Immunology Dr Swapnil Pawar
CVS Physiology Part 2 Dr Swapnil Pawar
Describe the cardiovascular events that occur during ventricular systole and diastole
The cardiac cycle is made up of two phases defined by the mechanical activity of cardiac muscles, systole which is ventricular contraction lasting about 300miliseconds and diastole which is ventricular relaxation and lasts about 500miliseconds. The cardiovascular events that occur during these phases can be subdivided into mechanical and electrochemical events:
Explain the Frank-Starling mechanism and its relationship to excitation-contraction coupling
The Frank-Starling mechanism states that the energy of contraction is proportional to the initial length of myocardial fibres. In the heart, this length of myocardial fibres is related to the end-diastolic volume. Therefore, up to a point, the force of contraction or stroke volume is increased by increasing venous return or preload. At a certain point, any increase in preload will exceed the heart’s contractile ability and result in no change or a decrease in stroke volume.
Excitation contraction coupling is the process by which an action potential results in a mechanical response, which in this case is myocardial contraction followed by relaxation. An action potential spreads over the muscle cell membrane and down the T tubule system causing L type calcium channel opening and calcium influx. This influx triggers the release of calcium from the sarcoplasmic reticulum through ryanodine receptors which causes a large increase in intracellular calcium concentration. The calcium then binds to troponin C causing a conformational change in tropomyosin so that a part of the actin molecule is exposed. This allows the head of myosin molecules to bind, leading to ATP hydrolysis, cross-bridging of the actin and myosin resulting in sliding of thick on thin filaments and thus muscle contraction.
Increasing preload increases the sarcomere length which increases troponin C calcium sensitivity. This increases the rate of cross-bridge attachment and detachment and the amount of tension developed by the muscle fibre thus increasing contractility. Increasing preload also optimises the overlap of actin and myosin and maximises cross-bridge formation.
Define cardiac output
Cardiac output is the volume of blood ejected by the heart per unit time and is the heart rate multiplied by the stroke volume. Normal cardiac output is usually between 4-8L/minute. Stroke volume is governed by preload, afterload and contractility. It is important to note that these main determinants of cardiac can influence each other. Due to the Frank-Starling mechanism, CO under normal unstressed conditions is altered mainly by factors affecting the peripheral circulation and venous return.
Outline the factors affecting heart rate, preload, afterload and contractility
Heart rate is affected by:
Preload is the myocardial sarcomere length just prior to contraction. Surrogate measures of preload are left ventricular end-diastolic pressure or volume. Preload is influenced by:
Afterload is the tension which needs to be generated in cardiac muscle before shortening will occur or the load against which the heart must eject blood. It is equal to ventricular wall stress which can be described by the law of Laplace where ventricular wall stress = ventricular transmural pressure x radius divided by 2 x wall thickness. Therefore, afterload is determined by these components:
Contractility is the intrinsic ability of myocardial fibres to shorten. It is influenced by the amount of intracellular calcium, with increased intra-cellular calcium causing increased inotropy. Determinants include:
List the cardiovascular effects of a sudden increase in afterload
Briefly outline the
determinants of myocardial oxygen demand
Normal myocardial oxygen consumption is high at approximately 8-10mls/100g/minute. In the last episode, we discussed the fact that the heart has a high oxygen extraction ratio and the mechanisms by which it regulates blood flow to facilitate oxygen demand.
The three major determinants of myocardial oxygen consumption are:
Minor determinants of oxygen demand are