Email: support@essaywriterpros.com
Call Us: US - +1 845 478 5244 | UK - +44 20 7193 7850 | AUS - +61 2 8005 4826

Drug-induced, toxicological – nitrates, antihypertensives, narcotics and sedatives, etc

Inotropes and vasopressors

The following is a very simplified approach to the choice of inotropes and vasopressors. More information can be found at the Critical Care Drug Manual – London Health Sciences Centre, UWO.

Inotropes

  1. Adrenergic (catecholamine)
    • Dobutamine – beta-agonist (ß1 >ß2). Increases contractility and HR. ß2 effect can sometimes decrease SVR and BP. ß1 effect can cause dysrhythmias. Start at 2.5 mcg/kg/min. Titrate upward by 2.5 mcg/kg/min until adequate cardiac index. Maximum 15 to 20 mcg/kg/min. Notify ICU Fellow or Attending if at 10 mcg/kg/min or higher.
    • Epinephrine -alpha and beta agonist (ß > alpha). Increases HR, CO, and SVR. Generally a second-line inotrope. A subset of patients who do not respond to dobutamine will respond to epinephrine. Potential detrimental effects include significant increases in myocardial oxygen consumption, increased lactic acidosis, arrhythmias. Start at 0.5 to 1.0 mcg/min and increase by these amounts until adequate cardiac index. Notify ICU Fellow or Attending if > 5 mcg/min and each increase of 5 mcg/min above that.
    • Dopamine – stimulates dopaminergic, beta, and alpha receptors in dose-dependent fashion. Inotropic effect (beta-effect) predominates in the 5 to 10 mcg/kg/min range. Notify ICU Fellow or Attending if at 10 mcg/kg/min or higher. There appears to be little benefit over Dobutamine as an inotrope. In low doses ( 2 – 4 mcg/kg/min) it has been purported to have beneficial renal protective effects (“renal-dose dopamine”). While it can increase urine output by several mechanisms, there is little evidence that it improves creatinine clearance or decreases the incidence of acute renal failure.
  2. Phosphodiesterase inhibitors
    • Milrinone – phosphodiesterase inhibitors decrease the metabolism (breakdown) of cAMP. cAMP is the “second messenger” that leads to increased calcium availability at the actin-myosin complexes and thus increased contractility. Beta-receptor stimulation leads to increases in cAMP. Thus the use of phosphodiesterase inhibitors “bypass” the beta-receptor. Milrinone increases cardiac output. It also decreases Pulmonary Vascular Resistance (PVR) and thus can be useful if pulmonary hypertension or significant right ventricular dysfunction is a problem. The bolus dose is 50 mcg/kg followed by an infusion between 0.375 and 0.75 mcg/kg/min. The half life of milrinone is several hours, unlike the catecholamines that have half-lives of a few minutes. When weaning milrinone, the rate of decreases should be slower and more gradual than with dobutamine or epinephrine. Reassess the patient 4 to 6 hours later to verify that he or she has tolerated the decrease.