Postoperative myocardial injury phenotypes and self-reported disability in patients undergoing noncardiac surgery: a multicentre observational study.

BACKGROUND: Postoperative myocardial injury (PMI) comprises a spectrum of mechanisms resulting in troponin release. The impact of different PMI phenotypes on postoperative disability remains unknown. METHODS: This was a multicentre prospective cohort study including patients aged ≥50 yr undergoing elective major noncardiac surgery. Patients were stratified in five groups based on the occurrence of PMI and clinical information on postoperative adverse events: PMI classified as myocardial infarction (MI; according to fourth definition), PMI plus adverse event other than MI, clinically silent PMI (PMI without adverse events), adverse events without PMI, and neither PMI nor an adverse event (reference). The primary endpoint was 6-month self-reported disability (assessed by WHO Disability Assessment Schedule 2.0 [WHODAS]). Disability-free survival was defined as WHODAS ≤16%. RESULTS: We included 888 patients of mean age 69 (range 53-91) yr, of which 356 (40%) were women; 151 (17%) patients experienced PMI, and 625 (71%) experienced 6-month disability-free survival. Patients with PMI, regardless of its phenotype, had higher preoperative disability scores than patients without PMI (difference in WHODAS; ß: 3.3, 95% confidence interval [CI]: 0.5-6.2), but scores remained stable after surgery (ß: 1.2, 95% CI: -3.2-5.6). Before surgery, patients with MI (n=36, 4%) were more disabled compared with patients without PMI and no adverse events (ß: 5.5, 95% CI: 0.3-10.8). At 6 months, patients with MI and patients without PMI but with adverse events worsened in disability score (ß: 11.2, 95% CI: 2.3-20.2; ß: 8.1, 95% CI: 3.0-13.2, respectively). Patients with clinically silent PMI did not change in disability score at 6 months (ß: 1.39, 95% CI: -4.50-7.29, P=0.642). CONCLUSIONS: Although patients with postoperative myocardial injury had higher preoperative self-reported disability, disability scores did not change at 6 months after surgery. However, patients experiencing myocardial infarction worsened in disability score after surgery.

Untreated preoperative depression is not associated with postoperative arrhythmias in CABG patients.

PURPOSE: The mechanism by which depression affects postoperative outcome may involve arrhythmias. The purpose of this study was to evaluate whether untreated depression is associated with an increased incidence of postoperative arrhythmias in patients undergoing coronary artery bypass graft surgery (CABG). METHODS: One hundred seven patients were assessed for signs of depression with the Prime-MD Patient Health Questionnaire (brief PHQ) one week before surgery and subsequently underwent Holter monitoring for 48-72 hr postoperatively. The incidences of atrial fibrillation (AF); supraventricular tachycardia (SVT); ventricular tachycardia (VT), defined as three or more consecutive beats at a cycle length less than 600 msec; ventricular fibrillation (VF); and average heart rate (HR) were recorded in patients with and without signs of depression. RESULTS: The incidence of preoperative untreated depression was 27% (29/107). Twenty patients had mild depression (brief PHQ score of 5-9), seven patients had moderate depression (a score of 10-14), and two patients had severe depression (a score of 20). The incidences of postoperative AF, SVT, and non-sustained VT in depressed and non-depressed patients were 37.9% vs 35.9%, respectively (P = 0.50), 34.4% vs 52.5%, respectively (P = 0.07), and 17.2% vs 37.1%, respectively (P = 0.04). The average (SD) postoperative HR was similar in both groups [95 (12) beats·min(-1) in depressed patients and 92 (10) beats·min(-1) in non-depressed patients, (P = 0.25)]. Multivariate regression analysis showed that older age, but not depression, was a risk factor for postoperative arrhythmia. CONCLUSIONS: Preoperative untreated depression is not related to postoperative arrhythmia in the early postoperative period in patients undergoing elective CABG. This trial was registered at clinicaltrials.gov (number: NCT00622024).

Non-invasive accurate measurement of arterial PCO2 in a pediatric animal model.

