Myocardial dysfunction following cardiopulmonary bypass: recovery patterns, predictors of inotropic need, theoretical concepts of inotropic administration.
Clinical myocardial dysfunction following cardiopulmonary bypass commonly occurs in patients with good preoperative ventricular function. Following separation from cardiopulmonary bypass, ventricular function improves initially, but then begins to worsen and reaches a nadir between 4 and 6 hours after surgery with full recovery occurring around 24 hours postoperatively. However, in patients with preoperative ventricular dysfunction, the depression of ventricular function is more severe and recovery is longer. Despite this high frequency of myocardial dysfunction, many patients do well without requiring pharmacologic intervention after cardiopulmonary bypass to augment contractility and peripheral perfusion. Factors that may predict the need for inotropic support in patients following cardiopulmonary bypass include low ejection fraction, older age, cardiac enlargement, female sex, the length of cardiopulmonary bypass and the duration of aortic cross-clamping. The patient with preoperative ventricular dysfunction has many of these preoperative and intraoperative predictors for inotropic support. The pharmacologic regimen to support the myocardium during the recovery period following cardiopulmonary bypass must take into consideration the pathophysiologic processes of chronic congestive heart failure and reperfusion injury. Reduction of cyclic adenosine monophosphate (cAMP) levels is a fundamental problem in congestive heart failure and results from either down-regulation of beta-receptors or a defect in the G-regulatory proteins controlling adenylyl cyclase production. This diminishes the effectiveness of agents dependent on cAMP to produce an inotropic response. However, amplification of the reduced cAMP produced by beta-agonists may occur in association with the inhibition of cAMP breakdown resulting from phosphodiesterase inhibitors. All inotropic agents are usually effective in reversing the reperfusion-induced stunned myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)
Royster
R L
RL
Department of Anesthesia, Bowman Gray School of Medicine, Winston-Salem, SC 27157-1009.
D000818:Animals; D002303:Cardiac Output, Low / Q000503:physiopathology; D002315:Cardiopulmonary Bypass / Q000009:adverse effects*; D002316:Cardiotonic Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D005260:Female; D005544:Forecasting; D006321:Heart / Q000503:physiopathology*; D006801:Humans; D009200:Myocardial Contraction / Q000187:drug effects / Q000502:physiology*; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology; D016276:Ventricular Function / Q000187:drug effects / Q000502:physiology*
D002316:Cardiotonic Agents