Brainscape's Knowledge GenomeTM

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


See full index

Anesthesia-phar > Antihypertensives & Diuretics > Flashcards

Antihypertensives & Diuretics Flashcards

1
Q

Adrenergic antagonists bind but do not ____.

A

activate adrenoceptors, thus preventing adrenergic agonist activity

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

Nonselective alpha antagonist

A

Phentolamine

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

Mixed antagonists

A

Labetalol

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

Nonselective beta antagonist

A

Propranolol

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

Selective beta 1 antagonists

A

Esmolol

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

Class and Clinical Use of Phentolamine

A

Class: Nonselective alpha antagonists

Clinical Use

  • Treatment of hypertension (especially related to excessive alpha antagonism: pheochromocytoma, clonidine withdrawal)
  • Minimize extravasation r/t norepinephrine infiltration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Mechanism of Action of Phentolamine & Route

A

Competitive antagonist of α1- and α2-receptors

Route: IV, SQ

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

Dosing of Phentolamine

A

IV: intermittent boluses (1-5 mg), followed by an infusion at 1-10 mcg/kg/min

SQ: 5 – 10 mg diluted in 10 mL of NS locally infiltrated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Onset and DOA of Phentolamine

A

Onset: 1 minute

Duration: 10 minutes

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

Metabolism and Excretion of Phentolamine

A

Metabolism: Hepatically metabolized

Elimination: Renally excreted

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

Phentolamine can cause ___.

A

reflex tachycardia for 2 – 15 minutes (until endogenous NE presence in the synaptic cleft is depleted from alpha 2 blockade)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Caution using phentolamine in patients with __.

A

CAD, MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Class, Clinical Use and Route of Labetalol

A

Class: Non-selective beta antagonist

Clinical Use: Used to treat tachycardia and hypertension

Route: IV

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

Mechanism of Action of Labetalol

A

Competitive antagonist of β1, β2 and α1 receptors

β-blockade: α-blockade ratio is 7:1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Dosing of Labetalol

A

Intermittent boluses: 5 – 20 mg

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

Onset and DOA of Labetalol

A

Onset: 5 minutes

DOA: 3 - 6 hours

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

Metabolism and Excretion of Labetalol

A

Metabolism: Hepatically metabolized

Elimination: Hepatically and renally excreted

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

Caution use of Labetalol in patients with ___.

A

bradycardia, hypotension, CHF, asthma and COPD

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

Labetalol may cause ___.

A

left ventricular failure, orthostatic hypotension, and bronchospasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Class, Clinical Use and Route of Propranolol

A

Class: Nonselective beta antagonist

Clinical Use: Used for tachycardia and hypertension by decreasing CO, HR, renin release and AV node conduction

Route: IV

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

Mechanism of Action of Propranolol

A

Competitive antagonist of β1 and β2 receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Dosing of Propranolol

A

Intermittent boluses: 0.5 mg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Onset and DOA of Propranolol

A

Onset: 5 minutes

DOA: 4 hours

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

Metabolism and Excretion of Propranolol

A

Metabolism

  • Hepatically metabolized
  • Extensive first pass effect (90%)
  • Highly protein bound (90%)

Elimination: Renally excreted

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Side effects of propranolol include _____.

A

bronchospasm, acute congestive heart failure, and bradycardia

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

Class, Clinical Use and Route of Esmolol

A

Class: Selective β1 antagonist

Clinical Use

  • Used to prevent or minimize tachycardia and hypertension in response to perioperative stimuli, such as intubation, surgical stimulation, and emergence
  • Emerging evidence suggests intraoperative esmolol infusions may decrease post operative opioid requirements

Route: IV

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

Mechanism of Action of Esmolol

A

Competitive antagonist of β1 receptors (inhibit β2 receptors at higher doses)

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

Dosing of Esmolol

A

Bolus: 0.5 mg/kg or 10 mg

Infusion: 50 mcg/kg/min (if desired, titrate up q 5 minutes to a max dose of 200 mcg/kg/min)

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

Onset and DOA of Esmolol

A

Onset: 1 - 2 minutes

DOA: 5 - 10 minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Metabolism and Excretion of Esmolol

A

Metabolism: Rapid hydrolysis by plasma esterase metabolism in RBCs

Elimination: Renally excreted

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

Caution use of Esmolol in patients with ___

A

bradycardia, hypotension, CHF, and bronchoconstriction

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

Direct Vasodilators include which drugs?

A

Hydralazine

Nitroprusside

Nitroglycerin

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

Agents that lower blood pressure include: ___

A

volatile anesthetics, sympathetic antagonists and agonists, calcium channel blockers, β-blockers, and angiotensin-converting enzyme inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Hypertensive emergency would be?

A

(blood pressure >180/120 mm Hg) with signs of organ injury (eg, encephalopathy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Prompt management of hypertension is critical following which types of procedures?

A

following cardiac and intracranial surgery and other procedures where excessive bleeding is a major concern.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Perioperative hypertension is often secondary to ____.

