Atlas of Clinical Electrocardiography

Normal cardiac rhythm generated at the sinoatrial node (Keith-Flack), with intact downstream conduction: Bachmann's bundle to the left atrium, internodal tracts, AV nodal delay, His-Purkinje system, and synchronized ventricular activation.

Normal sinus rhythm at a rate below 60 bpm. Physiological in trained athletes or during deep sleep; pathological in sick sinus syndrome, inferior ischemia, hypothermia, hypothyroidism, or under negative chronotropic drugs (beta-blockers, non-dihydropyridine calcium channel blockers).

Sinus rhythm at a rate above 100 bpm. Typical physiological response to exercise, fever, hypovolemia, anemia, hyperthyroidism, pain, anxiety, or adrenergic stimulation. Normal P wave morphology, though at very fast rates it may merge with the preceding T wave.

Physiological heart rate variation linked to the respiratory cycle: accelerates during inspiration (vagal withdrawal) and decelerates during expiration (increased vagal tone). Completely benign, common in young and healthy individuals. P wave morphology and PR interval remain identical in all cycles.

Intermittent failure of impulse conduction from the SA node into atrial myocardium. In Mobitz type I, the PP interval progressively shortens until a P-QRS cycle drops. In Mobitz type II, a complete P-QRS cycle drops without prior PP variation: the pause equals an exact multiple (typically 2x) of the baseline sinus cycle.

Transient cessation of automaticity in the sinoatrial node. The absence of sinus impulse creates a pause that is NOT a multiple of the baseline cycle. After the pause, a lower pacemaker takes over: typically the AV junction (escape rhythm at 40-50 bpm with narrow QRS and absent or retrograde P waves).

Structural dysfunction of the sinus node combining episodes of profound sinus bradycardia, sinus pauses or arrest, and paroxysms of atrial tachyarrhythmias (frequently atrial fibrillation or flutter). Often accompanied by chronotropic incompetence and symptomatic pauses upon tachycardia termination.

Ectopic beat originating in an atrial focus outside the SA node. Precocious P' wave with morphology distinct from the sinus P wave. It may conduct to ventricles with normal PR, conduct with aberration (bundle branch block morphology), or block in the AV node if it arrives during its refractory period. Followed by an incomplete compensatory pause.

Tachycardia originating in a single ectopic atrial focus firing by abnormal automaticity, triggered activity, or microreentry. Regular P' waves with morphology different from sinus P and identical to each other. The ventricular rate depends on AV conduction (1:1 at moderate rates, 2:1 or Wenckebach at high rates).

Supraventricular tachycardia characterized by ≥ 3 distinct P wave morphologies in the same lead, with irregular PP, PR, and RR intervals. Typical in elderly patients with acute pulmonary disease exacerbation (COPD), hypoxia, hypercapnia, or theophylline toxicity.

Macroreentrant circuit around the tricuspid annulus, dependent on the cavotricuspid isthmus (CTI). Counterclockwise activation generates negative 'sawtooth' F waves in inferior leads (II, III, aVF) and positive F waves in V1. Atrial rate ~300 bpm, typically with 2:1 AV block resulting in ventricular rate of ~150 bpm.

Atrial macroreentry that is either clockwise across the cavotricuspid isthmus (positive F waves in II, III, aVF) or independent of the isthmus, revolving around surgical scars, atriotomy incisions, or left atrial structures (peri-mitral, peri-pulmonary veins). Continuous undulating baseline with variable AV conduction.

Complete disorganization of atrial electrical activity with chaotic multiple wavelets, often initiated by pulmonary vein triggers. Total loss of effective atrial contraction. Absence of P waves; presence of irregular 'f' waves and completely irregular ventricular response ('irregularly irregular' rhythm).

Gradual shifting of the primary pacemaker between the SA node, different atrial foci, and the AV junction. Features ≥ 3 P wave morphologies at a normal or slow rate (< 100 bpm), with variable PR intervals. Typically benign and related to increased vagal tone.

Protective physiological pacemaker arising in the AV junction when the sinus node fails or is blocked. Regular rhythm at 40-50 bpm with narrow QRS complexes (unless preexisting bundle branch block). P waves are absent (buried in QRS) or retrograde (negative in II, III, aVF, preceding or following QRS).

Junctional pacemaker firing at 60-100 bpm due to enhanced automaticity or triggered activity. Common causes include digitalis toxicity, recent cardiac surgery, acute myocardial infarction (inferior), or severe myocarditis. Narrow QRS with absent, preceding, or following retrograde P waves.

