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CVS Physiology Part 2

Dr Swapnil Pawar December 1, 2019 361


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CARDIOLOGY PHYSIOLOGY

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:

Ventricular Systole:

  • Mechanical
    • Isovolumetric contraction
      • At the beginning of ventricular systole, the atrioventricular valves close, heard as the first heart sound, and the intraventricular pressure rises rapidly. This rise in pressure causes the AV valves to bulge into the atria causing a small rise in atrial pressure which corresponds to the c wave in the CVP trace. Isovolumetric contraction lasts about 50 milliseconds until the pressure in the left and right ventricles exceed the pressure in the aorta which is about 80mmHg, and the pulmonary artery, which is about 10mmHg respectively. This causes opening of the aortic and pulmonary valves which marks the beginning of ventricular ejection. There is no change in the volume of blood within the ventricles during this stage.
    • Ventricular ejection
      • This consists of an early rapid ejection phase lasting around 100miliseconds where about 70% of stroke volume is ejected and a prolonged reduced ejection phase lasting about 150miliseondswhere the remaining 30% is ejected. Intraventricular pressures rise to a maximum of about 120mmHg in the left ventricle and 25mmHg in the right ventricle. Atrial pressure initially reduces to 0 during rapid ejection as the AV ring is pulled downwards by ventricular contraction. This is seen on the CVP trace as the x descent. Atrial pressure then begins to rise as atrial volume increases and this is seen as the v wave which occurs in late systole/early diastole.
      • Approximately 70-90ml of blood is ejected by each ventricle during each cardiac cycle. There is about 50ml of blood remaining in each ventricle at the end of systole, otherwise known as end-systolic volume.
      • Ventricular ejection ends when the aortic and pulmonary valves close, heard as the second heart sound.
  • Electrochemical
    • The R wave of the ECG occurs at the beginning of an isovolumetric contraction
    • The T wave marks the end of ventricular systole and the start of isovolumetric relaxation
    • Phase 0, 1, 2 and 3 of the cardiac action potential occurs during ventricular systole. Phase 0 caused by the opening of fast sodium channels causes ventricular depolarisation and marks the beginning of ventricular systole. Phase 1, where there is closure of the fast sodium channels and opening of transient outward potassium channels, phase 2 where there is opening of L type calcium channels which is balanced by potassium efflux through delayed rectifier K channels, and phase 3 where there is closure of the L type calcium channels resulting in unopposed potassium efflux and repolarisation. Phase 3 marks the end of ventricular systole and the beginning of ventricular diastole.

Diastole:

  • Mechanical
    • Isovolumetric relaxation
      • This marks the beginning of diastole and occurs after the closure of the aortic and pulmonary valves which is responsible for the dicrotic notch. It lasts 30 – 60 milliseconds
      • The ventricular myocytes relax and the intraventricular pressure reduces rapidly but both the semilunar and atrioventricular valves are closed, meaning the volume within the ventricles remains constant.
      • Atrial pressure rises to 2mmHg in the RA and 5mmHg in the LA
    •  Ventricular filling
      • This phase begins when the pressure within the ventricles falls below atrial pressure causing the opening of the AV valves
      • There is a period of rapid filling which lasts for about 100milliseconds and corresponds to the y descent on the CVP trace. This is followed by a slow filling stage or ventricular diastasis lasting 200 milliseconds. During this stage the intraventricular pressure has risen which reduces the pressure gradient between the atria and the ventricles, thus reducing the rate of filling. The final stage is an atrial contraction or atrial systole which lasts about 100 milliseconds and corresponds to the a wave on the CVP trace.
      • During the rapid filling stage, about 75% of ventricular filling occurs, only 5% occurs during ventricular diastasis and about 20% occurs during atrial systole. At the end of diastole, there is approximately 120 – 130ml of blood within the ventricles, otherwise known as the end-diastolic volume.
      • During ventricular filling, atrial pressure is slightly higher than ventricular pressure and aortic and pulmonary pressures decrease as blood moves from the vasculature to the heart. When ventricular pressure rises above atrial pressure the mitral and tricuspid valves close, marking the beginning of ventricular systole.
  • Electrochemical
    • The p wave on the ECG represents atrial depolarisation and corresponds to atrial systole
    • The q wave occurs at the end of ventricular diastole and represents the beginning of ventricular depolarisation
    • Diastole corresponds to phase 4 of the cardiac myocyte action potential which is maintained by inward rectifier K channels in non-pacemaker cells

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:

