Michel Dauzat

Training is required to improve the reliability of esophageal Doppler to measure cardiac output in critically ill patients

Objectives: Assessment of and effect of training on reliability of esophageal Doppler (ED) versus thermodilution (TD) for cardiac output (CO) measurement.Design: Prospective study.Setting: Intensive care unit of a university hospital.Patients: 64 consecutive critically ill patients requiring a pulmonary artery catheter, sedation, and mechanical ventilation.Interventions: Esophageal Doppler CO measurements were performed by the same operator, whereas TD CO measurements were carried out by other independent operators. A training period involving the first 12 patients made the operator self-confident. In the remaining patients, the reliability of ED was assessed (evaluation period), using correlation coefficients and the Bland and Altman diagram. Between training and evaluation periods, correlation coefficients, biases, and limits of agreement were compared.Measurements and results: During training and evaluation periods, 107 and 320 CO measurements were performed in 11 out of 12 patients and in 49 out of 52 patients, respectively. Continuous CO monitoring was achieved in 6 out of 11 patients and in 38 out of 49 patients during training and evaluation periods, respectively. Between the two periods, correlation coefficients increased from 0.53 to 0.89 (p < 0.001), bias decreased from 1.2 to 0.1 l.min−1 (p < 0.001), and limits of agreement decreased from 3.2 to 2.2 l.min−1 (p < 0.001).Conclusion: A period of training involving no more than 12 patients is probably required to ensure reliability of CO measurement by ED.

Comparison of the diagnostic value of cardiac troponin I and T determinations for detecting early myocardial damage and the relationship with histological findings after isoprenaline-induced cardiac injury in rats

Cardiac troponins I (cTnI) and T (cTnT) have been shown to be highly sensitive and specific markers of myocardial cell injury. The purpose of this study was to investigate the diagnostic value of cTnI and cTnT with regard to creatine kinase (CK) and lactate dehydrogenase (LD) and to determine whether they can be used for early diagnosis of myocardial damage in rats, and to examine the relationship between cTnl and cTnT release with histological examinations, using isoprenaline-induced cardiac muscle damage as an experimental model in the rat. Eighteen Wistar rats per group were treated with a single dose of either isoprenaline (iso) or with normal saline as a control group. The anti-cTnI and cTnT monoclonal antibodies (mAbs) employed in the cTnI (Access) and cTnT (Elecsys) assays cross-react with cTnI and cTnT of the rat. A highly significant rise of cTnl or cTnT was found already 2 h after iso. The time-courses of cTnI and cTnT were monophasic in form. The highest cTnI (mean+/-S.D., 1.1+/-2.3 ng/ml) and cTnT (mean+/-S.D. 3.6+/-30 ng/ml) were found 4 h after iso. cTnI and cTnT significantly increased in iso-treated rats in comparison with controls whether the differences between 2-, 4- and 6-h levels and basal levels were considered or not. The areas under cTnl and cTnT curves (AUC) (0-6 h) and the maximal cTnI and cTnT (0-6 h) after iso were significantly different from the controls. For CK and LD, no elevation in comparison with controls could be detected (except a trend for LD whether or not the difference between 6-h levels and basal levels were considered (P=0.08) and for LD AUC (0-6 h) (P=0. 059)). Correlations between maximal cTnI and cTnT and AUC were 0.69 (P=0.0001) and 0.60 (P=0.0066), respectively. Histological examinations of iso-treated rats revealed acute focal or multifocal myofibrillar degeneration of the myocardial tissue in ten out of 14 rats and showed the earliest alterations 4 h after iso in one treated rat. Only four of the controls exhibited evidence of mild changes and slight mononuclear cell infiltration. cTnl and cTnT peak values to at least 0.35 and 1.3 ng/ml, respectively, were necessary to detect histological myocardial cell injury after iso. cTnI and cTnT were found to be early markers for diagnosing iso-induced myocardial damage in comparison with CK and LD. Elevations of cTnI and cTnT appeared to relate to the severity of histologic changes after myocardial injury. Although there was a difference in the absolute concentration of results between cTnI and cTnT assays, due to a lack of standardization and heterogeneity in the cross-reactivities of mAbs to various troponin I and T forms, cTnI and cTnT can be used as easily measurable target parameters for detection of cardiotoxic and/or cardiodegenerative effects in rats.

