Risk assessment and outcomes of vasoplegia after cardiac surgery.

OBJECTIVE: The aim of this study was to analyze risk factors and outcomes of vasoplegia after cardiac surgery based on our experience with almost 2000 cardiac operations performed at our institution. METHODS: We retrospectively analyzed patients who underwent cardiac surgery with cardiopulmonary bypass (CPB) between 2011 and 2013. Data were available for a total of 1992 patients. We defined vasoplegia as hypotension with persistently low systemic vascular resistance (<800 dyn/s/cm) and preserved Cardiac Index (>2.5). RESULTS: The rate of vasoplegia in our cohort was 20.3% (n = 405). The incidences of mild, moderate, and severe vasoplegia were 13.2, 5.7, and 1.5%, respectively. Factors that increased risk of vasoplegia included valve operations, heart transplants, dialysis-dependent renal failure, age >65, diuretic therapy, and recent myocardial infarction. B blocker therapy was protective against vasoplegia. CONCLUSION: Vasoplegic syndrome is still a frequently occurring adverse event following cardiac surgery. In high risk patients for vasoplegia, it may be sensible to proceed with preoperative volume loading (instead of diuresis), initiation of low dose vasopressin therapy if needed, and attempting to up titrate beta-blocker therapy.

Activation of complement factor B contributes to murine and human myocardial ischemia/reperfusion injury.

The pathophysiology of myocardial injury that results from cardiac ischemia and reperfusion (I/R) is incompletely understood. Experimental evidence from murine models indicates that innate immune mechanisms including complement activation via the classical and lectin pathways are crucial. Whether factor B (fB), a component of the alternative complement pathway required for amplification of complement cascade activation, participates in the pathophysiology of myocardial I/R injury has not been addressed. We induced regional myocardial I/R injury by transient coronary ligation in WT C57BL/6 mice, a manipulation that resulted in marked myocardial necrosis associated with activation of fB protein and myocardial deposition of C3 activation products. In contrast, in fB-/- mice, the same procedure resulted in significantly reduced myocardial necrosis (% ventricular tissue necrotic; fB-/- mice, 20 ± 4%; WT mice, 45 ± 3%; P < 0.05) and diminished deposition of C3 activation products in the myocardial tissue (fB-/- mice, 0 ± 0%; WT mice, 31 ± 6%; P<0.05). Reconstitution of fB-/- mice with WT serum followed by cardiac I/R restored the myocardial necrosis and activated C3 deposition in the myocardium. In translational human studies we measured levels of activated fB (Bb) in intracoronary blood samples obtained during cardio-pulmonary bypass surgery before and after aortic cross clamping (AXCL), during which global heart ischemia was induced. Intracoronary Bb increased immediately after AXCL, and the levels were directly correlated with peripheral blood levels of cardiac troponin I, an established biomarker of myocardial necrosis (Spearman coefficient = 0.465, P < 0.01). Taken together, our results support the conclusion that circulating fB is a crucial pathophysiological amplifier of I/R-induced, complement-dependent myocardial necrosis and identify fB as a potential therapeutic target for prevention of human myocardial I/R injury.

Mechanisms contributing to low orthostatic tolerance in women: the influence of oestradiol.

The impact of 17ß-oestradiol (E2) exposure on autonomic control of orthostasis in young women is unclear. We tested the hypothesis that autonomic cardiovascular regulation is more sensitive to E2 exposure in women with low orthostatic tolerance. Women underwent an initial maximal lower body negative pressure (LBNP) test to place them into a low (LT, n = 7, 22 ± 1 years old, body mass index 22 ± 1 kg m(-2)) or a high orthostatic tolerance group (HT, n = 7, 22 ± 1 years old, body mass index 24 ± 1 kg m(-2)). We then suppressed endogenous reproductive hormone production using a gonadotrophin-releasing hormone antagonist (GnRHant) for 10 days, with E2 administration during the last 7 days of GnRHant. We measured R-R interval and beat-by-beat blood pressure during the modified Oxford protocol, and changes in heart rate, blood pressure and forearm vascular resistance (FVR) during submaximal LBNP. During submaximal LBNP, FVR increased in HT (ANOVA P < 0.05) but not in LT (ANOVA P > 0.05), and stroke volume was lower in LT relative to HT at all levels of LBNP (P < 0.05). Compared with GnRHant, E2 administration shifted FVR lower in LT (ANOVA P < 0.05), with no effect in HT. Administration of E2 increased baroreflex control of heart rate (derived from the modified Oxford protocol) in LT (GnRHant 10.7 ± 2.5 ms mmHg(-1) vs. E2 16.1 ± 2.4 ms mmHg(-1), P < 0.05) but not in HT (GnRHant 13.4 ± 1.9 ms mmHg(-1) vs. E2 15.3 ± 2.4 ms mmHg(-1), n.s.). In conclusion, blunted peripheral vasoconstriction and lower stroke volume contribute to compromised orthostatic tolerance in women; this inability to vasoconstrict is further exacerbated by exposure to E2. Furthermore, E2 administration increases baroreflex-mediated heart rate responses to orthostasis in low orthostatic tolerant women, which is likely to be a compensatory mechanism for the blunted peripheral vascular resistance and lower central volume.

