INHALED NITRIC-OXIDE REVERSES THE INCREASE IN PULMONARY VASCULAR-RESISTANCE INDUCED BY PERMISSIVE HYPERCAPNIA IN PATIENTS WITH ACUTE RESPIRATORY-DISTRESS SYNDROME

被引:145
作者
PUYBASSET, L [1 ]
STEWART, T [1 ]
ROUBY, JJ [1 ]
CLUZEL, P [1 ]
MOURGEON, E [1 ]
BELIN, MF [1 ]
ARTHAUD, M [1 ]
LANDAULT, C [1 ]
VIARS, P [1 ]
机构
[1] HOP LA PITIE SALPETRIERE,DEPT ANESTHESIE,F-75013 PARIS,FRANCE
关键词
ANESTHETIC TECHNIQUES; MECHANICAL VENTILATION; ANESTHETICS; GASES; NITRIC OXIDE; CARBON DIOXIDE; PERMISSIVE HYPERCAPNIA; LUNG(S); ACUTE RESPIRATORY DISTRESS SYNDROME;
D O I
10.1097/00000542-199406000-00013
中图分类号
R614 [麻醉学];
学科分类号
100217 ;
摘要
Background: The aim of this prospective study was to determine if inhaled nitric oxide (NO) would reverse the increase in pulmonary arterial pressures and in pulmonary vascular resistance induced by acute permissive hypercapnia in patients with acute respiratory distress syndrome. Methods: In 11 critically ill patients (mean age 59 +/- 22 yr) with acute respiratory distress syndrome (Murray Score greater than or equal to 2.5), the lungs were mechanically ventilated with NO 2 ppm during both normocapnic and hypercapnic conditions. Four phases were studied: normocapnia (arterial carbon dioxide tension 38 +/- 6 mmHg, tidal volume 655 +/- 132 ml); normocapnia plus inhaled NO 2 ppm; hypercapnia (arterial carbon dioxide tension 65 +/- 15 mmHg, tidal volume 330 +/- 93 ml); and hypercapnia plus inhaled NO 2 ppm. Continuous recordings were made of heart rate, arterial pressure, pulmonary artery pressure, tracheal pressure, and tidal volume (by pneumotachograph). At the end of each condition, arterial pressure, pulmonary artery pressure, cardiac filling pressures, and cardiac output were measured. Simultaneous arterial and mixed venous blood samples were obtained to measure arterial oxygen tension, arterial carbon dioxide tension, mixed venous oxygen tension, arterial hemoglobin oxygen saturation, mixed venous hemoglobin oxygen saturation, pH, and blood hemoglobin and methemoglobin concentrations (by hemoximeter). In addition, plasma concentrations of catecholamines were measured with a radioenzymatic assay. In 5 patients, end-tidal carbon dioxide tension was measured with a nonaspirative infrared capnometer. Calculations were made of pulmonary vascular resistance index, systemic vascular resistance index, true pulmonary shunt, and alveolar dead space. Results: During hypercapnia, NO decreased pulmonary vascular resistance index from 525 +/- 223 to 393 +/- 142 dyn . s . cm(-5) m(-2) (P < 0.01), a value similar to that measured in normocapnic conditions (391 +/- 122 dyn . s . cm(-5) m(-2)). It also reduced mean pulmonary artery pressure from 40 +/- 9 to 35 +/- 8 mmHg (P < 0.01). NO increased arterial oxygen tension (inspired oxygen fraction 1) from 184 +/- 67 to 270 +/- 87 mmHg during normocapnia and from 189 +/- 73 to 258 +/- 101 mmHg during hypercapnia (P < 0.01). NO decreased true pulmonary shunt during normocapnia (from 34 +/- 3% to 28 +/- 4%, P < 0.001) but had no significant effect on it during hypercapnia (39 +/- 7% vs. 38 +/- 8.5%). In five patients, NO resulted in a decrease in alveolar dead space from 34 +/- 7% to 28 +/- 10% in normocapnic conditions and from 30 +/- 3% to 22 +/- 10% in hypercapnic conditions (P < 0.05). Conclusions: Inhaled NO completely reversed the increase in pulmonary vascular resistance index induced by acute permissive hypercapnia, It only partially reduced the pulmonary hypertension induced by acute permissive hypercapnia, probably because the flow component of the increase in pulmonary pressure (i.e., the increase in cardiac output) was not reduced by inhaled NO. A significant increase in arterial oxygenation after NO administration was observed during normocapnic and hypercapnic conditions. A ventilation strategy combining permissive hypercapnia and inhaled NO may reduce the potentially deleterious effects that permissive hypercapnia alone has on lung parenchyma and pulmonary circulation.
