title: Selective management of cardiovascular dysfunction in posttraumatic SIRS and sepsis.
abstract: Cardiovascular dysfunction associated with the systemic inflammatory response syndrome (SIRS) is caused by a combination of decreased myocardial contractility and low vascular resistance. The contribution of each of these components can be determined at the bedside, and directed therapy can be appropriately initiated. Over an 8-month period of time, 23 consecutive patients who experienced posttraumatic SIRS while still being monitored with a volumetric pulmonary artery catheter (PAC) were prospectively evaluated. Ventricular pressure-volume diagrams were constructed to quantify myocardial contractility and afterload. In a resuscitation protocol, dobutamine was administered to patients with an isolated decrease in contractility, and dopamine or epinephrine was instituted for the combination of reduced contractility and afterload. Variables describing cardiovascular function were measured at the time of resolution of initial shock resuscitation (BASE), at the onset of SIRS (ONSET), and after administration of inotropic or vasoactive agents (TREAT). ONSET was associated with a significant decrease in left ventricular power (LVP) (362 +/- 96 to 235 +/- 55 mmHg.L/min/m(2), P < 0.00001) and stroke work index (SWI) (4670 +/- 1213 to 3060 +/- 848 mmHg.mL/m, P < 0.00001) from BASE. Sixteen patients (70%) demonstrated predominantly decreased contractility, which returned to near BASE values after the administration of dobutamine. The remaining seven patients (30%) had both decreased contractility and afterload, which was treated with dopamine or epinephrine. LVP and SWI significantly increased (235 +/- 55 to 328 +/- 77 mmHg.L/min/m(2), P < 0.00001, and 3060 +/- 848 to 4554 +/- 1423 mmHg.mL/m(2), P < 0.00001, respectively) on the initiation of directed therapy. Specific cardiovascular abnormalities can be identified at the bedside, and this information can guide pharmacologic management. Directed therapy improves cardiovascular function.
authors.affiliation: Department of Surgery, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA.
authors.forename: R Shayn
authors.initials: RS
authors.lastname: Martin
authors.forename: Edward H
authors.initials: EH
authors.lastname: Kincaid
authors.forename: Hyde M
authors.initials: HM
authors.lastname: Russell
authors.forename: J Wayne
authors.initials: JW
authors.lastname: Meredith
authors.forename: Michael C
authors.initials: MC
authors.lastname: Chang
mesh_terms: D000328:Adult; D000368:Aged; D000465:Algorithms; D002316:Cardiotonic Agents / Q000627:therapeutic use; D002318:Cardiovascular Diseases / Q000188:drug therapy* / Q000209:etiology* / Q000503:physiopathology; D015331:Cohort Studies; D004280:Dobutamine / Q000627:therapeutic use; D004298:Dopamine / Q000627:therapeutic use; D004837:Epinephrine / Q000627:therapeutic use; D005260:Female; D006439:Hemodynamics; D006801:Humans; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction; D011446:Prospective Studies; D018805:Sepsis / Q000150:complications* / Q000503:physiopathology; D018746:Systemic Inflammatory Response Syndrome / Q000150:complications* / Q000503:physiopathology; D016277:Ventricular Function, Left
chemical_list: D002316:Cardiotonic Agents; D004280:Dobutamine; D004298:Dopamine; D004837:Epinephrine