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Advanced Pharmacology 2 > Final Exam Anesthesia Adjuncts > Flashcards

Final Exam Anesthesia Adjuncts Flashcards

1
Q

What occurs when agonists bind to one of the 3 beta receptor subtypes? (3)

A
  1. Activates adenylyl cyclase to produce caMP
  2. Enhances Ca++ influx
  3. Chronotropic, inotropic, and dromotropic effects
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2
Q

What is the selectivity of beta-antagonists dependent on?

A

Selectivity is dose dependent, which is lost at high doses of antagonists

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3
Q

Can competitive antagonists be displaced by higher doses?

A

yes

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4
Q

4 general benefits of beta blockers?

A
  1. May restored receptor responsiveness such as after desensitization from catecholamines (tachyphylaxis)
  2. Protect myocytes from perioperative ischemia and infarction
  3. Some may decrease arterial vascular tone and reduce afterload
  4. Decrease CO and inhibit renin release
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5
Q

Where do beta blockers delay conduction speed through?

A

The AV node

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6
Q

Which phase of depolarization do beta blockers effect?

A

decrease phase 4 depolarization

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7
Q

What would be the benefit of increasing diastolic perfusion time?

A

Gives more time for the perfusion of coronary arteries

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8
Q

4 Indications for Beta blocker administration?

A
  1. Excessive SNS stimulation from things such as noxious stimulus or acute cocaine ingestion
  2. Thyrotoxicosis
  3. Cardiac Dysrhythmias
  4. SCIP
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9
Q

Surgical Care Improvement Protocol (SCIP) for beta blockers

A

Beta blockers should be administered within 24 hours to all patients who are at risk for myocardial ischemia and patients who are already on beta-blockade therapy

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10
Q

3 examples of b1 selective agents?

A
  1. Atenolol
  2. Metoprolol
  3. Esmolol
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11
Q

Are all B1 receptors in the myocardium?

A

No, 75% of them are

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12
Q

Do B1 selective agents cause vasodilation or increased diastolic filling time?

A

No vasodilation but they do increase diastolic filling time

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13
Q

Cardiac selectivity, clearance route, active metabolites, elimination half time, protein binding and adult iv dose of propranolol?

A 
Cardiac Selectivity: no
Clearance: hepatic
E 1/2: 2-3 hours
Protein binding: highly (small Vd)
IV dose (mg): 1-10mg
Active metabolites: yes
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14
Q

Cardiac selectivity, clearance route, active metabolites, elimination half time, protein binding and adult iv dose of metoprolol?

A 
Cardiac Selectivity: yes
Clearance: hepatic
E 1/2: 3-4 hours
Protein binding: low
IV dose (mg): 1-15 mg
Active metabolites: no
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15
Q

Cardiac selectivity, clearance route, active metabolites, elimination half time, protein binding and adult iv dose of atenolol?

A 
Cardiac Selectivity: yes
Clearance: renal
E 1/2: 6-7 hours
Protein binding: low
IV dose (mg): 5-10 mg
Active metabolites: no
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16
Q

Cardiac selectivity, clearance route, active metabolites, elimination half time, protein binding and adult iv dose of esmolol?

A 
Cardiac Selectivity: yes
Clearance: plasma hydrolysis 
E 1/2: .15 hours (~9min)
Protein binding: low
IV dose (mg): 10-80 mg
Active metabolites: no
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17
Q

What receptor effect does propranolol (inderal) have?

A

Pure beta (B1=B2),there is no sympathomimetic activity

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18
Q

What is the difference per person of plasma concentration with inderal?

A

20x difference per person, oral doses range from 40mg-800mg/day

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19
Q

What other drugs does inderal have an effect on?

A

decreases clearance of amide LA’s and opioids

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20
Q

Which beta antagonist is the most B1 selective?

A

Atenolol (Tenormin)

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21
Q

What patients is tenormin useful for in the pre and postoperative setting?

A

Non-cardiac surgery in CAD patients, reduces complications for 2 years

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22
Q

Does tenormin potentiate insulin-induced hypoglycemia?

A

no

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23
Q

Why does tenormin show less fatigue than other beta blockers?

A

it does not enter the CNS

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24
Q

How is tenormin usually given?

A

5mg every 10 minutes IV

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25
Q

What are the two po forms of metoprolol

A
  1. Tartrate elimination 1/2 time is 2-3 hours, bid, qid dosing
  2. Succinate elimination 1/2 time is 5-7 hours, qd dosing
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26
Q

How is lopressor usually dosed?

A

1mg q 5 min IV in blocks of 5mgs

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27
Q

What does the selectivity of metoprolol (loppressor) give us?

A

bronchodilator, vasodilation and keeps metabolic effects of B2 receptors intact

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28
Q

Therapeutic effect and offset of esmolol (brevibloc)?

A

TE: 5 minutes
Offest: 10-30 minutes

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29
Q

What is esmolol useful in treating?

