A Clinical Update on Vasoactive Medication in the Management of Cardiogenic Shock

Abstract

This is a focused review looking at the pharmacological support in cardiogenic shock. There are a plethora of data evaluating vasopressors and inotropes in septic shock, but the data are limited for cardiogenic shock. This review article describes in detail the pathophysiology of cardiogenic shock, the mechanism of action of different vasopressors and inotropes emphasizing their indications and potential side effects. This review article incorporates the currently used specific risk-prediction models in cardiogenic shock as well as integrates data from many trials on the use of vasopressors and inotropes. Lastly, this review seeks to discuss the future direction for vasoactive medications in cardiogenic shock.

The Potential Synergistic Risk of Albuterol and Vasoactives in Acute Lung Injury Trials

“…The occurrence of cardiac adverse events can vary, and it depends largely on the vasoactive agent, dose, frequency, and other factors including drug-drug interaction. 7 Among vasoactive patients, 47.9% of patients received norepinephrine representing a large percentage in comparison to other vasoactives. Among the same group, 14.3% of albuterol developed cardiac adverse events (arrhythmias, atrial fibrillation, or myocardial infarction) whereas 11.3% of placebo developed cardiac adverse events ( P = .59).…”

A Comparison of Dobutamine, Norepinephrine, Vasopressin, and Hetastarch for the Treatment of Isoflurane-Induced Hypotension in Healthy, Normovolemic Dogs

“…According to the ‘Surviving Sepsis International Guidelines’, norepinephrine is strongly recommended as the first-line drug for treating vasodilatory shock through its α 1 and β 1 adrenergic actions that help to improve BP and CO [ 49 ]. In recent times, norepinephrine has been regarded as the most common first-line vasopressor for small animals to treat vasodilatory hypotension in emergency and critical care medicine [ 50 ]. Norepinephrine is a sympathomimetic amine derived from tyrosine and is structurally similar to epinephrine, although it lacks a methyl group on its nitrogen atom.…”

“…This chemical difference is attributed to its primary α 1 , α 2 , and β 1 adrenergic agonism. When compared to epinephrine, norepinephrine-associated peripheral vasoconstriction and venoconstriction in the venous beds (except the coronary vasculature) are more intense, while the β 1 activity is milder [ 20 , 50 ]. Increases in heart rate and myocardial contractility may be observed with β 1 agonism, but baroreceptor-reflex-mediated bradycardia is usually more common in response to α 1 - and α 2 -mediated vasoconstriction [ 20 , 43 ].…”

Inotropic support in cardiogenic shock: who leads the battle, milrinone or dobutamine?

“…Milrinone is a phosphodiesterase 3 inhibitor, simulating the stimulation of β1 and β2 receptors [ 28 ]. The properties that make this agent stand out from other inotropic agents are its ability to increase inotropism while generating a significant reduction in peripheral vascular resistance and pulmonary vascular resistance [ [20] , [21] , [22] ].…”