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Biomedical subjects

J L Fellahi

Publications and source records attributed to J L Fellahi.

13 recordsLinked to original sources
PubMed2001

Acute cor pulmonale in acute respiratory distress syndrome submitted to protective ventilation: incidence, clinical implications, and prognosis.

CONTEXT: The incidence of acute cor pulmonale (ACP), a frequent and usually lethal complication of acute respiratory distress syndrome (ARDS) during traditional respiratory support, has never been re-evaluated since protective ventilation gained acceptance. OBJECTIVE: We performed a longitudinal transesophageal echocardiographic (TEE) study to determine whether this incidence, and its severe implications for prognosis, might have changed in our unit as we altered respiratory strategy. DESIGN: Prospective open clinical study. SETTING: Medical intensive care unit of a university hospital. PATIENTS: Seventy-five consecutive ARDS patients given respiratory support with airway pressure limitation (plateau pressure < or =30 cm H2O). INTERVENTIONS: ACP was defined as a ratio of right ventricular end-diastolic area to left ventricular end-diastolic area in the long axis >0.6 associated with septal dyskinesia in the short axis during TEE examination. RESULTS: Normal right ventricular function was present in 56 patients, whereas right ventricular dysfunction was observed in 19 patients after 2 days of respiratory support. ACP was associated with pulmonary artery hypertension, increased heart rate, and decreased stroke index. Significant impairment of left ventricular diastolic function was also seen. All echo-Doppler abnormalities were reversible in patients who recovered, and the mortality rate was the same in both groups (32%). However, ACP patients who recovered required a longer period of respiratory support. A multivariate analysis individualized Paco2 level as the sole factor independently associated with ACP, suggesting that ACP development in ARDS is influenced by the severity of lung damage and/or the respiratory strategy. CONCLUSION: Evaluation of right ventricular function by TEE in a group of 75 ARDS patients submitted to protective ventilation revealed the persistence of a 25% incidence of ACP, resulting in detrimental hemodynamic consequences associated with tachycardia. However, ACP was reversible in patients who recovered and did not increase mortality.

APACHE↗
PubMed1999

[Postoperative patient management. Perioperative myocardial infarct].

A FREQUENT AND SEVERE EVENT: The incidence and the pathogenic mechanisms of cardiac complications in general surgery patients are now well described. Acute myocardial necrosis, the most frequent complication, is observed in 3 to 5% of patients at risk. Most are silent subendocardial lesions, but may have a short-term or mid-term life-threatening effect in these surgery patients. EARLY POSTOPERATIVE PERIOD: In most patients, cardiac events occur within 48 hours of surgery. Diagnosis is confirmed by elevated troponin I. The immediate postoperative period is characterized by increased left ventricular load and metabolic disturbances, increased release of catecholinergic mediators and hypercoagulability, factors related to the effect of anesthesia on circulation and surgical stimuli. These modifications compromise the energy balance in the myocardium and favor the development of left ventricular failure. ECG RECORDINGS: Continuous recordings in the postoperative period have shown that although the number of episodes of myocardial ischemia is not affected during surgery, their number doubles during the postoperative period, a factor predicting postoperative infarction. OPTIMAL CARE: Cardiovascular and anti-aggregate therapy should be adapted in patients with an underlying heart or coronary condition. Postoperative circulatory load and hyperaggregability should be controlled. This involves preventing hypothermia, intensive analgesia and, in some cases, cardiovascular therapy using beta blockers or alpha 2 agonists.

Combined Modality Therapy↗
PubMed1999

Hemodynamic effects of medical antishock trousers during mechanical ventilation.

PURPOSE: To compare the hemodynamic effects of medical antishock trousers (MAST) inflation in mechanically ventilated patients with normal and poor left ventricular function. METHODS: Twelve patients requiring respiratory support were divided into two groups according to baseline transesophageal echocardiography (TEE) measurements: normal left ventricular dimensions and fractional area of contraction (FAC=61 +/- 5%) (n=7) and dilated cardiomyopathy with reduced FAC (21 +/- 1%) (n=5). All patients were studied when two successive levels of load (mild load by inflation of the leg compartment of MAST at 50 cmH2O and high load by adding the abdominal compartment of MAST inflated at 30 cmH2O) were applied. Global left ventricular systolic function was assessed on the TEE transgastric short-axis view. End-systolic wall stress (ESWS) was used as an indicator of left ventricular afterload. RESULTS: Total respiratory, lung and chest wall compliances were reduced by 48%, 51% and 27% respectively at the high load level (P < 0.05). Whereas no hemodynamic changes occurred at mild load, the high load level produced an increase in left ventricular afterload as evidenced by concomitant increases in diastolic arterial blood pressure (66 +/- 6 to 79 +/- 6 mmHg, P < 0.05) and ESWS (69 +/- 12 to 74 +/- 12 Kdyn x cm(-2) x m(-2), P < 0.05). In patients with dilated cardiomyopathy, this increase in afterload impaired the left ventricular systolic function and end-systolic area increased (19.0 +/- 2.5 to 21.4 +/- 2.9 cm2 x m(-2), P < 0.05) while FAC decreased (22 +/- 2 to 16 +/- 2%, P < 0.05). Left ventricular end-diastolic area remained unchanged during the study in both groups. CONCLUSION: MAST inflation impairs respiratory mechanics and global left ventricular systolic function in cardiac patients without changes in left ventricular preload.

