Section 2 Review Flashcards
1
Q
Likely cause of edema if the venous return is blocked:
A
inc cap hydrostatic P
2
Q
What would the change in HR be if you inc. Ca++ current thru voltage activated Ca++ channels?
A
baroreflex decrease in HR
3
Q
Effects of cardiac gylcoside:
A
partial inhibition of the arc na/K pumps, inc activator pool Ca++, Inc force generation during systole, inc intracellular Ca++
4
Q
What would happen if at art P inc and there was a dec in inotropy?
A
SV decreases
5
Q
Regulation of s.m. involves:
A
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
6
Q
If a drug inc both mean pressure and arterial pulse what mode of action is it using?
A
increase SV
7
Q
a-1 receps primarily innervates:
A
s.m.
8
Q
Which neurotransmitter has higher affinity for the α1 receptor, noradrenaline or adrenaline
A
noradrenaline
9
Q
What happens when you activate a-1 receps?
A
contraction of s.m.
10
Q
What transmitter do B-2 receps interact w?
A
epinephrine
11
Q
What transmitter do a-1 receps interact w?
A
epi and norepi
12
Q
Physiological response of the activation of B-2 receps:
A
smooth muscle relaxation
13
Q
What effect does norepi have on B-2 receps?
A
none
14
Q
To what receps does epi bind?
A
α1, α2, β1, β2, and β3
15
Q
Activation of B-1 recep leads to:
A
Increase heart rate in SA node (chronotropic effect)
Increase atrial cardiac muscle contractility. (inotropic effect)
16
Q
T or F? Activation of B-1 recep leads to both a chronotropic effect and an inotropic effect.
A
T
17
Q
Chronotropic effect deal with:
A
heart rate
18
Q
Negative chronotropes:
A
Ca++ channel blocker, beta blockers, and
Acetylcholine
19
Q
Positive chronotropes:
A
Adrenergic agonists, Atropine, Dopamine, Epinephrine, Isoproterenol
20
Q
What do inotropes do?
A
alters the force or energy of muscular contractions
21
Q
One of the most important factors affecting inotropic state
A
Ca++ levels
22
Q
What do inotropic drugs typical alter?
A
Ca++ levels
23
Q
positive inotrpic drugs
A
Calcium Catecholamines Dopamine Epinephrine (adrenaline) Norepinephrine (noradrenaline) Angiotensin II Digitalis
24
Q
negative inotropic drugs:
A
Beta blockers and calcium channel blockers
25
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)
26
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)
27
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)
28
Calc CO from mean aortic BP, mean R atrial BP, systemic vascular R, and HR:
(Mean R atrial - Mean aortic BP)/R
29
Is the interstial V changed or unchanged? Decreased cap hydro P and dec cap osm P:
unchanged
30
Is the interstial V changed or unchanged? Decreased cap hydro P and inc lymph flow.
changed
31
Is the interstial V changed or unchanged? Decreased cap os P and dec lymph flow.
changed
32
inc cap hydo P and dec lymph flow.
changed
33
Inc cap hyrdo P and dec cap osm P:
changed
34
Effect of B-1 agonist:
Increase heart rate in SA node (chronotropic effect)
| Increase atrial cardiac muscle contractility. (inotropic effect)
35
Effect of agonist for precapillary alpha1 receps:
contraction of s.m.
36
Effect of mucurinic recep antagonist:
decreased autonomic m. contraction
37
What activates muscarinic receps?
AcH
38
Effect of muscarinic recep activation in the heart
slow heart rate and reduce contractile forces of atrium
39
Flux:
Permeability X conc gradient
40
In going for rest to exercise, the CO can increase __ times and the oxygen delivery to tissue can increase __ times.
5, 4
41
Convective flow in our system:
CO
42
Where to find fenestrated caps:
sk m.
43
Where to find sinusoidal caps:
liver
44
difference bw velocity and flow:
how fast something moves vs. how much of something moves
45
What type of fluid P is found in isf? negative, zero, positive?
negative, created by lymph uptakes of fluid
46
What maintains the shape of our tissues?
neg P is the isf's
47
What is not fxning properly in elephantiasis?
isf uptake into lymph vessels
48
net forces in vessels is always __ -___:
cap - isf
49
How is the P in the art and veins changed with edema?
both are increased
50
How is the R in the art and veins changed with edema?
Rv incr, Rart dec
51
Reabsorption will occur when __ pressure exceeds ___ pressure
osmotic, hydrostatic
52
How are cap and ifs's osmotic P's affected in edema?