A

intraoperative noxious stimulu

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30
Q

Initial dosing of brevibloc?

A

20-30mg IV

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31
Q

Drug interactions with cimetidine?

A

decreases 1st pass metabolism of metoprolol, causing it to last much longer

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32
Q

Drug interaction of beta blockers when concurrently administered with Ca++ channel blockers?

A

bradyarrhythmias and heart failure

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33
Q

Drug interaction of beta blockers and insulin?

A

Potentiate insulin effects and prevents glycogenolysis (B2 agonist activity), want to administer B1 antagonists instead of B2

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34
Q

Interaction of beta antagonists with anesthesia? (3)

A

Potential additive myocardial depression, greatest with enflurane, least with isoflurane, not significant between 1-2 MAC

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35
Q

2 examples of mixed beta/alpha antagonists

A
  1. Labetolol

2. Carvedilol

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36
Q

Receptors that labetalol effects?

A

selective alpha 1, non-selective b1 and b2 antagonist effects

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37
Q

What is the beta to alpha blocking ratio in IV form of labetalol?

A

1:7

38
Q

How does labetalol reduce systemic BP and what reflex is attenuated?

A

Reduction in SVR due to alpha 1 and b2 antagonistic effects, reflex tachycardia is attenuated by beta 1 blockade

39
Q

maximum effect time for IV labetalol?

A

5-10 minutes

40
Q

Usual dose of labetalol?

A

2.5-5 mg IV may increase to 10mg IV

41
Q

2 most common uses for sympathomimetics?

A
  1. Increase myocardial contactility

2. Increase systemic BP

42
Q

2 effects that may be seen in sympathomimetics lacking B1 specificity?

A
  1. Intense vasoconstriction

2. Reflex bradycardia

43
Q

MOA of sympathomimetics? (3)

A
  1. Activate directly or indirectly beta or alpha adrenergic G protein receptors
  2. cAMP enhance calcium influx to increase cytoplasmic concentrations
  3. Actin and myosin interact more forcefully
44
Q

4 direct acting sympathomimetics?

A

epinephrine, norepinephrine, phenylephrine, dopamine

45
Q

Action of indirect sympathomimetics?

A

Evoke the release of norepinephrine from postganglionic sympathetic nerve endings

46
Q

Most common indirect sympathomimetic?

A

Ephedrine

47
Q

5 effects seen with epinephrine?

A
  1. Alpha 1 and 2
  2. Cutaneous, splanchnic and renal bed vasoconstriction
  3. 2-10x more potent than norepinephrine in renal vessels
  4. B1 mediated increased HR and CO
  5. B2 mediated skeletal muscle vasodilation and bronchodilation
48
Q

Single dose of epinephrine and how long does it last?

A

2-8mcg lasts 1-5minutes

49
Q

Infusion dose of epinephrine and what receptor it primarily effects?

A
  1. 1-2mcg/min B2
  2. 4cg/min B1
  3. 10-20mcg/min Predominantly alpha
50
Q

Effects of Ephedrine?

A

Direct and indirect acting on alpha and beta adrenergic receptors

51
Q

4 characteristics of Ephedrine use

A
  1. Used in Inhaled or injected anesthetics sympathetic depression
  2. BP response much less intense, last 10x longer than epinephrine
  3. Causes increases in systolic, diastolic, heart rate and CO
  4. tachyphylaxis indicated depleted norpei stores
52
Q

What is the preferred sympathomimetic for parturients?

A

ephedrine, especially for hypotension s/p SAB, and does not effect uterine blood flow

53
Q

What did phenylephrine show in comparison to ephedrine in parturients?

A

equal BP response but higher umbilical pH in neonates

54
Q

Where does phenylephrine exert its effects more?

A

Venoconstriciton > arterial constriction

55
Q

Why does phenylephrine show less potency and longer lasting effects than epinephrine?

A
  1. Principally stimulates alpha 1 receptors

2. Indirectly releases small amount of norepinephrine

56
Q

3 instances in which phenylephrine is used to treat hypotension from?

A
  1. SNS blockade by regional anesthesia
  2. Inhaled/injected anesthetics
  3. CAD and AS d/t no tachycardic effects
57
Q

What side effect is seen with phenylephrine?

A

reflex bradycardia

58
Q

What does vasopressin stimulate?

A

Vascular V1 receptors to cause arterial vasoconstriction

59
Q

Effect of vasopressin on renal-collecting duct?

A

Increases its permeability, causing increased water to be reabsorbed

60
Q

What is vasopressin effective in?

A
  1. Reversing catecholamine-resistant hypotension

2. ACE-I resistant hypotension

61
Q

Side effects of Vasopressin? (3)

A
  1. Coronary artery vasoconstriction
  2. Stimulate GI smooth muscle to cause abd pain and N/V
  3. Decreased platelet counts and antibody formation
62
Q

What ion does Nitric Oxide cause a reduction in?

