Overview: Types of Heart Sounds

Before diving deep into pathology, it helps to have a mental map of ALL the sounds you might hear when auscultating the heart. This overview provides that framework—think of it as the "table of contents" for cardiac sounds. Understanding the categories and timing of different sounds will help you organize your approach to auscultation.

As you read through this overview, think about how each sound fits into the cardiac cycle. Every sound you hear has a mechanical origin—valves opening, valves closing, blood decelerating, or turbulent flow. When you understand the mechanism, remembering the timing becomes intuitive rather than requiring memorization.

Normal Heart Sounds

The normal heart produces two sounds per cardiac cycle: S1 and S2. These are the fundamental landmarks you'll use to orient yourself when listening to any patient. Everything else—murmurs, gallops, clicks—is defined by its relationship to S1 and S2.

S1 - First Heart Sound

S1 is created by the closure of the mitral and tricuspid valves (the AV valves) at the very start of systole. When the ventricles begin to contract, pressure rises rapidly. The instant ventricular pressure exceeds atrial pressure, the AV valves slam shut, producing S1. This sound marks the beginning of ventricular contraction and coincides with the carotid pulse—a useful trick for identifying S1 at the bedside.

S1 is loudest at the apex (the mitral area), where you're closest to the mitral valve. The mitral component (M1) contributes more to the sound than the tricuspid component (T1) because left ventricular pressure rises faster and higher. In practice, you hear M1 and T1 as a single sound. You've learned S1 in detail in the dedicated S1 section—refer back there for information about what makes S1 loud, soft, or variable.

S2 - Second Heart Sound

S2 marks the end of systole and the beginning of diastole. It's created by closure of the aortic and pulmonic valves (the semilunar valves) when ventricular pressure falls below arterial pressure and the ejected blood tries to flow backward. The valves catch this backward flow and snap shut, producing S2.

Unlike S1, the two components of S2—A2 (aortic closure) and P2 (pulmonic closure)—can often be heard separately, especially during inspiration. This "splitting" of S2 provides valuable diagnostic information about cardiac function. Physiologic splitting (wider during inspiration, single during expiration) is normal; abnormal splitting patterns (fixed, paradoxical, or wide) point to specific pathologies. You've learned S2 and its splitting patterns in detail in the dedicated S2 section.

Extra Heart Sounds (Gallops)

Beyond S1 and S2, you may hear additional sounds during diastole. These "gallops"—S3 and S4—are low-frequency sounds that occur during ventricular filling. Hearing them requires technique: use the bell of your stethoscope applied lightly at the apex, with the patient in the left lateral decubitus position to bring the heart closer to the chest wall.

S3 - Third Heart Sound

S3 occurs in early diastole, shortly after S2, during the rapid ventricular filling phase. When the AV valves open after S2, blood rushes passively from the atria into the ventricles. If this filling is particularly rapid or the ventricle is abnormally distended, the sudden deceleration of blood as it hits the ventricular wall creates a low-frequency vibration—the S3. Think of it like water rushing into a bucket and splashing against the sides.

The rhythm S1-S2-S3 sounds like "Ken-TUC-ky," with the emphasis on S2. Here's the clinically crucial point: S3 can be completely normal in certain populations, but is nearly always pathologic in others. In children, young adults under 40, athletes with high stroke volumes, and pregnant women, S3 represents vigorous filling into healthy, compliant ventricles—nothing is wrong. However, in adults over 40, S3 almost always indicates volume overload or ventricular dysfunction. In heart failure, the dilated, failing ventricle fills with too much blood, and the S3 you hear is a sign that the heart is struggling. Severe mitral or tricuspid regurgitation can also cause S3 by creating volume overload.

S4 - Fourth Heart Sound

S4 occurs in late diastole, just before S1, during the "atrial kick" phase. In normal physiology, the atrium contracts at the end of diastole to push the final 20-25% of blood into the ventricle. This atrial contraction is usually silent. However, when the ventricle is stiff and non-compliant, the atrium has to contract forcefully against this resistance, and this forceful contraction against a stiff wall creates the S4 sound.

