Section 2 Review Flashcards
Likely cause of edema if the venous return is blocked:
inc cap hydrostatic P
What would the change in HR be if you inc. Ca++ current thru voltage activated Ca++ channels?
baroreflex decrease in HR
Effects of cardiac gylcoside:
partial inhibition of the arc na/K pumps, inc activator pool Ca++, Inc force generation during systole, inc intracellular Ca++
What would happen if at art P inc and there was a dec in inotropy?
SV decreases
Regulation of s.m. involves:
reg of enabled myosin light-chain kinases, Ca-calmodulin interaction, Phosphorylation of myosin light gains, and voltage reg entry of Ca form the extracellular space
If a drug inc both mean pressure and arterial pulse what mode of action is it using?
increase SV
a-1 receps primarily innervates:
s.m.
Which neurotransmitter has higher affinity for the α1 receptor, noradrenaline or adrenaline
noradrenaline
What happens when you activate a-1 receps?
contraction of s.m.
What transmitter do B-2 receps interact w?
epinephrine
What transmitter do a-1 receps interact w?
epi and norepi
Physiological response of the activation of B-2 receps:
smooth muscle relaxation
What effect does norepi have on B-2 receps?
none
To what receps does epi bind?
α1, α2, β1, β2, and β3
Activation of B-1 recep leads to:
Increase heart rate in SA node (chronotropic effect)
Increase atrial cardiac muscle contractility. (inotropic effect)
T or F? Activation of B-1 recep leads to both a chronotropic effect and an inotropic effect.
T
Chronotropic effect deal with:
heart rate
Negative chronotropes:
Ca++ channel blocker, beta blockers, and
Acetylcholine
Positive chronotropes:
Adrenergic agonists, Atropine, Dopamine, Epinephrine, Isoproterenol
What do inotropes do?
alters the force or energy of muscular contractions
One of the most important factors affecting inotropic state
Ca++ levels
What do inotropic drugs typical alter?
Ca++ levels
positive inotrpic drugs
Calcium Catecholamines Dopamine Epinephrine (adrenaline) Norepinephrine (noradrenaline) Angiotensin II Digitalis
negative inotropic drugs:
Beta blockers and calcium channel blockers
Effect of partially compensated loss of blood for the P-V loop:
Volume decrease (graph shifts left), and pressure increases (to try and compensate for the BV dec)
Effect of an increase in after load in arterial pressure for the P-V loop:
EDV inc (graph extend to the R), pressure increases (graph extends higher in the P direction)
Effect of B1-blocker selective for vent working heart m. cells for the P-V loop:
Increase in V (shift to the R) and dec in pressure (shorter in P direction)
Calc CO from mean aortic BP, mean R atrial BP, systemic vascular R, and HR:
(Mean R atrial - Mean aortic BP)/R
Is the interstial V changed or unchanged? Decreased cap hydro P and dec cap osm P:
unchanged
Is the interstial V changed or unchanged? Decreased cap hydro P and inc lymph flow.
changed
Is the interstial V changed or unchanged? Decreased cap os P and dec lymph flow.
changed
inc cap hydo P and dec lymph flow.
changed
Inc cap hyrdo P and dec cap osm P:
changed
Effect of B-1 agonist:
Increase heart rate in SA node (chronotropic effect)
Increase atrial cardiac muscle contractility. (inotropic effect)
Effect of agonist for precapillary alpha1 receps:
contraction of s.m.
Effect of mucurinic recep antagonist:
decreased autonomic m. contraction
What activates muscarinic receps?
AcH
Effect of muscarinic recep activation in the heart
slow heart rate and reduce contractile forces of atrium
Flux:
Permeability X conc gradient
In going for rest to exercise, the CO can increase __ times and the oxygen delivery to tissue can increase __ times.
5, 4
Convective flow in our system:
CO
Where to find fenestrated caps:
sk m.
Where to find sinusoidal caps:
liver
difference bw velocity and flow:
how fast something moves vs. how much of something moves
What type of fluid P is found in isf? negative, zero, positive?
negative, created by lymph uptakes of fluid
What maintains the shape of our tissues?
neg P is the isf’s
What is not fxning properly in elephantiasis?
isf uptake into lymph vessels
net forces in vessels is always __ -___:
cap - isf
How is the P in the art and veins changed with edema?
both are increased
How is the R in the art and veins changed with edema?
Rv incr, Rart dec
Reabsorption will occur when __ pressure exceeds ___ pressure
osmotic, hydrostatic
How are cap and ifs’s osmotic P’s affected in edema?
Cap osm p decreases, isf osm p increases
inc in filtration can be caused by:
inc art P, inc ven P, dec arteriolar R
Explain edema due to starvation:
system starts to consume plasma proteins as food. Without plasma proteins, the osmotic force will decrease, causing more filtration than absorption.
How is lymph flow affected with edema?
dec
How much of an inc in mm Hg is there from the L atrium to the aorta?
