[Venous and arterial thromboembolism: autoimmune syndrome with heparin-induced thrombocytopenia. Unusual severe adverse reaction or the tip of the iceberg?].
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Biomedical subjects
Publications and source records attributed to T Fiore.
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BACKGROUND: Acute respiratory failure may develop in patients with chronic obstructive pulmonary disease because of intrinsic positive end-expiratory pressure (PEEPi) and increased resistive and elastic loads. Proportional assist ventilation is an experimental mode of partial ventilatory support in which the ventilator generates flow to unload the resistive burden (flow assistance: FA) and volume to unload the elastic burden (volume assistance: VA) proportionally to inspiratory muscle effort, and PEEPi can be counterbalanced by application of external PEEP. The authors assessed effects of proportional assist ventilation and optimal ventilatory settings in patients with chronic obstructive pulmonary disease and acute respiratory failure. METHODS: Inspiratory muscles and diaphragmatic efforts were evaluated by measurements of esophageal, gastric, and transdiaphragmatic pressures. Minute ventilation and breathing patterns were evaluated by measuring airway pressure and flow. Measurements were performed during spontaneous breathing, continuous positive airway pressure, FA, FA+PEEP, VA, VA+PEEP, FA+VA, and FA+VA+PEEP. RESULTS: FA+PEEP provided the greatest improvement in minute ventilation (89 +/- 3%) and dyspnea (62 +/- 2%). The largest reduction in pressure time product per breath of the respiratory muscles and diaphragm (44 +/- 3% and 33 +/- 2%, respectively) also was observed during FA+PEEP condition. When VA was added to this setting, a reduction in respiratory rate (50 +/- 3%), an increase in inspiratory time (102 +/- 6%), and a further reduction in pressure time product per minute (65 +/- 2% and 64% for the respiratory muscles and diaphragm, respectively) was observed. However, values of pressure time product per liter of minute ventilation during FA+VA+PEEP did not differ with those observed during FA+PEEP condition. Worsening of patient-ventilator interaction and breathing asynchrony occurred when VA was implemented. CONCLUSIONS: Application of PEEP to counterbalance PEEPi and FA to unload the resistive burden provided the optimal conditions in such patients. Ventilator over-assistance and patient-ventilator asynchrony was observed when VA was added to this setting. The clinical use of proportional assist ventilation should be based on continuous measurements of respiratory mechanics.
Recent data have suggested that the elastic properties of the chest wall (CW) may be compromised in patients with ARDS because of abdominal distension (4). We partitioned CW and lung (L) mechanics, assessed the role of abdominal distension, and verified whether the underlying disease responsible for ARDS affects the impairment of respiratory mechanics. Volume-pressure (V-P) curves (interrupter technique) were assessed in nine patients with surgical ARDS and nine patients with medical ARDS. Relative to nine patients undergoing heart surgery, V-P curves of the respiratory system (rs) and L of patients with surgical or medical ARDS showed a rightward displacement. V-P curves of the CW and the L showed an upward concavity in patients with medical ARDS and a downward concavity in patients with surgical ARDS. Although the CW and the abdomen (abd) V-P curves in patients with medical ARDS were similar to those obtained in patients undergoing heart surgery, they showed a rightward shift and a downward flattening in patients with surgical ARDS. In five of these patients, a reduction in static end-inspiratory pressure of the abd (69+/-4%), rs (30+/-3%), CW (41+/-2%), and L (27+/-3%) was observed after abdominal decompression for acute bleeding. Abdominal decompression therefore caused an upward and leftward shift of the V-P curves of the respiratory system, chest wall, lung, and abdomen. In conclusion we showed that impairment of the elastic properties of the respiratory system may vary with the underlying disease responsible for ARDS. The flattening of the V-P curve at high pressures observed in some patients with ARDS may be due to an increase in chest wall elastance related to abdominal distension. These observations have implications for the assessment and ventilatory management of patients with ARDS.
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We describe the very unusual case of a patient with a large, free-floating left-atrial thrombus secondary to severe mitral stenosis, in whom the peculiar symptoms and complications of a ball thrombus were absent. The patient's only symptom before the episode reported here was mild dyspnea, which was attributed to mitral stenosis. She experienced neither embolism nor syncope. While even her clinical signs did not indicate a left-atrial ball thrombus, both echocardiography and angiography showed a free-floating thrombus. Because of the risk of stroke and acute obstruction of the mitral valve, emergency surgery was performed upon diagnosis of the ball thrombus. The surgery, which consisted of removing the thrombus and replacing the mitral valve with a mechanical prosthesis, was uneventful. A computed tomographic brain scan prior to discharge did not detect any cerebral infarction.
