Atrial fibrillation (AFib) is the most common type of heart rhythm disorder, affecting millions of people worldwide. This condition is characterized by chaotic and disorganized electrical signals originating in the atria. Instead of a strong, coordinated contraction, the atria quiver rapidly, leading to a highly irregular and often fast heartbeat. This electrical chaos affects the basic sounds a doctor hears through a stethoscope, the familiar “lubb-dupp” of the heart. This article explores the physiological changes that occur during AFib and how they affect the first and second heart sounds.
Understanding the Normal “Lubb-Dupp”
The healthy heart produces two distinct sounds in a regular, predictable sequence, often described as “lubb-dupp.” The first heart sound, S1, represents the “lubb” and marks the beginning of systole (contraction). S1 is generated by the simultaneous closure of the mitral and tricuspid valves (the atrioventricular or AV valves). Their closure prevents blood from flowing backward into the atria when the ventricles begin to contract.
The second heart sound, S2, provides the “dupp” and signals the end of systole and the beginning of diastole (relaxation). This sound is created by the closure of the semilunar valves: the aortic and pulmonic valves. These valves snap shut after the ventricles have ejected blood, stopping backflow from the main arteries. In a normal, coordinated rhythm, the time interval and intensity of S1 and S2 are consistent from one beat to the next.
The Mechanism of Irregularity in Atrial Fibrillation
The fundamental issue in AFib is the disorganization of atrial electrical activity, which bombards the atrioventricular (AV) node with rapid, chaotic impulses. The AV node acts as the electrical gatekeeper between the atria and the ventricles. However, it cannot transmit all incoming signals, allowing only a random, variable number of impulses to pass through to the ventricles.
This irregular signal transmission causes the ventricles to contract at inconsistent intervals, resulting in an “irregularly irregular” rhythm. Because the time between contractions constantly changes, the period available for the ventricles to fill with blood (diastolic filling time) also varies dramatically with every beat. Short filling times mean the ventricles receive less blood, while longer filling times allow for greater volume.
The changing volume of blood in the ventricles directly impacts the contraction’s strength and stroke volume. A beat following a short filling time results in a weak contraction and a small stroke volume. Conversely, a beat following a long filling time is more forceful, resulting in a larger stroke volume.
S1 and S2 Sounds During AFib
The foundational S1 and S2 heart sounds are still present during atrial fibrillation because the underlying mechanical events of valve closure continue to occur. The ventricles still contract and relax, causing the AV and semilunar valves to close and generate sound. However, the chaotic rhythm profoundly alters how these sounds are heard.
The most characteristic auditory finding in AFib is the variable intensity of the S1 heart sound. The loudness of S1 depends on the position of the mitral and tricuspid valves just before the ventricles contract. Since the ventricular filling time changes with every beat, the valves are positioned differently at the start of each new systole.
A long filling time allows the AV valves to “float” closer to a closed position, resulting in a softer S1 when the ventricle contracts. Conversely, a short filling time means the valves are still wide open when stimulated, leading to a more forceful, louder snap when they close, creating an intensified S1 sound. This beat-to-beat variability in S1 intensity is a defining feature suggesting an irregularly irregular rhythm like AFib.
The S2 sound, marking the closure of the aortic and pulmonic valves, is generally present. Its intensity may fluctuate slightly depending on the variable force of the preceding ventricular contraction.
The extreme variability in stroke volume also leads to a clinical finding known as a pulse deficit. This deficit is the difference between the heart rate counted directly at the chest (the apical rate) and the pulse rate felt at a peripheral artery (such as the wrist). Beats following a very short ventricular filling time eject such a small volume of blood that the resulting pressure wave is too weak to be felt peripherally. The peripheral pulse is absent for that beat, creating the measurable difference that defines the pulse deficit.