K. Samii

Circulating cardiac troponin I in trauma patients without cardiac contusion

Objectives: To describe the evolution and the diagnostic value of cardiac troponin I (cTnI) and to relate its concentrations with the indicators of injury in trauma patients.Design: Prospective, observational study of 17 young, previously healthy, mechanically-ventilated patients during the early post-traumatic period in the Surgical ICU of a University Hospital.Methods: Serial measurements of serum cTnI, total creatine kinase activity (CKtot) and its isoenzyme MB (CK-MB) (on admission, 12 h later, then daily for 7 days), clinical data and repeated electrocardiographic (ECG) and transesophageal echocardiography (TEE) recordings.Results: Rhabdomyolysis was observed in all the patients with a significant relationship between CK-MB and CKtot. Despite the fact that no patient demonstrated ECG or TEE signs of myocardial contusion, elevated serum levels of cTnI were observed in six patients (35%) without obvious dilutional interference. As compared with the others, these patients exhibited a more frequent arterial hypotension (83% vs 18%, p=0.035), required greater volume expansion on day 1 (22,000 vs 8,500 ml, p=0.027) and usually demonstrated early (83% vs 9%, p=0.005) and late (66% vs 9%, p=0.028) multiple organ dysfunction syndrome.Conclusions: Taking into account the high reported sensitivity and specificity of cTnI dosage, the present results suggest cTnI can play a role in the evaluation of indirect myocardial injury following traumatic shock.

Transgastric, pulsed Doppler echocardiographic determination of cardiac output.

ObjectiveThe aim of this study was to evaluate the accuracy of cardiac output measurement with transesophageal echocardiography (TEE) using a transgastric, pulsed Doppler method in acutely ill patients.DesignCardiac output was simultaneously measured by thermodilution (TD) and a transgastric, pulsed Doppler method.SettingThe study was carried out in a surgical intensive care unit as part of the management protocol of the patients.PatientsThirty consecutive acutely ill patients with a Swan-Ganz catheter, mechanically ventilated, sedated and with a stable hemodynamic condition were included.MeasurementsPulsed Doppler TEE was performed using a transgastric approach in order to obtain a long axis view of the left ventricle. Cardiac output was calculated from the left ventricular outflow tract diameter, the velocity time integral of the blood flow profile and heart rate.ResultsOne patient was excluded because of the presence of aortic regurgitation and another, because of the impossibility of obtaining a transgastric view. Twenty-eight simultaneous measurements were performed in 28 patients. A clinically acceptable correlation and agreement were found between the two methods (Doppler cardiac output=0.889 thermodilution cardiac output +0.74l/min,r=0.975,p<0.0001).ConclusionTransgastric pulsed Doppler measurement across the left ventricular outflow tract with TEE is a very feasible and clinically acceptable method for cardiac output measurement in acutely ill patients.

Renal effects of low-dose dopamine during vasopressor therapy for posttraumatic intracranial hypertension

Objective: To investigate the effects of low-dose dopamine (Dop) on renal hemodynamics and function in patients with brain trauma receiving norepinephrine (NE). Design: Prospective clinical study. Setting: Surgical intensive care unit of a university hospital. Patients: 20 stable, non-septic, mechanically ventilated, sedated patients with brain trauma and normal renal function treated with intravenous NE (0.11–0.65 μg/kg per min) to maintain an adequate cerebral perfusion pressure (> 60 mm Hg). Interventions: Two successive 1-h study periods with NE alone then NE + Dop (2 μg/kg per min). During each period, creatinine (ClCREAT), sodium (ClNa), potassium (ClK), osmolar (ClOSM) and free water (ClH2O), clearances were measured in all the patients. Effective renal blood flow (ERBF, paraaminohippurate clearance) and glomerular filtration rate (GFR, inulin clearance) were measured in 7 of the 20 patients. Results: Dop during NE infusion induced increases in urine flow and natriuresis which were not correlated with possible changes in arterial pressure. ClCREAT, GFR and their difference remained unchanged, whereas ERBF tended to increase. Fractional sodium excretion [100 × (ClNa/ClCREAT) ] and ClK increased during Dop infusion. Conclusion: The mechanism of Dop-induced natriuresis during NE infusion in brain trauma patients seems mainly related to a direct tubular effect of the drug.

Effect of lignocaine in myocardial contusion: an experiment on rabbit isolated heart.

