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
How would preload be altered from standing to laying down
increases
How would a hemorrhage effect EDV?
decrease (less preload)
How does a decrease in preload effect SV?
decreases
How to get pos inotropic effect on heart m.:
stim n.s. to release norepi and activate B-1 receps
How si the blue curve (far left in the P-V) effected with a pos inotropic effect?
more forceful contraction
What type of effect leads to a more forceful contraction with every volume?
inotropic effect
T or F? SV increases with inotropy.
T.
What type of regulation is a change in the inotropic mechanism?
homeometric regulation
Which can produce a change in SV, inotropic mechanisms, preload mechanisms, or both?
both
How are after load and arterial pressure related?
dec art afterload, dec art p
How is the afterload affected with HBP?
it increases, harder to push blood out of ventricle
Where on the P-V graph is the after load?
upper R point (end of isovolumetric contraction)
How is isovolumetric contracted affected with a larger after load?
heart contracts isovolumetrically to a greater point
How is Sv affected with a larger after load?
SV decreases, less energy available for ejection? or less than ideal X-bridge alignment?
Anything that varies afterload will have an impact on:
Sv
Increase after load, ____ Sv.
dec
How will asteroid and Sv be affected with inotropic effectors?
Inc after load, dec SV
T or F? Chemical/Inotropic effects are both preload and after load independent.
T
These will all have neg inotropic effects:
ischemia, anesthetics, myopathy drugs (muscular weakness drugs)
These will all have pos inotropic effects:
NE/epi, syp stimulus, Beta agonist, cardiac glycosides
Body rxn to heart attack or ischemic heart disease:
CV decreases as a result (decreased inotropy). Response: kidney will retain volume and recover some of the SV
Bodies life saving response to hemorrhage:
(Losing BV, SV decreasing) Response: Inc Ca activation of the heart, produce a more forceful contraction to offset fall in SV. (increase inotropy)
Bodies life saving response to drug that constricts arterioles:
(raise in arterial blood pressure, increasing after load) Response: Increase preload to compensate.
When is the venomotor system activated?
when heart need more blood
How does the adrenal medulla regulated MAP?
inotropic and chronotropic effects (CO and art R)
Vagus n. sends BP info from:
aortic arch to the medulla
Glossopharyngeal n. sends BP info from:
carotid sinus to medulla
When the blood pressure is at 100, how many impulses per second are being produced and sent from the pressure receptors in the brain?
10
These receptors are related to the parasympathetic system:
Ach-M2
Predominant receptor in the heart:
M2
Receptor for heart m. contraction:
NE-B1
Receptor for precap R:
NE-a1
Receptor for venous compliance:
NE-a1
What receptors are involved in inotropy?
NE-B1 (only these?)
What receptors are involved in SA node?
Ach-M2 and NE-B1
What type of effect does para output to the SA node lead to?
neg chronotropic
sympathetic fibers go to:
the SA node, myocytes, precapillary resistance vessels, and postcapillary compliance vessels.
Sym input to SA Node:
stimulates norepinephrine Beta1 Receptor, increasing heart rate. (chronotropy)
Sym input to myocytes:
stimulates norepinephrine Beta1 Receptor, having an ionotropic and lusitropic effect, increasing contraction force and speed.
Sym input to precapillary Vessels:
stimulates norepinephrine Alpha1 Receptor, causing the vessels to constrict, increase resistance, increase pressure, and diminish flow.
Sym input to postcapillary Vessels:
stimulates norepinephrine Alpha1 Receptor, decreasing compliance, stiffen vessels, send more blood back to the heart.
Sym innervation effects these types of receptors:
a -1 (pre and post cap) and B-1 (beat, heart)
SV depends on:
Venomotor Tone and Inotropic State
Can the sym system have chronotropic effects?
yes
Can the parasym system have chronotropic effects?
yes
Can the sym system have inotropic effects?
yes
Can the parasym system have inotropic effects?
no
Will increasing the Depressor center activity have a pos or neg chronotropic effect?
negative
4 effects of the pressor center:
chrono (HR), ino (Ca++ levels), venous return, vasomotor tone
__ effects changer HR while __ effects change SV: (either changes CO)
chronotropic, inotropic
Does fear lead to sym or para effect?
para
Does anger lead to sym or para effect?
sym
Sym effects:
+ chrono, + ino, + vaso, +veno
T or F? When the sym system is activated the vessels in the arterial side and venous side are more contracted.
T
Parasym effects:
- chrono
How is the BP altered in response to cold or pain
increased
How is the BP altered in response to warmth, internal pain?
decreased
T or F? Veins can contract to decrease compliance.
T
Overlay control of the local control is done by:
The CNS (sympathetic outflow) “Neurogenic Control”
Vascular smooth muscle cells contain what type of receptor?
alpha1
alpha1 receptors are typically activated by the NT:
NE
Hormones that in inc contractility of precaps:
Angiotensin, ANP, Vasopressin, Epi
How are adenosine levels affected with a decin pH?
they inc
Why do adenosine levels increase during high metabolic rates?
bc ATP is being used for metabolism
Is adenosine a vasodilator or constritor?
dilator
How is total systemic flow affected by a decrease in resistance in arts?
overall flow increases
How would a decrease in afterload and an increase in preload affect SV?
