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Flashcards in Section 2 Review Deck (293):
1

Likely cause of edema if the venous return is blocked:

inc cap hydrostatic P

2

What would the change in HR be if you inc. Ca++ current thru voltage activated Ca++ channels?

baroreflex decrease in HR

3

Effects of cardiac gylcoside:

partial inhibition of the arc na/K pumps, inc activator pool Ca++, Inc force generation during systole, inc intracellular Ca++

4

What would happen if at art P inc and there was a dec in inotropy?

SV decreases

5

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

6

If a drug inc both mean pressure and arterial pulse what mode of action is it using?

increase SV

7

a-1 receps primarily innervates:

s.m.

8

Which neurotransmitter has higher affinity for the α1 receptor, noradrenaline or adrenaline

noradrenaline

9

What happens when you activate a-1 receps?

contraction of s.m.

10

What transmitter do B-2 receps interact w?

epinephrine

11

What transmitter do a-1 receps interact w?

epi and norepi

12

Physiological response of the activation of B-2 receps:

smooth muscle relaxation

13

What effect does norepi have on B-2 receps?

none

14

To what receps does epi bind?

α1, α2, β1, β2, and β3

15

Activation of B-1 recep leads to:

Increase heart rate in SA node (chronotropic effect)
Increase atrial cardiac muscle contractility. (inotropic effect)

16

T or F? Activation of B-1 recep leads to both a chronotropic effect and an inotropic effect.

T

17

Chronotropic effect deal with:

heart rate

18

Negative chronotropes:

Ca++ channel blocker, beta blockers, and
Acetylcholine

19

Positive chronotropes:

Adrenergic agonists, Atropine, Dopamine, Epinephrine, Isoproterenol

20

What do inotropes do?

alters the force or energy of muscular contractions

21

One of the most important factors affecting inotropic state

Ca++ levels

22

What do inotropic drugs typical alter?

Ca++ levels

23

positive inotrpic drugs

Calcium
Catecholamines
Dopamine
Epinephrine (adrenaline)
Norepinephrine (noradrenaline)
Angiotensin II
Digitalis

24

negative inotropic drugs:

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