Cardiac Physiology PDF - UM1011

Cardiac physiology UM1011 Dr Kathryn Taylor Lesson plan Review of heart structure and function Outline of how the heart is controlled (hormonal and neural influences) The pathway of the electrical activity in the heart...

Cardiac physiology UM1011 Dr Kathryn Taylor Lesson plan Review of heart structure and function Outline of how the heart is controlled (hormonal and neural influences) The pathway of the electrical activity in the heart Pressure and flow changes in the heart and circulation throughout a cardiac cycle The Cardiovascular System The heart: a dual pump within one organ. Each side has an atrium and ventricle The heart pumps from low pressure veins to high pressure arteries The output of right ventricle enters Pulmonary artery The output of left ventricle enters Aorta Output is under intrinsic control; can be extrinsically regulated by autonomic nerves and circulating hormones Blood pressure in the pulmonary circuit is approximately 28/8 mmHg Blood pressure in the systemic circuit is approximately 120/80mm Hg Guyton and Hall (2010) textbook of Medical Physiology p101 Using the numbers on this diagram see if you can put the correct sequence of events to the number from the 8 statements at the side Venous return to the right atrium Blood is ejected from the left ventricle into the aorta Blood is ejected from the right ventricle into the pulmonary artery. Blood flow from the lungs is returned to the heart via the pulmonary vein Mixed venous blood fills the right ventricle Blood flow from the organs is collected in the veins. Cardiac output is distributed among various organs Oxygenated blood fills the left ventricle - Heart Valves and Circulation of Blood Copyright © 2014 John Wiley & Sons, Inc. All rights reserved.  Duration of Atrial and Ventricular Diastole and Systole DOI: (10.1152/advan.00059.2019) Why do we need to understand the cardiac cycle? Heart failure by definition is: ‘The pathological state in which the heart is unable to pump blood at a rate required by metabolizing tissues or can do so only with an elevated filling pressure’. In adults it most frequently results from inability of the left ventricle to: Fill – Diastolic performance Eject blood – Systolic performance Heart Fail Clin. 2008 Jan; 4(1): 1–11  What is the Cardiac Cycle? The cardiac cycle can be described as a coordinated sequence of electrical and mechanical events occurring from the start of one heartbeat to the start of the next A single cardiac cycle includes a complete relaxation and contraction of both atria and ventricles Relaxation phase - DIASTOLE Contraction phase- SYSTOLE Changes in Pressure and Volume A series of pressure changes take place within the heart during the cardiac cycle that result in movement of blood through different chambers of the heart and body. Valves within the heart direct movement of blood Pressure changes are brought about by conductive electrochemical changes within the myocardium that result in contraction of cardiac muscle Conduction system of the heart  Sequence of Sequence of in cardiac depolarization depolarization in tissue cardiac tissue Cardiac Electrophysiology and the Electrocardiogram Cardiac Electrophysiology Lederer, and the W. Jonathan, Medical Physiology, Chapter Electrocardiogram 21, 483-506.e1 Lederer, W. Jonathan, Medical Physiology, Sequence Chapter of depolarization in 21, 483-506.e1 cardiac tissue. Sequence of © Copyright depolarization in©cardiac tissue. 2017 Copyright 2017 by Elsevier, Inc. All rights reserved. Copyright © 2017 Copyright © 2017 by Elsevier, Inc. All rights reserved.  Atrial contraction (mitral valve closes) Ventricular isovolumetric contraction—occurs when both valves are closed (aortic valve opens) Rapid ventricular ejection Slow ventricular ejection (aortic valve closes) Phases of the Ventricular isovolumetric relaxation occurs when both valves are closed (mitral valve opens) cardiac cycle Ventricular filling Diastasis Chambers and valves of the heart. A, During atrial contraction cardiac muscle in the atrial wall contracts, forcing blood through the atrioventricular (AV) valves and into the ventricles. B, Ventricular contraction Bottom illustration shows superior view of all four valves. PATTON, KEVIN T., PhD, Anatomy and Physiology, Adapted International Edition, 28, 637-664 PAPATTON, Copyright © KEVIN 2019 ©T., PhD, 2019, Anatomy Elsevier and Limited. All rights reserved. Physiology, Adapted International Edition, 28, 637-664 Copyright © 2019 © 2019, Elsevier Limited. All rights reserved. TTON, KEVIN T., PhD, Anatomy and Physiology, Adapted International Wiggers diagram shows relationship of pressure and volume over time Syncitial interconnecting cardiac muscle  Conduction in the heart – cardiac muscle Intercalated discs link muscle cells together and contain desmosomes and gap junctions Desmosomes hold the muscle