1 The reported incidence of myocardial contusion after blunt chest trauma varies from 16 to 76%. Of these patients, about 6% present a severe, life threatening contusion. We used an isolated heart preparation to examine the effect of lignocaine on myocardial performance after contusion. 2 Thirty hearts obtained from male New Zealand rabbits were perfused at constant flow according to the Langendorff technique and were divided into four groups. The following parameters were measured at frequent intervals for 60 min: mean coronary perfusion pressure (CPP), left ventricular diastolic pressure (LVDP), developed pressure (DP), dP/dtmax, dP/dtmin. 3 Group 1 (n = 6) served as control, group 2 (n = 7) received lignocaine for 20 min (15 μm for the first 10 min and 30 μm for the following 10 min), group 3 (n = 9) had a contusion leading to a 30–50% decrease in dP/dtmax and group 4 (n = 8) had the contusion and the lignocaine infusion was started 10 min after the contusion and stopped after 30 min. Lignocaine concentration was measured in the effluent. 4 Lignocaine alone moderately decreased contractility in group 2. In group 3, after contusion, DP, dP/dtmax, and dP/dtmin were markedly decreased during the 60 min recording period. In group 4, lignocaine infusion rapidly restored contractility. DP, dP/dtmax and dP/dtmin returned towards their basal values. This improvement of contractility remained stable, even after lignocaine infusion was discontinued. 5 In our rabbit isolated heart preparation, lignocaine at a low therapeutic concentration was able to restore contractility after contusion. These results need to be confirmed by other studies but this may lead to promising therapeutic intervention.

Intravenous nicardipine for treatment of intraoperative hypertension during abdominal surgery

Twenty patients, American Society of Anesthesiologists class I or II, who developed intraoperative hypertension (mean arterial pressure greater than 110 mm Hg) during abdominal surgery under balanced general anesthesia were randomly assigned to two groups. The nicardipine group (n = 10) received 5 mg of nicardipine hydrochloride, and the placebo group (n = 10) received 5 mL of nicardipine solvent injected intravenously over a 5-minute period in a blind manner. Arterial pressure was recorded for 15 minutes after the injection was started. If the mean arterial pressure did not decrease at least 10% at 15 minutes, the trial was opened and patients received 5 mg of nicardipine. None of the patients in the nicardipine group received nicardipine in an open manner, in contrast with 7 of the 10 patients in the placebo group (P less than 0.03, Fisher exact test). During both the blind period and the open trial, nicardipine induced a 34% decrease in systolic, diastolic, and mean arterial pressure. Minimal values of pressure were noted at 6 minutes; however, arterial pressure remained below the pre-nicardipine injection values and near preoperative values for 45 minutes. No severe hypotension was observed, but the nicardipine injection was stopped at 3 mg in two cases during the blind period because of the rate of pressure reduction. Heart rate remained unchanged during the decrease in arterial pressure in both groups. This study indicates that nicardipine is an effective, long lasting, and safe therapy for intraoperative hypertension during abdominal surgery.

Increase in the chronically monitored cerebrospinal fluid pressure after experimental brain injury in rats

The early effects of experimental brain injury with diffuse axonal lesions on intracranial pressure (i.c.p.), mean arterial pressure (MAP) and cerebral perfusion pressure (CPP) in rats have been already studied. The aim of this experiment was to examine the effects of brain injury on ICP, MAP and CPP during the first few days post-injury. In order to do that, an accurate technique of ICP measurement had to be developed. In a series of eight rats, a translumbar intrathecal catheter (TIC) was surgically introduced allowing repeated measurements of cerebrospinal fluid pressure (CSFP). Under anaesthesia, a second series of nine rats were equipped simultaneously with TIC and an intracranial fiberoptic device to measure ICP. Simultaneous measurements of CSFP and ICP were recorded for baseline values, than during and after jugular compression which was intended to induce an acute and significant increase in ICP. A third series of 53 rats having TIC received an experimental severe brain injury. MAP was measured non-invasively and CPP was calculated as CPP-MAP. CSFP, MAP and CPP were intermittently measured during 5-6 post-traumatic days and compared to the values obtained during ten control rats (SHAM). A clinical score was used to compare clinical condition. The results showed that the translumbar CSFP accurately measured ICP in rats having normal or acutely increased ICP. The experimental brain injury induced increased CSFP lasting up to 5-6 days, with increased MAP during the first 6 hours. CPP values were compromised at 24-48 hours. The clinical performance was reduced in the brain-injured rats. The translumbar technique of CSFP measurement reflected exact ICP in normal and acutely increased ICP in rats. Experimental brain injury with diffuse axonal lesions can increase lumbar CSFP in rats for many days.