Lecture 1_ Cardiac Cycle

It is the resistance the ventricle must overcome to eject blood during contraction.

The opening is driven by the pressure gradient when right and left atrial pressure exceed left ventricular pressure.

Regurgitant valves increase chamber volume, work, and diameter over time, leading to elevated pressures.

It is the lowest pressure in the arteries during ventricular filling.

It refers to the initial stretching of the cardiac muscle fibers before contraction.

Late systolic murmurs start mid-way between S1 and S2, peaking at S2, and are often related to mitral valve prolapse.

Early decrescendo diastolic murmurs occur after S2 and decrease sharply, commonly seen in aortic and pulmonic regurgitation.

In mid-to-late diastolic murmurs, the OS sound appears at the end of the murmur, indicating mild mitral or tricuspid stenosis.

Prolonged mid-to-late diastolic murmurs start mid-way between S2 and S1, with the OS sound appearing further from S1, often indicating severe mitral or tricuspid stenosis.

Stenotic valves increase chamber pressures, workload, and long-term wall thickness.

Right ventricular pressure must be lower than right atrial pressure for filling to occur.

Pressure decreases gradually from the aorta to the venae cavae.

The pressure in the pulmonary arteries is lower than in the systemic circulation.

The left ventricle is larger and thicker because it does more work by generating higher pressure to pump blood through the systemic circulation.

The phases are atrial contraction, isovolumetric contraction, rapid ventricular ejection, reduced ventricular ejection, isovolumetric relaxation, rapid ventricular filling, and reduced ventricular filling.

The pressure changes indicate the heart's mechanical activity and the phases of contraction and relaxation.

The ECG correlates with the electrical activity of the heart during the different phases of the cardiac cycle.

The heart sounds S1, S2, S3, and S4 correspond to specific events in the cardiac cycle such as valve closure and atrial contraction.

The closure occurs when pressure in the left ventricle exceeds that in the left atrium.

During isovolumic contraction, there is a rapid increase in ventricular pressure with no change in ventricular volume.

The aortic valve opens, marking the end of isovolumic contraction and the beginning of ejection.

The 'c' wave results from the bulging of the mitral valve into the atrium due to rising ventricular pressure.

Ejection begins when pressure in the ventricle exceeds pressure in the aorta and the aortic valve opens.

80% to 85% of the stroke volume is ejected during the rapid ejection phase.

Ventricular volume falls rapidly during the rapid ejection phase.

Ejection slows during the latter third of systole, known as the reduced ejection phase.

Aortic pressure exceeds ventricular pressure as the ventricle begins to relax, but ejection continues due to blood momentum.

The 'v' wave indicates an increase in atrial volume and pressure during ventricular systole.

Ventricular volume is at its minimum and muscle fibers begin to relax.

Ventricular repolarization occurs, indicated by the T wave.

The linear velocity of blood flow falls as pressure in the aorta exceeds that in the ventricle.

The oscillation of the aortic valve bulging into the ventricle and returning to its normal position causes the dicrotic notch.

Ventricular pressure falls rapidly, but volume does not change because no valves are open.

Atrial pressure exceeds ventricular pressure, leading to the opening of the AV valve.

Blood rapidly enters the relaxing ventricle after the AV valve opens.

The pressure in the atrium falls but remains above that in the ventricle until the next ventricular contraction.

The period of further reduced filling is referred to as diastasis.

Atrial contraction completes ventricular filling by ejecting about 20% of the volume into the ventricles.

The atrioventricular valves are open while the semilunar valves are closed during atrial contraction.

Atrial contraction causes a rise in atrial pressure, producing the a wave in the venous pulse.

In a healthy heart, left heart cardiac output and right heart cardiac output are equal.

S1 is caused by the closure of the mitral and tricuspid valves.

S2 is caused by the closure of the aortic and pulmonic valves.

Healthy heart valves make noise when they close.

S1 corresponds to mitral and tricuspid valve closure.

S2 corresponds to aortic and pulmonic valve closure.

The origin of the S3 heart sound is not valvular.

The S3 heart sound occurs just after the opening of the AV valves during the rapid filling of the ventricle.

