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Anesthesiologist Assistant > Cardiac Physiology Yr1FA23 > Flashcards

Cardiac Physiology Yr1FA23 Flashcards

1
Q

Each cycle of cardiac contraction and relaxation is initiated by

A

depolarization of the sinus node.

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2
Q

True/false: The cycle of cardiac contraction and relaxation being initiated by the sinus node is seen on the EKG?

A

FALSE

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3
Q

The P wave records

A

atrial depolarization and contraction.

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4
Q

The first part of the P wave reflects

A

right atrial activity; the second part reflects left atrial activity.

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5
Q

(the PR segment)

A

There is a brief pause when the electrical current reaches the AV node and the EKG falls silent

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6
Q

ventricular conducting system

A

(bundle of His, bundle branches, and Purkinje fibers)

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7
Q

The first part of the ventricles to be depolarized

A

the interventricular septum.

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8
Q

Ventricular depolarization generates what on the EKG

A

the QRS complex.

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9
Q

The wave of depolarization then spreads along the ventricular conducting system (bundle of His, bundle branches, and Purkinje fibers) and out into the

A

Ventricular Myocardium

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10
Q

The T wave records

A

repolarization of the ventricular myocardium

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11
Q

Is Atrial Repolarization seen on the EKG?

A

NO

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12
Q

the time from the start of atrial depolarization to the start of ventricular depolarization.

A

The PR interval

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13
Q

the time from the end of atrial depolarization to
the start of ventricular depolarization.

A

The PR segment

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14
Q

the time from the end of ventricular
depolarization to the start of ventricular repolarization.

A

The ST segment

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15
Q

the time from the start of ventricular
depolarization to the end of ventricular repolarization.

A

The QT interval

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16
Q

measures the time of ventricular depolarization.

A

The QRS interval

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17
Q

Alpha 1 Receptor Site

A

Vascular Smooth Muscle
Heart

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18
Q

Alpha 1 Receptor Action

A

Arterial Vasoconstriction

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19
Q

Alpha 2 Receptor Site

A

Vascular Smith Muscle
Presynaptic Nerve terminal

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20
Q

Alpha 2 Receptor Action

A

Vasoconstriction of venous capacitance vessels
Local feedback, inhibition of norepi release

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21
Q

Beta 1 Receptor Site

A

Heart

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22
Q

Beta 1 Receptor Action

A

Increased inotropic and chronotropic activity
Increased Av node conduction velocity

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23
Q

Beta 2 Receptor Site

A

Vascular smooth muscle
Bronchial smooth muscle

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24
Q

Beta 2 Receptor Action

A

Vasodilation of peripheral vasculature
Bronchodilation

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25
Q

D1 Receptor Site

A

post-synaptic
Vascular smooth muscle
(renal, Splanchnic, cerebral)
Renal Tubules

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26
Q

D2 Receptor Action

A

Decreased norepi release

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27
Q

D2 Receptor Site

A

Presynaptic sympathetic nerve terminals

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28
Q

D2 Receptor Action

A

Decreased norepi release

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29
Q

V1 Receptor Site

A

Vascular smooth muscle
platelets
Hepatocytes
myometrium

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30
Q

V1 Receptor Action

A

Vasoconstriction
Platelet aggregation
Glycogenolysis
Myometrial contraction

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31
Q

V2 Receptor Site

A

Basolateral membrane of collecting duct
Vascular endothelium
Vascular smooth muscle

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32
Q

V2 Receptor Action

A

INsertion of AQP-2 H2O channels in the apical membrane
induce AQP-2 synthesis
release of vwf and factor VII
vasodilation