Evaluation of cardiac troponin I and T levels as markers of myocardial damage in doxorubicin-induced cardiomyopathy rats, and their relationship with echocardiographic and histological findings

BACKGROUNDnCardiac troponins I (cTnI) and T (cTnT) have been shown to be highly sensitive and specific markers of myocardial cell injury. We investigated the diagnostic value of cTnI and cTnT for the diagnosis of myocardial damage in a rat model of doxorubicin (DOX)-induced cardiomyopathy, and we examined the relationship between serial cTnI and cTnT with the development of cardiac disorders monitored by echocardiography and histological examinations in this model.nnnMETHODSnThirty-five Wistar rats were given 1.5 mg/kg DOX, i.v., weekly for up to 8 weeks for a total cumulative dose of 12 mg/kg BW. Ten rats received saline as a control group. cTnI was measured with Access(R) (ng/ml) and a research immunoassay (pg/ml), and compared with cTnT, CK-MB mass and CK. By using transthoracic echocardiography, anterior and posterior wall thickness, LV diameters and LV fractional shortening (FS) were measured in all rats before DOX or saline, and at weeks 6 and 9 after treatment in all surviving rats. Histology was performed in DOX-rats at 6 and 9 weeks after the last DOX dose and in all controls.nnnRESULTSnEighteen of the DOX rats died prematurely of general toxicity during the 9-week period. End-diastolic (ED) and end-systolic (ES) LV diameters/BW significantly increased, whereas LV FS was decreased after 9 weeks in the DOX group (p<0.001). These parameters remained unchanged in controls. Histological evaluation of hearts from all rats given DOX revealed significant slight degrees of perivascular and interstitial fibrosis. In 7 of the 18 rats, degeneration and myocyte vacuolisation were found. Only five of the controls exhibited evidence of very slight perivascular fibrosis. A significant rise in cTnT was found in DOX rats after cumulative doses of 7.5 and 12 mg/kg in comparison with baseline (p<0.05). cTnT found in rats after 12 mg/kg were significantly greater than that found after 7.5 mg/kg DOX. Maximal cTnI (pg/ml) and cTnT levels were significantly increased in DOX rats compared with controls (p=0.006, 0.007). cTnI (ng/ml), CK-MB mass and CK remained unchanged in DOX rats compared with controls. All markers remained stable in controls. Analysis of data revealed a significant correlation between maximal cTnT and ED and ES LV diameters/BW (r=0.81 and 0.65; p<0.0001). A significant relationship was observed between maximal cTnT and the extent of myocardial morphological changes, and between LV diameters/BW and histological findings.nnnCONCLUSIONSnAmong markers of ischemic injury after DOX in rats, cTnT showed the greatest ability to detect myocardial damage assessed by echocardiographic detection and histological changes. Although there was a discrepancy between the amount of cTnI and cTnT after DOX, probably due to heterogeneity in cross-reactivities of mAbs to various cTnI and cTnT forms, it is likely that cTnT in rats after DOX indicates cell damage determined by the magnitude of injury induced and that cTnT should be a useful marker for the prediction of experimentally induced cardiotoxicity and possibly for cardioprotective experiments.

Non-invasive quantification of diaphragm kinetics using m-mode sonography.

PurposeThe standard conditions of spirometry (i.e., wearing a noseclip and breathing through a mouthpiece and a pneumotachograph) are likely to alter the ventilatory pattern. We used “time-motion” mode (M-mode) sonography to assess the changes in diaphragm kinetics induced by spirometry dunng quiet breathing.MethodsAn M-mode sonographic study of the nght diaphragm was performed before and dunng standard spirometry in eight patients without respiratory disease (age 34 to 68 yr).ResultsDuring spirometry, the diaphragm inspiratory amplitude (DIA) increased from 1.34 ± 0.18 cm to 1.80 ± 0.18 cm (P = 0.007), whereas the diaphragmatic mspiratory time (T1 diaph) increased from 1.27 ± 0.15 to 1.53 ± 0.23 sec, (P = 0.015), without change in diaphragmatic total time interval (Ttot diaph). Therefore, the diaphragm duty cycle (T1 diaph /Ttot diaph) increased from 38% ± 1% to 44% ± 4% (P = 0.023). The diaphragm inspiratory (DIV) and expiratory (DEV) motion velocity increased (P = 0.007).ConclusionM-mode sonography enabled us to demonstrate that the weanng of a nose clip and breathing through a mouthpiece and a pneumotachograph induce measurable changes in diaphragm kinetics.RésuméObjectifLes conditions de la spirométne standard (c.-à-d. le port du pince-nez et la respiration à travers un embout buccal et un pneumotacographe) sont susceptibles d’altérer la morphologie de la ventilation. Nous avons utilisé le mode «temps-amplitude» (mode M) de la sonographie pour évaluer les changements de la cinétique diaphragmatique provoqués par la spirométne pendant la respiration de repos.RésultatsPendant la spirométne, l’amplitude mspiratoire diaphragmatique augmentait de 1, 34 ± 0, 18 à 1, 80 ± 0, 18 cm (P = 0, 007), alors que le temps diaphragmatique mspiratoire (T1 diaph) augmentait de 1, 27 ± 0, 15 à 1, 53 ± 0, 23 sec (P = 0, 015), sans changement du temps diaphragmatique total (Ttot diaph). Par conséquent, le temps de l’activité diaphragmatique (T1 diaph/Ttot diaph) augmentait de 38 ± 1 % à 44 ± 4% (P = 0, 023). La vélocité de l’amplitude mspiratoire et expiratoire augmentait (P = 0, 007).ConclusionLa sonographie en mode M nous a permis de démontrer que le port du pince-nez et la respiration à travers un embout buccal et un pneumotacographe provoquent des changements tangibles de la cinétique diaphragmatique.

