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Basics Principles of Anesthesia > Hemodynamics > Flashcards

Hemodynamics Flashcards

1
Q

Why use adrenergic agonist?

A
  • Maintain organ perfusion
  • Tx of allergic rxn
  • Prolongs the effects of local anesthetics
  • CP resuciation
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2
Q

What are the SNS effects of adrenergic agonist at the pre junctional membrane?

A
  • Interferes w/NT synthesis, storage, release, metabolism or uptake
  • Stimulates NT release
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3
Q

What are the SNS effects of adrenergic agonist at the post junctional membrane?

A
  • Stimulates receptors
  • Blocks/inhibits the NT agonist
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4
Q

What is the function of direct acting adrenergic agonists?

A
  • Activate adrenergic receptor directly
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5
Q

Is the potency of direct acting synthetic non catecholamines less or more of less than catecholamines?

A

Less

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6
Q

What is the function of indirect acting adrenergic agonists?

A
  • Denervation/depletion effects
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7
Q

What are the sympathetic agonists?

A
  • Norepi
  • Epi
  • Isoproterenol
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8
Q

What is the order of potency of the sympathetic agonists?

A

NE > EPI> ISO

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9
Q

What are examples of selective adrenergic receptor agonists?

A
  • Phenylephrine
  • Clonidine
  • Dobutamine
  • Terbutaline
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10
Q

What receptor does phenylephrine work on?

A

A1 agonist

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11
Q

What is the catecholamine structure?

A
  • Benzene ring with an -OH group on the 3,4 position
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12
Q

What do naturally occuring catcholamines directly stimulate?

A

Adrenergic receptors

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13
Q

What are the 3 naturally occurring catecholamines?

A
  • Norepinephrine
  • Epi
  • Dopamine
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14
Q

Where is NE produced?

A
  • In the postganglionic neuron and adrenal medulla
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15
Q

Where is Epi produced?

A
  • In the adrenal medulla
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16
Q

Dopamine is a _____ acting neurotransmitter?

A
  • Centrally
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17
Q

What % of the adrenal medulla ouput is NE? What % is Epi?

A
  • NE = 20%
  • Epi = 80%
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18
Q

_____ is a precursor for the production of Epi and NE?

A

Dopamine

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19
Q

How do synthetic catecholamines function?

A
  • They mimic the effect of naturally occurring catecholamines at receptors
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20
Q

Which synthetic catecholamines mimic the effect of naturally occurring catecholamines at receptors?

A

Direct acting

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21
Q

What are the 2 types of synthetic non catecholamines?

A
  • Direct acting
  • Indirect acting
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22
Q

What is an example of an indirect acting synthetic non catecholamine?

A
  • Ephedrine
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23
Q

What are examples of direct acting synthetic non catecholamines?

A
  • Phenylephrine
  • Methoxamine
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24
Q

What is the prototype adrenergic agonist?

A
  • Adrenaline/Epinephrine
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25
Q

Can adrenaline be given exogenously?

A

Yes

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26
Q

Is adrenaline/epinephrine released in response to SNS activation?

A

Yes

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27
Q

Where is epinephrine made?

A

Adrenal medulla

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28
Q

What receptors are associated with the direct acting cardiovascular effects of epinephrine?

A

Beta 1, Beta 2, & Alpha 1 receptors

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29
Q

What are 2 synthetic catecholemines?

A
  • Ispoproteronolol
  • Dobutamine
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30
Q

What receptors are stimulated with epi dose of 1-2 mcg/min? What is the response?

A
  • B2 receptors in the periphery
  • causes vasodilation
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31
Q

What receptors are stimulated with epi dose of 2-5 mcg/min? What is the response?

A
  • B1 receptors in the heart
  • increase contractility
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32
Q

What receptors are stimulated with epi dose of 5-10 mcg/min? What is the response?

A
  • A1 receptors in the periphery
  • causes vasoconstriction
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33
Q

1:1000 of epi is _____ mg/ml

A

1mg/ml

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34
Q

1:10,000 of epi is _____ mg/ml

A

100 mcg/ml

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35
Q

1:100,000 of epi is _____ mcg/ml

A

10 mcg/ml

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36
Q

What are the respiratory effects of epinephrine?

A

Activation of B2 receptors in the lung smooth muscle > bronchodilation

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37
Q

What are the metabolic effects of epinephrine?

A

Increase serum glucose

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38
Q

What are the occular effects of epinephrine?

A

Mydriasis

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39
Q

What are the CNS effects of epinephrine?

