Medical School · Year 1 · Cardiovascular · includes a quiz and discussion video

Lecture 4: The Cardiac Cycle

Unit 1.7: Cardiovascular System

Learning Objectives

By the end of this lecture, students will be able to:

1. Describe the phases of the cardiac cycle and their hemodynamic events
2. Correlate electrical events (ECG) with mechanical events
3. Explain the pressure-volume relationships during the cardiac cycle
4. Describe the origin and characteristics of heart sounds
5. Explain the jugular venous pulse waveform
6. Apply cardiac cycle concepts to clinical scenarios

Overview of the Cardiac Cycle

The cardiac cycle encompasses the complete sequence of events from the beginning of one heartbeat to the beginning of the next. It is fundamentally divided into two phases: systole, during which the ventricles contract and eject blood, and diastole, during which the ventricles relax and fill with blood. At a normal resting heart rate of 75 beats per minute, the entire cycle lasts approximately 0.8 seconds.

The relative durations of systole and diastole have important physiological implications. Ventricular systole occupies approximately 0.3 seconds and diastole approximately 0.5 seconds at rest. As heart rate increases, both phases shorten, but diastole shortens proportionally more than systole. At a heart rate of 150 beats per minute, the total cycle time is halved to 0.4 seconds, with systole occupying 0.25 seconds and diastole only 0.15 seconds. This disproportionate shortening of diastole has clinical significance because diastole is when the coronary arteries receive most of their blood flow and when the ventricles fill. Extreme tachycardia compromises both coronary perfusion and ventricular filling, which can precipitate ischemia and reduce cardiac output.

<image>Panel A: Circular diagram representing one cardiac cycle at 75 bpm divided into systole (0.3 seconds in red) and diastole (0.5 seconds in blue). Panel B: Similar diagram at 150 bpm showing total duration of 0.4 seconds with systole at 0.25 seconds and diastole compressed to 0.15 seconds. Panel C: Bar graphs comparing absolute durations showing diastole shortens disproportionately (70% reduction) compared to systole (17% reduction). Panel D: Clinical note indicating consequences of reduced coronary filling time and decreased ventricular filling during tachycardia.</image>

Phases of the Cardiac Cycle

The cardiac cycle can be subdivided into seven distinct phases, four during ventricular systole and three during diastole. Understanding each phase requires tracking valve positions, pressure changes, and volume changes.

Isovolumetric contraction begins when the ventricles start contracting following electrical activation. The mitral valve has just closed as ventricular pressure exceeds atrial pressure. During this phase, all four valves are closed—the atrioventricular valves have just closed and the semilunar valves have not yet opened. Ventricular pressure rises rapidly while ventricular volume remains constant. This phase lasts approximately 0.05 seconds and ends when ventricular pressure exceeds aortic pressure, causing the aortic valve to open.

Rapid ejection follows aortic valve opening. Approximately 70 percent of the stroke volume is ejected during this initial portion of systole. Blood accelerates into the aorta, and aortic pressure rises to its peak systolic value. This phase lasts approximately 0.1 seconds.

Reduced ejection continues until the end of systole. The remaining 30 percent of stroke volume is ejected as myocardial contraction wanes. Ventricular pressure begins to fall even as ejection continues because the rate of relaxation begins to exceed the rate of contraction. This phase lasts approximately 0.15 seconds and ends when ventricular pressure falls below aortic pressure, causing the aortic valve to close.

Isovolumetric relaxation begins with aortic valve closure. Again, all four valves are closed. Ventricular pressure falls rapidly while volume remains constant. This phase lasts approximately 0.08 seconds and ends when ventricular pressure falls below atrial pressure, causing the mitral valve to open.

Rapid filling begins with mitral valve opening. Blood that has accumulated in the left atrium during ventricular systole rushes into the ventricle down the pressure gradient. Approximately 70 percent of ventricular filling occurs passively during this phase. The ventricle expands rapidly, and pressure rises only slightly. This phase lasts approximately 0.1 seconds.

Slow filling, or diastasis, is a period of pressure equilibration between the atrium and ventricle. Little blood flows because there is minimal pressure gradient. This phase contributes only about 5 percent of filling. Its duration is variable and shortens dramatically with tachycardia—it may virtually disappear at high heart rates.

Atrial systole, or the atrial kick, is the final contribution to ventricular filling. Atrial contraction, triggered by the P wave on the ECG, actively pushes blood into the ventricle, contributing approximately 25 percent of total filling in healthy individuals at rest. The atrial contribution becomes increasingly important at faster heart rates (when passive filling time is reduced) and in conditions where ventricular compliance is reduced (when active filling becomes essential).

