Microvascular response in patients with cardiogenic shock

Objective: To examine the mechanisms contributing to decreased microvascula r blood flow in cardiogenic shack by comparing patients with cardiogenic sh ock with critically ill controls and with patients with septic shock. Design: Prospective, consecutive entry of patients meeting the criteria for septic shock, cardiogenic shock, and critical illness without coexisting i nfection or shock. Setting: University hospital, medical intensive care unit, coronary care un it, and respiratory care unit. Patients: Eight patients with cardiogenic shock secondary to acute myocardi al infarction, six critically ill controls, and six patients with septic sh ock. Measurements and Main Results: Forearm blood flow was measured at rest and during reactive hyperemia by venous air plethysmography. Red cell deformabi lity was determined by filtration. Leukocyte aggregation was detected by th e leukergy test. Neutrophil CD11b/CD18 expression and soluble intercellular adhesion molecule-1 levels were also measured. In cardiogenic shock, forearm arterial resistance was significantly increas ed at rest and during reactive hyperemia compared with controls and patient s with septic shock. The response to reactive hyperemia was attenuated in c ardiogenic and septic shock patients, as measured by the absolute change in forearm blood flow from baseline, which was significantly less as compared with controls (p < .01). The percent change in forearm blood flow during r eactive hyperemia compared with forearm blood flow at rest was significantl y lower in cardiogenic shock (60 +/- 10) and in septic shock (50 +/- 11) co mpared with controls at baseline (145 +/- 20; p < .01). Red cell deformabil ity was significantly decreased in cardiogenic shock (1.2 +/- 0.2 mL/min; p < .05) and septic shock (1.1 +/- 0.2 mL/min; p < .05), compared with contr ols (1.8 +/- 0.1 mL/min). Neutrophil CD11b/CD18 expression, leukergy, and s erum intercellular adhesion molecule-1 levels in cardiogenic shock patients were not significantly different from controls. Conclusion: These data suggest that the response to reactive hyperemia is a ttenuated in cardiogenic shock. This appears to reflect increased vasoconst riction and an impaired capacity for vasodilation. Decreased erythrocyte de formability may also be important in limiting systemic microvascular flow. However, evidence supporting a role for neutrophil-endothelial cell interac tions was not observed.