A

Restlessness

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40
Q

What effect does epinephrine have on platelets?

A

Causes increased aggregation

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41
Q

Does norepinephrine have a strong direct acting effect on stimulating B1 receptors?

A
  • It has weak stimulation activity on B1
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42
Q

Does norepinephrine have a strong direct acting effect on stimulating B2 receptors?

A
  • No, it has little B2 agonist effects
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43
Q

Does norepinephrine have a strong direct acting effect on stimulating alpha receptors?

A
  • Yes, it is a POTENT alpha agonist
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44
Q

What are the CV effects of NE?

A
  • intense vasoconstriction
  • reduced CO
  • reduced renal blood flow
  • increased DBP
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45
Q

What receptors are associated with the direct acting effects of dopamine?

A
  • Dopa 1
  • B1 & 2
  • A1
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46
Q

At _____er doses, you see a dopaminergic response to dopamine?

A

lower

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47
Q

At _____ doses, you see a beta adrenergic response to dopamine?

A

medium

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48
Q

At _____er doses, you see a alpha adrenergic response to dopamine?

A

higher

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49
Q

At what dose of dopamine do you see D1 receptor response? What is the response?

A
  • seen at lower doses
  • vasodilation
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50
Q

At what dose of dopamine do you see B1 & B2 receptor response?

A

medium

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51
Q

At what dose of dopamine do you see A1 receptor response? What is the response?

A
  • seen at higher doses
  • increased SVR, decreased renal blood flow, increased risk of arrhythmias, & increased BP
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52
Q

_____ is seen in high doses of dopamine as a response to increased BP?

A

Reflex bradycardia

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53
Q

Is isoproterenol a synthetic or naturally occurring catecholamine?

A

A synthetic catecholamine

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54
Q

What receptors are associated with the direct acting effects of isoproterenol?

A

B1 & B2

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55
Q

What are the B1 CV effects of isoproterenol?

A

increased HR

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56
Q

Does increasing the HR cause an increase or decrease in the myocardial O2 consumption?

A

Increase

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57
Q

Is isoproterenol a strong or poor inotrope?

A

poor

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58
Q

What are the B2 CV effects of isoproterenol?

A
  • Skeletal muscle, renal & mesenteric vascular bed dilation
  • decreases DBP
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59
Q

What are the CNS effects of isoproterenol?

A

Stimulation

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60
Q

What are clinical uses of Isoproterenol?

A
  • Bronchodilator
  • Decrease PVR
  • Increase HR
  • Inotropy/chronotropy
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61
Q

What are common side effects of Isoproterenol?

A
  • Tachycardia
  • ventricular arrythmias
  • hypotension
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62
Q

Does Isoproterenol potentiate inhalation arrythmias?

A

Yes, it does

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63
Q

Is dobutamine a synthetic or naturally occurring catecholamine?

A

synthetic

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64
Q

Is dobutamine direct, indirect, or both?

A

Both, it is mostly direct with some indirect properties

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65
Q

What receptors are associated with the effects of dobutamine?

A

B1 & B2, Alpha

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66
Q

Is dobutamine a selective B1? Is it a weak B2?

A

Yes, it is a selective B1 and weak B2

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67
Q

Dobutamine has a dose dependent _____in CO & _____ in atrial filling pressures

A

Dobutamine has a dose dependent in INCREASE in CO & DECREASE in atrial filling pressures

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68
Q

Does dobutamine cause a major increase in HR & SVR? Does it increase myocardial O2 requirements?

A

No.

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69
Q

Does dobutamine increase or decrease SVR at low doses?

A

Decreases

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70
Q

Does dobutamine increase or decrease renal blood flow and CO?

A

Increases

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71
Q

What are common clinical uses of dobutamine?

A
  • cardiac failure
  • low cardiac output states
  • used in conjunction with vasodilators
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72
Q

What are common side effects of dobutamine?

A
  • sensitization to inhalation arrhythmias
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73
Q

Is ephedrine a synthetic non catecholemine or synthetic catecholemine?

A

synthetic non catecholemine

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74
Q

What is the most commonly used sympathomimetic?

A

Ephedrine

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75
Q

Is ephedrine a direct or indirect agonist? What percent is it?

A

mainly indirect, 70-80%

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76
Q

What receptors are associated with the indirect effects of ephedrine?

A

Non selective Beta and A1 receptors

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77
Q

What are common clinical uses of ephedrine?

