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CPR II Exam 1 > Lecture 11/12: Drugs for Shock/Hypertension and Hypertensive Emergencies > Flashcards

Lecture 11/12: Drugs for Shock/Hypertension and Hypertensive Emergencies Flashcards

1
Q

What is the initial treatment for Shock that is NOT cardiogenic in nature?

A

FLUID REPLACEMENT!
- give 20-40 mL/kg

Goal: to increase Jugular Venous Pressure slightly above normal (< 8 cm H2O)

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2
Q

What is the treatment for Anaphylactic Shock?

A
  • immediately give EPINEPHRINE

- can also give antihistamine and inhaled albuterol

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3
Q

What is the treatment for Hypovolemic Shock?

A
  • FLUIDS (usually do not need drugs)

Blood Loss < 15 - 30% –> give crystalloid
Blood Loss 30 - 40%+ –> give crystalloid AND blood

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4
Q

What receptors do these Vasopressors/Inotropes for Shock activate:

  1. Dopamine
  2. Norepinephrine
  3. Epinephrine
  4. Dobutamine
  5. Phenylephrine
  6. Vasopressor
A
  1. stimulates Beta at low doses, stimulates Alpha at high
  2. stimulates Alpha and Beta 1 receptors, NOT Beta 2
  3. stimulates Alpha, Beta 1, and Beta 2 receptors
  4. stimulates B1 receptors, vasodilates periphery
  5. stimulates Alpha receptors, reflexively dec. HR
  6. from posterior pituitary: V1 vasoconstrictor
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5
Q

What is the treatment for Cardiogenic Shock?

A
  • can use either norepinephrine OR dopamine, but NOREPINEPHRINE is SUPERIOR
  • can give dobutamine for refractory shock when low cardiac output despite adequate filling pressure
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6
Q

What is the treatment for Septic Shock?

A
  • start with BROAD SPECTRUM ANTIBIOTICS

Vasopressors:

  • NE is FIRST LINE CHOICE (can sub. EPI)
  • Dopamine if bradycardia occurs

Inotropic: DOBUTAMINE IS FIRST LINE CHOICE

low dose corticosteroid use improves shock reversal but NOT beneficial in absence of shock

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7
Q

Hydrochlorothiazide

What is its MOA, what is it used to treat, and what are 3 common toxicities of use? (H/H/S)

A

MOA: thiazide diuretic that blocks the NA/Cl cotransporter in the distal convoluted tubule and is used for hypertension (not effective in pts with low GFR)

Toxicities: hypokalemia (K-losing), hypomagnesemia, sulfonamide (not for hypersensitive pts)

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8
Q

What are chlorothiazide, chlorthalidone, and metolazone?

A
  • all are Thiazide diuretics

Chlorthalidone: prolonged (40-60 hr life) response preferred by some hypertension specialists

Metolazone: favorite of cardiologists as adjunct diuretic in congestive heart failure treatment

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9
Q

Furosemide

What is its MOA, what is it used for, and what are 4 common toxicities of use? (H/H/O/S)

What can it be used in that thiazides cannot?

A

MOA: loop diuretic that blocks Na/K/2Cl cotransporter in thick ascending limb of Henle causing massive fluid removal

use: heart failure edema (dec. preload) and hypertension (works in pts with LOW GFR)

Toxicities: hypokalemia, hypocalcemia (inc. kidney stone risk), ototoxicity (reversible), and sulfonamide

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10
Q

What are 3 other Loop Diuretic options? (T/B/EA)

A
  1. torsemide = longer half life, better absorption
    • some evidence that it works better in heart failure
  2. bumetanide = more predictable oral absorption
  3. ethacrynic acid = NON-sulfonamide (for pts. with sulfa allergy)
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11
Q

Amiloride

What is its MOA, what is it used for, and what is its major boxed warning?

What is Triamterene?

A

MOA: blocks epithelial sodium (ENaC) channels in the collecting duct, blocking the major pathway for K elimination

use: counteracts K loss induced by other diuretics in hypertension and heart failure

Toxicity: hyperkalemia (also hyperchloremic metabolic acidosis)

T: similar to amiloride (for edema and hypertension)

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12
Q

Spironolactone

What is its MOA, what are its two primary uses, and what are 3 common toxicities of use? (H/AH/GI)

What is eplerenone?

A

MOA: competitive antagonist of aldosterone receptors that blocks aldosterone promoting Na/K exchange in collecting duct and antagonizes pro-fibrotic effects

uses: K-sparing diuretic, reduced fibrosis in HFrEF and post-MI heart failure

Toxicities: hyperkalemia, amenorrhea/hirsutism, gynecomastia/impotence

E: more selective aldosterone antagonist

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13
Q

What are 4 ACE inhibitors that can be used to treat hypertension? (C/E/B/L)

What are two major toxicities they cause?

A

captopril

  • also enalapril (prodrug; enalaprilat is active), benazepril, lisonopril

Toxicities: cough (number one reason why they are NOT tolerated) and angioedema (swollen tongue = choking so stop ASAP)

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14
Q

What are 3 Angiotensin II Receptor blockers that can be used to treat hypertension? (L/V/C)

A

Losartan

  • also: valsartan (not prodrug; excreted in feces) and candesartan (irreversible binding)
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15
Q

What drug binds DIRECTLY to renin and what is it used for?

Why is it not commonly used?