The most common paroxysmal supraventricular tachycardia in adults with normal hearts. A functional circuit within the AV node utilizes an anterograde slow pathway and retrograde fast pathway. Retrograde P waves are buried inside or immediately after the QRS, mimicking a pseudo-r' in V1 or pseudo-S in inferior leads.

Paroxysmal SVT in patients with an accessory pathway (Kent bundle). The circuit conducts anterogradely through the normal AV node/His-Purkinje system (narrow QRS) and retrogradely through the accessory pathway. Retrograde P waves appear in the ST segment or early T wave with RP < PR (short-RP SVT).

Congenital presence of an anomalous muscular accessory pathway (Kent bundle) connecting atrium and ventricle, bypassing the AV node delay. Impulse travels faster through the pathway, preexciting ventricular myocardium: short PR interval (< 120 ms), initial slurring of QRS (delta wave), and widened QRS with secondary repolarization changes.

Less common form of AVRT in WPW (< 10%). The reentrant circuit conducts anterogradely down the accessory pathway (producing maximal preexcitation and very wide, bizarre QRS) and retrogradely up the AV node or a second accessory pathway. Can be difficult to distinguish on ECG from ventricular tachycardia.

Extremely dangerous emergency: chaotic atrial fibrillation impulses conduct anterogradely down an accessory pathway that lacks the decremental conduction properties of the AV node. Produces an irregularly irregular wide-QRS tachycardia at extremely rapid ventricular rates (> 200-300 bpm), with risk of degenerating into ventricular fibrillation. AV nodal blockers (adenosine, beta-blockers, verapamil, digoxin) are strictly contraindicated.

Premature ectopic impulse originating in ventricular myocardium. QRS is wide (≥ 120 ms) and bizarrely deformed, with T wave and ST segment directed opposite to the main QRS deflection. No preceding P wave; followed by a full compensatory pause.

≥ 3 consecutive ventricular complexes at a rate > 100 bpm with uniform QRS morphology. Usually caused by reentry around myocardial scar (post-infarction). Hallmarks include AV dissociation (independent P waves, fusion beats, capture beats) and extreme axis deviation.

Ventricular tachycardia with beat-to-beat variation in QRS morphology and axis. Commonly triggered by acute myocardial ischemia (coronary occlusion), severe electrolyte abnormalities, or catecholaminergic surge. Rapidly deteriorates into ventricular fibrillation and hemodynamic collapse.

Specific form of polymorphic ventricular tachycardia occurring in the setting of prolonged baseline QT interval (congenital or drug-induced). QRS complexes appear to twist their polarity and amplitude around the isoelectric baseline in an undulating fashion. Often triggered by an R-on-T premature ventricular beat after a pause ('short-long-short' sequence).

Chaotic, uncoordinated electrical activity of ventricular myocardium resulting in zero cardiac output, immediate loss of consciousness, and cardiac arrest. ECG displays irregular, shapeless undulations without identifiable P waves, QRS complexes, or T waves. Requires immediate electrical defibrillation.

Ventricular rhythm at 50-100 bpm (faster than ventricular escape, slower than ventricular tachycardia). Most commonly seen as a benign sign of successful myocardial reperfusion after primary PCI or thrombolysis in acute STEMI. Usually well tolerated, self-limiting, and requires no suppressive antiarrhythmic therapy.

Last-resort ventricular pacemaker firing when higher pacemakers (sinus, atrial, junctional) fail or complete infrahisian AV block prevents their conduction. Wide QRS (≥ 120 ms) at a slow, unstable rate of 20-40 bpm. Ineffective cardiac output, profound hemodynamic compromise, and high risk of progression to asystole.

Delay in conduction of the electrical impulse from atria to ventricles, usually at the AV node. Every P wave conducts to the ventricles (1:1 conduction), but the PR interval is abnormally prolonged (> 200 ms) and constant across all cycles. QRS morphology is typically normal.

Progressive prolongation of the PR interval in successive beats until a P wave fails to conduct (blocked P wave). The pause that follows is shorter than two normal cycles, and the cycle then restarts. Almost always located within the AV node; usually benign and reversible (vagal hypertonia, inferior STEMI, drugs).

Sudden failure of AV conduction with an intermittent dropped P wave WITHOUT prior PR interval prolongation. The block is located in the His bundle or bundle branches (infranodal). High risk of progression to complete infrahisian block and Stokes-Adams syncope; absolute indication for permanent pacemaker implantation.