A
  • Hypotension 2/2 anesthesia
  • sympathetic blockade (regional anesthesia)
  • inhalation or injected anesthetic agent
78
Q

What are the CV effects of ephedrine?

A

increases inotropy and dromotropy (increased conduction through AV node)

79
Q

Which receptors causes increase in inotropy and dromotropy in ephedirne?

A

mainly B1 stimulation and B2 is offset by A1 in vessels

80
Q

Does ephedrine increase or decrease fetal metabolic rate? Does it lead to acidosis or alkalosis?

A

Increase fetal metabolic rate and can lead to acidosis

81
Q

What are the resp effects of ephedrine?

A
  • stimulates respiration and bronchodilation (B2)
82
Q

What are the metabolic effects of ephedrine?

A

unlike epi, does NOT produce marked hyperglycemia

83
Q

What are the occular effects of ephedrine?

A

Mydriasis

84
Q

What are the CNS effects of ephedrine?

A

stimulation

85
Q

Can ephedrine cross the BBB?

A

Yes

86
Q

In terms of metabolism, does ephedrine has a slow or fast inactivation & excretion? Does this shorten or prolong the effects of the drug?

A

Slow inactivation & excretion which prolongs the effects of the drug

87
Q

Can tachyphylaxis occur with ephedrine?

A

Yes

88
Q

Is phenyleprhine a synthetic non catecholemine or synthetic catecholemine?

A

A synthetic non catecholemine

89
Q

Is phenyleprhine a direct or indirect acting agonist?

A

Direct acting

90
Q

What receptors are associated with the direct effects of phenylephrine?

A

A1 and B receptors

91
Q

Is the B receptor effect of phenylephrine minimal or large?

A

minimal

92
Q

What is the CV effect of phenylephrine?

A

Increases SVR

93
Q

What are the clinical uses of phenylephrine?

A

Hypotension/reduced SVR

94
Q

What are some scenarios related to our practice where phenylephrine would be used for the hypotension/decreased SVR?

A
  • SNS blockade post regional anesthesia
  • Injected/inhaled anesthetic agents
  • CPB
95
Q

Should you rapidly increase and decrease rate of a phenylephrine infusion?

A

No, that can cause roller coaster effect with BP (up & down)

96
Q

What is a potential side effect related to phenylephrine that you should be aware of?

A

Reflex bradycardia

97
Q

Is methoxamine a synthetic non catecholemine or synthetic catecholemine?

A

synthetic non catecholemine

98
Q

Is methoxamine a direct or indirect acting agonist?

A

direct acting

99
Q

What receptors are associated with the direct effects of methoxamine?

A

Stimulates A1

100
Q

What medication is the prototype pure alpha vasoconstrictor?

A

methoxamine

101
Q

What is the main clinical use of methoxamine?

A
  • arterial vasoconstriction during hypotension
102
Q

What is a common side effect of methoxamine?

A

decreased renal blood flow due to the intense ARTERIAL vasoconstriction

103
Q

Does methoxamine have a long duration of action?

A

Yes, up to 8hrs

104
Q

Dexmedetomidine is _____times more selective for alpha___ receptors

A

Dexmedetomidine is 7-10 times more selective for alpha 2 receptors

105
Q

What are the clinical indication for Dexmedetomidine?

A
  • hypnotic effects
  • sedation
  • analgesia
106
Q

Does dexmedetomidine increase or decrease catecholamines during anesthesia?

A

decreases

107
Q

Does dexmedetomidine increase or decrease MAC?

A

Decreases

108
Q

What is the most commonly used selective beta 2 agonist?

A

Proventil (Albuterol)

109
Q

What are selective beta 2 agonists used to treat?

A
  • bronchoconstriction
110
Q

How do selective beta 2 agonist affect labor?

A
  • stops premature labor by working as a tocolytic
111
Q

What is tocolytic referring to when talking about selective beta 2 agonist affect?

A

Uterine smooth muscle relaxation

112
Q

What are 3 examples of alpha antagonist medications?

A
  • Phentolamine
  • Phenoxybenzamine
  • Prazosin
113
Q

What condition does phentolamine treat?

A

Pheochromocytoma

114
Q

What is the onset of phentolamine? Quick, slow?

A

Quick

115
Q

What is the duration of phentolamine?

A

15-30 mins

116
Q

Phentolamine causes _____ tachycardia?

A

Phentolamine causes REFLEXIVE tachycardia

117
Q

When do you see the peak effect of Phenoxybenzamine?

A

1hr

118
Q

What is the 1/2 life of Phenoxybenzamine?

