Volumetric Capnography Monitoring and Effects of Epinephrine on Volume of Carbon Dioxide Elimination during Resuscitation after Cardiac Arrest in a Swine Pediatric Ventricular Fibrillatory Arrest

The aim of this study was to examine the use of volumetric capnography monitoring to assess cardiopulmonary resuscitation (CPR) effectiveness by correlating it with cardiac output (CO), and to evaluate the effect of epinephrine boluses on both end-tidal carbon dioxide (EtCO2) and the volume of CO2 elimination (VCO2) in a swine ventricular fibrillation cardiac arrest model. Planned secondary analysis of data collected to investigate the use of noninvasive monitors in a pediatric swine ventricular fibrillation cardiac arrest model was performed. Twenty-eight ventricular fibrillatory arrests with open cardiac massage were conducted. During CPR, EtCO2 and VCO2 had strong correlation with CO, measured as a percentage of baseline pulmonary blood flow, with correlation coefficients of 0.83 (p < 0.001) and 0.53 (p = 0.018), respectively. However, both EtCO2 and VCO2 had weak and nonsignificant correlation with diastolic blood pressure during CPR 0.30 (p = 0.484) (95% confidence interval [CI], –0.51–0.83) and 0.25 (p = 0.566) (95% CI, –0.55–0.81), respectively. EtCO2 and VCO2 increased significantly after the first epinephrine bolus without significant change in CO. The correlations between EtCO2 and VCO2 and CO were weak 0.20 (p = 0.646) (95% CI, −0.59–0.79), and 0.27 (p = 0.543) (95% CI, −0.54–0.82) following epinephrine boluses. Continuous EtCO2 and VCO2 monitoring are potentially useful metrics to ensure effective CPR. However, transient epinephrine administration by boluses might confound the use of EtCO2 and VCO2 to guide chest compression.

Effect of food intake on the ventilatory response to increasing core temperature during exercise

Food intake increases metabolism and body temperature, which may in turn influence ventilatory responses. Our aim was to assess the effect of food intake on ventilatory sensitivity to rising core temperature during exercise. Nine healthy male subjects exercised on a cycle ergometer at 50% of peak oxygen uptake in sessions with and without prior food intake. Ventilatory sensitivity to rising core temperature was defined by the slopes of regression lines relating ventilatory parameters to core temperature. Mean skin temperature, mean body temperature (calculated from esophageal temperature and mean skin temperature), oxygen uptake, carbon dioxide elimination, minute ventilation, alveolar ventilation, and tidal volume (VT) were all significantly higher at baseline in sessions with food intake than without food intake. During exercise, esophageal temperature, mean skin temperature, mean body temperature, carbon dioxide elimination, and end-tidal CO2 pressure were all significantly higher in sessions with food intake than without it. By contrast, ventilatory parameters did not differ between sessions with and without food intake, with the exception of VT during the first 5 min of exercise. The ventilatory sensitivities to rising core temperature also did not differ, with the exception of an early transient effect on VT. Food intake increases body temperature before and during exercise. Other than during the first 5 min of exercise, food intake does not affect ventilatory parameters during exercise, despite elevation of both body temperature and metabolism. Thus, with the exception of an early transient effect on VT, ventilatory sensitivity to rising core temperature is not affected by food intake.

Exercise physiology in pulmonary hypertension patients with and without congenital heart disease

Background Cardiopulmonary exercise testing allows the assessment of integrative cardiopulmonary response to exercise. Aims The aim of the study was to better understand the exercise physiology in pulmonary arterial hypertension related to adult congenital heart disease compared to non-adult congenital heart disease patients by means of cardiopulmonary exercise testing parameters. Methods The present is a multicentre retrospective study which includes pulmonary hypertension group 1 and group 4 patients. All subjects underwent full clinical and instrumental evaluation, including cardiopulmonary exercise testing and right heart catheterization. Results One hundred and sixty-seven pulmonary hypertension patients (93 women and 74 men, 57 adult congenital heart disease and 110 non-adult congenital heart disease) were enrolled. Adult congenital heart disease patients had higher pulmonary pressure (mean pulmonary arterial pressure: 59.8 ± 19.5 mmHg vs 44.6 ± 16.5 mmHg, p < 0.001) and lower pulmonary blood flow (pulmonary blood flow: 3.3 (2.1–4.3) l/min vs 4.5 (3.8–5.4) l/min, p < 0.001). At cardiopulmonary exercise testing they had lower peak oxygen uptake/kg (12.8 ± 3.8 ml/kg/min vs 15.5 ± 4.2 ml/kg/min, p < 0.001) and higher ventilation/carbon dioxide elimination slope (53.2 (43.3–64.8) vs 44.0 (34.6–51.6), p < 0.001). When patients were paired for gender and peak oxygen uptake ( ± 1 ml/kg/min), obtaining 44 pairs, adult congenital heart disease patients had higher pulmonary pressure (mean pulmonary arterial pressure: 58.4 ± 20.2 mmHg vs 42.8 ± 16.8 mmHg, p < 0.001) and ventilation/carbon dioxide elimination slope (51.2 (43.4–63.6) vs 44.9 (35.4–55.1), p = 0.033). Conclusions In pulmonary arterial hypertension-adult congenital heart disease patients, pulmonary pressure and ventilation/carbon dioxide elimination slope are higher compared to non-adult congenital heart disease pulmonary hypertension patients, while pulmonary blood flow and peak oxygen uptake are lower. After matching patients for gender and peak oxygen uptake, pulmonary pressure and ventilation/carbon dioxide elimination remain higher in adult congenital heart disease patients suggesting that the long-term adaptation to high pulmonary pressure, hypoxia and low pulmonary blood flow, as well as a persisting shunt has, at least partially, preserved exercise performance of pulmonary arterial hypertension-adult congenital heart disease patients.