Drug Box 3 Flashcards
Esmolol Name
Generic (Esmolol), Trade (Brevibloc)
Esmolol Classification
Cardioselective Beta Blocker/B-1 adrengeric receptor antagonist, Class II anti-arrhythmic agent
Esmolol Contraindication
Use esmolol with caution in patients with asthma; chronic obstructive pulmonary disease; atrioventricular heart block, or cardiac failure not caused by tachycardia; and diabetes
Esmolol Dose and route
SVT>loading:50 to 200 mcg/kg/min for 1 minute; follow by infusion of 50 mcg/kg/min for 4 minutes. If the desired effect is not achieved, repeat loading dose and increase infusion to 100 mcg/kg/min. May repeat the process up to a maximum of 300 mcg/kg/min. (Nagelhout handbook, pg 636)
- Loading dose: 50-300 mg/kg/min (Flood, pg 479 table)
- Single IV push- 5-10 mg (Dr. Hammons)
-10-80 mg IV (Flood, pg. 479 table)
Dosage forms:
10mg/mL in 10-mL vial for direct intravenous injection; 250 mg/mL in 10-mL ampule for intravenous infusion. Only administered IV. (Nagelhout handbook, pg 636)
Route IV
Esmolol MOA
By blocking adrengeric activity of epi and norepi, it decreases inotropic contractility, heart rate, and conduction. Esmolol increases atrioventricular refractory time decreases oxygen demand of the myocardium, and decreases atrioventricular conduction. A minor Beta 2 blockade has been reported with high IV infusion doses
Esmolol Onset
1-2 minutes
Esmolol Peak
5-6 minutes
Esmolol Duration
10-20 minutes
Labetalol Name
Trandate
Labetalol Classification
Combined α- and β-Adrenergic Receptor Antagonists
Labetalol Contraindications
bronchial asthma, 2nd-3rd degree heart block, hepatic failure
Labetalol Dose and route
Dose – IV: 0.1 - 0.5 mg/kg (Start with 5-10 mg)
Oral: 100-600 mg BID (Flood, p. 489)
5.) Route – IV, Oral
Labetalol MOA
exhibits selective α1 and non-selective β1- and β2-adrenergic antagonist effects. Presynaptic α2 receptors are spared by labetalol such that released norepinephrine can continue to inhibit further release of catecholamines via the negative feedback mechanism resulting from stimulation of α2 receptors.
Labetalol Elimination
metabolized by conjugation of glucuronic acid (enzyme that helps metabolize
drugs), with 5% of drug recovered in urine (Flood, p. 489)
Labetalol Onset
iv 1-3 min
oral 20-40 mins
Labetalol Peak
5-15min
Labetalol Duration
iv- 20mins- 2 hrs
oral- 4-12 hrs
Labetalol Misc
chronic bronchitis, emphysema, pre existing peripheral vascular disease, pheochromocytoma, and diabetes. It is contraindicated in bronchial asthma, overt heart failure, greater than first degree heart block, and hepatic failure
Metoprolol Name
Lopresor, Toprol XL
Metoprolol Classification
Beta-Blocker, Beta-1 Selective
Metoprolol Contraindication
COPD, CAD, Vulnerable to hypoglycemia
Metoprolol Dose and Route
Dose: Oral 50-400mg (Flood p. 479). Extended Release 50-150mg (Flood p.480) IV 1mg-15mg (Flood, p.479)
Route: PO or IV
Metoprolol MOA
Selective B1-Adrenergic receptor antagonist
Metoprolol Elimination
Absorbed from the gastrointestinal tract offset by sustabial hepatic first-pass-metabolism, only 40% of drug reaches systemic circulation
Metoprolol Onset
1-5 mins iv
Metoprolol Peak
iv- 20 mins
Metoprolol Duration
iv 5-7 hrs
Metoprolol Misc
Selectivity is dose related and large doses become non-selective antagonist B2 receptor as well as B1. (Flood p. 482)
Supply: 5mg/5ml or 1mg/ml
Neostigmine Name
Prostigmine
Neostigmine Classification
Anticholinesterase agent
Neostigmine Contraindications
Use with caution in patients with bradycardia, bronchial asthma, epilepsy, cardiac arrhythmias, peptic ulcer, peritonitis, or mechanical obstruction of the intestines or urinary tract
Neostigmine Dose and Route
Dose : 60 to 80 µg/kg (maximum 5mg)[dose cited from Flood, ignore other sources]
Myasthenia gravis PO 15-375 mg daily; IM 0.5-2 mg (Nagelhout Handbook P. 671)
maximum effective dose is in the 60 to 80 µg/kg range (Flood, 2016 P.335)
Dose range 25-75 mcg/kg (Nagelhout, 2018p.162)
5.) Route IV for reversal, IM or PO for myasthenia gravis (Nagelhout Handbook Page 671)
Neostigmine MOA
Mechanism of Action (MOA): It inhibits AChE by forming a drug-enzyme complex that degrades in the same manner as ACh-Cholinesterase complex, thereby increasing the concentration of endogenous ACh around the cholinoreceptors (Nagelhout hard copy textbook page 162 para 2). The ACh that accumulates at the NMJ competes with the residual molecules of NMBD for the available unoccupied nicotinic ACh receptors at the NMJ. (Flood hard copy textbook, P.334 last paragraph).
Neostigmine Elimination
Renal excretion accounts for about 50% of the excretion of neostigmine . Renal failure decreases the plasma clearance of neostigmine as much as, if not more than, that of the long-acting neuromuscular blockers