cells together tightly Gap junctions allow passage of action potentials from one cell to the next, very quickly – allows the cardiac muscle to function together as a syncytium Physiology of Cardiac Muscle Cardiac tissue has distinctive electrical characteristics Intercalated discs allow action potentials to pass to adjacent cells Myocardial cells can spontaneously depolarize- Automaticity Spontaneous depolarization generates a pacemaker potential Cardiac muscle as a Syncytium Heart composed of two syncytiums Atrial : constitutes the walls of the two atria Ventricular: walls of the two ventricles Atria separated from ventricles by fibrous tissue that surrounds the two atrio- ventricular valve openings What do you think the importance of this fibrous tissue is? The fibrous tissue that seats the cardiac valve lacks gap junctions and electrically isolates atria from ventricles: provides a border The action potential 1. Phases of the cardiac action potential are associated with changes in cell membrane permeability, mainly by Na + , K + , and Ca ++ ions. 2..Changes in cell membrane permeability alter the rate of movement of these ions across the membrane and thereby change the membrane voltage (V m ). 3. These changes in permeability are accomplished by the opening and closing of ion channels that are specific for individual ions.  PATTON, KEVIN T., PhD, Anatomy and Physiology, Adapted International Edition, 28, 637-664 Copyright © 2019 © 2019, Elsevier Limited. All rights reserved. Physiology Conti, C. Richard, MD, MACC, FESC, FAHA, Netter Collection of Medical Illustrations: Cardiovascular System, Section 2, 19-48 Copyright © 2014 Copyright © 2014 by Saunders, an imprint of Elsevier Inc. Electrophysiology Cells have a Resting potential : due to distribution of ions across the cell membrane The resting potential is negative inside the cell relative to the outside Ions that are contribute to the membrane potential are Na+ K+ Ca++ Transmembrane The is the electrical potential difference (voltage) between the inside and the outside potential (TMP) of a cell. When there is a net movement of +ve ions into a cell, the TMP becomes more +ve, and when there is a net movement of +ve ions out of a cell, TMP becomes more –ve. Ion channels Two main forces drive ions across cell membranes: Chemical potential: an ion will move down its concentration gradient. Electrical potential: an ion will move away from ions/molecules of like charge. Ion channels help maintain ionic concentration gradients and charge differentials between the inside and outside of the cardiomyocytes. Ionic Conductance Ionic movements or conductances across the myocardial membrane occur in response to the electrochemical potential gradient and are controlled by selective ion permeability Properties of cardiac ion channels Selectivity: they are only permeable to a single type of ion based on their physical configuration. Voltage-sensitive gating: a specific TMP range is required for a particular channel to be in open configuration; at all TMPs outside this range, the channel will be closed and impermeable to ions. Therefore, specific channels open and close as the TMP changes during cell depolarization and repolarization, allowing the passage of different ions at different times. Time-dependence: some ion channels (importantly, fast Na+ channels) are configured to close a fraction of a second after opening; they cannot be opened again until the TMP is back to resting levels, thereby preventing further excessive influx. Cardiac pacemakers The cells of the SAN depolarise over time, with movement of ions causing the resting membrane potential to gradually decrease (pacemaker potential) Once the membrane potential exceeds a threshold, an action potential is triggered This happens automatically every 0.8 seconds (approx.) at rest Although the SAN generates its own action The cells of the AVN do the same, but potentials, it can be influenced by sympathetic more slowly; the result of this is that an and parasympathetic nerves to do this faster or action potential is triggered in the AVN more slowly cells before they depolarise enough to trigger their own Excitation Contraction coupling Excitation-contraction coupling represents the process by which an electrical action potential leads to contraction of cardiac muscle cells. This is achieved by converting a chemical signal into mechanical energy via the action of contractile proteins. Calcium is the crucial mediator that couples electrical excitation to physical contraction by cycling in and out of the myocyte’s cytosol during each action potential. Pacemaker potentials At a membrane potential of about -60mV, ‘funny channels’ open in the SAN cell membrane Sodium enters the cell through the ‘funny channels’, taking a positive charge into the cell The inside of the cell becomes less negative in relation to the outside