65–74 = 1 · female sex 1) estimates a patient’s yearly stroke risk. Under the 2023 ACC/AHA/ACCP/HRS AF guideline, oral anticoagulation is recommended once that estimated annual stroke risk is ≥ 2%/year — conventionally mapped to a score of ≥ 2 in men / ≥ 3 in women. The cardioversion clock: if afib has lasted > 48 hours or the onset is unknown, restoring sinus rhythm can eject an atrial thrombus, so the patient is anticoagulated ≥ 3 weeks before and ≥ 4 weeks after cardioversion — or gets a TEE first to exclude a thrombus.

Day to day, rate control is first-line — a beta-blocker or calcium channel blocker, aiming for a chronic rate below 110 bpm; rhythm control (e.g., amiodarone) is not a first-line option in the acute setting. The classic bedside clue that the rate is uncontrolled is the apical–radial pulse deficit: in rapid afib some beats have stroke volume too weak to transmit to the wrist, so the apical count outruns the radial one. Controlled afib should have no deficit. Atrial flutter is the disciplined cousin — a macro-reentrant circuit driving the atria at about 300/min with classic 2:1 conduction giving a ventricular rate of 150/min — and it carries a similar stroke risk, the same CHA₂DS₂-VASc rule, and a ~95% cure rate with ablation of its circuit.

Ventricular tachycardia is a wide-complex rhythm of ≥ 3 consecutive beats above 100/min, and most of it grows in scarred myocardium — the majority of VT occurs with structural heart disease, triggered by electrolyte disturbances such as hypokalemia, hypocalcemia, and hypomagnesemia. The physiology is simple and brutal: a very fast ventricle has almost no time to fill, so preload and stroke volume collapse, cardiac output falls, and the coronary and cerebral circulations hypoperfuse — hypotension, syncope, then arrest. Sustained VT can degenerate into VF, which is often the terminal rhythm after prolonged VT.

VF is the end of organized activity: disorganized electrical chaos, uncoordinated contraction, and cessation of cardiac output — no P waves, no QRS, no T waves, just fibrillation waves. Coarse VF (waveforms ≥ 3 mm) generally responds better to defibrillation than fine VF. Left unshocked, it deteriorates to asystole — the flat line of no electrical or mechanical activity, with survival near 0–2%. One ventricular rhythm deserves its own reflex: torsades de pointes, a polymorphic VT twisting around the isoelectric line, grows out of a prolonged QT (QTc > 450 ms men / > 460 ms women; > 500 ms carries 2–3× the risk) — most often medication-induced — and its first-line treatment is IV magnesium, not the usual antiarrhythmics.