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Biomedical subjects

J F Monsallier

Publications and source records attributed to J F Monsallier.

At least 19 recordsLinked to original sources

Passive partitioning of respiratory volumes and time constants in ventilated patients.

If the thoracoabdominal partitioning of volumes in the mechanical respiratory apparatus was constant, one transducer of indirect spirometry should be sufficient to measure volume variations. To verify this hypothesis we used respiratory inductive plethysmography (RIP) in 16 paralysed patients, of whom eight had normal lungs and 8 had not, to measure: 1) the thoracoabdominal partitioning of volumes (400-1,200 ml) insufflated from either a syringe (Syr) or a ventilator (Vent); and 2) thoracic (Tho) and abdominal (Abd) time constants (T0.368) on spontaneous deflation to barometric pressure. In eleven additional subjects with normal lungs we measured only the time constants. 1) Correlation coefficients of the calibration lines were in all but one subject > 0.98. In all patients the error of volume was < +/- 10% when either one of two coils alone was used to assess volumes with no difference between the two coils; 2) Partitioning varied little with volumes (4 +/- 2%), but widely between subjects, with no group average significant difference between Syr and Vent; 3) T0.368 were identical for Tho and Abd except in one patient; 4) Partitioning and T0.368 were volume size independent. We conclude that, to measure volume variations and time constants in ventilated, paralysed patients, the use of either a thoracic or abdominal single coil RIP is justified. We also provide the normal range for time constant in 19 subjects (0.73 +/- 0.29 s).

Adult

Role of tricuspid regurgitation and left ventricular damage in the treatment of right ventricular infarction-induced low cardiac output syndrome.

To evaluate, in right ventricular (RV) myocardial infarction, the role of tricuspid regurgitation (TR) and left ventricular (LV) damage and the response to treatment of low cardiac output, 20 patients were prospectively studied. Volume infusion increased cardiac output only slightly (11%, p less than 0.001), despite a dramatic increase in ventricular filling pressures. Dobutamine (4 micrograms.kg-1.min-1) markedly increased cardiac output (24%, p less than 0.001) with a decrease in ventricular filling pressures. In the 5 patients with TR, dobutamine only modestly increased cardiac output (9 vs 26%, p less than 0.001), while stroke index and LV end-diastolic dimensions decreased in comparison (-5 vs 33% and -6 vs 9%, respectively, p less than 0.001). In the absence of TR (n = 15), there was no significant difference in response to volume expansion between patients with normal (n = 7) and depressed LV ejection fraction (n = 8). In contrast, dobutamine, in patients with depressed LV function, induced a greater increase in cardiac output (38 vs 17%, p less than 0.01) and RV ejection fraction (36 vs 12%, p less than 0.05). All patients with RV infarction-induced low cardiac output responded only modestly to volume loading. Dobutamine is particularly efficacious in patients without TR who have depressed LV function by improving RV function and, consequently, LV preload. In the 5 patients with TR, increasing RV contractility failed to improve the forward stroke volume by increasing the regurgitant fraction.

Adult

Is intensive care justified for patients with haematological malignancies?

The course of 260 adults with haematological malignancies admitted to a medical intensive care unit was studied to evaluate the value of life support techniques and to research predictive factors. The overall in the medical intensive care unit (MICU) and hospital mortality rates were respectively 43% (113 patients) and 57% (148 patients). Among survivors, 64% (49 patients) were still alive after 6 months and 44% (35 patients) after 1 year. Among 34 haemodialysed patients, the MICU mortality was 67% (23 patients) and among 111 mechanically ventilated patients 85% (94 patients). Prolonged mechanical ventilation, more than seven days, was performed in 11 of the 17 survivors and did not influence long term survival. No individual predictor of mortality was found comparing survivors and non-survivors. However, SAPS, intractable sepsis and failure of more than one organ system were significantly different in non-survivors (p less than 0.001). Among the 20 patients requiring both mechanical ventilation and haemodialysis, only two left the MICU and both died soon thereafter. We conclude that life support therapy should be initiated in patients with haematological disorders and that prolonged mechanical ventilation is compatible with long term survival. However, the combination of mechanical ventilation and haemodialysis is always associated with a poor prognosis and therefore the use of both techniques simultaneously for one patient is questionable.