  • Autonomic influence
    • HR is controlled by the SA node which is heavily influenced by vagal tone. Parasympathetic stimulation decreases heart rate
    • Sympathetic stimulation increases heart rate
  • Hormones such as thyroid hormones and catecholamines: increased levels of which cause the increased heart rate
  • Body temperature: hyperthermia causes the increased heart rate
  • Reflexes:
    • the Bainbridge reflex: increased right atrial pressure causes increased heart rate due to stimulation of atrial stretch receptors
    • The baroreceptor reflex: changes in blood pressure is detected by aortic and carotid baroreceptors, decrease in blood pressure increases sympathetic nerve activity which increases heart rate
  • Age and sex: heart rate is generally faster in females and in babies and slower in males and as age increases
  • Pharmacological: beta-blockers reduce heart rate

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:

  • Venous return
    • The mean systemic filling pressure is the average pressure within the circulation if there was no cardiac activity. The difference between this pressure and right atrial pressure is the gradient for venous return. The normal MSFP is about 7mmHg and increases with increased vasomotor tone or blood volume.
    • Increased venous return increases preload. Therefore, any increase in MSFP such as with increased blood volume, or any decrease in mean right atrial pressure such as with negative intrathoracic pressure, will increase venous return.
  • Heart rate: slower heart rates allow for greater diastolic time and therefore greater preload
  • Atrial contractile force: the atrial kick gives ventricles approximately 20% of their end-diastolic volume. Therefore, loss of this atrial kick such as in atrial fibrillation reduces preload.
  • Ventricular compliance
    • Increased ventricular compliance will increase filling for a given pressure and therefore increase preload
  • Pericardial compliance
    • Decreased compliance such as due to a large effusion will decrease ventricular filling and therefore preload
  • Valvular integrity
    • AV valvular stenosis will reduce ventricular filling and therefore reduce preload

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:

  • Ventricular transmural pressure is the difference between intraventricular pressure and pleural pressure
    • Intraventricular pressure is affected by:
      • Outflow tract impedance: increased impedance such as in aortic or pulmonary stenosis or hypertrophic obstructive cardiac myopathy will increase afterload
      • Pulmonary or systemic vascular resistance which is determined by the modified Hagen-Poiseuille equation where resistance = 8 x viscosity x vessel length divided by pi x vessel radius to the power of 4
        • Any increase in vascular resistance such as with vasoconstriction will increase afterload. Numerous drugs affect afterload by altering vascular resistance.
      • Arterial compliance: any decrease in arterial compliance will increase afterload
    • An increase in pleural pressure such as with positive pressure ventilation will decrease ventricular transmural pressure so decreases left ventricular afterload.
  • As the ventricular radius is increased such as with increased end-diastolic volume or with ventricular dilatation, afterload is increased
  • Ventricular thickness: as ventricular wall thickness increases such as with hypertrophy, afterload decreases

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:

  • Autonomic influences: sympathetic stimulation increases contractility while parasympathetic stimulation decreases contractility
  • Bowditch effect: contractility improves at faster heart rates
  • Anrep effect: myocardial contractility increases with increased afterload
  • Hormonal and metabolic: thyroid hormones, catecholamines, calcium and glucagon increase contractility while hypoxia, acidosis and hyperkalemia decrease contractility
  • Pharmacological: we use numerous drugs in ICU which affect contractility including positive inotropes such as milrinone and negative inotropes such as calcium channel blockers

List the cardiovascular effects of a sudden increase in afterload

  • Initially a decrease in left atrial pressure
  • Increase in end-systolic volume and initially a decrease in stroke volume. However, in a healthy heart, this will then lead to a secondary increase in end-diastolic volume and thus some increase in preload and increased contractility via the Frank-Starling mechanism
  • A small increase in contractility via the Anrep mechanism
  • Cardiac output: may reduce cardiac output depending on the extent of afterload increase and the health of the heart. In the healthy heart, and increase in afterload can usually be compensated for to some extent by increased preload and contractility
  • Ventricular end-systolic and end-diastolic pressure increases
  • Increased myocardial oxygen demand and myocardial work
  • Coronary blood flow: auto-regulated, will increase as it is tightly coupled to oxygen demand and an increased afterload increases oxygen demand
  • Systemic blood pressure: increased
  • Baroreceptors: stretched causing increased firing resulting in inhibition of sympathetic drive and increased vagal tone to reduce blood pressure

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:

  • Myocardial wall stress: as we outlined earlier, myocardial wall stress is determined by the law of Laplace where stress = transmural pressure x radius/ 2 x wall thickness. Increased wall tension increases oxygen demand.
  • Heart rate: increased heart rate increases oxygen demand.
  • Contractility: increased contractility increases oxygen demand

Minor determinants of oxygen demand are

  • Basal metabolism
  • External work performed: this is the energy expended to eject blood from the ventricle, otherwise known as volume work
  • Energy for electrical activation which only requires about 0.7ml oxygen/min/100g of myocardial tissue

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