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ANES 516B > Cardiovascular drugs > Flashcards

Cardiovascular drugs Flashcards

1
Q

BP =

A

CO x TPR

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2
Q

A pipe problem insinuates what type of issue with BP?

A

TPR

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3
Q

A pump problem implies what type of issue with BP?

A

CO

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4
Q

If your BP was low due to poor TPR, what drug class would be the best remedy?

A

Vasopressors

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5
Q

If your BP was low due to poor CO, what drug class would you use to remedy the problem?

A

Inotropes

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6
Q

By what means do inotropes increase CO to increase BP?

A

They improve contractility.

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7
Q

By what means do vasopressors increase TPR (SVR) to increase BP?

A

They increase vascular tone.

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8
Q

How does vasodilation affect cardiac filling pressures?

A

Vasodilation decreases cardiac filling pressures.

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9
Q

How does cardiac failure affect filling pressures?

A

Cardiac failure increases filling pressures.

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10
Q

By what means does spinal/epidural anesthesia cause hypotension?

A

They wipe out the SVR.

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11
Q

If your patient is undergoing an AAA and their CVP doubles during surgery, what do you suspect?

A

The heart is failing, and the CVP is likely increasing due to some kind of backup in flow.

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12
Q

How would spinal/epidural administration affect CVP?

A

Spinals and epidurals decrease SVR, which decreases cardiac filling pressures (therefore manifesting as a decrease in CVP).

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13
Q

How does calcium aid in causing muscular contraction in the heart?

A

Ca++ binds to troponin-C, a protein that sits on the surface of tropomyosin. Once troponin is bound, there is a conformational shift that allows the removal of tropomyosin from the actin surface. Once actin is exposed, myosin can bind to it. This is called cross-bridge cycling.

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14
Q

Where is intracellular Ca++ stored?

A

In the sarcoplasmic reticulum

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15
Q

The sarcoplasmic reticulum is in contact with the cell membrane via:

A

T-tubules

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16
Q

What spurs Ca++ release from the SR?

A

Electrical signals enter the SR from the cell membrane via T-tubules, exciting the SR and spurring the release of Ca++ into the cell. Ca++ release is a positive feedback loop in that the initial release of Ca++ encourages further release of Ca++ within the cell.

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17
Q

How does intracellular Ca++ reenter the SR to be stored?

A

Via nonvoltage-dependent Ca++ channels called ryanodine receptors

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18
Q

What are ryanodine receptors?

A

Nonvoltage-dependent Ca++ channels on the surface of the SR that regulate the reentry of Ca++ into the SR

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19
Q

When does relaxation of the cardiac tissue occur?

A

Relaxation takes place when Ca++ is pumped back into the SR via ATPase

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20
Q

What enzymes allow Ca++ to be pumped back into the SR through ryanodine receptors?

A

ATPase

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21
Q

Ca++ is not only pumped back into the SR after contraction; it is also pumped out of the cell. What mechanism is responsible?

A

Ca++ is pumped out of the cell via Na+/K+ ATPase and Na+/Ca++ exchange

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22
Q

What two processes remove Ca++ to the extracellular space?

A

First, Na+ is pumped into the cell via Na+/K+/ATPase pump. Then Ca++ is pumped out of the cell along with Na+ via Na+/Ca++ exchange.

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23
Q

What defines inotropy?

A

The quantity of intracellular Ca++

The maximum amount of tension the heart can develop

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24
Q

What term relates to the maximal amount of tension the heart can develop?

A

Inotropy

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25
Q

What term relates to the quantity of Ca++ within the cardiac cell?

A

Inotropy

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26
Q

What term relates to the rate of Ca++ delivery?

A

Chronotropy

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27
Q

What term relates to the rate of contraction?

A

Chronotropy

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28
Q

What is chronotropy?

A

The rate of contraction defined by the rate of Ca++ delivery

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29
Q

What is lusitropy?

A

The rate of muscle relaxation defined by the removal of intracellular Ca++

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30
Q

What term relates to the removal of intraceullar Ca++?

A

Lusitropy

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31
Q

What term relates to the rate of muscle relaxation?

A

Lusitropy

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32
Q

What determines the rate of contraction?

A

The rate of Ca++ delivery

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33
Q

What determines the rate of relaxation?

A

The rate of intracellular Ca++ removal

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34
Q

What determines the maximal tension that can develop in the heart?

A

Quantity of intracellular Ca++

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35
Q

What molecule is an important second messenger in muscle contraction?

