Cardiac Contractility Lecture Handout PDF
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Uploaded by FoolproofWilliamsite
University of St Andrews
Dr Alun Hughes
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Summary
This document presents a lecture overview of cardiac contractility and the events of the cardiac cycle, complete with diagrams of the heart and its components. Key learning outcomes include understanding force production, electrical activity timings, and interpreting pressure and volume diagrams. Focuses on the cardiovascular function of the heart.
Full Transcript
Learning outcomes To explain how force is produced in cardiac muscle, how it differs from skeletal muscle and how it can be influenced by the extrinsic sympathetic nerves. To relate the timings of the electrical activity of the heart to the resulting mechanical events of the cardiac cycle. To interp...
Learning outcomes To explain how force is produced in cardiac muscle, how it differs from skeletal muscle and how it can be influenced by the extrinsic sympathetic nerves. To relate the timings of the electrical activity of the heart to the resulting mechanical events of the cardiac cycle. To interpret cardiac volume/pressure diagrams and state how they differ between the left and right sides of the heart. 3. Cardiac contractility and the events of the cardiac cycle MD3001 Dr Alun Hughes 2 Cardiovascular physiology 1) 2) 3) 4) 5) 6) 7) 8) 9) Circulation of blood Physiological properties of the heart Cardiac contractility and the cardiac cycle Control of cardiac output Vasculature Microcirculation Control of blood pressure Control of blood volume Exercise and blood flow through special regions 3 Lecture overview Excitation/contraction coupling ANS effects on contractility Refractory period Events of the cardiac cycle 4 Contraction of cardiac muscle AP causes L-type dihydropyridine channels to open – Large influx of [Ca2+]e • only ~10% contributes to contraction – Cardiac muscle T-tubules 5x greater in diameter than sk. muscle (25x more volume) – Cardiac T-tubule mucopolysaccharides sequester Ca2+ DHP activation causes release of Ca2+ from sarcoplasmic reticulum via ryanodine release channels At res<ng heart rates, ↑[Ca2+]i due to influx and sarcoplasmic release is insufficient to cause maximal contractile force. Contraction of cardiac muscle Guyton p104 12th Ed P113 13th Ed Contraction of cardiac muscle Guyton p104 12th ed P113 13th ed ANS stimulation and contractility Sympathetic innervation – Throughout entire heart – Positive inotropic effect Noradrenaline on β1 receptors – ↑[cAMP]i – Enhances Ca2+ influx – Promotes storage and release of Ca2+ from sarcoplasmic stores – ↑ contrac<lity – ↑ speed of relaxa<on Parasympathetic innervation – Mostly to SA node – Innervates atria – Main effect is ↓ rate Refractory period of the heart Cardiac twitches involve all fibers of the myocardium Can not significantly summate contractions of cardiac muscle Refractory period due to inactivation of Na+ channels Skeletal muscle – Absolute refractory period 1-2ms – Period of contraction 20-100ms Cardiac muscle – – – – Absolute refractory period (ARP) ~245ms Relative refractory period (RRP) Period of supranormal excitability (SNP) Period of contraction 250ms Refractory period of the heart Guyton 12th ed. p103., 13th ed. p112 The heart as a pump Guyton p101 12th ed, p109 13th ed 11 Guyton p105 12th ed P114 13th ed Guyton p105 12th ed P114 13th ed Guyton p105 12th ed P114 13th ed Guyton p105 12th ed P114 13th ed Cardiac cycle Diastole – Period of relaxation Systole – Period of contraction Atria as primer pumps – ~80% of ventricular filling is passive due to normal blood flow – Atrial contraction ‘tops up’ remaining ~20% volume Ventricles as pumps – Isovolumic (isometric) period of contraction – Period of rapid ejection (1/3) when 70% of stroke volume ejected – Period of slow ejection (2/3) when remaining 30% ejected – Isovolumic (isometric) period of relaxation Blood pressure Blood pressure in the arteries oscillates Systolic blood pressure in the aorta – ~120 mmHg Diastolic blood pressure in the aorta – ~80 mmHg Pressure in pulmonary circulation is much lower – Much less resistance to flow – Right side of heart needs to do less work – Right ventricle walls contain less muscle mass Pulmonary systolic pressure – ~30 mmHg Pulmonary diastolic pressure – ~12 mmHg Cardiac output End systolic volume (ESV) Volume in ventricle at the end of systole End diastolic volume (EDV) Volume in ventricle at the end of diastole Stroke volume (SV) EDV-ESV. Quantity of blood expelled per beat (L) Cardiac output (CO) SV x HR. Volume of blood pumped by the heart (L/min) Guyton p109 12th ed, p118 13th ed. Main points Calcium handling in cardiac muscle allows for modulation of contractility The refractory period of cardiac muscle prevents tetany from occurring The heart functions as a pulsatile pump that produces oscillations in pressure CO is HR x SV 19 Learning outcomes To explain how force is produced in cardiac muscle, how it differs from skeletal muscle and how it can be influenced by the extrinsic sympathetic nerves. To relate the timings of the electrical activity of the heart to the resulting mechanical events of the cardiac cycle. To interpret cardiac volume/pressure diagrams and state how they differ between the left and right sides of the heart.