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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

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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
Pre-op hold for ACEIs:
One full day pre-op
26
S/E of ACEIs:
``` Intra-op hypotension** Granulocytopenia Angioedema* Proteinuria Cough* Hyperkalemia ```
27
Contraindications for ACEIs:
Renal artery stenosis
28
Cough/angioedema from ACEIs related to:
Bradykinin
29
Dosage of captopril:
12.5-25mg q8h
30
Onset and half-time of captopril:
Onset: 15 min | E1/2t: 2 hrs
31
Advantages of captopril:
Does not interfere with SNS outflow d/t short E1/2t
32
S/E of captopril:
``` Rash Loss of taste Antagonized by NSAIDs Hyperkalemia Angioedema ```
33
Enalapril vs. captopril:
Enalapril is IV; does not cause rash/renal insufficiency due to lacking sulfhydryl group
34
Elimination of lisinopril:
Administered in active form; excreted unchanged by kidney
35
Onset and duration of effect of enalapril/lisinopril/ramipril:
Enalapril/lisinopril: onset 60-120min, effect 18-30hrs Ramipril: onset 30-60min, effect 24-60hrs
36
MoA for ARBs:
Competitive binding to AT1 receptors to inhibit action of angiotensin II
37
S/E of ARBs:
Similar to ACEIs but less cough, no bradykinin accumulation
38
Contraindications for ARBs:
Renal artery stenosis | Pregnancy
39
Naming of ARBs:
-sartan
40
Drug class of hydralazine:
Phthalazine derivative
41
MoA of hydralazine:
Activates guanylate cyclase causing vasodilation (primarily arterial)
42
Dosage of hydralazine:
2.5 - 10mg IV
43
Peak, duration and half-time of hydralazine:
Onset: 10-20 minutes Duration: 6 hr E1/2t: 3 hrs
44
Elimination of hydralazine:
Extensive first-pass effect | IV: 15% excreted unchanged
45
S/E of hydralazine:
``` Reflex tachycardia Tolerance/tachyphylaxis Na+/H2O retention Angina w/ EKG changes Drug-induced lupus-like syndrome ```
46
Clinical use of hydralazine:
In combination with β-blocker and diuretic to limit SNS activation
47
MoA of minoxidil:
Directly relaxes arteriolar smooth muscle via influx of potassium --> hyperpolarization
48
Indications for minoxidil:
Severe HTN due to renovascular disease, renal failure, transplant rejection
49
Clinical use of minoxidil:
Combined with β-blocker and diuretic
50
PK of minoxidil:
90% oral absorption Peak: 1 hr E1/2t: 4 hrs 10% of drug excreted unchanged by kidneys
51
S/E of minoxidil:
``` ↑ HR ↑ renin, norepi Na+/H2O retention Pulmonary HTN Pericardial effusion/tamponade ```
52
EKG changes with minoxidil:
Flat/inverted T wave | Increased voltage of QRS
53
Indications for peripheral vasodilators:
Facilitate forward flow in AR, MR, HF Controlled hypotension in OR Treat hypertensive crisis
54
MoA of sodium nitroprusside:
Interacts with oxyhemoglobin to release NO and cyanide
55
Metabolism of sodium nitroprusside:
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
Cyanide toxicity occurs above this rate of sodium nitroprusside:
2 mcg/kg/min over long periods
57
Cyanide toxicity from SNP correlates to:
Lactate levels
58
Tx of cyanide toxicity from sodium nitroprusside:
D/c the SNP infusion 100% O2 Sodium bicarb Sodium thiosulfate 150 mg/kg over 15 min
59
Tx of severe cyanide toxicity:
Sodium nitrate 5 mg/kg (converts Hgb to metHgb which binds with cyanide)
60
S/s of thiocyanate toxicity:
``` N/V Tinnitus Fatigue Hyperreflexia Confusion Psychosis Miosis Seizure Coma ```
61
Dosage of sodium nitroprusside:
.3 - 10 mcg/kg/min IV
62
Max dose of sodium nitroprusside:
10 minute infusion
63
Onset/DOA of sodium nitroprusside:
Immediate onset | Short DOA
64
Clinical considerations for use of sodium nitroprusside:
Continues IV dosing | Use A-line!!
65
CV effects of sodium nitroprusside:
Direct venous and arterial dilation ↑ HR from baroreceptor reflex Intracoronary steal in areas of MI damage!