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收藏
页码:1254 / 1267
页数:14
相关论文
共 49 条
[1]   EFFECT OF HYPERCAPNIA AND HYPOCAPNIA ON MYOCARDIAL BLOOD-FLOW AND PERFORMANCE IN ANESTHETIZED DOGS [J].
ALEXANDER, CS ;
LIU, SM .
CARDIOVASCULAR RESEARCH, 1976, 10 (03) :341-348
[2]   EFFECT OF ACUTE RESPIRATORY AND METABOLIC ACIDOSIS ON CARDIAC OUTPUT AND PERIPHERAL RESISTANCE [J].
ANDERSEN, MN ;
MOURITZE.C .
ANNALS OF SURGERY, 1966, 163 (02) :161-&
[3]   ACTION OF CARBON-DIOXIDE ON HYPOXIC PULMONARY VASOCONSTRICTION IN THE RAT LUNG - EVIDENCE AGAINST SPECIFIC ENDOTHELIUM-DERIVED RELAXING FACTOR-MEDIATED VASODILATION [J].
BAUDOUIN, SV ;
EVANS, TW .
CRITICAL CARE MEDICINE, 1993, 21 (05) :740-746
[4]  
BAUER MA, 1986, AM REV RESPIR DIS, V134, P1203
[5]   EFFECT OF INHALED NITRIC-OXIDE DURING GROUP-B STREPTOCOCCAL SEPSIS IN PIGLETS [J].
BERGER, JI ;
GIBSON, RL ;
REDDING, GJ ;
STANDAERT, TA ;
CLARKE, WR ;
TRUOG, WE .
AMERICAN REVIEW OF RESPIRATORY DISEASE, 1993, 147 (05) :1080-1086
[6]   EFFECTS OF UNILATERAL HYPOXIA AND HYPERCAPNIA ON PULMONARY BLOOD FLOW DISTRIBUTION IN THE DOG [J].
BORST, HG ;
WHITTENBERGER, JL ;
BERGLUND, E ;
MCGREGOR, M .
AMERICAN JOURNAL OF PHYSIOLOGY, 1957, 191 (03) :446-452
[7]   INCREASED CARDIAC-OUTPUT INCREASES SHUNT - ROLE OF PULMONARY-EDEMA AND PERFUSION [J].
BREEN, PH ;
SCHUMACKER, PT ;
SANDOVAL, J ;
MAYERS, I ;
OPPENHEIMER, L ;
WOOD, LDH .
JOURNAL OF APPLIED PHYSIOLOGY, 1985, 59 (04) :1313-1321
[8]  
BRYAN CL, 1988, CLIN CHEST MED, V9, P141
[9]   DISTENSIBILITY AND PRESSURE-FLOW RELATIONSHIP OF THE PULMONARY CIRCULATION .2. MULTIBRANCHED MODEL [J].
BSHOUTY, Z ;
YOUNES, M .
JOURNAL OF APPLIED PHYSIOLOGY, 1990, 68 (04) :1514-1527
[10]   NO BANDWAGON, YET - INHALED NITRIC-OXIDE (NO) FOR NEONATAL PULMONARY-HYPERTENSION [J].
DAVIDSON, D .
AMERICAN REVIEW OF RESPIRATORY DISEASE, 1993, 147 (05) :1078-1079