antianginal drugs Flashcards
2 ways to decrease CVR
- increase cGMP, which prevents interaction of myosin w actin (nitrates)
- decrease intracellular Ca (CCB)
primary site for regulation of BF to the heart muscle
subendocardial network, essentially closed during systole. LV>RV
arteriole network in the heart
short matrix, resistant to compression creased by cardiac contraction. has decreased resistance to BF overall bc short
CPP safe range
CBF is autoregulated so that flow is independent of BPP as long as CPP is 50-150
4 major determinants of CVR
- metabolic (o2 demands, byproducts)
- autonomic nervous system
- endothelial modulation
- humoral
oxygen demand and CBF
linear relationship, MVo2 determined by contractility, heart rate (high HR = decreased flow), and wall tension (greater in endocardium than epicardium)
vasodilators for CBF
- low O2 is most influential metabolic factor
- causes AtP to degrade to adenosine, which vasodilates
- H, K, Co2, prostaglandins, lactate, NO
myogenic factors for CBF
stretch on BV wall leads to increase in SM contrax via opening of ion channels (Ca)
alpha SNS stim of CBF
alpha 1 - vasoconstriction of coronaries (also increases afterload, reflex bradycardia)
alpha 2 in endothelial cells increases release of NO –> vasodilation
net effect: modest decrease in flow
B SNS stim of CBF
B2 stim decreases epicardial and endocardial vasular resistance
b1 stim incr HR, contractility, Mvo2, metabolic vasodilation
net effect: increased flow
parasympathetic stim of CBF
- decrease epicardial and resistance vessel tone
- decreased HR, arterial BP, Mvo2 and metabolic vasoconstriction
- decrease in flow : net
humoral effects on CBF
ADH, angiotensin are coronary constrictors
others: catecholamines, thyroid hormone, adrenal hormones, glucagon, histamine, serotonin, prostaglandins, thromboxane, kinine, adenosine, VIP, arachodonic acid
enthothelial modulation of CBF
NO: released from endothelium in response to vessel stress, cGMP mediated (also inhibits PLT)
PGI2 and endothelium derived hyperpolarizing factor has dilation
-endothelin leads to vasoconstriction
