The impact of fatigue on the non-technical skills performance of critical care air ambulance clinicians.

BACKGROUND: The relationship between fatigue-related risk and impaired clinical performance is not entirely clear. Non-technical factors represent an important component of clinical performance and may be sensitive to the effects of fatigue. The hypothesis was that the sum score of overall non-technical performance is degraded by fatigue. METHODS: Nineteen physicians undertook two different simulated air ambulance missions, once when rested, and once when fatigued (randomised crossover design). Trained assessors blinded to participants' fatigue status performed detailed structured assessments based on expected behaviours in four non-technical skills domains: teamwork, situational awareness, task management, and decision making. Participants also provided self-ratings of their performance. The primary endpoint was the sum score of overall non-technical performance. RESULTS: The main finding, the overall non-technical skills performance rating of the clinicians, was better in rested than fatigued states (mean difference with 95% CI, 2.8 [2.2-3.4]). The findings remained consistent across individual non-technical skills domains; also when controlling for an order effect and examining the impact of a number of possible covariates. There was no difference in self-ratings of clinical performance between rested and fatigued states. CONCLUSION: Non-technical performance of critical care air transfer clinicians is degraded when they are fatigued. Fatigued clinicians may fail to recognise the degree to which their performance is compromised. These findings represent risk to clinical care quality and patient safety in the dynamic and isolated environment of air ambulance transfer.

Metabolic responses in ischemic myocardium after inhalation of carbon monoxide.

BACKGROUND: To clarify the mechanisms of carbon monoxide (CO) tissue-protective effects, we studied energy metabolism in an animal model of acute coronary occlusion and pre-treatment with CO. METHODS: In anesthetized pigs, a coronary snare and microdialysis probes were placed. CO (carboxyhemoglobin 5%) was inhaled for 200 min in test animals, followed by 40 min of coronary occlusion. Microdialysate was analyzed for lactate and glucose, and myocardial tissue samples were analyzed for adenosine tri-phosphate, adenosine di-phosphate, and adenosine mono-phosphate. RESULTS: Lactate during coronary occlusion was approximately half as high in CO pre-treated animals and glucose levels decreased to a much lesser degree during ischemia. Energy charge was no different between groups. CONCLUSIONS: CO in the low-doses tested in this model results in a more favorable energy metabolic condition in that glycolysis is decreased in spite of maintained energy charge. Further work is warranted to clarify the possible mechanistic role of energy metabolism for CO protection.

Contributions of myocardial ischemia and heart rate to ST segment changes in patients with or without coronary artery disease.

BACKGROUND: ST changes related to ischemia at different heart rates (HRs) have not been well described. We aimed to analyze ST dynamic changes by vectorcardiography (VCG) during pacing-induced HR changes for subjects with proven coronary artery disease (CAD) and without (non-CAD). METHODS: Symptomatic CAD patients scheduled for elective surgery were enrolled along with a non-CAD group. During anesthesia, both groups were placed at multiple ascending levels. VCG ST data, and in particular in ST change vector magnitude (STC-VM) from baseline, along with arterial and great coronary artery vein (GCV) blood samples were collected to determine regional myocardial lactate production. RESULTS: A total of 35 CAD and 10 non-CAD patients were studied over six incremental 10 beat/min HR increases. STC-VM mean levels increased in the CAD group from 9+/-5 to 131+/-37 microV (standard deviation) compared with non-CAD subjects with 8+/-3-76+/-34 microV. Myocardial ischemia (lactate production) was noted at higher HRs and the positive predictive value for STC-VM to detect ischemia was 58% with the negative predictive value being 88%. STC-VM at 54 microV showed a sensitivity of 88% and a specificity of 75% for identification of ischemia. CONCLUSIONS: Both HR and ischemia at higher HRs contribute to VCG ST elevation. Established ST ischemia detection concerning HR levels is suboptimal, and further attention to the effects of HR on ST segments is needed to improve electrocardiographic ischemia criteria.

Beat-to-beat change in "myocardial performance index" related to load.

