Systemic inflammatory response syndrome after cardiac operations.
BACKGROUND
A systemic inflammatory response after open heart operation may be responsible for hyperdynamic circulatory instability and organ dysfunction. To what extent mediator release is involved needs to be clarified.


METHODS
Ten patients with postoperative hyperdynamic circulatory dysregulation (group I) requiring application of alpha-constrictors and 10 patients with routine cardiac procedures and stable postoperative hemodynamic indices (group II) were analyzed for mediator release and metabolic and hemodynamic changes until the third postoperative day.


RESULTS
Group I patients showed a significantly increased cardiac index and decreased systemic vascular resistance after bypass (cardiac index, group I: 5.2 +/- 1.2 L.min-1.m-2, group II: 2.5 +/- 1.6 L.min-1.m-2; systemic vascular resistance, group I: 495 +/- 204 dyne.s. cm-5, group II: 1,356 +/- 466 dyne.s.cm-5) and at 3 hours (cardiac index, group I: 4.4 +/- 0.8 L.min-1.m-2, group II: 2.9 +/- 0.6 L.min-1.m-2; systemic vascular resistance, group I: 567 +/- 211 dyne.s.cm-5, group II: 1,053 +/- 273 dyne.s.cm-5). Significantly higher serum levels of interleukin-6 were assessed in group I (postbypass, group I: 6,812 +/- 9,293 pg/mL, group II: 295 +/- 303 pg/mL; 3 hours, group I: 3,474 +/- 5,594 pg/mL, group II: 286 +/- 296 pg/mL). Concentrations of elastase, tumor necrosis factor, soluble tumor necrosis factor receptor, and interleukin-8 were elevated in group I (not significant). Early postoperative levels of soluble E-selectin and soluble intercellular adhesion molecule were also higher in group I (not significant). Continuously increased levels of endotoxin could be detected in only 3 of 10 patients in group I. Severe lactic acidosis (> or = 5 mmol/L) occurred in group I only.


CONCLUSIONS
Postoperative hyperdynamic instability after open heart operations appears to be associated with a certain pattern of mediator release. In particular, interleukin-6 appears to be involved in circulatory dysregulation and metabolic derangement.
Cremer
J
J
Department of Thoracic and Cardiovascular Surgery, Hannover Medical School, Germany.
Martin
M
M
Redl
H
H
Bahrami
S
S
Abraham
C
C
Graeter
T
T
Haverich
A
A
Schlag
G
G
Borst
H G
HG
D000140:Acidosis, Lactic / Q000209:etiology; D000328:Adult; D000368:Aged; D001708:Biopterins / Q000031:analogs & derivatives / Q000097:blood; D001775:Blood Circulation; D002302:Cardiac Output; D006348:Cardiac Surgical Procedures / Q000009:adverse effects*; D002315:Cardiopulmonary Bypass / Q000009:adverse effects; D015815:Cell Adhesion Molecules / Q000097:blood; D019040:E-Selectin / Q000097:blood; D004731:Endotoxins / Q000097:blood; D005260:Female; D006439:Hemodynamics; D006801:Humans; D007155:Immunologic Factors / Q000502:physiology; D015850:Interleukin-6 / Q000097:blood; D016209:Interleukin-8 / Q000097:blood; D008297:Male; D008875:Middle Aged; D019798:Neopterin; D010196:Pancreatic Elastase / Q000097:blood; D018124:Receptors, Tumor Necrosis Factor / Q000032:analysis; D018746:Systemic Inflammatory Response Syndrome / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D014655:Vascular Resistance; D014662:Vasoconstrictor Agents / Q000627:therapeutic use
D015815:Cell Adhesion Molecules; D019040:E-Selectin; D004731:Endotoxins; D007155:Immunologic Factors; D015850:Interleukin-6; D016209:Interleukin-8; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D014662:Vasoconstrictor Agents; D001708:Biopterins; D019798:Neopterin; D010196:Pancreatic Elastase