A

24hrs

119
Q

Is prazosin a shorter or longer acting alpha antagonist?

A

shorter

120
Q

What are 4 examples of B2 blockers?

A
  • Propranolol
  • Labetolol
  • Esmolol
  • Metoprolol
121
Q

How do B2 blockers work in the body?

A
  • Oppose the effect of endogenous catecholamines at Beta receptors
122
Q

What are the 2 classification of B2 blockers?

A
  • Specific
  • Non specific
123
Q

Is labetolol specific or not specific to B1?

A

Not specific

124
Q

What is the alpha/beta blocker ratio of labetolol?

A

1:7

125
Q

What is the onset of labetolol?

A

2-5 mins

126
Q

Labetolol can be redosed q ____ mins

A

Labetolol can be redosed q 5-10 mins

127
Q

What is the 1/2 life of labetolol? Is it long?

A

> 5 hrs, yes its long

128
Q

Is esmolol specific or not specific to B1?

A

specific

129
Q

What is the onset of esmolol?

A

1-4 mins

130
Q

What is the duration of esmolol?

A

10-30 mins

131
Q

What is the 1/2 life of esmolol?

A
  • 9 min in adults
132
Q

Is metoprolol specific or not specific to B1?

A

specific

133
Q

What is the onset of metoprolol?

A
  • approx 5 mins
134
Q

What is the 1/2 life of metoprolol?

A

3-4 hrs

135
Q

What are 2 examples of Phosphodiesterase Inhibitor medicaitons?

A
  • Amrinone
  • Milrinone
136
Q

Amrinone and Milrinoine inhibit _____?

A

Amrinone and Milrinoine inhibit PDE 3

137
Q

What is the clinical indication of Amrinone?

A
  • CHF
  • Ventricular dysfunction
138
Q

Milrinone ____ myocardial contractility and causes peripheral _____ leading to an ____ CO

A

Milrinone INCREASES myocardial contractility and causes peripheral VASODILATION leading to an INCREASED CO

139
Q

Should a patient stop their MAOI 2-3 wks prior to surgery?

A

No, they can continue until sx

140
Q

Should you use direct or indirect acting agents in the presence of MAOIs?

A

Direct acting agents

141
Q

How do TCAs/SSRIs work in the body?

A
  • Inhibit the Uptake of NE/5HT Back Into Postganglionic Neurons.
142
Q

Should you avoid direct or indirect acting agents in the presence of TCAs/SSRIs?

A

Avoid indirect acting agents

143
Q

Anything which is a _____ to the SNS (Stress, Drugs) will potentially produce a _____ response and ______

A

Anything which is a STIMULANT to the SNS (Stress, Drugs) will potentially produce a HYPERTENSIVE response and ARRYTHMIAS

144
Q

How do anticholinesterases work in the body?

A
  • drugs which cause reversible inhibition of AChE
145
Q

What type of bonds are associated with anticholinesterases?

A

Edrophonium ionic bonds

146
Q

Which drugs will cause the formation of carbamyl esters?

A
  • Neostigmine
  • Pyridostigmine
  • Physostigmine
147
Q

What is the clincal use for anticholinesterases?

A
  • Tx of glaucoma, decreases IOP
148
Q

What can form after >6m of use of anticholinesterases?

A

Cataracts

149
Q

What class of drugs are considered synthetic quaternary ammonium compounds?

A

Anti-muscarinics

150
Q

What is an example of a synthetic quaternary ammonium compound?

A

glycopyrrolate

151
Q

What are 2 examples of naturally occurring anitmuscarinic tertiary amines?

A
  • Atropine
  • Scopalamine
152
Q

What are the clinical indication for anitmuscarinic

A
  • preop medication
  • NM blockade reversal
  • prevention of reflex mediated bradycardia
153
Q

How do antimuscarinics work in the body?

A

reversible bind to muscarinic receptor > inablity of ACH from to access the receptor

154
Q

What chemical group is necessary for anitmuscarinic activity?

A

An ester group

155
Q

Antimuscarinics increase or decrease _____ & ______ secretions

A

Antimuscarinics DECREASE BRONCHIAL & SALVIVARY secretions

156
Q

Do Antimuscarinics have occular and cardiac effects?

A

Yes

157
Q

Do Antimuscarinics have decrease or increase GI motility and urinary effects?

A

Decrease

158
Q

What effect do Do Antimuscarinics have on gastric secretion of H+?

A

An inhibitory effect

159
Q

What effect do Antimuscarinics have on secretions?

