Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardiopulm/Renal Exam 2 > Hypertension Drugs > Flashcards

Hypertension Drugs Flashcards

1
Q

Phentolamine: Pharmacokinetics

A
  • Short half life of 19 mins (blocks alpha receptor)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Phentolamine: Adverse Effects

A
  • Acute and prolonged HYPOTENSIVE EPISODES
  • ORTHOSTATIC HYPOTENSION
  • TACHYCARDIA, and
  • CARDIAC ARRHYTHMIAS;
  • weakness, dizziness, flushing, NASAL STUFFINESS, nausea, vomiting, and DIARRHEA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Phenoxybenzamine: MOA

A

non-competitive antagonist (blocks alpha receptor)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Phenoxybenzamine: Adverse Effects

A

many adverse effects similar to phentolamine, plus MIOSIS and occasionally causes severe allergic reactions (e.g., ANGIOEDEMA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Prazosin: MOA (non emphasized)

A

competitive antagonist of postsynaptic alpha1-adrenergic receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Prazosin: Effects (non emphasized)

A

vasodilationof veins and

arterioles leads to a decrease in total peripheral resistance and blood pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Prazosin: Clinical Applications

A

• Hypertension
- a late choice in JNC8 due to ALLHAT data showing > LIKELIHOOD OF STROKE AND CHF with DOXAZOSIN in comparison to CHLORTHALIDONE

• For PTSD nightmares; Raynaud syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Prazosin: Toxicities

A
  • palpitations, edema, ORTHOSTATIC HYPOTENSION, syncope
  • dizziness,headache, drowsiness, depression, nervousness
  • decreased energy, weakness
  • nausea, diarrhea, constipation
  • urinaryfrequency, “RETROGRADE” EJACULATION, priapism
  • blurred vision, reddened sclera
  • nasal congestion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Similar to prazosin (but differ with respect to α1a, α1b and α1d subtype selectivity)… marketed for benign prostatic
hypertrophy and also used to help kidney stones pass

  • potential one drug solution for old man in wheelchair with BPH and hypertension…
A

tamsulosin, terazosin, (doxazosin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Clonidine: MOA (non-emphasized)

A

alpha2- adrenergic

receptor agonist, crosses blood- brain barrier

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Clonidine: Effects

A

• IV administration produces a transient increase in blood pressure

• Then get reduced sympathetic outflow from the CNS
- produces a decrease in peripheral resistance, renal vascular resistance, heart rate, and blood pressure

  • Produces pain relief
  • Beneficial for ADHD to reduce hyperactivity, impulsiveness, and distractibility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Clonidine: Clinical Applications (non-emphasized)

A
  • oral Immediate release tablets or transdermal patch for management of hypertension
  • extended release tablets for treatment of ADHD
  • continuous epidural administration as adjunctive therapy with opioids for treatment of severe cancer pain
  • off-label includes: opioid withdrawal, postherpetic neuralgia, smoking cessation, Tourette syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Clonidine: Pharmacokinetics (non-emphasized)

A

oral, transdermal patch and epidermal solution formulations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Clonidine: Toxicities

A
  • Drowsiness
  • Xerostomia (dry mouth)
  • REBOUND HYPERTENSION IF DOSE IS MISSED
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

α-methyldopa: MOA

A

selective agonist for α2-adrenergic receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

α-methyldopa: Effects (non-emphasized)

A

used as sympatholytic for hypertension due to reduced sympathetic outflow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

α-methyldopa: Clinical Applications

A

• For management of moderate to severe hypertension

  • Not recommended for initial therapy of primary hypertension
  • Continues to have a role in otherwise difficult to treat hypertension

• Remains a drug of choice for gestational hypertension (aka pregnancy-induced hypertension)
- (labetalol and long- acting nifedipine also used for gestational hypertension)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

α-methyldopa: Pharmacokinetics

A

oral and IV forms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

α-methyldopa: Toxicities

A 
There is a lot 
• angina pectoris aggravation
• Bell’s palsy
• Amenorrhea
• Sore or “black” tongue,
  • POSITIVE COOMBS TEST
  • SLE-LIKE SYNDROME
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Propranolol: MOA

A

NONSELECTIVE beta-adrenergic blocker (class II antiarrhythmic); competitively blocks response to beta1- and beta2- adrenergic stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Propranolol: Effects

A
  • beta1 blockade decreases heart rate, myocardial contractility, blood pressure, and myocardial oxygen demand
  • beta2 blockade effects include blunting of bronchodilation and vasodilation in skeletal muscle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Propranolol: Clinical Applications (non-emphasized)