OBJECTIVE: To examine the effects of external positive end-expiratory pressure (PEEP) on right ventricular function in chronic obstructive pulmonary disease (COPD) patients with intrinsic PEEP (PEEPi). DESIGN: Prospective study. SETTING: General intensive care unit in a university teaching hospital. PATIENTS: Seven mechanically ventilated flow-limited COPD patients (PEEPi = 9.7 +/- 1.3 cmH2O, mean +/- SD) with acute respiratory failure. INTERVENTION: Hemodynamic and respiratory mechanic data were collected at four different levels of PEEP (0-5-10-15 cmH2O). MEASUREMENTS AND RESULTS: Hemodynamic parameters were obtained by a Swan-Ganz catheter with a fast response thermistor. Cardiac index (CI) and end-expiratory lung volume (EELV) reductions started simultaneously when the applied PEEP was approximately 90% of PEEPi measured on 0 cmH2O (ZEEP). Changes in transmural intrathoracic pressure (PEEPi,cw) started only at a PEEP value much higher (120%) than PEEPi. The reduction in CI was related to a decrease in the right end-diastolic ventricular volume index (RVEDVI) (r = 0.61; p < 0.001). No correlation between CI and transmural right atrial pressure was observed. The RVEDVI was inversely correlated with PEEP-induced changes in EELV (r = -55; p < 0.001), but no with PEEPi,cw (r = -0.08; NS). The relationship between RVEDVI and right ventricular stroke work index, considered an index of contractility, was significant in three patients, i.e., PEEP did not change contractility. In the other patients, an increase in contractility seemed to occur. CONCLUSIONS: In COPD patients an external PEEP exceeding 90% of PEEPi causes lung hyperinflation and reduces the CI due to a preload effect. The reduction in RVEDVI seems related to changes in EELV, rather than to changes in transmural pressures, suggesting a lung/heart volume interaction in the cardiac fossa. Thus, in COPD patients, application of an external PEEP level lower than PEEPi may affect right ventricular function.
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PEEP is indicated in patients with COPD only to unload the respiratory muscles from the auto-PEEP resulting from expiratory flow limitation. If auto-PEEP is not caused by flow limitation, application of PEEP will cause further hyperinflation, worsening respiratory mechanics, muscle activity, and hemodynamics. To assess the presence of expiratory flow limitation correctly, to measure auto-PEEP correctly, and to identify the maximal PEEP level to be used, measurements of flow and opening pressure must be obtained during a brief period of suspended respiratory muscle activity (obtained by sedation) with the patient's own breathing pattern reproduced accurately.
The objective of this study was to compare patient-ventilator interaction during pressure-support ventilation (PSV) and proportional-assist ventilation (PAV) in the course of increased ventilatory requirement obtained by adding a dead space in 12 patients on weaning from mechanical ventilation. With PSV, the level of unloading was provided by setting the inspiratory pressure at 20 and 10 cmH2O, whereas with PAV the level of unloading was at 80 and 40% of the elastic and resistive load. Hypercapnia increased (P < 0.001) tidal swing of esophageal pressure and pressure-time product per breath at both levels of PSV and PAV. During PSV, application of dead space increased ventilation (VE) during PSV (67 +/- 4 and 145 +/- 5% during 20 and 10 cmH2O PSV, respectively, P < 0.001). This was due to a relevant increase in respiratory rate (48 +/- 4 and 103 +/- 5% during 20 and 10 cmH2O PSV, respectively, P < 0.001), whereas the increase in tidal volume (VT) played a small role (13 +/- 1 and 21 +/- 2% during 20 and 10 cmH2O PSV, respectively, P < 0.001). With PAV, the increase in VE consequent to hypercapnia (27 +/- 3 and 64 +/- 4% during 80 and 40% PAV, respectively, P < 0.001) was related to the increase in VT (32 +/- 1 and 66 +/- 2% during 80 and 40% PAV, respectively, P < 0.001), respiratory rate remaining unchanged. The increase in pressure-time product per minute and per liter consequent to acute hypercapnia and the sense of breathlessness were significantly (P < 0.001) higher during PSV than during PAV. Our data show that, after hypercapnic stimulation of the respiratory drive, the capability to increase VE through changes in VT modulated by variations in inspiratory muscle effort is preserved only during PAV; the compensatory strategy used to increase VE during PSV requires greater muscle effort and causes more pronounced patient discomfort than during PAV.
