What are the features and causes of ventricular bigeminy and trigeminy?

Ventricular Bigeminy and Trigeminy: Features and Causes

Electrocardiographic Features

Ventricular bigeminy is diagnosed on ECG by identifying a repetitive pattern where every normal sinus beat is followed by a premature ventricular complex (PVC), creating characteristic paired complexes. 1

Bigeminy Characteristics

• Broad QRS complexes (>110 ms) that are premature relative to the expected sinus rhythm 2
• No evidence of pure atrioventricular conduction through the normal pathway 2
• Compensatory pause following the PVC, which may be full, more than, or less than compensatory 2
• Discordant QRS and T wave axis in the ectopic beats 2
• Apical-radial pulse deficit on physical examination, where premature beats fail to generate sufficient stroke volume to produce a palpable peripheral pulse 3
• Effective bradycardia despite normal underlying sinus rate, as PVCs don't generate adequate forward flow 3

Trigeminy Characteristics

• Pattern of two normal sinus beats followed by one PVC, or one sinus beat followed by one PVC in a repeating triplet pattern 2
• Variable coupling intervals between bigeminy and trigeminy patterns, with bigeminy typically showing shorter coupling intervals and trigeminy showing longer coupling intervals 4
• Distribution patterns can be quantified using the ratio of trigeminy to bigeminy postextrasystolic intervals (T/B-PEI), which determines the interectopic intervals 5

Critical Diagnostic Pitfalls

• Do not mistake blocked atrial bigeminy for sinus bradycardia - carefully examine T waves for hidden blocked P waves 1
• Avoid inaccurate heart rate estimation due to effective bradycardia from non-conducted premature beats 1
• Never dismiss bigeminy as benign without excluding structural heart disease through comprehensive evaluation 1

Causes and Underlying Mechanisms

Structural Heart Disease (Most Important to Exclude)

• Ischemic heart disease including acute myocardial infarction or chronic coronary artery disease 6
• Cardiomyopathy of any etiology (dilated, hypertrophic, or restrictive) 6
• Valvular heart disease including mitral valve prolapse, aortic stenosis, or regurgitation 6
• Heart failure with reduced or preserved ejection fraction 6
• Prior myocardial infarction with ventricular scar tissue 6

Metabolic and Electrolyte Abnormalities

• Hypokalemia - critically important reversible cause 6
• Hypomagnesemia - frequently overlooked but treatable 6
• Hypocalcemia or hypercalcemia 6
• Thyroid disorders including hyperthyroidism 6

Heightened Adrenergic States

• Excessive catecholamine stimulation from stress, anxiety, or exercise 6
• Catecholaminergic polymorphic ventricular tachycardia (CPVT) - exercise-induced PVCs in bigeminy represent a high-risk pattern 3

Toxic and Pharmacologic Causes

• Drug-induced arrhythmias from QT-prolonging medications 6
• Caffeine, alcohol, and stimulants including cocaine and amphetamines 6
• Digitalis toxicity - classic cause of ventricular bigeminy 7

Mechanistic Considerations

• Ventricular parasystole may be the mechanism, especially in "dome type" bursts showing gradual shortening of coupling intervals 8
• Re-entry circuits around areas of myocardial scar or fibrosis 7
• Enhanced automaticity from ectopic ventricular foci 2
• Concealed bigeminy - PVCs separated by an odd number of sinus beats, which has the same clinical implications as overt ventricular bigeminy 7

Idiopathic Causes

• Benign PVCs in structurally normal hearts - generally infrequent and benign, particularly common in elderly patients 2
• Right ventricular outflow tract (RVOT) or left ventricular outflow tract (LVOT) ectopy in otherwise healthy individuals 2

High-Risk Features Requiring Urgent Evaluation

QTc >500 ms with bigeminy indicates extremely high risk for torsades de pointes and warrants immediate intervention. 1, 3

• Bigeminy in the setting of acute myocardial infarction indicates ongoing electrical instability 1, 3
• Polymorphic PVC patterns suggesting multiple ectopic foci or ischemia 6
• Symptoms of reduced cardiac output including syncope, presyncope, or severe fatigue 3
• Evidence of structural heart disease on physical examination (jugular venous distention, rales, gallops, peripheral edema) 6

Clinical Presentation Patterns

Burst Patterns

• Dome type bursts show gradual shortening of VPC coupling intervals with regular cycle length (185 ± 40 seconds) 8
• Horizontal type bursts demonstrate fixed coupling intervals with irregular cycle length (210 ± 63 seconds) 8
• Both burst types are associated with transient increases in sinus rate and abbreviated VPC-VPC intervals 8

Hemodynamic Consequences

• Reduced cardiac output by up to 50% due to ineffective premature contractions 3
• Symptoms of low cardiac output states including fatigue, exercise intolerance, and lightheadedness 3
• Relative hypertension with wide pulse pressure may be observed 6