Heart Blocks, Bradyarrhythmias & Electrolyte ECG Changes

Conduction system and normal intervals

Pathway. The impulse travels SA node → atria → AV node, where it is delayed to allow ventricular filling → His bundle → right and left bundle branches (the left splits into anterior and posterior fascicles) → Purkinje fibers. The PR interval mainly reflects AV nodal delay. A wide QRS means slow muscle-to-muscle conduction or a blocked bundle.

Pacemaker hierarchy. The SA node (60–100/min) overrides slower pacemakers. If it fails or conduction is blocked, a junctional or ventricular escape rhythm takes over, and the lower the focus, the slower and less reliable the rhythm.

AV blocks

First degree and Mobitz I. In first-degree block every impulse is conducted, only slowly; it is asymptomatic and needs no treatment. In Mobitz I, each beat meets an increasingly refractory AV node, so the PR lengthens until one P wave is blocked, and then the cycle restarts. RR intervals shorten before the pause, producing grouped beating. The nodal site explains its links to inferior MI (the AV nodal artery usually arises from the RCA), vagal tone during sleep or in trained athletes, and AV-nodal drugs. It is usually benign and responds to atropine.

Mobitz II. The PR interval is constant, and beats drop without warning because the disease is in the His–Purkinje system; bundle branch block often coexists. It can progress abruptly to complete block with syncope, so a permanent pacemaker is indicated even without symptoms. Atropine acts on the node and is unlikely to help. When conduction is 2:1, a single strip cannot separate Mobitz I from Mobitz II; a narrow QRS favors a nodal site.

Third-degree (complete) block. Atria and ventricles beat independently: P waves march through at their own regular rate, faster than the escape rhythm. Atria contracting against closed tricuspid valves produce cannon a waves in the jugular pulse, and S1 varies in intensity. With inferior MI the block is usually nodal, the escape is narrow, and it often resolves. With anterior MI it reflects extensive septal necrosis, the escape is wide and slow, and the outlook is worse. Lyme carditis often resolves with ceftriaxone, with temporary pacing as a bridge. Neonatal lupus is permanent: maternal anti-Ro/SSA antibodies cross the placenta and damage the fetal conduction system. In a young adult with unexplained heart block, consider sarcoidosis.

Bundle branch and fascicular blocks

Fascicular blocks. The anterior fascicle of the left bundle is long and thin, so it fails most often. Left anterior fascicular block shifts the axis to about −45° or beyond, with qR in I and aVL, rS in II, III and aVF, and a QRS under 120 ms. Left posterior fascicular block is rare and shifts the axis to the right. RBBB plus left anterior fascicular block is a bifascicular block, classically seen in Chagas cardiomyopathy.

Sinus bradycardia and sick sinus syndrome

Sinus bradycardia. Normal P waves at under 60/min. Causes are vagal (trained athletes, sleep), metabolic (hypothyroidism, hypothermia), neurologic (raised ICP) and ischemic (inferior MI). Drug causes include β-blockers, verapamil and diltiazem, digoxin, amiodarone, clonidine and ivabradine. Ivabradine lowers heart rate by blocking the funny current (If, HCN channels) in the SA node without reducing contractility.

Hypothermia. Cold slows the SA node and lengthens PR, QRS and QT. A positive hump at the J point (the Osborn or J wave) grows as core temperature falls. Shivering artifact and AF are common, and below about 28 °C the risk of VF rises.

Sick sinus syndrome. Age-related fibrosis of the SA node causes sinus bradycardia, pauses or arrest, SA exit block, and chronotropic incompetence (heart rate fails to rise with exertion). In tachy-brady syndrome, bursts of AF, flutter or atrial tachycardia alternate with bradycardia, and a long pause often follows the end of a tachycardia and causes syncope. A pacemaker treats the slow side and makes it safe to give AV-nodal blockers for the fast side.

Treating bradycardia. Atropine blocks M2 receptors on the SA and AV nodes, speeding the sinus rate and AV nodal conduction. It helps sinus bradycardia and Mobitz I but not His–Purkinje disease. Unstable bradycardia that does not respond is treated with transcutaneous pacing or a dopamine or epinephrine infusion. Mobitz II, complete block and symptomatic sick sinus syndrome need a permanent pacemaker.

Electrolyte ECG changes

Hyperkalemia. A high extracellular K+ makes the resting membrane potential less negative, which inactivates fast Na+ channels and slows phase 0 and conduction. Repolarization also speeds up, producing tall, narrow, peaked T waves. The ECG progresses from peaked T waves to PR prolongation and P-wave flattening, then QRS widening, a sine-wave pattern as QRS and T merge, and finally VF or asystole. Bradycardia and AV block may occur along the way. The ECG stage matches the serum level only loosely.

With ECG changes, give IV calcium first. It stabilizes the membrane within minutes but does not lower K+. Next shift K+ into cells with insulin plus glucose and β2-agonists, then remove it with loop diuretics, K+ binders or dialysis.

Hypokalemia and hypomagnesemia. Low K+ flattens or inverts T waves, depresses the ST segment and brings out U waves, producing a long QU interval. It raises the risk of ectopy, torsades and digoxin toxicity, because digoxin binds the Na+/K+-ATPase more avidly when K+ is low. Hypomagnesemia often coexists and must be corrected, or K+ cannot be kept replete.

Calcium. Calcium changes act mainly on the plateau (phase 2). Hypocalcemia lengthens the ST segment and therefore the QT, which risks torsades. It shows neuromuscular irritability: perioral tingling, tetany, and Chvostek and Trousseau signs, classically after thyroid or parathyroid surgery. Hypercalcemia shortens the ST segment and the QT and depresses neuromuscular function, causing confusion, polyuria and kidney stones.