The effects of vasopressin on systemic hemodynamics in catecholamine-resistant septic and postcardiotomy shock: a retrospective analysis.
We retrospectively investigated the effects of continuous arginine vasopressin (AVP) infusion on systemic hemodynamics, acid/base status, and laboratory variables in patients (mean age [mean +/- SD]= 66.3 +/- 10.1 yr) with catecholamine-resistant septic (n = 35) or postcardiotomy shock (n = 25). Hemodynamic and acid/base data were obtained before; 30 min after; and 1, 4, 12, 24, 48, and 72 h after the start of AVP infusion. Laboratory examinations were recorded before and 24, 48, and 72 h after the start of AVP infusion. For statistical analysis, a mixed-effects model was used. The overall intensive care unit mortality was 66.7%. AVP administration caused a significant increase in mean arterial pressure (+29%) and systemic vascular resistance (+56%), accompanied by a significant decrease in heart rate (-24%) and mean pulmonary arterial pressure (-11%) without any change in stroke volume index. Norepinephrine requirements could be reduced by 72% within 72 h. During AVP infusion, a significant increase in liver enzymes and total bilirubin concentration and a significant decrease in platelet count occurred. Arginine vasopressin was effective in reversing systemic hypotension. However, adverse effects on gastrointestinal perfusion and coagulation cannot be excluded.


CONCLUSIONS
In this retrospective analysis, the influence of a continuous infusion of an endogenous hormone (arginine vasopressin) on systemic hemodynamics and laboratory variables was assessed in patients with vasodilatory shock unresponsive to conventional therapy. Arginine vasopressin was effective in reversing systemic hypotension. However, adverse effects on gastrointestinal perfusion and coagulation cannot be excluded.
Dünser
M W
MW
Division of General and Surgical Intensive Care Medicine, Department of Anesthesia and Critical Care Medicine, The Leopold Franzens University of Innsbruck, Austria.
Mayr
A J
AJ
Ulmer
H
H
Ritsch
N
N
Knotzer
H
H
Pajk
W
W
Luckner
G
G
Mutz
N J
NJ
Hasibeder
W R
WR
D000136:Acid-Base Equilibrium / Q000187:drug effects; D000368:Aged; D006348:Cardiac Surgical Procedures / Q000009:adverse effects*; D002395:Catecholamines / Q000627:therapeutic use*; D003422:Critical Care; D004351:Drug Resistance; D005260:Female; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D008297:Male; D008954:Models, Biological; D009638:Norepinephrine / Q000627:therapeutic use; D011183:Postoperative Complications / Q000188:drug therapy* / Q000503:physiopathology; D012189:Retrospective Studies; D012769:Shock / Q000188:drug therapy* / Q000503:physiopathology; D012772:Shock, Septic / Q000188:drug therapy* / Q000503:physiopathology; D013318:Stroke Volume / Q000187:drug effects; D017741:Survivors; D014662:Vasoconstrictor Agents / Q000627:therapeutic use*; D014667:Vasopressins / Q000627:therapeutic use*
D002395:Catecholamines; D014662:Vasoconstrictor Agents; D014667:Vasopressins; D009638:Norepinephrine