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44 Cards in this Set
- Front
- Back
Three types of cardiac muscle |
atrial, ventricular, and excititory/conductive fibers
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Duration of cardiac muscle contraction compared to skeletal muscle
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much longer in cardiac
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Cardiac muscle arrangment
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latticework of cells connected in series and parallel
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intercalated discs
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cell membranes that separate cardiac cells (contain gap junctions)
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average V of AP in ventricular muscle fiber
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105 mV (from -85 to +20)
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time ventricular cells remain depolarized
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0.2 seconds
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Channels that cause cardiac AP
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1)Fast sodium channels (also in skeletal muscle) 2) Slow calcium channels
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After onset of AP, how much does K+ permeability change
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decreases 5 fold
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velocity of AP across atrial and ventricular muscle fibers
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0.3 to 0.5 m/s (1/250 the speed of nerve fibers and 1/10 of skeletal muscle)
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Purkinje fiber AP velocity
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as much as 4 m/s
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Normal ventricular refractory period
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0.25 to 0.3 s
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Normal atrial refractory period
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0.15 s
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Skeletal vs. cardiac sarcoplasmic reticulum
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cadiac is less developed (Ca stored in T tubules)
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What keeps Ca in T tubules
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eletronegatively charged mucopolysaccarides
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What is T tubule Ca concentration dependent on
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extracellular fluid Ca concentration
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Legth of AP delay from atria to ventricles
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0.1 s
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P wave cause
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spread of depolarization through atria
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QRS wave cause
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depolarization of ventricles (about .16 s after P wave onset)
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T wave
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repolarization of ventricles
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acute sign of heart failure
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SOB
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pressure changes in atria - a wave
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atrial contraction
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pressure changes in atria - c wave
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ventricles contract (slight backflow and valves bulging backwards)
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pressure changes in atria - v wave
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slow flow of blood into atria while valves closed
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First third of diastole
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rapid filling of ventricles
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Last third of diastole
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atria contract (additional 20 percent ventricular filling)
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Isometric/Isovolumic contration in ventricles
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Beginning of systole before valves (aortic and pulmonary) open
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Isometric/Isovolumic relaxation in ventricles
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beginning of diastole before atrioventricular values open
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End systolic volume and end diastolic volume
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40-50 mL and 110-120 mL
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papillary muscle
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pull valve toward ventricles to prevent bulging too far backwards
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volume-pressure work/external work
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move blood from low pressure veins to high pressure arteries (major proportion of E)
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kinetic energy of blood flow
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accelerate blood to its velocity of ejection (minor proportion of E)
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What happens to systolic pressure with a fill V of over 150-170mmHg
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decreases-actin and myosin filaments are pulled far enough apart that the strength of each contraction becomes less than optimal
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maximum systolic right and left ventricular pressure
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right = 60-80mmHg; left = 250-300mmHg
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Preload
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degree of tension on muscle when it begins to contract
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Afterload
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load against which the muscle exerts its contractile force
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Maximum efficiency of normal heart
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20-25 percent (most energy converted to heat)
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Liters pumped per minute at rest and exercise
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4-6 L/min at rest (4-7 times this during exercise)
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Frank-Starling mechanism
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intrinsic ability for heart to adapt to increasing volumes of inflowing blood (stretch = greater contraction = greater quantity of blood pumped)
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Sympathetic stimulation of heart
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Can raise pulse from resting 70 to 180-200; also can double force of contration
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No sympathetic stimulation causes…
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decrease of cardiac pumping by 30% (there is generally always sympathetic stimulation)
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parasympathetic stimulation
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can stop heartbeat for few seconds, decreases contratile strength 20-30% (most fibers in atria)
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excess potassium
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heart become dilated and flaccid; heart rate slows; can vlock impulse from atria to ventricles
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excess calcium
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toward spastic contration(kept in narrow range in body - rarely seen)
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calcium deficiency
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cardiac flaccidity (kept in narrow range in body - rarely seen)
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