Every other P wave is blocked in the AV conduction system: one P conducts, the next is blocked. Because two consecutive conducted PR intervals are never seen, it cannot be categorized as Mobitz I or II by PR behavior alone. High-grade AV block requiring careful assessment of QRS width (narrow = likely nodal; wide = likely infranodal).

No P waves reach the ventricles: atria and ventricles beat completely independently (complete AV dissociation). Sinus P waves march through the tracing with constantly varying PR intervals. Prognosis depends on the escape rhythm: junctional escape gives narrow QRS at 40-60 bpm; ventricular escape gives wide QRS at 20-40 bpm and is unstable.

Total interruption of AV conduction located below the His bundle (in both bundle branches or all three fascicles). Accompanied by a low, wide, unstable ventricular escape pacemaker at 20-40 bpm. Severe hemodynamic compromise with syncope, heart failure, and immediate risk of asystole.

The right ventricle does not receive impulse via the right bundle branch and activates late, cell-to-cell across the septum from the left ventricle. QRS duration ≥ 120 ms with typical rSR' ('rabbit ears') pattern in V1-V2 and wide, slurred S wave in I, aVL, and V6. Secondary repolarization changes in right precordial leads.

Complete block in the main trunk of the left bundle branch. Ventricular activation is drastically altered: the septum activates from right to left, and the left ventricle activates late and slowly. Wide QRS (≥ 120 ms), broad notched or slurred R waves in I, aVL, V5-V6, and deep QS or rS in V1-V2. Normal septal q waves in lateral leads disappear.

Block in the thin anterior fascicle of the left bundle branch. Activation of the left ventricle proceeds first through the posterior fascicle (inferior and rightward) and then anteriorly and leftward. Results in marked left axis deviation (between -45° and -90°), qR complexes in I and aVL, and rS complexes in II, III, and aVF with normal or slightly prolonged QRS (< 120 ms).

Block in the broad posterior fascicle of the left bundle branch. Ventricular activation proceeds first anterosuperiorly and then posteroinferiorly and rightward. Results in marked right axis deviation (between +90° and +180°), rS in I and aVL, and qR in II, III, and aVF with QRS < 120 ms. Other causes of right axis deviation (RV hypertrophy, acute PE) must be excluded.

Concomitant block of two of the three main ventricular conduction fascicles: complete right bundle branch block (RBBB) plus left anterior fascicular block (LAFB). ECG shows typical RBBB pattern in V1 (rSR') combined with marked left axis deviation (-45° to -90°). Only the left posterior fascicle remains functional.

Block of the right bundle branch combined with left posterior fascicular block. ECG shows typical RBBB in V1 (rSR') with marked right axis deviation (+90° to +180°), in the absence of right ventricular hypertrophy or pulmonary disease. Only the left anterior fascicle conducts.

Disease involving all three fascicles: bifascicular block (typically RBBB + LAFB or LPFB) combined with first-degree AV block (prolonged PR, reflecting delay in the remaining fascicle or AV node). High risk of progression to complete infrahisian block.

Total absence of electrical and mechanical ventricular activity ('flatline'). No cardiac output, no pulse, no blood pressure: clinical cardiac arrest. May present occasional isolated P waves ('ventricular standstill'). Requires immediate CPR and epinephrine; electrical defibrillation is ineffective and contraindicated.

Presence of organized electrical activity on ECG (sinus, bradycardia, bundle branch block, or other rhythms) in a patient with no palpable arterial pulse and no effective cardiac output. Caused by reversible profound mechanical or metabolic collapse (hypovolemia, hypoxia, tension pneumothorax, tamponade, pulmonary embolism, acidosis).

Involvement of the left main trunk before bifurcation. Compromises the entirety of the left ventricle (LAD + LCx). Cardiogenic shock and extreme risk. ST elevation in aVR >= V1 with deep diffuse multilead depression (I, II, aVL, V4-V6).

Occlusion prior to the origin of the 1st septal (S1) and 1st diagonal (D1). Massive anteroseptal infarction with high risk of bifascicular block (RBBB + LAFB) and shock. ST elevation in V1-V4, I, aVL, and aVR with marked reciprocal depression in III > II.

Occlusion distal to S1 but prior to D1. Involves the anterior and high lateral wall with preservation of the upper basal septum. ST elevation in V1-V4, I, aVL with reciprocal depression in inferior leads (II, III, aVF).

