L4 Cardiac Muscle & Electrical Activity I PDF
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These lecture notes detail cardiac muscle and electrical activity, covering components of the cardiovascular system, the heart's location, pulmonary and systemic circulations, and the cardiac cycle. The notes also discuss cardiac muscle structure, myocardial cells, and excitation-contraction coupling.
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Lecture 04 Cardiac Muscle & Electrical Activity I 1 Components of Cardiovascular System Heart – Muscular pump which creates pressure head to push blood through blood vessels Blood vessels – Conduits which permit blood flow from heart t...
Lecture 04 Cardiac Muscle & Electrical Activity I 1 Components of Cardiovascular System Heart – Muscular pump which creates pressure head to push blood through blood vessels Blood vessels – Conduits which permit blood flow from heart to cells and back to the heart – Arteries, arterioles, capillaries, venules, veins Blood 2 Location of the Heart Located in thoracic cavity – Diaphragm separates abdominal cavity from thoracic cavity Size of fist Weighs approximately 250 – 350 g 3 Pulmonary and Systemic Circulations Pulmonary capillaries – Blood entering lungs = deoxygenated blood – Oxygen diffuses from tissue to blood – Blood leaving lungs = oxygenated blood Systemic capillaries – Blood entering tissues = oxygenated blood – Oxygen diffuses from blood to tissue – Blood leaving tissues = deoxygenated blood 4 5 Cardiac Cycle/Heartbeat Rhythmic contraction and relaxation generates heart pumping action – Contraction pushes blood out of heart into vasculature – Relaxation allows heart to fill with blood Wave of contraction spreads through cardiac muscle 1. Both atria contract as a unit 2. Both ventricles contract as a unit 6 Cardiac Cycle Contraction increases pressure while relaxation decreases pressure – Pressure difference drives blood flow (pressure gradient). Blood moves from area of higher pressure to area of lower pressure Pressure within chambers of heart varies during cardiac cycle – Atrial contraction precedes ventricle contraction – Atrial pressure > ventricular pressure – Blood flows simultaneously from both atria into both ventricles – When ventricles contract, blood flows from ventricles to arteries 7 Cardiac Muscle Contain actin and myosin arranged in sarcomeres similar to skeletal muscle cells – Contract via sliding-filament mechanism Myocardial cells are short, branched and join neighbouring cells to create a complex network Adjacent myocardial cells joined by intercalated discs containing gap junctions 8 Myocardial Cells Gap junctions are fluid filled channels that allow action potentials spread rapidly from cell to cell Therefore, myocardial cells contract almost simultaneously – Cardiac muscle is a syncytium – “All or nothing” property 9 Cardiac Muscle Contraction Contraction of skeletal muscle requires external stimulation by somatic motor nerves Specialized noncontractile myocardial cells, autorhythmic or pacemaker cells are responsible for triggering the contraction of cardiac muscle Cell membranes spontaneously depolarize and generate APs which spread into surrounding contractile myocardial cells 10 Sinoatrial Node Autorhythmic cells are concentrated in the sinoatrial node located in the right atrium near the opening of the superior vena cava Spontaneous depolarizations generated here pass into surrounding myocardial cells and generate contraction as follows: – Atrial myocardial cells – Pause (fibrous layer) – Ventricular myocardial cells – Atrial syncytium & ventricular 11 syncytium Cardiac Conduction System Spontaneous APs generated by the autorhythmic cells in the SA node spread to surrounding atrial contractile myocytes and then spread to the ventricles through the cardiac conduction system 12 Atrial Conduction Impulses spread through atrial fibres at rate of 1 m/sec Specialized fibres, known as Bachmann’s bundle, conduct the impulse from right into left atrium Impulses then spread to the atrioventricular (AV) node 13 Atrioventricular Conduction AV node is located on the base of the right atrium near the interatrial septum – Normally the only route of conduction from atria to ventricles Conduction velocity slows to 0.05 m/sec – This results in a delay between atrial and ventricular excitation/contraction – Permits optimal ventricular filling during atrial contraction 14 Ventricular Conduction AV node conducts to the bundle of His, then to the bundle branches. The bundle branches subdivide into a complex network called the Purkinje fibres. These conduct impulses into both ventricles Conduction velocity is of the range 1 – 4 m/sec in Purkinje fibres. This is due to their large cell size (diameter: 80 mM) compared to myocytes (diameter: 15 mM) 15 Autorhythmic Cells Location of these cells: – 1 Sinoatrial (SA) node in right atrium. Most important location, APs generated here spread over entire cardiac tissue. 70-80 APs/min – 2 Atrioventricular (AV node). Are only generated if SA node is destroyed as rate of firing is slower, 40-60 APs/min – 3 Pacemaker cells are also located in the Purkinje fibres, 30-40 AP/min. Again, APs generated by SA node will normally inhibit autorhythmic activity of these cells Cardiac Action Potentials Two types of action potentials in individual cells in cardiac tissue – Fast response Atrial and ventricular myocytes (contractile and conductive cells) – Slow response autorhythmic cells in sinoatrial (SA) node and atrioventricular (AV) node 17 Cardiac Action Potentials Phase 0: Upstroke Phase 1: Early repolarization Phase 2: Plateau Phase 3: Repolarization Phase 4: Final repolarization ERP: Effective refractory period RRP: Relative refractory period 18 Myocardial Contractile Cells Arrival of AP at a contractile myocardial cell opens voltage- gated Na+ channels (rapid depolarization) Voltage-gated Ca2+ channels also open more slowly At +20 mV, Na+ channels close and K+ channels open; repolarization begins Slow inward diffusion of Ca2+ then balances outward diffusion of K+ plateau phase Ca2+ channels close and K+ channels complete repolarization 19 Fast Response Action Potential K+ K+ K+ Myocardial Cell Contraction Inward movement of extracellular Ca2+ during depolarization also opens Ca2+ channels on the sacroplasmic reticulum – Extracellular Ca2+ is used to initiate contraction in myocardial cells rather than intracellular stores Increase in intracellular [Ca2+] triggers contraction in an identical mechanism to skeletal muscle During repolarization, Ca2+ is transported out of the cell and relaxation occurs 21 Excitation-Contraction Coupling 22 Cardiac Muscle Contraction 23 Skeletal Muscle Contraction A.P. in skeletal muscle cell is fast (20 msec) – No plateau phase Cell has repolarised before associated contraction has begun Cell is responsive to further stimuli during contraction – Summation of contraction (B) – Tetany (C & D) 24 Myocardial Cell Contraction The length of an AP in a myocardial cell (250 msec) is much longer than an AP in a skeletal muscle cell (20 msec) due to plateau phase The duration of the AP is almost as long as the associated contraction Myocardial cells are refractory during almost their entire contraction Summation of contraction cannot occur so tetany in cardiac muscle is also prevented 25 Ca2+ Channels Number of different types in cardiac muscle but the predominant are L-type Ca2+ channels (long-lasting) Opening these channels increases conductance – The large concentration gradient drives the influx of Ca2+ As well as prolonging the action potential, the Ca2+ influx also triggers the contraction of muscle fibres – The greater the influx of Ca2+, the stronger the contraction 26 In the Clinic Ca2+ channel antagonists such as verapamil and diltiazem decrease the duration of the action potential and also diminish the contractility of the myocardial cells Increasing concentrations of diltiazem diminish contractile strength of the heart 27