Shannon-Induction Of Anesthesia For The CV Patient Flashcards

1
Q

Patients with ___tension display an exaggerated response to induction agents and laryngoscopy —> more extreme ___tension to laryngeal stimulation, but also an increased ___tensive reaction to induction agents

A

Patients with hypertension display an exaggerated response to induction agents and laryngoscopy —> more extreme hypertension to laryngeal stimulation, but also an increased hypotensive reaction to induction agents

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2
Q

Administering ___ or arterial ___ (i.e.: nitroprusside) can decrease the hyperdynamic sympathetic response to laryngoscopy

A

Administering beta blockers or arterial dilators (i.e.: nitroprusside) can decrease the hyperdynamic sympathetic response to laryngoscopy

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3
Q

Use of ___ IV prior to intubation blunts the laryngeal reflex with intubation

A

Lidocaine IV

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4
Q

Propofol MOA—direct ___ agonist

A

GABA-A

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5
Q

Propofol induction dose ___-___ mg/kg in healthy patient; often much ___ (lower/higher) for CV patients

A

1-2 mg/kg in healthy patient; often much lower for CV patients

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6
Q

Two compartment model for propofol distribution in the body—propofol rapidly distributes to ___ and highly ___ areas following IV injection in one circulation time; propofol rapidly redistributes into ___ compartments, circulates to less perfused areas, concentration ___ (increases/decreases) and ___ (slow/rapid) awakening occurs

A

Propofol rapidly distributes to brain and highly perfused areas following IV injection in one circulation time; propofol rapidly redistributes into peripheral compartments, circulates to less perfused areas, concentration decreases and rapid awakening occurs

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7
Q

Propofol is rapidly metabolized in the ___

A

Liver

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8
Q

Metabolism of propofol—extrahepatic metabolism sites (due to metabolism exceeding hepatic blood flow) results in tissue uptake of Propofol into areas including possibly the ___; need your patient to be ___ to metabolize this out!

A

Possibly the lungs; need your patient to be breathing to metabolize this out!

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9
Q

Benefits of propofol—___ (slow/fast) onset; relatively ___ (short/long) half life; mild anti___ effects; very few serious ___ effects

A

Fast onset; relatively short half life; mild antiemetic effects; very few serious side effects

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10
Q

Propofol CNS effects—___ (increases/decreases) cerebral blood flow, CMRO2

A

Decreases cerebral blood flow, CMRO2

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11
Q

Propofol CV effects—___ (increases/decreases) BP, cardiac output, SVR; dose dependent ___ (increase/decrease) in BP within ___ minutes after induction

A

Decreases BP, cardiac output, SVR; dose dependent decrease in BP within 10 minutes after induction

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12
Q

Etomidate MOA—___ agonist

A

GABA

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13
Q

Etomidate induction dose = ___-___mg/kg

A

0.2-0.3 mg/kg

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14
Q

Metabolism of etomidate = ___ hydrolysis

A

Ester hydrolysis—this is why the duration of action is so short

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15
Q

Etomidate CV effects—hemodynamic ___ is achieved—___ (changes/no changes) in HR, pulmonary artery pressure, SVR, CO, and BP; acts as an alpha 2B adrenoreceptor agonist, which leads to a ___ (increase/decrease) in BP; no significant ___mias associated with etomidate

A

HD stability is achieved—no significant changes in HR, PA pressure, SVR, CO, and BP; acts as an alpha 2B adrenoreceptor agonist, which leads to an increase in BP; no significant arrhythmias associated with etomidate

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16
Q

Etomidate CNS effects—dose dependent ___ (increase/decrease) in cerebral blood flow and CMRO2

A

Decrease

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17
Q

Etomidate CNS effects—awakening occurs ___-___ minutes after administration

A

5-15 minutes

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18
Q

Etomidate side effects—___ on injection; ___ and ___; thrombo___; myoclonia may resemble ___ like activity, but does not cause them; ___ suppression

A

Pain on injection; nausea and vomiting; thrombophlebitis; myoclonia may resemble seizure like activity, but does not cause seizures; adrenocortical suppression

