Core Concepts/Cardiac Anatomy & Physiology

Cardiac Anatomy & Physiology

Before we dive into heart sounds, you need to understand the mechanical events that create them. Think of this chapter as building your foundation – everything else will make more sense once you grasp these basics. By the end of this section, you should be able to visualize exactly what's happening inside the heart at any point in the cardiac cycle.

Cardiac Chambers & Valves

Your heart has four chambers working in beautiful synchrony. The atria are the receiving chambers – they collect blood and prime the ventricles. The ventricles are the powerhouses that pump blood to your lungs (right ventricle) and the rest of your body (left ventricle).

Here's a question to consider before we go further: why do you think the left ventricle is so much thicker than the right? The answer lies in the pressures each must generate. The right ventricle only needs to push blood through the low-resistance pulmonary circulation, while the left ventricle must overcome the much higher resistance of the systemic circulation. More work requires more muscle.

This difference in wall thickness becomes clinically important. When the right ventricle faces chronically elevated pulmonary pressures (pulmonary hypertension), it hypertrophies to compensate – sometimes becoming as thick as the left ventricle. This is called "cor pulmonale" and changes the physical exam findings you'll detect, including a right ventricular heave and louder right-sided heart sounds.

The Valve System

Between these chambers sit four crucial valves. Understanding their structure will help you understand why certain diseases cause specific sounds.

Atrioventricular (AV) Valves

The AV valves sit between the atria and ventricles, preventing blood from flowing backward when the ventricles contract. On the left side, the mitral valve has two leaflets (which is why it's sometimes called the bicuspid valve). On the right side, the tricuspid valve has three leaflets, as its name suggests.

What makes the AV valves fascinating is their support structure. Unlike simple flaps, these valves are anchored by chordae tendineae – thin, tendinous cords that connect the leaflet edges to papillary muscles projecting from the ventricular walls. When the ventricles contract, the papillary muscles also contract, pulling on the chordae and preventing the leaflets from flipping backward into the atria. Think of it like an umbrella being held in place during a windstorm – the ribs prevent the fabric from inverting.

Why This Matters Clinically

When a papillary muscle ruptures (often after a heart attack that cuts off its blood supply), the valve leaflet loses its anchor and flips backward with each heartbeat, causing acute severe mitral regurgitation. This is a surgical emergency. Understanding the anatomy helps you understand why the patient suddenly develops a loud murmur and flash pulmonary edema.

Semilunar Valves

The semilunar valves guard the exits from the ventricles. The aortic valve sits between the left ventricle and the aorta, typically with three cusps (though bicuspid aortic valves, with only two cusps, are the most common congenital cardiac anomaly, affecting 1-2% of the population). The pulmonic valve sits between the right ventricle and the pulmonary artery, also with three cusps.

Unlike the AV valves, the semilunar valves don't need chordae or papillary muscles. Their cup-shaped cusps fill with blood that tries to flow backward after ventricular ejection ends, and this back-pressure pushes them shut. It's an elegant passive mechanism – no active muscular support required.

Think About This: If semilunar valves close passively from back-pressure, what happens when aortic pressure drops very low (as in severe hypotension)?

The valve may not close as firmly because there's less back-pressure to push it shut. This is one reason why aortic regurgitation can worsen in the setting of vasodilation – less afterload means less diastolic aortic pressure and potentially less competent valve closure.

The Cardiac Cycle

Now let's walk through what happens during each heartbeat. This is where the magic happens, and understanding it will let you predict exactly when different heart sounds and murmurs occur.

Systole: The Contraction Phase

Systole begins when the ventricles start contracting. But the first phase, called isovolumetric contraction, is special: all four valves are closed. The AV valves just slammed shut (creating S1), but ventricular pressure hasn't yet risen high enough to push open the semilunar valves. It's like squeezing a closed water balloon – the pressure rises but nothing flows. This phase is brief, lasting only about 50 milliseconds.

Once ventricular pressure exceeds the pressure in the great arteries (about 80 mmHg in the aorta, about 10 mmHg in the pulmonary artery), the semilunar valves pop open and ventricular ejection begins. Blood flows from the ventricles into the aorta and pulmonary artery. The volume ejected with each beat – typically 60-80 mL in a healthy adult – is called the stroke volume.

Diastole: The Relaxation Phase

Diastole begins when the ventricles stop contracting and start relaxing. Ventricular pressure drops rapidly, and when it falls below aortic pressure, blood briefly tries to flow backward. This back-flow catches the aortic valve cusps and snaps them shut, creating S2. The same happens at the pulmonic valve a fraction of a second later.

Now we're in isovolumetric relaxation – again, all valves are closed, but this time pressure is falling rather than rising. This phase ends when ventricular pressure drops below atrial pressure, at which point the AV valves open.