A

Decreased intercellular Ca++ ions, causing vasodilation

63
Q

7 instances in which Nitric Oxide is involved

A
  1. Cardiovascular tone relaxation
  2. Platelet regulation
  3. CNS neurotransmitter
  4. GI smooth muscle relaxation
  5. Immune modulation
  6. Effector molecule for volatile anesthetics
  7. Pulmonary artery vasodilation
64
Q

How do nitro-vasodilators work to reduce systemic blood pressure?

A
  1. Decreased SVR (arterial vasodilators)

2. Decreased venous return (venous vasodilators), which helps to alleviate pulmonary/systemic congestion

65
Q

Effect of sodium nitroprusside?

A

causes relaxation of arterial and venous vascular smooth muscle

66
Q

Describe the onset and duration of sodium nitroprusside

A

Immediate onset, transiet duration, requires arterial line monitoring and continuous administration

67
Q

Effect of sodium nitroprusside on oxyhemoglobin?

A

dissociated immediately upon contact, causing methemoglobin and releases cyanide and NO

68
Q

Initial dose and titrated dose of sodium nitroprusside?

A

Initial: 0.3mcg/kg/min
Titrated: 10mcg/kg/min

69
Q

Uses of SNP?

A
  1. Production of controlled hypotension in Aortic surgery
  2. Production of controlled hypotension in Pheochromocytoma
  3. Production of controlled hypotension in Spine surgery
  4. HTN emergencies in carotid surgery
70
Q

When do we see Cyanide toxicity with SNP use?

A

With higher IV doses

71
Q

Why do Cyanide radicals accumulate with SNP use?

A

Sulfur donors/methemoglobin is exhausted

72
Q

When should we suspect cyanide toxicity in patients who SNP is being used?

A
  1. Increased doses needed
  2. Increased mixed-venous sats (tissues not oxygenating)
  3. Metabolic acidosis
  4. CNS dysfunction/change in LOC occurs
73
Q

What does nitroglycerin act on and what does it cause?

A

Acts on venous capacitance vessels and large coronary arteries causing venous pooling, relaxation of arterial vascular smooth muscle in high doses

74
Q

Relate tachyphylaxis and nitroglycerin (3)

A
  1. Dose dependent and duration dependent (24 hours0
  2. Limit vasodilation
  3. Drug free interval 12-15 hours reverses tolerance, but may see rebound ischemia
75
Q

Initial dose of nitroglycerin

A

0.5-1 mcg/kg/min or IVP boluses

76
Q

What is the effect of nitroglycerin in acute MI?

A

receives pulmonary congestion, reduces O2 requirements and limits MI size

77
Q

4 instances in which nitroglycerin is useful

A
  1. Acute MI
  2. Acute HTN
  3. Controlled Hypotension (less potent than SNP)
  4. Sphincter of Oddi spasm
78
Q

What is hydralazine?

A

Direct, systemic arterial vasodilator

79
Q

Effect of hydrazine? (2)

A
  1. Decreases ITP (inositol triphosphate), reducing Ca++ release
  2. Extreme hypotension, rebound tachycardia
80
Q

Onset time of hydralazine?

A

peak plasma concentration 1 hour

81
Q

Initial dose of hydralazine?

A

2.5mg IV

82
Q

Which Ca++ channel blockers have selective AV node effects?

A

Phenylalkylamines and Benzothiazepines

83
Q

Which Ca++ channel blocker has selective arteriolar bed effects?

A

Dihydropyrmidines

84
Q

MOA of Ca++ channel blockers?

A
  1. Bind to receptor on voltage-gated L-type calcium channels

2. Decreases calcium influx, inhibits excitation-contraction coupling

85
Q

Effects of CCB? (4)

A
  1. Decreased vascular smooth muscle and contractility
  2. Peripheral vasodilation d/t reduction in SVR and systemic blood pressure
  3. Increased coronary blood flow
  4. Decreased speed of conduction through the AV node
86
Q

Which CCBs show reduction in HR?

A

Verapamil and diltiazem

87
Q

Which CCB shows the greatest coronary artery vasodilation?

A

nicardipine

88
Q

Which CCBs show marked peripheral artery dilation?

A

nifedipine and nicardipine

89
Q

Which CCBs do not effect the SA node or AV node conduction?

A

nifedipine and nicardipine

90
Q

Describe nicardipine’s effect on hypertension?

A

provides short term control

91
Q

Dose, increase titration, decrease dose of nicardipine?

A
  1. 5 mg/hour (50mL/hr)
  2. Increase 2.5 mg/hr (25 mL/hr) to max of 15 mg/hr (150 mL/hr)
  3. Decrease to 3 mg/hr
92
Q

How much nicardipine is decreased 30 minutes after D/C?

A

50% drug decrease 30 minutes after D/C

Advanced Pharmacology 2 (5 decks)

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