Physics of Heart Sounds & Murmurs

Now that you understand what normal heart sounds are and when they occur, let's dive into the why. Understanding the physics behind heart sounds will transform you from someone who memorizes findings to someone who can reason through any cardiac exam.

Here's a counterintuitive question to consider: if a patient has severe aortic stenosis, would you expect their murmur to be louder or softer than someone with moderate stenosis?

Counterintuitively, the murmur may be softer in severe stenosis. As the valve becomes critically narrowed, cardiac output drops—there's simply less blood flowing across the valve. Less flow means less turbulence, despite the high velocity. This is the "orifice size paradox": moderate disease is often louder than severe disease. Never judge severity by murmur intensity alone.

What Is a Heart Sound?

At its most basic, a heart sound is vibration. When valves snap shut, when blood decelerates suddenly, or when turbulent flow occurs, these events create vibrations in the cardiac structures and blood column. These vibrations transmit through the chest wall to your stethoscope.

The Frequency Spectrum

Heart sounds and murmurs occur across a range of frequencies:

Low frequency (20-100 Hz): S3, S4, mitral stenosis rumble, tricuspid stenosis
Medium frequency (100-500 Hz): S1, S2, most murmurs
High frequency (>500 Hz): Aortic regurgitation, mitral regurgitation, clicks

Your ear can detect roughly 20-20,000 Hz, but your stethoscope (and the chest wall) filters out many frequencies. This is why technique matters – the diaphragm filters out low frequencies, while the bell (when applied lightly) preserves them.

Why Laminar Flow Is Silent

Normal blood flow is laminar – smooth, parallel layers sliding past each other like cars in separate lanes on a highway. Laminar flow creates minimal vibration and is essentially silent.

Think about it: your blood is always flowing through your heart, yet you only hear sounds at specific moments (valve closure, turbulent flow). The flow itself, when laminar, doesn't create sound.

Turbulence: The Source of Murmurs

Murmurs occur when blood flow becomes turbulent – chaotic, swirling, with eddies and vortices. This creates vibrations across a range of frequencies that you can hear.

What Creates Turbulence?

Several factors promote turbulent flow:

High velocity – Fast-moving blood is more likely to become turbulent
Narrow orifice – Blood accelerates as it passes through a constriction (like water through a nozzle)
Sudden change in diameter – Abrupt widening or narrowing disrupts laminar flow
Low viscosity – Thinner blood (anemia) flows more turbulently
Irregular surfaces – Damaged or irregular valve surfaces disrupt smooth flow

Reynolds Number (Conceptual)

The Reynolds number is a dimensionless value that predicts whether flow will be laminar or turbulent. You don't need to calculate it, but understanding the concept helps:

Re = (velocity × diameter) / viscosity

What this tells us:

↑ Velocity → ↑ Re → more turbulent
↑ Diameter → ↑ Re → more turbulent (but this is complex in valves)
↓ Viscosity (anemia) → ↑ Re → more turbulent

When Re is low (<2000), flow is laminar. When Re is high (>4000), flow is turbulent. In between is a transitional zone.

Clinical Application: Anemia

Anemic patients often have systolic flow murmurs not because they have structural heart disease, but because their blood has lower viscosity (less hemoglobin = less viscous). This increases the Reynolds number, creating turbulent flow across normal valves. Treat the anemia, and the murmur often disappears.

Flow, Velocity, and Pressure Gradients

This is fundamental to understanding murmurs. Let's build this step by step.

The Basic Equation: Ohm's Law for Fluids

Flow = ΔP / Resistance

Where:

Flow = volume of blood moving per unit time (cardiac output)
ΔP = pressure gradient (difference between upstream and downstream pressure)
Resistance = opposition to flow (determined by valve area, vessel diameter, blood viscosity)

Velocity vs. Volume Flow

This distinction is crucial:

Volume flow (Q): How much blood moves per minute (e.g., 5 liters/min)
Velocity (v): How fast the blood is moving at a particular point (e.g., 1 meter/second)

Relationship: Q = v × A (where A = cross-sectional area)

For a given volume flow, if you decrease the area (stenotic valve), velocity must increase to maintain the same flow. This is why stenotic lesions create high-velocity jets.

The Garden Hose Analogy

Imagine a garden hose. When you put your thumb over the opening (decrease the area), the same amount of water comes out per minute (volume flow), but it comes out much faster (higher velocity) and travels farther. That high velocity creates turbulence—the water sprays chaotically. The same principle applies to blood flowing through stenotic valves.

Murmur Intensity Principles

Now we get to the really practical stuff. What makes a murmur louder or softer?

Principle 1: Pressure Gradient Matters

↑ Pressure gradient → ↑ Velocity → Louder murmur

The greater the pressure difference across a valve, the faster the blood flows, the more turbulent it becomes, and the louder the murmur.

Example: In aortic regurgitation, the murmur is loudest in early diastole when the aortic-to-LV pressure gradient is maximal. As diastole progresses and LV pressure rises, the gradient decreases, and the murmur becomes softer (decrescendo pattern).

Principle 2: The Orifice Size Paradox

This is counterintuitive and clinically crucial:

Mild-to-moderate stenosis:

Moderate narrowing of valve orifice
High velocity jet (blood accelerates through smaller opening)
Good cardiac output (heart can still push adequate flow through)
Result: LOUD murmur

Severe stenosis:

Critically narrow valve orifice
Cardiac output DROPS (can't push enough blood through)
Lower volume flow → less turbulence despite high velocity
Result: Softer murmur or even silent

Critical Clinical Pearl: Loud ≠ Severe

This is one of the most important concepts in cardiology: A loud murmur does NOT mean severe disease, and a soft murmur does NOT mean mild disease.