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33
Q

V3/V1B Receptor Site

A

Anterior Pituitary gland

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34
Q

V3/ V1B Receptor Action

A

Release of ACTH
Prolactin
Endorphins

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35
Q

Norepinephrine Dose

A

0.02-.2 mg/kg/min

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36
Q

Norepinephrine Receptors

A

A1>B1& B2

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37
Q

Norepinephrine Inotropy

A

+

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38
Q

Norepinephrine Chronotropy

A

+

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39
Q

Norepinephrine SVR effects

A

+

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40
Q

Norepinephrine PVR Effects

A

+

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41
Q

Phenylephrine Dose

A

0.02-0.3 mcg/kg/min

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42
Q

Phenylephrine Receptors

A

Alpha1

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43
Q

Phenylephrine Inotropy Effects

A

<->

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44
Q

Phenylephrine Chronotropy effects

A

-

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45
Q

Phenylephrine SVR Effects

A

+

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46
Q

Phenylephrine PVR Effects

A

+

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47
Q

Vasopressin Dose

A

0.02-0.5 units/kg/hr

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48
Q

Vasopressin Receptors

A

V1 V2

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49
Q

Vasopressin Inotropy

A

<->

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50
Q

Vasopressin Chronotropy effects

A

<->

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51
Q

Vasopressin SVR Effects

A

+

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52
Q

Vasopressin PVR Effects

A

+

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53
Q

Nitroprusside Dose

A

0.2-5 mcg/kg/min

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54
Q

Nitroprusside Receptors

A

Increase cGMP in vascular myocytes

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55
Q

Nitroprusside Inotropy

A

<->

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56
Q

Nitroprusside Chronotropy

A

<->
+

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57
Q

Nitroprusside SVR

A

-

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58
Q

Nitroprusside PVR

A

-

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59
Q

Nicardipine Dose

A

0.5-5 mcg/kg/mni

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60
Q

Nicardipine Receptors

A

Calcium Channel Blocker

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61
Q

Nicardipine Inotropy

A

<->

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62
Q

Nicardipine Chronotropy

A

<->

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63
Q

Nicardipine SVR

A

-

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64
Q

Nicardipine PVR

A

-

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65
Q

Nitroglycerin Dose

A

0.2-10 mcg/kg/min

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66
Q

Nitroglycerin Receptors

A
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67
Q

Nitroglycerin Inotropy

A
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68
Q

Nitroglycerin Chronotropy

A
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69
Q

Nitroglycerin SVR

A
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70
Q

Nitroglycerin PVR

A
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71
Q

Epinephrine Dose

A

0.02-0.2 mcg/kg/min

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72
Q

Epinephrine Receptors

A

A1A2B1B2

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73
Q

Epinephrine Inotropy

A

+

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74
Q

Epinephrine Chronotropy

A

+

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75
Q

Epinephrine SVR

A

+

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76
Q

Epinephrine PVR

A

+

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77
Q

Epinephrine high-dose Inotropy

A

+

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78
Q

Epinephrine high-dose Chronotropy

A

+

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79
Q

Epinephrine high-dose SVR

A

<->

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80
Q

Epinephrine High-dose PVR

A

<->

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81
Q

Dopamine low dose

A

2-5 mcg/kg/min

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82
Q

Dopamine mid dose

A

5-10 mcg/kg/min

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83
Q

Dopamine high dose

A

> 10 mcg/kg/min

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84
Q

Dopamine low dose Receptors

A

D1, D2

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85
Q

Dopamine mid dose receptors

A

B1, B2> A1

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86
Q

Dopamine high dose receptors

A

A1>B1, B2

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87
Q

Dopamine low dose inotropy

A

same

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88
Q

Dopamine low dose chronotropy

A

same

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89
Q

Dopamine low dose SVR

A

same
Reduces

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90
Q

Dopamine low dose PVR

A

Same,
Reduces

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91
Q

Dopamine mid dose Inotropy

A

+

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92
Q

Dopamine mid dose chronotropy

A

+

93
Q

Dopamine mid dose SVR

A
94
Q

Dopamine Mid dose PVR

A

<->

95
Q

Dopamine high dose Inotropy

A

+

96
Q

Dopamine high dose chronotropy

A

+

97
Q

Dopamine high dose SVR

A

+

98
Q

Dopamine high dose PVR

A

+

99
Q

Milrinone Loading Dose

A

25-75 mcg/kg

100
Q

Milrinone Receptors

A

PDE3 Inhibitor
Increased cAMP

101
Q

Milrinone infusion dose

A

0.25-0.75 mcg/kg/min

102
Q

Milrinone Inotropy

A

+

103
Q

Milrinone Chronotropy

A

+

104
Q

Milrinone PVR

A

-

105
Q

Milrinone SVR

A

-

106
Q

Dobutamine Dose

A

2-20 mcg/kg/min

107
Q

Dobutamine Receptors

A
108
Q

Dobutamine Inotropy

A

+

109
Q

Dobutamine Chronotropy

A

+

110
Q

Dobutamine SVR

A

-

111
Q

Dobutamine PVR

A

-

112
Q

Function of Systemic circulation

A

Delivers oxygen to all body cells and carries away wastes

113
Q

OXygenated blood is pumped to all body tissues via

A

The Aorta

114
Q

Deoxygenated blood is pumped to the lungs via

A

Pulmonary arteries

115
Q

Function of Pulmonary arteries

A

Eliminates CO2 via the lungs and oxygenates the blood

116
Q

Deoxygenated blood returns to the heart via

A

Vena Cava

117
Q

Oxygenated blood returns to the heart via

A

Pulmonary Veins

118
Q

General function of the CV system

A

Transporting nutrients to the body tissues
Transporting waste products away
Transporting hormones from one part of the body to another
Temperature regulation

119
Q

When valves are open, what is the skeletal muscle doing?