A type of voltage – gated calcium channels open, and calcium enters the cell slowly The cell continues to depolarise gradually (pacemaker potential) When the threshold is reached, another type of voltage- gated calcium channels opens and calcium enters the cell rapidly this results in rapid depolarisation – the cardiac action potential Pacemaker Action Potentials : Channels Membrane potential drifts towards threshold on its own Funny channels – voltage gated , Na+ enters cell, depolarizES Transient –type T- type Ca++ channels open briefly at low depolarization, -50mV- Long lasting – open at a threshold of -40 – Ca++ enters cell, full deplolarisation Repolarisation is due to K+ Voltage gated K+channels Open at peak, 10 mV , K+ leaves the cell- Repolarisation Cardiac action potential Action potential of cardiac muscles  The initial influx of Ca2+ into myocytes through L-type Ca2+ channels during phase 2 of the action potential is insufficient to trigger contraction of myofibrils. This signal is amplified by the CICR mechanism, which triggers much greater release of Ca2+ from the sarcoplasmic reticulum. Calcium The cell membrane of cardiomyocytes, called sarcolemma, contains invaginations (T-tubules) that induced bring L-type Ca2+ channels into close contact with ryanodine receptors, specialized Ca2+ release receptors in the sarcoplasmic reticulum (SR). calcium release When Ca2+ enters the cells through L-type channels, ryanodine receptors change conformation and induce a larger release of Ca2+ from abundant SR stores. Large levels of intracellular Ca2+ act on tropomyosin complexes to induce myocyte contraction. Calcium–induced calcium release  Introduction 1901- Dutch Physiologist –William Einthoven developed a galvanometer to show that a tracing can be produced as ACTION POTENTIALS spread between negatively and positively charged electrodes. 3 rd electrode – ground current He demonstrated how tracings varied according to the location of positive and negative electrodes- 3 angles or leads with heart in the middle- EINTHOVENS TRIANGLE Einthoven's Triangle is a useful imaginary triangle spanning the trunk which can quickly give an idea about which lead will best show certain electrical activity. http://ahajournals.org by on October 13, 2020  Conduction and ECG As action potentials travel through the heart The ECG is an electrical trace resulting from action potentials in muscle, the produce electrical currents that can all the heart muscle fibres be detected using electrodes on the body surface The trace varies depending on: a) The direction of travel b) Whether the cells are depolarising or repolarising c) The size of the change in potential ECG unlabelled  Events of the cardiac cycle Becker DE. Fundamentals of electrocardiography interpretation. Anesth Prog. 2006;53(2):53-64. doi:10.2344/0003-3006(2006)53[53:FOEI]2.0.CO;2  A vector is a physical quantity having both magnitude and direction in space During an action potential movement of Electrical electrically charged particles generates an electrical vector Vectors Depolarization propagates through the myocardium creating small deplolarizing wave fronts – the average at any one time represents the main electrical vector- that is the average direction of the impulse The ECG therefore represents the electrical vectors of the cardiac cycle.  The baseline of the ECG is the isoelectric line and denotes resting membrane potential P wave represents depolarization of the atrial muscle cells- it does not represent contraction of the muscle or firing of the SA node – P wave We assume that the SA node fires at the start of the P wave and atrial contraction begins at the peak of the P wave. Atrial repolarization is too minor in amplitude to be recorded by surface electrodes.  QRS represents depolarization of ventricular muscle Q – Initial downward deflection R –initial upward deflection S- downward deflection and return to QRS Complex baseline- isoelectric point Contraction commences at PEAK of the R portion of the complex In contrast to Atrial contraction this can be confirmed clinically by palpating a pulse  PR interval Measured from the beginning of the P wave to the beginning of the R portion of the QRS complex PR interval starts with atrial muscle depolarization ends with the start of ventricular depolarization –it is assumed that the impulse passes through the AV node into the ventricle during this interval Used to determine if impulse conduction from the atria to ventricles is normal So a prolonged PR interval may suggest AV block is present  PR Segment The flat line between the end of the P wave and the onset of the QR complex is the PR segment- it reflects the slow impulse conduction through the AV node. The PR segment serves as a baseline – reference line or isoelectric line of the ECG TRACE. The amplitude of and deflection /wave is measured using the PR segment as the baseline. Cardiac volumes End diastolic volume (EDV) – volume of blood in the ventricles at the end of diastole: approx. 