EKG Interpretation & The Cardiac Cycle: A Complete Guide
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Physiology11 min readAI-Generated6 views

EKG Interpretation & The Cardiac Cycle: A Complete Guide

The EKG is one of the most powerful diagnostic tools in medicine — and it looks terrifying to most students. But the EKG is just a graphical record of the heart's electrical activity. Once you understand what each wave represents physiologically, you can interpret any tracing systematically. This guide walks you through everything: from the cardiac cycle to full EKG interpretation.

AI-generated content. This guide was written by MedAI's AI and is intended as a study aid. Always cross-reference with your official course materials, textbooks, and instructor guidance before your exam.

The Cardiac Conduction System

The heart generates and propagates its own electrical impulses through a specialized conduction system. The sequence of activation determines the waveform pattern on the EKG.

StructureFunctionIntrinsic RateEKG Correlate
SA Node (sinoatrial)Primary pacemaker of the heart; right atrium near SVC60–100 bpmSets the heart rate; precedes P wave
AV Node (atrioventricular)Delays signal transmission to ventricles (~100ms); allows atrial filling40–60 bpmPR interval (0.12–0.20 sec)
Bundle of HisConducts signal from AV node to bundle branches40–60 bpmPart of PR interval
Bundle Branches (R & L)Rapidly conduct signal down interventricular septum~40 bpmPart of QRS complex
Purkinje FibersFinal rapid distribution to ventricular myocardium20–40 bpmCompletes QRS complex

EKG Waveforms: What Each One Means

Wave/IntervalDuration (Normal)RepresentsAbnormality
P wave<120 msAtrial depolarizationAbsent: atrial fibrillation; Peaked (>2.5mm): right atrial enlargement
PR interval120–200 msConduction through AV node>200 ms: 1st-degree AV block; progressively longer then dropped: 2nd-degree Mobitz I (Wenckebach); fixed dropped beats: Mobitz II; no relationship: 3rd-degree
QRS complex<120 msVentricular depolarization>120 ms: bundle branch block, ventricular tachycardia, hyperkalemia
ST segmentIsoelectric (flat)Plateau phase of ventricular AP (phase 2)Elevation: STEMI, pericarditis, Brugada. Depression: NSTEMI, ischemia, digitalis effect
T waveUpright in most leadsVentricular repolarizationInverted: ischemia, RBBB, LVH. Peaked: hyperkalemia. Flattened: hypokalemia
QT interval<440 ms (corrected)Total ventricular depolarization + repolarizationProlonged QTc: risk of Torsades de Pointes (VTach). Drugs: quinidine, haloperidol, macrolides, fluoroquinolones
U waveSmall, after T waveLate repolarization (Purkinje fibers?)Prominent U wave: hypokalemia

The 5-Step EKG Interpretation

1) Rate (count large boxes: 300/# boxes between R waves). 2) Rhythm (regular? P before every QRS?). 3) Axis (quadrant method: QRS polarity in leads I and aVF). 4) Intervals (PR, QRS, QTc). 5) Waveform changes (ST elevation/depression, T-wave inversion, Q waves).

The Cardiac Cycle: Pressure, Volume & Valves

The cardiac cycle is the sequence of mechanical events that accompany each heartbeat. Heart sounds, murmurs, and the EKG all map directly onto specific events in the cycle.

PhaseValve StatusPressure ChangeEKGSound
Late diastole (filling)Mitral + tricuspid OPEN; Aortic + pulmonic CLOSEDLV pressure low, filling from LAAfter T wave; P wave beginsS4 if present (atrial kick)
Isovolumetric contractionALL VALVES CLOSEDLV pressure rises rapidly; volume constantQRS to start of ejectionS1 (mitral + tricuspid close) — beginning of systole
Ejection (systole)Aortic + pulmonic OPEN; Mitral + tricuspid CLOSEDLV pressure > aortic pressure; SV ejected; volume fallsST segmentEjection click (stenotic valve) if present
Isovolumetric relaxationALL VALVES CLOSEDLV pressure falls rapidly; volume constantT waveS2 (aortic + pulmonic close) — beginning of diastole; A2 before P2
Rapid filling (early diastole)Mitral + tricuspid OPENBlood rushes into ventricle from pressure gradientAfter T waveS3 (if present: volume overload, heart failure, mitral regurgitation)

High-Yield Arrhythmias

ArrhythmiaEKG FindingsCauseTreatment
Atrial FibrillationNo P waves; irregularly irregular rhythm; fibrillatory baselineHypertension, valvular disease, thyrotoxicosis, alcohol ("holiday heart")Rate control (β-blockers, CCBs); rhythm control (cardioversion); anticoagulation (stroke prevention)
Atrial Flutter"Sawtooth" flutter waves at 300 bpm; regular ventricular rate (150 bpm with 2:1 block)Right atrial macro-reentryCardioversion; ablation; anticoagulation
Ventricular Tachycardia (VT)Wide QRS (>120ms) ≥3 beats at >100 bpm; AV dissociation; fusion beatsMI scar reentry; cardiomyopathyStable: amiodarone. Unstable: synchronized cardioversion
Ventricular Fibrillation (VF)Chaotic, no organized complexesIschemia, electrolyte disturbanceImmediate DEFIBRILLATION (unsynchronized). No pulse = VF or pulseless VT
Torsades de PointesVT with rotating axis ("twisting of points"); prolonged QTcProlonged QT (drugs, hypokalemia, hypomagnesemia)Magnesium sulfate IV; correct electrolytes; remove offending drug
1st-degree AV blockPR > 200ms; every P followed by QRSIncreased vagal tone, digoxin, myocarditisUsually none required
3rd-degree AV blockComplete AV dissociation; P and QRS independentInferior MI (right coronary artery), Lyme disease, structuralPermanent pacemaker

STEMI Localization by EKG Leads

Affected TerritoryOccluded ArteryEKG Leads with ST ElevationReciprocal Changes
Inferior wallRCA (90%) or LCxII, III, aVFI, aVL (lateral)
Lateral wallLCx or diagonal branch of LADI, aVL, V5-V6II, III, aVF
Anterior wallLAD (diagonal branches)V1-V4II, III, aVF
Posterior wallRCA or LCxTall R in V1-V2 + ST depression V1-V3ST elevation in V7-V9 (posterior leads)
RV infarctProximal RCAST elevation in V1, V4RClassic: inferior STEMI + hypotension + JVD + clear lungs

Hyperkalemia EKG Changes (Know in Order)

As K⁺ rises: (1) Peaked T waves (K 5.5–6.5) → (2) Widened QRS (K 6.5–7.5) → (3) Sine wave pattern (K >7.5) → (4) VF / asystole. TREATMENT: Calcium gluconate (stabilizes membrane), then insulin+glucose (shifts K into cells), then kayexalate/dialysis (removes K).

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