<image>Panel A: Isovolumetric contraction with all valves closed and rising LV pressure, followed by rapid ejection phase with aortic valve open showing 70% stroke volume ejected. Panel B: Reduced ejection phase with aortic valve open showing remaining 30% stroke volume, followed by isovolumetric relaxation with all valves closed and falling pressure. Panel C: Rapid filling phase with mitral valve open showing 70% ventricular filling, slow filling/diastasis with 5% filling, and atrial systole contributing 25% filling. Panel D: Aligned ECG trace showing P wave before atrial systole, QRS at isovolumetric contraction start, T wave during ejection, with duration bars for each phase.</image>

Pressure Changes During the Cardiac Cycle

Understanding pressure changes is essential for interpreting hemodynamic data and recognizing abnormalities. The left and right hearts operate in parallel but generate different pressures.

In the left heart, the left atrium maintains low pressures with subtle fluctuations. The a wave (approximately 10 mmHg) results from atrial contraction. The v wave (approximately 12 mmHg) reflects atrial filling during ventricular systole when the mitral valve is closed. Mean left atrial pressure is approximately 8 mmHg.

Left ventricular pressure swings dramatically during the cardiac cycle. End-diastolic pressure is approximately 8 to 12 mmHg, reflecting the filling pressure at the end of diastole. Systolic pressure rises rapidly during isovolumetric contraction, then reaches a peak of approximately 120 mmHg during ejection before falling during reduced ejection and returning to diastolic levels.

Aortic pressure closely follows left ventricular pressure during ejection but maintains a minimum diastolic pressure of approximately 80 mmHg due to arterial compliance and peripheral resistance. The mean aortic pressure is approximately 93 mmHg. The dicrotic notch in the aortic pressure tracing marks aortic valve closure.

The right heart generates much lower pressures because pulmonary vascular resistance is only one-tenth of systemic vascular resistance. Right atrial pressures are similar in pattern to left atrial pressures but lower in magnitude (mean approximately 4 mmHg). Right ventricular systolic pressure is approximately 25 mmHg, and diastolic pressure approximately 4 mmHg. Pulmonary artery pressure is approximately 25/10 mmHg with a mean of 15 mmHg.

Valve opening and closing are determined by pressure gradients. The mitral valve closes when left ventricular pressure exceeds left atrial pressure at the onset of systole. The aortic valve opens when left ventricular pressure exceeds aortic diastolic pressure. The aortic valve closes when aortic pressure exceeds left ventricular pressure at the end of systole. The mitral valve opens when left atrial pressure exceeds left ventricular pressure at the end of isovolumetric relaxation.

<image>Panel A: Left atrial pressure trace in blue showing a wave (~10 mmHg at atrial contraction) and v wave (~12 mmHg during ventricular systole). Panel B: Left ventricular pressure trace in red showing diastolic pressure (~8-12 mmHg), rapid rise during isovolumetric contraction, and peak systolic pressure (~120 mmHg). Panel C: Aortic pressure trace in orange paralleling LV during ejection with dicrotic notch at aortic valve closure and diastolic pressure (~80 mmHg), with vertical lines marking valve events (MVC, AVO, AVC, MVO). Panel D: Right heart pressure traces at same scale showing lower magnitudes for comparison.</image>

The Wiggers Diagram

The Wiggers diagram is a comprehensive graphical representation of the cardiac cycle that simultaneously displays multiple variables aligned in time. Understanding this diagram is fundamental to integrating cardiac physiology.

The diagram typically includes the electrocardiogram, showing the P wave, QRS complex, and T wave that initiate and correlate with mechanical events. Atrial depolarization (P wave) precedes atrial contraction by a short interval. Ventricular depolarization (QRS complex) precedes ventricular contraction. Ventricular repolarization (T wave) occurs during the ejection phase.

Pressure tracings show aortic pressure with its systolic peak and diastolic nadir, left ventricular pressure with its dramatic rise and fall, and left atrial pressure with its characteristic waveform. The pressure relationships define when valves open and close.

Left atrial pressure shows several important features. The a wave coincides with atrial systole and reflects the pressure generated by atrial contraction. The c wave is a small notch coinciding with the onset of ventricular systole, caused by bulging of the mitral valve leaflets back toward the atrium and transmitted carotid pulsation. The x descent follows the c wave and reflects atrial relaxation and descent of the atrioventricular ring during ventricular ejection. The v wave represents atrial filling during ventricular systole when the mitral valve is closed. The y descent follows mitral valve opening and represents passive emptying of the atrium into the ventricle.

