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Communications to the Editor |

Vasopressin and Cardiac Performance FREE TO VIEW

William L. Jackson, Jr, MD; Andrew F. Shorr, MD, MPH
Author and Funding Information

Affiliations: Walter Reed Army Medical Center Washington, DC,  St. Paul’s Hospital Vancouver, BC, Canada

Correspondence to: William L. Jackson, Jr., MD, Walter Reed Army Medical Center, Building 2, Room 3M12, 6900 Georgia Ave NW, Washington, DC; e-mail: wl_jackson@yahoo.com



Chest. 2002;121(5):1723-1724. doi:10.1378/chest.121.5.1723-a
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To the Editor:

We read with interest the review by Holmes and associates1 in CHEST (September 2001). Their article prompted us to review our experience with this agent. We retrospectively identified patients treated with vasopressin for septic shock at our institution from January 2000 to June 2001. These seven patients had a median age of 63 years and a mean (± SD) APACHE (acute physiology and chronic health evaluation) II score of 28.2 ± 11.7. All patients demonstrated a drop in cardiac index with use of vasopressin (mean dosage, 0.08 ± 0.06 U/min). The cardiac index was 3.9 ± 2.4 L/min/m2 prior to start of the infusion and 2.7 ± 1.9 L/min/m2 4 h after initiation (p = 0.014). The stroke volume index declined similarly (31.6 ± 17.1 mL/beat/m2 vs 22.9 ± 17.3 mL/beat/m2; p = 0.032). No significant changes in heart rate were observed. Notably, six patients subsequently required the addition of inotropic agents (dobutamine in four patients and milrinone in two patients). As the article suggests, while vasopressin appears to be an effective vasoconstrictor, the potential for a decrease in cardiac output should be anticipated with use of this agent. However, as our data show, such decreases may not be solely rate related.

In addition, we submit that the literature on cardiac performance with vasopressin in patients with septic shock is not entirely as uniform as the authors imply. For example, the authors describe a study by Malay et al,2in which vasopressin exerted no significant effect on cardiac index. Tsuneyoshi et al3 recently reported 16 patients with septic shock treated with continuous vasopressin infusion in whom no significant change in cardiac index was noted. Both of these trials utilized “physiologic” (0.04 U/min) doses of vasopressin, which might theoretically minimize the potential for coronary ischemia, and excluded patients with baseline myocardial dysfunction. While these are small studies, the variable response of cardiac output to vasopressin demonstrated thus far in human trials likely indicates that septic shock is sufficiently heterogeneous that predicting individual responses to such infusions is not straightforward. In particular, while use of vasopressin appears to allow for withdrawal of other vasoactive medications,2,4 in patients with sepsis-associated myocardial depression, addition of inotropes may be required. Randomized, controlled trials will be instrumental in assessing both the efficacy of and specific indications for vasopressin in patients with septic shock.

The views expressed in this communication are those of the authors and do not reflect the official policy or position of the Department of the Army, Department of Defense, or the US Government.

Holmes, CL, Patel, BM, Russell, JA, et al (2001) Physiology of vasopressin relevant to the management of septic shock.Chest120,989-1002
 
Malay, MB, Ashton, RC, Jr, Landry, DW, et al Low-dose vasopressin in the treatment of vasodilatory septic shock.J Trauma1999;47,699-703
 
Tsuneyoshi, I, Yamada, H, Kakihana, Y, et al Hemodynamic and metabolic effects of low-dose vasopressin infusions in vasodilatory septic shock.Crit Care Med2001;29,487-493
 
Landry, DW, Levin, HR, Gallant, EM, et al Vasopressin deficiency contributes to the vasodilation of septic shock.Circulation1997;95,1122-112
 
To the Editor:

We thank Dr. Jackson and Dr. Shorr for their thorough discussion, in response to our recent review1of the effects of vasopressin on cardiac performance. We also conducted a retrospective review in our institution of 50 patients who had received vasopressin for hemodynamic support in septic shock.2 In the subset of patients with a pulmonary artery catheter in place, we found a mean decrease in cardiac index of 11% at 4 h of treatment with vasopressin infusion. This effect appeared to be dose related; doses > 0.03 U/min were significantly associated with a decrease in the cardiac index (p = 0.0026).

We agree that the potential for a decrease in cardiac index should be anticipated at higher than physiologic doses of vasopressin. We also agree that the use of vasopressin in septic shock should await the results of a randomized controlled trial that assesses both mortality and hemodynamic outcomes.

References
Holmes, CL, Patel, BM, Russell, JA, et al Physiology of vasopressin relevant to management of septic shock.Chest2001;120,989-1002
 
Holmes, CL, Walley, KR, Chittock, DR, et al The effects of vasopressin on hemodynamics and renal function in severe septic shock: a case series.Intensive Care Med2001;27,1416-1421
 

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References

Holmes, CL, Patel, BM, Russell, JA, et al (2001) Physiology of vasopressin relevant to the management of septic shock.Chest120,989-1002
 
Malay, MB, Ashton, RC, Jr, Landry, DW, et al Low-dose vasopressin in the treatment of vasodilatory septic shock.J Trauma1999;47,699-703
 
Tsuneyoshi, I, Yamada, H, Kakihana, Y, et al Hemodynamic and metabolic effects of low-dose vasopressin infusions in vasodilatory septic shock.Crit Care Med2001;29,487-493
 
Landry, DW, Levin, HR, Gallant, EM, et al Vasopressin deficiency contributes to the vasodilation of septic shock.Circulation1997;95,1122-112
 
Holmes, CL, Patel, BM, Russell, JA, et al Physiology of vasopressin relevant to management of septic shock.Chest2001;120,989-1002
 
Holmes, CL, Walley, KR, Chittock, DR, et al The effects of vasopressin on hemodynamics and renal function in severe septic shock: a case series.Intensive Care Med2001;27,1416-1421
 
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