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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Artifacts or mechanical problems may cause data which suggest poor myocardial performance during emergence from cardiopulmonary bypass (CPB). Transducer and monitoring equipment malfunctions, damping of the arterial blood pressure tracing, effects of drugs, hypercarbia, inordinately high intrathoracic pressure, cardiac tamponade, and others are all possible culprits. It is important to have a systematic plan for evaluating and interpreting the signs and data that are evident. Causes of hypotension after CPB include low hematocrit, hypercarbia, sympathetic inhibition, vasodilator action, anaphylaxis or anaphylactoid reactions, protamine reactions, and impaired myocardial performance. Impaired myocardial performance can be attributable to rate and rhythm disturbances, inadequate ventricular preload, inappropriately elevated right and left ventricular afterload, and decreased myocardial contractility. Common causes of hypoxemia include a malfunctioning ventilator system, pulmonary problems such as atelectasis and shunt, anemia, and inordinately high utilization of oxygen.
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PMID:The anesthesiologist's response to a low-output state after cardiopulmonary bypass: etiologies and remedies. 213 54

The hemodynamic effects of changes in PaCO2 during intermittent positive pressure ventilation (IPPV) were studied in nine dogs with acute cardiac tamponade. During steady state light thiopental anesthesia, measurements were performed during hypocarbia (24.0 +/- 2.6), normocarbia (40.4 +/- 2.4), and hypercarbia (56.8 +/- 3.1 mm Hg; mean +/- SD). The study was carried out at a standardized level of cardiac tamponade that gave a 60% reduction in cardiac output (CO) at normocarbia. Changes in airway pressure were avoided by adding CO2 to the inspiratory gas to obtain the desired PaCO2. Hypercarbia increased pericardial pressure 2-4 mm Hg and significantly decreased CO. During hypocarbia CO increased as pericardial pressure decreased 3-6 mm Hg. These findings are the reverse of changes seen when tamponade is not present. The changes in pericardial pressure most likely influence myocardial tone and cardiac volume and, thus, CO. The results suggest that patients with cardiac tamponade requiring general anesthesia should not breathe spontaneously if there is any danger of respiratory depression and hypercarbia.
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PMID:Effects of hypo-, normo-, and hypercarbia in dogs with acute cardiac tamponade. 640 55

Recent reports have suggested that increases in venoarterial difference in PCO2 (VAPCO2) and arteriovenous difference in pH (AVpH) represent valuable markers of tissue hypoxia in shock states associated with low cardiac output. We compared the values of VAPCO2 and AVpH with that of blood lactate in their relationship to changes in O2 uptake (VO2) and O2 delivery (DO2) during an acute reduction in blood flow induced by cardiac tamponade. In 13 anesthetized and mechanically ventilated dogs, a catheter was inserted into the pericardium to inject saline and to measure the intrapericardial pressure. VO2 was derived from expired gas analysis. DO2 was calculated by the product of the thermodilution cardiac index and the arterial O2 content. The critical DO2 (DO2crit) was found at 9.9 +/- 1.8 ml/kg.min. VAPCO2 and AVpH, which were 7.1 +/- 4.6 mm Hg and 0.028 +/- 0.025 U, respectively, at baseline, progressively increased to reach 17.5 +/- 6.6 mm Hg and 0.114 +/- 0.054 U, respectively, at DO2crit (both p < 0.01). Below DO2crit they increased more dramatically. These changes were related to both arterial hypocapnia and mixed venous hypercapnia. CO2 excretion decreased from 5.8 +/- 2.0 ml/kg-min at baseline to 3.9 +/- 0.9 ml/kg.min at DO2crit (p < 0.01). End-tidal CO2 tension significantly fell below DO2crit. Lactate levels increased from 2.1 +/- 0.5 to 3.5 +/- 0.5 mmol/L at DO2crit (P < 0.01) and to 6.9 +/- 2.1 mmol/L (p < 0.01) at the end of the study. There was no statistically significant difference between the DO2crit calculated for VAPCO2, AVpH, lactate, or VO2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Arteriovenous differences in PCO2 and pH are good indicators of critical hypoperfusion. 821 40