ABSTRACT
Cardiopulmonary bypass (CPB) is one of the methods used in myocardial revascularization and can be associated with adverse events that are uncommon, but CPB induces high morbidity and mortality. Cardiac surgery and CPB activate a systemic inflammatory response characterized by tissular lesions, cells movements and blood flow toward the interstice where the harmful stimulus has begun, under the influence of the mediators. The systemic inflammatory response may be initiated during cardiac surgery by a number of processes, including blood contact with the foreign surface of the CPB apparatus, development of ischemia and reperfusion injury, and presence of endotoxemia. In the course of cardiac surgery using CPB, all three processes are present and contribute concurrently to the systemic inflammatory response. The term "systemic inflammatory response syndrome" (SIRS) has been proposed to describe an entity that continually overlaps with normal postoperative physiology. A frequent complication of SIRS is the development of organ dysfunction, including acute lung injury, shock, renal failure, and multiple organ dysfunction syndrome. Finally, long-term survival in patients developing SIRS may also be adversely affected. The purpose of this review is to examine and understand the pathological mechanisms for inflammatory response that occur following cardiopulmonary bypass.
Subject(s)
Cardiac Surgical Procedures , Extracorporeal Circulation , Complement Activation , Cytokines/metabolism , Extracorporeal Circulation/adverse effects , Extracorporeal Circulation/instrumentation , Extracorporeal Circulation/mortality , Fibrinolysis , Humans , Infections/etiology , Myocardial Reperfusion Injury/etiology , Risk Factors , Systemic Inflammatory Response Syndrome/etiology , Systemic Inflammatory Response Syndrome/physiopathology , Time FactorsABSTRACT
OBJECTIVE: We evaluated the precision of the perfusion and ventricular function through cardiac scintigraphy 99mTc-MIBI SPECT synchronized to the electrocardiogram to differentiate the ventricular damage of ischemic origin from the dilated cardiomyopathy. METHODS: Thirty patients with myocardial damage with ejection fraction =30% were included. We analyzed the prognostic value of clinical, angiographic, and 99mTc-MIBI SPECT variables. RESULTS: We studied 30 patients with myocardial damage, 26 men (86.7%) and 4 women (13.3%), with an average age of 45.7 +/- 9.3 years. The diagnosis established by cardiac catheterization was dilated cardiomyopathy in 17 patients (56.6%) and 13 with ischemic cardiomyopathy (43.4%). The study by cardiac scintigraphy 99mTc-MIBI SPECT synchronized to the electrocardiogram established the diagnosis of dilated cardiomyopathy in 18 patients, with a sensitivity of 100% and specificity of 92%. The predictive positive value was 100% and the predictive negative value 94.4%. CONCLUSIONS: Cardiac scintigraphy 99mTc-MIBI SPECT synchronized to the electrocardiogram differs in the etiology of the myocardial damage produced by dilated cardiomyopathy from that of ischemic origin in a noninvasive way and with high sensitivity and specificity.