A 
• hypertension
• angina pectoris
• pheochromocytoma
• essential tremor supraventricular
arrhythmias 
• ventricular tachycardias
• prevention of myocardial infarction
• migraine headache prophylaxis
• off-label: akathisia, antipsychotic-induced; performance anxiety; thyroid storm / thyrotoxicosis; tremor, lithium-induced
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Propranolol: Pharmacokinetics

A

given orally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Propranolol: Toxicities

A
  • bronchospasm, dyspnea
  • COLD EXTREMITIES (ESPECIALLY INFANTS) – The reason B-blockers are contraindicated if peripheral vascular disease

• bradycardia, AV conduction
disturbance, congestive heart failure, cardiogenic shock, hypotension, syncope

  • disrupted sleep with nightmares, drowsiness/fatigue, agitation
  • hyperglycemia or hypoglycemia; hyperkalemia; hyperlipidemia
  • abdominal pain, diarrhea, constipation, etc.
  • conjunctival hyperemia, decreased visual acuity, mydriasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Atenolol: MOA

A

• competitive β1-selective adrenergic receptor antagonist

• little or no effect on
β2- receptors except at high doses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Atenolol: Effects

A

beta1 blockade decreases heart rate, myocardial contractility, blood pressure, and myocardial oxygen demand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Atenolol: Clinical Applications

A
  • treatment of hypertension, alone or in combination with other agents
  • management of angina pectoris

• secondary prevention
postmyocardial infarction

• off-label: atrial fibrillation (rate control); cardiac risk reduction during surgery; pediatric hypertension; acute ethanol withdrawal (in combination with a benzodiazepine); supraventricular arrhythmias; unstable angina; ventricular arrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Atenolol: Pharmacokinetics

A
  • PO: rapid but incomplete absorption

* not lipophilic, does not cross BBB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Atenolol: Toxicities (non-emphasized)

A
  • bradycardia (persistent), cardiac failure, chest pain, cold extremities, complete atrioventricular block, edema, hypotension, Raynaud’s phenomenon, second degree atrioventricular block
  • confusion, fatigue, headache, insomnia, lethargy, nightmares
  • constipation, diarrhea, nausea
  • impotence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

another widely used beta1-selective blocker, shorter half-life than atenolol but available in extended release form; more lipid soluble so more likely to produce adverse CNS effects (e.g., lethargy/confusion, nightmares)

A

metoprolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

notable for having highest beta1-selectivity

A

bisoprolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Captopril: MOA

A

competitive inhibitor of

angiotensin- converting enzyme (ACE)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Captopril: Effects

A
  • prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor and mitogen for cardiovascular remodeling
  • lowers levels of angiotensin II –> Increased plasma renin activity and decreased aldosterone secretion
  • Lowers BP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Captopril: Clinical Applications (non-emphasized)

A
  • hypertension, add thiazide or loop diuretic if additional lowering is needed at max recommended dose
  • acute hypertension (urgency/emergency)
  • heart failure with reduced ejection fraction
  • LV dysfunction following MI
  • diabetic nephropathy
  • off-label: aldosteronism (diagnosis), delay the progression of nephropathy and reduce risks of cardiovascular events HT + DM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Captopril: Pharmacokinetics

A
  • Rapidly absorbed, ~60% bioavailability
  • Substrate of CYP2D6 (major)
  • excreted primarily in urine, 40-50% as unchanged drug
  • t1/2: ~1.7 hrs, longer in renal impairment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Captopril: Toxicities

A

• COUGH

  • hypotension
  • headache
  • drowsiness
  • dizziness, orthostatic dizziness

• ANGIOEDEMA, anaphyllactoid reactions

  • loss of/altered taste (especially captopril among class)
  • rare cholestatic jaundice
  • rare agranulocytosis, neutropenia, anemia, pancytopenia, thrombocytopenia
  • myalgia, weakness
  • polyuria, renal failure, renal insufficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

another early ACEI, a prodrug with active form (enalaprilat) available for IV

A

enalapril (enalaprilat)

38
Q

now widely used ACE inhibitor, longer half life permitting 1X/day dosing

A

benazepril

39
Q

now widely used ACE inhibitor, longer half life permitting 1X/day dosing

A

lisonopril

40
Q

Losartan: MOA

A

competitive nonpeptide angiotensin II receptor antagonist

41
Q

Losartan: Effects (non-emphasized)

A

• blocks the vasoconstrictor and aldosterone- secreting effects of angiotensin II

• induces a more complete
inhibition of the renin- angiotensin system than ACE inhibitors

• does not affect the response to bradykinin

42
Q

Losartan: Clinical Applications (non-emphasized)