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19
Q

Etomidate side effects—adrenocortical suppression—inhibits 11B-___, which is essential in the body’s production of ___steroids and ___corticoids; the effects of a single etomidate dose can last for ___ hours; can cause increases in morbidity and mortality in patients on prior ___ therapy and/or patients in a ___ state

A

Inhibits 11B-hydroxylase, which is essential in the body’s production of corticosteroids and mineralocorticoids; the effects of a single etomidate dose can last for 72 hours; can cause increases in morbidity and mortality in patients on prior steroid therapy and/or patients in a septic state

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20
Q

Ketamine MOA—noncompetitive ___ antagonist; inhibits ___; depressant effect on ___ nuclei, which blocks afferent signals of pain perception to the ___ and ___

A

Noncompetitive NMDA antagonist; inhibits glutamate; depressant effect on thalami nuclei, which blocks afferent signals of pain perception to the thalamus and cortex

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21
Q

Ketamine causes a ___ state where the patient feels separated from the ___

A

Catatonic state where the patient feels separated from the environment

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22
Q

Ketamine has ___ and ___ effects

A

Amnesic and analgesic effects

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23
Q

Ketamine inhibits ___ factor alpha—may be responsible for its anti___ and anti___analgesic effects

A

Inhibits tumor necrosis factor alpha—may be responsible for its anti-inflammatory and antihyperanalgesic effects

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24
Q

Metabolism of ketamine = ___ metabolizes ketamine into ___

A

Liver metabolizes ketamine into norketamine metabolite

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25
Q

Norketamine has ___-___% the activity of ketamine

A

20-30%

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26
Q

Ketamine CNS effects—airway reflexes maintain ___; ___ (increase/decrease) in salivary gland secretions; ___ (increase/decrease) in skeletal muscle tone; ___ (increase/decrease) in CBF, CMRO2, ICP; causes ___ waves on EEG

A

Airway reflexes maintain intact; increase in salivary gland secretions (give glycopyrrolate); increase in skeletal muscle tone (may have no purposeful movements); increase in CBF, CMRO2, ICP (give with a GABA agonist to counterract…i.e.: propofol, etomidate); causes theta waves on EEG

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27
Q

Ketamine CV effects—indirect ___mimetic—use with caution in patients where an increase in ___ could be detrimental; ___ (increase/decrease) in myocardial contractility, may ___ (increase/decrease) myocardial oxygen consumption; ___ (increase/decrease) in BP, HR, CO, CVP

A

Indirect sympathomimetic—use with caution in patients where an increase in HR could be detrimental; increase in myocardial contractility, may increase myocardial oxygen consumption; increase in BP, HR, CO, CVP

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28
Q

Benefits of ketamine—___ properties; potent ___

A

Analgesic properties; potent bronchodilator

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29
Q

Side effects of ketamine—emergence ___; night___; ___ations

A

Emergence delirium, nightmares, hallucinations

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30
Q

Caution using ketamine in patients with ___tension, ___ heart failure, and ___ ICP—the benefits of a stable hemodynamic profile may be outweighed by the potential for overstimulation of ___ release/___ (increase/decrease) in myocardial oxygen consumption

A

Caution using ketamine in patients with hypertension, congestive heart failure, and increased ICP—the benefits of a stable hemodynamic profile may be outweighed by the potential for overstimulation of catecholamine release/increase in myocardial oxygen consumption

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31
Q

Ketamine is usually used in CV cases as an adjunct for multimodal analgesia, but not as a primary induction agent—T/F?

A

True

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32
Q

Dexmedetomidine MOA—alpha 2 receptor ___ (agonist/antagonist)

A

Agonist

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33
Q

Precedex dose—infusion loading dose of ___mcg/kg over ___ minutes; infusion ___-___ mcg/kg/hr

A

Loading dose of 1 mcg/kg over 10 minutes; infusion 0.2-1.5 mcg/kg/hr

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34
Q

In CABG, precedex loading dose ___ (is/is not) used

A

Is not used—precedex is often just an adjunct sedative for time on bypass/transport to ICU at a drip rate of 0.4 mcg/kg/hr