SV inc leading to an increase in CO
Increase in metabolic demand in tissues can lead to this problem:
p drop in arterial system, dec after load, inc preload, inc SV, and inc CO
How would an increase in venous flow affect the preload?
increase preload
supply of blood brought up to meet the demands of the body:
Active hyperemia
Occlude vessel, vasodilator metabolite conc elevates Release occlusion → overshoot of blood flow necessary to wash out added metabolites → brings system back to normal.
reactive hyperemia
Thin filament regulation is used for __ and thick filament regulation is used for __.
cardiac muscle, smooth muscle
Mech of control for s.m.:
ca entry into cytosol, bind calmodulin to MLCK, activates MLCK,MLCK phosphorylates myosin, poshorylated M-A
Why do X-bridges break when Ca leaves the cell?
my is dephosphorylated by MLC Phosphatase
do cAMP and cGMP kinase activate or deactivate MLCKinase?
deactivate
Ways to control X-bridge formation:
ca levels in cel, MLCK availability, presence of cAMP and cGMP
After depol of a cell, Ca enters and binds:
calmodulin and MLCK (leads to contraction)
What receptors can be found in vascular s.m. cells
a-1 (NE) and B2 (epi)
What pathway leads to the release of Ca from the SR in the vascular smooth muscle cell?
IP3
How does adenosine operates on K system?
Increase in K conductance → hyperpolarization → closes Ca channels → decrease in Ca entry → relaxation of smooth muscle
Overall result of adenosine:
relaxation of smooth muscle
Release of Ca from SR is regulated by:
a-1 receptors activated by NE
What produces cAMP in vascular smooth muscle cells?
B-2 receptro acted on by Epi
Overall result of Epi attaching to B-2 receptor in vascular smooth muscle cells:
relaxes the cell (only s.m. cells controlling blood flow, not all vas s.m. cells)
T or F? NE-a-1 receptors on located on both sides of the capillary bed.
T
How, if at all, is the BV in the peripheral tissues affected with sym stimulation to the post capillary vessels?
decreases
How is venous compliance affected with sym stimulation to the post cap venules?
decreases
How is the driving force of flow changed with sym stim of the precap arterioles?
not chnages (check)
How is BV in the tissue space affected with sym stimulation of the precap vessels?
it decreases bc the pressure in the cap drops
Peripheral flow depends on what types of control?
local and neural controls
Sym activation of the heart during exercise uses what NT and what receptor?
NE, B-1
Sym activation of the precap vessels to muscles during exercise is via what NT and what receptor?
epi, B2 (leads to vasodilation) local metabolites lead to vasoconstriction as well) B2 activates cAMP which inhibits MLCK, leads to relaxed s.m. (dilation)
Sym activation of the precap and post cap vessels peripheral tissues (not muscle) during exercise is via what NT and what receptor?
NE, a-1
What receptors increase in heart rate and ionotropy during exercise?
Beta1 receptors.
What opposes the dilation of vessels to the skmm. expected with sym stimulation during exercise?
local metabolites overwhelm the spy control of the aa.
Is vasodilation or vasoconstriction favored during exercise?
vasodilation
Is venoconstriction or venodilation favored during exercise?
venoconstriction
Why can the body regulate flow from one circuit, independent of the other
CVS is assembled in parallel
Pressure required to pump blood through pulmonary circulation:
20 mm Hg
Driving force of blood flow through pulmonary system:
15 mm Hg (P gradient) (20, 15, 5, 93, 2)
Calc P from volume and stiffness:
V X stiffness
Calc P from volume and compliance:
V/Compliance
How are stiffness and compliance related?
inversely
Calc stiffness from P and V:
p/V
How much fluid in a balloon will drain?
Only the stress volume
Why can our heart pump all fluid out and not just the stress volume like a balloon?
the pressure gradient
T or F? With each pump of the heart the EDV is the maximum unstressed volume.
F. More than just the stressed volume was ejected so there is some filling that is required before we are at the stressed volume
T or F? Blood is ejected from ventricles as soon as active tension starts.
F. Soon thereafter, isovolumetric contraction must first take place
The venous compartment is ___x more compliant than the arterial compartment
19
On which side of the system does most of the stressed volume reside, venous or arterial?
venous
What are the unstressed and stressed V’s of the heart?
4.4L and 5L
What is the mean circulatory pressure?
10 mm Hg
If flow through cap beds was completely blocked, P would increase/decrease in the arteries? What about veins?
inc, dec
T or F? If flow through the cap beds is blocked, the Pa will rise higher than the Pv is going to fall due to the difference in compliance.
T
Pressure difference are measured at these 2 spots for systemic flow pressure gradient measurements:
R atrium, aorta
What is the driving force/pressure gradient for the systemic system?