90 mm Hg (5-95 mm Hg)
How much of an inc in mm Hg is there from the R atrium to the pulmonary a.?
18 mm Hg (2-20 mm Hg)
How do the SV of the L and R ventricles compare in the steady state?
SV R ventricle = SV L ventricle
How does the systemic R compare to the pulmonary?
sys = 6 times higher
How does the systemic P gradient compare to the pulmonary?
sys = 6 times higher
The L ventricles works about __ times harder than the R ventricle.
6
which heart chamber(s) create the lub and dub sounds?
L ventricle for both: “lub” - a-v valve in L vent, “dub” - semilunar valve in L vent
Which close first, the semilunar valves or the a-v valves of the L ventricle?
a-v
T or F? A larger P gradient is required to fill during diastole.
F. small
Is mitral valve closing the 1st or 2nd sound?
1st
Ej fraction:
SV/ EDV part/whole each stroke/total filling each time
Length of cardiac cycle in ECG:
R wave to R wave (peak to peak)
Where in the ECG is isovolumetric contraction?
imm after the under/after shoot of the R wave
Where in the ECG is isovolumetric relaxation?
after small hill (created by systole)
What does the R-R interval indicate?
the length of the cardiac cycle
diastole in the ECG:
after hill of after/under shoot of the R wave
What fraction of the cardiac cycle is diastole?
2/3
Which valves close directly before isovolumetric contraction?
a-v valve (check)
This causes a small bump in ventricular filling:
atrial kick
Is phase 1 diastole or systole?
diastole
What causes the increase in pressure in the L ventricle during isovolumetric contraction?
mechanical contraction (ventricular wall tension)
How is L ventricular pressure changing during isovolumetric relaxation?
decreasing
Are inotropic factors preload and after load dependent or independent?
independent?
HR can increase __ times.
3
SV can increase __ times.
2
Is the length-tenstion relationship preload-dependent or afterload-dependent?
preload-dependent
Is the force-velocity relationship preload-dependent or afterload-dependent?
afterload-dependent
T or F? Every depolarized cell leads to intracellular Ca2+ increase, which leads to contraction.
T
When actin and myosin bind does the spring stretch or decrease in length?
stretch
What creates active tension in the myosin/actin network?
the binding of the actin/myosin
T or F? Actin binds to myosin and not the opposite way.
F. myosin bind actin
Which has a Ca binding site, troponin or tropomyosin?
troponin
What blocks the binding site on G-actin?
tropomyosin
Under what chemical condition will tropomyosin block the head region of myosin from attaching to the binding site on actin?
Low Ca++ conc
To where does Ca++ bind to help expose the binding sites?
to Troponin C molecule
T or F? Myosin has ATPase activity.
T
All muscles can generate Fmax force of:
5x10^3
Another name for Ca form the SR:
activator Ca++
Ca released from the SR is:
graded
What terminates contraction of the heart?
move of Ca++ back into the SR
T or F? The Na/Ca exchanger works to inc intracellular Ca++ conc.
to expel Ca from the cell.
Does the Na/Ca exchanger fxn during diastole or systole?
diastole
What type of channels are DHPR’s?
Voltage-gated at SL
What channels are involved in the release of trigger Ca++?
DHPR channels
What channels are involved in the release of activator Ca++?
Ryanodine channels
When does actin/myosin contraction terminate?
following electrical recovery of the myocyte and the return of cytosolic calcium to a diastolic level
How many X-bridges are activated in heart muscle at rest?
about 1/2
Which neurotransmitters have a positive inotropic effect?
epi and norepi
The activation of Beta receptors will:
increase cAMP and the exposure of PKA
4 targets of PKA:
phosphorylates: volt-dep Ca channels (L-type), Ry Channels (opens), phospholambon (PLB) which increases uptake of Ca into the SR, Troponin (decreasing Ca affinity)
Which are L-type ca channels, voltage-gated or Ry?
voltage-gated
What causes the positive inotropic effect?
phosphorylation of Ca channels and Ryanadine release channels
What effect will a decrease in Na have on the heart muscle?
positive inotropic, inc Ca in cells, taken into SR, extra Ca will cause more forceful contraction (same duration of H contraction)
Another way to describe overstretch of sarcomere so that very few X-bridges are formed
very little active tension
What does the systolic isometric max curve represent?
ideal sarcomere length and the quick decrease in P thereafter
What prevents an ideal X-bridge formation at the completely unstretched state of the sarcomere?
steric hinderance
Where in the P-V do the a-v and SL valves close?
a-v: EDV (bottom R of graph), SL: ESV (upper L of graph)
At what point in the P-V loop is the ventricle finished contracting?
ESV: upper left point
How to calculate after load pressure using a P-V loop:
diff bw the highest point on P-V loop and the upper right point (end of isovolumetric contraction)
Where can you determine the preload volume?
bottom right point of P-V loop (EDV)
What type of regulation is a change in the preload volume?
heterometric regulation
How would your EDV and SV be altered from standing to laying down?
both increase
