The effects of inhaled nitric oxide on pulmonary vascular resistance in patients after total cavopulmonary connection.
- Author:
Zong-tao YIN
1
;
Hong-yu ZHU
;
Ren-fu ZHANG
;
Nan-bin ZHANG
;
Zeng-wei WANG
;
Han-dong GONG
;
Jun WANG
;
Heng-chang SONG
Author Information
- Publication Type:Journal Article
- MeSH: Administration, Inhalation; Adolescent; Adult; Arteriovenous Shunt, Surgical; methods; Cardiac Output; drug effects; Child; Child, Preschool; Female; Humans; Male; Nitric Oxide; administration & dosage; therapeutic use; Postoperative Period; Pulmonary Artery; physiology; surgery; Time Factors; Vascular Resistance; drug effects; Vasodilator Agents; administration & dosage; therapeutic use; Venae Cavae; surgery
- From: Chinese Journal of Surgery 2005;43(10):647-649
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the effects of inhaled nitric oxide (NO) on pulmonary vascular resistance in patients after total cavopulmonary connection (TCPC).
METHODSFifty-two patients after TCPC were evaluated, of them 24 patients were administered with inhaled nitric oxide in the early postoperative period. The cardiac index (CI) and pulmonary vascular resistance (PVR) were compared before and after inhaled NO.
RESULTSIn experimental group, after inhaled NO, partial pressure of oxygen in artery/fraction of inspired oxygen increased from 161 +/- 17 to 193 +/- 23 (t = 2.75, P < 0.01); CI from (2.86 +/- 0.24) L.min(-1).m(-2) to (3.13 +/- 0.22) L.min(-1).m(-2) (t = 2.25, P < 0.05); PVR decreased from (4.2 +/- 0.5) U/m(2) to (3.8 +/- 1.4) U/m(2) (t = 2.29, P < 0.05); central venous pressure (CVP) from (17.0 +/- 1.8) mm Hg to (15.0 +/- 1.1) mm Hg, decreased 11.7%. Compared with the control group, respirator time decreased from (86 +/- 27) h to (54 +/- 18) h (t = 2.29, P < 0.05); ICU time from (6 +/- 2) d to (4 +/- 2) d (t = 2.32, P < 0.05); But hydrothorax drainage and length of stay had no significant difference.
CONCLUSIONSThough inhaled NO, there is no significant long-term effects in patients after TCPC, but it may play an important role in the management of low cardiac output syndrome and high cava pressure caused by reactive elevated pulmonary vascular resistance in the early postoperative period of TCPC.
