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Human Phys

Anatomy of the heart

QuestionAnswer
Veins of the heart Left pulmonary artery - to the lungs Lefft pulmonary vein - blood from lungs to left atrium Aorta - over heart from left ventricle, oxygenated blood to body Superior/inferior vena cava - bring deoxygenated blood to heart
Anatomy of heart - muscle that contracts and pumps blood around body - valves ensure one way flow - conduction system: specialised myocytes lose ability to contract - fibrous skeleton
Heart skeleton Collagenous and elastic fibres Concentrated in fibrous rings around the valves Provides structural support Anchors the cardiomyocytes, gives them something to pull against Right AV valve has three cusps Left AV valve has 2 cusps
Heart skeleton Semilunar valves- Pulmonary and aortic valves, cusps are pushed open and closed by changes in pressure as the heart contracts and relaxes Tendinous chords connect the valves to the wall of the heart, to prevent flipping of cusps
Conducting system of the heart 1. SA node generates spontaneous action potentials 2. Action potentials spreads through the conducting system to other heart cells in Atria 3. AV node fires
Conducting system of the heart 4. Subendocardial conducting network distributes excitation through ventricular myocardium - Specialised cardiomyocytes Fibres are large in diameter Fewer myofibrils Contract less forcefully Contains lots of gap junctions AP travel quickly
Conducting system of the heart 5. Rest of ventricular cells activated by cell-to-cell spread of impulse through gap junctions
The heartbeat Organised into bundles that spiral around the heart forming the vortex of the heart When heart contracts produces a twisting motion enhancing the ejection of blood
The heartbeat Beats on average 60-70 times minute at rest Pumps 5L blood Under control of ANS Regulates cardio-activity to meet physiological demand
The heartbeat Spontaneous electrical activity- Autorhythmic Depolarisation/repolarisation the cell membranes causes the heart to contract/relax rhythmically Depolarization: rapid change in membrane potential from –ve to +ve causes the opening of ion channels.
Why does the sa node fire spontaneously? - no resting stabe action potential Membrane potential starts at -60mV and drifts upwards gradually depolarising
Pacemaker and threshold potential PACEMAKER POTENTIAL- due to a inflow of Na+ but no movement of K+ At THRESHOLD POTENTIAL of -40mV, voltage gated Ca2+ channels open, Ca2+ flows in from ECF
Polarisation Membrane is rapidly depolarised- ACTION POTENTIAL K+ channels open and K+ leaves the cell- REPOLARISATION phase of the action potential
Myocardium action potentials Resting potential of -90mV Voltage gated Na+ channels open Rapid depolarisation Na+ channels close at about +30 mV
Myocardium action potentials Ca2+ enters through slow channels prolong depolarisation creating a plateau Ca2+ channels close Ca2+ transported out of the cell. Rapid outflow of K+ returns membrane to resting potential
Parasympathetic control Fibres terminate on SA and AV nodes Reduces rate and force of contraction Mediated via ACETYLCHOLINE This lengthens the interval between pacemaker potentials, hence slowing heart rate
Sympathetic control Fibres terminate on SA and AV nodes Increases heart rate/ strength Dilates coronary arteries: increase blood supply Mediated via NORADRENALINE  Makes the pacemaker potential steeper, hence increasing the heart rate
Heart rates ECGs can see heart rhythm disorders and normal rhythms - tachycardia: fast rhythm - brachycardia: slow rhythm
Heart rates First degree AV node block, it can be a sign of coronary artery disease Indication that there is a blockage somewhere between the AV node and the ventricles
Atropine - anticholinergic - treats brachycardia - inhibits Ach effect on sa node - increases heart rate
Propanolol - beta blockers - treats hbp and irregular heart rates - blocks adrenaline to increase pacemaker firing rate - decreases heart rate
During exercise - heart rate increases Proprioceptors in the muscles and joints transmit signals to the cardiac centres Sympathetic output from the cardiac centres then increases - more blood flow
During exercise Heart rate and stroke volume rises, cardiac output rises which compensates for the venous return Sustained program of exercise causes hypertrophy of the ventricles which increases the stroke volume
During exercise This allows the heart to beat more slowly and still maintain a normal resting cardiac output
The action potentials and the ECG SA node is the primary pacemaker of the heart Cells of the SA node fire spontaneously generating APs that spread through the atria Electrical coupling of neighbouring cells (Gap junctions)
The action potentials and the ECG AP in one cell triggers AP in neighbour Impulses reach AV node AV bundle/ Subendocardial conducting network Ventricles contracts
Composite recording of all the action potentials produced by the nodes and the cells of the myocardium Each waves corresponds to a certain event of the electrical cycle
Cardiac cycle and the ECG - interval 1. P-R SA nodes fires, AP spread across the atrial myocardium atrial systole
Cardiac cycle and the ECG - interval 1. P-R AP reaches AV node. Fibrous skeleton prevents the signals from entering through any other route. The AV node has fewer gap junction (PR interval) allows ventricles to fill up, delay between atrial and ventricular contraction
Cardiac cycle and the ECG - interval 2. Q-T Ventricles contract (ventricular systole) Ventricle pressure increases, forces AV valves shut, blood leaves through semi-lunar valves into aorta and pulmonary trunk.
Cardiac cycle and the ECG - interval 3. T-P Ventricular diastole - T wave, repolarization. All 4 chambers relax. Muscle is electrically silent
Created by: reub8n
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