A

pain, anxiety, hypoxemia, hypercapnia, distended bladder, and failure to continue baseline antihypertensive medications.

37
Q

Blood pressure is the product of ____.

A

cardiac output and systemic vascular resistance. Agents that lower blood pressure reduce myocardial contractility or produce vasodilatation of the arterial and venous capacitance vessels, or both.

38
Q

Class and Clinical Use of Sodium Nitroprusside

A

Class: Direct peripheral arterial vasodilator; Non-selective, relaxation of arterial & venous smooth muscle

Clinical Use: Reliable antihypertensive

39
Q

Dosing of Sodium Nitroprusside

A

Infusion: 0.3–10 mcg/kg/min

40
Q

Mechanism of Action of Sodium Nitroprusside

A

As NTP is metabolized by iron, it releases nitric oxide and cyanide. NO activates guanylyl cyclase which synthesizes (cGMP), decreases intracellular calcium, which causes smooth muscle dilation

41
Q

Onset and DOA of Sodium Nitroprusside

A

Onset: 1 minute

DOA: 3 – 5 minutes

42
Q

Metabolism of Sodium Nitroprusside

A

An iron (Fe2+) electron of oxyhemoglobin binds to NTP then unstable NTP radical and methemoglobin then unstable NTP radical decomposes into 5 cyanide ions

Cyanide ions can:

  1. bind to methemoglobin to form cyanmethemoglobin
  2. undergo a reaction in the liver and kidney catalyzed by the enzyme rhodanese: thiosulfate + cyanide → thiocyanate
  3. bind to tissue cytochrome oxidase, which interferes with normal oxygen utilization and results in cyanide toxicity
43
Q

Elimination of Sodium Nitroprusside

A

Thiocyanate is slowly cleared by the kidney

44
Q

Caution use of Sodium Nitroprusside in patients with __

A

aortic stenosis, hypertrophic cardiomyopathy, increased ICP, hypotension, heart failure

45
Q

Sodium Nitroprusside may cause ___

A

headache, tachycardia and bronchodilation

46
Q

Patients who receive sodium nitroprusside may experience a build-up of ___

A

thiocyantate, which may lead to thyroid dysfunction, muscle weakness, nausea, hypoxia, and an acute toxic psychosis

47
Q

Special considerations for Sodium Nitroprusside

A
  • Dilation of coronary arterioles may result in an intracoronary steal
  • Reductions in pulmonary artery pressure and the hypoxic pulmonary vasoconstriction mechanism may decrease lung perfusion
  • Large doses of NTP may lead to methemoglobinemia and is treated with methylene blue to reduce methemoglobinemia to hemoglobin
  • NTP must be protected from light because of photodegradation
  • Patient’s on NTP infusions benefit from arterial line monitoring
48
Q

How is cyanide toxicity caused? What are the characteristics?

A

Cyanide toxicity can occur with cumulative daily dose of NTP greater than 500 mcg/kg or if an infusion rate greater than 2 mcg/kg/min for more than a few hours.

Cyanide toxicity is characterized by metabolic acidosis, cardiac arrhythmias, and increased venous oxygen content

49
Q

Treatment of Cyanide Toxicity

A

Mechanical ventilation with 100% oxygen

•administering sodium thiosulfate or 3% sodium nitrite

To oxidize hemoglobin to methemoglobin

50
Q

Class, Clinical Use and Route of Nitroglycerin

A

Class: Peripheral vasodilator, with venous dilation predominating over arterial dilation

Clinical Use: Nitroglycerin relieves myocardial ischemia, coronary vasospasm, hypertension, ventricular failure, used for controlled hypotension

Route: IV, SL, transdermal

51
Q

Dosing of Nitroglycerin

A

IV Infusion: 5 – 100 mcg/min

SL: 0.4 mg

52
Q

Why is NTG less effective with arterial vasodilation than NTP?

A

less release of nitric oxide

53
Q

Onset and DOA of Nitroglycerin

A

Onset: 2 – 5 minutes

DOA: 5 – 10 minutes

54
Q

Metabolism and Excretion of Nitroglycerin

A

Metabolism: Nitroglycerin undergoes rapid reductive hydrolysis in the liver and blood by glutathione-organic nitrate reductase. One metabolic product is nitrite, which can convert hemoglobin to methemoglobin

Elimination: Renally excreted

55
Q

What is the ideal agent for MIs and why?

