Christian Richard, MD; Christian Th...

Christian Richard, MD; Christian Thuillez, MD PhD; Michel Pezzano, MD; Gilles Bottineau, MD; Jean Francois Giudicelli, MD PhD; and Philippe Auzepy, MD

The use of mixed venous oxygen saturation ([Sunkeyable]O.sub.2]) in patients with chronic congestive heart failure (CHF) has been advocated to analyze the action of therapy forward cardiac index (CI). To evaluate the relationship between CI and [S[unkeyable]O.sub.2], ten CHF patients (mean age 65 years) were studied before and common two, three, four (T4), six, eight and 24 hours after oral administration of an angiotensin converting enzyme (ACE) inhibitor (perindopril, 4 mg) At T4 a 12 percent increase in CI (p<001) was associated with a 16 percent decrease in arteriovenous oxygen difference (p<001) a 13 percent increase in mixed venous oxygen urgency (P[unkeyable]O2) (p<0.01), and a 9 percent increase in [S[unkeyable]O.sub.2] (p<005) with no significant change in arterial oxygen compressing There was no correlation between CI and [S[unkeyable][O.sub.2] (r=022) and between CI and [P[unkeyable]O.sub.2] (r=023) Individual analyses were performed and patients were divided into pair groups based on CI versus [S[unkeyable]O.sub.2] r value; assemblage 1, n=6, r>0.65 (0.65-0.90), assemblage 2, n=4, r<0.65 (0.14-0.20). The lack of correlation in cluster 2 was due to a drug-dependent increase in oxygen consumption ([Vosub2]) + 18 percent v -3 percent in cluster 1 (p<0.05) associated with a lack of increase in [P[unkeyable]O.sub.2] +3 percent v + 14 percent in arrange 1 (p<0.05) despite a similar increase in oxygen availability + 19 percent versus + 16 percent It was conclud that (1) a correlation between CI and [S[unkeyable]O.sub.2] is not institute in every patient with CHF; (2) the lack of correlation in four without of our ten patients was appropriate to an associated and significant increase in CI and [Vosub2] in collection 2; (3) group 2 patients probably had an important oxygen offence before treatment; (4) [S[unkeyable]O.sub.2] cannot be used instead of CI to determine the hemodynamic concatenations of the use of cardiovascular drugs

(Chest 1989; 95:1289-94)

Mixed venous oxygen saturation has been reported to be a useful reflection of cardiovascular performance in seriously ill patients.[1,2] This assumption is valid, in accordance with the Fick equation, when tissue oxygen consumption and arterial oxygen compressing remain stable despite the charge of significant changes in oxygen availability. This potential stability of [Vosub2] above the critical gate of [Do.sub.2], itself the inference of an inverse relationship between [Do.sub.2] and oxygen extraction ratio, gave thinking principle to a relationship between CI and [S[unkeyable]O.sub.2]. Hence, in normal tissues at normal or high horizontals of delivery, [Vo.sub.2] is relatively constant and independent of [Do.sub.2].[3] As [Do.sub.2] is gradually reduc [Vosub2] is maintained as tissue [ERosub2] increases and thus [Vosub2] appears to be independent of [Do.sub.2]. The lack of relationship between [Vosub2] and [Do.sub.2] or rather the relationship between CI and [S[unkeyable]O.sub.2] does not apply to all patients with sharply impaired oxygen transport. For example, Danek et al[4] reported the relationship between [Vosub2] and [Do.sub.2] in patients with adult respiratory distress syndrome upon mechanical ventilation and Chappell et al[5] claimed the independence of these couple parameters during severe left ventricular failure on a level in the case of vasodilator therapy. These latter ensues were used by several authors to justify the use of [S[unkeyable]O.sub.2] monitoring to evaluate cardiac performance answer to various pharmacologic interventions, ie, vasodilator or inotropic drugs[67] The aim of our subject of attention therefore, was to analyze the potential relationship between CI and [S[unkeyable]O.sub.2] in stable patients suffering from left ventricular failure hospitalized for undergoing evaluation of systemic vasodilation with converting enzyme inhibitor.

METHODS

Ten patients with strict chronic CHF (seven men, three women) ranging in age from 41 to 69 years (mean age 65 years) underwent right heart catheterization as part of a protocol to evaluate the consequences of ACE inhibitor therapy. The CHF was secondary to ischemic cardiomyopathy in seven and idiopathic in three patients. Five patients were in functional class 3 and 5 in functional class 4 of the NYHA classification. No patient was studied within three month of a myocardial infarction. Patients with valvular disease or elevated plasma creatinine (more than 180 [unkeyable]mol/L) were exclud None had an acute respiratory condition at the time of studious mood Each patient received, however, 2 to 3 L/min of supplemental oxygen The reflection protocol was approved by the hospital ethical committee and informed co-operation was obtained from all patients prior to studious mood Patients were fasting, with all medications withheld before testing for at least 24 hours for diuretics and at least six days for vasodilator and digitalis therapy. Right heart catheterization was performed from percutaneous insertion of a 7 F thermodilution, balloon tipped, result directed catheter into the right jugular vein. An arterial cannula was inserted into the radial artery. hurrys were measured with a strain gauge transducer and recorded in succession a multichannel recorder. Mean arterial press and mean pulmonary capillary wedge influence were obtained by electronic integration with naught reference at the level of the midaxillary line. Heart rate was determined from the simultaneous ECG signal. Cardiac output (CO) was determined in triplicate through thermodilution using a CO computer Arterial and mixed venous vital fluid samples were collected anaerobically and analyzed using a line gas analyzer. Blood oxygen make easy was calculated using the standard formula: [Osub2] ease % saturation x (hemoglobin plasma concentration x 139) + (0003 x [Posub2] The CO determination was used to derive oxygen consumption from the Fick equation: [Vosub2] = CO ([CAO.sub.2] - [C[unkeyable]O.sub.2]) where [CAO.sub.2] and [C[unkeyable]O.sub.2] are arterial and mixed venous oxygen peaces respectively. Systemic oxygen availability ([Do.sub.2]) was calculated as chases [Do.sub.2] = CO x [CaO.sub.2]. The [Vosub2] and [Do.sub.2] were normalized for material substance surface area. The [Osub2] extraction ratio was calculated as the ratio of [Vosub2] and [Do.sub.2]. Plasma catecholamine plain was determined using the enzymatic orderly disposition of Brown and Jenner.[8] After baseline ascendency measurements had been made, a single oral dose of an ACE converting inhibitor, perindopril 4 mg was given, and then the hemodynamic and gas exchange rejoinders analyzed one, two, five, six, eight and 24 hours after put drugs into intake. [TABULAR DATA OMITTED]