determined by: coronary blood flow and oxyhemoglobin dissociation (very minor)
autoregulatory system
blood flow is mainly a function of vessel radius (Poiseuille equation)
Poiseuille equation: Q = (Pp p r4) / (8 l h ) where Pp = perfusion pressure, h = viscosity
other factors in equation are minor
75% of oxygen extracted from blood, so hard to increase oxygen this way
autoregulation: intrinsic tendency of organ to maintain constant blood flow independent of perfusion pressure by varying vascular resistance
flow vs perfussion pressure curve has large range where flow independent of pressure
probably mediated by metabolic control
physical factors
ventricular contractions tend to constrict vessels
in LV can even result in reversal of flow
LV flow mostly in diastole; RV flow mostly in systole
tachycardias, or inc LV contractility can effect blood flow in diseased heart
neural factors
sympathetic nerves: initial coronary vasoconstriction followed by vasodilation
with alpha blockers, only see dilation
with beta blockers, only see constriction
parasympathetic: vasodilation, but not much of an effect in heart
coronary reflexes
large vessel coronary spasm: could be from unopposed stim of alpha receptors
myogenic factors
hypothesis states that there is an intrinsic mech in the vessel walls of arteries and arterioles which responds to increase in internal pressure by contracting (unproven)
metabolic factors
: basic idea is that reduced bloodflow causes vasodilation by accumulation of vasodilator metabolites in the tissue or decreased nutrient supply - autoregulation
oxygen: little direct role in autoregulation, elaboration of other metabolites influenced by O2
carbon dioxide: coronary vasodilator that is 50% less potent than hypoxia (small effect); could be mediated though pH change and subsequent potentiation of adenosine
ATP: potent vasodilator; has not been found in hypoxic perfused hearts, so prob little role
prostaglandins: potent, released from hypoxic hearts; require some O2 for synth, so anoxia shuts down this effect
adenosine: potent; blocks Ca entry into cell; probably main autoregulator of coronary blood flow
potent vasodilator
adequate intracellular source of ATP
readily crosses membranes
can be rapidly inactivated (deamination, incorporation into nucleotides)
present in normal myocardium, increased in hypoxia or increased O2 requirements
concentrations reached are capable of producing observed effects