Adult↗
PubMed1999

Improved prognosis of acute respiratory distress syndrome 15 years on.

OBJECTIVE: Evaluation of the impact of low-volume, pressure-limited ventilation on the recovery rate of acute respiratory distress syndrome (ARDS). DESIGN: Prospective observational clinical study with historical control. SETTING: University hospital intensive care unit (ICU). PATIENTS: We studied two groups of, respectively, 33 and 37 ARDS patients separated by 15 years ("historical", June 1978-April 1981, and "recent", October 1993-June 1996). METHOD: ARDS was defined as the presence of bilateral chest infiltrates and a PaO(2)/FIO(2) ratio of less than 200 mmHg under controlled ventilation regardless of PEEP level. Any cardiac participation was excluded by right heart catheterization in the "historical" group and by echo-Doppler examination in the "recent" group. The origin of ARDS was principally pulmonary (ARDS(p)) in both groups (26/33 and 29/37, respectively), and secondarily extrapulmonary (ARDS(exp)) (7/33 and 8/37, respectively). In the "historical" group, normocapnia was the major goal for respiratory support and was achieved in all patients regardless of airway pressure levels. In contrast, end-inspiratory plateau pressure in the "recent" group was limited to 30 cmH(2)O under respiratory support, regardless of PaCO(2) level. The "historical" and "recent" ARDS groups were compared with regard to therapeutic procedure and outcome. RESULTS: Normalization of PaCO(2) (36 +/- 6 mmHg) in the "historical" group required high airway pressure (end-inspiratory plateau pressure at 39 +/- 4 cmH(2)O) and high tidal volume (13 ml/kg). Respiratory support used in the "recent" group was less aggressive, with lower airway pressure (end-inspiratory plateau pressure 25 +/- 4 cmH(2)O) and tidal volume (9 ml/kg) resulting in "permissive" hypercapnia (51 +/- 10 mmHg). Mortality rates significantly decreased from 64 % in the "historical" group to 32 % in the "recent" group (p < 0.01). This decrease concerned only ARDS(p), which was markedly predominant in both groups. CONCLUSION: Mortality due to ARDS of pulmonary origin has declined in our unit over the last 15 years. Low-volume, pressure-limited (protective) ventilation seems the most likely reason for improved survival, despite hypercapnia.

Adult↗
PubMed1999

Pericardial cardiac troponin I release after coronary artery bypass grafting.

UNLABELLED: Pericardial fluid can reflect the composition of cardiac interstitium in myocardial ischemia. This study investigated the hypothesis that pericardial cardiac troponin I (CTnI) measurements could be a more accurate marker of perioperative myocardial infarction (MI) than serum CTnI after coronary artery bypass grafting (CABG). Postoperative arterial and pericardial blood samples were taken in 102 subjects undergoing elective CABG allocated to one of three groups according to the 12-lead electrocardiogram (ECG) abnormalities observed during the first postoperative 24 h: Group 1 = normal ECG; Group 2 = nonspecific ECG abnormalities; and Group 3 = perioperative Q-wave MI. Peak pericardial CTnI concentrations were much higher than peak serum concentrations in all subjects and significantly greater in Group 3 than in Groups 1 and 2 (1,318 +/- 1,810 ng/mL vs 367 +/- 339 ng/mL and 558 +/- 608 ng/mL, respectively; P < 0.01). However, no significant difference between groups occurred at any time for pericardial/serum CTnI ratios, indicating that time courses of CTnI were not different in pericardial fluid and serum. A significant correlation was found between serum and pericardial CTnI concentrations (R = 0.70, P < 0.001). Pericardial CTnI was not more accurate than serum CTnI in predicting Q-wave MI as shown by the low value of the area under the receiver-operator characteristic curve (= 0.71). Peak and early pericardial CTnI were also not accurate in predicting an increase of serum CTnI greater than a cutoff value of 19 ng/mL. Thus, pericardial CTnI measurements were less useful than serum CTnI measurements in the diagnosis of perioperative MI after CABG. IMPLICATIONS: Although cardiac troponin I concentrations were much higher in pericardial fluid than in serum and significantly increased in subjects who experienced perioperative Q-wave myocardial infarction, pericardial cardiac troponin I measurements were of less value than serum cardiac troponin I measurements for the diagnosis of perioperative myocardial infarction after coronary artery bypass grafting and cannot be recommended in routine clinical practice.