Doppler study of fasting and postprandial resistance indices in the superior mesenteric artery in healthy subjects and patients with cirrhosis

We assessed the resistance index (RI) in the superior mesenteric artery under fasting and postprandial conditions in healthy subjects and in patients with cirrhosis to determine whether the amount of change in the RI reflects the presence or severity of liver dysfunction.

CO assessment by suprasternal Doppler in critically ill patients: comparison with thermodilution

Objective: Comparison of suprasternal Doppler (SST) and thermodilution (TD) for the measurement of cardiac output (CO) in critically ill patients.¶Design: Prospective study.¶Setting: Intensive care unit of a university hospital.¶Patients and participants: 65 consecutive critically ill patients requiring a pulmonary artery catheter.¶Interventions: Paired CO measurements were made simultaneously using SST and TD by two independent operators. The time to obtain a CO value by SST was measured. Correlation coefficients and the linear regression equation were determined. A Bland and Altman diagram was plotted. A Bland and Altman diagram was also plotted for the level of cardiac index (CI) values (low: CI < 2.5 l min–1 m–2; normal: 2.5 ≤ CI ≤ 4.5 l min–1 m–2; high: CI > 4.5 l min–1 m–2).¶Measurements and results: In seven patients SST failed to measure CO. In the remaining 58 patients 314 paired CO measurements were performed. The mean time to measure CO by SST was 73 ± 45 s. The equation of linear regression was: SSTCO = 0.84 TDCO + 1.39. The correlation coefficient was 0.84. The bias between SST and TD was –0.2 ± 1.4 l min–1. Biases were –0.23 ± 0.50, –0.20 ± 0.68, and 0.25 ± 0.92 l min–1 m–2 for low, normal, and high levels of CI, respectively.¶Conclusion: SST does not accurately measure CO but allows a rapid assessment of CI level in critically ill patients.

Pulmonary gas exchange capacity is reduced during normovolaemic haemodilution in healthy human subjects

PurposeTo test the hypothesis that a physiological compensatory mechanism maintains respiratory gas exchange during normovolaemic haemodilution.MethodsPulmonary gas exchange capacity was evaluated in seven healthy subjects by measuring the lung diffusion of carbon monoxide (DLCO). During the measurement, various breath-holding times, inspiratory volumes, and sitting or supine positions, were randomly selected in an attempt to alter pulmonary capillary perfusion. KCO was calculated as the percentage of theoretical values of the ratio of DLCO by alveolar volume and normalized by sex, age, and height. Normovolaemic haemodilution (NH) was performed by bleeding an average blood volume of 1 L with simultaneous Dextran 60 replacement to obtain an haematocrit below 35%.ResultsAfter NH, haemoblogin concentration [Hb] decreased from 14.94 ± 0.96 to 12.5 ± 0.98 g · dl−1 (P < 0.001). KCO decreased (P < 0.02) but remained closely correlated to [Hb] at every lung volume (< 0.02). Breathholding time and body position had no effect.ConclusionModerate NH impairs pulmonary gas exchange capacity in awake, resting healthy subjects. There is no evidence of any compensatory mechanism since the KCO vs [Hb] relationship is unchanged.RésuméButVérifier l’hypothèse d’un mécanisme physiologique compensateur maintenant la capacité d’échanges respiratoires lors de l’hémodilution normovolémique.MéthodesNous avons évalué les échanges gazeux respiratoires par la mesure du transfert du CO (DLCO) chez sept sujets sains au cours d’une hémodilution normovolémique (NH). Différents temps d’apnée, volumes inspiratoires, et postures ont été sélectionnés aléatoirement afin de modifier la perfusion capillaire pulmonaire. Les résultats ont été normalisés en fonction de l’âge, du sexe, et de la taille par l’expression en pourcentage des valeurs théoriques du KCO (rapport de DLCO sur le volume alvéolaire). La NH a été réalisée par soustraction d’une quantité moyenne de 1 L de sang, remplacée par du Dextran 60.RésultatsAprès NH, le taux d’hémoglobine [Hb] a diminué de 14,94 ± 0,96 à 12,5 ± 0,98 g · dla−1 (P < 0,001). KCO diminuait (P < 0,02) mais restait étroitement corrélé à [Hb] (P < 0,02) quelque soit le volume pulmonaire. Le temps d’apnée et la position étaient sans effet.ConclusionLa NH modérée diminue la capacité d’échanges respiratoires chez le sujet sain, éveillé et au repos. Il ne paraît pas exister de mécanisme compensateur, puisque la pente de la relation entre KCO et [Hb] n’est pas modifiée.