Reversal of Vasodilatory Shock: Current Perspectives on Conventional, Rescue, and Emerging Vasoactive Agents for the Treatment of Shock

Jonathan H. Chow, MD; Ezeldeen Abuelkasem, MBBCh, MSc; Susan Sankova, MD; Reney A. Henderson, MD; Michael A. Mazzeffi, MD, MPH; Kenichi A. Tanaka, MD, MSc


Anesth Analg. 2019;130(1):15-30. 

In This Article

Dobutamine for Concomitant Vasodilatory Shock and Cardiac Dysfunction

Cardiac dysfunction is found in over 50% of patients with septic shock and in up to 90% of patients with culture-proven septic shock.[53] Dobutamine has been used for cardiogenic shock for decades, and, not surprisingly, there has been much interest in the use of dobutamine to augment cardiac output when vasodilatory shock is complicated by underlying cardiac dysfunction. Because it can cause hypotension and increase myocardial oxygen demand, dobutamine is another agent that should not be used indiscriminately in vasodilatory shock.


Dobutamine is a synthetic catecholamine that is typically used as an inotrope for heart failure.[54] It is most commonly found as a racemic mixture, and the enantiomers have different adrenergic effects. The negative enantiomer (−) predominantly acts as an α1 receptor agonist with weak β1 and β2 receptor interaction. Conversely, the positive enantiomer (+) predominately acts as β1 and β2 receptor agonists and an α1 receptor antagonist.[55] In the cardiovascular system, racemic dobutamine targets myocardial α1 and β1 receptor activation to cause increased contractility.[55,56] In other organ systems, dobutamine decreases vascular smooth muscle resistance and causes increased organ perfusion through α1 receptor inhibition and β2 receptor activation.

Clinical Studies

There are variations in the response to dobutamine in patients with septic shock. Some studies have shown improved oxygen delivery, mesenteric perfusion, and microcirculation perfusion due to the β2 effects of the drug.[55] For this reason, dobutamine was frequently used in early goal–directed therapy (EGDT) protocols to maximize oxygen delivery and cardiac output.[57–59] These RCTs did not detect any significant mortality differences between the EGDT and standard-of-care groups. Another large-scale RCT of dobutamine for augmenting cardiac output in septic shock found that, although dobutamine did successfully increase cardiac output from baseline, it did not result in any significant improvement in mortality.[60] Furthermore, when comparing the use of NE plus dobutamine versus Epi alone in septic shock, there was also no difference in 28-day mortality (RR, 0.86; 95% CI, 0.65–1.14; P = .31), time to successful hemodynamic resuscitation (log-rank P = .67), and time to vasopressor withdrawal (log rank P = .09) between the 2 groups.[61]

One retrospective study propensity matched 526 patients receiving inotropes during septic shock and found that the use of dobutamine, Epi, or multiple inotropes was associated with an increase in 90-day mortality.[62] However, this was a retrospective study, and the conclusions must be critically evaluated as there were significant differences in the baseline dose of NE between the groups, as well as large differences in baseline Sequential Organ Failure Assessment (SOFA) and Acute Physiology and Chronic Health Evaluation (APACHE) II scores.

Unclear Role in Vasodilatory Shock

Dobutamine's role in septic shock remains unclear. The Surviving Sepsis Guidelines stipulate that dobutamine only be used in patients with low cardiac output and adequate blood pressure reserve.[29] Although dobutamine can augment cardiac output and splanchnic blood flow, it also increases myocardial oxygen demand and can cause hypotension.[63,64] Both increase the risk of developing cardiac ischemia and dysrhythmias and are reasons for caution when administering this drug during vasodilatory shock.