A

cAMP

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36
Q

How will an increase in cyclic AMP affect muscle contractility?

A

It will increase intracellular Ca++ release, which increases contractility.

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37
Q

What role does cyclic AMP play in contractility?

A

cAMP is a second messenger that spurs SR to release Ca++.

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38
Q

What receptors are known as “effectors of SNS”?

A

Adrenergic receptors

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39
Q

Medications that work by activating adrenergic receptors are known as:

A

sympathomimetics

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40
Q

What effect is mediated by alpha 1 receptors?

A

Vasoconstriction

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41
Q

Alpha 1 receptors mediate what effect?

A

Vasoconstriction

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42
Q

What class of adrenergic receptors are involved in vasoconstriction?

A

Alpha adrenergic receptors

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43
Q

Which alpha adrenergic receptors are involved in inhibition of presynaptic NE release?

A

Alpha 2 receptor

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44
Q

Effects of alpha 2 receptor activation include

A

Vasoconstriction

Inhibition of presynaptic NE release

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45
Q

T/F: alpha 1 adrenergic receptor activation inhibits presynaptic release of NE.

A

False; alpha 2 action

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46
Q

T/F: alpha 2 adrenergic receptors are strictly involved in vasoconstriction.

A

False; alpha 2 receptor activation causes vasoconstriction, but it also causes inhibition of NE release.

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47
Q

Effects of beta 1 receptor activation?

A

Increased myocardial chronotropy + inotropy

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48
Q

What class of adrenergic receptors increase myocardial inotropy when activated?

A

Beta receptors

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49
Q

Activatation of B1 receptors causes:

A

Increased myocardial chronotropy + inotropy

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50
Q

Activation of which beta receptor causes increase in myocardial chronotropy?

A

B1 receptor

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51
Q

Which type of adrenergic receptor is involved in vasodilation in vessels and lungs?

A

B2

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52
Q

B2 causes vasodilation in:

A

vessels and lungs

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53
Q

T/F: alpha2 receptors cause vasodilation.

A

False; alpha2 receptors causes vasoconstriction. B2 receptors cause vasodilation in vessels and lungs.

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54
Q

What type of beta receptor acts strictly on the heart?

A

B1 receptors

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55
Q

What does it mean to say that B1 receptor activation increases myocardial chronotropy and inotropy?

A

It increases HR + contractility of the heart.

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56
Q

If you wanted to fix a “pump” problem, you would adminster a drug that worked on which variety of adrenergic receptor?

A

Beta

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57
Q

If you wanted to fix a “pipe” problem, you would adminsiter a drug that worked on which variety of adrenergic receptor?

A

Alpha

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58
Q

T/F: both B1 and B2 serve to increase HR.

A

True.

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59
Q

What types of drugs activate alpha and beta adrenergic receptors?

A

Sympathomimetics

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60
Q

T/F: All clinically used catecholamines work via adrenergic receptors and are therefore sympathomimetics.

A

True

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61
Q

Are catecholamines sympathomimetics?

A

All of the catecholamines that we use in the clinical setting are sympathomimetics.

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62
Q

What two structures make up a catecholamine?

A

Catechol ring + ethylamine tail

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63
Q

Ethylamine + catechol =

A

Catecholamine

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64
Q

T/F: catecholamines are made up of an ethylamine ring and a catechol tail.

A

False: catechol ring and ethylamine tail

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65
Q

The ethylamine tail of a catecholamine has wait nitrous molecule attached to it?

A

NH2

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66
Q

T/F: All catetcholamines are endogenous.

A

False; some catecholamines are synthetic.

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67
Q

Are catecholamines endogenous or synthetic?

A

Both.

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68
Q

Are all sympathomimetics catecholamines?

A

No, but for our purposes, all catecholamines are sympathomimetics.

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69
Q

Name some examples of endogenous catecholamines:

A

Norepi, epi, dopamine

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70
Q

Name some examples of synthetic catecholamines:

A

Isoproteronol

Dobutamine

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71
Q

All catecholamines work via what type of receptor?

A

Adrenergic receptor

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72
Q

Mechanism of action of beta agonists?

A

Beta agonists bind to beta receptors on the cell membrane, stimulating adenylyl cyclase. Activated adenylyl cyclase then converts ATP to additional cAMP, enhancing Ca++ release from the SR and increasing contractility.

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73
Q

By what means do beta agonists increase contractility (inotropy) in the heart?

A

Beta agonists bind to beta receptors, activating adenylyl cyclase and triggering synthesis of cAMP from ATP. Increased concentrations of cAMP encourages higher amounts of Ca++ release from SR, increasing contractility.

