Vasoactive drugs Flashcards
Only inotrope that can be bolused
adrenaline in cardiac arrest
Adrenaline receptors and effects at low / high dose?
ß and α adrenoreceptors. Positive Inoptope
In a low dose infusion the ß effects predominate, leading to an increase in heart rate, contractility and cardiac output.
In high doses the α effects predominate,
leading to vasoconstriction and an increase in blood pressure.
Adrenaline disadvantages
Excessive tachycardia, dysrhythmias, myocardial ischaemia, hyperglycaemia, lactic acidosis (which is usually transient)
How long onset of action ionotropes
All inotropes/vasopressors work within 1-2 minutes and their effect wears off within minutes
Noradrenaline receptors and effects?
- α1 vasoconstriction and increasing SVR. -> increases BP (perfusion pressure).
- ß1 contractility and heart rate.
noradrenaline disadvantages
Excessive vasoconstriction seen as blue/ black peripheries, dysrhythmias, myocardial ischaemia
main uses noradrenaline
improvement of BP in septic shock.
Used in neuro ICU patients to increase BP to maintain cerebral perfusion pressure.
main uses adrenaline
cardiac arrest
anaphylaxis (stabilise mast cells and prevent further histamine release as well as treat hypotension.)
Shock of unknown origin
Dopamine receptors
α, ß, and dopamine receptors to varying degrees.
non specific inotrope/vasopressor that can be used to increase cardiac output and SVR.
Dopamine disadvantages
Excessive tachycardia and dysrhythmias
When use dopamine
positive inotrope to increase cardiac output and provide vasoconstriction at higher doses.
Rx of Bradycardia -5-10mcg/kg/min (B1 receptor ↑HR)
Rx of Shock: 10-20mcg/kg/min (B1+A1 - ↑CO and vasoconstriction)
Used in septic shock in some centres.
Dobutamine receptors ? effect?
ß receptors leading to an increase in heart rate and contractility together with vasodilatation mediated via the ß2 receptors.
The net effect is an increase in cardiac output
Dobutamine disadvantages
Hypotension, tachycardia
Dobutamine uses
Low cardiac output states especially cardiogenic shock
how does GTN work ?
In a low dose it acts as a venodilator, thus offloading the heart and reducing preload.
In higher doses it acts as an arterial dilator, thus reducing afterload.
The net effect is to improve the function of the myocardium and cardiac output by reducing both preload and afterload.
It also causes relaxation of the coronary arteries and is therefore useful in angina.