Left ventricular volume changes from end-diastolic volume (EDV, approximately 120 mL) to end-systolic volume (ESV, approximately 50 mL). The stroke volume is the difference, approximately 70 mL.

Heart sounds appear on the phonocardiogram. S1 coincides with mitral and tricuspid valve closure at the onset of systole. S2 coincides with aortic and pulmonary valve closure at the end of systole.

<image>Panel A: ECG trace showing P wave, QRS complex, and T wave aligned with pressure traces showing aortic pressure (peak ~120 mmHg, dicrotic notch), left ventricular pressure, and left atrial pressure with a, c, v waves and x, y descents. Panel B: Left ventricular volume trace showing filling from ESV (~50 mL) to EDV (~120 mL) then ejection back to ESV with stroke volume indicated. Panel C: Phonocardiogram showing S1 at mitral/tricuspid closure and S2 at aortic/pulmonary closure. Panel D: Vertical shading distinguishing systole (pink) from diastole (blue) with seven phases labeled across the bottom.</image>

The Pressure-Volume Loop

The pressure-volume loop is a powerful graphical tool that plots left ventricular pressure against left ventricular volume throughout the cardiac cycle. Each complete cardiac cycle traces one counterclockwise loop.

The four segments of the loop correspond to the major phases of the cardiac cycle. The bottom segment, from point A to point B, represents ventricular filling. The mitral valve is open, and the ventricle fills from end-systolic volume (approximately 50 mL at point A) to end-diastolic volume (approximately 120 mL at point B). Pressure rises only slightly during filling in a normal, compliant ventricle.

The right vertical segment, from B to C, represents isovolumetric contraction. Both valves are closed, so volume is constant while pressure rises rapidly from end-diastolic pressure (approximately 12 mmHg) to aortic diastolic pressure (approximately 80 mmHg).

The top segment, from C to D, represents ejection. The aortic valve is open, and volume decreases as blood is ejected. Pressure first rises to peak systolic pressure, then begins to fall even as ejection continues.

The left vertical segment, from D to A, represents isovolumetric relaxation. Both valves are closed, volume is constant at end-systolic volume, and pressure falls rapidly until it drops below atrial pressure and the mitral valve opens.

Several important values can be derived from the loop. End-diastolic volume (EDV) is the maximum volume reached, approximately 120 mL. End-systolic volume (ESV) is the minimum volume, approximately 50 mL. Stroke volume (SV) is EDV minus ESV, approximately 70 mL, represented by the width of the loop. Ejection fraction (EF) is stroke volume divided by EDV, normally 55 to 70 percent.

The area enclosed by the loop represents stroke work—the external work performed by the ventricle in ejecting blood against arterial pressure. This equals the integral of pressure times volume change and reflects the energy expenditure per beat.

<image>Panel A: Pressure-volume loop axes showing volume (0-150 mL) on x-axis and pressure (0-150 mmHg) on y-axis with counterclockwise loop traced through four phases. Panel B: Filling phase (A to B) curving rightward as volume increases to EDV (~120 mL) with minimal pressure rise, and isovolumetric contraction (B to C) rising vertically to aortic diastolic pressure (~80 mmHg). Panel C: Ejection phase (C to D) curving leftward with peak pressure (~120 mmHg) then isovolumetric relaxation (D to A) dropping vertically, with stroke volume as loop width and ejection fraction calculation shown. Panel D: Loop area shaded as stroke work with end-systolic pressure-volume relationship (ESPVR) drawn as diagonal line through point D indicating contractile state.</image>

Heart Sounds

Heart sounds are produced by vibrations in the heart, blood, and surrounding structures associated with valve closure and blood flow. The normal heart produces two audible sounds per cycle.

The first heart sound (S1) occurs at the onset of ventricular systole and is caused by closure of the atrioventricular valves—the mitral and tricuspid valves. S1 marks the beginning of systole and is described as "lub" in the traditional "lub-dub" characterization. It is normally heard best at the apex. S1 has two components: M1 from mitral valve closure occurs first because the left ventricle begins contracting slightly before the right, and T1 from tricuspid valve closure follows immediately. The two components are usually heard as a single sound because they are nearly simultaneous.

