Front Lines of Thoracic Surgery

Front Lines of Thoracic Surgery collects up-to-date contributions on some of the most debated topics in today's clinical practice of cardiac, aortic, and general thoracic surgery,and anesthesia as viewed by authors personally involved in their evolution. The strong and genuine enthusiasm of the authors was clearly perceptible in all their contributions and I'm sure that will further stimulate the reader to understand their messages. Moreover, the strict adhesion of the authors' original observations and findings to the evidence base proves that facts are the best guarantee of scientific value. This is not a standard textbook where the whole discipline is organically presented, but authors' contributions are simply listed in their pertaining subclasses of Thoracic Surgery. I'm sure that this original and very promising editorial format which has and free availability at its core further increases this book's value and it will be of interest to healthcare professionals and scientists dedicated to this field

An investigation into the effects of commencing haemodialysis in the critically ill

<b>Introduction:</b> We have aimed to describe haemodynamic changes when haemodialysis is instituted in the critically ill. 3 hypotheses are tested: 1)The initial session is associated with cardiovascular instability, 2)The initial session is associated with more cardiovascular instability compared to subsequent sessions, and 3)Looking at unstable sessions alone, there will be a greater proportion of potentially harmful changes in the initial sessions compared to subsequent ones. <b>Methods:</b> Data was collected for 209 patients, identifying 1605 dialysis sessions. Analysis was performed on hourly records, classifying sessions as stable/unstable by a cutoff of >+/-20% change in baseline physiology (HR/MAP). Data from 3 hours prior, and 4 hours after dialysis was included, and average and minimum values derived. 3 time comparisons were made (pre-HD:during, during HD:post, pre-HD:post). Initial sessions were analysed separately from subsequent sessions to derive 2 groups. If a session was identified as being unstable, then the nature of instability was examined by recording whether changes crossed defined physiological ranges. The changes seen in unstable sessions could be described as to their effects: being harmful/potentially harmful, or beneficial/potentially beneficial. <b>Results:</b> Discarding incomplete data, 181 initial and 1382 subsequent sessions were analysed. A session was deemed to be stable if there was no significant change (>+/-20%) in the time-averaged or minimum MAP/HR across time comparisons. By this definition 85/181 initial sessions were unstable (47%, 95% CI SEM 39.8-54.2). Therefore Hypothesis 1 is accepted. This compares to 44% of subsequent sessions (95% CI 41.1-46.3). Comparing these proportions and their respective CI gives a 95% CI for the standard error of the difference of -4% to 10%. Therefore Hypothesis 2 is rejected. In initial sessions there were 92/1020 harmful changes. This gives a proportion of 9.0% (95% CI SEM 7.4-10.9). In the subsequent sessions there were 712/7248 harmful changes. This gives a proportion of 9.8% (95% CI SEM 9.1-10.5). Comparing the two unpaired proportions gives a difference of -0.08% with a 95% CI of the SE of the difference of -2.5 to +1.2. Hypothesis 3 is rejected. Fisher’s exact test gives a result of p=0.68, reinforcing the lack of significant variance. <b>Conclusions:</b> Our results reject the claims that using haemodialysis is an inherently unstable choice of therapy. Although proportionally more of the initial sessions are classed as unstable, the majority of MAP and HR changes are beneficial in nature

Cerebral oxygenation during induction of therapeutic hypothermia after cardiac arrest

Introduction Induced mild hypothermia (32 to 34°C) improves survival and neurological outcome after CA. Near-infrared spectroscopy (NIRS) measures cerebral tissue oxygen saturation (SctO2 ). As of today, no data are available on SctO2 monitoring during therapeutic hypothermia (TH). Therefore, SctO2 was measured in this study during the fi rst 36 hours after CA. Methods After IRB approval, data were collected from 23 patients. Cold saline (30 ml/kg) was administered as soon as possible after hospital admission. TH (33°C) was induced by endovascular or surface cooling and maintained for 24 hours. All patients were sedated (propofol/ remifentanil) for the duration of TH. NIRS sensors were bilaterally applied to the frontotemporal area before start of TH. Patients were monitored during induction, maintenance and recovery of TH. Results Of 23 patients, 11 patients did not survive until hospital discharge due to post-ischemic brain damage. Twelve patients survived until hospital discharge, of whom eight without any neurological impairment. Temperature at admission was 34.6°C (±0.5°C). Patients reached the target temperature of 33°C, 4 hours after induction of TH. Two patients died during maintenance of TH due to refractory hemodynamic shock. In all patients, SctO2 values started above 65%. Two and a half hours after induction of TH, SctO2 values decreased with 9% (±3%). The decrease in cerebral oxygenation during induction of TH was not associated with a major change in hemodynamic parameters (MAP before induction of TH: 79 mmHg ± 19; at 33°C: 82 mmHg ± 9), nor with a major change in systemic oxygenation (SpO2 before TH: 99% ± 1; at 33°C: 97%  ±  3). In patients who survived until hospital discharge, SctO2 returned to baseline values, 3.5 hours after induction of TH, before the target temperature of 33°C was reached. In patients who did not survive the hospital stay, SctO2 remained lower than baseline values until the target temperature was reached. In these nonsurvivors, SctO2 values did only return to baseline values during maintenance of TH (10 hours after induction of TH). During maintenance of TH and rewarming (0.3°C), no further signifi cant changes in SctO2 values were observed. Conclusion Noninvasive monitoring revealed a decrease in cerebral oxygenation during induction of mild hypothermia in patients after cardiac arrest. We observed a diff erence in oxygenation between hospital survivors and nonsurvivors