Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To examine whether CPB influences pulmonary vascular sensitivity to CO2, we compared the effect of slight induced hypocarbia and hypercarbia on pulmonary circulation before and after CPB in ten mechanically ventilated patients undergoing CABG. Hypocarbia was produced by increasing tidal volume slightly and hypercarbia was then induced by adding CO2 to the inspired gas mixture. In another ten patients, hypercarbia was produced after CPB by decreasing ventilator rate and the cardiopulmonary responses to hypercarbia, produced by the two methods of CO2 elevation, were compared. Slight respiratory acidosis induced by CO2 inhalation did not change PVR before CPB but effected a 50 percent increase after CPB. Hypercarbia induced by alveolar hypoventilation after CPB increased PVR by 40 percent. During the increased CO2 production after hypothermic CPB, pulmonary vasoconstriction would be expected to occur and impair right ventricular performance. Therefore, tight control of PaCO2 with appropriate adjustment of ventilatory support is mandatory.
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PMID:Pulmonary vascular resistance before and after cardiopulmonary bypass. The effect of PaCO2. 249 21

Forty-eight hour old anesthetised and ventilated neonatal piglets were cannulated in order to measure pressure, blood gases and cardiac outputs (CO) from which pulmonary (PVR) and systemic (SVR) vascular resistances were calculated. After baseline measurements had been made inspired gases were altered to produce hypoxemia and hypercapnia, to raise PVR. Animals then received Prostaglandin E1 (PGE1), Tolazoline (TOL), and Prostacyclin (PGI2) in varying dosages until PVR was reduced or the dosage no longer tolerated. With "hypoxia" CO, PVR and pulmonary artery (PA) pressures rose; aortic pressure also rose although SVR tended to fall. PGE1 (5microgram/kg/min) and PGI2 (1.0 microgram/kg/min) both produced a significant fall in PVR. The decrease in PVR with TOL (1 mg/kg/10 minutes and 2 mg/kg/1 hour) was less consistent and in surviving animals did not achieve statistical significance by multivariate analysis. SVR fell with all drugs although the change with TOL was again non-significant. With both PGI2 and TOL there was a trend for CO to rise and, although this did not reach significant levels, it restricted the drop in arterial pressure to approximately control levels. The fall in arterial pressure with PGE1 was greater. The death rate with treatment with TOL was much higher than that seen with the other two drugs. Circulatory changes in a group of animals with normal blood gases treated with PGI2 (1 microgram/kg/min) were similar to those seen with the hypoxic group.
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PMID:Comparative studies on the hemodynamic effects of prostaglandin E1 prostacyclin, and tolazoline upon elevated pulmonary vascular resistance in neonatal swine. 703 18

The purpose of this observational study was to determine whether hypercarbia or oxygen desaturation occurred during our current regimens of deep sedation or general anaesthesia of infants and children undergoing cardiac catheterization. Data were gathered prospectively from 50 consecutive infants and children aged 4 months to 12 years undergoing cardiac catheterization. Several anaesthetists used the following regimens, which were not randomized: 1) propofol. 1.5-2.0 mg.kg-1 and fentanyl 1 microgram.kg-1 IV over 2 min for induction, followed by propofol infusion of 100-150 micrograms.kg-1.min-1; 2) fentanyl 2-3 micrograms.kg-1 and midazolam 0.1-0.2 mg.kg-1 IV over 10-15 min; 3) ketamine 8 mg.kg-1 IM, or 4) same as regimens 1 or 2, plus pancuronium, intubation and controlled ventilation. Regimens 1, 2, and 3 were associated with spontaneous ventilation through the natural airway. End-tidal carbon dioxide tension (PetCO2), SpO2, and respiratory rate were monitored for 60 min. The three regimens employing spontaneous ventilation through the natural airway were associated with both statistically and clinically significant increases in PetCO2 and decreases in SpO2. This raises the possibility that acute exacerbation of PAP and PVR may occur in pulmonary hypertensive patients. In contrast, PetCO2 and SpO2 did not change significantly from baseline in the controlled ventilation group.
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PMID:Changes in carbon dioxide tension and oxygen saturation during deep sedation for paediatric cardiac catheterization. 883 83