Adult

Failure of teicoplanin therapy in two neutropenic patients with staphylococcal septicemia who recovered after administration of vancomycin.

A report is given on two neutropenic patients with staphylococcal septicemia caused by Staphylococcus haemolyticus and Staphylococcus aureus (both strains methicillin-resistant) who failed to respond to therapy with teicoplanin. Both strains were resistant to teicoplanin (MIC 16 and 8 mg/l respectively), but remained sensitive to vancomycin (MIC 2 and 4 mg/l respectively). Replacement of teicoplanin with vancomycin led to full recovery of both patients and their discharge from hospital. These two cases emphasize the importance of clinical and microbiological monitoring of patients with staphylococcal septicemia, even when glycopeptides are used for treatment.

Adult

Right ventricular performance in patients with acute respiratory failure.

To examine the right ventricular response to acute respiratory failure, serial studies of biventricular performance were analysed in 34 such patients, specifically detailing the role of associated underlying disease. During the initial study, the 34 patients with acute respiratory failure had a higher right ventricular end-diastolic volume than the control group (+21%), associated with a decrease in right ventricular ejection fraction, abnormalities which tended to return to normal values in the 15 survivors. In the 9 patients who died of refractory hypoxemia with severe pulmonary hypertension, the right ventricular dilation allowed to maintain stroke volume. In contrast, in 8 patients who died of septic shock, biventricular function was progressively altered (right and left ventricular ejection fraction = -37% and -35%). In 4 patients who died of cardiogenic shock (viral myocarditis), the cardiac function was the lowest (right and left ventricular ejection fraction = -59% and -60%). Only patients with acute respiratory failure associated with septic shock or viral myocarditis are unable to maintain their stroke volume.

Acute Disease

Right ventricular dysfunction in patients with septic shock.

Using a rapid computerized thermodilution method, we examined the evolution of right ventricular performance in 23 patients with septic shock. Nine survived the episode of septic shock. The other 14 patients died of refractory circulatory shock. Significant right ventricular systolic dysfunction, defined as decreased ejection fraction (-39%) and right ventricular dilation (+38%) was observed in all patients with septic shock. However, in the survivors, increased right ventricular preload may prevent hemodynamic evidence of right ventricular pump failure by utilizing the Frank-Starling mechanism to maintain stroke volume. Conversely, in the nonsurvivors, right ventricular dysfunction was more prononced two days after the onset of septic shock, leading to a fall in stroke. In the last patients, a decrease in contractility appears to be the major factor accounting for decreased right ventricular performance, as evidenced by the marked increase in end-systolic volume (+27%) without significant change in pulmonary artery pressure, during the later stage of septic shock. The observed right ventricular pump failure then appears associated with an alteration in diastolic mechanical properties of this ventricle, as suggested by a leftward displacement of the individual pressure-volume curves.

Adult

Causes of error of respiratory pressure-volume curves in paralyzed subjects.

Respiratory pressure-volume (PV) curves are commonly obtained in paralyzed patients by relating airway pressure to volume changes of a syringe (Vsyr). This is based on the implicit assumption that changes in thoracic volume (Vtho) and Vsyr are equal. We undertook to verify this assumption through simultaneous measurements of Vtho by respiratory inductive plethysmography and Vsyr in six comatose, paralyzed, intubated patients. At any constant Vsyr, Vtho fell and was smaller on deflation than on inflation during inflation-deflation (ID) cycle. The rate of fall was 110 +/- 64 (SD) ml/min. During ID cycles lasting 76 +/- 7 s, thoracic PV curves showed less hysteresis and a larger compliance on deflation than PVsyr curves (12 +/- 2 vs. 18 +/- 6% and 73 +/- 13 vs. 67 +/- 12 ml/cmH2O, P less than 0.05). With PVsyr curves, hysteresis increased and compliance on deflation decreased with increasing rate of fall of Vtho. We submit that the difference between changes in Vsyr and Vtho is best explained by gas exchange and should be taken into account when performing PV curves with a syringe in paralyzed patients.

Adult

Individual free fatty acids and lactate uptake in the human heart during severe sepsis.