Cap osm p decreases, isf osm p increases
53
inc in filtration can be caused by:
inc art P, inc ven P, dec arteriolar R
54
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.
55
How is lymph flow affected with edema?
dec
56
How much of an inc in mm Hg is there from the L atrium to the aorta?
90 mm Hg (5-95 mm Hg)
57
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)
58
How do the SV of the L and R ventricles compare in the steady state?
SV R ventricle = SV L ventricle
59
How does the systemic R compare to the pulmonary?
sys = 6 times higher
60
How does the systemic P gradient compare to the pulmonary?
sys = 6 times higher
61
The L ventricles works about __ times harder than the R ventricle.
6
62
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
63
Which close first, the semilunar valves or the a-v valves of the L ventricle?
a-v
64
T or F? A larger P gradient is required to fill during diastole.
F. small
65
Is mitral valve closing the 1st or 2nd sound?
1st
66
Ej fraction:
SV/ EDV part/whole each stroke/total filling each time
67
Length of cardiac cycle in ECG:
R wave to R wave (peak to peak)
68
Where in the ECG is isovolumetric contraction?
imm after the under/after shoot of the R wave
69
Where in the ECG is isovolumetric relaxation?
after small hill (created by systole)
70
What does the R-R interval indicate?
the length of the cardiac cycle
71
diastole in the ECG:
after hill of after/under shoot of the R wave
72
What fraction of the cardiac cycle is diastole?
2/3
73
Which valves close directly before isovolumetric contraction?
a-v valve (check)
74
This causes a small bump in ventricular filling:
atrial kick
75
Is phase 1 diastole or systole?
diastole
76
What causes the increase in pressure in the L ventricle during isovolumetric contraction?
mechanical contraction (ventricular wall tension)
77
How is L ventricular pressure changing during isovolumetric relaxation?
decreasing
78
Are inotropic factors preload and after load dependent or independent?
independent?
79
HR can increase __ times.
3
80
SV can increase __ times.
2
81
Is the length-tenstion relationship preload-dependent or afterload-dependent?
preload-dependent
82
Is the force-velocity relationship preload-dependent or afterload-dependent?
afterload-dependent
83
T or F? Every depolarized cell leads to intracellular Ca2+ increase, which leads to contraction.
T
84
When actin and myosin bind does the spring stretch or decrease in length?
stretch
85
What creates active tension in the myosin/actin network?
the binding of the actin/myosin
86
T or F? Actin binds to myosin and not the opposite way.
F. myosin bind actin
87
Which has a Ca binding site, troponin or tropomyosin?
troponin
88
What blocks the binding site on G-actin?
tropomyosin
89
Under what chemical condition will tropomyosin block the head region of myosin from attaching to the binding site on actin?
Low Ca++ conc
90
To where does Ca++ bind to help expose the binding sites?
to Troponin C molecule
91
T or F? Myosin has ATPase activity.
T
92
All muscles can generate Fmax force of:
5x10^3
93
Another name for Ca form the SR:
activator Ca++
94
Ca released from the SR is:
graded
95
What terminates contraction of the heart?
move of Ca++ back into the SR
96
T or F? The Na/Ca exchanger works to inc intracellular Ca++ conc.
to expel Ca from the cell.
97
Does the Na/Ca exchanger fxn during diastole or systole?
diastole
98
What type of channels are DHPR's?
Voltage-gated at SL
99
What channels are involved in the release of trigger Ca++?
DHPR channels
100
What channels are involved in the release of activator Ca++?
Ryanodine channels
101
When does actin/myosin contraction terminate?
following electrical recovery of the myocyte and the return of cytosolic calcium to a diastolic level
102
How many X-bridges are activated in heart muscle at rest?
about 1/2
103
Which neurotransmitters have a positive inotropic effect?
epi and norepi
104
The activation of Beta receptors will:
increase cAMP and the exposure of PKA
105
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)
106
Which are L-type ca channels, voltage-gated or Ry?
voltage-gated
107
What causes the positive inotropic effect?
phosphorylation of Ca channels and Ryanadine release channels
108
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)
109
Another way to describe overstretch of sarcomere so that very few X-bridges are formed
very little active tension
110
What does the systolic isometric max curve represent?
ideal sarcomere length and the quick decrease in P thereafter
111
What prevents an ideal X-bridge formation at the completely unstretched state of the sarcomere?
steric hinderance
112
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)
113
At what point in the P-V loop is the ventricle finished contracting?
