BRS cardiovascular physiology
Terms
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-
stressed volume
definition? - blood volume contained in systemic arteries
- site of highest resistance in the cardiovascular system
- arterioles
- vessels with largest total cross sectional and surface area of circulation
- capillaries
- vessels regulated by the autonomic system
- arterioles and venules
- vessels with highest proportion of the blood
- veins
-
unstressed blood volume
definition? - blood volume in the veins
-
relationship between:
blood velocity
blood flow
cross sectional area - v = Q/A
-
relationship between:
blood flow
pressure gradient
resistance - Q = dP/R
-
relationship between :
Resistance
viscosity
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
-
anemia:
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) - preload
- end diastolic volume/venous filling presure
- afterload
- 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
-
Adenosine
Hypoxia - cerebral vasoactive metabolite control of circulation
-
CO2
H+ - muscular vasoactive metabolite control of circulation
-
Lactate
K+
Adenosine - 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