Conflicting data are available on the relative contribution of the chest wall (cw) to the intrinsic positive end-expiratory pressure of the total respiratory system (PEEPi,rs) in patients with chronic obstructive pulmonary disease (COPD). In order to assess the chest wall and lung contribution to the elastic properties of the respiratory system in COPD patients during acute ventilatory failure, using the "interrupter technique", static inflation volume-pressure (V-P) curves of the total respiratory system (rs), lung (L) and cw were obtained in seven mechanically-ventilated COPD patients during application of zero end-expiratory pressure (ZEEP) and different levels (0-15 cmH2O) of PEEP. On ZEEP, PEEPi,rs was present in all patients (range 10.5-13.1 cmH2O), to which PEEPi,cw and PEEPi,L contributed 17 +/- 2 and 83 +/- 1%, respectively. The static V-P curves of the rs, L, and cw on ZEEP were concave toward the horizontal axis, indicating that elastance increased with inflating volume. Application of PEEP did not affect lung and chest wall mechanics until PEEP levels exceeding 90% of PEEPi,cw on ZEEP (critical value of PEEP (Pcrit)). At PEEP levels higher than Pcrit, and relative to the V-P curves on ZEEP, we observed that: 1) the V-P curve of the rs showed an initial shift along the curve on ZEEP followed by a downward displacement with inflating volume; 2) the V-P curve of the L was shifted along the curve on ZEEP throughout inflating volume; and 3) the V-P curve of the cw was initially displaced along the curve on ZEEP, whilst a downward displacement appeared at higher lung volume. In conclusion, our data show that, in chronic obstructive pulmonary disease patients with flow limitation, the increase in pleural pressure does not make a significant contribution to the intrinsic positive end-expiratory pressure of the total respiratory system. However, during tidal ventilation, a substantial increase in elastance of the chest wall is present. The critical values of positive end-expiratory pressure below which there are no changes in chest wall and lung mechanics amount to 90% of the total PEEPi,rs on ZEEP. Positive end-expiratory pressure levels higher than such critical value cause important alterations of the elastic properties of the lung and chest wall.
BACKGROUND: In patients with acute respiratory distress syndrome (ARDS), the ventilatory approach is based on tidal volume (VT) of 10-15 ml/kg and positive end-expiratory pressure (PEEP). To avoid further pulmonary injury, decreasing VT and allowing PaCO2 to increase (permissive hypercapnia) has been suggested. Effects of 10 cmH2O of PEEP on respiratory mechanics, hemodynamics, and gas exchange were compared during mechanical ventilation with conventional (10-15 ml/kg) and low (5-8 ml/kg) VT. METHODS: Nine sedated and paralyzed patients were studied. VT was decreased gradually (50 ml every 20-30 min). Static volume-pressure (V-P) curves, hemodynamics, and gas exchange were measured. RESULTS: During mechanical ventilation with conventional VT, V-P curves on PEEP 0 (ZEEP) exhibited an upward convexity in six patients reflecting a progressive reduction in compliance with inflating volume, whereas PEEP resulted in a volume displacement along the flat part of this curve. After VT reduction, V-P curves in the same patients showed an upward concavity, reflecting progressive alveolar recruitment with inflating volume, and application of PEEP resulted in alveolar recruitment. The other three patients showed a V-P curve with an upward concavity; VT reduction increased this concavity, and application of PEEP induced greater alveolar recruitment than during conventional VT. With PEEP, cardiac index decreased by, respectively, 31% during conventional VT and 11% during low VT (P < 0.01); PaO2 increased by 32% and 71% (P < 0.01), respectively, whereas right-to-left venous admixture (Qs/Qt) decreased by 11% and 40%, respectively (P < 0.01). The greatest values of PaO2, static compliance, and oxygen delivery and the lowest values of Qs/Qt (best PEEP) were obtained during application of PEEP with low VT (P < 0.01). CONCLUSIONS: Although PEEP induced alveolar hyperinflation in most patients during mechanical ventilation with conventional VT, at low VT, there appeared to be a significant alveolar collapse, and PEEP was able to expand these units, improving gas exchange and hemodynamics.
Synchronized intermittent mandatory ventilation (SIMV) intermixes assisted and spontaneous breaths. Its ability as a weaning technique has been questioned on the basis that patients show little adaptation to ventilator assistance. We studied inspiratory effort and patient-ventilator interaction at different levels (SIMV, 100, 50, and 0%) of flow-triggered SIMV versus pressure-triggered SIMV in patients during the weaning period. The two triggering systems were evaluated during constant flow and constant pressure mandatory SIMV breaths. Inspiratory effort was estimated as the esophageal pressure time product (PTP) per breath (PTP/b) and per minute (PTP/min). The PTP/b and PTP/min of both mandatory and spontaneous breaths were significantly lower during flow triggering than during pressure triggering SIMV, irrespective of the ventilatory mode. During pressure-triggered SIMV PTP/b and PTP/min were identical for mandatory and spontaneous breaths, whereas during flow-triggered SIMV PTP/b and PTP/min were significantly lower for mandatory than for spontaneous breaths. This difference was greatest when flow triggering and constant pressure ventilation were associated. These data show that flow triggering reduces inspiratory effort during both mandatory and spontaneous SIMV breaths and obtains a better patient-ventilator interaction.