BACKGROUND: This study was designed to assess the relationship of the "myocardial performance index" (MPI) to the beat-by-beat change in pre-load with static or unchanged contractile status. METHODS: Eight anesthetized juvenile pigs were studied using direct measurement of the left ventricular pressure and volume. Transient inflation of a vena cava balloon catheter produced controlled pre-load alterations. Consecutive beats were analyzed, grouped for first, second, third, etc. during the pre-load alteration, and evaluated for the change in MPI during the same contractile status with a controlled pre-load alteration. Two pharmacologic inotropic interventions were also included to generate several myocardial conditions in each animal. RESULTS: MPI demonstrated a strong linear relationship to the pre-load and after-load. MPI increased progressively during decreasing end-diastolic volume, mostly related to changes in ejection time. MPI was observed at the same level for three different myocardial function conditions (all eight animals), with a different relationship between MPI and pre-load noted for each observation. CONCLUSIONS: MPI is strongly load dependent, and can vary widely in value for the same contractile status if the load is varied. The use of this index in critically ill patients should be limited in this respect. Further work is needed to establish the relationship of MPI to load and contractile status.

Streptozotocin induced diabetes in minipig: a case report of a possible model for type 1 diabetes?

Studies on the pathogenic process in type 1 diabetes are often performed in animal models. Low-dose administration of streptozotocin has been used to induce diabetes with pathological alterations similar to human type 1 diabetes in the animals. Rodent models are frequently used but there is a need of developing new models including larger animals. In this study we wanted to investigate to what extent a minipig was sensitive to low-dose streptozotocin for induction of diabetes with features of human Type I diabetes. A female Göttingen minipig received two low-doses (40 mg/kg) of streptozotocin with an 11-day interval. Serum was analysed for the presence of the enzyme glutamic acid decarboxylase, isoform 65, (GAD65) and autoantibodies against glutamic acid decarboxylase, isoform 65 (GAD65A), isoform 67 (GAD67A), insulinoma antigen 2 (IA-2) and insulin (IAA). Pancreas tissue was fixated in formaldehyde and was sent for pathoanatomical examination. The minipig became hyperglycaemic after the second injection of streptozotocin. The pathoanatomical examination showed atrophy of the beta-cell population, depletion of insulin with preserved glucagon content. There was no sign of insulitis. Both GAD65 and GAD65A were detected while GAD67A and IAA were absent. It is concluded that chronic diabetes developed after low-dose streptozotocin injection in a female minipig with the characteristics of the end stage of type 1 diabetes. This pilot study suggests that minipigs show promise as a model to induce diabetes by injections of low-dose streptozotocin.

Analysis of left ventricular systolic function during elevated external cardiac pressures: an examination of measured transmural left ventricular pressure during pressure-volume analysis.

BACKGROUND: Variations or disturbances in intrathoracic and extracardiac pressures (ECP) occur in critically ill and anaesthetised patients. There are uncertainties concerning the analysis of left ventricular pressure-volume relationship (LVPVR) and the calculation of systolic function parameters when conducted without reference to transmural left ventricular pressure (LVPtm) in the setting of elevated ECP. METHODS: In 7 anaesthetised adult pigs, we measured LVPVR using conductance volumetry and tip manometry along with measurement of pericardial and other intrathoracic pressures. Experimental pericardial infusion and pleural insufflation were performed. Transient controlled preload reductions were accomplished using balloon occlusion of the inferior vena cava. Preload recruitable stroke work (PRSW) was calculated using both intracavitary left ventricular pressure (LVPic) and LVPtm, and differences were tested for using a paired t-test. RESULTS: The pericardial and pleural interventions produced significant elevations in ECP. No difference in PRSW calculated using LVPic and LVPtm was detected. CONCLUSION: These results suggest that LVPtm need not be measured and included in LVPVR analysis of systolic function when there is significant external cardiac pressure. To be able to employ LVPVR analysis of systolic function without reference to LVPtm is important for simplified application in the clinical setting, particularly when elevated extracardiac pressures are suspected, or have been therapeutically induced, as with continuous positive pressure ventilation.

