Thoracoabdominal aortic aneurysm repair: results of conventional open surgery.

OBJECTIVES: The aim of this study is to report our experience in the surgical repair of thoracoabdominal aortic aneurysms (TAAAs) over the last 27 years against the background of evolving surgical techniques. METHODS: We reviewed the prospectively collected data of 571 patients who underwent open TAAA repair between 1981 and 2008. Data were analysed using univariate and multivariate analysis (logistic regression). Pre-, intra- and postoperative risk factors were used to develop risk models for in-hospital mortality, spinal cord deficit and renal failure. Recent published series were used to highlight the different treatment modalities and explore results. RESULTS: Seventy patients (12.3%) died in the hospital, the 30-day mortality was 8.9%, 37 patients (6.5%) required postoperative dialysis and 47 patients (8.3%) developed paraplegia or paraparesis. The incidence of paraplegia in the left heart bypass group was 4.4%. The predictors for hospital mortality were increasing age (odds ratio 1.096 per year, 95% confidence interval (CI): 1.05-1.14) and the need for haemodialysis (odds ratio 10, 95% CI: 4.7-21.1). For postoperative spinal cord deficit, we found three protecting factors: age above 75 years (odds ratio 0.14, 95% CI: 0.19-1.09), the presence of a post-dissection aneurysm (odds ratio 0.4, 95% CI: 0.17-0.94) and the combined use of cerebrospinal fluid drainage and motor-evoked potentials (odds ratio 0.28, 95% CI: 0.14-0.56). The urgency of procedure (odds ratio 4, 95% CI: 1.8-9) and preoperative serum creatinine level (odds ratio 1.007 per micromole per litre, 95% CI: 1.0-1.01) were significant risk factors for renal failure. CONCLUSIONS: Open TAAA repair intrinsically has substantial complications, of which spinal cord ischaemia and renal failure are the most devastating, despite major progress in our understanding of the pathophysiology and operative strategy. An overview of the results of recently published series is given along with an analysis of our data.

Continuous monitoring of haemodynamic parameters in humans during the early phase of simulated diving with and without breathholding.

This study examined the integrative changes of blood pressure (BP) and stroke volume (SV) leading to the initial biphasic heart rate (fc) response (first 15 s) in simulated diving manoeuvres with and without breathholding (BH). Simulated diving was studied in ten young healthy volunteers by application of a gel-filled pack at 0 degree C and 18 degrees C on the forehead with and without BH. Beat-by-beat and second-to-second fc, BP, SV, and total peripheral vascular resistance (TPR) were followed by continuous non-invasive monitoring. In all conditions (BH with forehead cooling at 0 degree and 18 degrees C) there was an early rise in BP triggering the first tachycardial response (fc acceleration) which was immediately counteracted by the concurrent further increase of SV leading to the second phase of early bradycardic response (fc deceleration). Furthermore, the continuous beat-by-beat and second-to-second monitoring allowed the documentation of a highly significant increase of TPR within the first few seconds of the manoeuvres. Our data further indicated that the differences in haemodynamics observed during the stimuli at different temperatures was overruled by BH. Detailed comparisons of the beat-by-beat and second-to-second analyses were unable to show that one method was better than the other. Using continuous non-invasive monitoring of haemodynamic variables during simulated diving manoeuvres it was possible to provide better insights into the physiological principles and meaning of the diving reflex in humans.

Hyperventilation is not diagnostically specific to panic patients.

It has been claimed that hyperventilation is a cause of panic attacks in patients suffering from panic disorder (PD), and various studies have, in fact, documented low resting CO2 in PD patients. However, most comparisons have been made using non-psychiatric controls. Since increased ventilation is a common concomitant of distress, the relevance of using healthy/non-anxious control groups may be questioned. Respiratory peculiarities of PD patients may actually just reflect background anxiety rather than a diagnostically specific feature. In order to explore the possible diagnostic specificity of hyperventilation, as well as increased respiratory rate and respiratory variability, to PD patients, capnographic patterns were analyzed from PD patients, non-panic disorder anxiety patients, and healthy controls. Capnographic data were obtained while subjects were resting, watching an exciting film, relaxing, and being exposed to idiosyncratically relevant fearful imagery. Findings were robust. As found in most studies, PD patients had lower resting CO2 than healthy controls; however, that of non-panic disorder anxiety patients was just as low as PD patients. The exciting film and fearful imagery produced consistent increases in distress and concomitant increases in respiratory rate, variability of end-tidal CO2, and decreases in end-tidal CO2. However, this was similar in all three groups. Data suggest that hyperventilation is not specific to PD patients.