*Two pumps in series, each with a weaker chamber and a stronger chamber

*Each of the four chambers of the heart receives the same flow (CO).

*The right heart pumps this CO into a low resistance (pulmonary) circulation, and is not required to generate as high a pressure as the left heart which is pumping the same CO into the systemic circulation with about 10X the resistance of the pulmonary circulation.

*Each side of the heart has a relatively weak pump (atrium) which has no inflow valve and a large (low resistance) outflow valve.

*The atrium fills a stronger pump chamber (ventricle) that must generate enough pressure to force the CO through the circulation its services. To generate this pressure the ventricle is heavily muscled and has both an outflow valve to direct the blood flow into the circulation it services and an inflow valve to prevent backflow of the blood under high pressure into the atrium.

*Blood in both the pulmonary and systemic circulations is under pressure, forcing it back towards the right and left atrium respectively. As there are no inflow valves in the atria, they are continuously being filled with blood.

*When the AV valves are open after the ventricles have ejected their stroke volume, the pressure of the blood in the atria causes the ventricles to be filled passively.

*When the atria contract there is a further increase in the atrial blood pressure and further ventricular filling takes place. This is really "topping-off", and while advisable, it is not essential for life, e.g. individuals survive atrial fibrillation.

*Ventricles are required to generate a significant pressure to drive the stroke volume into the circulations.

*Ventricles need to be rapidly filled from the low pressure atria - advantage of a wide, low resistance inflow valve (tricuspid/mitral) - disadvantage of a wide low resistance valve holding under pressure (need for chordae tendinae and papillary muscles).

*To generate a high pressure the ventricles need to contract in a forceful, coordinated manner (importance of the conducting system).

*The smaller, higher resistance outflow valve (pulmonic/aortic) effective at preventing backflow - don't need papillary muscles and chordae tendinae

*Ventricular inflow AV valves (tricuspid and mitral)

*Ventricular outflow valves (pulmonic and aortic)

*For a valve to open, the pressure of the blood upstream must be greater than that downstream.

*For a valve to close, the pressure of the blood downstream must be greater than that upstream. Because blood flow will occur from high to low pressure this causes a backflow of blood which catches the valve cusps and closes it.

*Stenosis = narrowing. Increased resistance makes it harder to get the stroke volume through the valve, requiring more pressure generation in the upstream chamber to maintain the same stroke volume.

*Insufficiency - incomplete closure. Causes a backflow (leak) when the valve is supposed to be closed.

*Electrical (visualized as ECG)

*Mechanical (coordinated muscle tension development)

*Pressure development (results as blood is squeezed by contracting muscles.

*Flow occurs when valves open and pressure gradient drives the blood flow.

*Valves serve to direct flow in one direction and keep blood in the ventricles as pressure is developed to the point where it exceeds the pressure downstream.

*Cardiac cycle is the events occur from the beginning of one heartbeat to the next

*Each cycle is initiated by action potential generated in SA node

*Each cycle consists of diastole (period of relaxation) and systole (period of contraction)

A) Atrial systole

B) Isovolumic contraction (isometric)

C) Rapid ventricular ejection

D) Reduced ventricular ejection

E) Isovolumic relaxation (isometric)

F) Rapid ventricular filling

G) Reduced ventricular filling

*The atria contract - preceded by the P wave on the ECG

*This is the "topping off" of the ventricles - final phase of ventricular filling

*volume is the end-diastolic volume

*corresponds to the a wave in the venous pulse because the increase in atrial pressure is reflected back to the veins

*At the end of phase A/beginning of phase B is where the mitral valve closes (as soon as LV pressure is higher than LA pressure) - sound of mitral valve closing is the first heart sound aka the "lub"

*since both the mitral and aortic valves are closed there is no change in ventricular volume

*the ventricles contract and increase ventricular pressure (volume is constant)

*this corresponds to QRS complex (ventricular depolarization) on the ECG - atria repolarization also occurs during QRS

*since the atria are continuously filled with blood, the atrial pressures increase (remember the valves are closed)

*as soon as LV pressure is higher than the aortic pressure the aortic valve opens and blood flows into the aorta

*ventricles are still contracting

*both ventricular and aortic pressure increase and reach their maximum

*ventricular volume decreases rapidly

*this corresponds to the ST segment on the ECG

*LA pressure slowly increases as blood flows in from the pulmonary vein

*Venous pulse decreases because a smaller volume of blood is being returned to the RA (more blood is in the aorta and arteries, etc.)

