Cardiovascular Physiology II

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Cardiac Cycle

The heart is two pumps (left and right) that work together by using repetative contractions (systole) and relaxation (diastole) of the heart chambers. Blood moves through the circulatory system from high to low pressures, heart contractions produce pressure.

LATE DIASTOLE: both sets of chambers are relaxed and ventricles fill passively (AV valves open)

ARTIAL SYSTOLE: ~80% of the ventricle is full but atrial contractions forces blood into the ventricle. (AV valves open)

ISOVOLUMIC VENTRICULAR CONTRATION: AV valves pushed close (muscles develop tension but do not shorten) but not enough pressure to open semi lunar valves. (All valves closed)

VENTRICULAR EJECTION: semi lunar valves open and eject blood as the ventricle pressure is greater than the aorta and pumonary artery (semi lunar valves open).

ISOVOLUMIC VENTRICULAR RELAXATION: pressure falls so blood flows back closing semi lunar valves (All valves closed)

Valves in the heart open and close in response to pressure. The sound of the heart is caused by AV valve and aortic valve closing. Heart murmurs mean the hearts valves are damaged.

Cardiac Output

Stroke Volume (SV centimills) is the amount of blood EJECTED from VENTRICLE during a single heartbeat = End diastolic volume (EDV) - End systolic volume (ESV)

Cardiac Output (CO) amount of BLOOD PUMPED in ONE MINUTE used to measure heart performance = Stroke Volume (SV) x Heart rate (HR)

At rest: 70ml x 70bpm = 4900ml.min-1 therefore as the normal blood volume id ~5L the entire blood volume passes through the heart every minute at rest. During exercise this can rise to 20-25 litres per minute.

Control

INTRINSIC REGULATION: response of ventricular muscle to EDV changes which increase with stoke volume

Preload: (volume of blood in ventricle just before contraton) passive atrial filling (dependant on venous pressure) followed by atrial contraction that causes ventricular filling. If right atrial pressure increases so does ventricular filling. This results in increased output, increasing myocardial work and O2 requirement.

Afterload: (arterial pressure against which ventricles pump) the peripheral BP a ventricular contraction must overcome. Increased afterload compensated for by ventricular contraction and cardiac output. Ventricular hypertrophy is a result of long term increases in arterial pressure.

EXTRINSIC REGULATION: the effect of the hearts nerve supply on it s activity. The ANS regulates cardiac output by:

Parasympathetic stimulation decreases HR (SA node) release of Ach

Sympathetic stimulation increase HR (SA node) release of noradrenaline

Increasing cardiac muscle contraction force

Intrinsic regulation changes stroke volume where as extrinsic regulation changes heart rate and stoke volume.