A
  • Treatment of diabetic nephropathy
  • HT,alone or in combination with other antihypertensives
  • Hypertension with left ventricular hypertrophy to reduce risk of stroke
  • CKD and HT regardless of race or diabetes status, to improve kidney outcomes
  • Heart failure if intolerant of ACE inhibitors
  • Off-label: Marfan syndrome
43
Q

Losartan: Pharmacokinetics

A

t1/2 = 2 hours

44
Q

Losartan: Toxicities (non-emphasized)

A
  • Adverse effects more common in those with diabetic nephropathy
  • Hypotension, first-dose hypotension, orthostatic hypotension
  • Fatigue, dizziness, fever
  • Hypoglycemia, hyperkalemia
  • Diarrhea,gastritis, nausea, weight gain
  • anemia

• weakness,back/knee
pain

• Cough (< ACEI) bronchitis, nasal congestion

45
Q

t1/2 ~ 6 -10 hrs, noteworthy in that NOT A PRODRUG requiring activation, excreted primarily in feces as unchanged drug

A

valsartan

46
Q

t1/2 5-9 hrs, noteworthy for its relatively IRREVERSIBLE BINDING4

A

candesartan

47
Q

Aliskiren: MOA

A

Direct renin inhibitor,

resulting in blockade of the conversion of angiotensinogen to angiotensin I

48
Q

Aliskiren: Effects

A
  • Decreases the formation of angiotensin II (Ang II), a potent blood pressure- elevating peptide (via direct vasoconstriction, aldosterone release, and sodium retention)
  • ACE inhibitor and ARB therapy can potentially be offset by increases in plasma renin actvitity (PRA), which is blocked by direct renin inhibitors
49
Q

Aliskiren: Clinical Applications

A

Treatment of hypertension, alone or in combination with other antihypertensive agents

50
Q

Aliskiren: Pharmacokinetics

A
  • oral route, poor absorption
  • see maximum effects in 2 weeks
  • t1/2 ~ 24 hrs
51
Q

Aliskiren: Toxicities

A
  • few…
  • skin rash (1%),rarely other hypersensitivity reactions
  • diarrhea (2%)

• >300% increase in creatine
phosphokinase (1%)

  • increased blood urea nitrogen, increased serum creatinine
  • hyperkalemia, especially if combined or predisposing factors such as renal dysfunction or diabetes mellitus
  • cough (1%)
52
Q

Which drug is new, expensive, no obvious benefits, some evidence of increased risk of adverse events?

A

Aliskiren

53
Q

Are ACE inhibitors contraindicated in pregnancy?

A

YES

54
Q

Nifedipine: MOA

A

• prototypical dihydropyridine calcium channel blocker

55
Q

Nifedipine: Effects

A
  • causes relaxation of coronary vascular smooth muscle –> coronary vasodilation
  • FREQUENCY – INDEPENDENT … NOT CARDIOACTIVE
56
Q

Nifedipine: Clinical Applications

A
  • management of chronic stable or vasospastic angina
  • treatment of hypertension
  • off-label: HYPERTENSIVE EMERGENCY IN PREGNANCY; PULMONARY HYPERTENSION
57
Q

Nifedipine: Toxicities

A

Common:
• flushing
•peripheral edema
• headache

Also see:
• palpitations
• gingival hyperplasia

58
Q

dihydropyridine CCB with use limited to CAD and HT, but very widely used in part due to long t1/2 of 30-50 hrs

A

amlodipine

59
Q

Verapamil: MOA

A

non-dihydropyridine CCB

60
Q

Verapamil:

A
  • produces relaxation of coronary vascular smooth muscle and coronary vasodilation
  • FREQUENCY – DEPENDENT (I.E., CARDIOACTIVE)
61
Q

Verapamil: Clinical Applications

A
  • IV: supraventricular tachyarrhythmia
  • Oral, treatment of:
  • primary hypertension
  • angina pectoris
  • supraventricular tachyarrhythmia

• off-label: episodic migraine prevention (adults); hypertrophic cardiomyopathy

62
Q

Verapamil: Toxicities

A

Common:
• headache
• gingival hyperplasia
• constipation

Also see: 
• peripheral edema
• CHF/pulmonary edema
• hypotension, fatigue, dizziness, lethargy
• AV block, bradycardia
• flushing
• rash
• dyspepsia
• flu-like syndrome
63
Q

Diltiazem: MOA

A

non- dihydropyridine calcium channel blocker

64
Q

Diltiazem: Effects

A
  • producing a relaxation of coronary vascular smooth muscle and coronary vasodilation
  • FREQUENCY – DEPENDENT (I.E., CARDIOACTIVE)
65
Q

