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N929 - Anesthesia Pharmacology > CV Drugs II > Flashcards

CV Drugs II Flashcards

1
Q

Ephedrine Class

A
  • NT Releaser

- Alpha- & Beta-Adrenergic Receptor Agonist

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2
Q

Ephedrine MOA

A
  • direct –> acts directly at alpha and beta adrenergic receptors to create effect
  • indirect –> acts to increase the amount of NT released (specifically NE)
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3
Q

Ephedrine PK/PD

A

DOA: 15-60 min

-DOA prolonged in elderly

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4
Q

Ephedrine Dose/Route

A

IV bolus: 0.1-0.2 mg/kg OR 5-25 mg

*can give in 5 mg increments

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5
Q

Ephedrine Clinical uses

A

hypotension

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6
Q

Ephedrine Effects/Considerations

A

can cause tachyphylaxis which depletes stores of catecholamines with repeated doses

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7
Q

Phenylephrine Class

A

Alpha Adrenergic Agonist

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8
Q

Phenylephrine MOA

A
  • direct acting only

- binds to the alpha adrenergic receptor and exerts same effect as endogenous catecholamine

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9
Q

Phenylephrine PK/PD

A

DOA: 5-10 min

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10
Q

Phenylephrine dose/route

A

IV bolus: 50-200 mcg

IV infusion: 20-100 mcg/min

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11
Q

Phenylephrine clinical uses

A
  • hypotension

- nasal intubation or NP tube placement as nasal spray to vasoconstrict –> decrease bleeding risk

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12
Q

Alpha Adrenergic Antagoinst Drugs

A

Phentolamine
Prazosin
Yohimbine
Phenoxybenzamine

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13
Q

Alpha Adrenergic Antagoinst MOA

A
  • bind selectively to alpha receptors and interfere with ability of catecholamines to cause a response
  • phentolamine, prazosin, yohimbine = competitive antagonism
  • phenoxybenzamine = covalent bond
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14
Q

Alpha Adrenergic Antagoinst clinical uses

A
  • HTN
  • BPH (benign prostatic hypertrophy)
  • pheochromocytoma (non-selective agents)
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15
Q

Alpha Adrenergic Antagoinst effects/considerations

A

CV Effects:
-alpha 1 –> decreased PVR, decreased BP, postural hypotension (d/t failure of venoconstriction upon standing
-alpha 2 –> increases NE release from nerve terminals, resultant tachycardia from stimulation of beta receptors
GU effects – blockade in prostate and bladder cause muscle relaxation and ease micturition
-miosis
-increased nasal congestion

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16
Q

Phenoxybenzamine Class

A

Non-selective Alpha-Adrenergic Antagonist

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17
Q

Phenoxybenzamine MOA

A
  • covalent bond to alpha receptor

- non-selective but higher affinity for alpha 1 vs alpha 2

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18
Q

Phenoxybenzamine PK/PD

A

-pro-drug (i.e., inactive until something in body activates it
Onset: 1 hour
E1/2: 24 hrs

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19
Q

Phenoxybenzamine Dose/Route

A

PO: 0.5-1.0 mg/kg (preop for BP control for pheo)

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20
Q

Phenoxybenzamine Clinical Uses

A
  • preop for patients with pheochromocytoma (PO)

- potential use for patients with Raynaud’s

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21
Q

Phenoxybenzamine Effects/Considerations

A
  • decreased SVR, vasodilation

- less tachycardia (due to less alpha2)

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22
Q

Phentolamine Class

A

Non-selective Alpha-Adrenergic Antagonist

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23
Q

Phentolamine MOA

A

non-selective, equal affinity for alpha1 and alpha2

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24
Q

Phentolamine Dose/Route

A

IV: 30-70 mcg/kg
SubQ: 2.5-5 mg

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25
Q

Phentolamine Clinical Uses

A
  • intraoperative management of HTN emergencies (Pheo manipulation or autonomic hyperreflexia)
  • extravascular admin of sympathomimetic agents (subQ to minimize necrosis)
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26
Q

Phentolamine Effects/Considerations

A
  • peripheral vasodilation and a decrease in SVR

- reflex mediated and alpha2 associated increase in HR and CO

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27
Q

Prazosin Class

A

Selective Alpha1-Adrenergic Antagonist

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28
Q

Prazosin MOA

A

selective for alpha1

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29
Q

Prazosin Clinical Uses

A
  • preop prep for pheo
  • essential HTN (in combo with thiazides)
  • decrease afterload in pt with HF
  • Raynaud phenomenon
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30
Q

Prazosin Effects/Considerations

A
  • less likely to cause tachycardia

- dilates both arterioles and veins

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31
Q

Yohimbine Class

A

Selective Alpha2-Adrenergic Antagonist

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32
Q

Yohimbine MOA

A
  • selective for alpha 2
  • higher affinity for alpha2 vs alpha1
  • increases release of NE from post-synaptic neuron
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33
Q

Yohimbine Clinical Uses

A
  • orthostatic hypotension

- impotence

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34
Q

Terazosin & Tamsulosin Class

A

Selective Alpha1-Adrenergic Antagonist

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35
Q

Terazosin & Tamsulosin MOA

A

long acting selective alpha 1a

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36
Q

Terazosin & Tamsulosin Clinical Uses

A

BPH

37
Q

Terazosin & Tamsulosin effects/considerations

A
  • biggest concern orthostatic hypotension
  • Tamsulosin HIGHLY selective for receptors in urogenital tract so less of a problem with orthostatic hypotension but can still occur
38
Q

Beta-Adrenergic Receptor Antagonist Drugs

A 
Propranolol 
Metoprolol 
Atenolol 
Esmolol 
Timolol 
Nadolol 
Betaxolol
Labetalol
39
Q

Beta-Adrenergic Receptor Agonist MOA

A
  • derivatives of isoproterenol, so possess some sympathomimetic effects
  • selective binding to beta receptors
  • competitive and reversible inhibition – large doses of agonists will completely overcome antagonism
  • chronic use – associated with up-regulation (if stop, exaggerated respose to SNS)
40
Q

Beta-Adrenergic Receptor Antagonist clinical use

A
  • HTN
  • management of angina
  • decrease mortality in treatment of post MI patients
  • used periop and preop for patients at risk for MI
  • suppression of tachyarrhythmias
  • prevention of excessive SNS activity
41
Q

Beta-Adrenergic Receptor Antagonist CV Effects

A
  • bradycardia
  • decreased contractility
  • decreased conduction velocity
  • improve O2 supply/demand balance
  • vasoconstriction in skeletal muscles, PVD symptoms increased
42
Q

Beta-Adrenergic Receptor Antagonist resp effects

A
  • bronchoconstriction

- can provoke bronchospasm in patients with asthma or COPD

43
Q

Beta-Adrenergic Receptor Antagonist effect on JG cells

A

decreased renin release; indirect way of decreasing BP

44
Q

Beta-Adrenergic Receptor Antagonist effect on pancreas

A

decreased stimulation of insulin release by epi/NE at B2; masks symptoms of hypoglycemia at B1 (bc no increased HR)

45
Q

Beta-Adrenergic Receptor Antagonist effect on eyes

A

decreased IOP, especially in glaucoma due to decreased aqueous humor production

46
Q

Beta-Adrenergic Receptor Antagonist other effects/considerations

A
  • chronic use  decreased concentration of HDLs increase risk for CAD
  • distribution of extracellular potassium-inhibit uptake of potassium into sk muscles
  • interaction with anesthetics  decrease BP with induction agents
  • nervous system fatigue, lethargy
  • N/V/D
47
Q

Beta-Adrenergic Receptor Antagonist relative contraindications

A

pre-existing AV heart block or HF; RAD, DM (without BG monitoring), hypovolemia

48
Q

Propranolol Class

A

Non-selective Beta Blocker

49
Q

Propranolol MOA

A

about equal for beta1 and beta2

50
Q

Propranolol PK/PD

A
  • extensive 1st pass with oral admin (90-95%)
  • protein bound (90-95%)
  • metabolized in liver
  • E1/2 2-3 hours
  • increased in low hepatic blood flow states
  • decreased clearance of amide Las due to decrease in hepatic blood flow inhibiting metabolism in liver – risk of systemic toxicity of LAs
51
Q

Propranolol dose/route

A

IV bolus: 0.05 mg/kg OR 1-10 mg (give slowly 1 mg q 5 min)

52
Q

Propranolol effects/considerations

A

-beta1 –> decreased HR and contractility
-beta2 –> increased vascular resistance
-decreased clearance of amide local anesthetics (particularly bupivacaine)
-decreased pulmonary clearance of fentanyl
-Goal HR 55-60bpm
CV Effects:
-decreased HR, contractility, CO (especially prominent during exercise and sympathetic outflow)
-increased PVR, increased coronary vascular resistance
-decreased MVO2
-reduction in renin release

53
Q

Metoprolol Class

A

Beta 1 Selective Blocker

54
Q

Metoprolol MOA

A

selective for beta 1, selectivity is dose related

55
Q

Metoprolol PK/PD

A
  • 60% first pass effect
  • metabolized in liver
  • IV onset 3 min
  • E1/2 3-4 hrs
56
Q

Metoprolol dose/route

A

PO: 50-400 mg

IV bolus: 1-15 mg

57
Q

Metoprolol clinical use

A

benefit for patients with COPD, asthma, lung disease

58
Q

Metoprolol effects/considerations

A
  • inotropic and chronotropic depressant

- beta 2 receptors remain intact (bronchial dilation, vasodilation, metabolic effects)

59
Q

Atenolol Class

A

Beta1 selective receptor blocker

60
Q

Atenolol MOA

A

most selective for beta1

61
Q

Atenolol PK/PD

A
  • E1/2 7-6 hours
  • not metabolized in liver
  • excreted via renal system, E1/2 increased markedly in patients with renal disease
62
Q

Atenolol clinical use

A
  • advantageous for those who need beta 2 receptor activity

- oral to treat HTN

63
Q

Atenolol effects/considerations

A
  • least CNS effects

- longer lasting antihypertensive effects

64
Q

Esmolol (breviblock) class

A

Beta 1 Selective Blocker

65
Q

Esmolol PK/PD

A
  • rapid onset and short DOA
  • onset 60 seconds
  • E1/2 9 min
  • DOA 10-30 min
  • metabolized by plasma esterase (less than 1% drug excreted in urine unchanged); not same as esterases responsible for succ
  • poor lipid solubility
66
Q

Esmolol clinical use

A
  • used for treatment of HTN and tachycardia associated with laryngoscopy
  • useful in treating hyperdynamic effects of  pheochromocytoma, thyrotoxicosis, thyroid storm
67
Q

Timolol class

A

non-selective beta-blocker

68
Q

Timolol clinical use

A

tx of glaucoma – decreases IOP by decreasing production of aqueous humor

69
Q

Timolol effects/considerations

A
  • decreased BP
  • decreased HR
  • increased airway resistance
70
Q

Nadolol class

A

Non-Selective Beta Blocker

71
Q

Nadolol PK/PD

A
  • no significant metabolism
  • renal/biliary elimination
  • E1/2 20-40 hours
72
Q

Nadolol dose

A

1x daily

73
Q

Betaxolol class

A

Beta 1 Cardio Selective Blocker

74
Q

Betaxolol PK/PD

A

-E1/2 11-22 hours

75
Q

Betaxolol dose

A

1x daily

76
Q

Betaxolol clinical use

A
  • tx of HTN

- topical for glaucoma

77
Q

Betaxolol effects/considerations

A
  • less risk of bronchospasm than timolol

- good choice for asthmatics with glaucoma

78
Q

Labetolol Class

A

Combined Non-Selective Antagonist

79
Q

Labetolol MOA

A
  • alpha1, beta1, beta2
  • IV beta to alpha blockade 7:1
  • PO beta to alpha blockade 3:1
80
Q

Labetolol PK/PD

A
  • metabolism conjugated with glucuronic acid
  • > 5% of drug recovered unchanged in urine
  • E1/2 5-8 hrs; prolonged in liver disease
  • not affected by renal dysfunction
81
Q

Labetolol dose/route

A

IV dose: 0.1-0.5 mg/kg (small increments)

-usually 5mg at a time for mild HTN in OR

82
Q

Labetolol clinical uses

A
  • mild HTN in OR
  • hypertensive crisis
  • can be used in hypotensive technique without an increased HR
83
Q

Labetolol effects/considerations

A
  • max drop in BP 5-10 min after IV admin
  • decreases systemic BP (alpha1) with attenuated reflex tachy (beta2)
  • decreased HR, SVR, HR
  • CO not affected
  • can cause orthostatic hypotension, bronchospasm, heart block, CHR, bradycardia
84
Q

Clonidine & Dexmedetomidine Class

A

Alpha 2 Receptor Agonist

85
Q

Clonidine & Dexmedetomidine MOA

A
  • reduce sympathetic outflow from vasomotor centers in brainstem; centrally acting selective partial alpha2 adrenergic agonist
  • site of action –> CNS non-adrenergic binding sites and alpha2 receptor agonism
86
Q

Clonidine & Dexmedetomidine PK/PD

A
  • avail as PO or transdermal patch

- 50/50 hepatic metabolism and renal excretion

87
Q

Clonidine & Dexmedetomidine clinical use

A
  • HTN
  • induce sedation
  • decrease anesthetic requirements
  • improve peri-op hemodynamics
  • analgesia
88
Q

Clonidine & Dexmedetomidine effects/considerations

A
  • BP reduction from decreased CO due to decreased HR and peripheral resistance
  • rebound HTN with abrupt cessation
  • SE –> bradycardia, sedation, xerostomia, impaired concentration, nightmares, depression, vertigo, EPS, lactation in men
  • withdrawal syndrome –> occurs with doses of >1.2 mg/day; occurs 18 hours after acute discontinuation of drug; lasts 24-72 hrs; treatment of rectal or transdermal clonidine

N929 - Anesthesia Pharmacology (12 decks)

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