Antihypertensives Flashcards

1
Q

Metoprolol MOA

A

B1 blocker

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2
Q

Labetalol MOA

A

A1, B1, B2 blocker

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3
Q

Esmolol MOA

A

B1 blocker

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4
Q

Nicardipine MOA

A

Dihydropyridine CBB

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5
Q

Hydralazine MOA

A

Arteriolar Dilator

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6
Q

Fendolopam MOA

A

Dopamine type 1 agonist

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7
Q

Nitroprusside MOA

A

NO donor

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8
Q

Nitroglycerine MOA

A

NO donor

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9
Q

Metoprolol Dose

A

1-5mg

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10
Q

Labetalol Dose

A

5-20 mg bolus

0.5-2 mg/min infusion

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11
Q

Esmolol Dose

A

50-300 mcg/kg/min infusion

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12
Q

Nicardipine Dose

A

100 mcg bolus

5-15 mg/hr infusion

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13
Q

Hydralazine Dose

A

2.5-20 mg IV bolus

onset: 10-20 min
duration: 3-6 hrs

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14
Q

Fendolopam Dose

A

0.05-1.6 mcg/kg/min infusion

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15
Q

Nitroprusside Dose

A
  1. 25-10 mcg/kg/min infusion
    - metabolism involves interaction with oxyHgb to form methemoglobin which is an unstable radical which breaks down releasing cyanide. high doses (>2mcg/kg/min) may result in cyanide accumulation
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16
Q

Nitroglycerine Dose

A

5-300 mcg/kg/min

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17
Q

A patient known to be taking verapamil was given dantrolene in the OR for suspected MH. Complications associated with these medications administered in tandem include?

A

Cardiovascular collapse & increased potassium levels

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18
Q

Sympathomimetics with the greatest affinity for the alpha receptors?

A

phenylephrine

norepinepherine

19
Q

HTN meds that should be used with caution in coronary artery disease?

A

hydralazine
nitroprusside

-reflex tach can worsen the metabolic demand on the heart

20
Q

Sodium nitroprusside vasodilates with the help of which active mediator?

A

NO

21
Q

Deflourination and renal toxicity is a complication associated with which antihypertensive:

A

Hydralazine

22
Q

labetalol –> IV and Oral beta/alpha ratios

A

IV: 3-1
Oral: 7-1

23
Q

Which of the following is NOT mainly an adrenergic receptor ANTAGONIST? (esmolol, prazosin, labetalol, clonidine, propranolol)

A

clonidine

24
Q

Anti-hypertensive drug classes

A
Diuretics
Sympatholytics (alpha & beta blockers)
Vasodilators
CCBs
ACE-Is / ARBs
25
Q

Thaizide Diuretics for HTN

A
Hydrochlorothiazide (HydroDIURIL)
Chlorthalidone (Hygroton)
Chlorothiazide (Diuril)
Indapamide (Lozol)
Metolazone (Zaroxolyn)
26
Q

K+ Sparing Diuretics for HTN

A

Amiloride (Midamor)
Spironolactone (Aldactone)
Triamterene (Dyrenium)

27
Q

Loops Diuretics for HTN

A

Furosemide (Lasix), Bumetanide (Bumex), Ethacrynic acid (Edecrin)
Torsemide (Demadex)

28
Q

Methods to manage hypertension (4)

A
  • central & peripheral control of SNS
  • RAAS
  • tone of vascular sm. muscle
  • fluid balance (Na+ & H2o)
29
Q

ACE-Is for HTN

A

“PRIL”

captopril, enalapril, benazepril, fosinopril, lisinopril, quinapril, r spirapril, moexipril, perindopril, trandolapril

30
Q

ARBs for HTN

A

“SARTAN”

losartan, valsartan, candesartan, eprosartan, irbesartan, telmisartan

31
Q

CCBs for HTN

A

verapamil, diltiazem, nifedipine, nicardipine, isradipine, amlodipine, felodipine

32
Q

Vasodilators for HTN

A

hydralazine
minoxidil
sodium nitroprusside
nitroglycerine

33
Q

ACE-I MOA

A

-block the conversion of ATI to ATII, since ATII is a potent vasoconstrictoror

34
Q

ACE-I Side effects

A

cough, angioedema, rash, ARF, hyperkalemia, taste disturbances, teratrogenic, NSAIDS antagonize effects

35
Q

ARB MOA

A

-competitive inhibition, block ATII from binding at its receptor sites

36
Q

CCB MOA

A
  • interfere with Ca++ influx across myocardial and vascular sm. muscle cell membranes
  • interfere by binding to alpha1 subunit (verapamil), modulating the shape of the channel (amlodipine), act on alpha1 subunit - mechanism unknown (diltizem)
37
Q

CV effects of CCBs

A
  • decreased myocardial contractility
  • decreased HR
  • decreased activity/rate of AV node conduction
  • vascular sm. muscle relaxation, vasodilation, and decrease BP
  • decrease coronary resistance and increase CBF
38
Q

Vasodilators work at the vascular wall to promote vasodilation by “donating” what endogenous mediator?

A

Nitric oxide (NO)

Donated NO diffuses through the vascular endothelium to smooth muscle where it (2 nd messenger) activates soluble guanylate cyclase –> GTP –> cGMP

Ex: Hydralazine, sodium nitroprusside, nitroglycerine

39
Q

Sodium nitroprusside (SNP) has 3 toxicities:

A

1) cyanide toxicity (risk at >2mcg/kg/min)
2) Methemoglobinemia (risk at > 10 mg/kin/min)
3) Effects of high thiocyanate concentrations

40
Q

SNP cyanide toxicity diagnosis

A

Should be suspected when tachyphylaxis occurs, despite maximal infusion rates
– Metabolic acidosis
– Mixed venous PO2 increases reflecting the inability of tissues to utilize O2
– CNS dysfunction: seizures

41
Q

SNP cyanide toxicity treatment

A

Treatment
– Immediately discontinue SNP
– Administer 100% O2
– NaHCO 3 for metabolic acidosis

– Sodium thiosulfate 150 mg/kg over 15 min
• Converts cyanide to thiocyanate (nontoxic)

– If severe, sodium nitrite 5 mg/kg
• Converts hemoglobin to methemoglobin allowing the conversion of cyanide to cyanomethemoglobin

– Hydroxocobalamin (Vit B12a) 25 mg/hr
• Binds cyanide to form cyanocobalamin (B12)

42
Q

SNP methemoglobinemia toxicity treatment

A
  • unlikely unless doses exceed 10mg/kg/min to produce 10% methemoglobin
  • screen patients receiving high doses of SNP when evidence of impaired oxygenation despite adequate arterial oxygenation and CO
43
Q

Anesthetic implications of CCBs - drug interactions

A
  • potentiate effects of NMBs, impair reversal
  • may increase risk of local anesthetic toxic reactions during regional anesthesia
  • administration of dantrolnene in the presence of CCBs may result in hyperkalemia and CV collapse
44
Q

vasodilators effects on arteries vs veins

A

SNP - A=V

NTG - A>V