Rapid filling follows. Blood that has been accumulating in the atria rushes into the ventricles. This is the fastest filling phase and accounts for about 70-80% of ventricular filling. In some conditions, this rapid rush of blood creates an audible sound – S3, the third heart sound.

After rapid filling, there's a period of diastasis – a slow-filling phase where blood trickles passively from atria to ventricles. At normal heart rates, this phase provides time for the coronary arteries to perfuse the myocardium (remember, coronary filling occurs primarily during diastole).

Finally, the atria contract in what's called the atrial kick. This active contraction pushes the final 20-30% of blood into the ventricles, topping off the tank just before the next systole. When the ventricle is stiff and non-compliant, this forceful atrial contraction against resistance creates an audible sound – S4, the fourth heart sound.

Clinical Pearl

In atrial fibrillation, there's no organized atrial contraction, so patients lose the atrial kick. This explains why AFib patients often feel more fatigued – they lose about 20% of their cardiac output. It also explains why you can never hear an S4 in a patient with AFib – there's no atrial contraction to create it. If you think you hear an S4 in someone with AFib, recheck the rhythm; either you're wrong about the sound or wrong about the rhythm.

Pressure Curves: The Wiggers Diagram

The relationship between left ventricular, left atrial, and aortic pressures is crucial for understanding heart sounds. The Wiggers diagram – a classic representation of these pressure curves over time – is worth understanding deeply.

Key Pressure Relationships

Phase Valve Status Pressure Relationship What Happens
Ventricular filling Mitral open, Aortic closed LA > LV Blood flows from atrium to ventricle
Isovolumetric contraction All valves closed LV rising rapidly Pressure builds, no flow
Ejection Mitral closed, Aortic open LV > Aorta Blood flows into aorta
Isovolumetric relaxation All valves closed LV falling rapidly Pressure drops, no flow

Why Pressure Gradients Matter

Every murmur you'll ever hear is created by blood flowing through a pressure gradient. When blood moves from a high-pressure zone to a low-pressure zone through a narrowed or incompetent valve, it becomes turbulent, and turbulent flow creates sound.

Stenotic lesions create murmurs during the normal flow phase – blood trying to flow forward through a narrowed valve encounters resistance and becomes turbulent. Regurgitant lesions create murmurs during the phase when the valve should be closed – blood flows backward through an incompetent valve down its pressure gradient.

The Foundation of Everything

If you remember one thing from this section: Murmurs occur when there's turbulent blood flow across a pressure gradient. Understanding which pressures are higher than others at different points in the cardiac cycle will let you predict when murmurs occur and reason through unusual findings.

Right Heart Dynamics

Everything we just discussed applies to the right heart too, with one key difference: pressures are much lower. The right ventricle pumps against pulmonary vascular resistance (normally very low), while the left ventricle pumps against systemic vascular resistance (much higher). Normal right ventricular systolic pressure is about 25 mmHg compared to the left ventricle's 120 mmHg.

This pressure difference has important implications for auscultation. Right-sided murmurs are generally softer than left-sided ones because lower pressure gradients create less turbulent flow. A tricuspid regurgitation murmur is typically quieter than mitral regurgitation, even with similar valve pathology.

The right heart's lower pressures also explain why right-sided murmurs respond differently to respiration. During inspiration, negative intrathoracic pressure increases venous return to the right heart, filling it more and increasing flow across right-sided valves. Right-sided murmurs get louder with inspiration. Left-sided murmurs don't show this same effect because blood pools in the pulmonary vasculature during inspiration, actually decreasing return to the left heart slightly.

When pulmonary hypertension develops, right heart pressures rise and can approach left-sided pressures. This changes the examination findings – right-sided murmurs become louder, P2 becomes accentuated, and the entire right heart examination becomes more prominent.

Putting It All Together

With this foundation in place, you're ready to understand why heart sounds occur when they do. S1 happens because the AV valves close at the start of systole. S2 happens because the semilunar valves close at the start of diastole. S3 occurs during rapid filling if the ventricle is dilated or non-compliant. S4 occurs during atrial contraction if the ventricle is stiff.

You can also begin to predict murmur timing. A murmur that occurs during systole (between S1 and S2) is either ejection through a stenotic semilunar valve or regurgitation through an incompetent AV valve. A murmur that occurs during diastole (after S2, before the next S1) is either filling through a stenotic AV valve or regurgitation through an incompetent semilunar valve.

Test Your Understanding

Before moving on, make sure you can answer these questions: During which phase of the cardiac cycle is left ventricular pressure higher than aortic pressure? During which phase is left atrial pressure higher than left ventricular pressure? At what moment does the mitral valve close, and what heart sound does this create?

LV > Aorta: During the ejection phase of systole, when blood is being pumped from the ventricle into the aorta.

LA > LV: During diastole (ventricular filling), when the mitral valve is open and blood flows from atrium to ventricle.

Mitral valve closure: At the very beginning of systole, when ventricular pressure first exceeds atrial pressure. This creates the first heart sound, S1.