The second heart sound (S2) occurs at the end of ventricular systole and is caused by closure of the semilunar valves—the aortic and pulmonary valves. S2 marks the end of systole and is described as "dub." It is heard best at the base of the heart. S2 also has two components: A2 from aortic valve closure normally occurs first, and P2 from pulmonary valve closure follows.

Physiologic splitting of S2 occurs during inspiration. Inspiration increases venous return to the right heart, prolonging right ventricular ejection time and delaying P2. Simultaneously, pooling of blood in the pulmonary vasculature reduces return to the left heart, shortening left ventricular ejection and causing earlier A2. The net result is that A2 and P2 move apart during inspiration, creating audible splitting. During expiration, the components move back together.

Extra heart sounds include S3 and S4. The third heart sound (S3) occurs in early diastole during rapid ventricular filling. It is normal in children and young adults but in older adults suggests heart failure with volume overload. S4 occurs in late diastole during atrial contraction and results from atrial contraction forcing blood into a stiff, non-compliant ventricle. It is heard in left ventricular hypertrophy, ischemia, and other conditions that reduce ventricular compliance.

<image>Panel A: Phonocardiogram aligned with cardiac cycle showing S1 at systole onset and S2 at systole end, with S1 components M1 and T1 nearly simultaneous and S2 components A2 and P2 shown. Panel B: Mechanism of physiologic splitting during inspiration showing increased RV filling, prolonged RV ejection (delayed P2), decreased LV filling, shortened LV ejection (earlier A2) widening A2-P2 interval. Panel C: S3 timing in early diastole during rapid filling phase with ventricle rapidly expanding, and S4 in late diastole with atrium contracting against stiff LV wall. Panel D: Summary table of S3 associations (normal in youth, heart failure in adults) and S4 associations (LVH, ischemia, hypertension).</image>

Jugular Venous Pulse

The jugular venous pulse (JVP) provides a visible and measurable window into right atrial hemodynamics. The internal jugular vein transmits pressure waves from the right atrium, and careful examination reveals waveform components that reflect specific cardiac events.

The a wave is the dominant positive wave and corresponds to right atrial contraction. It occurs just before S1 and reflects the pressure rise in the right atrium as it contracts to complete ventricular filling. The timing of the a wave can be confirmed by noting that it precedes the carotid pulse.

The c wave is a small positive wave that follows the a wave. It has two causes: bulging of the tricuspid valve leaflets back toward the atrium at the onset of ventricular systole, and transmitted pulsation from the adjacent carotid artery. It is often difficult to visualize clinically.

The x descent is a negative wave (falling pressure) that follows the c wave. It represents atrial relaxation and the descent of the atrioventricular ring during ventricular ejection, which increases right atrial volume and decreases pressure.

The v wave is a positive wave during ventricular systole. It reflects filling of the right atrium from venous return while the tricuspid valve is closed. The v wave peaks just after S2, coinciding with tricuspid valve opening.

The y descent follows the v wave and represents passive emptying of the right atrium into the right ventricle after the tricuspid valve opens. It corresponds to the rapid filling phase of ventricular diastole.

Several clinical abnormalities produce characteristic JVP findings. Prominent a waves (cannon a waves) occur when the atrium contracts against a closed tricuspid valve, as in complete heart block or ventricular tachycardia with AV dissociation. Absent a waves are seen in atrial fibrillation, where there is no organized atrial contraction. Prominent v waves suggest tricuspid regurgitation, where blood regurgitates into the right atrium during ventricular systole. A steep y descent is characteristic of constrictive pericarditis, where the stiff pericardium limits ventricular expansion but allows rapid early filling.

The height of the JVP reflects right atrial pressure. It is measured as the vertical distance from the sternal angle to the top of the venous pulsation, with 5 centimeters added to account for the distance from the sternal angle to the right atrium. Normal JVP is less than 8 centimeters of water.

<image>Panel A: JVP waveform aligned with ECG showing a wave preceding QRS at atrial contraction, c wave at systole onset, x descent during atrial relaxation, v wave rising during ventricular systole, and y descent after tricuspid opening. Panel B: Clinical examination technique with patient reclined at 45 degrees, internal jugular vein visible, measurement from sternal angle to column top plus 5 cm for right atrium distance. Panel C: Pathological waveforms showing cannon a waves when atrium contracts against closed valve with AV dissociation on ECG. Panel D: Giant v waves merging with c wave in tricuspid regurgitation and steep y descent in constrictive pericarditis.</image>

Cardiac Output and Its Determinants

Cardiac output is the volume of blood pumped by the heart per unit time. It represents the product of heart rate and stroke volume.

