Lecture Details[edit | edit source]
Julia Choate; Week 10 MED1022; Physiology
Lecture Content[edit | edit source]
Heart is made of myocardium, lined by endocardium and on the outer surface by epicardium. Contraction is shortening of sarcomeres. Ca binds to troponin, alters tropomyosin, exposes myosin binding site on actin chain. Cardiac output (L/minute) = stroke volume (L/contraction) x heart rate (contractions/minute). Usually about 5 litres. Distribution of blood in exercise changes greatly to skeletal muscle. In CAD output is decreased.
Strength of cardiac contraction/stroke volume is altered by change in muscle cell length (EDV) and changes in calcium release (contractility). Stroke volume = strength of ventricular contraction; = EDV - end systolic volume. Relation between EDV and SV = Frank-Starling relation. It describes the relationship between myocardial stress and stroke volume. EDV causes increased pressure in ventricle, increased pressure stretches heart muscle fibres, increased length in muscle fibres increases rate of contraction. The greater the stretch in diastole, the greater the stroke work in systole. Control of stroke volume by EDV is an intrinsic property of the heart. Increased venous return causes an increase in stroke volume. Main determinants are filling time and venous pressure. It is important to match right and left sides of the heart.
Contractility is a change in contractile energy not due to changes in muscle length (EDV). The amount of Ca released depends on how much Ca is stored in the SR and how much Ca enters the cell through voltage dependant Ca channels. If more Ca is released there is a stronger contraction, if less there is a weaker contraction. Sympathetic stimulation eg by noradrenaline acts on beta receptors on cardiac muscle cells to increase Ca entry and release from the SR.