Antihypertensives & Diuretics Flashcards
1
Q
Adrenergic antagonists bind but do not ____.
A
activate adrenoceptors, thus preventing adrenergic agonist activity
2
Q
Nonselective alpha antagonist
A
Phentolamine
3
Q
Mixed antagonists
A
Labetalol
4
Q
Nonselective beta antagonist
A
Propranolol
5
Q
Selective beta 1 antagonists
A
Esmolol
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
7
Q
Mechanism of Action of Phentolamine & Route
A
Competitive antagonist of α1- and α2-receptors
Route: IV, SQ
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
9
Q
Onset and DOA of Phentolamine
A
Onset: 1 minute
Duration: 10 minutes
10
Q
Metabolism and Excretion of Phentolamine
A
Metabolism: Hepatically metabolized
Elimination: Renally excreted
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)
12
Q
Caution using phentolamine in patients with __.
A
CAD, MI
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
14
Q
Mechanism of Action of Labetalol
A
Competitive antagonist of β1, β2 and α1 receptors
β-blockade: α-blockade ratio is 7:1
15
Q
Dosing of Labetalol
A
Intermittent boluses: 5 – 20 mg
16
Q
Onset and DOA of Labetalol
A
Onset: 5 minutes
DOA: 3 - 6 hours
17
Q
Metabolism and Excretion of Labetalol
A
Metabolism: Hepatically metabolized
Elimination: Hepatically and renally excreted
18
Q
Caution use of Labetalol in patients with ___.
A
bradycardia, hypotension, CHF, asthma and COPD
19
Q
Labetalol may cause ___.
A
left ventricular failure, orthostatic hypotension, and bronchospasm
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
21
Q
Mechanism of Action of Propranolol
A
Competitive antagonist of β1 and β2 receptors
22
Q
Dosing of Propranolol
A
Intermittent boluses: 0.5 mg
23
Q
Onset and DOA of Propranolol
A
Onset: 5 minutes
DOA: 4 hours
24
Q
Metabolism and Excretion of Propranolol
A
Metabolism
- Hepatically metabolized
- Extensive first pass effect (90%)
- Highly protein bound (90%)
Elimination: Renally excreted
25
Side effects of propranolol include \_\_\_\_\_.
bronchospasm, acute congestive heart failure, and bradycardia
26
Class, Clinical Use and Route of Esmolol
**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
27
Mechanism of Action of Esmolol
Competitive antagonist of β1 receptors (inhibit β2 receptors at higher doses)
28
Dosing of Esmolol
**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)
29
Onset and DOA of Esmolol
Onset: 1 - 2 minutes
DOA: 5 - 10 minutes
30
Metabolism and Excretion of Esmolol
Metabolism: Rapid hydrolysis by **plasma esterase metabolism in RBCs**
Elimination: Renally excreted
31
Caution use of Esmolol in patients with \_\_\_
bradycardia, hypotension, CHF, and bronchoconstriction
32
Direct Vasodilators include which drugs?
Hydralazine
Nitroprusside
Nitroglycerin
33
Agents that lower blood pressure include: \_\_\_
volatile anesthetics, sympathetic antagonists and agonists, calcium channel blockers, β-blockers, and angiotensin-converting enzyme inhibitors
34
Hypertensive emergency would be?
(blood pressure \>180/120 mm Hg) with signs of organ injury (eg, encephalopathy)
35
Prompt management of hypertension is critical following which types of procedures?
following cardiac and intracranial surgery and other procedures where excessive bleeding is a major concern.
36
Perioperative hypertension is often secondary to \_\_\_\_.
pain, anxiety, hypoxemia, hypercapnia, distended bladder, and failure to continue baseline antihypertensive medications.
37
Blood pressure is the product of \_\_\_\_.
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
Class and Clinical Use of Sodium Nitroprusside
Class: Direct peripheral arterial vasodilator; Non-selective, relaxation of arterial & venous smooth muscle
Clinical Use: Reliable antihypertensive
39
Dosing of Sodium Nitroprusside
Infusion: 0.3–10 mcg/kg/min
40
Mechanism of Action of Sodium Nitroprusside
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
Onset and DOA of Sodium Nitroprusside
Onset: 1 minute
DOA: 3 – 5 minutes
42
Metabolism of Sodium Nitroprusside
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
Elimination of Sodium Nitroprusside
Thiocyanate is slowly cleared by the kidney
44
Caution use of Sodium Nitroprusside in patients with \_\_
aortic stenosis, hypertrophic cardiomyopathy, increased ICP, hypotension, heart failure
45
Sodium Nitroprusside may cause \_\_\_
headache, tachycardia and bronchodilation
46
Patients who receive sodium nitroprusside may experience a build-up of \_\_\_
thiocyantate, which may lead to thyroid dysfunction, muscle weakness, nausea, hypoxia, and an acute toxic psychosis
47
Special considerations for Sodium Nitroprusside
* 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
How is cyanide toxicity caused? What are the characteristics?