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74
Q

What is the primary method of activating beta receptors?

A

Catecholamines

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75
Q

What catecholamines act as beta agonists?

A

Epi, norepi, dobutamine, and isoproteronol

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76
Q

T/F: epinephrine is the most clinically effective beta agonist.

A

False; no B-agonist has been proven to be more effective than another.

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77
Q

T/F: epinephrine activates alpha and beta receptors equally.

A

True.

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78
Q

What must you keep in mind when choosing to treat with catecholamines.

A

Each catecholamine will effect alpha and beta adrenergic receptors differently, so you must decide which effects you want and which you must avoid.

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79
Q

What is an appropriate rate for a norepi drip?

A

1-20 mcg/min

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80
Q

What is an appropriate rate for a dopamine drip?

A

2-20 mcg/kg/min

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81
Q

What is an appropriate rate for an epinephrine drip?

A

1-20 mcg/min

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82
Q

What is an appropriate rate for a dobutamine drip?

A

2-10 mcg/kg/min

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83
Q

What is an appropriate rate for an isoproterenol drip?

A

1-5 mcg/min

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84
Q

Which catecholamine drips are weight dependent?

A

Dobutamine

Dopamine

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85
Q

1-20 mcg/min

A

Epi or norepi

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86
Q

2-20 mcg/kg/min

A

Dopamine

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87
Q

2-10 mcg/kg/min

A

Dobutamine

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88
Q

1-5 mcg/min

A

Isoproterenol

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89
Q

Which catecholamine is a strong non-selective beta agonist with no effects on alpha?

A

Isoproterenol

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90
Q

Does isoproterenol have greater affinity for B1 or B2 receptors?

A

Equally strong affinity for both

91
Q

Isoproterenol only works on what type of adrenergic receptors?

A

Beta

92
Q

Based on receptor activation, what type of drug is norepi?

A

A vasopressor and an inotrope

93
Q

Is norepi a stronger vasopressor or a stronger inotrope?

A

A stronger vasopressor

94
Q

Which catecholamine has no B2 effects, meaning it does not cause vasodilation in the lungs or vessels?

A

Norepi

95
Q

Which catecholamine has an equally strong effect on beta 1, beta 2, and alpha 1 receptors?

A

Epi

96
Q

Which inotropes also have vasopressive effects? Which is stronger in that regard?

A

Dopamine + dobutamine; dopamine is a stronger vasopressor than dobutamine

97
Q

Name some adverse effects of norepinephrine.

A

Norepi acts on B1 and A1 receptors. Its strong effects on A1 receptors can increase SVR so much that CO decreases.

98
Q

Which catecholamine is the agent of choice in anaphylaxis?

A

Epi

99
Q

Which catecholamine is prone to causing arrythmias?

A

Epi

100
Q

T/F: norepi is arrhythmogenic.

A

False; epi is arrhythmogenic.

101
Q

Which catecholamine is largely indirectly acting?

A

Dopamine: mild inotrope and moderate vasopressor

102
Q

Which catecholamine is prone to causing moderate tachycardia?

A

Dobutamine

103
Q

Dobutamine may cause:

A

moderate tachycardia

104
Q

Which catecholamine is prone to causing severe tachycardia, arrhythmias, and decreased SVR?

A

Isoproteronol. It is a strong beta agonist, which may increase HR to the point of arrhythmia and decreased SVR.

105
Q

Adverse effects of isoproteronol:

A

Severe tachycardia
Arrhythmias
Decreased SVR

106
Q

What do phosphodiesterases do?

A

They break down cyclic nucleotides like cAMP and cGMP.

107
Q

T/F: phosphodiesterases only break down cAMP.

A

False; break down cGMP as well

108
Q

What are cyclic nucelotides?

A

Second messengers that activate protein kinases and open ion channels.

109
Q

What do cyclic nucleotides open? What do they activate?

A

Open ion channels

Activate protein kinases

110
Q

If cyclic nucleotides activate protein kinases and open ion channels, what do phosphodiesterases do?

A

They break down cyclic nucleotides and therefore prevent the activation of protein kinases to open ion channels.

111
Q

How many PDE families are known?

A

11

112
Q

T/F: PDE families include a vast number of cell types.

A

True.

113
Q

Name three common PDE III inhibitors.

A

Amrinone
Milrinone
Enoximone

114
Q

What type of drug is amrinone?