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35
Q

Precedex metabolism—extensive ___ metabolism

A

Hepatic

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36
Q

Precedex CNS effects—dose-dependent sedation that resembles natural ___; ___ (does/does not) cause respiratory depression; ___ (does/does not) interfere with EEG monitoring; ___ (does/does not) change CMRO2; ___ (increase/decrease) in CBF d/t cerebral vaso___

A

Dose-dependent sedation that resembles natural sleep; does not cause respiratory depression; does not interfere with EEG monitoring; does not change CMRO2; decrease in CBF d/t cerebral vasoconstriction

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37
Q

Precedex CV effects—___tension and ___cardia —> result of alpha 2 ___ and systemic vaso___; can occasionally see transient ___tension with loading dose/___ (low/high) maintenance rate (rare to see); no direct effect on myocardial ___

A

Hypotension and bradycardia —> result of alpha 2 stimulation and systemic vasodilation; can occasionally see transient hypertension with loading dose/high maintenance rate (rare to see); no direct effect on myocardial contractility

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38
Q

Fentanyl MOA—___ agonist

A

Opioid

39
Q

Fentanyl dose—dependent on technique—standard ___-___ mcg/kg; can give doses up to ___ mcg/kg for induction

A

Standard 5-10 mcg/kg; can give doses up to 100 mcg/kg for induction

40
Q

Fentanyl metabolism—___ metabolism into ___ (active/inactive) metabolites

A

Hepatic metabolism into inactive metabolites

41
Q

Fentanyl CNS effects—___ and ___ properties; ___gesia; can cause ___ (increased/decreased) ICP if respiratory depression induced ___carbia occurs

A

Sedative and euphoric properties; analgesia; can cause increased ICP if respiratory depression induced hypercarbia occurs

42
Q

Fentanyl CV effects—___cardia; ___ effect on blood pressure; ___ (does/does not) affect myocardial contractility or baroreceptor function; these traits are why a high dose fentanyl induction can be useful for CABG patients where the need for rapid extubation postoperatively is not an issue—very stable cardiac profile

A

Bradycardia; no effect on BP; does not affect myocardial contractility or baroreceptor function

43
Q

Tabletop rescue drugs—phenylephrine MOA—direct acting alpha ___ agonist; virtually no ___ stimulation

A

Direct acting alpha 1 agonist; virtually no beta stimulation

44
Q

Phenylephrine—unopposed alpha stimulation can elicit a ___ reflex, causing reflex ___cardia with administration; useful for patients in which an increase in ___ is not desired, but an increase in ___ is necessary

A

Unopposed alpha stimulation can elicit a baroreceptor reflex, causing reflex bradycardia with administration; useful for patients in which an increase in heart rate is not desired, but an increase in BP is necessary

45
Q

Phenylephrine dose—syringes come in ___ mcg/ml; administer ___-___ mcg intervals to treat BP

A

Syringes come in 80 mcg/ml; administer 80-160 mcg intervals to treat BP

46
Q

Phenylephrine infusion—usually comes ___mg/___ml (peripheral strength concentration—a heavier concentration may be used via central line in ICU, so always check the bag)—start infusion at ___mcg/kg/min

A

Usually comes 20 mg/250 ml—start infusion at 0.02mcg/kg/min

47
Q

Tabletop rescue drugs—ephedrine MOA—synthetic non___ ___mimetic; stimulates ___ and ___ receptors directly; indirectly causes a release of endogenous ___

A

Synthetic noncatecholamine sympathomimetic; stimulates alpha and beta receptors directly; indirectly causes a release of endogenous catecholamines

48
Q

Ephedrine—causes dose dependent ___ (increase/decrease) in BP, cardiac output, HR, and SVR; acts in a similar manner to ___, only carries a ___ (shorter/longer) duration of action and ___ (does/does not) increase glucose levels like ___ can

A

Causes dose dependent increase in BP, cardiac output, HR, and SVR; acts in a similar manner to epi, only carries a longer duration of action and does not increase glucose levels like epi can

49
Q

Ephedrine dosing—comes in vials of ___mg/ml —> mix 1 ml of ephedrine with ___ ml of NS for a concentration of ___mg/ml; dose in ___-___mg increments IV

A

Comes in vials of 50 mg/ml —> mix 1 ml of ephedrine with 9 ml of NS for a concentration of 5 mg/ml; dose in 5-10 mg increments IV

50
Q

Ephedrine—can see ___phylaxis with subsequent dosing due to depletion of ___ stores

A

Can see tachyphylaxis (diminished response to successive doses of a drug) with subsequent dosing due to depletion of catecholamine stores

51
Q

You will see an increase in effectiveness of ephedrine over time—T/F?

