Maintaining core normothermia decreases the duration of postanesthetic recovery and may, therefore, reduce costs of care.

In patients with acute respiratory distress syndrome (ARDS), permissive hypercapnia is a strategy to decrease airway pressures to prevent ventilator-induced lung damage by lowering tidal volumes and tolerating higher arterial carbon dioxide tension. However, in experimental studies hypercapnia impairs myocardial contractility and hemodynamic function. We investigated the effect of short-term permissive hypercapnia on myocardial contractility and hemodynamics in patients with ARDS. We hypothesized that the administration of tromethamine (THAM), a buffer which does not increase carbon dioxide production, would modify these changes. In 12 patients with ARDS, permissive hypercapnia was implemented for 2 h with a target Pa(CO(2))of 80 mm Hg. Patients were randomized to have respiratory acidosis corrected by THAM (pH-corrected group), or not corrected (pH-uncorrected group). Hemodynamic responses were measured, and transesophageal echocardiography (TEE) was used to determine myocardial contractility. Permissive hypercapnia resulted in significant decreases in systemic vascular resistance (SVR) and increases in cardiac output (Q). Myocardial contractility decreased in both groups but significantly less in the pH-corrected group (approximately 10%) than in the pH-uncorrected group (approximately 18%, p < 0.05). Mean arterial pressure decreased and mean pulmonary arterial pressure increased significantly only in the pH-uncorrected group. All values returned to baseline conditions 1 h after permissive hypercapnia was terminated. Our study demonstrates a reversible depression of myocardial contractility and hemodynamic alterations during rapid permissive hypercapnia which were attenuated by buffering with THAM. This may have applicability to the clinical strategy of permissive hypercapnia and allow the benefit of decreased airway pressures to be realized while minimizing the adverse hemodynamic effects of hypercapnic acidosis.

No abstract

No abstract

utations in the gene encoding fibrillin are the cause of Marfan syndrome, an autosomal dominant disorder with skeletal, ocular, and cardiovascular complications. The leading cause of premature death in patients with Marfan syndrome is progressive dilatation of the aortic root and ascending aorta, resulting in aortic regurgitation and acute aortic dissection. 1,2 From the Departments of Cardiothoracic Surgery a and Cardiothoracic and Vascular Anaesthesia,

In a case of catheter-induced superior vena cava thrombosis with septicemia and pulmonary embolism, bedside TEE was very helpful to make the correct diagnosis early, assess thrombus size during anticoagulation, and monitor cardiac performance and thrombus disposition during central venous catheter removal.

No abstract

Every perioperative transoesophageal echo (TEE) study should generate a written report. A verbal report may be given at the time of the study. Important findings must be included in the written report. Where the perioperative TEE findings are new, or have led to a change in operative surgery, postoperative care or in prognosis, it is essential that this information should be reported in writing and available as soon as possible after surgery. The ultrasound technology and methodology used to assess valve pathology, ventricular performance and any other derived information should be included to support any conclusions. This is particularly important in the case of new or unexpected findings. Particular attention should be attached to the echo findings following the completion of surgery. Every written report should include a written conclusion, which should be comprehensible to physicians who are not experts in echocardiography.