A

PDE III inhibitor

115
Q

What type of drug is milrinone?

A

PDE III inhibitor

116
Q

What type of drug is enoximone?

A

PDE III inhibitor

117
Q

Enoximone is a:

A

PDE III inhibitor

118
Q

Milrinone is a:

A

PDE III inhibitor

119
Q

Amrinone is a:

A

PDE III inhibitor

120
Q

Loading dose of amrinone?
Infusion rate?
Duration?

A

LD: 1 mg/kg
IR: 2-10 mcg/kg/min
Duration: 2 hours

121
Q

Loading dose of milrinone?
Infusion rate?
Duration?

A

LD: 0.05 mg/kg
IR: 0.5 mcg/kg/min
Duration: 30 minutes

122
Q

Loading does of enoximone?
Infusion rate?
Duration?

A

LD: 0.5 mg/kg
IR: 10 mcg/kg/min
Duration: 1 hour

123
Q

Which PDE III inhibitor is excreted by the liver?

A

Enoximone

124
Q

Enoximone is excreted by the

A

liver.

125
Q

Where do Ca++ sensitizers work?

A

Work on the interaction of troponin and Ca++ or the response of the myofilaments to Ca++ binding

126
Q

What is the major benefit to using Ca++ sensitizers instead of catecholamines or PDE inhibitors?

A

Ca++ sensitizers do not increase intracellular Ca++ levels, so they are less arrythmogenic and do not increase O2 consumption.

127
Q

PDE family 1 is found where? What do they regulate?

A

They are found in smooth muscle cells, likely regulating proliferation in vascular tissue.

128
Q

Which family is found in smooth muscle cells? What is its action there?

A

PDE 1

Likely regulates proliferation in vascular tissue

129
Q

PDE family 3 is found where?

A

Type A is found in CV system and platelets.

Type B is found in liver/adipose and may be activated by insulin.

130
Q

Which PDE family is of most interest for this topic?

A

PDE 3, Type A

131
Q

Where is Type A PDE 3 family found?

A

CV system + platelets

132
Q

Where are PDE 4 found?

A

In inflammatory cells

133
Q

Which PDE family may play a role in COPD and arthritis?

A

PDE 4

134
Q

What is the most prominent family of PDE? Where are they found?

A

PDE 5; found in the penis

135
Q

T/F: PDE inhibitors work synergistically with B agonists.

A

True

136
Q

T/F PDE inhibitors work synergistically with B antagonists.

A

False; work synergistically with B agonists

137
Q

Effects of PDE inhibitors in cardiac myocytes?

A

They inhibit the breakdown of cAMP, which increases cAMP concentrations to increase Ca++ release to incrase contractility.

138
Q

T/F: PDE inhibitors have effects both in cardiac myocytes and in vascular tissue.

A

True

139
Q

What are the effects of PDE inhibitors in vascular tissue?

A

Increase cyclic nucleotides to cause smooth muscle relaxation
They decrease PA pressures and decrease SVR

140
Q

PDE inhibitors are known as

A

inodilators because of their inotropic effects in the heart and their vasodilator effects in vascular tissue

141
Q

Effect of PDE inhibitors on PA pressures?

A

Decrease PA pressures

142
Q

What class of drug is effective in management of pulmonary hypertension?

A

PDE inhibitors

143
Q

What effects do PDE inhibitors have on SVR

A

Increased cyclic AMP in vascular tissue causes smooth muscle relaxation and decreases SVR

144
Q

T/F: PDE inhibitors have a strictly inotropic effect.

A

False

145
Q

By what PDE family do PDE inhibitors cause vasodilation?

A

PDE 3

146
Q

Conventional inotropes are known as:

A

Ca++ mobilizers

147
Q

T/F: Ca++ sensitizers increase O2 consumption.

A

False; they do not increase the amount of Ca++ in the cell, so they do not add any work to the cell

148
Q

What are the benefits to the fact that Ca++ sensitizers do not increase Ca++ levels in the cell?

A

Less arrhythmogenic

Do not increase O2 consumption

149
Q

Any drug that ends in “-endan” is a:

A

Ca++ sensitizer

150
Q

Name two Ca++ sensitizers.

A

Pimobendan

Levosimendan

151
Q

Which Ca++ sensitizer is used as a longterm treatment for CHF?

A

Pimobendan

152
Q

Pimobendan is used as a long term treatment for

A

CHF

153
Q

T/F: Levosimendan increases troponin-C affinity to Ca++.