A

False—you will see a decrease in effectiveness of ephedrine over time

52
Q

Tabletop rescue drugs—epinephrine—MOA—strong alpha ___ sympathomimetic catecholamine; dose dependent stimulation of ___ and ___ receptors

A

Strong alpha 1 sympathomimetic catecholamine; dose dependent stimulation of B1 and B2 receptors

53
Q

Epinephrine is used to treat patients in ___ states where there is poor tissue oxygen ___ and ___tension

A

Used to treat patients in shock states where there is poor tissue oxygen delivery and hypotension

54
Q

Epinephrine is used when patients are unresponsive to ___ (direct/indirect) acting sympathomimetics

A

Indirect acting sympathomimetics

55
Q

Epinephrine causes marked increase in ___tropy, heart ___, and conduction ___

A

Marked increase in inotropy, heart rate, and conduction velocity

56
Q

Epinephrine also increases myocardial oxygen ___

A

Consumption—need to watch your oxygen supply/demand balance

57
Q

Epi is rarely used in CV anesthesia outside of an arrest situation, but it is important to always have readily available for a patient who may be hypotensive and unresponsive to other tabletop rescue drugs—T/F?

A

True

58
Q

Epi comes in ___mg/ml vial doses

A

1 mg/ml vial

59
Q

Epi heavy concentration = ___mcg/ml

A

100 mcg/ml—mix 1 ml vial of epi in 9 ml of NS dilutent

60
Q

Epi lite concentration = ___mcg/ml

A

10 mcg/ml—mix 1 ml of epi “heavy” mixture in 9 ml of NS dilutent

61
Q

Tabletop rescue drugs—vasopressin—MOA—endogenous hormone produced in the ___, stored in the ___ pituitary gland; release is stimulated by ___ (increased/decreased) osmolality and ___volemia

A

Endogenous hormone produced in the hypothalamus, stored in the posterior pituitary gland; release is stimulated by increased osmolality and hypovolemia

62
Q

Vasopressin is also known as ___

A

ADH

63
Q

Vasopressin is a potent ___

A

Vasoconstrictor—second line usage after catecholamine vasopressors

64
Q

Vasopressin dosing—comes in vials ___ units/ml

A

20 units/ml

Mix 1 ml with 19 ml NS for a concentration of 1 unit/ml

65
Q

Vasopressin dosing—dose in increments of ___ unit at a time

A

1 unit at a time

66
Q

Vasopressin infusion dose—___units/min

A

0.04 units/min

67
Q

Vasopressin complications—___ ischemia, ___ (increased/decreased) cardiac output, digital ___, cardiac ___ at elevated doses

A

GI ischemia, decreased cardiac output, digital necrosis, cardiac arrest at elevated doses

68
Q

Tabletop rescue drugs—esmolol—MOA—beta ___ selective ___onist

A

Beta 1 selective antagonist

69
Q

Esmolol metabolism—___

A

Nonspecific plasma esterases

70
Q

Esmolol has an extremely ___ (slow/quick) onset and ___ (short/long) half-life

A

Extremely quick (2 min or less) onset and short half-life

^^^ this is d/t its metabolism but nonspecific plasma esterases

71
Q

Esmolol is useful to transiently treat ___ heart rate without carrying lasting effects that may cause subsequent ___ BP

A

Useful to transiently treat elevated heart rate without carrying lasting effects that may cause subsequent low BP

72
Q

Esmolol is often used alongside induction agents to prevent an increase in ___ during laryngoscopy

A

Prevent an increase in HR

73
Q

Esmolol concentration—___mg/ml in a ___ ml vial

A

10 mg/ml in a 10 ml vial (so total of 100 mg in the vial)