The rhythm S4-S1-S2 sounds like "TEN-nes-see," with the emphasis on S1. Unlike S3, which can be normal, S4 is always pathologic. It indicates decreased ventricular compliance—meaning the ventricle doesn't relax and fill properly. Common causes include left ventricular hypertrophy from hypertension, hypertrophic cardiomyopathy (HCM), acute myocardial ischemia (the ischemic muscle becomes stiff), and aortic stenosis (which causes LV hypertrophy). If you hear an S4, you should think about what's making the ventricle stiff.

Murmurs

Murmurs are prolonged sounds created by turbulent blood flow. Unlike the brief, discrete sounds of S1, S2, or gallops, murmurs have duration—they occupy a portion of the cardiac cycle. The key to categorizing murmurs is their timing relative to S1 and S2, which tells you when in the cardiac cycle the turbulence is occurring and therefore what's causing it.

Systolic Murmurs (between S1 and S2)

Systolic murmurs occur during ventricular contraction. There are two main categories, distinguished by their shape and mechanism. Ejection murmurs have a crescendo-decrescendo (diamond-shaped) pattern. They're caused by blood being ejected through a narrowed opening—either stenotic semilunar valves (aortic stenosis, pulmonic stenosis) or increased flow across a normal valve. The murmur starts soft as ejection begins, peaks at maximum flow, then fades as flow decreases.

Regurgitant murmurs are holosystolic or pansystolic—they span the entire duration of systole at relatively constant intensity. These occur when blood leaks backward through an incompetent AV valve (mitral regurgitation, tricuspid regurgitation) or through an abnormal communication like a ventricular septal defect (VSD). The pressure gradient between the chambers exists throughout systole, so the turbulent flow—and the murmur—is continuous from S1 to S2.

Diastolic Murmurs (between S2 and S1)

Diastolic murmurs occur during ventricular filling and are always pathologic—there are no innocent diastolic murmurs. Early diastolic murmurs are decrescendo in shape, starting immediately after S2 and fading through diastole. They're caused by semilunar valve regurgitation (aortic regurgitation, pulmonic regurgitation). The pressure gradient is highest right after S2 (when aortic/pulmonary pressure is maximal) and decreases as diastole progresses, hence the decrescendo pattern.

Mid-diastolic murmurs are rumbling, low-frequency sounds occurring during passive ventricular filling. The classic example is mitral stenosis, where blood must flow through a narrowed mitral orifice. Tricuspid stenosis produces a similar rumble on the right side. These low-frequency rumbles are notoriously difficult to hear and require the bell of the stethoscope applied lightly. They may have presystolic accentuation (getting louder just before S1) when atrial contraction forces blood through the stenotic valve.

Continuous Murmurs

Continuous murmurs are present throughout systole AND diastole, typically peaking around S2 (when the pressure gradient is maximal) but persisting through both phases of the cardiac cycle. They occur when there's a connection between high-pressure and low-pressure systems with a pressure gradient that exists continuously—not just during systole or diastole.

The classic example is patent ductus arteriosus (PDA), where the aorta connects directly to the pulmonary artery. Since aortic pressure exceeds pulmonary pressure throughout the cardiac cycle, blood flows continuously through the ductus, creating a continuous "machinery" murmur. Arteriovenous fistulas and the benign venous hum are other causes of continuous murmurs. Don't confuse a continuous murmur with a to-and-fro murmur (separate systolic and diastolic components, as in combined AS and AR)—in a continuous murmur, the sound never completely stops.

Clicks and Snaps

Clicks and snaps are brief, high-frequency sounds that stand out from the lower-pitched gallops and most murmurs. They're created by specific valve pathology and provide important diagnostic information.

Ejection Clicks

Ejection clicks are brief, sharp sounds occurring in early systole, immediately after S1. They're caused by the sudden tensing or "doming" of a stenotic but still mobile semilunar valve as it opens. Think of it like snapping open an umbrella—the sudden halting of valve motion creates a sharp sound. Ejection clicks occur in aortic stenosis (heard best at the apex) and pulmonic stenosis (heard at the left upper sternal border).