66
CNS effects of sodium nitroprusside:
↑ CBF | ↑ ICP
67
Pulmonary effects of sodium nitroprusside:
Attenuation/blunting of hypoxic vasoconstriction
68
Hemologic effects of sodium nitroprusside:
Increase in GMP inhibits platelet aggregation
69
Clinical uses for sodium nitroprusside:
Controlled hypotension HTN crisis Cardiac disease
70
Controlled hypotension dosing of sodium nitroprusside:
0.3 - 0.5mcg/kg/min
71
HTN crisis dosing of sodium nitroprusside:
1-2 mcg/kg IV bolus
72
MoA of nitroglycerin:
Vasodilation via generation of NO (glutathione pathway)
73
Tx of methemoglobinemia:
Methylene blue 1-2mg/kg IV over 5 min
74
Half-time of nitroglycerin:
1.5 minutes
75
CV effects of nitroglycerin:
``` Venodilation ↓ ventricular EDP ↓ CO Minimal change in HR ↑ in coronary blood flow to ischemic areas! ```
76
Tolerance to nitroglycerin is seen after:
24 continuous hours of tx
77
CNS effects of nitroglycerin:
↑ ICP | Headache
78
Pulmonary effects of nitroglycerin:
↓ PVR Bronchial dilation Inhibition of pulmonary hypoxic vasoconstriction
79
Coagulation effects of nitroglycerin:
Inhibition of plt aggregation
80
GI effects of nitroglycerin:
Relaxation of GI smooth muscle
81
Benefits of nitroglycerin for angina:
↓ venous return to heart, thus ↓ ventricular EDP ↓ myocardial O2 reqs
82
Benefits of nitroglycerin for cardiac failure:
↓ preload Relieves pulm edema Limits MI damage
83
Controlled hypotension dosing and contraindication for nitroglycerin:
4-5 mcg/kg/min IV Not recommended in cranial surgery pre-dura opening
84
Sphincter of Oddi dosing of nitroglycerin:
200 mcg (1ml) IV bolus
85
PK of isosorbid:
Good oral absorption Oral DOA: 6 hrs Sublingual DOA: 2 hrs
86
S/E of isosorbid:
Orthostatic hypotension
87
Active metabolite of isosorbid:
isosorbid-5-mononitrate
88
MoA of trimethaphan:
Ganglionic blocker and peripheral vasodilator Blocks ANS and venodilates
89
Onset of trimethaphan:
Rapid
90
Dose of trimethaphan:
10-200 mcg/kg/min IV
91
Clinical effects of trimethaphan:
↓ BP, CO, SVR
92
Increased HR from trimethaphan due to:
PSNS blockade, NOT reflex
93
S/E of trimethaphan:
Mydriasis, ↓ GI activity, urinary retention (anticholinergic)
94
Phosphodiesterase inhibitors work by:
Inhibition of breakdown of intracellular cAMP/cGMP, causing vascular smooth muscle relaxation and inotropy
95
Avoid concurrent use of phosphodiesterase inhibitors and:
Nitrates
96
Indications for phosphodiesterase inhibitors:
Heart failure
97
Examples of CCBs:
Verapamil Diltiazem Nifedipine
98
MoA of CCBs:
Bind to receptor on voltage-gated Ca2+ channels maintaining them in closed/inactive state
99
CCBs that work on the AV node:
Phenyl-alkyl-amines | Benzothiazepines
100
CCBs that work on the arterial beds:
1,4-dihydropyridines
101
Importance of L-type Ca2+ channel:
Determines vascular tone and cardiac contractility
102
Clinical effects of CCBs:
↓ contractility, HR, SA node activity, conduction across AV node ↓ SVR/BP (due to vascular smooth muscle relaxation)
103
S/E of CCBs:
Cancer Prolonged bleeding Cardiac issues Constipation
104
Inhalational agents + CCBs =
Myocardial depression/vasodilation
105
NMBs + CCBs =
Potentiation of the NMBs
106
Verapamil + β-blockers =
Myocardial depression
107
Verapamil + LA =
Increased risk of LA toxicity
108
Verapamil + dantrolene =
Hyperkalemia and potential cardiac collapse
109
Digoxin + CCBs =
Decreased clearance of digoxin
110
H2 blockers + CCBs =
Potentially increased plasma levels of CCBs due to altered hepatic enzyme activity
111
Tx of CCB toxicity:
IV administration of calcium or dopamine
112
Vascular indications for CCBs:
``` Systemic HTN Pulmonary HTN Cerebral arterial spasm Raynaud's Migraine ```
113
Non-vascular indications for CCBs:
Bronchial asthma Esophageal spasms Dysmenorrhea Premature labor
114
Structure of verapamil:
Levoisomer specific for slow Ca2+ channel
115
Site of action of verapamil:
AV node
116
Clinical effects of verapamil:
Depresses AV node Negative chronotropic effect on SA node Negative inotropic effect on myocardium Vasodilation of coronary and systemic arteries
117
Indications for verapamil:
``` SVT Vasospastic angina HTN Hypertrophic cardiomyopathy Maternal/fetal tachydysrhythmias Premature labor ```
118
PK of verapamil:
Highly protein bound Extensive first pass effect Peak: 30-45 minute (oral) 15 min (IV) E1/2t: 6-12 hrs
119
Site of action for nifedipine:
Peripheral arterioles
120
Verapamil vs. nifedipine:
Nifedipine has greater coronary/peripheral vasodilator effect
121
SA/AV node effects of nifedipine:
Little to no effect
122
Indications for nifedipine:
Angina
123
PK of nifedipine:
``` 90% protein bound Hepatic metabolism Excreted in urine Effect: 20 min (oral) Peak: 60-90 min (oral) E1/2t: 3-7 hrs ```
124
S/E of nifedipine:
``` Vertigo Headache Flushing Hypotension Parasthesias Muscle weakness Renal dysfunction ```
125
Abrupt d/c of nifedipine can cause:
Coronary vasospasm
126
Class of drug of diltiazem:
Benzothiazepine derivative
127
Site of action of diltiazem:
AV node
128
Potency of diltiazem:
Between verapamil and nifedipine
129
Clinical uses of diltiazem:
Same as verapamil
130
Dosage of diltiazem:
0.25 - 0.35 mg/kg over 2 min; can repeat in 15 min IV infusion: 10 mg/hr
131
PK of diltiazem:
``` 70-80% protein bound Excreted in bile and urine Onset: 15 min (oral) Peak: 30 min E1/2t: 4-6 hrs ```
132
Indications for centrally acting agents:
``` HTN Sedation ↓ anesthesia reqs Improve peri-op hemodynamics Analgesia ```
133
MoA of clonidine:
BP ↓ from ↓ HR, SVR
134
Abrupt cessation of clonidine causes:
Rebound HTN
135
S/E of clonidine:
``` Bradycardia Sedation Xerostomia Impaired concentration Nightmares Depression Vertigo EPS Lactation (men) ```
136
PK of clonidine:
50/50 hepatic metabolism, renal excretion
137
Withdrawal syndrome from clonidine:
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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