Occlusion in the middle third of the LAD distal to D1. Anteroapical infarction circumscribed to the mid-anterior wall and apex. Prominent ST elevation in V2-V4 with subtle reciprocal changes in inferior leads.

Occlusion in the distal third of the anterior descending artery. Involves solely the apical cap of the left ventricle. Moderate ST elevation in V3-V6 without reciprocal depression in inferior leads.

Type III LAD anatomy (long / wrapping): wraps around the apex and supplies the lower third of the posterior groove. Causes simultaneous anterior (V3-V5) and inferior (II, III, aVF with II > III) ST elevation, with characteristic reciprocal depression in aVL.

Isolated occlusion of the first diagonal branch of the LAD. Involves high lateral wall and mid-anterolateral portion. ST elevation in I, aVL and occasionally V2 with marked reciprocal depression in III and aVF.

Occlusion of the second diagonal. Supplies the mid-lateral and low anterolateral wall. Elevation in aVL, V5, and V6.

Occlusion of the first obtuse marginal branch. Supplies the mid and superior free lateral wall of the left ventricle.

Occlusion of the second obtuse marginal branch. Supplies low posterolateral and lateral apical walls.

Occlusion of the acute marginal artery. Infarction circumscribed to the right ventricular free wall without LV involvement. ST elevation in V1, V3R, and V4R with normal inferior leads.

Isolated occlusion of the posterolateral branch. Involves basal inferolateral segments and posterior wall.

Proximal circumflex occlusion before OM1. In right dominance it produces posterolateral infarction (I, aVL, V5-V6, V7-V9) with anterior mirror changes in V1-V3. In left dominance it additionally compromises the complete inferior wall (II, III, aVF with II >= III).

Distal circumflex occlusion in the left atrioventricular groove. Involves posterolateral and posterior basal walls.

Proximal occlusion of right coronary artery prior to RV branches and acute marginal. Inferior LV infarction (III > II, aVF) with RV extension (V1, V3R, V4R) and reciprocal depression in I and aVL. High risk of hypotension and AV block.

Occlusion in the middle third of the right coronary artery distal to RV branches but before the crux. Isolated diaphragmatic LV infarction without RV involvement. ST elevation in III > II and aVF.

Occlusion in the distal third of the RCA right before bifurcation into PDA and PLB. Involves basal inferior wall.

Occlusion of the posterior descending artery in the posterior interventricular groove. Inferoseptal and posterior infarction. In right dominance it arises from RCA; in left dominance from distal LCx. Frank elevation in V7-V9 and inferior leads, with anterior mirror image in V1-V3.

Classic transmural epicardial injury pattern with upward convex ST-segment elevation and reciprocal changes in opposite leads.

J-point depression of 1 to 3 mm with upsloping continuation into tall, peaked, symmetrical hyperacute T-waves in precordial leads (V1-V6), alongside ST elevation in aVR (0.5 to 1 mm). Critical subtotal occlusion of proximal LAD.

Biphasic T waves (+/- with initial positive and terminal negative phase) in V2-V3 with isoelectric or minimally elevated ST (< 1 mm). Represents critical stenosis (>90%) of proximal LAD during reperfusion or post-ischemic period. Requires urgent coronary angiography to prevent impending massive anterior infarction.

Deeply inverted T waves (<= -0.4 mV), symmetrical and acuminated in V2-V4 with isoelectric ST. Accounts for 75% of Wellens cases due to critical proximal LAD stenosis in pain-free intervals.

Acute inferior wall infarction in patients with severe multivessel disease or concomitant LAD lesion. ECG characteristics: 1) ST elevation isolated to lead III (without elevation in lead II or aVF); 2) ST depression in V4-V6 with positive T wave; 3) ST elevation in aVR; 4) ST in V1 higher than in V2 (V1 > V2).

Giant monophasic fusion of QRS complex, ST segment and T wave into a single triangular deflection ('shark-fin'). Indicates massive hyperacute transmural ischemia with extreme risk of ventricular fibrillation and cardiogenic shock.

Modified Sgarbossa-Smith criteria for diagnosing transmural infarction in the presence of LBBB: 1) Concordant ST elevation >= 1 mm in leads with positive QRS (I, aVL, V5, V6); 2) Concordant ST depression >= 1 mm in V1-V3; 3) Excessive discordance with ST/S ratio >= 0.25 in leads with negative QRS (V1-V3).

Assessment of acute transmural infarction in right ventricular paced rhythm (LBBB-like morphology with preceding pacing spike): Concordant ST elevation >= 1 mm or excessive discordance ST/S >= 0.25.