A

Contracted skeletal muscle

120
Q

When valves are closed, what is the skeletal muscle doing?

A

Relaxed skeletal muscle

121
Q

In cardiac Action potential, Phase 0

A

fast, voltage-gated Na+ channels open. K+ channels close

122
Q

In phase 0 of Cardiac AP, is it fast or slow

A

Fast

123
Q

In phase 0 of Cardiac AP, what are the Na+ and K+ Channels doing?

A

Voltage- GatedNa+ channels open
K+ channels close

124
Q

Describe Phase 1 of Cardiac AP

A

transient outward rectifier potassium channels (Ito) open briefly

125
Q

Describe Phase 2 of Cardiac AP

A

slow L-type Ca2+ channels
open (plateau).

126
Q

Phase 3 of Cardiac AP

A

Ca2+ channels close. K+ channels re-open

127
Q

Phase 4 of Cardiac AP

A

Resting Membrane Potential is re-established (K+ channels stay open)

128
Q

RMP of Cardiac AP

A

-90

129
Q

Phase 0 Membrane potential (mV)

A

-90-+20

130
Q

Phase 1 membrane potential (mV)

A

+20

131
Q

Phase 2 Membrane Potential (mV)

A

+10

132
Q

Phase 3 Membrane Potential (mV)

A

-20

133
Q

Plateau phase

A

actin / myosin molecules remain activated for 300ms.
Ca2+ enters here

134
Q

Ca2+ entering during plateau phase helps

A

activate the muscle for sustained, forceful contraction.

135
Q

Absolute Refractory Period (Definition)

A

all inactivation gates are closed no electrical stimulus will elicit another action potential.

136
Q

Absolute Refractory period runs from

A

Runs from phase 0 through most of phase 3.

137
Q

True or False: Heart Muscle can be tetanized

A

FALSE
Because of the long refractory period, heart muscle cannot be tetanized

138
Q

Relative Refractory Period

A

Some inactivation gates are open
An action potential can be elicited but a higher stimulus voltage is required and not all channels participate.

139
Q

In the SA Node, timing of depolarization to depolarization is

A

Intrinsic HR

140
Q

In the SA Node, Pacemaker potential is due to

A

gradual drop in K+ conductance and and an increase in Na+ conductance “the funny current” (If).

141
Q

Electrical Properties of the SA Node

A

gradual drop in K+ conductance and and an increase in Na+ conductance “the funny current” (If).

142
Q

The heartbeat originates in

A

The SA Node

143
Q

After the SA node, where does the electicity conduct through?

A

and spreads over the heart by cell to cell conduction through a complex pathway

144
Q

Why is the SA Node the pacemaker?

A

because it has the fastest rhythm.
It is the first structure to show electrical activity with each beat.

145
Q

Order of conductance of electricity through the heart

A

SA Node
AV Node
AV Bundle
Left and Right Bundle Branches
Purkinje Fibers
Ventricular Myocardium

146
Q

Atrial Conduction Velocity

A

1-1.2 m/S

147
Q

AV Node conduction Velocity

A

0.02-0.05 m/s

148
Q

AV Bundle Conduction Velocity

A

1.2-2.0 m/s

149
Q

Bundle Branches and Purkinje Fibers’ Conduction Velocity

A

2.0-4.0 m/s

150
Q

Ventricular Myocardium Conduction Velocity

A

0.3-1.0 m/s

151
Q

SA Node Rate of discharge (B/min)s

A

60-100 B/min

152
Q

AV Node Rate of Discharge

A

40-55 B/min

153
Q

Bundle Branches/ Purkinje Fibres Rate of Discharge

A

25-40 B/min

154
Q

Which tissue has the slowest conduction Velocity?

A

AV Node

155
Q

Why is the AV node the slowest in conduction?

A

It has small diameter cells, few gap junctions and slow phase zero

156
Q

Which structure conducts the fastest in Cardiac AP?

A

Purkinje FIbers

157
Q

Why are the Purkinje Fibers the fastest for conduction?