Coronary haemodynamics and myocardial metabolism of nonesterified fatty acids (NEFA) and lactate were studied in 11 patients with severe sepsis, and compared to 10 control subjects. Coronary sinus blood flow was evaluated by thermodilution. Arterial and coronary sinus blood samples were collected for the measurement of lactate and total and individual NEFA concentrations both in septic and control patients. There was an increase in lactate and total NEFA arterial concentrations with a marked increase in palmitic and linolenic acids. The uptake of the main NEFA (C14:0 to C18:2) was significantly decreased. In the control group, individual NEFA uptake was proportional to their arterial concentrations. This relationship was not observed in patients with sepsis: there was no preferential extraction of any particular NEFA. Furthermore, in patients with sepsis, myocardial oxygen consumption did not correlate with NEFA, but only with lactate uptake. Alterations in NEFA uptake were found to be constant during severe sepsis and are consistent with major disturbances in myocardial metabolism.

Coronary Circulation

Bedside evaluation of right ventricular performance using a rapid computerized thermodilution method.

In 34 patients, we assessed the reproducibility and accuracy of a new, computerized, thermodilution method that determines right ventricular ejection fraction (RVEF). We compared the results from this new algorithm with simultaneous results from the conventional plateau thermodilution method and from both first-pass and gated nuclear techniques. Using this new method improved the reproducibility of thermal determinations of RVEF. Although the thermal values were lower, the correlations between thermal and nuclear measurements were close [r = .92 (first-pass technique), r = .81 (gated technique)]. This new method seems particularly appropriate for serial monitoring of RV performance.

Adult

Coronary hemodynamics and myocardial metabolism of lactate, free fatty acids, glucose, and ketones in patients with septic shock.

To investigate disturbances in the coronary circulation and myocardial metabolism during septic shock, we examined coronary sinus blood flow and myocardial substrate extraction in 40 patients with septic shock and 13 control patients. Patients with coronary artery disease were excluded from this study. The global hemodynamic pattern of the septic patients was characterized by a lower stroke volume, despite an elevated cardiac index. Coronary sinus blood flow was high (187 +/- 47 vs 130 +/- 21 ml/min in the control group, p less than .001) due to marked coronary vasodilation, especially in the subgroup of nonsurvivors. In contrast to the control group, myocardial lactate uptake was elevated, while that of free fatty acids, glucose, and ketone bodies was diminished in patients with septic shock. These findings were especially prominent in the nonsurvivors. Expressed as oxygen equivalents, the contribution of free fatty acids as an energy source of the myocardium was markedly diminished in septic patients (12% vs 54% in the control group, p less than .005), while that of lactate was increased (36% vs 12%, p less than .01). The observed shift in myocardial substrate extraction was associated with a discrepancy between measured myocardial oxygen consumption and that calculated chemically from commonly available exogenous substrates: 41% of myocardial oxygen consumption was not explained by the utilization of commonly available substrates extracted from coronary circulation in all patients with septic shock.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

Mechanisms of decreased left ventricular preload during continuous positive pressure ventilation in ARDS.

Continuous positive pressure ventilation is associated with a reduction in left ventricular preload and cardiac output, but the mechanisms responsible are controversial. The decrease in left ventricular preload may result exclusively from a decreased systemic venous return due to increased pleural pressure, or from an additional effect such as decreased left ventricular compliance. To determine the mechanisms responsible, we studied the changes in cardiac output induced by continuous positive pressure ventilation in eight patients with the adult respiratory distress syndrome. We measured cardiac output by thermodilution, and biventricular ejection fraction by equilibrium gated blood pool scintigraphy. Biventricular end-diastolic volumes were then calculated by dividing stroke volume by ejection fraction. As positive end-expiratory pressure increased from 0 to 20 cm H2O, stroke volume and biventricular end-diastolic volumes fell about 25 percent, and biventricular ejection fraction remained unchanged. At 20 cm H2O positive end-expiratory pressure, volume expansion for normalizing cardiac output restored biventricular end-diastolic volumes without markedly changing biventricular end-diastolic transmural pressures. The primary cause of the reduction in left ventricular preload with continuous positive pressure ventilation appears to be a fall in venous return and hence in right ventricular stroke volume, without evidence of change in left ventricular diastolic compliance.

Adult