A

False; it does nothing to affect affinity of Ca++ to Troponin C; instead, it binds to Troponin C to stabilize the troponin/Ca++ conformational change

154
Q

How does Levosimendan aid in contractility?

A

It binds to troponin in a Ca++-dependent manner and stabilizes the troponin/Ca++ conformational change

155
Q

How do Ca++ levels affect action of levosimendan?

A

The more Ca++ present, the more stabilizing activity of levosimendan.

156
Q

Which increases O2 consumption more, milrinone or levosimendan.

A

Levosimendan does nothing to increase Ca++ levels in the cell, so it does not increase O2 consumption as much as milrinone, a PDE III inhibitor.

157
Q

What is the overall goal of vasopressors?

A

To increase SVR

158
Q

Two groups of vasopressors?

A

Non-catecholamines

Catecholamines

159
Q

Within the vasopressor realm, what are the two kinds of non-catecholamines?

A

Sympathomimetics

Non-sympathomimetics

160
Q

T/F: cAMP is an important second messenger for alpha receptors within the vasculature.

A

F; cAMP is only significant in myocardial activity.

161
Q

What is the second messenger for alpha receptors on vasculature?

A

IP3-DAG pathway

162
Q

By what means does A1 receptor activation increase intracellular Ca++ concentration? What is the effect?

A

Activation triggers the IP3-DAG pathway, which increases Ca++ concentration and causes smooth muscle relaxation.

163
Q

A1 receptors are present where?

A

On systemic and pulmonary vasculature

164
Q

A1 receptors are present on what vasculature?

A

Systemic and pulmonary

165
Q

What catecholamine has the most prominent affects on A1 receptors?

A

Norepi

166
Q

Which catecholamine has greater effects on A1 receptors, dopamine or epi?

A

They have equal effects

167
Q

Which catecholamine has no effect on alpha 1 receptors?

A

Isopropenterol

168
Q

Name two non-catecholamine sympathomimetics:

A

Phenylephrine

Methoxamine

169
Q

What type of drug is phenylephrine?

A

Pure, direct acting a agonist

170
Q

Is phenylephrine a catecholamine?

A

No, it is a non-catecholamine

171
Q

IV bolus of phenylephrine?
Time of onset?
Duration?
Infusion rate?

A

Bolus: 1-2 mcg/kg
Onset: 30 s
Duration: 2-3 minutes
IR: 25 - 100 mcg/min

172
Q

Is the phenylephrine drip rate weight-dependent?

A

No, it is 25-100 mcg/min.

173
Q

What type of drug is methoxamine?

A

Pure, direct acting A agonist

174
Q

T/F: methoxamine is a catecholamine.

A

False; it is a non-catecholamine.

175
Q

Bolus of methoxamine?
Onset?
Duration?

A

Bolus: 5-10 mg
Onset: 1 minute
Duration: 5-10 minutes

176
Q

Which is longer acting, phenylephrine or methoxamine?

A

Methoxamine

177
Q

What type of drug is ephedrine?

A

An indirect acting alpha agonist

A non-catecholamine sympathomimetic

178
Q

Which non-catecholamine sympathomimetic causes NE release from neurons?

A

Ephedrine

179
Q

Issue with chronic use of ephedrine?

A

Ephedrine prevents the reuptake of NE into neurons via granules yet perpetuates the release of NE from neurons. Therefore, NE stores are eventually depleted.

180
Q

T/F: ephedrine has no beta activity.

A

False; it has very little beta activity, but it does have beta activity.

181
Q

What inactivates ephedrine in the liver?

A

MAO in liver inhibits ephedrine.

182
Q

What inactivates ephedrine in the liver?

A

MAO

183
Q

What population group may experience prolonged effects of ephedrine? Why?

A

Those who are on MAO inhibitors (anti-depressants) because MAO inactivates ephedrine in the liver; without that inactivation step, expect a prolonged effect.

184
Q

How is ephedrine excreted?

A

40% is excreted unchanged in the urine

185
Q

What percentage of ephedrine is excreted unchanged in the urine?

A

40%

186
Q

Ephedrine is contraindicated in what patient population?

A

Those on MAO inhibitors, a type of antidepressant.

Prolonged effect of ephedrine could deplete NE stores.

187
Q

What type of drug is vasopressin?

A

A non-sympathomimetic vasopressor

188
Q

T/F: vasopressin has strong alpha adrenergic activity.

A

False; it works on V recepors

189
Q

Does vasopressin utilize alpha receptors?

A

No

190
Q

Name a drug that is a non-sympathomimetic vasopressor.