A

It has small diameter cells, few gap junctions and FASTphase zero

158
Q

Atrial , ventricular, and Bundle of His tissue conduct at what velocity

A

1m/sec

159
Q

What is the only pathway to the Ventricles in Conduction?

A

The AV Node

160
Q

The paucity of gap junctions in the AV node also causes a safety factor

A

(the amount of current passed to the next cell/the amount of current needed to reach threshold).

161
Q

AV node is vulnerable to Injury from

A

disease which can cause loss of conduction to the ventricles.
(Heart block)

162
Q

Ablation of the fast-conducting tissue below the AV bundle is very serious. Why?

A

the spontaneous rate for Purkinje fibers is dangerously low

163
Q

Ablation of the AV node slows the heart rate down to that of

A

the next highest pacemaker (below the node)

164
Q

Baroreceptors in_______detect changes in blood

A

Carotid Sinus and Carotid arch

165
Q

Rising pressure stretches receptors
Leads to

A

Parasympathetic Activation

166
Q

Decreasing pressure leads to

A

less stretch on receptors ->sympathetic activation

167
Q

Why can heart muscle not be tetanized?

A

Because of the long refractory period

168
Q

In SA Node conduction, is the sharp spike present?

A

Sharp spike is absent (no fast Na+ channels). Phase 0 from slow Ca++ channels

169
Q

In SA Node conduction, how does pacemaker potential occur?

A

Pacemaker potential is due to gradual drop in K+ conductance and and an increase in Na+ conductance “the funny current” (If).

170
Q

In the SA Node conduction, how is depolarization timed?

A

Timing of depolarization to depolarization is intrinsic HR

171
Q

Why is the SA Node the pacemaker of the heart?

A

Because it has the fastest rhythm.
It is the first structure to show electrical activity with each beat.

172
Q

How is the rate of Cardiac Pacemakers slowed?

A

-The Vagus nerve secretes Ach (Parasympathetic activation
-Ach increases K+ conductance at KAch channels, which hyperpolarizes the SA Node cells and opposes the Funny Current (Lf)
-CAMP is also decreased

173
Q

How is the rate of Cardiac Pacemakers increased?

A
  • Sympathetic nerves secrete norepinephrine which acts at beta receptors on SA node leading to increased cAMP
  • cAMP opens the hyperpolarization-activated cyclic nucleotide-gated (HCN) sodium channels which increases If (funny current) during phase 4, thus increasing speed of depolarization.
174
Q

Describe Sympathetic Neural Regulation of the heart:

A

Sympathetic stimulation :
Increases HR
Decreases AV Node ERP
Decreased PR
Increased Contractility (SV)

175
Q

How are the Supraventricular and Purkinje Fibers innervated?

A

Vagal Innervation

176
Q

How is everywhere bu the supraventricular and Purkinje fibers innervated?

A

Sympathetic Innervation

177
Q

Receptors on Sympathetic Ganglia

A

AcH- NIcotinic

178
Q

Receptors on Sympathetic nerves

A

Norepinephrine

179
Q

Describe Vagal Neural Regulation of the heart:

A

Decreased HR
Increased AV Node ERP
Increased PR

180
Q

What is the largest current in the heart?

A

Sodium Current

181
Q

What is the status of Sodium channels at RMP?

A

Na+ Channels are closed at RMP

181
Q

Has Alpha/Beta Subunits that are sensitive to cAMP-Dependent protein Kinase

A

Sodium Current

182
Q

Regenerated spread of the action potential depends largely on what?

A

The magnitude of the Na+ Current

183
Q

The depolarization caused by Na+ also activates what?

A

Lca
Ik

184
Q

What inactivates the Na+ Channels in the heart

A

Sodium-Channel Blockers

185
Q

L-Type Calcium channels are inactivated by

A

Dihydropyridines
Phenylalkylamines
Benzothiazepines

186
Q

This current is activated by voltage, Deactivated by time

A

L-Type Calcium Channels

186
Q

At RMP, what is the status of L-Type Calcium channels?

A

Closed at RMP

187
Q

Why are Cardiac Action Potentials twice as long as skeletal muscle APs?

A

Because the K+ channels open so slowly

188
Q

How is the K+ Repolarization current divided?

A

IKA- Rapid
IK- Slow

189
Q

Early outward / A-type current

A

Found in atrial and ventricular muscle. Activated by depolarization and deactivated quickly. Contributes to phase 1

190
Q

G-protein activated current

A

Ach to receptor to GIRK K channels resulting in outward K current. Prominent in SA and AV nodal cells

191
Q

KATP channels in the sinoatrial node contribute to

A

HR Control

192
Q

When fully activated, KATP channels can cause cardiac electrical activity to

A

STOP;
Contractile Failure

193
Q

KATP channels play a role in

A

heart rate control, adaptation to hypoxia, and cardiac excitability

194
Q

Where is the Funny Current found?

