Hemodynamic Consequences of Arrhythmias
Bradycardia, whether of atrial or ventricular origin, decreases cardiac output and thereby decreases arterial pressure. The reduced pressure can result in syncope (i.e., fainting) and other symptoms related to hypotension.
Tachycardia of atrial or ventricular origin reduces stroke volume and cardiac output particularly when the ventricular rate is greater than 160 beats/min. The stroke volume becomes reduced because of decreased ventricular filling time and decreased ventricular filling (preload) at high rates of contraction. Furthermore, if the tachyarrhythmia is associated with abnormal ventricular conduction, the synchrony and therefore effectiveness of ventricular contraction will be impaired leading to reduced ejection. Another consequence of tachycardia is increased myocardial oxygen demand. This can cause angina (chest pain), particularly in patients having underlying coronary artery disease. Finally, chronic states of tachycardia can lead to systolic heart failure. In fact, one animal model used for studying dilated cardiomyopathy induces ventricular failure by rapidly pacing the ventricles for a few weeks.
Atrial fibrillation abolishes the contribution of atrial contraction to ventricular filling. Normally, under low, resting heart rates, atrial contractions account for about 10% of ventricular filling. However, during exercise when heart rate is elevated and ventricular filling time is reduced, atrial contraction can contribute up to 40% of ventricular filling. Therefore, atrial fibrillation generally has relatively minor hemodynamic consequence at rest, but can significantly limit normal increases in ventricular stroke volume and cardiac output during exercise. This may cause shortness of breath (exertional dyspnea) and impaired perfusion of active muscles, which will limit exercise capacity. Furthermore, in some cardiac pathologies such as ventricular hypertrophy in which ventricular compliance is reduced, atrial contraction contributes significantly to ventricular filling even at rest. Therefore, in these patients, atrial fibrillation can significantly affect resting cardiac output. Of major concern with atrial fibrillation is the increased risk of thrombus formation within the atria and the release of these thrombi into the pulmonary or systemic circulations, which can lead to pulmonary embolism or cerebral stroke. For this reason, patients with atrial fibrillation are commonly placed on anticoagulants such as coumadin. Atrial fibrillation also produces ventricular tachycardia because more impulses pass through the AV node. This is often treated with drugs (e.g., digoxin, calcium-channel blockers, beta-blockers) to reduce the number of impulses passing through the AV node, thereby reducing ventricular rate.
Ventricular fibrillation causes cardiac output to go to zero, and therefore leads to death unless it is quickly converted to a rhythm compatible with sustaining life.