130ml at rest End systolic volume (ESV) – volume of blood in the ventricles at the end of systole : approx. 60ml at rest Stroke volume (SV) amount of blood ejected from the ventricles in one beat SV = EDV - ESV Cardiac output Cardiac = Stroke x heart Mild exercise Output volume rate Typical SV = 100ml Typical HR = 100bpm Cardiac output = 10Lmin-1 Moderate exercise Typical SV = 130ml Typical HR = 150bpm Cardiac output = 19.5Lmin-1  Regulation of Stroke Volume The more the heart fills Venous return is increased with blood, the more during physical activity due to Preload (the extent of the muscle is stretched the skeletal muscle pump stretch of the heart muscle) If the artery walls are stiff e.g. The higher the arterial due to aging, then they stretch Afterload (the pressure pressure, the lower the less when blood is pumped into against which the heart need stroke volume them, increasing pressure and to pump, to expel blood) afterload The more forcefully the Inotropic agents such as Contractility (the ability of muscle contracts, the adrenalin , and the influence of the muscle to produce a more blood is expelled the sympathetic nervous system force) increase contractility Frank –Starling mechanism Force of contraction is proportional to the INITIAL fibre length in diastole So : an increase in blood returning to the heart increases End Diastolic Volume- which causes ‘extra” stretching – this causes an increase in the next contraction The heart will pump out whatever volume it receives ( within limits) Physiological basis of Starlings Law Increased stretch of ventricular muscle results in increased overlap of actin and myosin filaments so that a greater number of cross bridges are formed Length tension relationship states that there is an optimal sarcomere length for maximum contraction Increased stretch increases the sensitivity of the contractile proteins to Ca++ Intracellular calcium required to generate 50 % max tension is lower when muscle fibre is stretched Why is Frank-Starling effect important? Allows the heart to adapt its pumping capacity to changes in venous return and to changes in arterial blood pressure Helps to match the output of right and left sides of the heart Neural control of the heart rate Neural control of the heart is regulated by sympathetic and parasympathetic divisions of the autonomic nervous system, both opposing each other to maintain cardiac homeostasis by regulating : heart rate (HR), conduction velocity, force of contraction, and coronary blood flow Sympathetic hyperactivity and diminished parasympathetic activity are the characteristic features of many cardiovascular disease states including hypertension, myocardial ischemia, and arrhythmias that result in heart failure (HF) Effect of sympathetic and parasympathetic stimulation on the sinoatrial (SA) node action potential. A, The normal firing pattern of the SA node is shown. B, Sympathetic stimulation increases the rate of phase 4 depolarization and increases the The effects of the autonomic nervous system on - the heart are called Chronotrophic effects. Positive chronotrophic effects are increases in heart rate- most important example is sympathetic nervous system – Norephinephrine released from sympathetic nerve fibres activates Beta 1 receptors in the SA node, activation of the Beta 1 receptors in the SA node produces an increase in the Na funny channels this increases the rate of phase 4 depolarization. In addition, there is an increase in intracellular Ca2+ channels so that less depolarization is required to reach threshold so more action potentials are fired – increasing the heart rate. Negative Chronotrophic effects- decrease heart rate- Acetycholne released from parasympathetic nerve fibres activate Muscarinic receptors in the SA node. This has 2 effects to decrease the heart rate. Costanzo, Linda S., PhD, Physiology, Chapter 4, 117-188  Neural factors affecting the heart Resting HR is about 70bpm (reduced from about 100bpm by ‘vagal tone’ The sympathetic NS increases both heart rate and contractility The parasympathetic NS decreases heart rate but has little effect on contractility Effects of autonomic NS on pacemaker cells Parasympathetic NS (slows heart rate) Sympathetic NS (increases heart rate) Decreases rate of influx of Na+ through the funny ØIncreases rate of influx of channels, and slow Ca2+ Na+ and Ca2+ influx This means it takes longer for the pacemaker ØThis means that pacemaker potential to reach the potentials develop quickly, threshold for an action so cardiac action potentials potential happen more quickly  Decreased sympathetic/increased Cardiovascular control parasympathetic activity centre Baroreceptors (carotid artery) Heart muscle and SAN Increased blood Stimulus reduced