ESV: upper left point
114
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)
115
Where can you determine the preload volume?
bottom right point of P-V loop (EDV)
116
What type of regulation is a change in the preload volume?
heterometric regulation
117
How would your EDV and SV be altered from standing to laying down?
both increase
118
How would preload be altered from standing to laying down
increases
119
How would a hemorrhage effect EDV?
decrease (less preload)
120
How does a decrease in preload effect SV?
decreases
121
How to get pos inotropic effect on heart m.:
stim n.s. to release norepi and activate B-1 receps
122
How si the blue curve (far left in the P-V) effected with a pos inotropic effect?
more forceful contraction
123
What type of effect leads to a more forceful contraction with every volume?
inotropic effect
124
T or F? SV increases with inotropy.
T.
125
What type of regulation is a change in the inotropic mechanism?
homeometric regulation
126
Which can produce a change in SV, inotropic mechanisms, preload mechanisms, or both?
both
127
How are after load and arterial pressure related?
dec art afterload, dec art p
128
How is the afterload affected with HBP?
it increases, harder to push blood out of ventricle
129
Where on the P-V graph is the after load?
upper R point (end of isovolumetric contraction)
130
How is isovolumetric contracted affected with a larger after load?
heart contracts isovolumetrically to a greater point
131
How is Sv affected with a larger after load?
SV decreases, less energy available for ejection? or less than ideal X-bridge alignment?
132
Anything that varies afterload will have an impact on:
Sv
133
Increase after load, ____ Sv.
dec
134
How will asteroid and Sv be affected with inotropic effectors?
Inc after load, dec SV
135
T or F? Chemical/Inotropic effects are both preload and after load independent.
T
136
These will all have neg inotropic effects:
ischemia, anesthetics, myopathy drugs (muscular weakness drugs)
137
These will all have pos inotropic effects:
NE/epi, syp stimulus, Beta agonist, cardiac glycosides
138
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
139
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)
140
Bodies life saving response to drug that constricts arterioles:
(raise in arterial blood pressure, increasing after load) Response: Increase preload to compensate.
141
When is the venomotor system activated?
when heart need more blood
142
How does the adrenal medulla regulated MAP?
inotropic and chronotropic effects (CO and art R)
143
Vagus n. sends BP info from:
aortic arch to the medulla
144
Glossopharyngeal n. sends BP info from:
carotid sinus to medulla
145
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
146
These receptors are related to the parasympathetic system:
Ach-M2
147
Predominant receptor in the heart:
M2
148
Receptor for heart m. contraction:
NE-B1
149
Receptor for precap R:
NE-a1
150
Receptor for venous compliance:
NE-a1
151
What receptors are involved in inotropy?
NE-B1 (only these?)
152
What receptors are involved in SA node?
Ach-M2 and NE-B1
153
What type of effect does para output to the SA node lead to?
neg chronotropic
154
sympathetic fibers go to:
the SA node, myocytes, precapillary resistance vessels, and postcapillary compliance vessels.
155
Sym input to SA Node:
stimulates norepinephrine Beta1 Receptor, increasing heart rate. (chronotropy)
156
Sym input to myocytes:
stimulates norepinephrine Beta1 Receptor, having an ionotropic and lusitropic effect, increasing contraction force and speed.
157
Sym input to precapillary Vessels:
stimulates norepinephrine Alpha1 Receptor, causing the vessels to constrict, increase resistance, increase pressure, and diminish flow.
158
Sym input to postcapillary Vessels:
stimulates norepinephrine Alpha1 Receptor, decreasing compliance, stiffen vessels, send more blood back to the heart.
159
Sym innervation effects these types of receptors:
a -1 (pre and post cap) and B-1 (beat, heart)
160
SV depends on:
Venomotor Tone and Inotropic State
161
Can the sym system have chronotropic effects?
yes
162
Can the parasym system have chronotropic effects?
yes
163
Can the sym system have inotropic effects?
yes
164
Can the parasym system have inotropic effects?
no
165
Will increasing the Depressor center activity have a pos or neg chronotropic effect?
negative
166
4 effects of the pressor center:
chrono (HR), ino (Ca++ levels), venous return, vasomotor tone
167
__ effects changer HR while __ effects change SV: (either changes CO)
chronotropic, inotropic
168
Does fear lead to sym or para effect?
para
169
Does anger lead to sym or para effect?
sym
170
Sym effects:
+ chrono, + ino, + vaso, +veno
171
T or F? When the sym system is activated the vessels in the arterial side and venous side are more contracted.
T
172
Parasym effects:
- chrono
173
How is the BP altered in response to cold or pain
increased
174
How is the BP altered in response to warmth, internal pain?
decreased
175
T or F? Veins can contract to decrease compliance.
