Get the terms right:
- inotropes – increase myocardial contractility (inotropy)
— e.g. adrenaline, dobutamine
- vasopressors -vasoconstriction leading to increased systemic and/or pulmonary vascular resistance (SVR, PVR)
— e.g. noradrenaline, vasopressin,vasopressin, methylene blue
- inodilators – inotropic effects + vasodilation leading to decreased systemic and/or pulmonary vascular resistance (SVR, PVR)
— e.g. milrinone, levosimendan
- some agents don’t fit these categories easily!
— e.g. dopamine
we will focus on adrenaline, noradrenaline, dobutamine, dopamine.
All are endogenous cathecholamines except dobutamine – synthetics
Adrenaline : beta > alpha
Noradrenaline : alpha > beta
Dopamine: D receptor> beta > alpha (multitude dose response)
1-5 = D receptor 1+2
- Vasodilation at peripheral mesenteric and renal vascular bed.
- D2 receptors are also found on presynaptic adrenergic neurons, where their activation interferes with norepinephrine release.
5-10 = beta
>10 = alpha + aldosterone
Dobutamine: beta 1 & beta 2
UNDIFFERENTIATED SHOCK- NORAD, NORAD, NORAD
Dobutamine and Dopamine : prone to cause arrhythmias
Dobutamine will increase myocardial oxygen consumption despite low chronotophic effect which make it unsuitable for situation that induction of myocardial ischemia is harmful.
Combination of smaller dose of inotropes and vasopressor is advantageous compare to single agent with higher dose to prevent dose related adverse effect.