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The Heart
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Location Heart Rests on diaphragm situated in mediastinum
Two thirds lies to left of midline
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Pericardium Heart enclosed and held in place by pericardium
Two layers: Outer fibrous layer Attached to diaphragm Prevents overstretching Inner serous layer Outer parietal layer Fused to fibrous pericardium visceral layer (epicardium) Attached to surface of heart Pericardial cavity filled with fluid reduces friction.
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Heart wall Heart wall has three layers:
epicardium (visceral layer of serous pericardium) myocardium (cardiac muscle tissue) Bulk of heart tissue Provides pumping action Endocardium Continuous with endothelial lining of blood vessels
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Heart chambers - Atria Right atrium receives blood from
Superior vena cava Inferior vena cava Coronary sinus passes blood into right ventricle via tricuspid valve Left atrium receives blood from: pulmonary veins passes blood into right ventricle via bicuspid valve
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Heart chambers - ventricles
Right ventricle Passes blood through pulmonary valve into pulmonary trunk Left ventricle Passes blood through aortic valve into ascending aorta
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Myocardial function Thickness of myocardium varies between chambers according to function Atria deliver blood to ventricles thin walled Right ventricle pumps blood short distance to lungs against low resistance Relatively thin wall Left ventricle Pumps blood to all tissues except lungs against high resistance Thick wall
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Atrio-ventricular valves
tricuspid valve right side bicuspid valve left side Valve eversion prevented by: Chordae tendinae Papillary muscles
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Semilunar valves Semilunar valves
prevent blood flow back into ventricles Made up of three crescent-moon shaped cusps right ventricle pulmonary semilunar valve left ventricle aortic semilunar valve
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Systemic circulation Systemic circulation
Oxygen-rich blood enters ascending aorta from left ventricle Divides into progressively smaller arteries Arterioles Capillaries EXCHANGE IN TISSUES Venules Veins Empty into right atrium
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Pulmonary circulation
Blood enters pulmonary trunk Branches into right and left pulmonary arteries Arterioles Capillaries GAS EXCHANGE Venules Pulmonary veins Empty into left atrium
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Coronary circulation Coronary arteries branch from ascending aorta
carry oxygenated blood to the myocardium Pulsatile blood flow Little flow during systole deoxygenated blood returns to the right atrium primarily via the coronary sinus Thin walled vein with no smooth muscle to alter diameter
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Histology of cardiac tissue
Cardiac muscle fibres connected via intercalated discs Contain desmosomes and gap junctions large mitochondrial content same arrangement of contractile protein as skeletal muscle small sarcoplasmic reticulum Small intracellular Ca2+ reserve Contract according to sliding filament mechanism
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Conduction system Cardiac muscle can contract without extrinsic stimulation Autorhythmic fibres Act as pacemaker Form conduction system
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Conduction system Components of the hearts conduction system are:
sinoatrial node (pacemaker) Spontaneously depolarise (100 times/min) Rate of depolarisation modified by neurotransmitters from ANS atrioventricular node Spontaneous depolarisation times/min Conduction slows at AV node Delay allows atria time to contract bundle of HIS right and left bundle branches conduction myofibers (Purkinje fibers)
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Cardiac action potential
Action potential occurs in three phases: Depolarisation Resting membrane potential –90mV Moves toward firing threshold Opens voltage-gated sodium channels Close rapidly Plateau Voltage-gated slow Ca2+ channels open in sarcolemma and sarcoplasmic reticulum Balances slow K+ outflow Repolarisation Voltage-gated K+ channels open Voltage-gated slow Ca2+ channels close
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Electrocardiogram Electrocardiogram (ECG)
Composite record of action potentials produced by all heart fibres during one beat P wave - atrial depolarisation QRS complex - ventricular depolarisation atrial repolarisation hidden by QRS complex T wave - ventricular repolarisation
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Cardiac cycle Cardiac cycle All events associated with one heartbeat
Atrial systole Atria contract Contributes ~25ml to ventricles Most blood enters ventricles during ventricular diastole Ventricular systole Ventricles contract Isovolumetric contraction until pressures in pulmonary trunk and aorta overcome Both ventricles eject same volume of blood Relaxation period Atria and ventricles relaxed As ventricular pressure falls below atrial pressure AV valves open and ventricular filling commences With increasing HR relaxation period shortens considerably atrial and ventricular systole only shorten slightly
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Cardiac output Cardiac output
volume of blood ejected by left or right ventricle per minute CO = stroke volume (mL/beat) x heart rate (beats/min) Average CO approx 5.25 L/min (70 mL/beat x 75 beats/min) Similar to total blood volume of ~5 litres (male) Cardiac reserve maximal CO – resting CO
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Stroke volume Stroke volume (SV) depends on:
volume of blood ejected by a ventricle during systole depends on: Preload Degree of stretch prior to contraction Contractility Forcefulness of contraction Afterload Pressure that must be exceeded before ejection of blood from ventricles can occur
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Stroke volume Preload Contractility Afterload
Frank-Starling law of the heart Greater stretch (preload) increases force of contraction Preload proportional to end-diastolic volume (EDV) EDV determined by: Duration of ventricular diastole (filling time) Venous return Frank-Starling law equalises output from both ventricles Contractility Forcefulness of contraction Positive inotropic agents usually increase contractility by promoting Ca2+ inflow Negative inotropic agents usually reduce contractility by blocking Ca2+ channels Afterload Pressure that must be exceeded before ejection of blood from ventricles can occur
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Heart rate Several factors contribute to regulation of heart rate:
(1) Autonomic regulation (medullary CV centre) Receives input from higher brain centres and variety of sensory receptors Proprioceptors Chemoreceptors Baroreceptors Sympathetic output increases heart rate and contractility Parasympathetic impulses decrease heart rate Little effect on contractility does not innervate ventricular myocardioum
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Heart rate Several factors contribute to regulation of heart rate:
(2) Chemical regulation Cardiac activity depressed by Hypoxia Acidosis Alkalosis Hormones Catecholamines and thyroid hormones increase HR and contractility Cations Alterations in balance of K+, Na+ and Ca2+ alter HR and contractility
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Heart rate Several factors contribute to regulation of heart rate:
(3) Other factors Age U shaped curve Gender Female HR higher Physical fitness Resting bradycardia Body temperature Increase causes SA node to discharge more rapidly
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