The PCO2 in arterial blood (PaCO2) is a good parameter for monitoring ventilation and acid-base changes in ventilated patients, but its measurement is invasive and difficult to obtain in small children. Attempts have been made to use the partial pressure of CO2 in end-tidal gas (PETCO2), as a noninvasive surrogate for PaCO2. Studies have revealed that, unfortunately, the differences between PETCO2 and PaCO2 are too variable to be clinically useful. We hypothesized that end-inspiratory rebreathing, previously shown to equalize PETCO2 and PaCO2 in spontaneously breathing humans, would also be effective with positive pressure ventilation. Eight newborn Yorkshire pigs were mechanically ventilated via a partial rebreathing circuit to implement end-inspiratory rebreathing. Arterial blood was sampled and tested for PaCO2. A variety of alveolar ventilations resulting in different combinations of end-tidal PCO2 (30-50 mmHg) and PO2 (35-500 mmHg) were tested for differences between PETCO2 and PaCO2 (PET-aCO2). The PET-aCO2 of all samples was (mean ± 1.96 SD) 0.4 ± 2.7 mmHg. Our study demonstrates that, in ventilated juvenile animals, end-inspiratory rebreathing maintains PET-aCO2 to what would be a clinically useful range. If verified clinically, this approach could open the way for non-invasive monitoring of arterial PCO2 in critically ill patients.

The interaction of carbon dioxide and hypoxia in the control of cerebral blood flow.

Both hypoxia and carbon dioxide increase cerebral blood flow (CBF), and their effective interaction is currently thought to be additive. Our objective was to test this hypothesis. Eight healthy subjects breathed a series of progressively hypoxic gases at three levels of carbon dioxide. Middle cerebral artery velocity, as an index of CBF; partial pressures of carbon dioxide and oxygen and concentration of oxygen in arterial blood; and mean arterial blood pressure were monitored. The product of middle cerebral artery velocity and arterial concentration of oxygen was used as an index of cerebral oxygen delivery. Two-way repeated measures analyses of variance (rmANOVA) found a significant interaction of carbon dioxide and hypoxia factors for both CBF and cerebral oxygen delivery. Regression models using sigmoidal dependence on carbon dioxide and a rectangular hyperbolic dependence on hypoxia were fitted to the data to illustrate this interaction. We concluded that carbon dioxide and hypoxia act synergistically in their control of CBF so that the delivery of oxygen to the brain is enhanced during hypoxic hypercapnia and, although reduced during normoxic hypocapnia, can be restored to normal levels with progressive hypoxia.

End-inspiratory rebreathing reduces the end-tidal to arterial PCO2 gradient in mechanically ventilated pigs.

PURPOSE: Noninvasive monitoring of the arterial partial pressures of CO(2) (PaCO(2)) of critically ill patients by measuring their end-tidal partial pressures of CO(2) (PETCO(2)) would be of great clinical value. However, the gradient between PETCO(2) and PaCO(2) (PET-aCO(2)) in such patients typically varies over a wide range. A reduction of the PET-aCO(2) gradient can be achieved in spontaneously breathing healthy humans using an end-inspiratory rebreathing technique. We investigated whether this method would be effective in reducing the PET-aCO(2) gradient in a ventilated animal model. METHODS: Six anesthetized pigs were ventilated mechanically. End-tidal gases were systematically adjusted over a wide range of PETCO(2) (30-55 mmHg) and PETO(2) (35-500 mmHg) while employing the end-inspiratory rebreathing technique and measuring the PET-aCO(2) gradient. Duplicate arterial blood samples were taken for blood gas analysis at each set of gas tensions. RESULTS: PETCO(2) and PaCO(2) remained equal within the error of measurement at all gas tension combinations. The mean ± SD PET-aCO(2) gradient (0.13 ± 0.12 mmHg, 95% CI -0.36, 0.10) was the same (p = 0.66) as that between duplicate PaCO(2) measurements at all PETCO(2) and PETO(2) combinations (0.19 ± 0.06, 95% CI -0.32, -0.06). CONCLUSIONS: The end-inspiratory rebreathing technique is capable of reducing the PET-aCO(2) gradient sufficiently to make the noninvasive measurement of PETCO(2) a useful clinical surrogate for PaCO(2) over a wide range of PETCO(2) and PETO(2) combinations in mechanically ventilated pigs. Further studies in the presence of severe ventilation-perfusion (V/Q) mismatching will be required to identify the limitations of the method.