Chapter A9: Atlas of Cardiac Arrhythmias

Respiratory sinus arrhythmia, a physiologic finding in a healthy young adult. The rate of the sinus pacemaker is relatively slow at the beginning of the strip during expiration, then accelerates during inspiration and slows again with expiration. Changes are due to cardiac vagal tone modulation with breathing.

Sinus tachycardia (110/min) with first-degree AV “block” (conduction delay) with PR interval = 0.28 s. The P wave is visible after the ST-T wave in V₁−V₃ and superimposed on the T wave in other leads. Atrial (nonsinus) tachycardias may produce a similar pattern, but the rate is usually faster.

Sinus rhythm (P wave rate about 60/min) with 2:1 AV (second-degree) block causing marked bradycardia (ventricular rate of about 30/min). LVH is also present, along with left atrial abnormality.

Sinus rhythm (P wave rate about 60/min) with 2:1 (second-degree) AV block yielding a ventricular (pulse) rate of about 30/min. Left atrial abnormality. RBBB with left anterior fascicular block. Possible inferior MI.

Marked junctional bradycardia (25 beats/min). Rate is regular with a flat baseline between narrow QRS complexes, without evident P waves. Patient was on atenolol, with possible underlying sick sinus syndrome. The serum potassium was slightly elevated at 5.5 mEq/L.

Sinus rhythm at a rate of 64/min (P wave rate) with third-degree (complete) AV block yielding an effective heart (pulse) rate of 40/min. The slow, narrow QRS complexes indicate an AV junctional escape pacemaker. Left atrial abnormality.

Sinus rhythm at a rate of 90/min with advanced second-degree AV block and possible transient complete heart block with Lyme carditis.

Multifocal atrial tachycardia with varying P-wave morphologies and P-P intervals; right atrial overload with peaked P waves in II, III, and aVF (with vertical P-wave axis); superior QRS axis; slow R-wave progression with delayed transition in precordial leads in patient with severe chronic obstructive lung disease.

Sinus rhythm in a patient with Parkinson’s disease. Tremor artifact, best seen in limb leads. This tremor artifact may sometimes be confused with atrial flutter/fibrillation. Borderline voltage criteria for LVH are present.

Atrial tachycardia with atrial rate of about 200/min (note lead V₁), 2:1 AV block (conduction), and one premature ventricular complex. Also present: LVH with intraventricular conduction delay and slow precordial R-wave progression (cannot rule out prior anterior MI).

Atrial tachycardia with 2:1 block. P-wave rate is about 150/min, with ventricular (QRS) rate of about 75/min. The nonconducted (“extra”) P waves just after the QRS complex are best seen in lead V₁. Also, note incomplete RBBB and borderline QT prolongation.

Atrial tachycardia (180/min with 2:1 AV block [see lead V₁]). LVH by precordial voltage and nonspecific ST-T changes. Digitalis toxicity was present. Slow R-wave progression (V₁−V₄) raises consideration of prior anterior MI.

AV nodal reentrant tachycardia (AVNRT) at a rate of 150/min. Note subtle “pseudo” R waves in lead aVR due to retrograde atrial activation, which usually occurs nearly simultaneous with ventricles in AVNRT. Left-axis deviation consistent with left anterior fascicular block (hemiblock) is also present.

Atrial flutter with 2:1 AV conduction. Note typical atrial flutter waves, partly hidden in the early ST segment, seen, for example, in leads II and V₁.

Atrial flutter with atrial rate 300/min and variable (predominant 2:1 and 3:1) AV conduction. Typical flutter waves are best seen in lead II.

Wide complex tachycardia. Atrial flutter with 2:1 AV conduction (block) and LBBB, not to be mistaken for VT. Typical atrial flutter activity is clearly present in lead II, at a cycle rate of about 320/min, yielding an effective ventricular rate of about 160/min.

AF with LBBB. The ventricular rhythm is erratically irregular. Coarse fibrillatory waves are best seen in lead V₁, with a typical LBBB pattern.

AF with complete heart block and a junctional escape mechanism causing a slow regular ventricular response (45/min). The QRS complexes show an intraventricular conduction delay with left-axis deviation and LVH. Q-T (U) prolongation is also present.

AF with right-axis deviation and LVH. Tracing suggests biventricular hypertrophy in a patient with mitral stenosis and aortic valve disease.

WPW preexcitation pattern, with triad of short PR, wide QRS, and delta waves. Polarity of the delta waves (slightly positive in leads V₁ and V₂ and most positive in lead II and lateral chest leads) is consistent with a right-sided bypass tract.

AF in patient with the WPW syndrome and antegrade conduction down the bypass tract leading to a wide complex tachycardia. Rhythm is “irregularly irregular,” and rate is extremely rapid (about 230/min). Not all beats are preexcited.

Accelerated idioventricular rhythm (AIVR) originating from the LV and accounting for RBBB morphology. ST elevations in the precordial leads from underlying acute MI.

Prolonged (0.60 s) QT interval in a patient with a hereditary (congenital) long QT syndrome. Note the broad T waves with notching (or possibly U waves) in the precordial leads. This characteristic may identify patients with long QT syndrome at increased risk for torsade de pointes and syncope and sudden death.

Monomorphic VT at rate of 170/min. The RBBB morphology in V₁ and the R:S ratio <1 in V₆ are both suggestive of VT. The morphology of the VT is suggestive of origin from the left side of the heart, near the base (RBBB with inferior/rightward axis). Baseline artifact is present in leads V₁−V₃.