Page 572 - ACCCN's Critical Care Nursing

Management of Shock 549

TABLE 20.7 Inotrope drug actions and characteristics 70-73

Drug Action Dose range Physiological effect Nursing considerations
dobutamine Synthetic adrenergic agonist 100–2000 µg/min Inotropy CVC administration
β 1 -agonist Vasodilation Arrhythmia risk
β 2 -agonist ↑↑Cardiac output Excess dilation may cause
↑Blood pressure hypotension
↑Heart rate
dopamine Dopaminergic ‘Inotropic’ dose Mainly inotropic CVC administration
β 1 -agonist 5–10 µg/kg/min ↑Blood pressure Tachycardia
α-agonist (at higher doses) ‘High’ dose ↑Cardiac output Arrhythmia risk
10–20 µg/kg/min Inotrope Risk peripheral vascular
Vasoconstriction dominates compromise
↑↑Blood pressure
levosimendan Calcium sensitiser Loading: 6–12 µg/kg over Inotropy Tachycardia
10 min Vasodilation Arrhythmia risk
Infusion 0.05–0.2 µg/kg/min ↑↑Cardiac output Risk hypokalaemia
(maximum 24–48 hours’ use) Risk Q-T prolongation
Excess dilation may cause
hypotension
Half-life 5 days
adrenaline Sympathomimetic 1–20 µg/min or higher Potent inotrope and Tachycardia common
α-agonist constrictor Arrhythmia risk
β 1 -agonist ↑Cardiac output Risk peripheral vascular
β 2 -agonist ↑↑Blood pressure compromise
↑↑Heart rate Myocardial work
milrinone Phosphodiesterase inhibitor Loading: 50–75 µg/kg Inotropy Vasodilation may be
Infusion: 0.375–0.75 µg/kg/min Potent vasodilator marked
↑↑Cardiac output Observe for hypotension
↓Blood pressure
noradrenaline Sympathomimetic 1–20 µg/min or higher Potent inotrope and Reflex bradycardias
α-agonist constrictor Arrhythmia risk
β 1 -agonist ↑↑Blood pressure Risk peripheral vascular
little effect on β 2 -receptors ↑coronary artery blood flow compromise
vasopressin vascular (V-1) receptors 0.1–0.4 µg/min Inotropy Check liver function
renal (V-2) receptors ↑SVR
↑vasoconstrictor
↑ = increase; ↓ = decrease.

because of additional vasoactive actions (either vasodila- myocardial pumping and an increased cardiac output.
tion or constriction) (see Table 20.7). Selection of an ino- The effect on blood pressure is variable, as the opposing
tropic agent is therefore partly based on inotropic potency actions of increased contractility and vasodilation are not
as well as the desired effect on vascular resistance: uniform in potency, and occur with differing effects
between patients. Inodilators are generally selected when
● vasodilation in addition to inotropy (inodilator effect) a patient has an elevated afterload and low cardiac
favours cardiac output, but may compromise blood output. By reducing afterload, left ventricular emptying
70
pressure 70 is favoured with a reduction in cardiac contractility,
● vasoconstriction in addition to inotropy (inoconstric- reducing myocardial oxygen demand. Inodilators are
tor effect) improves blood pressure, but may at times therefore preferred in ischaemic cardiogenic shock. 71–73
compromise left ventricular emptying and cardiac
output. In contrast, inoconstrictors constrict the vasculature,
resulting in increased preload and afterload while also
70
All inotropes present a paradox in the treatment of car- increasing myocardial contractility. These increases, par-
diogenic shock, as they have the potential to raise heart ticularly in afterload, generally result in a raised blood
rate, increase myocardial oxygen demands, and increase pressure, but the impact on cardiac output is less predict-
the frequency of arrhythmias to a greater or lesser extent. able. An increase in cardiac output is often seen with
Monitoring is used to identify heart rate, rhythm and the these agents, but the increase in afterload may become
development of ST segment or T wave changes. limiting to left ventricular emptying when there is signifi-
cant contractile impairment. Inoconstrictors are therefore
The vasodilation seen with inodilator agents may reduce generally selected when the afterload and resultant blood
both preload and afterload, leading to more effective pressure are more severely compromised than the cardiac