Heart-lung interactions during positive pressure ventilation: left ventricular pressure-volume momentary response to airway pressure elevation.

BACKGROUND: Left ventricular (LV) pressure and volume changes are known to occur in response to positive airway pressure (PAP). We aimed to further describe the immediate LV response to increased PAP as demonstrated in successive heart cycles with LV pressure and volume alterations. We postulated that these acute systematic LV events during institution of PAP can follow a distinct pattern that would allow calculation of parameters of systolic function, including end-systolic elastance (Ees) and preload recruitable stroke work (PRSW). We also aimed to examine the relationship of PAP-derived Ees and PRSW to the same parameters derived from vascular occlusion. METHODS: Eight anesthetized adult pigs were studied with invasive circulatory measurements including LV pressure and volume (conductance). The PAP intervention was an airway pressure plateau of 15 cm H2O for 6 s (APP). Venous occlusion was performed by transient balloon inflation in the inferior vena cava (IVCO). Ees and PRSW were derived for each APP and IVCO intervention. RESULTS: Central circulatory variables during APP and IVCO are reported. LV systolic function parameters could be derived from each of the heart-lung interactions during APP sequences. Ees and PRSW derived from APP showed a significant positive bias in relation to those derived from the IVCO sequence. CONCLUSIONS: We conclude that the heart-lung interactions during APP of the magnitude and duration shown here can allow derivation of Ees and PRSW. These parameters are not interchangeable with Ees and PRSW derived from IVCO.

Improvement in mitral regurgitation after aortic valve replacement.

This study sought to determine whether there is a quantitative improvement in mitral regurgitation (MR) after aortic valve replacement (AVR) for aortic stenosis (AS) and, if so, the mechanisms for this change. MR frequently accompanies AS. The addition of mitral valve replacement to AVR significantly increases the risk of surgery. Although previous studies have suggested a qualitative improvement in MR severity after AVR, semiquantitative analysis of this improvement has not been documented nor have the underlying mechanisms been examined. We evaluated 28 patients who had undergone 2-dimensional echo and color flow Doppler imaging an average of 1.5 +/- 2.5 months before and 2.5 +/- 4.2 months after AVR. Maximum MR area, MR percentage (MR area/left atrial area), mitral annular area, left atrial area, aortic gradient, and parameters of left ventricular geometry were measured to evaluate MR severity and to assess functional mechanisms for improvement in MR. There was a significant decrease in MR area (5.5 +/- 2.8 cm2 vs 2.5 +/- 1.9 cm2, p < or =0.0001) and MR percentage (25 +/- 11% vs 12 +/- 10% after operation, p < or =0.0001) between preoperative and postoperative studies. There was a significant reduction in aortic gradient, mitral annular area, left atrial area, and left ventricular length postoperatively. In univariate analysis, MR improvement was related to the lower preoperative left ventricular fractional area change (p = 0.027) and to the changes in fractional area change (p = 0.001) and left ventricular systolic area (p = 0.001). Thus, improvement in MR after AVR is related to changes in left ventricular function postoperatively. These data suggest that reduction in MR is due not only to decreased intraventricular pressure, but also to changes in ventricular morphology.

Systemic embolization complicating right ventricular myocardial infarction.

We describe a patient in whom multiple episodes of pulmonary and systemic embolization occurred in the setting of right ventricular infarction. The mechanism of paradoxical embolization was determined based on transesophageal echocardiographic findings that included right atrial spontaneous contrast, appendage thrombosis, patent foramen ovale with right-to-left atrial shunting, and absence of left ventricular thrombosis. Recurrent thromboembolization was prevented by percutaneous placement of a "clam-shell" occluder across the patent foramen. This clinical scenario may be more common than previously believed and is best detected with transesophageal echocardiography. Early identification of this condition can lead to prompt treatment and prevention of subsequent thromboembolic morbidity.