Jean-Louis Hébert

The Influence of Tidal Volume on the Dynamic Variables of Fluid Responsiveness in Critically Ill Patients

Respiratory-related variabilities in stroke volume and arterial pulse pressure (&Dgr;%Pp) are proposed to predict fluid responsiveness. We investigated the influence of tidal volume (Vt) and adrenergic tone on these variables in mechanically ventilated patients. Cyclic changes in aortic velocity–time integrals (&Dgr;%VTIAo, echocardiography) and &Dgr;%Pp (catheter) were measured simultaneously before and after intravascular volume expansion, and Vt was randomly varied below and above its basal value. Intravascular volume expansion was performed by hydroxyethyl starch (100 mL, 60 s). Receiver operating characteristic curves were generated for &Dgr;%VTIAo, &Dgr;%Pp and left ventricle cross-sectional end-diastolic area (echocardiography), considering the change in stroke volume after intravascular volume expansion (≥15%) as the response criterion. Covariance analysis was used to test the influence of Vt on &Dgr;%VTIAo and &Dgr;%Pp. Twenty-one patients were prospectively included; 9 patients (43%) were responders to intravascular volume expansion. &Dgr;%VTIAo and &Dgr;%Pp were higher in responders compared with nonresponders. Predictive values of &Dgr;%VTIAo and &Dgr;%Pp were similar (threshold: 20.4% and 10.0%, respectively) and higher than that of left ventricle cross-sectional end-diastolic area at the appropriate level of Vt. &Dgr;%Pp was slightly correlated with norepinephrine dosage. &Dgr;%Pp increased with the increase in the level of Vt both before and after intravascular volume expansion, contrasting with an unexpected stability of &Dgr;%VTIAo. In conclusion, &Dgr;%VTIAo and &Dgr;%Pp are good predictors of intravascular fluid responsiveness but the divergent evolution of these two variables when Vt was increased needs further explanation.

Incidence and Significance of Cardiac Troponin I Release in Severe Trauma Patients

Background:The incidence and significance of troponin I release and its mechanism are unknown in severe trauma patients. The characteristics of this release were prospectively studied in such patients and correlated with presence of shock, existence of myocardial contusion, and outcome. Methods:During a 24-month period, serial electrocardiogram recordings and troponin I measurements were performed in all trauma patients admitted at a surgical intensive care unit. The diagnosis of a significant myocardial contusion was made on electrocardiographic criteria. According to the time course of troponin I, three groups of patients were defined a priori: very transient (≤ 12 h) and limited release (troponin I < 2 &mgr;g/l), transient (≤ 36 h) and significant release (troponin I ≥ 2 &mgr;g/l), and sustained (> 36 h) and significant release (troponin I > 2 &mgr;g/l). In the last group, coronary artery angiography was performed. Results:The incidence of troponin I release was 12% (95% confidence interval [CI], 9.6–14.4%) in 728 patients. A significant myocardial contusion was found in 35 patients (5%; 95% CI, 3.4–6.6%) and may occur in the absence of chest trauma and without troponin I release. Sensitivity, specificity, and positive and negative predictive values of troponin I for the diagnosis of myocardial contusion were 63, 98, 40, and 98%, respectively. Troponin I release was observed in 54 early (> 48 h) survivors (7%; 95% CI, 5.6–9.6%) without preexisting coronary artery disease. A sustained and significant release of troponin I (17 patients) was frequently associated with chest trauma (82%) and constantly with electrocardiographic abnormalities. A coronary artery injury was found in 7 patients (2 major and 5 minor vascular injuries) (1% of the whole group; 95% CI, 0.4–2.0%). Mortality was similar in early survivors with (15%; 95% CI, 7–27%) or without (12%; 95% CI, 9–14%) troponin I release. The odds ratio for late mortality was 1.32 (95% CI, 0.61–2.85) in patients with troponin I release. Conclusions:Serial electrocardiogram recordings and troponin I assessments may be proposed for initial screening in high-risk trauma patients to detect anatomical cardiac injuries through the time course of circulating protein. Troponin I release does not have a prognosis value in trauma patients.

Chapter 63 – Ventricular Tachycardia in Arrhythmogenic Right Ventricular Cardiomyopathies

Identification of arrhythmogenic right ventricular dysplasia (ARVD) resulted from surgical antiarrhythmic treatment of ventricular tachycardia (VT). 1