Factors contributing to burnout among perfusionists in the United States.

INTRODUCTION: As the job climate continues to change, many perfusionists are faced with high employee turnover rates, working longer hours, and increased stress related to more complex surgeries. Understanding the sources of professional burnout and stress may allow the formulation of a strategy to help prevent such negative outcomes. The purpose of this study was to determine the current level of stress and burnout among perfusionists. METHODS: A questionnaire was constructed with the use of SurveyMonkey®. Invitations requesting participation in the survey were distributed by electronic mail to members of PerfList and PerfMail. To assess burnout, components of the well-established Maslach Burnout Inventory (MBI) tool were used. RESULTS: At p<0.05, job demand variables such as stress level, conflict, call duties, hours worked, and case load were all shown to have a statistically significant relationship to burnout. CONCLUSION: The study found that, among the various factors, job demands were the most likely culprit contributing to burnout. Stress level and conflict, in particular, had the strongest association to burnout.

Systemic inflammatory response syndrome (SIRS) following emergency cardiopulmonary bypass: a case report and literature review.

A complication of emergency resuscitation is the development of the Systemic Inflammatory Response Syndrome (SIRS). In the past, this has been identified as multiple organ failure, with symptoms similar to sepsis. The hallmark of this syndrome is peripheral vasodilation, which is associated with a breakdown of capillary membranes and the accumulation of excess interstitial fluid. This case report discusses the development of SIRS in a patient following emergency cardiopulmonary bypass (CPB). The patient was a 53 year old male with significant left main coronary artery disease who developed sudden bradycardia and hypotension in the operating room and was emergently placed on cardiopulmonary bypass. During CPB, the patient was peripherally vasodilated, and required continuous alpha-adrenergic support to maintain normal systemic vascular resistance. In addition, metabolic acidosis was present despite high flow rates, high hematocrit, addition of colloids, and hemoconcentration. Despite excellent neurological and myocardial recovery following surgery, the patient died one week later in renal and hepatic failure. Several mechanisms for the development of this syndrome have been hypothesized. One of these theories is that the ischemic injury in the gastrointestinal tract disturbs the gut barrier function and allows enteric bacterial endotoxins to pass into the circulation producing sepsis-like symptoms. Other theories relate to the release patterns of cytokines associated with CPB. These mechanisms and the treatment of SIRS with new pharmacological agents and perfusion techniques are reviewed.

ATP-sensitive potassium channel activation before cardioplegia. Effects on ventricular and myocyte function.

BACKGROUND: Pretreatment with potassium channel openers (PCOs) has been shown to provide protective effects in the setting of myocardial ischemia. The goal of the present study was to examine whether PCO pretreatment would provide protective effects on left ventricular (LV) and myocyte function after cardioplegic arrest. METHODS AND RESULTS: The first study quantified the effects of PCO pretreatment on LV myocyte contractility after simulated cardioplegic arrest. LV porcine myocytes were randomly assigned to 3 groups: (1) normothermic control: 37 degrees C x 2 hours (n = 116); (2) cardioplegia: K+ 24 mEq/L, 4 degrees C x 2 hours followed by reperfusion and rewarming (n = 62); and (3) PCO/cardioplegia: 5 minutes of PCO treatment (50 mumol/L, SR47063, 37 degrees C; n = 94) followed by cardioplegic arrest and rewarming. Myocyte contractility was measured after rewarming by videomicroscopy. The second study determined whether the effects of PCO pretreatment could be translated to an in vivo model of cardioplegic arrest. Pigs (weight 30 to 35 kg) were assigned to the following: (1) cardioplegia: institution of cardiopulmonary bypass (CPB) and cardioplegic arrest (K+ 24 mEq/L, 4 degrees C x 2 hours) followed by reperfusion and rewarming (n = 8); and (2) PCO/cardioplegia: institution of CPB, antegrade myocardial PCO perfusion without recirculation (500 mL of 50 mumol/L, SR47063, 37 degrees C), followed by cardioplegic arrest (n = 6). LV function was examined at baseline (pre-CPB) and at 0 to 30 minutes after separation from CPB by use of the preload-recruitable stroke work relation (PRSWR; x 10(5) dyne.cm/mm Hg). LV myocyte velocity of shortening was reduced after cardioplegic arrest and rewarming compared with normothermic control (37 +/- 3 vs 69 +/- 3 microns/s, P < 0.05) and was improved with 5 minutes of PCO treatment (58 +/- 3 microns/s). In the intact experiments, the slope of the PRSWR was depressed in the cardioplegia group compared with baseline with separation from CPB (1.07 +/- 0.15 vs 2.57 +/- 0.11, P < 0.05) and remained reduced for up to 30 minutes after CPB. In the PCO-pretreated animals, the PRSWR was higher after cessation of CPB when compared with the untreated cardioplegia group (1.72 +/- 0.07, P < 0.05). However, in the PCO pretreatment group, 50% developed refractory ventricular fibrillation by 5 minutes after CPB, which prevented further study. CONCLUSIONS: PCO pretreatment improved LV myocyte contractile function in an in vitro system of cardioplegic arrest. The in vivo translation of this improvement in contractile performance with PCO pretreatment was confounded by refractory arrhythmogenesis. Thus the application of PCO pretreatment as a protective strategy in the setting of cardiac surgery may be problematic.