pressure Reduced heart rate (and stroke volume)  Increased sympathetic/decreased Cardiovascular control parasympathetic activity centre Chemoreceptors (carotid body) Heart muscle and SAN Increased PCO2 and/or Stimulus reduced decreased PO2 Increased heart rate and stroke volume Systemic hypertension represents the pressure of the blood as it moves through the arterial system. BP = CO x SVR. BP is determined by CO (HRXSV) and the resistance the blood encounters as it moves through the arterial system. Systolic BP is largely determined by characteristics of SV being ejected by the heart and the ability of aorta to stretch to accommodate the SV Diastolic pressure is determined by the energy that is stored in the elasticity of fibres that are stretched during systole  Elastic tissue in blood vessel walls is stretched when blood is pushed into the vessels The elasticity ‘absorbs’ the pressure, preventing a very sharp rise in pressure in the vessel (which would happen if the vessel wall was less elastic) Elastic tissue Between heart beats, the elastic tissue recoils, putting continuous pressure on the blood inside the vessels and thus continuous blood flow Without the elastic recoil, pressure would fall dramatically between beats, as would blood flow Elastic arteries (Windkessel vessels) The heart is pumping the blood intermittently. However, the blood flow in the aorta is continuous. This effect is called Windkessel’s effect. Elastic arteries are called Windkessel’s vessels because of their abundant elastic tissue. Systemic Blood pressure Note TA - total cross-sectional area of the vessels RR - relative resistance Blood Pressure Blood pressure is regulated by A baroreceptor reflex; is regulated by stretch –sensitive sensory nerve root endings located in the carotid sinuses and aortic arch. Autonomic and As arterial pressure rises the rate of firing of these neurons increases, causing a decrease in heart rate and arterial hormonal pressure This is the primary mechanism for blood pressure in an mechanisms acute setting and acts as the buffer in changes to posture and acute changes in blood volume. If blood pressure remains elevated it can reset or downregulation the reflex to a higher setpoint Long term blood pressure is maintained mainly through the Renin-angiotensin- aldosterone mechanism. Vasoconstriction Vasodilation Contraction of smooth muscle in the relaxation of smooth muscle in the vessel walls, also precapillary vessel walls, also precapillary sphincters in arterioles sphincters in arterioles Causes narrowing of the diameter of Causes widening of the diameter of the the blood vessel blood vessel Caused by sympathetic nerve activity Caused by withdrawal of sympathetic and the hormone angiotensin II nerve activity and locally released chemicals e.g. nitrous oxide and lactic Increases the resistance of blood acid vessels to blood flow decreases the resistance of blood vessels to blood flow  Arterioles play a major role in the control of blood flow to organs or tissues. The constriction of arterioles increases the resistance and decreases Arterioles the blood flow while dilation of arterioles decreases the resistance (Resistant and increases the blood flow. vessels) Thus, blood flow is primarily regulated by altering the radius of arterioles. According to Poiseuille’s law, the rate of flow is proportional to the fourth power of the radius, i.e. r^4. Control of blood flow to the organs Arterial Blood pressure and age § Arterial pressure is the product of cardiac output and peripheral resistance. § It is affected by conditions that affect either or both of these factors. § There is general agreement that blood pressure rises with advancing age, § but the magnitude of this rise is uncertain because hypertension is a common disease and its incidence also increases with advancing age. Control of Blood Pressure Regulation of blood pressure by sympathetic system activation. Citation: Chapter 13 Systemic Arterial Hypertension and Antihypertensive Drugs, Elmoselhi A. Cardiology: An Integrated Approach; 2017. Available at: https://accessmedicine.mhmedical.com/content.aspx?sectionid=171661773&bookid=2224 Accessed: November 17, 2020 Copyright © 2020 McGraw-Hill Education. All rights reserved  Age-related changes Main change with age is increased stiffness of large arteries due to arteriosclerotic lesions and calcification Decreased baroreceptor sensitivity Less well understood and Increased responsiveness to sympathetic nervous system activity very variable Alteration in RAA system relationships  Essential / idiopathic hypertension- 95% of all cases A modifiable risk factor for Cardiovascular Disease No single hypothesis- some studies suggest early elevations in blood volume and cardiac output early in life might initiate increased resistance in in the systemic vasculature. All forms involve haemodynamic mechanisms- an