Aged↗
PubMed1998

Does positive end-expiratory pressure ventilation improve left ventricular function? A comparative study by transesophageal echocardiography in cardiac and noncardiac patients.

STUDY OBJECTIVES: Positive end-expiratory pressure (PEEP) has been proposed to improve cardiac output in patients with left ventricular (LV) dysfunction. This study was designed to compare quantitative global and regional LV performance in response to PEEP in patients with normal and poor LV function. DESIGN: A prospective clinical trial. SETTING: Adult medical ICU in a university hospital. PATIENTS: Twelve critically ill patients requiring respiratory support and divided into two groups according to baseline transesophageal echocardiographic (TEE) measurements: normal LV dimensions and fractional area of contraction (FAC=61+/-5%) (n=7) and dilated cardiomyopathy with reduced FAC (21+/-1%) (n=5). MEASUREMENTS AND RESULTS: All patients were studied when two successive levels of PEEP (best PEEP as the highest value of respiratory compliance and high PEEP as best PEEP+10 cm H2O) were applied. Global systolic LV performance and quantitative regional wall motion analysis performed by the centerline method were assessed on the TEE transgastric short-axis view. End-systolic wall stress (ESWS) was used as a reliable indication of LV afterload. PEEP reduced LV dimensions asymmetrically in both groups of patients and septolateral diameter significantly decreased without affecting global LV systolic performance. Additionally, high PEEP produced a significant impairment in septal kinetics as evidenced by the centerline method. High PEEP also decreased ESWS for all patients (-27% in normal group and -23% in cardiac group, p<0.05) without significant improvement in global systolic LV performance (FAC: +2% in normal group and +0% in cardiac group; not significant). CONCLUSIONS: PEEP cannot be recommended routinely to improve LV performance in patients with severe dilated cardiomyopathy.

Adult↗
PubMed1997

[Management of severe amiodarone-induced pneumopathy using inhaled nitric oxide].

Treatment of amiodarone-induced pulmonary toxicity generally consists in simply discontinuing the drug with subsequent improvement in clinical condition and radiologic abnormalities. Corticosteroid therapy, when used, may accelerate recovery. Early diagnosis is however necessary and mandates the immediate cessation of the drug otherwise diffuse interstitial and alveolar damage can develop and lead to acute respiratory distress syndrome with a high rate mortality. To our knowledge, the use of inhaled nitric oxide to improve arterial oxygenation in amiodarone-induced ARDS has not yet been described. Here we report the case of a patient in whom 2 ppm inhaled nitric oxide in association with mechanical ventilation dramatically improved a life-threatening hypoxemia. We therefore submit that inhaled nitric oxide could be of benefit in patients with amiodarone-induced ARDS.

Administration, Inhalation↗
PubMed1995

Mechanisms of increased myocardial contractility with hypertonic saline solutions in isolated blood-perfused rabbit hearts.

Hypertonic saline improves organ perfusion and animal survival during hemorrhagic shock because it expands plasma volume and increases tissue oxygenation. Because both decreased and increased myocardial performance have been reported with hypertonic saline, the effects of hyperosmolarity and the mechanism accounting for it were investigated in isolated blood-perfused rabbit hearts. Coronary blood flow (CBF), myocardial contractility, relaxation, and oxygen consumption were measured during administration of blood perfusates containing 140-180 mmol sodium concentrations ([Na+]). In two other series of experiments, the role of Na(+)-Ca2+ exchange in the inotropic effect of hyperosmolarity (160 mmol sodium concentration) and hypertonicity (sucrose) were also investigated. Hypertonic [Na+] induced a significant increase in contractility and relaxation, combined with a coronary vasodilation. Myocardial oxygen consumption (MVO2) increased at all hypertonic [Na+] without significant change in coronary venous oxygen tension (PVO2) and content (CVO2). Amiloride (0.3 mmol) inhibited the improved contractility observed with 160 mmol sodium. Similar Na(+)-Ca2+ exchanger blockade did not inhibit the inotropic effect of sucrose. These results confirm the positive inotropic effect of hypertonic [Na+]. The inhibition of this improvement by amiloride suggests that calcium influx through the sarcolemna could be the major mechanism of this effect.