A

SA, AV and Purkinje fibers

195
Q

How is the Funny Current Mediated?

A

by a nonspecific anion channel called HCN… Hyperpolarization activated Cyclic Nucleotide Gated channel

196
Q

Funny Current conducts which currents?

A

Both Na and K

197
Q

Does the Funny Current conduct at positive potentials?

A

No
Does not conduct at positive potentials

198
Q

The funny current is activated by hyperpolarization during what phase of the Cardiac Action Potential?

A

phase 4 of the cardiac action potential, which is also known as diastolic depolarization

199
Q

Where is the SA Node located?

A

Sits in RA near the junction of SVC

200
Q

SA Node size in comparison to other atrial muscle fibers:

A

Smaller than the other atrial muscle fibers

201
Q

Cardiac muscle differs from skeletal muscle in that

A

It has Slow L-Type Calcium Channels

202
Q

Phase 0 in the SA Nodal cells is due to

A

Slow Calcium channels

203
Q

The slowest conduction velocity occurs in the :

A

AV Node

204
Q

What is true about aortic Arch baroreceptors?

A

Stretching of the receptors occurs when arterial pressure suddenly rises

205
Q

All are true about the sympathetic nervous system EXCEPT:
A- Norepi acts on Beta receptors to increase cAMP
B. Activation of the sympathetic nervous system leads to increased heart rate.
C. Increased cAMP leads to Activation of K+ channels that hyperpolarize the cell membrane and increase the activity of the “Funny Current” during phase 4
D. Increased cAMP and increased opening of hyperpolarization-actiated cyclic nucleotide-gated (HCN) Sodium channels that increase activity of the “Funny Current” during Phase 4

A

C.
Increased cAMP leads to activation of K+ Channels that hyperpolarize the cell membrane and increase the activity of the “Funny Current” during Phase 4

206
Q

All is true about the sympathetic ns Except:
A- Norepi acts on Beta Receptors to increase cAMP
B. Activation of the SNS leads to increased HR
C. Increased cAMP leads to activation of K+channels that hyperpolarize the cell membrane and increase the activity of the “Funny Current” during phase 4
D. Increased cAMP and increased opening of hyperpolarization-activated cyclic necleotide-gated (HCN) sodium channels that increase activity of the “Funny Current” During Phase 4

A

C.
Increased cAMP leads to activation of K+channels that hyperpolarize the cell membrane and increase the activity of the “Funny Current” during phase 4

207
Q

Select the true statement about L-Type Calcium Channels:
A: Present in the heart and vasculature
B. They are activated by voltage and deactivated by time
C. They are open at very negative membrane potential
D. They are inhibited by Beta Blockers

A

B.
They are activated by voltage and deactivated by time

208
Q

True or False: Fast Sodium channels open during Phase 0 of the AP in the SA Node

A

FALSE

209
Q

The AV Node:
A: Is located near the Mitral Valve
B. Conducts very quickly
C. Gives RIse to Purkinje Fibers
D. Has an intrinsic pacemaker rate of 300 bpm

A

C. Gives rise to Purkinje fibers

210
Q

Which leads would you see changes in for a bundle branch block?

A

Anterior

Anterior leads are leads V1, V2, V3, and V4. For a left bundle branch block you will see a “beach chair” formation in these leads and in a right bundle branch block you will see “bunny ears” in these leads.

211
Q

Which of the following is an EKG change seen with hyperkalemia?

A. Sine wave

B. U wave

C. Peaked T waves

D. QRS widening

E. P wave flattening

F. A, C, D, E

G. All of the above

A

F. A, C, D, E

U waves are seen in hypokalemia not hyperkalemia. Changes seen with hyperkalemia are often progressive, starting with peaked t waves. This progresses to QRS widening and p wave flattening with the sine wave (and eventually torsades) following.

212
Q

what arrhythmia reflects U waves on the EKG?

A

Hypokalemia

213
Q

In which of the following scenarios is a pacemaker NOT indicated?

