cardiovascular Flashcards
cardiac output in moderate exercise
12.5 L/min
CO at rest
5 L/min
maximal CO in exercise
25-30 L/min
CO equation
HR x StV
venous return effect on CO
increase
increase in SNS activity on CO
increased activity increases HR which increases CO
exercise effect on PNS and CO
PNS inhibited, HR increase
how does cardiac hypertrophy develop
prolonged exercise, left ventricle is larger so StV increases
what is the inner layer of the arteriole called
tunica intima
what is the middle layer of the arteriole called
tunica media
what is the outer layer of the arteriole called
tunica externa
constant flow rate equation
blood flow velocity x cross-sectional area
what does flow (Q) refer to
vol of fluid passing a given cross sectional area of vessel per unit time
poiseulles law
flow is proportional to vessel radius, and difference in inflow and outflow pressure but its inversely proportional to length of vessel and velocity of blood
peripheral resistance equation
pressure difference / Q
autorythmic cells
the cells of the heart that act as a pacemaker
SAN
- 8mm long 2mm thick
- fast firing cells
- NO RESTING POTENTIAL
phase 0 of SAN
upstroke of AP less steep than myocyte
phase 3 of SAN
plateau not sustained
phase 4 of SAN
membrane potential deviates from K+ equilibrium potential
3 factors affecting StV
- End diastolic volume
- Aortic pressure
- contractality
5 things affecting HR
- intrinsic rate
- SNS
- PNS
- hormones
- extra and intracellular ions
what is systolic blood pressure
force exerted onto the walls of arteries by the heart when it beats
what determines the systolic blood pressure
aortic elasticity (increases it)
what is diastolic blood pressure
arterial pressure when heart not beating - determined by peripheral resistence
StV equation
end diastolic vol - end systolic vol
pulse pressure equation
systolic BP - Diastolic BP
mean BP equation
Diastolic BP + 1/3 pulse pressure
Q equation
mean BP/ total peripheral resistance
factor affecting peripheral resistance
blood vessel radius
Mean BP equation
CO x TPR
PNS control of BP
ACh binds to M receptors and decreases HR
SNS control of BP
NA binds to b-adrenoceptors and increases HR and force
alpha 1 and 2 adrenoceptors on vasculature
NA binds and causes vasoconstriction
beta 2 adrenoceptros on vasculature
NA binds and causes vasodilation
baroreceptors on BP
in carotid arteries - sense changes in transmural pressure
clinical hypertension
defined as a rise in arterial pressure which is significant enough to raise instance of stroke, heart attack/failure
essential hypertension
no cause, significant risk
secondary hypertension
renal disease, hyperthyroidism, pregnancy and drug use
what pharmacological intervention reduces BP by reducing TPR via vasodilation
Ca2+ channel blockers
what pharmacological intervention reduces BP by reducing TPR via vasoconstriction
alpha adrenoceptors, angiotensin II
what pharmacological intervention reduces BP by reducing CO
diuretics, beta 1 and 2 adrenoceptor antagonists
phentolamine
non selective alpha adrenoceptor antagonist
phentolamine side effects
postural hypertension, high HR and cold extremeties
angiotensin II
pepide with activity in vasculature, kidneys and adrenal cortex
angiotensin II in adernal cortex
acts on zona glomerulosa cells, stimulating aldosterone secretion and synthesis
bradykinin
vasodilator
what is a pro of AT1 receptor antagonists
they block angiotensin II without effecting bradykinin
what do ca2+ channel blockers do
inhibit voltage-mediated Ca2+ channels on vascular smooth muscle
what is the effect of Ca2+ channel blockers on BP
increase vasodilation so decrease BP
where are beta 1 receptors found
heart
where are beta 2 receptors found
lungs and blood vessels