An important clinical pearl: ejection clicks disappear when the valve becomes heavily calcified and immobile. A patient with severe calcific aortic stenosis may have no ejection click because the valve can no longer "snap" open—it's essentially frozen. Additionally, ejection clicks can occur with dilated great vessels (aortic or pulmonary dilation) even without valve stenosis, as the dilated vessel "snaps" during early ejection.

Mid-Systolic Click

The mid-systolic click is the hallmark sound of mitral valve prolapse (MVP). It occurs in mid-to-late systole when the redundant mitral valve leaflets "flip" or prolapse backward into the left atrium. The click represents the sudden tensing of the chordae tendineae as they reach maximum stretch and abruptly halt the prolapsing leaflets.

What makes MVP clinically fascinating is that the click timing is dynamic—it moves with maneuvers that change ventricular volume. When preload decreases (standing, Valsalva), the LV is smaller, and the leaflets prolapse earlier in systole—the click moves closer to S1. When preload increases (squatting), the LV is fuller, the leaflets prolapse later, and the click moves closer to S2. If prolapse is significant enough to cause regurgitation, you'll hear a late systolic murmur following the click.

Opening Snap

The opening snap (OS) is a high-frequency sound in early diastole, heard shortly after S2. It's the classic sound of mitral stenosis. When the stenotic mitral valve opens at the beginning of diastole, the fused leaflets "snap" open abruptly, creating a sharp sound. The valve must be stenotic (narrowed) but still mobile for an opening snap to occur—heavily calcified, immobile valves don't produce this sound.

The timing of the opening snap relative to S2 provides prognostic information. A short S2-OS interval indicates severe stenosis: when left atrial pressure is very high (severe stenosis causes severe LA pressure elevation), the mitral valve is forced open earlier in diastole, moving the OS closer to S2. Conversely, a longer S2-OS interval suggests milder stenosis. This is a useful bedside gauge of severity before you get an echocardiogram.

Other Sounds

Pericardial Friction Rub

The pericardial friction rub is caused by inflamed pericardial surfaces rubbing against each other. Normally, the visceral and parietal pericardium glide smoothly, separated by a thin layer of lubricating fluid. In pericarditis, inflammation makes these surfaces rough, and they create a scratchy, grating sound with each heartbeat—like leather rubbing against leather or walking on fresh snow.

The classic friction rub has up to three components corresponding to atrial systole, ventricular systole, and ventricular diastole (early rapid filling). However, you may hear only one or two components. The rub is best heard with the diaphragm of the stethoscope, with the patient leaning forward and holding their breath in expiration—this brings the heart closer to the chest wall. Importantly, friction rubs are evanescent: they may come and go as the amount of pericardial fluid fluctuates. If a large effusion develops, the fluid separates the pericardial surfaces and the rub disappears.

Prosthetic Valve Sounds

Mechanical prosthetic valves produce distinct clicking sounds as their components open and close. Unlike bioprosthetic (tissue) valves, which are relatively quiet, mechanical valves create audible clicks that patients can sometimes hear themselves. The character and timing of these sounds depend on the valve type (ball-and-cage, tilting disc, bileaflet) and position (aortic vs. mitral).

Monitoring prosthetic valve sounds is clinically important. A change in sound intensity or character may indicate valve dysfunction—thrombus formation, pannus ingrowth, or leaflet malfunction. Patients with mechanical valves should have baseline documentation of their valve sounds, and any change warrants investigation with echocardiography or fluoroscopy. You'll learn more about prosthetic valve assessment in Module 3.

Summary: Timing is Everything

Quick Recall

1. S3 vs S4: Which indicates volume overload and which indicates a stiff ventricle?

2. An opening snap is heard in early diastole. What condition should you suspect?

3. A mid-systolic click is nearly pathognomonic for what condition?

This overview gives you the mental framework. In Module 2, you'll learn each pathologic sound in detail—what causes it, how to recognize it, and what it means clinically.