Cardiac Output = Heart Rate × Stroke Volume

At rest, with a heart rate of 70 beats per minute and stroke volume of 70 mL, cardiac output is approximately 5 liters per minute. This precisely matches the oxygen demands of the tissues under resting conditions. During exercise, cardiac output can increase to 20 to 25 liters per minute in healthy individuals, primarily through increases in both heart rate and stroke volume.

Stroke volume is determined by three major factors: preload, afterload, and contractility.

Preload is the stretch on the ventricular muscle fibers at the end of diastole, determined by end-diastolic volume. The Frank-Starling mechanism describes the relationship between preload and contractile force: increased preload stretches the sarcomeres toward their optimal length, improving the overlap of actin and myosin filaments and increasing the force of contraction. This mechanism has several important physiological functions. It matches right and left ventricular output, ensuring that any increase in right ventricular output is met by a corresponding increase in left ventricular output. It allows the heart to adapt to changes in venous return. The Frank-Starling curve plots stroke volume against end-diastolic volume, showing that stroke volume increases as preload increases, up to a plateau.

Afterload is the resistance against which the ventricle must eject blood. For the left ventricle, this is primarily determined by aortic pressure and systemic vascular resistance. For the right ventricle, it is pulmonary artery pressure. Increased afterload makes it more difficult for the ventricle to eject blood, increasing end-systolic volume and reducing stroke volume if contractility remains constant. The ventricle must generate higher pressure to open the aortic valve and sustain ejection against higher resistance.

Contractility, or inotropy, is the intrinsic strength of cardiac muscle contraction independent of preload and afterload. Increased contractility shifts the Frank-Starling curve upward and leftward, producing greater stroke volume at any given preload. Contractility is increased by sympathetic stimulation, circulating catecholamines, and positive inotropic drugs such as digitalis and dobutamine. It is decreased by heart failure, acidosis, hypoxia, and negative inotropic drugs such as beta-blockers.

<image>Panel A: Central equation CO = HR x SV with heart rate regulation showing sympathetic (increases) and parasympathetic (decreases) inputs. Panel B: Preload panel with Frank-Starling curve showing increasing SV with increasing EDV on ascending limb, and sarcomere diagram showing stretch optimizing actin-myosin overlap. Panel C: Afterload panel showing increased afterload from constricted aorta or elevated pressure reduces stroke volume with increased ESV. Panel D: Contractility panel with family of Frank-Starling curves showing baseline, shifted-up curve with positive inotropy (catecholamines, digitalis), and shifted-down curve with negative inotropy (heart failure, acidosis, beta-blockers).</image>

Pressure-Volume Loops in Disease

The pressure-volume loop changes characteristically in various cardiovascular conditions, providing insight into the hemodynamic consequences of disease.

Increased preload, as occurs with volume overload from mitral or aortic regurgitation or fluid administration, shifts the loop rightward. End-diastolic volume increases, and according to the Frank-Starling mechanism, stroke volume also increases (wider loop). The heart is operating at a higher filling volume.

Increased afterload, as occurs with systemic hypertension or aortic stenosis, shifts the loop upward and rightward. The ventricle must generate higher pressure to eject blood. End-systolic volume increases because the ventricle cannot eject blood as effectively against the higher resistance. Stroke volume initially decreases, though compensatory mechanisms may restore it over time. The area of the loop (stroke work) increases, reflecting greater energy expenditure.

Increased contractility, as occurs with sympathetic stimulation or positive inotropic drugs, steepens the end-systolic pressure-volume relationship (ESPVR), the line connecting the upper-left corners of loops at various preloads. The loop shifts leftward with decreased end-systolic volume and increased stroke volume at any given preload and afterload.

Heart failure with reduced contractility produces the opposite changes. The ESPVR becomes flatter. End-systolic volume increases because the weakened ventricle cannot eject blood effectively. Stroke volume decreases. The loop becomes narrower, reflecting reduced stroke work. Ejection fraction falls.

Diastolic dysfunction, as seen in heart failure with preserved ejection fraction (HFpEF), alters the filling portion of the loop. The ventricle is stiff and non-compliant, so filling requires higher pressures. The diastolic pressure-volume relationship shifts upward and leftward. Filling is impaired, and the patient develops symptoms of congestion despite normal ejection fraction.