90 mm Hg
T or F? Each of the circulatory system is driven by the same driving force
T (force of the aorta)
Will total resistance always be more or less than the smallest individual resistance?
less
The central/pulmonary system is arranged in __ and the systemic system is arranged in____.
series, parallel
All elements in series/parallel are supplied by the same pressure reservoir
parallel
All elements in series/parallel will have the same amount of flow through each element.
series
Circuits in parallel/series allow for different flow through different areas.
parallel
Which series type allows you to sum the individual resistance to get the total resistance of the circuit?
series
T or F? P drops in both the arterial and venous sides of the circulation.
T
Where is the largest P drop?
arterioles
What % of the BV is in the high pressure reservoir?
20%
What % of the BV is in the low pressure reservoir?
65%
T or F? The P in the arterial system is extremely high and constant.
T
As resistance increases, flow:
decreases
If you decrease resistance, flow:
increases
Flow equation involving vessel radius:
(pressure gradient X r^4)/ (viscosity X L)
Resistance = (involves tube length and radius)
(tube length X viscosity)/(radius^4)
Flow is indirectly proportional with both:
tube length and viscosity
Blood is __x more viscous than water.
2
it takes __x more pressure to generate flow in blood than water.
2
Increasing radius K will increase flow through K, what effect will this have on flow through M?
no effect (this is why the parallel setup is so genius, we can selectively increase and decrease flow to certain parts of our body as needed)
systemic R = ?
18 mm HgL/min
pulmonary R = ?
3 mm Hg/L/min
How do APs spread through cardiac mm.?
gap junctions
How do the APs differ bw myocardial cells and the cells of the SA node?
longer Aps in the myocardial cells
Automaticity of the SA node, AV node, and parking fibers
70-80 BPM, 40-50 BPM, and 25-35 BPM
Which is the main pacemaker of the heart. AV or SA node
SA
Are SA and VA nodes slow or fast conducting?
slow
During excitation of the myocardial cell, there is activation of __, inactivation of __, and slow __ activation
Na, K, Ca
Where are concentrations of Na, K, and Ca higher and lower in the myocardial cell?
K higher in, Na higher out, Ca higher out
What does the long plateau of the AP in the myocardial cell allow for?
full contraction
What channels are responsible for the long plateau of the AP in the myocardial cells?
Ca channels
What channels are responsible for the fast repolarization of the AP in the myocardial cells?
K channels
What type of channels do normal fast conducting cells use?
a lot of Na channels. (Purk and working myocaridum)
What type of channels do normal slow conducting cells use?
a few Ca channels (no Na channels)
What type of cells have normal fast conducting fibers?
Purk and working myocaridum
What type of cells have normal slow conducting fibers?
AV and SA nodes
Which cells use Ca channels to increase the duration of the AP?
AV and SA node cells
Are cells of the AV and SA node narrow or wide?
narrow
Do cells of the AV and SA node how a short or long space/length constant?
short (impulse conducts slowly)
What will happen if Ca channels are blocked in the SA or VA nodal cells?
slowed conduction rate
Automaticity in pacemaker cells is mediated through these specific receptors
(M1-receptor-ACh), (Beta1-receptor-NE)
T or F? Heart will always produce a SV into the arterial system that is greater than the outflow from the arterial system.
T
During diastole, pressure in ventricle:
falls
T or F? Heart will always produce a SV into the arterial system that is less than the outflow from the arterial system.
F. greater than.
What maintains the pressure of the system during diastole?
elastic recoil, extra energy in walls from systole
How does flow across capillaries vary through systole and diastole?
it doesn’t, it remains more or less constant
Which phase of the P vs. time graph tells us about the heart?
rising pressure phase
Which phase of the P vs. time graph tells us about the systemic circulation?
Falling pressure phase
If you decrease arteriole resistance how will arteriolarrRun-off be effected?
Increased
Relationship bw compliance, Sv and Pulse pressure:
P(p) = Sv/Compliance
In steady state these are both constant:
art flow and avg art P
Everything that can change the pressure of the arteries has to do with:
Stroke Volume, Heart Rate, and Arterial Resistance
How will pulse P and MAP be affected be a suddenly decreased SV?
both decrease (pulse P for only one stroke)
How will pulse P and MAP be effected with dec art R?
dec MAP, inc pulse P
Why will pulse P increase with dec art R?
dec after load, inc preload, and inc SV
Increase HR fro 30-60 BPM, affect on PP and MAP:
inc MAP, dec PP (shorter cycle length, less filling time, dec Sv/ inc after load, dec SV)
Increase HR fro 60-120 BPM, affect on PP and MAP:
inc MAP, dec PP (shorter cycle length, less filling time, dec Sv/ inc after load, dec SV)
Increase HR fro 120-300 BPM, affect on PP and MAP:
dec MAP and dec PP (MAP bc HR is so fast that SV is approaching 0, PP bc of dec SV)
Decrease in arterial compliance, affect on MAP and PP:
MAP does not change (not compliance dependent), inc PP due to inc compliance)
What to be cautious of even if an older pt has a normal BP:
could be reduced SV due to high R, high after load from stiff vessels, indicating fragile arterial system
