TRACHEOMOTOR RESPONSE TO CARDIOPULMONARY BYPASS - INFLUENCE OF LUNG DEFLATION AND CARDIAC DISTENSION
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BYRICK, RJ
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UNIV TORONTO, ST MICHAELS HOSP, DIV CARDIOVASC SURG, TORONTO M5B 1W8, ONTARIO, CANADAUNIV TORONTO, ST MICHAELS HOSP, DIV CARDIOVASC SURG, TORONTO M5B 1W8, ONTARIO, CANADA
BYRICK, RJ
[1
]
YCAS, JO
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UNIV TORONTO, ST MICHAELS HOSP, DIV CARDIOVASC SURG, TORONTO M5B 1W8, ONTARIO, CANADAUNIV TORONTO, ST MICHAELS HOSP, DIV CARDIOVASC SURG, TORONTO M5B 1W8, ONTARIO, CANADA
YCAS, JO
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]
SALERNO, TA
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UNIV TORONTO, ST MICHAELS HOSP, DIV CARDIOVASC SURG, TORONTO M5B 1W8, ONTARIO, CANADAUNIV TORONTO, ST MICHAELS HOSP, DIV CARDIOVASC SURG, TORONTO M5B 1W8, ONTARIO, CANADA
SALERNO, TA
[1
]
机构:
[1] UNIV TORONTO, ST MICHAELS HOSP, DIV CARDIOVASC SURG, TORONTO M5B 1W8, ONTARIO, CANADA
The pressure within the water-filled cuff of an endotracheal tube (PTE) was used as a measure of tracheal smooth muscle tone in 10 patients undergoing cardiopulmonary bypass (CPB). Pulmonary artery pressure (PPA) and left atrial pressure (PLA) were also monitored. Institution of CPB, with acute reduction of pulmonary blood flow and lung deflation, caused no significant change in PTE. Crystalloid cardioplegic administration without left ventricular decompression (VENT) resulted in statistically significant increases of PPA (from 1.33 .+-. 0.15 to 1.88 .+-. 0.2 kPa) (P < 0.05) and of PLA (from 1.2 .+-. 0.11 to 2.2 .+-. 0.31 kPA) (P < 0.05). Coincident with these changes a statistically significant increase in PTE (from 4.95 .+-. 0.21 to 5.24 .+-. 0.27 kPa) (P < 0.05) was detected. This increase in PTE was significantly greater than the small random variations noted in PTE prior to cardioplegic infusion with constant PLA and PPA. Thus, miminal tracheomotor constriction in response to cardioplegia administration occurred. Larger increases in PTE were noted during cardiac compression suggesting that the water-filled cuff could have detected larger increases if they had occurred. These transient changes do not reflect clinically detectable increases in airway resistance at the termination of CPB when lung ventilation is started. Neither of these 2 physiological stimuli, lung deflation or cardioplegia administration, cause clinically significant increases of large airway tone during CPB.