A

Nitroglycerin

  • Decrease preload will reduce myocardial oxygen demand and increases endocardial perfusion
  • Redistributes coronary blood flow to ischemic areas of the subendocardium
  • Relieves coronary vasospasm
56
Q

Special considerations for Nitroglycerin

A
  • Headache, tachycardia can occur
  • Tolerance may develop with prolonged use
  • Caution in patients with aortic stenosis, hypertrophic cardiomyopathy, increased ICP, hypotension, heart failure
57
Q

Class, Use and Route of Hydralazine

A

Class: Direct acting arterial vasodilator

Clinical Use: Hypertension

Route: IV

58
Q

Mechanism of Action of Hydralazine

A

Activate guanylate cyclase to increase cGMP

59
Q

Dosing for Hydralazine

A

Intermittent boluses: 2.5 – 20 mg

60
Q

Onset and DOA of Hydralazine

A

Onset: 15 minutes

DOA: 2 – 4 hours

61
Q

Metabolism and Excretion of Hydralazine

A

Metabolism: Hepatically metabolized

Elimination: Renally excreted

62
Q

Hydralazine may result in ___

A

reflexive tachycardia

63
Q

Caution use of Hydralazine in patients with ___

A

aortic stenosis, hypertrophic cardiomyopathy, increased ICP, hypotension, heart failure

64
Q

Class, Clinical Use and Route of Nicardipine

A

Class: Calcium channel blocker

Clinical Use: treatment of angina, hypertension, arrhythmias, peripheral vascular disease, esophageal spasm, cerebral vasospasm, and controlled hypotension

Route: IV

65
Q

Mechanism of Action of Nicardipine

A

By blocking the influx of Ca, it depress electrical impulses in the sinoatrial (SA) and atrioventricular (AV) nodes, resulting in negative chronotropic and inotropic effects and increasing coronary and systemic vasodilation

66
Q

Dosing of Nicardipine

A

5 mg/hr, increased by 2.5 mg/h every 15 min up to 15 mg/hr

67
Q

Onset and DOA of Nicardipine

A

Onset: 1 – 5 min

DOA: 3 – 6 hr

68
Q

Metabolism and Excretion of Nicardipine

A

Metabolism: Hepatically metabolized

Elimination: Renally excreted

69
Q

Nicardipine may cause ___. Caution in patients with ___.

A

May cause reflexive tachycardia

Caution in patients with an acute MI, heart failure, bradycardia, hypotension and on dantrolene

70
Q

The kidneys are responsible for ___ and have a major influence on ___.

A

Responsible for regulating volume and composition of body fluids & have a major influence on blood pressure

71
Q

The nephron is a ___. List the structures within it.

A

The nephron is the functional unit

Structures: glomerulus and the renal tubule.

The components of the renal tubule are Bowman’s capsule (which encapsulates the glomerulus), the proximal tubule, the loop of Henle, the distal tubule, and the collecting duct.

72
Q

Class, Clinical Use and Route of Furosemide

A

Class: Loop diuretics

Clinical Use: Treatment for hypertension, heart failure, peripheral and pulmonary edema, ICP, and renal failure

Route: IV, PO

73
Q

Mechanisms of Action of Furosemide

A

Inhibits reabsorption of Na, Cl, and 2K in the thick ascending loop of Henle

74
Q

Dosing of furosemide

A

Start with 5 mg and titrate up as needed

75
Q

Onset and DOA of Furosemide

A

Onset: 5 minutes

DOA: 2 hours

76
Q

Metabolism and Excretion of Furosemide

A

Metabolism: Hepatically metabolized

Elimination: Renally excreted

77
Q

Considerations for Use of Furosemide

A

Hypotension

Electrolyte abnormalities (decrease K, Mg and Cl levels)

Ototoxic

Potentiates neuromuscular blockers

78
Q

Class, Clinical Use and Route of Mannitol

A

Class: Osmotic diuretic

Clinical Use: Increased ICP, renal perfusion

Route: IV

79
Q

Mechanism of Action of Mannitol

A

increase the osmolarity of plasma drawing in fluid from ICF & ECF & out of the brain; ­increased plasma mannitol is filtered, not reabsorbed which draws fluids & electrolytes (Na, Cl, bicarb) into urine & then increases UOP

Occurs in the proximal tube

80
Q

Dose, Onset and DOA of Mannitol

A

Dosing (IV)

•0.25-1 g/kg over 30-60 mins

Onset: 15 minutes

DOA: 3 – 6 hours

81
Q

Metabolism and Elimination of Mannitol

A

Metabolism: Not metabolized

Elimination: Renally excreted (100% unchanged)

82
Q

Mannitol puts the patient at risk for ___

A

Risk for hypovolemia, electrolyte abnormalities, pulmonary edema

83
Q

Class, Clinical Use and Route of Hydrochlorothiazide

A

Class: Thiazide diuretic

Clinical Use: Treatment for hypertension, often given with beta antagonists

Route: PO

84
Q

Mechanism of Action of Hydrochlorothiazide

A

Inhibits reabsorption of Na & Cl in the ascending loop, proximal & distal tubules

85
Q

Dosing of Hydrochlorothiazide

A

25 – 100 mg PO/day

86
Q

Onset and DOA of Hydrochlorothiazide

A

Onset: 2 hours

DOA: 6 hours

87
Q

Metabolism and Excretion of Hydrochlorothiazide

A

Metabolism: Not metabolized

Elimination: Renally excreted (100% unchanged)

88
Q

Considerations for Hydrochlorothiazide

A

Risk for hypovolemia, electrolyte abnormalities, pulmonary edema

Potentiates neuromuscular blockade

Anesthesia-phar (18 decks)

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