Amiloride↗
PubMed1995

Inhibition of platelet aggregation by inhaled nitric oxide in patients with acute respiratory distress syndrome.

BACKGROUND: Nitric oxide inhibits platelet adhesion and aggregation in vitro. The aim of this prospective study was to assess the platelet antiaggregating activity of nitric oxide administered to patients with acute respiratory distress syndrome (ARDS) at increasing concentrations. METHODS: In six critically ill patients (mean age 37 +/- 16 yr) with ARDS (lung injury severity score > or = 2.2), the lungs were mechanically ventilated with inhaled nitric oxide (1, 3, 10, 30, and 100 ppm) randomly administered. Patients with cardiac dysrhythmias, septic shock, an underlying hemostasis disorder (constitutive or acquired), a platelet count less than 100 Giga/l, or a decreased platelet aggregation and those treated with antiplatelet or anticoagulant agents were excluded. Platelet aggregation was measured without nitric oxide and at each nitric oxide concentration in platelet-rich plasma issued from radial artery. Ivy bleeding time using a horizontal incision was simultaneously performed. RESULTS: After nitric oxide, a non-dose-dependent but statistically significant decrease in ex vivo platelet aggregation induced by three aggregating agents was observed: adenosine diphosphate = -56 +/- 18%, collagen = -37 +/- 18%, and ristocetin = -45 +/- 18% (P < 0.05). In each individual, Ivy bleeding time remained within normal values measured in healthy volunteers, and variations after nitric oxide did not correlate with changes in platelet aggregation. Simultaneously, arterial oxygenation improved significantly and pulmonary artery pressure decreased significantly. CONCLUSIONS: In patients with ARDS and without preexisting coagulation disorders, the beneficial effects of inhaled nitric oxide on arterial oxygenation and pulmonary circulation are associated with a significant inhibition of platelet aggregation. This antithrombotic effect is not associated with a significant prolongation of the bleeding time.

Acute Disease↗
PubMed1995

[Analgesia with intra-articular injection of buprenorphine after surgery of the shoulder].

The effect of 10 ml of intra-articular buprenorphine (0.30 mg) or normal saline on postoperative pain after shoulder surgery was studied in a randomized, prospective, double-blind study in 30 ASA I-II patients receiving general anaesthesia. The pain scores (Five Point Scale ranging from "no pain" to "unbearable pain" and Visual Analog Pain Scale) 1, 2, 3, 4, 6 and 24 hours after surgery, time to first analgesic use and total 6-hours and 24-hours analgesic requirements were recorded. VAPS was significantly lower in the buprenorphine group compared with placebo-treated patients one hour after surgery (p < 0.05). The time to first analgesic use was longer and total 6-h opioid requirements were lower in the buprenorphine group when compared with the control group (p < 0.05). No significant differences were detected in total 24-h analgesic requirements between the two groups. These results indicate that intra-articular injection of buprenorphine after shoulder surgery provides short analgesia. This effect may be mediated by systemic absorption.

Adolescent↗
PubMed1992

[The intravascular transfer of glycine during percutaneous kidney surgery].

Transurethral prostatic resection using a 1.5% glycine solution causes a well known clinical and metabolic syndrome called TURP-syndrome. Recent development of percutaneous renal surgery is responsible of several similar accidents. In a prospective study of 150 patients (mean age: 35 +/- 10) subjected to a percutaneous nephrolithotomy, the natremia and the amino acid content of the plasma were measured preoperatively and immediately postoperatively by chromatography. The study shows that there is a post-nephrolithotomy syndrome in two per cent. This syndrome contains a hemodilution with hyponatremia and reabsorption of irrigation fluid. Glycolemia, serinemia and threoninemia increase significantly. These modifications have a good correlation between them except for the natremia. Variability of results in this study and in the literature is explained by difficulty and duration of surgery, volume of glycol used, increasing intrarenal pressures and sudden opening of vessels peroperatively. The gravity of post-nephrolithotomy syndrome requires to change the irrigate solute and use normal saline solution when it is possible.

Adolescent↗