A. Second degree heart block type I

B. Second degree heart block type II

C. Third degree heart block

D. Third degree heart block caused by lyme disease

E. A and B

F. A and D

A

F. A and D

Third degree heart block caused by lyme disease IS reversible when treated with corticosteroids and antibiotics and may not indicate need for a pacemaker. Second degree heart block type I (wenckebach) rarely progresses to third degree heart block and is usually transient and benign. It also does not indicate need for a pacemaker. Type II second degree heart block on the other hand often progresses to third degree heart block and needs a pacemaker.

214
Q

What is the fastest conduction system of the heart? What is the slowest?

A: SA node; AV node

B: purkinje fibers; AV node

C: AV node; SA node

D: SA node; purkinje fibers

A

B: purkinje fibers; AV node

This question is looking at conduction velocity NOT the rate of pacemaker discharge (BPM)

215
Q

When discussing neural regulation of the heart, the right vagus nerve innervates what structure?

A: purkinje fibers

B: AV node

C: SA node

D: myocardium

A

C: SA node

The right vagus nerve innervates the SA node and the left vagus nerve innervates the AV node and purkinje fibers. There is sympathetic innervation everywhere in the heart.

216
Q

What leads do you look at to determine axis?

A: aVR, I

B: aVL, III

C: aVF, I

D:aVF, II

A

C: aVF, I

217
Q

If lead I is positive and lead aVF is negative, what is the axis?

A: Left axis deviation

B: Normal axis

C: Right axis deviation

D: Extreme right axis deviation

A

A: Left axis deviation

218
Q
  1. Which of the following is represented by the Q wave?

A. Atrial depolarization

B. Atrial repolarization

C. Ventricular depolarization

D. Septal depolarization

A

D. Septal depolarization

219
Q
  1. Which of the following will carotid massage/vagal maneuver terminate?

A. A flutter

B. A fib

C. PAT

D. AVNRT

A

D. AVNRT

Carotid massage should not regularly be done, but is theoretically only helpful in terminating SVTs such as AVNRT. It can be useful in determining if a rhythm is atrial flutter as the ratio to atrial/ventricular depolarizations will become longer (i.e. 1:2 to 1:3 or 1:4).

220
Q
  1. In which of the following arrhythmias would your patient most likely be on anticoagulation?

A. SVT

B. A flutter

C. A fib

D. V tach

A

C. A fib

Pretty much all a fib patients will be on anticoagulants as the quivering atria can allow blood to move slowly and form clots.

221
Q
  1. Which of the following arrhythmias is defibrillation (NOT synchronized cardioversion) used for?

A. A fib

B. A flutter

C. V tach

D. F fib

E. Asystole

F. Pulseless electrical activity (PEA)

G. A and B

H. C and D

I. A, B, E, F

J. C, D, E, F

K. All of the above

A

H. C and D

A fib and A flutter require synchronized cardioversion or else this can lead to R on T phenomenon and cause torsades. Asystole and PEA are non-shockable rhythms and you cannot use defibrillation or synchronized cardioversion on these patients.

222
Q

Non-Shockable Rhythms

A

PEA
Asystole

223
Q

Your patient in the ICU is found to have metabolic acidosis (pH< 7.35). Which way is their oxyhemoglobin curve shifted: left or right?

A

Right
With metabolic acidosis there is an increase in H+ ions which shifts the curve to the right. Anything that “increases” will shift the curve to the right (increased offloading of O2/decreased affinity) and anything that “decreases” will shift the curve to the left (decreased offloading of O2/increased affinity)

224
Q

The Frank Starling curve relates:

a. Stroke volume and preload

b. Preload and afterload

c. Afterload and force of contraction

A

a. Stroke volume and preload

The greater the heart muscle is stretch during filling (PRELOAD/ left ventricular end diastolic pressure), the greater the force of contraction and the greater the quantity of blood pumped into the aorta (SV). The greater the preload (up until a certain point), the more the myosin and actin before aligned and the greater the contraction.

225
Q

At low doses, dopamine acts of what receptors?

a. Alpha 1 receptors

b. Beta 1 receptors

c. Beta 2 receptors

d. Dopamine receptors

A

d. Dopamine receptors

2-5 mcg/kg/min D1, D1
5-10 mcg/kg/min B1>B2>A1
>10mcg/kg/min A1>B1, B2

226
Q
  1. Which of the following drugs would be the most useful in treating ventricular tachycardia?

a. Procainamide

b. Labetalol

c. Verapamil

d. Phenytoin

A

A- Procainamide

Class I antiarrhythmics are particularly useful in treating ventricular arrhythmias (wide QRS). Amiodarone and sotalol would be appropriate alternatives.

227
Q
A

Anesthesiologist Assistant (12 decks)

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