A

Vasopressin

191
Q

By what means does vasopressin cause vasoconstriction?

A

Activation of V1 receptors

192
Q

Which drug acts on V1 receptors? What is the action of V1 receptors?

A

Vasopressin

V1 receptors release Ca++ to cause SM contraction

193
Q

Second messenger in vasopressin mechanism of action?

A

DAG-IP3

194
Q

What types of drugs utilize DAG-IP3 as a second messenger?

A

Those that work on alpha receptors and v-receptors.

195
Q

Where are V1 receptors located? V2? V3?

A

V1: vascular smooth muscle
V2: kidneys
V3: CNS

196
Q

Where are V2 receptors located? Their activation results in?

A

Located in the kidney.

Activation results in increased water permeability and dilatation of renal endothelium

197
Q

Activation of what V receptor results in increased water retention and dilalation of renal endothelium?

A

V2 receptors

198
Q

Activation of what V receptor results in increased ACTH release?

A

V3

199
Q

Where are V3 receptors located?

A

Pitutarity gland (CNS)

200
Q

T/F: the principle role of vasopressin is regulation of vascular tone.

A

False; more important effects in V3 and V2 receptors than in V1 receptors.

201
Q

Physiological level of vasopressin the body:

A

5-10 pmol/L

202
Q

What disorder can cause vasopressin levels to double or triple in the body?

A

Onset of sepsis

203
Q

Affect of onset of sepsis on vasopressin levels?

A

Doubles/triples

204
Q

What happens to vasopressin levels as sepsis continues (no longer onset phase)?

A

Vasopressin levels decrease dramatically to 1/3 of normal levels.

205
Q

What is a proper infusion rate to replace vasopressin the event of prolonged sepsis or CPB?

A

4-6 units/hr infusions

206
Q

When might you give your patient a vasopressin drip of 4-6 units/hr?

A

In the event of prolonged sepsis or CPB

207
Q

Where are alpha receptors located?

A

In periphery and in lungs

208
Q

Vasopressin causes intense vasoconstriction. What are some risks that comes with that?

A

Myocardial ischemia
Decreased CO
Mesenteric ischemia
Digital necrosis

209
Q

Why might vasopressin be beneficial in the case of pulmonary HTN?

A

Its effects are less severe in pulmonary vasculature because V receptors are not in the lungs

210
Q

What may you give if your patient’s MAP is below 50 mmHg and they are on a norepi drip of greater than 35 mcg/min?

A

Methylene blue

211
Q

Methylene blue may treat what problem associated w/ high rates of norepi infusion?

A

Refractory vasodilation

212
Q

Why does a norepi infusion cause refractory vasodilation?

A

It has strong alpha effects

213
Q

T/F: methlyene blue may be administered in the event that your patient has very low MAPs with a high infusion rate of norepi, but only as a rescue measure.

A

True.

214
Q

Why is methylene blue effective in the treatment of refractory vasodilation?

A

NO activates guanylate cyclase to increase levels of cGMP in the body and cause smooth muscle relaxation. Methylene blue inhibits guanylate cyclase, preventing the proliferation of cyclic nucelotides.

215
Q

Methylene blue inhibits:

A

guanylate cyclase

216
Q

Guanylate cyclase is inhibited by:

A

Methylene blue

217
Q

To treat refractory vasodilation, what bolus dose of methylene blue should you give?
Over what amount of time?

A

Bolus: 1.5 - 2 mg/kg

Give over 10-60 minutes.

218
Q

Methylene blue adminsitration causes minimal side effects at what dose limit?

A

<2 mg/ kg

219
Q

What are mild side effects you may see in your patient upon administration of methylene blue?

A

Transient decrease in SpO2 monitoring

Mild skin and urine discoloration

220
Q

High doses of methylene blue may cause:

A

hyperbilirubinemia + hemolytic anemia

221
Q

What population should never receive methylene blue? Why?

A

Patients on SSRIs shouldn’t receive methylene blue because it may cause serotonin syndrome.

222
Q

What symptoms define serotonin syndrome?

A

Hypotension
Tachycardia
Hyperthermia

223
Q

Your 24 yo patient presents with BP 65/40, HR 100, 92 SpO2, and a rash. What do you suspect? How should you treat it?

A

Anaphylaxis

Treat with epinephrine.

224
Q

High CVP indicate what issue, pump or pipe?

A

High CVP indicates that the heart isn’t pumping like it should. Give a beta agonist to remedy.

ANES 516B (3 decks)

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