Severe AS with poor cardiac output produces a soft murmur because reduced flow means less turbulence. A small VSD creates a very loud murmur because high velocity jets through a tiny hole generate intense turbulence. A large VSD with Eisenmenger syndrome may have no murmur at all—once pulmonary pressures equalize with systemic pressures, there's no gradient and no turbulent flow. Acute severe MR may be surprisingly soft because LA pressure rises quickly, reducing the regurgitant gradient.

Never judge severity by murmur intensity alone. Always correlate with hemodynamics, symptoms, and imaging.

Principle 3: Volume Flow Effects

↑ Volume flow across a valve → ↑ Velocity → Louder murmur (even if valve is normal)

High-output states amplify murmurs or create flow murmurs across normal valves:

Anemia
Pregnancy
Thyrotoxicosis
Fever/sepsis
Arteriovenous fistula
ASD (increased flow across pulmonic valve)

Sound Transmission Through Tissues

A murmur generated at the valve must travel through cardiac tissue, chest wall, and air to reach your stethoscope. Several factors affect this transmission.

Tissue Density and Conduction

Dense tissues conduct sound better:

Bone conducts well (why AS is heard at the suprasternal notch)
Muscle and solid organs conduct reasonably well
Fluid conducts well but may muffle high frequencies
Air conducts poorly (why COPD/emphysema muffles heart sounds)
Fat dampens sound (obesity makes everything quieter)

Why Murmurs Radiate

Murmurs radiate along the path of blood flow and areas where turbulence is maximal:

AS: Blood flows up into aorta → radiates to carotids
MR: Regurgitant jet aims posteriorly into LA → radiates to axilla and back
AR: Blood flows back down into LV → radiates down left sternal border
PS: Blood flows toward lungs → radiates to back

Why Certain Conditions Muffle Sounds

Condition	Mechanism	Clinical Context
Pericardial effusion	Fluid layer dampens transmission	Distant, muffled sounds + Beck's triad if tamponade
Obesity	Thick adipose tissue absorbs sound	May miss subtle murmurs; consider echo if high clinical suspicion
COPD/Emphysema	Hyperinflated lungs (air) between heart and chest wall	Listen at epigastrium or subxiphoid area instead
Pleural effusion	Fluid layer on affected side	Asymmetrically decreased sounds
Pneumothorax	Air in pleural space on affected side	Unilateral decrease in heart and breath sounds

Pitch and Frequency: What They Tell You

The frequency content of a murmur gives you clues about the underlying pathology.

High-Frequency Murmurs (Use Diaphragm)

Characteristics: Created by high-velocity jets across high-pressure gradients

Examples:

Aortic regurgitation – High aortic pressure drives blood back into LV at high velocity
Mitral regurgitation – High LV-to-LA pressure gradient during systole
Tricuspid regurgitation – Same principle, right heart
VSD – High LV-to-RV pressure gradient

Quality: Blowing, harsh

Low-Frequency Murmurs (Use Bell)

Characteristics: Created by relatively low-velocity flow, often across stenotic AV valves during diastole (lower pressure gradients)

Examples:

Mitral stenosis – Low-pressure gradient from LA to LV during diastole
Tricuspid stenosis – Low-pressure gradient, right heart
S3 and S4 – Low-frequency vibrations from ventricular filling

Quality: Rumbling

Medium-Frequency Murmurs

Examples:

Aortic stenosis – High flow, but through narrowed orifice creates mixed frequencies
Pulmonic stenosis – Similar to AS but right-sided

Quality: Harsh, rough

Why This Matters Clinically

If you're using the diaphragm and you hear a murmur, but your attending says "now use the bell," and suddenly you hear a loud rumble you were missing – you just found mitral stenosis. The pitch tells you which stethoscope component to use, and using the right one means you don't miss pathology.

Putting Physics Into Practice

Let's apply these principles to clinical scenarios:

Scenario 1: The Paradox of Severity

You find: Soft grade 2/6 systolic murmur at RUSB + pulsus parvus et tardus + syncope

Physics explanation: Severe AS → critically narrowed valve → reduced cardiac output → less volume flow → softer murmur despite critical stenosis

Action: Urgent echo and cardiology consult. The soft murmur is misleading – this is severe disease.

Scenario 2: The Pregnant Patient

You find: Grade 2/6 systolic murmur at LUSB in pregnant woman, previously healthy

Physics explanation: Pregnancy → ↑ cardiac output + ↓ blood viscosity (dilutional anemia) → ↑ flow velocity across normal pulmonic valve → benign flow murmur

Action: Reassurance. This is physiologic. It will resolve postpartum.

Scenario 3: The VSD That Disappeared

You find: Infant who had a loud harsh murmur at 1 month now has no murmur at 6 months

Physics explanation: Small VSD closed spontaneously (common). OR, large VSD developed Eisenmenger syndrome (pulmonary HTN equalizes RV and LV pressures → no gradient → no murmur). Check for cyanosis!

Action: Echo to determine which scenario. Very different prognoses.

Key Takeaways

Murmurs are created by turbulent flow, not laminar flow. Turbulence increases with higher velocity, narrower orifices, and lower viscosity (such as in anemia). Pressure gradients drive murmur intensity—the greater the gradient, generally the louder the murmur. However, severe disease can be paradoxically quiet if cardiac output drops (the orifice size paradox), which is why you should never judge severity by murmur intensity alone.

High-frequency murmurs from regurgitant lesions are best heard with the diaphragm, while low-frequency murmurs from stenotic AV valves require the bell applied lightly. Remember that anything between the heart and your stethoscope—obesity, COPD, pericardial effusion—can muffle what you hear.

Understanding these physics principles transforms you from a passive listener into an active diagnostician who can reason through unusual findings and avoid common pitfalls. This is the foundation for everything that follows.