PhysioEX notes Autorhythmicity- heart’s ability to trigger its own contractions Phase O- a lot like depolarization in neuronal action potentials. Sodium channels open, increase of sodium INTO cell. Phase 1- sodium channels close, potassium channels close, decrease in potassium and sodium. Calcium channels open, increase of calcium into cell. Phase 2- Plateau phase, membrane still depolarized (contract). Potassium channels closed, L-type calcium channels stay open. Lasts 0. 2 seconds/200 milliseconds.
Phase 3- second set of potassium channels open, potassium decrease. Failing membrane potential cause calcium channels to close, calcium decrease to cell. Membrane repolarizes to resting potential. Phase 4- resting membrane potential is reached until next depolarization from neighboring cardiac pacemaker cells. Total cardiac AP last 0. 25-0. 3 seconds or 250-300 milliseconds Wave Summation- occurs when a skeletal muscle is stimulated with such frequency that muscle twitches overlap and result in a stronger contraction than a single muscle twitch.
When enough of these twitches occur at a frequent rate, muscle reaches fused tetanus, or smooth movement. Individual twitches cannot be distinguished. Tetanus occurs in skeletal muscle because skeletal muscle has a relatively short absolute refractory period(a period during which APs cannot be generated no matter how strong the stimulus). Cardiac muscles has a relatively long refractory perios and is thus incapable of wave summation. Cardiac muscle is incapable of reacting to any stimulus before middle of phase 3 and will not respond to a normal cardiac stimulus efore phase 4. Absolute refractory period- time between the beginning of the cardiac AP and middle of phase 3. Relative refractory period- time between absolute refractory period and phase 4. Total refractory period = 200-250 milliseconds. Almost as long as the contraction of the cardiac muscle. Vagus Nerve Stimulation The autonomic nervous system has two branches: Sympathetic- fight or flight Parasympathetic- resting and digesting At rest, parasympathetic is more active. Sympathetic is more active when needed, during exercise or confronting danger.
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Both supply nerve impulses to the heart. Sympathetic stimulation increases rate and force of contraction. Parasympathetic stimulation decreases rate without changing force of contraction. Vagus nerve carries signal to heart (cranial nerve X). Excessive vagal stimulation causes heart to stop beating. Ventricles will start beating after short time. Resumption of heartbeat is called Vagal Escape. Result of sympathetic reflexes or initiation of rhythim by Purkinje fibers. SA node is cluster of autorhythimic cardiac cells in right atrium. SA has fastest rate of spontaneous depolarization.
Determineds heart rate and is referred to as pacemaker. SA node generates 100 Aps per minute. Humans are homeothermic- maintaining an internal body temperature at 35. 8 to 38. 2C regardless of outside temperature. When external temp is elevated, hypothalamus signals heat releasing mechanisms (sweat, vasodilation). In extreme external temperatures, body cannot compensate and hyperthermia (elevated body temperature) or hypothermia(decreased body temperature) occurs. Frog is poikilothermic- internal body temperature changes with external environment temperatures.
Ringer’s solution/irrigation- essential electrolytes (chloride, sodium potassium, calcium and magnesium), keeps isolated, intact heart viable. Sympathetic nerve fibers release norepinephrine (noradrenaline) and epinephrine (adrenaline) at cardiac synapses. Norepinephrine and epinephrine increase frequency of AP by binding to B1 adrenergic receptors embedded in plasma membrane of SA cells. cAMP second messenger mechanism, bing of ligand opens sodium and calcium channels, increasing rate of depolarization and shortening period of repolarization, increasing heart rate.
Parasympathetic NS usually dominates; releases acetylcholine at cardiac synapses. ACH decreases frequency of AP by binding to muscarinic cholinergic receptors in plasmas membrane of SA cells. ACH indirectly opens potassium channels and closes calcium and sodium channels, decreasing rate of depolarization and decreasing heart rate. Cholinergic- chemical modifiers that inhibit, mimic or enhance action of ACH. Adrenergic- chemical modifiers that inhibit, mimic or enhance action of epinephrine. If the modifiers works like a neurotransmitter, it is an agonist.
If the modifier works opposite of a neurotransmitter, it is an antagonist. Resting cell membrane favors movement of potassium more than sodium or calcium. Resting membrane potential is determined by ratio of extracellular and intracellular concentrations of potassium. Phase 0 (rapid depolarization)- sodium moves in Phase 1 (small repolarization) – sodium movement decreases Phase 2 (plateau) – Potassium movement out decreases, Calcium moves in Phase 3 (repolarization)- potassium moves out, calcium movement decreases Phase 4 (resting potential) – potassium moves out, little sodium or calcium moves in
Calcium channel blockers used to treat high BP and abnormal HR. Block calcium movement in all phases of cardiac action potentials. Result- depolarization rate and force of contraction reduced. Modifiers that affect HR are chronotropic Modifiers that affect force of contraction are inotropic. Modifiers that lower HR are negative chronotropic Modifiers that increase HR are positive chronotropic Modifiers that decrease force of contraction are negative inotropic Modifiers that increase force of contraction are positive inotropic
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