Diltiazem: Clinical Applications

A

IV:
• control of rapid ventricular rate in patients with atrial fibrillation or atrial flutter

• conversion of paroxysmal supraventricular tachycardia (PSVT)

Oral:
• primary hypertension
• chronic stable angina or angina from coronary artery spasm

• off-label: anal fissures (topical); atrial fibrillation (rate control) (oral); stable narrow-complex tachycardia uncontrolled or unconverted by adenosine or vagal maneuvers or if SVT is recurrent (injection); hypertrophic cardiomyopathy; Raynaud phenomenon; hypertension (children)

66
Q

Diltiazem: Toxicities

A

Common:
• edema
• headache

Also seen:
• Atrioventricular block, bradycardia, hypotension, extrasystoles, flushing, palpitations
• dizziness, pain, nervousness
• skin rash
• gout
• dyspepsia, constipation, vomiting, diarrhea
• injection site reaction
• weakness, myalgia
• rhinitis, pharyngitis, dyspnea bronchitis, cough

67
Q

Direct Vasodilator:

Hydralazine: MOA

A

• Direct vasodilation of arterioles (with little effect on veins)

68
Q

Direct Vasodilator:

Hydralazine: Effects

A

• Decreases systemic

resistance

69
Q

Direct Vasodilator:

Hydralazine: Clinical Applications

A
  • Heart failure with reduced ejection fraction

* HYPERTENSIVE EMERGENCY IN PREGNANCY

70
Q

Direct Vasodilator:

Hydralazine: Pharmacokinetics

A

• oral or IV administration

71
Q

Direct Vasodilator:

Hydralazine: Toxicities

A
  • Cardiovascular: Angina pectoris, flushing, orthostatic hypotension, palpitations, paradoxical hypertension, peripheral edema, tachycardia, vascular collapse
  • Central nervous system: Anxiety, chills, depression, disorientation, dizziness, fever, headache, increased intracranial pressure, psychotic reaction
  • Dermatologic: Pruritus, rash, urticaria
  • Gastrointestinal: Anorexia, constipation, diarrhea, nausea, paralytic ileus, vomiting
  • Genitourinary: Dysuria, impotence
  • Hematologic: Agranulocytosis, eosinophilia, erythrocyte count reduced, hemoglobin decreased, hemolytic anemia, leukopenia
  • Neuromuscular and skeletal: Muscle cramps, peripheral neuritis, rheumatoid arthritis, tremor, weakness
  • Ocular: Conjunctivitis, lacrimation
  • Respiratory: Dyspnea, nasal congestion
  • Miscellaneous: Diaphoresis, DRUG-INDUCED LUPUS-LIKE SYNDROME
72
Q

Direct Vasodilator:

Nitroprusside: MOA

A

causes peripheral vasodilation by direct action on VENOUS and ARTERIOLAR smooth muscle

73
Q

Direct Vasodilator:

Nitroprusside: Effects

A

• reduces peripheral resistance

• will increase cardiac
output by decreasing afterload

74
Q

Direct Vasodilator:

Nitroprusside: Clinical Applications

A

• management of hypertensive crises

• acute
decompensated heart failure (HF)

• controlled hypotension to
reduce bleeding during surgery

• off-label… hypertension
during acute ischemic stroke

75
Q

Direct Vasodilator:

Nitroprusside: Pharmacokinetics

A
  • Administered IV

* t1/2 = 2 mins

76
Q

Direct Vasodilator:

Nitroprusside: Toxicities

A

• Cardiovascular: flushing, hypotension (excessive), palpitations, substernal distress, tachycardia

• Central nervous system:
apprehension, dizziness, headache, intracranial pressure increased, restlessness

  • Dermatologic: rash
  • Endocrine and metabolic: metabolic acidosis due to cyanide toxicity, hypothyroidism
  • Gastrointestinal: abdominal pain, ileus, nausea, retching, vomiting
  • Hematologic: methemoglobinemia, platelet aggregation decreased
  • Neuromuscular and skeletal, ocular: muscle twitching and miosis due to thiocyanate toxicity
  • Otic: tinnitus due to thiocyanate toxicity
  • Respiratory: hyperoxemia due to cyanide toxicity
77
Q

Direct Vasodilator:

Minoxidil: MOA

A
  • produces vasodilation by directly relaxing arteriolar smooth muscle, with little effect on veins
  • stimulationof hair growth
78
Q

Direct Vasodilator:

Minoxidil: Effects

A

lowers arteriolar

vascular resistance

79
Q

Direct Vasodilator:

Minoxidil: Clinical Applications

A

• treatment of hypertension that is symptomatic or associated with target organ damage, and is not manageable with maximum therapeutic doses of a diuretic plus 2 other antihypertensives

• Use in milder degrees of
hypertension is not recommended because the benefit-risk ratio in such patients has not been defined.

