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ARCHIVED: Pharmacology for Nurse Anesthesia > Exam 3: Drugs for Hypertension and Vascular Tone > Flashcards

Exam 3: Drugs for Hypertension and Vascular Tone Flashcards

1
Q

HTN tx threshold without DM/renal disease:

A

140/90

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2
Q

HTN tx threshold with DM/renal disease:

A

130/80

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3
Q

First-line tx for HTN:

A

Thiazide diuretic (without “compelling indication”)

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4
Q

Best drugs for HTN in pts with heart failure:

A

Thiazide + β-blocker or ACEI

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5
Q

Best drugs for HTN in pts with MI:

A

β-blocker

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6
Q

Best drugs for HTN in pts with high CVD risk:

A

Thiazide, β-blocker, ACEI, CCB

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7
Q

Best drugs for HTN in pts with DM:

A

Thiazide + ACEI

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8
Q

Best drugs for HTN in pts with CKD:

A

ACEI or ARB

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9
Q

Best drugs for HTN in pts with recurrent strokes:

A

Thiazide + ACEI

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10
Q

Best drugs for HTN in pts with isolated systolic HTN:

A

Thiazide + CCB

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11
Q

Define hypertensive urgency:

A

DBP > 120 with evidence of end organ damage

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12
Q

Tx for hypertensive urgency:

A

↓ DBP to 100-105 within 24 hours with clonidine

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13
Q

Define hypertensive crisis:

A

DBP > 120 with evidence of end organ failure

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14
Q

Tx for hypertensive crisis:

A

↓ DBP to 100-105 asap using NTG, NTP, labetalol, fenoldapam

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15
Q

Effects of angiotensin II:

A

Vasoconstriction (arterial)
Na+ retention
Thirst/ADH secretion
Aldosterone secretion

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16
Q

Effect of aldosterone:

A

↑ Na+ reabsorption

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17
Q

ACEIs are 2nd-line therapy for pts with:

A

HTN
CHF
Mitral regurg

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18
Q

ACEIs are more effective in pts with:

A

DM

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19
Q

ACEIs delay the progression of:

A

Renal disease

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20
Q

AT-1 and AT-2 receptors are:

A

GPCRs

AT-1 effects > AT-2 effects

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21
Q

AT-1 receptor effects:

A

Vasoconstriction, esp. in glomerular afferent arterioles
↑ norepi release
Proximal tubule reabsorption of Na+
Aldosterone secretion

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22
Q

MoA of ACEIs:

A

Block conversion of angiotensin I to II via interaction with zinc ion

Works on ACE in endothelium

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23
Q

Clinical effects of ACEIs:

A

↓ arterial pressure

↓ cardiac load

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24
Q

Indications for ACEIs:

A 
HTN
Cardiac failure
Post-MI
Diabetic neuropathy
CRI
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25
Q

Pre-op hold for ACEIs:

A

One full day pre-op

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26
Q

S/E of ACEIs:

A 
Intra-op hypotension**
Granulocytopenia
Angioedema*
Proteinuria
Cough*
Hyperkalemia
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27
Q

Contraindications for ACEIs:

A

Renal artery stenosis

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28
Q

Cough/angioedema from ACEIs related to:

A

Bradykinin

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29
Q

Dosage of captopril:

A

12.5-25mg q8h

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30
Q

Onset and half-time of captopril:

A

Onset: 15 min

E1/2t: 2 hrs

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31
Q

Advantages of captopril:

A

Does not interfere with SNS outflow d/t short E1/2t

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32
Q

S/E of captopril:

A 
Rash
Loss of taste
Antagonized by NSAIDs
Hyperkalemia
Angioedema
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33
Q

Enalapril vs. captopril:

A

Enalapril is IV; does not cause rash/renal insufficiency due to lacking sulfhydryl group

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34
Q

Elimination of lisinopril:

A

Administered in active form; excreted unchanged by kidney

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35
Q

Onset and duration of effect of enalapril/lisinopril/ramipril:

A

Enalapril/lisinopril: onset 60-120min, effect 18-30hrs

Ramipril: onset 30-60min, effect 24-60hrs

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36
Q

MoA for ARBs:

A

Competitive binding to AT1 receptors to inhibit action of angiotensin II

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37
Q

S/E of ARBs:

A

Similar to ACEIs but less cough, no bradykinin accumulation

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38
Q

Contraindications for ARBs:

A

Renal artery stenosis

Pregnancy

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39
Q

Naming of ARBs:

A

-sartan

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40
Q

Drug class of hydralazine:

A

Phthalazine derivative

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41
Q

MoA of hydralazine:

A

Activates guanylate cyclase causing vasodilation (primarily arterial)

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42
Q

Dosage of hydralazine:

A

2.5 - 10mg IV

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43
Q

Peak, duration and half-time of hydralazine:

A

Onset: 10-20 minutes
Duration: 6 hr
E1/2t: 3 hrs

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44
Q

Elimination of hydralazine:

A

Extensive first-pass effect

IV: 15% excreted unchanged

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45
Q

S/E of hydralazine:

A 
Reflex tachycardia
Tolerance/tachyphylaxis
Na+/H2O retention
Angina w/ EKG changes
Drug-induced lupus-like syndrome
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46
Q

Clinical use of hydralazine:

A

In combination with β-blocker and diuretic to limit SNS activation

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47
Q

MoA of minoxidil:

A

Directly relaxes arteriolar smooth muscle via influx of potassium –> hyperpolarization

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48
Q

Indications for minoxidil:

A

Severe HTN due to renovascular disease, renal failure, transplant rejection

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49
Q

Clinical use of minoxidil:

A

Combined with β-blocker and diuretic

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50
Q

PK of minoxidil:

A

90% oral absorption
Peak: 1 hr
E1/2t: 4 hrs
10% of drug excreted unchanged by kidneys

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51
Q

S/E of minoxidil:

A 
↑ HR
↑ renin, norepi
Na+/H2O retention
Pulmonary HTN
Pericardial effusion/tamponade
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52
Q

EKG changes with minoxidil:

A

Flat/inverted T wave

Increased voltage of QRS

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53
Q

Indications for peripheral vasodilators:

A

Facilitate forward flow in AR, MR, HF
Controlled hypotension in OR
Treat hypertensive crisis

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54
Q

MoA of sodium nitroprusside:

A

Interacts with oxyhemoglobin to release NO and cyanide

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55
Q

Metabolism of sodium nitroprusside:

A

Transfer of electron from iron in oxyhemoglobin to SNP yields metHgb + unstable SNP radical with 5 cyanide ions

One cyanide reacts with metHgb to form nontoxic product

Remainder metabolized by liver/kidney to thiocyanate

56
Q

Cyanide toxicity occurs above this rate of sodium nitroprusside:

A

2 mcg/kg/min over long periods

57
Q

Cyanide toxicity from SNP correlates to:

A

Lactate levels

58
Q

Tx of cyanide toxicity from sodium nitroprusside:

A

D/c the SNP infusion
100% O2
Sodium bicarb
Sodium thiosulfate 150 mg/kg over 15 min

59
Q

Tx of severe cyanide toxicity:

A

Sodium nitrate 5 mg/kg (converts Hgb to metHgb which binds with cyanide)

60
Q

S/s of thiocyanate toxicity:

A 
N/V
Tinnitus
Fatigue
Hyperreflexia
Confusion
Psychosis
Miosis
Seizure
Coma
61
Q

Dosage of sodium nitroprusside:

A

.3 - 10 mcg/kg/min IV

62
Q

Max dose of sodium nitroprusside:

A

10 minute infusion

63
Q

Onset/DOA of sodium nitroprusside:

A

Immediate onset

Short DOA

64
Q

Clinical considerations for use of sodium nitroprusside:

A

Continues IV dosing

Use A-line!!

65
Q

CV effects of sodium nitroprusside:

A

Direct venous and arterial dilation
↑ HR from baroreceptor reflex
Intracoronary steal in areas of MI damage!