T
176
Overlay control of the local control is done by:
The CNS (sympathetic outflow) “Neurogenic Control”
177
Vascular smooth muscle cells contain what type of receptor?
alpha1
178
alpha1 receptors are typically activated by the NT:
NE
179
Hormones that in inc contractility of precaps:
Angiotensin, ANP, Vasopressin, Epi
180
How are adenosine levels affected with a decin pH?
they inc
181
Why do adenosine levels increase during high metabolic rates?
bc ATP is being used for metabolism
182
Is adenosine a vasodilator or constritor?
dilator
183
How is total systemic flow affected by a decrease in resistance in arts?
overall flow increases
184
How would a decrease in afterload and an increase in preload affect SV?
SV inc leading to an increase in CO
185
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
186
How would an increase in venous flow affect the preload?
increase preload
187
supply of blood brought up to meet the demands of the body:
Active hyperemia
188
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
189
Thin filament regulation is used for __ and thick filament regulation is used for __.
cardiac muscle, smooth muscle
190
Mech of control for s.m.:
ca entry into cytosol, bind calmodulin to MLCK, activates MLCK,MLCK phosphorylates myosin, poshorylated M-A
191
Why do X-bridges break when Ca leaves the cell?
my is dephosphorylated by MLC Phosphatase
192
do cAMP and cGMP kinase activate or deactivate MLCKinase?
deactivate
193
Ways to control X-bridge formation:
ca levels in cel, MLCK availability, presence of cAMP and cGMP
194
After depol of a cell, Ca enters and binds:
calmodulin and MLCK (leads to contraction)
195
What receptors can be found in vascular s.m. cells
a-1 (NE) and B2 (epi)
196
What pathway leads to the release of Ca from the SR in the vascular smooth muscle cell?
IP3
197
How does adenosine operates on K system?
Increase in K conductance → hyperpolarization → closes Ca channels → decrease in Ca entry → relaxation of smooth muscle
198
Overall result of adenosine:
relaxation of smooth muscle
199
Release of Ca from SR is regulated by:
a-1 receptors activated by NE
200
What produces cAMP in vascular smooth muscle cells?
B-2 receptro acted on by Epi
201
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)
202
T or F? NE-a-1 receptors on located on both sides of the capillary bed.
T
203
How, if at all, is the BV in the peripheral tissues affected with sym stimulation to the post capillary vessels?
decreases
204
How is venous compliance affected with sym stimulation to the post cap venules?
decreases
205
How is the driving force of flow changed with sym stim of the precap arterioles?
not chnages (check)
206
How is BV in the tissue space affected with sym stimulation of the precap vessels?
it decreases bc the pressure in the cap drops
207
Peripheral flow depends on what types of control?
local and neural controls
208
Sym activation of the heart during exercise uses what NT and what receptor?
NE, B-1
209
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)
210
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
211
What receptors increase in heart rate and ionotropy during exercise?
Beta1 receptors.
212
What opposes the dilation of vessels to the skmm. expected with sym stimulation during exercise?
local metabolites overwhelm the spy control of the aa.
213
Is vasodilation or vasoconstriction favored during exercise?
vasodilation
214
Is venoconstriction or venodilation favored during exercise?
venoconstriction
215
Why can the body regulate flow from one circuit, independent of the other
CVS is assembled in parallel
216
Pressure required to pump blood through pulmonary circulation:
20 mm Hg
217
Driving force of blood flow through pulmonary system:
15 mm Hg (P gradient) (20, 15, 5, 93, 2)
218
Calc P from volume and stiffness:
V X stiffness
219
Calc P from volume and compliance:
V/Compliance
220
How are stiffness and compliance related?
inversely
221
Calc stiffness from P and V:
p/V
222
How much fluid in a balloon will drain?
Only the stress volume
223
Why can our heart pump all fluid out and not just the stress volume like a balloon?
the pressure gradient
224
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
225
T or F? Blood is ejected from ventricles as soon as active tension starts.
F. Soon thereafter, isovolumetric contraction must first take place
226
The venous compartment is ___x more compliant than the arterial compartment
19
227
On which side of the system does most of the stressed volume reside, venous or arterial?
venous
228
What are the unstressed and stressed V's of the heart?
4.4L and 5L
229
What is the mean circulatory pressure?
10 mm Hg
230
If flow through cap beds was completely blocked, P would increase/decrease in the arteries? What about veins?
inc, dec
231
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
232
Pressure difference are measured at these 2 spots for systemic flow pressure gradient measurements:
R atrium, aorta
233
What is the driving force/pressure gradient for the systemic system?
