Physiology of the Heart

PHYSIOLOGY OF THE HEART Measuring pressure and flow • • • • • Total energy within a vessel can be separated into potential energy (pressure) and kinetic energy (flow) in addition to gravity Most potential energy required to overcome resistance and thus flow is proportional to pressure differences o Energy lost in overcoming resistance is lost as heat and (irreversible) A (93) = Potential Energy + Kinetic Energy B (97) = Potential energy – kinetic energy C (95) = Potential Energy o The best indicator of pressure within a chamber Bernoulli’s Principle • • • • • Total energy = kinetic energy of flow + potential energy + heat of overcoming resistance Decreasing diameter will result in increasing velocity → pressure loss due to conversion of potential energy to kinetic energy Similarly kinetic energy is released as diameter increases However even with changes in diameter there will still be a loss of energy due to heat Above the heart, there is a need to overcome gravity which results in decreasing pressure. From below the heart gravity assists and thus there is an increase in pressure. o Increasing pressure results in increasing flow o A minimum pressure is required for flow to exist o A minimum pressure called the critical closing pressure is also required to ensure that vessels do not collapse on themselves o This curve is non-linear in vivo because of: ▪ Auto regulation – renal, cerebral ▪ Vascular Tone ▪ Anomalous Viscosity of Blood Autoregulation – Local/intrinsic mechanism • Renal Blood flow regulates itself through: o Myogenic response: Increasing blood pressure will cause vasoconstriction, decreasing BP will cause vasodilation o Preserving renal blood flow to maintain glomerular filtration etc. o Normally this is essential for balancing pressure and flow however in bad cases it will cause hypertension Myogenic Responsiveness (vascular tone) • Varied by o Local Mechanism (auto regulation) o Circulating hormones o Autonomic nervous system ▪ Increased noradrenaline will cause vasoconstriction Viscosity of Blood • • As haematocrit increases viscosity will also increase, thus decreasing flow Low flow rates will increase adherence of adjacent RBCs to vessel walls which will can increase viscosity further by 10x Cardiac output: matching of venous return and cardiac output Cardiac output (mL/min) = Stroke volume (mL/beat) X Heart rate (beats/min) Stroke Volume = End Diastolic Volume (EDV) – End systolic volume (ESV) • • • Cardiac output is the flow of blood (L/min) pumped by the heart Affected by external factors (neural inputs, circulating hormones, state of arterial and venous circulations) and internal factors (autoregulatory mechanisms, cardiac muscle proteins and calcium) Most importantly: CO is determined by heart rate, preload, afterload and cardiac contractility o Heart rate is the main cause of changes in cardiac output at low-level exercise (e.g. walking). It is controlled by vagal (parasympathetic) and sympathetic nervous inputs to the sinoatrial node (the SA node). As the heart rate increases and the cardiac cycle time shortens, the diastolic filling time shortens more than the systolic ejection time which may reduce cardiac output in patients with impaired ventricular filling. o Stroke Volume is determined by 3 factors: ▪ Preload is the load or stretch on myocardial muscle fibres just before contraction (end diastolic volume). Increasing the EDV increases the cardiac output (Starling’s Law) due an increased length-tension relationship of each sarcomere in the myocardial fibres (particularly in LV). Increased sarcomere length causes increased sensitivity to Ca of the myocardial proteins (particularly troponin C) → increased force of contraction at each AP. ▪ Afterload is the stress of the ventricles to contract during ejection → resistance to flow in the pulmonary and systemic arteries • Increasing afterload reduces the cardiac output ▪ Contractility (or ionotropic state) is the capacity of muscle fibres to contract at any given preload and afterload → determined by the interaction between cytosolic calcium and the cardiac contractile proteins • Influenced by SNS and drugs