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The effects of positive end-expiratory pressure (PEEP) on static ("rapid airway occlusion" technique) and dynamic ("constant flow" technique) volume-pressure (V-P) curves were studied in 19 patients with adult respiratory distress syndrome (ARDS). To describe the shape of both curves, the nonlinear coefficient of a second-order polynomial equation fitted to the static (static nonlinear coefficient) and dynamic (dynamic nonlinear coefficient) V-P curves on zero end-expiratory pressure (ZEEP) was used. Two distinct patterns were observed: (1) in ten patients, the static and dynamic V-P curves on ZEEP exhibited a convex shape with a progressive decrease in slope with increasing inflation volume (nonlinear coefficients: negative). In these patients PEEP induced a volume displacement along the static and dynamic V-P curves on ZEEP (hyperinflation). (2) In nine patients, the static and dynamic V-P curves on ZEEP showed a concave shape with a progressive increase in slope with increasing volume (nonlinear coefficients: positive) and PEEP shifted both curves upward along the volume axis (alveolar recruitment). A correlation (p < 0.0001) between static and dynamic nonlinear coefficients was found at all levels of PEEP. Both static and dynamic nonlinear coefficients on ZEEP were correlated (p < 0.0001) with the amount of lung volume recruited with PEEP, and the variations of cardiac index (CI), O2 delivery (DO2), right-to-left venous admixture (Qs/Qt), and PaO2 with PEEP. Besides, the effects of PEEP on Cl, DO2, Qs/Qt, and PaO2 were less pronounced (p < 0.001) in patients with convex V-P curves than in patients with concave V-P curves.(ABSTRACT TRUNCATED AT 250 WORDS)
Diltiazem is a dihydropyridinic calcium-antagonist which acts an arterial muscle, producing an increase in vascular capacity. We administered it intraoperatively in 2 patients subjected to kidney transplantation, to asses the maximal vascular reserve of the transplanted organ. After 2' and 10' from administration of Diltiazem, Color Doppler Ultrasound showed a 30% increase in mean flow in the renal artery and 13% reduction in the intraparenchymal resistance rates with respect to the basal parameters. Systemic arterious pressure remained unchanged. This result was associated with an improvement in the perfusion of the transplanted organ.
Dynamic hyperinflation and intrinsic positive end-expiratory pressure (PEEPi) are observed in patients with chronic obstructive pulmonary disease (COPD) and flow limitation. Several reports suggest that PEEP levels approaching PEEPi reduce inspiratory load due to PEEPi, without further hyperinflation. Hence PEEP should not increase intrathoracic pressure or affect hemodynamics and gas exchange. To verify this hypothesis, the effects of PEEP (0 to 15 cm H2O) on respiratory mechanics, hemodynamics, and gas exchange were studied in nine COPD patients during controlled mechanical ventilation. PEEP levels approaching PEEPi (9.8 +/- 0.5 cm H2O) did not affect the expiratory flow/volume relationship, confirming the presence of flow limitation. PEEP levels of 5 and 10 cm H2O did not change lung volume and PEEPi in the respiratory system (PEEPtot,rs) and chest wall (PEEPtot,cw) or affect hemodynamics and gas exchange. When applied PEEP overcame PEEPi, changes in lung volume and the expiratory flow/volume relationship were observed. PEEPtot,rs and PEEPtot,cw also increased. Under these circumstances, PEEP increased static elastance in both the respiratory system and the chest wall, reducing cardiac index and affecting hemodynamics and gas exchange. Our data show that in mechanically ventilated COPD patients with PEEPi due to flow limitation, PEEP levels exceeding the 85% of PEEPi (Pcrit) caused further hyperinflation and compromised hemodynamics and gas exchange.
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The authors critically examine the preoperative management, the various anaesthetic techniques, the perioperative undesired effects in eighty six ASA I-II paediatric patients (age 6 months-11 years) submitted to ambulatorial anaesthesia for minor surgery or endoscopy. The importance of the psychological approach to patients and parents is enhanced. The preoperative screening included physical examination, ECG and simple laboratory tests. Various anaesthetic techniques (tracheal intubation and muscle relaxation with mechanical ventilation or spontaneous breathing) and many variously combined anaesthetic drugs (propofol 2 mg/kg, ketamine 1.5 mg/kg, diazepam 0.15 mg/kg, thiopental 3-4 mg/kg, halothane 1-2 MAC, fentanyl 1 microgram/kg) were employed depending on the quality of the surgical procedure and the conditions and the age of the patient. The results show that arousal was always rapid and smooth. The residual analgesia was sufficient in 74 cases; the other patients received rectal paracetamol 250 mg. No major complication was observed and only 6 patients were discharged 1 day later on account of vomiting or low Steward score. In conclusion outpatient paediatric anaesthesia has no contraindication for ASA I-II patients, shows no major complication and is well accepted by the patients and their patients.