Flashcards in Section 2 Review 2 Deck (79):
Responses to a therapeutic level of a cardiac glycodeside?
inc SV, ince MAP, inc Art PP
Response to an agent that selectively reduces arteriolar resistance:
inc SV, dec MAP, inc PP
Which patron best describes the response to hemmorhage?
dec Sv, dec MAP, dec PP
Inc both MAP and PP means you what increased:
In response to hemmorhage HR is increased by:
activation of b-1 recipes on SA-node
* 2 vasc beds in parallel, flow through each is the same. Cut the R of 1 in half and double the R in the other, total flow:
will be greater than the control ?
Effect of metabolites released into tissues on flow and mean cap p:
increase total flow and inc mean cap P in the tissue
How will blood flow to the myocardium change with increased fitness levels?
coronary blood flow will decrease
T or F? inc HR is most responsibel for the inc in the working of the heart m. during exercise.
How would the PV loop be changed with the addition of a pos inotropic agent?
same preload, inc P build up during isovolumetrtic contraction, increased Sv
How is PV loop effected with chronic reduction in the inotropic state of the heart (dev. of heart failure)
heart can't pump as much, increased preload, graph shifted to the R and smaller in the y direction
If a drug dec MAP and inc PP, what is the mode of action?
dec art R
How will arterial pulse pressure be effected with a decrease in arteriolar R?
it will increase
Will the application of a M rec agonist lead to an increase or decrease venous compliance?
Will going from laying down to a standing position lead to an increase or decrease venous compliance?
Would a beta recep agonist lead to an increase or decrease venous compliance?
Would a selective agonist for precap a-1 recpes lead to an increase or decrease venous compliance?
Would a a-1 recep antagonist lead to an increase or decrease venous compliance?
Are metabolites vasodilators or vasoconstrictors?
vasodilators. this makes sense, if anything builds up that normally isn't there, you're body wants to clear it)
In the presence of sever hemorrhage the baro-reflex mediated mechanism most responsible for the recruitment of myocyte cross bridges is:
Activation of beta-1 receptors on myocytes.
Effect of inc HR on SV:
Effects of cardiac glycosides:
increase force of contraction, dec HR
How do cardiac glycosides work?
inhibit the Na-K pump, inc activator pool of Ca, inc force of ven contraction, inc intracellular Na levels (initiating depol.)
Which is troponin dependent, sk m. or s.m.?
Calcium binding protein involved in s.m. contraction:
What is invloved in the phosphorylation of myosin in s.m. cell contraction?
3 methods to dec Ca conc in s.m. cell after contraction is over:
ATP in SR, ATP out of cell, Na Ca exchanger (against Ca gradient)
The only way to activate sk.m. contraction:
how to activate s.m. contraction:
AP, NTs, hormones, paracrines, NE, AcH, stretch
What type of rec does IP3 interact with:
G-protein coupled rec
How is Ca released from the SR?
What type of channels are involved in entry of Ca into s.m. cells?
voltage gated (L-type)
What would cause blood flow to normal regions of the myocardium to be increased, while blood flow distal to the stenotic artery to not change if a pt w/ stenosis was given a vasodilator agent?
The arterioles in the stenotic region were already maximally dilated due to chronic under-perfusion and build up of vasodilator metabolites.
How will a circulation model tracing change with an inc in art R?
same HR, more forceful contract (larger amplitude wave on bottom and top of tracing)
body response to an alpha-1 receptor agonist:
Dec HR and inotropic state of the myocardium
What do an increase in venous hydrostatic pressure lead to?
Will vasoconstriction lead to edema?
When do you hear the first heart sound?
at the end of ventricular filling
What would happen to a P-V loop if the Ca channels of the cardiac working muscle were blocked?
the preload would increase, the Sv decrease, and the force of contraction decreases. these would make the loo[p narrower, shorter and shifted to the R. The U L portion of the graph will never touch toe solid curve bc it can't generate the nec. force
How would the P-V loop be effected if you block the alpha-1 receptors of systemic arterioles?
no resistance in the systemic arterioles, decrease in arterial pressure, decrease in after load, more blood returning faster so an increase in preload.
Activation of a-1 receps in s.m. leads to __ while activation of B-2 receps in s.m. leads to:
increased tissue flow, in excess of metabolic demand, following the release for arterial occlusion
How would partial inhibition of the Na-K pump affect the cell?
increase intracellular Ca levels
Would increasing vasomotor tone increase or decrease SV?
dec (inc vasomotor tone --> inc arterial BP --> inc afterload
response to hemorrhage
a primary dec cardiac output, a secondary dec in art P and inc in HR and R
a drug causes an inc in art systolic P and dec in art diastolic P (inc in art pulse P). What physiological responses account for these changes?
inc SV and inc art R
What does the P wave correspond with on the EcG?
right before the little hill that represents the atrial, extra push of blood into the L ventricle
Why is a person w/ a stenosis asymptotical initially?
the R2 coronary R (art R) decreases to compensate or the inc R1 R (the stenosis)
How to calculate PP:
how to calculate mean arterial P:
[1/3(PP) + d] ...... (PP=s-d)
Slow depol during this phase enable pacemaking activity by the cell:
Phase 4 (RMP)
This phase is assoc with QRS complex of the ECG:
Phase 0 (rapid depolarizaton)
This phase is imp in excitation-contraction coupling:
Phase 2 (plateau)
What is phase 1?
What is phase 3?
T or F? The RMP is prop to the ratio of the K conc across the membrane for both cardiac and sk.m..
T or F? The force of m. contraction is prop to the cytosolic Ca conc. for both cardiac and sk.m..
Through which heart structure does the AP travel most slowly through?
AV node fibers
What will a dec in MAP w/ reflexes intact result in?
inc in HR
Does atropine decrease or increase HR?
What change happens in the cap bed if the arterioles are constricted?
reabsorption > filtration
What physiological changes alter MAP?
SV, HR, arterial resistance (not sig. though)
What causes hyperemia in sk. m. during light exercise?
an inc in vasodilator metabolites
T or F? Coronary blood flow is primarily under neural control.
F. characterized by autoregulation
T or F? A persons HR decreases when they stand.
T or F? The central V.P. will inc when a person stands.
Does R atrial P increase or dec with exercise?
What can an ECG tell you about cardiac activation?
Hr, sequence of activation of the myocardium, delay bw the excitation of the atria and the ventricles, duration of the ventricular excitation
2 beds in parallel: double R in one and halve the other. Net flow?
Greater than control ( Flow = 1/R(a) + 1/R(b) )
T or F? Ca binds troponin-C subunit of actin in s.m.
F. in sk. m., not s.m.
What would happen if you block the a-1 receps on venous s.m. cells?
constriction (act of these leads to vasodilation)
What would phosphorylation of volt-gated Ca channels in cardiac ventricular cells lead to?
Mech responsible for adjusting HR from laying down to standing:
dec activation of muscarinic receps on the SA-node cells (removing para sym depression and allowing to rise to the rate it would be w/o any influence?)
How would a dec in art P and an inc in venous compliance affect SV?
it wouldn't. It would remain the same
Changes resulting form the loss of a limb:
Resting metabo decreases, resting CO dec, resting MAP remains the same, total BV dec
These dec if a limb is lost:
resting metabo, resting CO, total BV
How is resting MAP effected with the loss of a limb?
What physio change can lead to a dec in MAP and an inc in arterial PP?
dec art R