The anesthesia patient with acute coronary syndrome.

This article reviews the current state of knowledge of the pathophysiology, diagnosis, and treatment of acute coronary syndrome outside and during the perioperative period. It highlights some aspects of relevance for the anesthesiologist caring for these patients. Perioperative modalities for the management of patients suffering from this syndrome, the major guidelines and the evidence behind them, and possible avenues for future research is explored.

Prophylactic amiodarone versus lidocaine for prevention of reperfusion ventricular fibrillation after release of aortic cross-clamp.

BACKGROUND AND OBJECTIVE: Ventricular fibrillation is common after aortic cross-clamp release in patients undergoing open-heart surgeries. The aim of the study was to evaluate the efficacy of the prophylactic administration of 150 mg amiodarone by way of the pump 2 min before release of aortic cross-clamp in preventing ventricular fibrillation. METHODS: The present study is a prospective, randomized, controlled and blinded study performed at a teaching university hospital where 120 patients undergoing coronary bypass graft surgery were randomly assigned to three groups. Each group received either 150 mg of amiodarone or 100 mg lidocaine or isotonic saline by way of pump 2 min before release of the aortic cross-clamp. The frequency of occurrence of ventricular fibrillation and the subsequent required defibrillation counter shocks were determined in all groups. RESULTS: The frequency of occurrence of ventricular fibrillation was significantly higher in both the amiodarone (48%) and the control group (45%) as compared with the lidocaine group (20%) with no statistically significant difference between the amiodarone and the control groups. Furthermore, when ventricular fibrillation occurred, the percentage of patients requiring defibrillation counter shocks was significantly higher in both the amiodarone (58%) and control (61%) groups as compared with the lidocaine group (13%) with no difference between the amiodarone and the control groups, despite a significant decrease in the defibrillation counter shocks energy requirements in the amiodarone group. CONCLUSION: The present study showed no difference between amiodarone (150 mg) and placebo in preventing ventricular fibrillation after release of aortic cross-clamp. In addition, the use of lidocaine was able to reduce the incidence of ventricular fibrillation as compared with both amiodarone and placebo.

The relationship between the photoplethysmographic waveform and systemic vascular resistance.

OBJECTIVE: The objective of this study was to determine the relationship between systemic vascular resistance (SVR), finger & ear photoplethysmographic measurements in 14 adult patients undergoing coronary artery bypass grafting (CABG). METHODS: Patients were monitored with photoplethysmographs of the finger and ear and continuous cardiac output (QT) via thermodilution catheter. The relationship between SVR, finger plethysmographic amplitude, width and ear plethysmographic amplitude, width was assessed with linear regression. RESULTS: The finger plethysmographic amplitude had a low correlation r value = -0.15, while finger plethysmographic width had a better correlation r value = 0.56. The correlation between SVR and ear plethysmographic amplitude and width were -0.24 and 0.62 respectively. Using receiver operating characteristic analysis the ear plethysmographic width had both better sensitivity and specificity than the finger plethysmographic width in identifying high and low SVR. Using a multiple regression analysis, SVR was estimated from the pulse oximeter waveforms: SVR calculated = 27.27 + (3978.53 x Ear pulse oximeter width) - (8.91 x Ear pulse oximeter area) + (1986.3 x Finger pulse oximeter width). Bland-Altman analysis was used the bias was 29.8 dynes s cm(-5), standard deviation was 587.3, upper and lower limit of agreement were 1204.45, and -1144.8 dynes s cm(-5) respectively. CONCLUSION: The data indicate that pulse width of finger and ear plethysmographic tracing are more sensitive to changes in SVR than the other indices. An appreciation of changes in pulse width may provide valuable evidence with respect to changes in peripheral vascular tone.