66
Q

CNS effects of sodium nitroprusside:

A

↑ CBF

↑ ICP

67
Q

Pulmonary effects of sodium nitroprusside:

A

Attenuation/blunting of hypoxic vasoconstriction

68
Q

Hemologic effects of sodium nitroprusside:

A

Increase in GMP inhibits platelet aggregation

69
Q

Clinical uses for sodium nitroprusside:

A

Controlled hypotension
HTN crisis
Cardiac disease

70
Q

Controlled hypotension dosing of sodium nitroprusside:

A

0.3 - 0.5mcg/kg/min

71
Q

HTN crisis dosing of sodium nitroprusside:

A

1-2 mcg/kg IV bolus

72
Q

MoA of nitroglycerin:

A

Vasodilation via generation of NO (glutathione pathway)

73
Q

Tx of methemoglobinemia:

A

Methylene blue 1-2mg/kg IV over 5 min

74
Q

Half-time of nitroglycerin:

A

1.5 minutes

75
Q

CV effects of nitroglycerin:

A 
Venodilation
↓ ventricular EDP
↓ CO
Minimal change in HR
↑ in coronary blood flow to ischemic areas!
76
Q

Tolerance to nitroglycerin is seen after:

A

24 continuous hours of tx

77
Q

CNS effects of nitroglycerin:

A

↑ ICP

Headache

78
Q

Pulmonary effects of nitroglycerin:

A

↓ PVR
Bronchial dilation
Inhibition of pulmonary hypoxic vasoconstriction

79
Q

Coagulation effects of nitroglycerin:

A

Inhibition of plt aggregation

80
Q

GI effects of nitroglycerin:

A

Relaxation of GI smooth muscle

81
Q

Benefits of nitroglycerin for angina:

A

↓ venous return to heart, thus ↓ ventricular EDP

↓ myocardial O2 reqs

82
Q

Benefits of nitroglycerin for cardiac failure:

A

↓ preload
Relieves pulm edema
Limits MI damage

83
Q

Controlled hypotension dosing and contraindication for nitroglycerin:

A

4-5 mcg/kg/min IV

Not recommended in cranial surgery pre-dura opening

84
Q

Sphincter of Oddi dosing of nitroglycerin:

A

200 mcg (1ml) IV bolus

85
Q

PK of isosorbid:

A

Good oral absorption
Oral DOA: 6 hrs
Sublingual DOA: 2 hrs

86
Q

S/E of isosorbid:

A

Orthostatic hypotension

87
Q

Active metabolite of isosorbid:

A

isosorbid-5-mononitrate

88
Q

MoA of trimethaphan:

A

Ganglionic blocker and peripheral vasodilator

Blocks ANS and venodilates

89
Q

Onset of trimethaphan:

90
Q

Dose of trimethaphan:

A

10-200 mcg/kg/min IV

91
Q

Clinical effects of trimethaphan:

A

↓ BP, CO, SVR

92
Q

Increased HR from trimethaphan due to:

A

PSNS blockade, NOT reflex

93
Q

S/E of trimethaphan:

A

Mydriasis, ↓ GI activity, urinary retention (anticholinergic)

94
Q

Phosphodiesterase inhibitors work by:

A

Inhibition of breakdown of intracellular cAMP/cGMP, causing vascular smooth muscle relaxation and inotropy

95
Q

Avoid concurrent use of phosphodiesterase inhibitors and:

96
Q

Indications for phosphodiesterase inhibitors:

A

Heart failure

97
Q

Examples of CCBs:

A

Verapamil
Diltiazem
Nifedipine

98
Q

MoA of CCBs:

A

Bind to receptor on voltage-gated Ca2+ channels maintaining them in closed/inactive state

99
Q

CCBs that work on the AV node:

A

Phenyl-alkyl-amines

Benzothiazepines

100
Q

CCBs that work on the arterial beds:

A

1,4-dihydropyridines

101
Q

Importance of L-type Ca2+ channel:

A

Determines vascular tone and cardiac contractility

102
Q

Clinical effects of CCBs:

A

↓ contractility, HR, SA node activity, conduction across AV node

↓ SVR/BP (due to vascular smooth muscle relaxation)

103
Q

S/E of CCBs:

A

Cancer
Prolonged bleeding
Cardiac issues
Constipation

104
Q

Inhalational agents + CCBs =

A

Myocardial depression/vasodilation

105
Q

NMBs + CCBs =

A

Potentiation of the NMBs

106
Q

Verapamil + β-blockers =

A

Myocardial depression

107
Q

Verapamil + LA =

A

Increased risk of LA toxicity

108
Q

Verapamil + dantrolene =

A

Hyperkalemia and potential cardiac collapse

109
Q

Digoxin + CCBs =

A

Decreased clearance of digoxin

110
Q

H2 blockers + CCBs =

A

Potentially increased plasma levels of CCBs due to altered hepatic enzyme activity

111
Q

Tx of CCB toxicity:

A

IV administration of calcium or dopamine

112
Q

Vascular indications for CCBs:

A 
Systemic HTN
Pulmonary HTN
Cerebral arterial spasm
Raynaud's
Migraine
113
Q

Non-vascular indications for CCBs:

A

Bronchial asthma
Esophageal spasms
Dysmenorrhea
Premature labor

114
Q

Structure of verapamil:

A

Levoisomer specific for slow Ca2+ channel

115
Q

Site of action of verapamil:

116
Q

Clinical effects of verapamil:

A

Depresses AV node
Negative chronotropic effect on SA node
Negative inotropic effect on myocardium
Vasodilation of coronary and systemic arteries

117
Q

Indications for verapamil:

A 
SVT
Vasospastic angina
HTN
Hypertrophic cardiomyopathy
Maternal/fetal tachydysrhythmias
Premature labor
118
Q

PK of verapamil:

A

Highly protein bound
Extensive first pass effect
Peak: 30-45 minute (oral) 15 min (IV)
E1/2t: 6-12 hrs

119
Q

Site of action for nifedipine:

A

Peripheral arterioles

120
Q

Verapamil vs. nifedipine:

A

Nifedipine has greater coronary/peripheral vasodilator effect

121
Q

SA/AV node effects of nifedipine:

A

Little to no effect

122
Q

Indications for nifedipine:

123
Q

PK of nifedipine:

A 
90% protein bound
Hepatic metabolism
Excreted in urine
Effect: 20 min (oral)
Peak: 60-90 min (oral)
E1/2t: 3-7 hrs
124
Q

S/E of nifedipine:

A 
Vertigo
Headache
Flushing
Hypotension
Parasthesias
Muscle weakness
Renal dysfunction
125
Q

Abrupt d/c of nifedipine can cause:

A

Coronary vasospasm

126
Q

Class of drug of diltiazem:

A

Benzothiazepine derivative

127
Q

Site of action of diltiazem:

128
Q

Potency of diltiazem:

A

Between verapamil and nifedipine

129
Q

Clinical uses of diltiazem:

A

Same as verapamil

130
Q

Dosage of diltiazem:

A

0.25 - 0.35 mg/kg over 2 min; can repeat in 15 min

IV infusion: 10 mg/hr

131
Q

PK of diltiazem:

A 
70-80% protein bound
Excreted in bile and urine
Onset: 15 min (oral)
Peak: 30 min
E1/2t: 4-6 hrs
132
Q

Indications for centrally acting agents:

A 
HTN
Sedation
↓ anesthesia reqs
Improve peri-op hemodynamics
Analgesia
133
Q

MoA of clonidine:

A

BP ↓ from ↓ HR, SVR

134
Q

Abrupt cessation of clonidine causes:

A

Rebound HTN

135
Q

S/E of clonidine:

A 
Bradycardia
Sedation
Xerostomia
Impaired concentration
Nightmares
Depression
Vertigo
EPS
Lactation (men)
136
Q

PK of clonidine:

A

50/50 hepatic metabolism, renal excretion

137
Q

Withdrawal syndrome from clonidine:

A

Occurs with doses > 1.2mg/day
18 hrs after acute D/D
Lasts 24-72 hrs
Tx: rectal/transdermal clonidine

ARCHIVED: Pharmacology for Nurse Anesthesia (20 decks)

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