Cardiac Control 1, 2, and 3 -Cardiac Output and Arterial Pressure Flashcards
Degree of myocardial stretch during diastole is determined by what interaction?
diastolic pressure and chamber compliance (measured by chamber architecture and myocardial properties)
At upper ranges, a given increment in LVEDP produces a larger/same/smaller increment of LV end diastolic volume.
smaller –> myocardial diastolic force-length relationship is non linear
During ventricular contraction, which myocytes shorten the most and contribute the most to cavity volume reduction?
subendocardial myocytes shorten more than the epicardial surface
The load that ventricular muscle must overcome during systole to eject.
Ventricular afterload
How is the extent of cardiac muscle shortening during systole related to the load opposing it?
inversely –> increasing afterload decreases extent to which cardiac muscle can shorten, thereby decreasing stroke volume
T/F as a ventricle ejects during systole, the wall force increases as pressure increases and the ventricle volume decreases
F –> b/c volume goes down, wall force goes down despite pressure increase (a larger ventricle has larger wall force) –> AKA the ventricle has to produce less force to maintain the same/greater pressure outflow
At what point is systolic wall stress greatest?
at onset of ejection as ventricular volume is largest
During ejection LV pressure increases in the first half of systole and wall stress increases/decreases –> why?
decreases b/c of larger effect of decrease in LV dimension
What is the increased inotropic state of cardiac muscle?
cardiac muscle can increase force at any given length
What determines ventricular stroke volume?
EDV-ESV
What determines EDV?
preload as measured by EDP and diastolic force-length relationship
What determines ESV?
Afterload as measured by peak systolic pressure and end systolic force-length relationship AND inotropic state (Which shifts the end systolic force-length relationship)
What happens to stroke volume if: end diastolic volume is kept constant and arterial pressure is decreased
increase
What happens to stroke volume if: load is kept constant and end diastolic volume is increased
increase
What happens to stroke volume if: arterial pressure increases,
decreases
What enables greater shortening form the same EDV against the same pressure?
increased inotropy
What two factors increase inotropy?
increased intrinsic heart rate, beta adrenergic input
What impairs inotropy?
metabolic abnormality
How is inotropy mediated?
calcium release
T/F LVEF is load/intropy independent
F
What happens to LVEF if: increase preload within limits
increase
What happens to LVEF if: increase afterload
decrease
What happens to LVEF if: decrease afterload
increase
What happens to LVEF if: increase inotropic state holding other variables constant
increase
_____ is determined by preload, afterload, and inotropic state.
stroke volume
_____ is determined by atrial pressure and ventricular diastolic dimension.
preload
_____ is determiend by arterial vascular resistance, cardiac output, and ventricular diastolic and systolic dimension.
afterload
_____ is determined by autonomic input to SA node.
heart rate
What provides the potential energy that drives systemic blood flow to all systemic tissues?
systemic arterial pressure
How do we calculate systemic vascular resistance/SVR?
mean arterial pressure/cardiac output = MAP/CO
What are the short term systemic arterial pressure sensors?
arterial/ventricular/atrial baroreceptors
What are the long term systemic arterial pressure sensors?
renal baroreceptors
Where are arterial baroreceptors located and how are they mediated?
carotid sinus and aortic arch –> cationic channels that respond to stretch
What nerves are the afferents for arterial baroreceptors?
9 and 10
What nerves are efferents component from arterial baroreceptors to heart and vessels?
sympa/parasympathetics
What happens to the firing rate of arterial baroreceptors as they are stretched more?
increases
What happens to the firing rate of arterial baroreceptors as they are stretched statically?
decays
What do atrial baroreceptors sense?
atrial distension –> intravascular volume –> will release anp if too much iv volume to cause diuresis
What do renal baroreceptors do?
release renin which leads to angiotensin production –> arterial vasoconstriction and retention of Na+ and H2O
What happens to SA node rate? beta adrenergic stimulation
increase
What happens to SA node rate? muscarinic stimulation
decrease
What happens to AV node refractoriness and conduction velocity? beta adrenergic stimulation
reduced refract., increase conduction velocity
What happens to AV node refractoriness and conduction velocity? muscarinic stimulation
increased refract., reduced conduction velocity
What happens to the ventricles when stimulated by beta adrenergics?
increased inotropy
What receptors mediate adrenergic vasoconstriction and in what tissues does this occur?
alpha adrenergic: renal, mesenteric, cutaneous
What are the three natriuretic peptides?
atrial, btype, ctype
What releases ANP and what is its function?