80
Q

Direct Vasodilator:

Minoxidil: Pharmacokinetics

A

t1/2 = ~4hrs

81
Q

Direct Vasodilator:

Minoxidil: Toxicities

A
  • Cardiovascular: ECG changes (T- wave changes 60%), edema (reversible, 7% to 10%), PERICARDIAL EFFUSION (OCCASIONALLY WITH TAMPONADE, 3%), angina pectoris, cardiac failure, pericarditis, tachycardia
  • Dermatologic: hypertrichosis (80%)
  • Endocrine and metabolic: sodium retention, water retention, weight gain
  • Gastrointestinal: Nausea, vomiting

• Hematologic and oncologic:
transient decreased in hematocrit due to hemodilution

  • Hepatic: ascites, increased serum alkaline phosphatase
  • Respiratory: pulmonary edema
82
Q

IV Antihypertensive Drugs For Hypertensive Emergencies

CCB — dihydropyridines:
Nicardipine: Contraindication

A

Contraindicated in advanced aortic stenosis; no dose adjustment needed for elderly

83
Q

IV Antihypertensive Drugs For Hypertensive Emergencies

CCB — dihydropyridines:
Clevidipine: Contraindication

A

Contraindicated in patients with soybean, soy product, egg, and egg product allergy and in patients with defective lipid metabolism (eg, pathological hyperlipidemia, lipoid nephrosis or acute pancreatitis)

84
Q

IV Antihypertensive Drugs For Hypertensive Emergencies

Vasodilators — Nitric-oxide dependent:
Sodium nitroprusside: Caution

A

Intra-arterial BP monitoring recommended to prevent “overshoot.” Lower dosing adjustment required for elderly. Cyanide toxicity with prolonged use can result in irreversible neurological changes and cardiac arrest; thiosulfate is antidote

85
Q

IV Antihypertensive Drugs For Hypertensive Emergencies

Vasodilators — Nitric-oxide dependent:
Nitroglycerin: Cautions

A

Use only in patients with acute coronary syndrome and/or acute pulmonary edema. Do not use in volume-depleted patients

86
Q

IV Antihypertensive Drugs For Hypertensive Emergencies

Vasodilators — direct:
Hydralazine: Cautions

A

BP begins to decrease within 10–30 min, and the fall lasts 2–4 h. Unpredictability of response and prolonged duration of action do not make hydralazine a desirable first-line agent for acute treatment in most patients

87
Q

IV Antihypertensive Drugs For Hypertensive Emergencies

Adrenergic blockers, beta1 selective:
Esmolol: Contraindication

A

Contraindicated in patients with concurrent beta-blocker therapy, bradycardia, or decompensated HF. Monitor for bradycardia. May worsen HF. Higher doses may block beta-2 receptors and impact lung function in reactive airway disease

88
Q

IV Antihypertensive Drugs For Hypertensive Emergencies

Adrenergic blockers, combined alpha-1 selective and non selective beta :
Labetalol: Contraindication

A

Contraindicated in reactive airways disease or chronic obstructive pulmonary disease. Especially useful in hyperadrenergic syndromes. May worsen HF and should not be given in patients with secon- or third-degress heart block or bradycardia

89
Q

IV Antihypertensive Drugs For Hypertensive Emergencies

Adrenergic blockers, nonselective alpha:
Phentolamine: Uses

A

Used in hypertensive emergencies induced by catecholamine excess (pheochromocytoma, interactions between monamine oxidase inhibitors and other drugs or food, cocaine toxicity, amphetamine overdose, or clonidine withdrawal)

90
Q

IV Antihypertensive Drugs For Hypertensive Emergencies

Dopamine1-receptor agonist:
Fenoldopam: Contraindication

A

Contraindicated in patients at risk of increased intraocular pressure (glaucoma) or intracranial pressure and those with sulfite allergy

91
Q

IV Antihypertensive Drugs For Hypertensive Emergencies

ACE inhibitor:
Enalaprilat: Contraindication

A

Contraindicated in pregnancy and should not be used in acute MI or bilateral renal artery stenosis. Mainly useful in hypertensive emergencies associated with high plasma renin activity. Dose not easily
adjusted. Relatively slow onset of action (15 min) and unpredictability of BP response

Cardiopulm/Renal Exam 2 (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions