Control Heart Rate and Synchronise Heart Rhythm
A new AV-block or atrial fibrillation is common after cardiac surgery.68–70 Temporary epicardial pacemaker wires are routinely implanted during surgery for ventricular pacing in case of postoperative third degree AV-block. In cases of severe intraoperative bradycardia or asystole, temporary atrial pacing may be useful for better haemodynamic stability; an increase in heart rate increases cardiac output if AV synchrony is maintained.71 As a general rule, the more physiological stimulation applied (AAI>DDD>VVI), the better the result on cardiac output.
Atrial fibrillation impairs ventricular filling thereby potentially contributing to the shock state.72,73 In patients with haemodynamic instability, conversion into sinus rhythms must be attempted by direct current electrical cardioversion. Synchronised cardioversion with anterior-posterior electrode positioning and high initial biphasic energy of 200 joules is recommended.72,74 Prior to this, electrolytes are supplemented to obtain high plasma levels (magnesium >1.0 mmol/l; potassium 4.5–5.5 mmol/l).72,75,76
Improve Contractility
Inotropes are used in patients with low cardiac output due to impaired cardiac contractility.5 Details on recommended drugs and dosages are listed in Table 3.
Dobutamine has mainly 1-adrenergic properties and increases contractility with little effect on peripheral vascular 2-receptors causing some degree of vasodilatation. Although improving oxygen delivery was beneficial perioperatively4,75 and during the early phase of shock,8 circulatory stimulation with dobutamine to supra-normal values (cardiac index > 4.5 l/min/m2, oxygen delivery >600 ml/min/m2) was associated with an adverse outcome in patients with established multi-organ failure.78,79 This might be due to the fact that excessive adrenergic stimulation has adverse metabolic effects (augmented energy demands, hyperglycaemia, lipolysis, muscle wasting),80–82 impairs splanchnic haemodynamics,83,84 causes arrhythmia,85 stimulates inflammation86,87 and promotes stress cardiomyopathy.88,89 Dobutamine is also associated with eosinophilia and fever,90 and its use for longer than 72 hours may lead to tolerance.
Adrenaline has potent effects on inotropy and chronotropy via-adrenergic receptors and produces vasoconstriction via -adrenergic receptors.91 A dose of only 0.03 μg/kg/min adrenaline compared with placebo resulted in a significant increase of cardiac output and in a significant rise in MAP.92 In a small pilot study, adrenaline and the combination of dobutamine-noradrenaline improved both cardiac output and oxygen delivery in patients with cardiogenic shock but a transient lactic acidosis, an increase in insulin requirements, impairments in gastric mucosa perfusion, (supra-)ventricular arrhythmia and an increased myocardial oxygen consumption were observed in the adrenaline group.57 The adrenaline-induced increase in lactate levels may mislead to excessive fluid loading or other potentially harmful shock therapies.57
Milrinone is a phosphodiesterase type III inhibitor and augments the intracellular concentration of cAMP. In comparison to dobutamine, milrinone is considered to be more effective in patients under-blockade.80,90 The effects of milrinone on right ventricular ejection fraction were comparable with the inhalational nitric oxide at 20 ppm.93 However, systemic vasodilation limits the use of milrinone in shock. A loading dose (50 mcg/kg) might profoundly worsen hypotension and is not recommended in ICU patients. The half-life of 50 minutes is longer in comparison with dobutamine or adrenaline and hypotensive effects will be prolonged if renal function is impaired.90
In summary, -mimetic inotropes increase contractility but can have serious adverse effects. Hence, their use should be limited to the lowest dose and the shortest duration necessary. The use of Levosimendan will be discussed in a planned future article for Cardiac Failure Review.