Why Not Dobutamine?

Why Not Dobutamine?

PGY3 Neil McCormack


A patient rolls into the emergency room. You don’t need this. You’ve got a lot of other patients. This patient however is in shock. They are hypotensive and with a decreased mental status. You need to give them something and the attending asks what vasopressors you would like. “Why not dobutamine” the intern asks. With a sigh and a heavy eye roll you turn away. But… Why not dobutamine?



Dobutamine            Dobutamine is a synthetic catecholamine used primarily for cardiac stress testing outside of the hypotensive patient (8). This is due to the positive inotropic effects it plays on the heart. Dobutamine acts via a 3:1 selective agonist effect on β1 and β2 receptors respectively. This causes increased contractility of the heart (9). There is, however, a side effect of reflexive decrease in systemic vascular resistance (SVR) causing potential for worsening of hypotension. This is not seen in higher doses of dobutamine and the reason for this is because of dobutamine’s partial α1 agonist effect (9). Given this information, we can intuitively think that giving dobutamine would be a good option for use in a hypotensive patient. But what does the literature say?

There have been a few studies that look at the use and effectiveness of dobutamine in the setting of hypotension (1, 2, 9, 10, 12, 13). Partially due to the α1 partial agonist effect, dobutamine is not a first line recommended treatment option alone in patients with septic or hypovolemic shock (3, 4, 9). It has been proposed as a first line treatment for sepsis patients if used in conjunction with another vasopressor (example: norepinephrine) to prevent the reflexive SVR decrease and hypotension. In the absence of using multiple vasopressors, dopamine and norepinephrine have been listed as the first line drugs of choice for septic shock patients. According to the “Surviving Sepsis” guidelines (3, 4), norepinephrine is the first line vasopressor of choice for sepsis patients. However, dobutamine is the recommended inotropic agent to be used in combination to improve cardiac output (without going to supranormal levels of cardiac output) (3).



But what if this patient has a bad heart? The evidence for use of dobutamine in patients with cardiogenic shock is more favorable (7, 12, 14). Patients who need inotropic support primarily are recommended to undergo dobutamine therapy as their vasopressor of choice in the beginning. This is due to the positive effect that dobutamine has on the contractility of the heart muscle itself. It has been shown as well that dobutamine appears to have a more favorable effect on right ventricular (RV) contractility than on left ventricular (LV) though it is effective in both settings (14). The downside of dobutamine alone is, as mentioned, it is only a partial α1 agonist and thus, if the blood pressure does not respond to the increased inotropic effects, a second line agent will need to be added. In a trial looking at epinephrine vs dobutamine/norepinephrine, there was no difference in the overall outcomes of patients but the epinephrine patients had more side effects (including arrhythmias).

What does all this mean? Well what this means is that the intern may have, in fact, been correct to suggest that we use dobutamine for our now hypotensive patient. It all depends on the suspected cause (IE: cardiogenic vs septic vs other causes of hypotension). It is important to keep in mind, though, that unless this patient has a purely cardiogenic cause (such as severe heart failure), they may also require a second pressure support in order to maintain a healthy blood pressure.



1) Bangash, Mansoor N, Ming-Li Kong, and Rupert M Pearse. “Use of Inotropes and Vasopressor Agents in Critically Ill Patients.” British Journal of Pharmacology 165, no. 7 (April 2012): 2015–33. doi:10.1111/j.1476-5381.2011.01588.x.

2) Beale, Richard J., Steven M. Hollenberg, Jean-Louis Vincent, and Joseph E. Parrillo. “Vasopressor and Inotropic Support in Septic Shock: An Evidence-Based Review.” Critical Care Medicine 32, no. 11 Suppl (November 2004): S455–65.

3) Campaign, Surviving Sepsis. “Leitlinienempfehlungen Zur Sepsistherapie.” Sepsis Und MODS, 2015, 377.

4) Dellinger, R. Phillip, Mitchell M. Levy, Jean M. Carlet, Julian Bion, Margaret M. Parker, Roman Jaeschke, Konrad Reinhart, et al. “Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock: 2008.” Critical Care Medicine 36, no. 1 (January 2008): 296–327. doi:10.1097/01.CCM.0000298158.12101.41.

5) Huang, Xuan, Shu Lei, Mei-fei Zhu, Rong-lin Jiang, Li-quan Huang, Guo-lian Xia, and Yi-hui Zhi. “Levosimendan versus Dobutamine in Critically Ill Patients: A Meta-Analysis of Randomized Controlled Trials.” Journal of Zhejiang University. Science. B 14, no. 5 (May 2013): 400–415. doi:10.1631/jzus.B1200290.

6) Levy, Bruno, Pierre Perez, Jessica Perny, Carine Thivilier, and Alain Gerard. “Comparison of Norepinephrine-Dobutamine to Epinephrine for Hemodynamics, Lactate Metabolism, and Organ Function Variables in Cardiogenic Shock. A Prospective, Randomized Pilot Study.” Critical Care Medicine 39, no. 3 (March 2011): 450–55. doi:10.1097/CCM.0b013e3181ffe0eb.

7) Lewis, Tyler, Caitlin Aberle, Diana Esaian, and John Papadopoulos. “EFFICACY AND SAFETY OF MILRINONE VERSUS DOBUTAMINE IN CARDIOGENIC SHOCK.” Critical Care Medicine 43, no. 12 Suppl 1 (December 2015): 34. doi:10.1097/01.ccm.0000473960.43621.41.

8) Miller, Todd D., J. Wells Askew, and Nandan S. Anavekar. “Noninvasive Stress Testing for Coronary Artery Disease.” Heart Failure Clinics 12, no. 1 (January 2016): 65–82. doi:10.1016/j.hfc.2015.08.006.

9) Müllner, M., B. Urbanek, C. Havel, H. Losert, F. Waechter, and G. Gamper. “Vasopressors for Shock.” The Cochrane Database of Systematic Reviews, no. 3 (2004): CD003709. doi:10.1002/14651858.CD003709.pub2.

10) Rudis, M. I., M. A. Basha, and B. J. Zarowitz. “Is It Time to Reposition Vasopressors and Inotropes in Sepsis?” Critical Care Medicine 24, no. 3 (March 1996): 525–37.

11) Smith, Maria A. “Use of Vasopressors in the Treatment of Cardiac Arrest.” Critical Care Nursing Clinics of North America 17, no. 1 (March 2005): 71–75, xi. doi:10.1016/j.ccell.2004.09.010.

12) Steltzer, H., P. Simon, A. N. Owen, M. Thalmann, and A. F. Hammerle. “The Effects of Dobutamine Therapy in Critically Ill Patients Measured by Transoesophageal Echocardiography and Intracardiac Monitoring.” Anaesthesia 49, no. 5 (May 1994): 432–37.

13) “Vasopressors and Inotropes in Shock.pdf,” n.d.

14) Vincent, J. L., C. Reuse, and R. J. Kahn. “Effects on Right Ventricular Function of a Change from Dopamine to Dobutamine in Critically Ill Patients.” Critical Care Medicine 16, no. 7 (July 1988): 659–62.


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