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BRS cardiovascular physiology


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stressed volume

blood volume contained in systemic arteries
site of highest resistance in the cardiovascular system
vessels with largest total cross sectional and surface area of circulation
vessels regulated by the autonomic system
arterioles and venules
vessels with highest proportion of the blood
unstressed blood volume

blood volume in the veins
relationship between:

blood velocity
blood flow
cross sectional area
v = Q/A
relationship between:

blood flow
pressure gradient
Q = dP/R
relationship between :

length of vessel
radius of blood vessel
R = (8n*l)/(pi*r^4)

R = resistance
n = viscosity
l = length
r^4 = radius to fourth power
if blood vessel radius decreases by factor of 2, what change in resistance?
increased by 16 (2^4)
Reynold's number
predicts whether blood flow will be laminal or turbulent
effect on reynold's number
increased (decreased viscosity)
capacitance (compliance), defining equation
C = V/P

V= volumr
P = pressure
vessels across which the greatest pressure decrease occures
arterioles (because site of highest resistance)
most important determinant of pulse pressure
stroke volume
atrial depolarization on EKG
P wave
interval from atrial depolarization to ventricular depolarization
PR interval
represents depolarization of ventricle on EKG
QRS complex
interval representing entire period of depolarization and repolarization of ventricle
QT interval
isoelectric segment when entire ventricle is deplarized
ST segment
represents ventricular repolarization on EKG
T wave
normally is the pacemaker of heart
SA node
SA nodal action potential phases (#'s)
0 (Ca++)
3 (K+)
4 (Na+ current, I*f*)
Bowditch staircase
increased heart rate increases strength of contraction in a stepwise fashion b/c as intracellular Ca++ increases over several beats
post extrasystolic potentiation
the beat *following* an extrasystolic beat has increased strength of contraction

***increased intracellular Ca++
mechanisms by which beta receptors increase strength of contraction
increased Ca++ into cell during plateau

increased activity of Ca++ of SR (phospholambam, therefore more Ca++ accumulated)
end diastolic volume/venous filling presure
aortic pressure
y intercept of venous return curve
mean systemic pressure
clockwise rotation of venous return curve
decrease total peripheral resistance
Type I hyperlipidemia
high chylomicrons
Type IIa hyperlipidemia
high LDL
Type IIb hyperlipidemia
high LDL and VLDL
Type III hyperlipidemia
high chylomicrons and IDL (intermediate density lipoprotein)
Type IV hyperlipidemia
high triglycerides
Type V hyperlipidemia
very similar to Type I (high cholymicrons), but with high VLDL
stroke work equation
stroke work = stroke volume * aortic pressure
coronary vasoactive metabolite control of circulation
cerebral vasoactive metabolite control of circulation
muscular vasoactive metabolite control of circulation
pulmonary vasoactive metabolite control of circulation
hypoxia constricts
vascular effects of histamine
arteriolar vasodilation
venous vasoconstriction

**effect of increasing capillary pressure->edema
vascular effects of bradykinin
arteriolar vasodilation
venous vasoconstriction

**increased capillary pressure -> edema
serotonin vascular effects
arteriolar vasoconstriction in response to blood vessel damage

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