Shock is a state of inadequate perfusion that affects vital organs. Cardiogenic shock (CS) predisposes patients to various arrhythmias. The adverse effect depends on intervention and pharmacogenomics. This narrative review sheds light on treatment strategies for arrhythmias caused by milrinone and dobutamine when managing CS. Dobutamine, through beta-1 agonism, and milrinone, by phosphodiesterase-3 inhibition, increase cardiac contractility by enhancing the availability of calcium to the myocardium. Dobutamine is also a beta-2 agonist, and milrinone is a phosphodiesterase-3 inhibitor; both result in peripheral vasodilation, leading to their use preferentially in patients with CS with normotensive blood pressure. To narrow down relevant literature, various electronic databases, including PubMed, Google Scholar, and Cochrane Library, were searched. The review revealed limited evidence favoring either milrinone or dobutamine as the preferred inotropic agent for managing CS, but it did reveal that though hospital stays using dobutamine were shorter, mortality from its induced arrhythmias led to an increase in all-cause mortality rates. Both proarrhythmic agents triggered ventricular and supraventricular tachyarrhythmias, some requiring cardioversion while others are non-sustained and managed medically or symptomatically. Though neither agent has a specific reversal agent, the effect of dobutamine was seen to be successfully aborted using intravenous ultrashort half-life beta-blockers (such as esmolol). The findings accentuated the critical need for a tailored approach to managing these iatrogenic arrhythmias, emphasizing clinical vigilance and individualized patient care.
Keywords: cardiogenic shock; dobutamine; heart failure; milrinone; vasopressor.
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