atria –> response to atrial stretch as in hypervolemia and exercise –> leads to increased GFR, reduced Na reabsorption, reduced renin secretion, increased smooth muscle relaxation
What releases BNP and what is its function?
ventricles –> response to ventricular stretch –> similar actions as ANP
What releases CNP and what is its function?
produced in vascular endothelium –> no diuretic activity, physiologic role less certain
Adrenergic stimulation leads to venous constriction/dilation
constriction –> repartitions blood volume to central circulation, augments cardiac preload
Muscarinic stimulation leads to venous constriction/dilation
dilation –> distributes blood into large veins, reduces cardiac preload
What is the effect of gravitation/standing up on perfusion pressures?
upper body: lower pressure
lower body: higher pressure
*impaired venous return
What is the effect of hemorrhage on systemic arterial pressure?
loss of iv volume causes loss of preload –> reduced cardiac output
What is the fick cardiac output technique
measure CO by using oxygen as indicator –> CO = VO2/AVO2D = oxygen consumption/concentration difference is the arteriovenous oxygen difference
What is thethermal dilution technique
catheter with tip thermistor positioned in main pulmonary artery –> colled by injected bolus of iced saline coming from right atrium –> CO calculated by integrating area under time termpreature curve –> small area = high CO, larg area = low CO
What is normal mixed venous O2 sat?
75%
A low CO will result in a low/high mixed O2 sat?
low
Why does the reduction in diastolic filling time due to increased heart rate not reduce preload/stroke volume?
because most filling occurs during first 1/3 of diastole so high hear rates don’t really impair diastolic filling
How do you overcome reduced ventricular ejection/stroke volume due to increase in afterload due to increased arterial pressure?
inotropic stimulation
What is the pressure effect of increased local metabolic rate?
decrease local vascular resistance to match local flow to metabolic requirements –> reduced systemic vascular resistance –> decrease pressure
inadequate blood flow to a tissue leading to metabolic derangement or cell necrosis
ischemia
The majority of systemic vascular resistance occurs at the level of the _______
systemic arterioles
Do medium sized arteries make an important contribution to vascular resistance?
no –> have flow-mediated vasodilation (endothelially regulated)
Can blood get to venules without entering a capillary bed?
yes direct shunt between arteriole and venule
What regulates arteriolar diameter?
tone of vascular smooth muscle
Do vascular smooth muscle cells cycle between systole and diastole?
no –> but can exhibit chronic changes in basal tone –> controlled by cytosolic calcium concentration (increase calcium = increase basal tone)
How is flow resistance related to arteriolar diameter?
r^4 –> subtle changes in arteriolar diameter can cause large changes in vascular resistance
What is the difference between intrinsic and extrinsic control of VSMCs?
intrinsic control is based on the tissue’s local requirements whereas extrinsic control has to do with circulation’s overall requirements
What are three effectors of intrinsic VSMC autoregulation?
myogenic autoregulation, endothelium mediated autoregulation, metabolic mediated autoregulation
How does myogenic vascular autoregulation occur?
increase in arterial inflow pressure leads to increased SMC tone –> via stretch activated calcium channels (e.g. renal vascular bed)
How does endothelium mediated vascular autoregulation occur?
increased endothelial shear stress –> activation of endothelial receptors –> NO release –> reduce SMC tone (mostly in distributing arteries vs. resistance vessels)
How does metabolic mediated vascular autoregulation occur?
increased tissue metabolic activity leads to reduced SMC tone (possibly via adenosine)
Resistance provided by vascular beds is effectively in series/parallel.
parallel –> different resistances determine the partitioning of blood flow
What happens to systemic vascular resistance/SVR in: hypertension
disease process sets SVR to an abnormally high level leading to sustained elevation of systemic arterial pressure
What happens to systemic vascular resistance/SVR in: CHF
normal homeostatic response to decreased CO increases SVR increases load on an already poorly functioning heart
What happens to systemic vascular resistance/SVR in: sepsis
loss of normal SVR regulation mediated by circulating cytokines –> inappropriate opening of metarterioles (bypass capillaries), low systemic arterial pressure in setting of increased CO–> tissue ischemia in setting of increased blood flow
What happens to systemic vascular resistance/SVR in: shock
low CO –> fall in systemic arterial pressure –> reduction in organ perfusion –> vasoconstriction of renal/cutaneous/GI beds to increase systemic vascular resistance –> restoration of systemic arterial pressure at the price of possible organ dysfunction (kidneys and liver)
