Cardiovascular phys Review Flashcards
What changes in blood volume distribution normally occur immediately when moving from supine to standing?
Blood volume transfers from central reservoirs → pools in highly compliant large veins of the lower extremity
A-V difference in pressure is 85 approximately and this stays the same when you go to standing from laying. but what does change/increases is the actual pressure the further you are from the heart b/c of the hydrostatic pressure, but at the head its lower
why does walking decrease venous pressure in the foot?
one way valves and muscles pumping
what effect does the venous pooling in a patients lower extremity upon standing prior to compensation have on her cardio output and arterial blood pressure
CO decreases
arterial blood pressure decreases
b/c VR decreases–> decrease CVP –> decreased EDV–> decreased SV–> decreased CO
MAP= COxTPR so decrease CO and decrease MAP
MAP = what?
CO x TPR
or
MAP = DB + 1/3 PP
considering cerebral circulation and its ability to autoregulate, why would a patient lose consciousness ?
what is the driving force for blood flow?
the driving force for blood flow is a pressure gradient
even though resistance to flow can be decreased via autoregulation/vasodilation, a sufficient driving for (MAP) must be maintained for adequate flow
her sudden severe drop in MAP was below the autoregulatory limit of her cerebral circulation and thus blood flow (and O2 supply) was compromised
what is Ohm’s law?
flow = pressure gradient/resistance
CO = what?
MAP/TPR
if a patient’s BP dropped to 95/65 when she fainted what is her MAP?
MAP = CO x TPR
MAP = DB + 1/3(PP)
65 + 1/3 (95-65)
= 75
when someone goes from laying to standing, what is the firing rate of their high pressure aortic and carotid baroreceptors
what is the integration center where the baroreceptor firing rate information is processed
firing decreases
integration center is? –> medulla
what are the effects of a normal reflexive response to hypotension
standing–> blood pools in veins –> decrease in MAP–> decrease in baroreceptor firing–> baroreceptor reflex –> increase sympathetic output and decrease parasympathetic output
- Heart –> increase HR, contractility –> increase CO
- arterioles–> TPR increase b/c of constriction
- veins –> Constriciton of veins–> increased VR –> increase SV –> increase CO
what are some factors that influence the degree of orthostatic response?
total blood volume
vascular distensibility
skeletal muscle tone ; strength and rate of intermittent contraction of sk. musc.
temperature
initial HR
initial myocardial contractility
how does a double dose of nitroglycerin affect the ability of baroreceptor response to correct for postural hypotension?
arterioles and veins–> antagonized sympathetic vasoconstrictor effects on arterioles and veins –> results in further pooling of blood within LE when a patient goes from supine to standing
effect on cardiac tissue? no direct effect on cardiac tissue
reflexive increase in HR and contractility remain intact
during which phase of the cardiac cycle does the left ventricular myocardium receive majority of blood flow ?
diastole
left coronary artery is filled most during this time
what is the cause of the angina in a patient doing yardwork/exercise that has a stenotic LAD?
he had decreased oxygen delivery from a stenotic LAD –> ischemia
which specific factors increase O2 demand in a patient at rest?
exercise?
rest–> HR, force of contraction, afterload increased, HTN
exercise?
–> increase in HR
how does increased afterload affect O2 demand?
increased wall stress
what is ventricular wall stress/tension ?
force acting on myocardial fibers, tends to pull fibers apart
energy must be expended to oppose wall stress
what is Laplace law?
wall stress is related to transmural pressure, radius and wall thickness
wall stress is directly proportional to…
pressure (systolic ventricular pressure)
radius (radius of ventricular chamber)
wall stress is indirectly proportional to ….
wall thickness of ventricle
so aortic regurg–> increases ventricualr wall stress
aortic stenosis increases wall stress
dilated ventricular chamber increases wall stress
systemic HTN increases wall stress
what is the normal mechanism by which O2 supply is increased in order to meet demand of the exercising heart?
with increased tissue metabolism–> increased release of metabolic vasodilators/autoregulation (adenosine, PCO2, NO, H+, prostaglandins) –> dilation of arterioles –> decreased resistance creates increased blood flow–> Increase O2 and nutrient supply to tissue as long as metabolism is increased
what is the Fick calculation
Myocardial O2 consumption can be calculated by the Fick Principle if coronary blood flow (CBF) is known and arterial/venous O2 content is known.
Fick calculation also be used to determine cardiac output (CO) if whole-body oxygen consumption (VO2) and arterial/venous O2 content is known
What is this patient’s myocardial O2 consumption (MVO2)?
Coronary Blood flow = 100 ml/min
Arterial O2 = .2 ml O2/ml blood
Venous O2 = .1 ml O2/ml blood
MVO2 = CBF x (AO2 - VO2)
100 x (.2 - .1)
=10 mL o2/min
Q = VO2 / A - VO2 difference Q = CO or flow
why was autoregulation of a patient’s coronary circulation (who has an occlusion of his LAD) during exertion insufficient to meet his myocardial oxygen demand when doing yard work or stress test?
even at rest this patient is maximally vasodilated
a portion of his arteriolar dilating capacity (coronary reserve) was already utilized at rest in order to compensate for the resistance to flow caused by his stenotic LAD
If a patient with a LAD stenosis were prescribed a vasodilator, would blood flow to ischemic tissue downstream of the stenosis likely increase or decrease?
may actually decrease
“Coronary Steal”
If arterioles are already maximally dilated in response to ischemia, vasodilator action likely to only affect vessels in nonischemic vascular beds
An additional reduction in perfusion pressure can further compromise blood flow to ischemic tissue downstream of stenosis
which vasodilator effects could be beneficial for a patient with angina upon exertion
decrease peripheral resistance –> decrease afterload–> decrease wall tension –> decrease myocardial oxygen demand