Determinants of Aortic Pressure Variation During Positive-Pressure Ventilation in Man
To define the relation between systolic arterial pressure (SAP) changes during ventilation and left ventricular (LV) performance in humans. Prospective repeat-measures series. University of Pittsburgh Medical Center Operating Room. Fifteen anesthetized cardiac surgery patients before and after cardi...
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Published in | Chest Vol. 116; no. 1; pp. 176 - 186 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
Northbrook, IL
Elsevier Inc
01.07.1999
American College of Chest Physicians |
Subjects | |
Online Access | Get full text |
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Summary: | To define the relation between systolic arterial pressure (SAP) changes during ventilation and left ventricular (LV) performance in humans.
Prospective repeat-measures series.
University of Pittsburgh Medical Center Operating Room.
Fifteen anesthetized cardiac surgery patients before and after cardiopulmonary bypass when the mediastinum was either closed or open.
Positive-pressure ventilation.
SAP and LV midaxis cross-sectional areas were measured during apnea and then were measured for three consecutive breaths. SAP increased during inspiration, this being the greatest during closed chest conditions (p < 0.05). Changes in SAP could not be correlated with changes in either LV end-diastolic areas (EDAs), end-systolic areas, or stroke areas (SAs). If SAP decreased relative to apnea, the decrease occurred during expiration and was often associated with increasing LV EDAs and SAs. SAP often decreased after a positive-pressure breath, but the decrease was unrelated to SA deficits during the breath. Increases in SAP were in phase with increases in airway pressure, whereas decreases in SAP, if present, followed inspiration. No consistent relation between SAP variation and LV area could be identified.
In this patient group, changes in SAP reflect changes in airway pressure and (by inference) intrathoracic pressure (as in a Valsalva maneuver) better than they reflect concomitant changes in LV hemodynamics. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0012-3692 1931-3543 |
DOI: | 10.1378/chest.116.1.176 |