<image>Panel A: Increased preload/volume overload with loop shifted rightward showing increased EDV, slightly increased SV (wider loop), and ESV relatively unchanged. Panel B: Increased afterload/pressure overload with loop shifted upward (higher peak pressure), increased ESV, slightly decreased SV, and increased stroke work area. Panel C: Increased contractility with steeper ESPVR line, loop shifted leftward with decreased ESV and increased SV at same EDV. Panel D: Heart failure/decreased contractility with flatter ESPVR, loop shifted rightward with increased ESV and EDV, decreased SV (narrower loop), and diastolic dysfunction showing elevated filling pressures with preserved EF.</image>

Clinical Applications

Understanding the cardiac cycle illuminates the pathophysiology of common cardiovascular conditions.

Heart failure can be classified by ejection fraction. Heart failure with reduced ejection fraction (HFrEF, EF less than 40%) represents systolic dysfunction, where the ventricle cannot contract effectively. The pressure-volume loop shows increased end-systolic volume, reduced stroke volume, and a flattened ESPVR. Heart failure with preserved ejection fraction (HFpEF, EF 50% or greater) represents diastolic dysfunction, where the ventricle cannot relax and fill properly. Ejection fraction is normal, but filling pressures are elevated, causing pulmonary congestion.

Valvular heart disease alters hemodynamics predictably. Aortic stenosis creates a pressure gradient across the valve, requiring the left ventricle to generate much higher pressure to eject blood into the aorta. This pressure overload causes concentric left ventricular hypertrophy. Aortic regurgitation allows blood to leak back from the aorta into the left ventricle during diastole, causing volume overload. The ventricle dilates and total stroke volume increases, though forward stroke volume may be reduced. Mitral stenosis impedes left atrial emptying, causing left atrial enlargement, elevated left atrial pressure, and pulmonary congestion. Mitral regurgitation allows blood to regurgitate into the left atrium during systole, causing both atrial and ventricular volume overload.

Arrhythmias affect the cardiac cycle in specific ways. Atrial fibrillation eliminates the organized atrial contraction (atrial kick), reducing ventricular filling by 15 to 25 percent. This is particularly detrimental when ventricular compliance is reduced. Tachycardia shortens diastole more than systole, reducing filling time and potentially reducing stroke volume if preload falls. Bradycardia prolongs diastole, allowing more filling time, but may reduce cardiac output if heart rate falls too low.

Cardiac tamponade occurs when fluid accumulates in the pericardial space and compresses the heart. External pressure limits ventricular filling during diastole. All diastolic pressures equilibrate. Pulsus paradoxus—an exaggerated fall in systolic blood pressure during inspiration—is a hallmark finding.

<image>Panel A: Heart failure PV loops comparing HFrEF (wide loop shifted right with flat ESPVR, low EF) and HFpEF (nearly normal loop with elevated diastolic pressures, preserved EF). Panel B: Valvular disease diagrams showing aortic stenosis (pressure gradient, LV hypertrophy), aortic regurgitation (regurgitant jet, dilated LV), mitral stenosis (narrowed orifice, LA enlargement), and mitral regurgitation (regurgitant jet, LA and LV dilation). Panel C: Arrhythmias showing atrial fibrillation with loss of a wave and 25% atrial contribution to filling, and tachycardia with shortened diastole and reduced filling. Panel D: Cardiac tamponade with pericardial effusion compressing heart, equalized diastolic pressures, and pulsus paradoxus on arterial tracing.</image>

Summary

The cardiac cycle consists of systole (ventricular contraction and ejection) and diastole (ventricular relaxation and filling). Seven phases can be identified: isovolumetric contraction, rapid ejection, reduced ejection, isovolumetric relaxation, rapid filling, slow filling (diastasis), and atrial systole.

The pressure-volume loop plots LV pressure against LV volume throughout the cycle. Key values include end-diastolic volume (approximately 120 mL), end-systolic volume (approximately 50 mL), stroke volume (approximately 70 mL), and ejection fraction (55 to 70%). The area enclosed represents stroke work.

Heart sounds correlate with valve events: S1 from atrioventricular valve closure at the onset of systole, S2 from semilunar valve closure at the end of systole. S3 and S4 are extra sounds associated with rapid filling and atrial contraction into a stiff ventricle, respectively.

The jugular venous pulse waveform includes the a wave (atrial contraction), c wave (tricuspid bulging), x descent (atrial relaxation), v wave (atrial filling), and y descent (passive atrial emptying).

Cardiac output equals heart rate times stroke volume. Stroke volume is determined by preload (Frank-Starling mechanism), afterload, and contractility. The Frank-Starling mechanism ensures that increased venous return produces increased stroke volume, matching right and left ventricular output.

Key Terms

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