increase in cardiac output and/or peripheral vascular resistance, enhanced sympathetic nervous system activity, kidney function in terms of salt /Na and water balance. In chronic hypertension Cardiac output and blood volume are often normal, the hypertension therefore is Hypertension sustained by an elevation of the systemic vascular resistance rather than by increase in cardiac output. This increased output is caused by a thickening in vascular walls and lumen. There is evidence to suggest changes in vascular endothelial function may cause increases in vascular tone, e.g. in hypertensive patients endothelium produces less NO and the smooth muscle has decreased sensitivity to NO. Dysfuntional endothelium due to enhanced oxygen free radical and decreased NO bioavailabilty also seen in hyperinsulinaemia and Hyperglycaemia in Type 2 Diabetes.  Secondary hypertension; 5-10 % of all cases , Has an identifiable cause; Among the most common causes are kidney disease. i.e. renovascular hypertension, adrenal cortical disorders, pheochromocytomia Anatomic considerations, coarction, narrowing of the aorta or chronic changes in vascular structure i.e. vascular hypertrophy Effects of hypertension on the body Stroke due to brain haemorrhage Damage to capillaries in the eye, eyesight damage oedema Left ventricular hypertrophy (heart muscle becomes enlarged and stiffened) resulting in reduced pumping ability of the heart – heart failure Damage to kidney blood vessels – renal failure Injury to artery walls precipitating atherosclerosis  Excess salt consumption Risk factors Overweight/obesity Alcohol consumption Inactivity Modifiable Smoking Essential hypertension Age Race Genetic factors Unmodifiable Renal disease Secondary Excess aldosterone Hypertension Phaeochromocytoma Other disorders  The response to injury hypothesis states that the initial event in the pathogenesis of atherosclerosis is injury to the epithelium. A variety of Injurious agents produce an Atherosclerosis; inflammatory response in which leucocytes, primarily monocytes, migrate to the area of Response to injury injury. hypothesis The result is retention and oxidation of lipoproteins and transformation of monocytes into macrophages that ingest lipid, particularly oxidized low density lipoproteins (LDL). These form the fatty streak that is an early sign of atherosclerosis but not the first. Atherosclerosis Ischaemic heart disease Peripheral Cerebro- Athero- arterial vascular disease scelerosis disease Reno- vascular disease Formation of an atherosclerotic plaque Heterogeneity of atherosclerotic plaques. Cross-section of a coronary artery cut just distal to a bifurcation. The plaque to the left (circumflex branch) is fibrotic with a dense calcification, whereas the plaque to the right (marginal branch) contains a large lipid-rich necrotic core covered by a thin fibrous cap that is disrupted with mural thrombosis. The lumen contains contrast medium injected postmortem. Trichrome, staining collagen blue and thrombus red. Citation: CHAPTER 32 ATHEROTHROMBOSIS: DISEASE BURDEN, ACTIVITY, AND VULNERABILITY, Fuster V, Harrington RA, Narula J, Eapen ZJ. Hurst's The Heart, 14e; 2017. Available at: https://accessmedicine.mhmedical.com/content.aspx?bookid=2046&sectionid=176555141 Accessed: October 07, 2020 Copyright © 2020 McGraw-Hill Education. All rights reserved http://wwwf.imperial.ac.uk/~ajm8/BioFluids/Pictures/ Atherosclerosis development Injury to vascular endothelium caused by inflammation or physical stress Lipoprotein deposition – low density lipoprotein (LDL) is deposited on the endothelium, of damage blood vessels where it is oxidised. The modified LDL enters the tunica intima of the artery and is ingested by macrophages, which then become lipid-filled foam cells and cause a ‘fatty streak’ in the arterial wall, which increases in size and starts to narrow the artery Inflammatory reaction: The modified LDL acts as an antigenic and attracts inflammatory cells into the arterial wall. Inflammatory mediators are released and attract more lymphocytes to the area Cap formation: Smooth muscle cells migrate to the surface of the plaque creating a “fibrous cap”. When this cap is thick, the plaque is stable, however thin capped atherosclerotic plaques are thought to be more prone to rupture or erosion causing thrombosis. The Plaque may become calcified and hard. Learning Objectives Outline the physiological mechanism of contraction of the heart, the actions of the papillary muscles and cardiac valves Explain the role of the hormonal and nervous system on cardiac output explaining the function of individual structures Identify the role of the heart in body fluid dynamics, contrast systemic and pulmonary circulations and describe the electrophysiology of cardiac muscle and its regulation Outline the causes and physiological basis of hypertension and its consequences for health