A

decrease secretions by the exocrine glands

160
Q

What is the effect called that is related to decreased secretions by exocrine glands?

A

antisialagogue effect

161
Q

In terms of secretions management, order these antimuscarinics from most effective to least: Glycopyrrolate, Scopolamine, Atropine?

A

Scopolamine> Glycopyrrolate> Atropine

162
Q

Antimuscarinics block the ___2 receptor resulting in the ______ of _____ reuptake

A

Antimuscarinics block the M2 receptor resulting in the INHIBITION of NE reuptake

163
Q

How do Antimuscarinics affect the P-R interval? What is the effect on A-V conduction?

A
  • Antimuscarinics DECREASE the P-R interval
  • Antimuscarinics INCREASE the A-V conduction
164
Q

In terms of blocking the M2 receptor to inhibit NE reuptake, order these antimuscarinics from most effective to least: Glycopyrrolate, Scopolamine, Atropine

A

Atropine> Glycopyrrolate> Scopolamine

165
Q

In reference to antimuscarinics, can the tertiary amines (scopalamine & atropine) cross the blood brain barrier?

A

Yes

166
Q

Do antimuscarinics cause central anticholinergic delirium?

A

Yes

167
Q

Which antimuscarinics cause sedation, amnesia, confusion, & hallucinations?

A

Naturally occurring tertiary amines - Scopalamine & atropine

168
Q

Between scopalmaine and atropine, order them from greatest to least in regards to sedation, amnesia, confusion, & hallucinations?

A

Scopalamine > atropine

169
Q

At high does what effects does atropine have?

A

ocular effects

170
Q

Why is Glycopyrrolate a good choice for antimuscarinic?

A

Glycopyrrolate does NOT cause sedation, amnesia, confusion, & hallucinations

171
Q

What are the ocular effects of antimuscarinics?

A

Mydriasis

172
Q

What is Mydriasis?

A

Pupil dilation w/no accommodation

173
Q

In terms of degree of mydriasis, order these antimuscarinics from most to least: Glycopyrrolate, Scopolamine, Atropine

A

Scopolamine> Atropine> Glycopyrrolate

174
Q

What are the respiratory effects of antimuscarinics?

A

Relax the smooth muscle of the bronchioles

175
Q

In terms of bronchiole relaxation, order these antimuscarinics from most to least: Glycopyrrolate, Scopolamine, Atropine

A

Atropine > Scopalamine = Glycopyrrolate

176
Q

Do antimuscarinics increase or decrease GI motility, LES pressure, and gastric acid H+ secretions?

A

Decrease

177
Q

Do antimuscarinics increase or decrease the tone of the bladder sphincter? Does this cause an inability or ability to void?

A

Antimuscarinics INCREASE bladder tone causing an INABILITY to void

178
Q

What is an antimuscarinic overdose called?

A

Central anticholinergic syndrome

179
Q

How do you treat Central anticholinergic syndrome?

A

Give physostigmine 15-60 mcg/kg

180
Q

Which population is more likely to suffer from Central anticholinergic syndrome?

A

Elderly and peds

181
Q

What are the symptoms of Central anticholinergic syndrome?

A

A range of restlessness and confusion > sedation and unconsciousness

182
Q

How many mg of elemental calcium are in calcium chloride? What % solution is it?

A
  • 27 mg
  • 10%
183
Q

How many mg of elemental calcium are in calcium gluconate? What % solution is it?

A
  • 9 mg
  • 10%
184
Q

What is the clinical use of calcium?

A

In situations where the ionized ca 2+ is <0.8 mmol/L

185
Q

How does calcium affect BP? Does it increase or decrease inotropy?

A
  • Increases BP
  • Increases inotropy
186
Q

Can administration of calcium aggravate/increase cell injury? Why?

A

Yes, it can cause tissue injury

187
Q

Can calcium cause tissue injury? If yes, how do you avoid this?

A

Yes, you can avoid tissue injury by giving it centrally.

188
Q

What are examples of non selective direct acting adrenergic agonists?

A
  • Isoproterenol
  • epinephrine
  • norepinephrine
  • oxymetazoline
189
Q

What is an example of a mixed acting adrenergic agonist?

A

Ephedrine

190
Q

What are examples of indirect acting adrenergic agonists?

A
  • Releasing agents (amphetamine, tyramine)
  • Uptake inhibitors (cocaine)
  • MOAIs (selegiline)
  • COMT inhibitors (COMT)

Basics Principles of Anesthesia (6 decks)

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