BIOL 431 - LEC 3

Intrinsic conduction system ( 1%), Contractile tissue (99%)

specialized cardiac muscle that doesn’t rely on NS for stim, can beat w/o nerve impulse, NS modifys intrinsic pace of heart (stim = increase in HR)

Stable resting membrane (needs stim from NS to fire), 2 sources for Ca2+, contraction is 250msec, refractory is 250msec, function = self excitatory results in pacemaker potential

rely on presence of gap junction for coordination, non contractile tissue ( few myo-filaments actin/myosin, function = Disttributes impulses (AP) throughout heart in orderly & sequential fashion, Starts at atria and moves to ventricles

Found in auto0rythmic cells, results in them being self excitable ( can develop AP without stim), this constant depolarization = pacemaker potential

caused by increased Na permeability, membrane potential hits a certain point (+) = AP generated—> after repolarization Na again begins to leak —> repeats 75x/min at SA node

Na leaks in while K+ usually leak out —> however k efflux is thought to decrease —> upsets charge balance across membrane —> depolarization —> threshold of -40mV reached —> voltage reg fast Ca gates open —> Ca rushes in from exytracellulr fluid —> greater depolarization —-> Ca responsible for final depoliration in auto rhythmic cells only —> repolarization occurs when k moves out.

SA node (sinoatrial node), AV node (atrioventricular Node), Atrioventricular bundle, R & L bundle branches, Purkinje fibers

located in R atrium wall near superior vena cava, uncontrolled rate = 100bpm (fastest depolarization), w/ neuronal and hormonal influence 75 bpm, SA node set rate (pacemaker), This is known as sinus rythm

Once AP produced by SA node spreads over atria via gap junctions along the INTERNODAL pathway and stimulates AV node, Delay AP by 0.1 sec, located at base of interatrial septum, 50 bpm *occurs if AV becomes the pacemaker

From AV node travels down bundle of his, From superior margin of interventricular septum, separates into 2 branches 1/2 way down, Depole rate = 30 bpm

the branching of the bundle of his in the intervenvular septum, travel down toward apex, each cover walls evenly, depole rate = 30 bpm

Emerge from bundle branches, barrel shaped cardiac muscle, enter myocardium @ apex, spread upward within ventricular walls —>passes into cells of myocardium to stim excitation of muscle cells —> AP then spreads via gap junction to neighboring cells —> contraction spreads from apex runs supeiorly in a wave towards atria. **total time for depolarization = 0.22 seconds from SA node to depole of last ventricular muscle cell

stable resting membrane, sliding of filaments is = to skeletal muscle, Once stim by intrinsic conduction system Ca is released causing contraction, *in cardiac muscle Ca channels are in sarcolema (found in extracelulalr fluid (20%)) and sarcoplasmic reticulum (80%)

Depoliration, Plateau, Repolorization

normal resting potential = -90mV —> Voltage reg fast Na+ open —> perm of Na increases —> influx of Na —> rapid depole to +30mV —> Na channels close

Depole = slow Ca+ open in sarcolema —> perm of Ca increases —> Ca in cytosol stimulate initial contraction —> Ca entering cytosol also triggers openings of Ca gates in SR —> burst of Ca leading to extended contraction —> K+ perm decreases for 250msec —> time required for blood ejection from ventricles

after delay voltage K+ open —> INcreas in K perm —> K efflux to outside cell —> Ca channels begin to close stopping influx of Ca —-> as K leaves cells become more (-)—> Na starts pumpmoing out before contraction terminates

Autonomic NS, and Chemical regulation

sympathetic NS & parasympathetic NS

cardiac accelerators nerves = centers located in medulla aoblongata —> pass down spinal chord to SA node, AV node, and myocardium —> norepinephrine is realeased —> binds to beta 1 receptors on cardiac muscle —> 2 effects: 1. SA & AV Node increases rate of spontaneous depole = increases HR, 2. increased perm of Ca in contractile fibers through voltage Ca = increased ejection blood volume during systole

cardiac inhibitory center in Medulla, parasympathetic fibers travel down Vagus nerve to SA node an AV node and Atrium —> Acetycolene releasesed —> effects; hyperpolorization of SA & AV node -> stim of K+ gates = k released -> hyperpolorization = slower HR

Epinephrine, norepinephrine, thyroid hormones

increase HR and volume similar to sympathetic, released from adrenal medulla during stress, excitement, excerise

Increases HR by increasing cell metabolism, symptoms of hyperthyroidism is tachycardia, hypothyroidism = bradycardia (low thyroid hormones)