A

Aliskiren –> direct renin inhibitor that can be used for hypertension (can block renin inc. that could possibly offset ACEi/ARB therapy)

  • NOT COMMONLY USED because it is new/expensive, has no obvious benefits, and might have evidence of inc. risk of adverse events
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16
Q

What are 2 dihydropyridine and 2 non-dihydropyridine Calcium Channel Blockers that can be used in pts. with hypertension?

Which drug will show inc. HR and contractility?

A

D: nifedipine (prototype) and amlodipine (very widely used due to long half life of 30-50 hrs)
- Nifedipine has inc. HR/contractility due to primarily affecting vasculature (SNS reflex occurs)

ND: verapamil and diltiazem

CCBs are important first line therapy drugs for hypertension

17
Q

What are the 4 front line oral drug classes used to treat hypertension? (TD/Ai/A/C)

A
  1. Thiazide or thiazide-type diuretics
  2. ACE inhibitors
  3. ARBs
  4. CCBs - dihydropyridines AND non-dihydropyridines
18
Q

What are the alpha 1, alpha 2, beta 1, and beta 2 adrenergic receptors responsible for in the Sympathetic Baroreceptor Reflex?

A

a1: on blood vessels = vasoconstriction
a2: brain/periphery = dec. sympathetic tone

B1: inc. HR and contractility, stimulate renin secretion by kidneys
B2: dilate skeletal muscle vasculature

19
Q

What Prazosin used to treat and what are two of its major toxicities? (OH/RE)

What is tamsulosin/terazosin/doxazosin used to treat?

A

P: blocks a1 receptors to vasodilate veins/arterioles in pts. with hypertension but has many adverse effects

TE: orthostatic hypotension, retrograde ejaculation

T/T/D: similar to prazosin but marketed for BPH and to help kidney stones pass
- one drug solution for old man in wheelchair with BPH and hypertension

20
Q

What are Clonidine and a-methyldopa used for?

What are 2 toxicities found with each drug?

A

C: alpha-2 receptor agonist that causes reduced sympathetic outflow once in brainstem (transient inc. in BP after IV though)
- TE: drowsiness, xerostomia, REBOUND HTN if missed a dose

aM: selective a2 receptor agonist for moderate-severe HTN and is a drug of choice for GESTATIONAL HTN (along with labetalol and nifedipine)
- TE: positive Coombs test, SLE-like syndromes

21
Q

What Beta Blocker used for hypertension is nonselective and why is it contraindicated with Peripheral Vascular Disease?

What are 3 competitive B1-selective blockers (A/M/B) and what are they used for?

A

beta 1 receptor antagonists block both cardiac and juxtaglomerular cells (no renin release)

Propranolol - nonselective antagonist that slows HR/contractility but blunts vascular vasodilation
CI: can cause cold extremities, especially in infants
- also causes bronchospasm and bradycardia

Atenolol, metoprolol, bisoprolol (has highest beta-1 selectivity) –> treat HTN and angina pectoris (dec. HR)

22
Q

What happens if a2-agonists or Beta-blockers are stopped abruptly?

A
  • cause REBOUND HYPERTENSION

B1 blockers –> cardiac stimulation to normal SNS tone
a2 agonists –> excessive SNS tone

23
Q

Hydralazine and Hypertension

What is its MOA and what 3 things is it used for?

What is a major toxicity it can cause?

A

MOA: direct arteriole vasodilator that decreases systemic resistance

use: HFrEF intolerant to ARB/ACEi, HFrEF in African Americans, HTN emergency in pregnancy

T: drug-induced lupus-like syndrome

24
Q

Nitroprusside and Hypertension

What is its MOA and what is it used for?

What is a major toxicity it can cause?

A

MOA: peripheral vasodilation by direct action on venous AND arteriolar SM that reduced peripheral resistance and inc. CO by decreasing afterload

use: hypertensive crises and acute decompensated HF

T: metabolic acidosis due to CYANIDE TOXICITY

25
Q

Minoxidil and Hypertension

What is its MOA and what is it used for?

A

MOA: direct vasodilation by directly relaxing arteriolar SM and can stimulate HAIR GROWTH; lowers arteriolar vascular resistance

use: treatment of HTN that is symptomatic and NOT manageable with maximum therapeutic doses of diuretic plus 2 other antihypertensives

26
Q

What are 3 conditions that suggest bilateral renovascular hypertension rather than primary hypertension? (FPE/RF/RCCF)

A
  1. Flash Pulmonary Edema
  2. Progressive Renal Failure
  3. Refractory Congestive Cardiac Failure
27
Q

What drugs would be used for each of these classes in a Hypertensive Emergency:

  1. CCB - dihydropyridines (N/C)
  2. Vasodilators - NO dependent (N/N)
  3. Vasodilators - direct (H)
  4. Beta-1 selective blocker (E)
A
  1. nicardipine and clevidipine
  2. sodium nitroprusside and nitroglycerin
  3. hydralazine
  4. esmolol
28
Q

What drugs would be used for each of these classes in a Hypertensive Emergency:

  1. alpha-1/nonselective Beta blocker (L)
  2. nonselective alpha blocker (P)
  3. D1 receptor agonist (F)
  4. ACE Inhibitor (E)
A
  1. labetalol
  2. phentolamine
  3. fenoldopam
  4. enalaprilat

CPR II Exam 1 (15 decks)

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