Cardiac surgery and cardiopulmonary bypass (CPB) may initiate a clinical state of hyperdynamic circulation that is presumed to be due to activation of inflammatory mediators. This state of high cardiac indices/low SVR is considered analogous to the systemic inflammatory response syndrome (SIRS); however its epidemiology and clinical significance have not yet been elucidated. We hypothesized that a persistent inflammatory response to CPB leads to systemic vasodilatation and accompanying high cardiac indices requiring vasopressor therapy.


Data was collected prospectively for 8492 patients undergoing CPB from 1995–1999. Patients were included if they required vasopressor infusions (norepinephrine, phenylephrine, vasopressin) to maintain clinically acceptable mean arterial blood pressure on admission to the Intensive care unit. We analyzed pre-operative factors, perioperative events and outcome in isolated valve and coronary artery bypass surgery (CABG). Groups were compared by ANOVA for continuous and logistic regression for dichotomous variables.


1075 patients (12.6%) manifested with vasodilatory shock following CPB. Although preoperative demographics and ICU admission scores were similar amongst groups for CABG patients, hyperdynamic patients following valvular surgery more frequently had a history of previous MI or poor LV function (9.4 vs 3.9% and 10 vs 4.8%, P < 0.001). Intubation time, CPB and aortic cross clamp times as well as ICU and hospital stay were statistically increased in the hyperdynamic group (P < 0.001). The hyperdynamic patients had statistically significant reductions in hematocrit (P < 0.001) and platelets (P < 0.001); this was associated with an increased incidence of return to the OR for bleeding/tamponade (9.4 vs 2%, P < 0.001). Although overall morbidity was increased (5.7 vs 2.5%, P < 0.001), this was not accompanied by significant increases in mediastinitis or blood stream infections (P = 0.09), ARDS (P = 0.25) or MODS (P = 0.09).


Hyperdynamic circulation, presumably secondary to a CPB induced inflammatory response, is associated with increased postoperative hemorrhage and morbidity but not with increased susceptibility to MODS. Elucidation of unique mechanisms regulating systemic vasodilatation following CPB may point to novel strategies that attenuate CPB mediated inflammation.