A premature ventricular contraction (PVC) is a common type of irregular heartbeat often felt as a “skipped beat” or flutter in the chest. These extra heartbeats arise from an abnormal electrical impulse in the heart’s lower chambers, temporarily disrupting the normal rhythm. Because PVCs occur frequently in many healthy individuals, understanding their mechanism and significance is crucial to determine if they are harmless or indicate a serious underlying issue.
Defining the Premature Ventricular Contraction
The heart’s electrical system typically begins in the sinoatrial (SA) node, the natural pacemaker located in the upper right atrium. This impulse travels through the atria and down to the ventricles, the lower pumping chambers, prompting a coordinated contraction that pushes blood throughout the body. This orderly sequence is known as normal sinus rhythm.
A PVC occurs when an electrical signal originates prematurely from an ectopic focus within the ventricles, bypassing the normal conduction pathway. Because the impulse starts in the ventricles, the resulting contraction is often disorganized and happens before the chamber has fully filled with blood. This premature contraction is followed by a brief, compensatory pause as the heart resets its rhythm.
The physical feeling of a “skipped beat” is not the PVC itself, but the pause that follows it. When the next normal beat occurs after this longer pause, the ventricle has had more time to fill with blood, resulting in a more forceful contraction felt as a strong thump or palpitation.
Common Triggers and Underlying Causes
PVCs can be prompted by a wide range of factors, including external triggers and underlying cardiac conditions. Common lifestyle triggers involve substances that increase adrenaline levels in the body, such as excessive intake of caffeine, alcohol, or nicotine. Certain medications, like decongestants, are also known to provoke these extra beats.
Non-cardiac states, including heightened anxiety, emotional stress, fatigue, or sleep deprivation, can also contribute to PVC frequency. Imbalances in electrolytes, particularly low levels of potassium or magnesium, can destabilize the heart muscle’s electrical activity. Addressing these triggers often reduces the occurrence of the extra beats.
PVCs may also be a symptom of existing cardiac pathology, which is a more concerning scenario. Structural heart conditions, such as prior myocardial infarction (heart attack), can leave scar tissue that interferes with electrical signals. Cardiomyopathies (dilated or hypertrophic forms) and heart failure also increase the likelihood of PVCs. The presence of underlying heart disease is a key factor in determining the significance and potential danger of the PVCs.
Assessing the Significance of PVCs
The danger posed by a PVC depends almost entirely on the health of the underlying heart muscle. In individuals with a structurally normal heart—meaning no history of heart attack, heart failure, or other heart disease—infrequent, isolated PVCs are considered benign and carry an excellent prognosis. These are often asymptomatic or cause only mild palpitations, posing no significant risk of sudden cardiac events.
PVCs become more concerning when they are frequent, occur in patterns (such as consecutive beats or runs), or are associated with pre-existing structural heart disease. A high frequency, known as the PVC “burden,” is a specific measure used for risk stratification. A PVC burden exceeding 10% to 15% of the total daily heartbeats begins to raise clinical concern.
This high burden, particularly exceeding 20%, can independently lead to PVC-induced cardiomyopathy. This condition involves the weakening of the heart muscle caused by constant, disorganized electrical activity. Fortunately, this form of cardiomyopathy is often reversible if the PVCs are successfully suppressed with treatment.
To assess PVC significance, a doctor typically begins with a standard 12-lead electrocardiogram (ECG) to identify the PVC morphology. Ambulatory monitoring, such as a 24-hour Holter monitor, is then used to quantify the PVC burden and capture patterns. An echocardiogram is routinely performed to provide an ultrasound image of the heart’s structure, confirming underlying heart disease and measuring pumping function. In complex cases, a cardiac magnetic resonance imaging (MRI) scan may provide a more detailed assessment of the heart tissue.
Management Approaches
The management strategy for PVCs is determined by the risk assessment, including the patient’s symptoms, PVC frequency, and the presence of structural heart disease. For patients with few or no symptoms and a structurally normal heart, the approach is observation and reassurance. In these benign cases, avoiding known triggers like excessive caffeine, alcohol, and stress is the primary intervention.
When PVCs are symptomatic, causing bothersome palpitations, or when the burden is high enough to risk cardiomyopathy, active treatment is warranted. The first line of medical therapy involves prescription medications, such as beta-blockers or non-dihydropyridine calcium channel blockers. These drugs suppress the ectopic beats by dampening the effect of adrenaline on the heart and slowing the heart rate.
For patients whose PVCs are refractory to medication or who develop PVC-induced cardiomyopathy, catheter ablation may be recommended. During this procedure, a specialized cardiologist uses a catheter to deliver radiofrequency energy to the precise location in the ventricle where the abnormal electrical signal originates. This targeted approach eliminates the ectopic focus, which significantly reduces the PVC burden and can potentially restore normal heart function.