Antihypertensives Flashcards
Metoprolol MOA
B1 blocker
Labetalol MOA
A1, B1, B2 blocker
Esmolol MOA
B1 blocker
Nicardipine MOA
Dihydropyridine CBB
Hydralazine MOA
Arteriolar Dilator
Fendolopam MOA
Dopamine type 1 agonist
Nitroprusside MOA
NO donor
Nitroglycerine MOA
NO donor
Metoprolol Dose
1-5mg
Labetalol Dose
5-20 mg bolus
0.5-2 mg/min infusion
Esmolol Dose
50-300 mcg/kg/min infusion
Nicardipine Dose
100 mcg bolus
5-15 mg/hr infusion
Hydralazine Dose
2.5-20 mg IV bolus
onset: 10-20 min
duration: 3-6 hrs
Fendolopam Dose
0.05-1.6 mcg/kg/min infusion
Nitroprusside Dose
- 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
Nitroglycerine Dose
5-300 mcg/kg/min
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?
Cardiovascular collapse & increased potassium levels
Sympathomimetics with the greatest affinity for the alpha receptors?
phenylephrine
norepinepherine
HTN meds that should be used with caution in coronary artery disease?
hydralazine
nitroprusside
-reflex tach can worsen the metabolic demand on the heart
Sodium nitroprusside vasodilates with the help of which active mediator?
NO
Deflourination and renal toxicity is a complication associated with which antihypertensive:
Hydralazine
labetalol –> IV and Oral beta/alpha ratios
IV: 3-1
Oral: 7-1
Which of the following is NOT mainly an adrenergic receptor ANTAGONIST? (esmolol, prazosin, labetalol, clonidine, propranolol)
clonidine
Anti-hypertensive drug classes
Diuretics Sympatholytics (alpha & beta blockers) Vasodilators CCBs ACE-Is / ARBs
Thaizide Diuretics for HTN
Hydrochlorothiazide (HydroDIURIL) Chlorthalidone (Hygroton) Chlorothiazide (Diuril) Indapamide (Lozol) Metolazone (Zaroxolyn)
K+ Sparing Diuretics for HTN
Amiloride (Midamor)
Spironolactone (Aldactone)
Triamterene (Dyrenium)
Loops Diuretics for HTN
Furosemide (Lasix), Bumetanide (Bumex), Ethacrynic acid (Edecrin)
Torsemide (Demadex)
Methods to manage hypertension (4)
- central & peripheral control of SNS
- RAAS
- tone of vascular sm. muscle
- fluid balance (Na+ & H2o)
ACE-Is for HTN
“PRIL”
captopril, enalapril, benazepril, fosinopril, lisinopril, quinapril, r spirapril, moexipril, perindopril, trandolapril
ARBs for HTN
“SARTAN”
losartan, valsartan, candesartan, eprosartan, irbesartan, telmisartan
CCBs for HTN
verapamil, diltiazem, nifedipine, nicardipine, isradipine, amlodipine, felodipine
Vasodilators for HTN
hydralazine
minoxidil
sodium nitroprusside
nitroglycerine
ACE-I MOA
-block the conversion of ATI to ATII, since ATII is a potent vasoconstrictoror
ACE-I Side effects
cough, angioedema, rash, ARF, hyperkalemia, taste disturbances, teratrogenic, NSAIDS antagonize effects
ARB MOA
-competitive inhibition, block ATII from binding at its receptor sites
CCB MOA
- 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)
CV effects of CCBs
- 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
Vasodilators work at the vascular wall to promote vasodilation by “donating” what endogenous mediator?
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
Sodium nitroprusside (SNP) has 3 toxicities:
1) cyanide toxicity (risk at >2mcg/kg/min)
2) Methemoglobinemia (risk at > 10 mg/kin/min)
3) Effects of high thiocyanate concentrations
SNP cyanide toxicity diagnosis
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
SNP cyanide toxicity treatment
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)
SNP methemoglobinemia toxicity treatment
- 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
Anesthetic implications of CCBs - drug interactions
- 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
vasodilators effects on arteries vs veins
SNP - A=V
NTG - A>V