90 mm Hg
234
T or F? Each of the circulatory system is driven by the same driving force
T (force of the aorta)
235
Will total resistance always be more or less than the smallest individual resistance?
less
236
The central/pulmonary system is arranged in __ and the systemic system is arranged in____.
series, parallel
237
All elements in series/parallel are supplied by the same pressure reservoir
parallel
238
All elements in series/parallel will have the same amount of flow through each element.
series
239
Circuits in parallel/series allow for different flow through different areas.
parallel
240
Which series type allows you to sum the individual resistance to get the total resistance of the circuit?
series
241
T or F? P drops in both the arterial and venous sides of the circulation.
T
242
Where is the largest P drop?
arterioles
243
What % of the BV is in the high pressure reservoir?
20%
244
What % of the BV is in the low pressure reservoir?
65%
245
T or F? The P in the arterial system is extremely high and constant.
T
246
As resistance increases, flow:
decreases
247
If you decrease resistance, flow:
increases
248
Flow equation involving vessel radius:
(pressure gradient X r^4)/ (viscosity X L)
249
Resistance = (involves tube length and radius)
(tube length X viscosity)/(radius^4)
250
Flow is indirectly proportional with both:
tube length and viscosity
251
Blood is __x more viscous than water.
2
252
it takes __x more pressure to generate flow in blood than water.
2
253
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)
254
systemic R = ?
18 mm HgL/min
255
pulmonary R = ?
3 mm Hg/L/min
256
How do APs spread through cardiac mm.?
gap junctions
257
How do the APs differ bw myocardial cells and the cells of the SA node?
longer Aps in the myocardial cells
258
Automaticity of the SA node, AV node, and parking fibers
70-80 BPM, 40-50 BPM, and 25-35 BPM
259
Which is the main pacemaker of the heart. AV or SA node
SA
260
Are SA and VA nodes slow or fast conducting?
slow
261
During excitation of the myocardial cell, there is activation of __, inactivation of __, and slow __ activation
Na, K, Ca
262
Where are concentrations of Na, K, and Ca higher and lower in the myocardial cell?
K higher in, Na higher out, Ca higher out
263
What does the long plateau of the AP in the myocardial cell allow for?
full contraction
264
What channels are responsible for the long plateau of the AP in the myocardial cells?
Ca channels
265
What channels are responsible for the fast repolarization of the AP in the myocardial cells?
K channels
266
What type of channels do normal fast conducting cells use?
a lot of Na channels. (Purk and working myocaridum)
267
What type of channels do normal slow conducting cells use?
a few Ca channels (no Na channels)
268
What type of cells have normal fast conducting fibers?
Purk and working myocaridum
269
What type of cells have normal slow conducting fibers?
AV and SA nodes
270
Which cells use Ca channels to increase the duration of the AP?
AV and SA node cells
271
Are cells of the AV and SA node narrow or wide?
narrow
272
Do cells of the AV and SA node how a short or long space/length constant?
short (impulse conducts slowly)
273
What will happen if Ca channels are blocked in the SA or VA nodal cells?
slowed conduction rate
274
Automaticity in pacemaker cells is mediated through these specific receptors
(M1-receptor-ACh), (Beta1-receptor-NE)
275
T or F? Heart will always produce a SV into the arterial system that is greater than the outflow from the arterial system.
T
276
During diastole, pressure in ventricle:
falls
277
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.
278
What maintains the pressure of the system during diastole?
elastic recoil, extra energy in walls from systole
279
How does flow across capillaries vary through systole and diastole?
it doesn't, it remains more or less constant
280
Which phase of the P vs. time graph tells us about the heart?
rising pressure phase
281
Which phase of the P vs. time graph tells us about the systemic circulation?
Falling pressure phase
282
If you decrease arteriole resistance how will arteriolarrRun-off be effected?
Increased
283
Relationship bw compliance, Sv and Pulse pressure:
P(p) = Sv/Compliance
284
In steady state these are both constant:
art flow and avg art P
285
Everything that can change the pressure of the arteries has to do with:
Stroke Volume, Heart Rate, and Arterial Resistance
286
How will pulse P and MAP be affected be a suddenly decreased SV?
both decrease (pulse P for only one stroke)
287
How will pulse P and MAP be effected with dec art R?
dec MAP, inc pulse P
288
Why will pulse P increase with dec art R?
dec after load, inc preload, and inc SV
289
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)
290
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)
291
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)
292
Decrease in arterial compliance, affect on MAP and PP:
MAP does not change (not compliance dependent), inc PP due to inc compliance)
293
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