*ventricles begin to repolarize, marked by the T wave on the ECG

*because the ventricles are no longer contracting the ventricular pressure decreases

*blood still flows into the aorta because the aortic valve is still open (as long as LV pressure is above aortic pressure)

*aortic pressure starts to fall because blood is flowing to the systemic circulation faster than blood is coming from the LV

*the minimum ventricular volume is reached

*remember LA pressure is still increasing as the atria are continuously being filled

*phase begins after the ventricles are fully repolarized, marked by the end of the T wave on the ECG

*when LV pressure decreases below aortic pressure the aortic valve closes - along with the closing of the pulmonic valve this is the 2nd heart sound aka the "dub"

*since the ventricles are relaxed and no longer contracting the LV pressure decreases

*since all the valves are closed the ventricular volume remains constant

*volume at the end of phase is considered the end-systolic volume because systole is ending

*when ventricular pressure decreases to its lowest point below left atrial pressure the mitral valve opens

*ventricular volume increases rapidly

*ventricular pressure remains low because the ventricle is relaxed and compliant

*rapid flow produces the third heart sound (normal in children, absent in adults, presence in adults indicates volume overload)

*atrial pressure decreases as blood flows from atria to ventricles

*aortic pressure decreases as blood runs off from the aorta into the arterial tree, to the veins, and back to the heart

*ventricles remain relaxed and the ventricles fill slower

*aka diastasis and is the longest phase of the cardiac cycle

*aortic pressure continues to decrease

Mitral and Tricuspid valves close ->first heart sound (S1) - "lub"

Aortic and pulmonic valves close -> second heart sound (S2) - "dub"

Timing

*S1 to S2 = Systole

*S2 to S1 = Diastole

S3 - sound of rapid flow of blood from the atria to the ventricles. (phase F)

*normal in children but not heard in normal adults

*in adults S3 indicates volume overload as in congestive heart failure or advanced mitral or tricuspid regurgitation

S4 - additional volume being added to the ventricles during phase A - the "topping off"

*not audible in normal adults but it may be heard in ventricular hypertrophy where ventricle compliance is decreased

*narrowing of the aortic valve

*Causes: Senile degeneration; congenital deformity; rheumatic heart diseases

*Increase left ventricular pressure to overcome resistant of small valve opening and drive blood flow

*Large systolic pressure gradient between LV and Aorta (common > 100 mmHg) - aortic pressure is decreased because less blood is there (downstream of the resistance)

*Long term effect

a) LV hypertrophy (concentric) -> decreased compliance

b) LA hypertrophy

*Major consequences:

1- Congestive heart failure

2- Angina (imbalance of O2 supply & demand)

3- Syncope during exercise

*Abnormal heart sounds

1) Diminish S2

2) Ejection systolic murmur

*narrowing of the mitral valve

*Mainly due to acute rheumatic fever

*Increase pressure gradient between LA and LV

*Increase LA pressure and volume -> increase pulmonary venous and capillary pressure -> increase work load on right heart -> congestive heart failure (dyspnea - difficulty breathing, hemoptysis - coughing up blood)

*Decrease LV filling -> decrease LV end-diastolic volume -> decrease stroke volume and cardiac output

*Pulmonary hypertension -> overload in right atrium -> stretch atrial conductive fibers -> atrial fibrillation

*Abnormal heart sounds:

1) Opening snap (OS) follows S2

2) Diastolic murmur

*From diseases of aortic leaflets (e.g. rheumatic) or dilatation of the aortic roots (e.g. aneurysm)

*Abnormal amount of blood regurgitate from the aorta to the LV during diastole

*Increase stroke volume according to Frank-Starling mechanism

*Acute AR -> normal size LV -> increase LV diastolic pressure -> increase LA pressure -> dyspnea and pulmonary edema

*Chronic AR -> LV dilatation (eccentric hypertrophy -> due to increased LV volume and pressure high systolic arterial pressure (due to high stroke volume) and reduce aortic diastolic pressure (reduced because not all of the volume is going to the periphery) -> widened pulse pressure [eventually patient develop heart failure]

*Abnormal heart sounds

Early diastolic murmur

*Structural abnormalities due to ischemic heart disease, infection, etc.

*Abnormal amount of blood regurgitate to the LA

*Effects:

Increase LA volume & pressure

Reduce LV cardiac output

Overloaded LV during diastole

*Acute MR

High LA pressure -> pulmonary congestion and edema

*Chronic MR

Increase LA size & compliance

normal LA pressure & pulmonary venous pressure

Low cardiac output -> fatigue

*Abnormal heart sound: Holosystolic murmur