The S3 heart sound is produced by rapid filling of a very compliant ventricle.

The S3 heart sound is a normal finding in children and young adults.

In older adults, the presence of S3 often indicates volume overload and is a sign of cardiac disease.

In volume overload, the left ventricle dilates, increasing chamber size and compliance, leading to the S3 sound during rapid ventricular filling.

The origin of the S4 heart sound is not valvular.

The S4 heart sound occurs during atrial contraction at the end of the filling phase.

The S4 heart sound is produced when the atrium contracts against a stiff ventricle due to concentric hypertrophy.

The S4 heart sound is a low frequency sound.

In pressure overload, the ventricle hypertrophies, leading to thickened walls and reduced compliance, which causes the S4 sound during atrial contraction.

The S4 heart sound coincides with a rise in atrial pressure during the atrial kick.

The two general types of cardiac valve defects are stenosis and regurgitation.

Valvular stenosis is usually caused by thickening and increased rigidity of the valve leaflets, often accompanied by calcification.

Valvular stenosis results in high resistance to flow and a large pressure gradient across the valve.

During valvular insufficiency, the valve leaflets do not completely seal, causing regurgitation of blood into the proximal chamber.

A common example of regurgitation is aortic valve insufficiency, where blood regurgitates from the aorta into the left ventricle after ventricular ejection.

A valvular murmur occurs when blood flow through a diseased valve.

Ejection type systolic murmurs occur between S1 and S2 with intensity increasing sharply from S1 and decreasing sharply before S2, commonly seen in aortic and pulmonary stenosis.

Pansystolic murmurs maintain almost constant intensity between S1 and S2, typically associated with mitral and tricuspid regurgitation and ventricular septal defects.

The phases are Atrial systole, Isovolumic ventricular contraction, Rapid ventricular ejection, Reduced ventricular ejection, Isovolumic ventricular relaxation, Rapid ventricular filling, and Reduced ventricular filling.

Preload is the ventricular wall tension at the end of diastole, reflecting the stretch on the ventricular fibers just before contraction.

Afterload is the ventricular wall tension during contraction, representing the force that must be overcome for the ventricle to eject its contents.

Contractility is the property of heart muscle that accounts for changes in the strength of contraction, independent of preload and afterload.

Stroke volume is the volume of blood ejected from the ventricle during systole, calculated as end-diastolic volume minus end-systolic volume.

Ejection fraction is the fraction of end-diastolic volume ejected from the ventricle during each systolic contraction, with a normal range of 55%-75%.

Cardiac output is the volume of blood ejected from the ventricle per minute, calculated as stroke volume multiplied by heart rate.

Compliance describes the pressure-volume relationship during filling, reflecting the ease or difficulty with which a chamber can be filled.

Increased preload leads to an increase in stroke volume while afterload and contractility are held constant.

Increased afterload results in a decrease in stroke volume while preload and contractility are held constant.

Increased contractility causes an increase in stroke volume while preload and afterload are held constant, and the ESPVR slope increases.

It indicates the beginning of ventricular ejection when pressure exceeds aortic pressure.

It marks the end of ventricular ejection and the start of isovolumic relaxation.

It indicates the beginning of ventricular filling after isovolumic relaxation.

It marks the end of ventricular filling and the start of isovolumic contraction.

It is the phase where blood is expelled from the ventricle into the aorta.

It is the phase where the ventricle fills with blood from the atrium.

It is the phase where the ventricle relaxes without changing volume after ejection.

It is the phase where the ventricle contracts without changing volume before ejection.

It is the volume of blood in the ventricle at the end of filling before contraction.

It is the volume of blood remaining in the ventricle after ejection.

It is the amount of blood ejected from the ventricle during each heartbeat.

It is the peak pressure in the arteries during ventricular ejection.

Narrowing of the aortic valve (aortic stenosis) is indicated by these pressures.

The pressure before is always increased, while the pressure after is always normal or decreased.

Constriction of pulmonary arterioles is indicated by the elevated pressures in the pulmonary artery and right ventricle.

Pressure before the stenotic valve is increased, while pressure after is normal or decreased.