Hemodynamics of LeVeen Shunt Pulmonary Edema
| Autor: | Steven B. Heymsfield, Joseph D. Ansley, Layton F. Rikkers, John R. Darsee, B F Nordlinger, J T Fulenwider, G Ivey |
|---|---|
| Rok vydání: | 1981 |
| Předmět: |
Male
Peritoneovenous Shunt medicine.medical_specialty Cardiac output medicine.medical_treatment Pulmonary Edema Afterload Furosemide Internal medicine medicine Humans Pulmonary Wedge Pressure Cardiac Output Pulmonary wedge pressure business.industry Hemodynamics Ascites Stroke Volume Middle Aged Pulmonary edema medicine.disease Diuresis Peritoneovenous shunt medicine.anatomical_structure Anesthesia Circulatory system Cardiology Vascular resistance Female Vascular Resistance Surgery business Vascular Surgical Procedures Research Article medicine.drug |
| Zdroj: | Annals of Surgery. 194:189-192 |
| ISSN: | 0003-4932 |
| DOI: | 10.1097/00000658-198108000-00013 |
| Popis: | In order to characterize the circulatory changes which may lead to pulmonary edema following the surgical placement of a LeVeen peritoneovenous shunt, intraoperative hemodynamic studies were performed on five consecutive patients without clinical evidence of cardiac disease undergoing shunt insertion. Within 30 minutes after opening the peritoneovenous shunt, there was a marked increase in pulmonary capillary wedge pressure, cardiac output, and stroke work index, and a sharp decline in both pulmonary and systemic vascular resistances. In three patients, pulmonary edema did not occur; in one patient, pulmonary edema occurred transiently but responded to furosemide administration. In these four patients, systemic vascular resistance continued to drop over the ensuing hours and the elevated pulmonary capillary wedge pressure also decreased appropriately with furosemide. The fifth patient developed persistent pulmonary edema. In this subject, systemic vascular resistance continued to rise and the elevated pulmonary capillary wedge pressure did not respond to intravenous furosemide. This study suggests that uncomplicated LeVeen peritoneovenous shunt insertion may result in a drop in systemic vascular resistance which lowers left ventricular afterload, and, thus, may protect most patients from pulmonary edema. In contrast, a continued rise in systemic vascular resistance and afterload may contribute to pulmonary edema refractory to diuretic therapy and should probably be treated with a parenteral afterload-reducing agent. |
| Databáze: | OpenAIRE |
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