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44 Cards in this Set

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