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
Treatment of Cyanide Toxicity
Mechanical ventilation with 100% oxygen
•administering sodium thiosulfate or 3% sodium nitrite
To oxidize hemoglobin to methemoglobin
50
Class, Clinical Use and Route of Nitroglycerin
**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
Dosing of Nitroglycerin
IV Infusion: 5 – 100 mcg/min
SL: 0.4 mg
52
Why is NTG less effective with arterial vasodilation than NTP?
less release of nitric oxide
53
Onset and DOA of Nitroglycerin
Onset: 2 – 5 minutes
DOA: 5 – 10 minutes
54
Metabolism and Excretion of Nitroglycerin
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
What is the ideal agent for MIs and why?
Nitroglycerin
## Footnote
* 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
Special considerations for Nitroglycerin
* Headache, tachycardia can occur
* Tolerance may develop with prolonged use
* Caution in patients with aortic stenosis, hypertrophic cardiomyopathy, increased ICP, hypotension, heart failure
57
Class, Use and Route of Hydralazine
Class: Direct acting arterial vasodilator
Clinical Use: Hypertension
Route: IV
58
Mechanism of Action of Hydralazine
Activate guanylate cyclase to increase cGMP
59
Dosing for Hydralazine
Intermittent boluses: 2.5 – 20 mg
60
Onset and DOA of Hydralazine
Onset: 15 minutes
DOA: 2 – 4 hours
61
Metabolism and Excretion of Hydralazine
Metabolism: Hepatically metabolized
Elimination: Renally excreted
62
Hydralazine may result in \_\_\_
reflexive tachycardia
63
Caution use of Hydralazine in patients with \_\_\_
aortic stenosis, hypertrophic cardiomyopathy, increased ICP, hypotension, heart failure
64
Class, Clinical Use and Route of Nicardipine
**Class**: Calcium channel blocker
**Clinical Use**: treatment of angina, hypertension, arrhythmias, peripheral vascular disease, esophageal spasm, cerebral vasospasm, and controlled hypotension
**Route**: IV
65
Mechanism of Action of Nicardipine
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
Dosing of Nicardipine
5 mg/hr, increased by 2.5 mg/h every 15 min up to 15 mg/hr
67
Onset and DOA of Nicardipine
Onset: 1 – 5 min
DOA: 3 – 6 hr
68
Metabolism and Excretion of Nicardipine
Metabolism: Hepatically metabolized
Elimination: Renally excreted
69
Nicardipine may cause \_\_\_. Caution in patients with \_\_\_.
May cause reflexive tachycardia
Caution in patients with an acute MI, heart failure, bradycardia, hypotension and on dantrolene
70
The kidneys are responsible for ___ and have a major influence on \_\_\_.
Responsible for regulating volume and composition of body fluids & have a major influence on blood pressure
71
The nephron is a \_\_\_. List the structures within it.
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
Class, Clinical Use and Route of Furosemide
**Class**: Loop diuretics
**Clinical Use**: Treatment for hypertension, heart failure, peripheral and pulmonary edema, ICP, and renal failure
**Route**: IV, PO
73
Mechanisms of Action of Furosemide
Inhibits reabsorption of Na, Cl, and 2K in the thick ascending loop of Henle
74
Dosing of furosemide
Start with 5 mg and titrate up as needed
75
Onset and DOA of Furosemide
Onset: 5 minutes
DOA: 2 hours
76
Metabolism and Excretion of Furosemide
Metabolism: Hepatically metabolized
Elimination: Renally excreted
77
Considerations for Use of Furosemide
Hypotension
Electrolyte abnormalities (decrease K, Mg and Cl levels)
Ototoxic
Potentiates neuromuscular blockers
78
Class, Clinical Use and Route of Mannitol
**Class**: Osmotic diuretic
**Clinical Use**: Increased ICP, renal perfusion
**Route**: IV
79
Mechanism of Action of Mannitol
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
Dose, Onset and DOA of Mannitol
Dosing (IV)
•0.25-1 g/kg over 30-60 mins
Onset: 15 minutes
DOA: 3 – 6 hours
81
Metabolism and Elimination of Mannitol
Metabolism: Not metabolized
Elimination: Renally excreted (100% unchanged)
82
Mannitol puts the patient at risk for \_\_\_
Risk for hypovolemia, electrolyte abnormalities, pulmonary edema
83
Class, Clinical Use and Route of Hydrochlorothiazide
**Class**: Thiazide diuretic
**Clinical Use**: Treatment for hypertension, often given with beta antagonists
**Route**: PO
84
Mechanism of Action of Hydrochlorothiazide
Inhibits reabsorption of Na & Cl in the ascending loop, proximal & distal tubules
85
Dosing of Hydrochlorothiazide
25 – 100 mg PO/day
86
Onset and DOA of Hydrochlorothiazide
Onset: 2 hours
DOA: 6 hours
87
Metabolism and Excretion of Hydrochlorothiazide
Metabolism: Not metabolized
Elimination: Renally excreted (100% unchanged)
88
Considerations for Hydrochlorothiazide
Risk for hypovolemia, electrolyte abnormalities, pulmonary edema
Potentiates neuromuscular blockade
