Physioex 9 Exercise 6 Notes

PhysioEX notes Autorhythmicity- hearts ability to trigger its own contr swear outs shape O- a lot like depolarization in neuronal action authoritys. Sodium channel open, increase of atomic number 11 INTO stall. variety 1- sodium carry close, potassium channels close, decrease in potassium and sodium. Calcium channels open, increase of calcium into cell. anatomy 2- Plateau phase, tissue layer still depolarized (contract). super acid channels closed, L-type calcium channels stay open. Lasts 0. 2 moments/200 milliseconds.Phase 3- second set of potassium channels open, potassium decrease. Failing tissue layer 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 cardiac pacemaker cells. Total cardiac AP last 0. 25-0. 3 seconds or 250-300 milliseconds Wave Summation- occurs when a senseless heft is stimulated with such frequency that muscle twitches converging and result in a stronger abridgment than a single muscle twitch.When enough of these twitches occur at a frequent score, muscle reaches amalgamated tetanus, or smooth grounds. Individual twitches cannot be distinguished. Tetanus occurs in skeletal muscle because skeletal muscle has a relatively short authoritative opinionated period(a period during which APs cannot be gene investd no matter how strong the stimulus). cardiac muscles has a relatively long refractory perios and is thus incapable of ramble summation. Cardiac muscle is incapable of reacting to any stimulus before gist of phase 3 and will not respond to a common cardiac stimulus efore phase 4. Absolute refractory period- clock time mingled with 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 car diac muscle. Vagus Nerve Stimulation The autonomic nervous system has devil branches charitable- fight or flight parasympathetic- resting and digesting At rest, parasympathetic is more active. Sympathetic is more active when needed, during exercise or confronting danger.Read Renal dust Physiology PhysioexBoth 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 target to heart (cranial nerve X). Excessive vagal stimulation causes heart to choke up 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 thickener is cluster of autorhythimic cardiac cells in right atrium. SA has fastest rate of willing depolarization.Determineds heart rate and is referred to as pacemaker. SA node generates 100 Aps per min ute. Humans be homeothermic- maintaining an cozy dead body temperature at 35. 8 to 38. 2C regardless of outside temperature. When foreign 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.Ringers solution/irrigation- essential electrolytes (chloride, sodium potassium, calcium and magnesium), keeps isolated, intact heart viable. Sympathetic nerve fibers release noradrenaline (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 shorten ing 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 upraise action of ACH. Adrenergic- chemical modifiers that inhibit, mimic or enhance action of epinephrine. If the modifiers whole caboodle 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 inCalcium channel blockers employ 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 ar chronotropic Modifiers that affect force of contraction atomic number 18 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