19.3 Cardiac Cycle

Cardiac Cycle

The cardiac cycle describes the complete sequence of contraction and relaxation events that occur during one heartbeat. Each cycle lasts about 0.8 seconds at a resting heart rate of 75 bpm, and every phase depends on precise pressure changes and valve timing to move blood in the right direction.

Blood Pressure and Cardiovascular Flow

Blood pressure is the driving force that moves blood through the cardiovascular system. Without a pressure difference between two points, blood simply won't flow.

• Pressure gradient determines both direction and rate of flow. Blood always moves from areas of higher pressure to areas of lower pressure. A larger pressure difference means faster flow.
• Higher blood pressure generally increases blood flow, while lower blood pressure reduces it. Chronically elevated pressure is called hypertension; abnormally low pressure is hypotension.
• Resistance opposes blood flow and is influenced mainly by blood vessel diameter. Narrowed vessels (as in atherosclerosis) increase resistance, which raises blood pressure upstream and reduces flow downstream. Dilated vessels (vasodilation) decrease resistance, lowering blood pressure and increasing flow.
• Cardiac output (CO) also influences blood pressure and flow. CO equals heart rate multiplied by stroke volume: $CO = HR \times SV$. During exercise, CO rises, increasing blood pressure and flow. In heart failure, CO drops, reducing both.
• Afterload is the pressure the ventricle must overcome to eject blood (think of it as the resistance the ventricle pushes against). Higher afterload, such as from chronic hypertension, makes the ventricle work harder and can reduce stroke volume over time.

Phases of the Cardiac Cycle

The cardiac cycle has two main events: systole (contraction) and diastole (relaxation). These happen in a coordinated sequence across the atria and ventricles.

1. Atrial systole — The atria contract, pushing the final portion of blood into the ventricles. The AV valves (tricuspid and mitral) are open during this phase. This "atrial kick" contributes roughly 20% of ventricular filling; the other 80% flows in passively during diastole.

2. Isovolumetric contraction — The ventricles begin contracting. All four valves are closed (AV valves just shut, semilunar valves haven't opened yet). Ventricular pressure rises rapidly, but volume doesn't change because there's no outflow path.

3. Ventricular ejection — Once ventricular pressure exceeds pressure in the aorta and pulmonary trunk, the semilunar valves (aortic and pulmonary) open. Blood is ejected into the great vessels. The AV valves remain closed, preventing backflow into the atria.

4. Isovolumetric relaxation — The ventricles relax. The semilunar valves snap shut as ventricular pressure drops below arterial pressure. All four valves are again closed, and ventricular volume stays constant momentarily.

5. Ventricular filling — Ventricular pressure drops below atrial pressure, so the AV valves open. Blood flows passively from the atria into the ventricles. Most filling happens early and rapidly, then slows until the next atrial systole completes the cycle.

Systole vs. Diastole in Heart Chambers

The atria and ventricles don't contract at the same time. Their systole and diastole phases are staggered so that one set of chambers fills while the other ejects.

• Atrial systole occurs at the same time as late ventricular diastole. The atria squeeze blood into the already-relaxing ventricles.
• Atrial diastole occurs during ventricular systole and continues through most of ventricular diastole. While the ventricles are contracting and then relaxing, the atria are passively refilling with blood from the venae cavae (right side) and pulmonary veins (left side).

This overlapping timing is what makes the heart so efficient. The atria serve as both receiving chambers and priming pumps for the ventricles.

Heart Sounds and Valve Actions

The heart sounds you hear through a stethoscope are produced by valve closures, not by the valves opening.

• S1 ("lub") — Caused by closure of the AV valves (mitral and tricuspid). This marks the beginning of ventricular systole. It's typically the louder, longer sound.
• S2 ("dub") — Caused by closure of the semilunar valves (aortic and pulmonary). This marks the end of ventricular systole and the beginning of ventricular diastole. It's shorter and sharper than S1.
• S3 — A soft, low-pitched sound heard just after S2 during rapid ventricular filling. It can be normal in children and young athletes but in older adults may indicate volume overload or heart failure.
• S4 — Heard just before S1, caused by forceful atrial contraction pushing blood into a stiff, non-compliant ventricle. S4 is generally considered abnormal and is associated with conditions like ventricular hypertrophy.

Ventricular Volumes and Cardiac Function

Two key volume measurements define how much blood the ventricles handle each beat:

• End-diastolic volume (EDV) — The volume of blood in the ventricle at the end of filling, just before contraction. A typical value is about 120 mL.
• End-systolic volume (ESV) — The volume of blood remaining in the ventricle after contraction. A typical value is about 50 mL.
• Stroke volume (SV) — The amount of blood ejected per beat: $SV = EDV - ESV$. Using the values above, that's about 70 mL per beat.

Preload refers to the degree of stretch on the ventricular muscle fibers just before contraction. It's directly related to EDV: more blood in the ventricle means more stretch on the walls.

The Frank-Starling law explains why this matters. When venous return increases and the ventricle fills with more blood (higher EDV), the cardiac muscle fibers are stretched further. This greater stretch produces a stronger contraction and a larger stroke volume. The heart automatically matches its output to the volume of blood returning to it, without needing any neural input. Think of it like stretching a rubber band further before releasing it: more stretch, more snap.