74
Q

Esmolol dosing—administer in increments of ___-___mg at a time

A

Administer in increments of 10-30 mg at a time

75
Q

Tabletop rescue drugs—nitroglycerin—MOA—direct vaso___, venous ___ (more/less than) arterial; caused by an induced release of vascular ___

A

Direct vasodilator, venous more than arterial; caused by an induced release of vascular nitric oxide

76
Q

Nitroglycerin causes veno___; used to treat elevated ___, prevent ___, and treat ___ during anesthesia

A

Venodilation; used to treat elevated BP, prevent angina, and treat ischemia during anesthesia

77
Q

Nitroglycerin decreases myocardial wall ___, cardiac ___ pressures, ___load, and myocardial ___ requirements

A

Decreases myocardial wall tension, cardiac filling pressures, preload, and myocardial oxygen requirements

78
Q

Nitroglycerin concentration—nitro “lite” vials obtained from pharmacy come ___mcg/ml in a ___ ml vial—dose in increments of ___ mcg at a time

A

40mcg/ml in a 10 ml vial (so 400 mcg in whole vial)—dose in increments of 40 mcg at a time

79
Q

Nitroglycerin infusion—UPMC Hamot infusion is 400 mcg/ml in a 250 ml bottle—infusion rate is typically started at ___mcg/min in a heart room

A

5 mcg/min

80
Q

Rescue infusions—norepinephrine MOA—potent alpha ___ sympathomimetic; little activity on ___ receptor at low doses (this increases some with higher doses)

A

Potent alpha 1 sympathomimetic; little activity on B1 receptor at low doses

81
Q

Norepinephrine infusion—causes ___ (increased/decreased) coronary artery perfusion pressure d/t increase in ___ BP; vaso___ causes a ___ (increase/decrease) in preload; ___ (increases/decreases) SVR

A

Causes increased coronary artery perfusion pressure d/t increase in diastolic BP; vasoconstriction causes an increase in preload; increases SVR

82
Q

___ is a first line choice for infusion when a vasopressor is indicated in a cardiac case

A

Norepinephrine

83
Q

Norepinephrine infusion concentration—___mg/250 ml; titration of infusion starting at ___ mcg/kg/min

A

16 mg/250 ml; titration of infusion starting at 0.02 mcg/kg/min

84
Q

Rescue infusions—dobutamine MOA—synthetic sympathomimetic ___; primarily a ___ agonist with some ___ effects

A

Synthetic sympathomimetic amine; primarily a beta 1 agonist with some B2 effects

85
Q

Dobutamine increases ___tropy, cardiac ___; BP may slightly increase or remain the same; decreases ___ d/t peripheral vaso___, decreases ___ pressure

A

Dobutamine increases inotropy, cardiac output; BP may slightly increase or remain the same; decreases SVR d/t peripheral vasodilation, decreases pulmonary artery pressure

86
Q

Dobutamine infusion dosing—___-___ mcg/kg/min

A

0.5-20 mcg/kg/min

87
Q

Rescue infusions—milrinone MOA—___ inhibitor; prevents the breakdown of ___

A

Phosphodiesterase 3 inhibitor; prevents the breakdown of cAMP

88
Q

Milrinone causes ___ (positive/negative) inotropic action and vaso___ without producing ___cardia

A

Positive inotropic action and vasodilation without producing tachycardia

89
Q

Vasodilation occurs within milrinone because in the smooth muscle, cAMP causes an efflux of ___ which results in ___ of the muscle

A

Efflux of calcium which results in relaxation of the muscle

90
Q

Milrinone ___ (increases/decreases) preload and afterload

A

Decreases

91
Q

Milrinone causes pulmonary vaso___

A

Vasodilation

92
Q

Milrinone improves ___ function; causes acceleration of ___ uptake by the sarcoplasmic reticulum

A

Improves LV function; causes acceleration of calcium uptake by the sarcoplasmic reticulum

93
Q

Milrinone is eliminated via the ___; caution in patients with ___ disease; buildup may cause ___

A

Via the kidneys; caution in patients with kidney disease; buildup may cause arrhythmias

94
Q

Milrinone infusion dosing—start infusion at ___mcg/min up to ___mcg/min

A

0.375 mcg/min up to 0.75 mcg/min