Independent lung ventilation in patients with unilateral pulmonary contusion. Monitoring with compliance and EtCO(2).

OBJECTIVE: a) to describe a non-barotraumatic ventilatory setting for independent lung ventilation (ILV); b) to determine the utility of single lung end-tidal CO(2) (EtCO(2)) monitoring to evaluate the ventilation to perfusion (V/Q) matching in each lung during ILV and for ILV weaning. DESIGN: prospective study. SETTING: general intensive care unit in a university teaching hospital. PATIENTS: twelve patients with unilateral thoracic trauma needing ILV. INTERVENTIONS AND RESULTS: ILV was started with each lung ventilated with the same tidal volume (Vt): plateau airway pressure (Pplat) was 34.2+/-3.2 cmH2O in diseased lungs (DL) and 18.1+/-1.9 cmH2O in normal lungs (NL) ( P<0.01). Static compliance (Cst) was 9.9+/-1.1 ml/cmH(2)O in DL and 19.3+/-1.7 ml/cmH(2)O in NL ( P<0.01). EtCO2 was 22.5+/-2.2 mmHg in DL and 36.6+/-1.9 mmHg in NL ( P<0.01). PaO(2)/FiO(2) was at 151+/-20. PEEP was applied on the DL and each lung was ventilated with a Vt that developed Pplat < or =26 cmH2O. With this setting, Vt given to the NL was unchanged, whereas it was reduced in the DL (238+/-30 ml vs 350+/-31 ml; P<0.01). Cst and EtCO2 were still significantly lower in the DL ( P<0.01, respectively), while the PaO(2)/FiO(2) ratio remained unchanged. Vt was then progressively increased in the DL as Pplat decreased, but remained unchanged in the NL. ILV was discontinued when Vt, Cst and EtCO(2) were the same in each lung. PaO(2)/FiO(2) ratio had then increased to 295+/-18. CONCLUSIONS: a) during ILV, adequate oxygenation and a reduction in V/Q mismatch can be obtained by setting Vt and PEEP to keep Pplat below a safe threshold for barotrauma; b) measurement of single lung EtCO2 can be useful to evaluate progressive V/Q matching.

Effect of mechanical ventilation on inflammatory mediators in patients with acute respiratory distress syndrome: a randomized controlled trial.

CONTEXT: Studies have shown that an inflammatory response may be elicited by mechanical ventilation used for recruitment or derecruitment of collapsed lung units or to overdistend alveolar regions, and that a lung-protective strategy may reduce this response. OBJECTIVE: To test the hypothesis that mechanical ventilation induces a pulmonary and systemic cytokine response that can be minimized by limiting recruitment or derecruitment and overdistention. DESIGN AND SETTING: Randomized controlled trial in the intensive care units of 2 European hospitals from November 1995 to February 1998, with a 28-day follow-up. PATIENTS: Forty-four patients (mean [SD] age, 50 [18] years) with acute respiratory distress syndrome were enrolled, 7 of whom were withdrawn due to adverse events. INTERVENTIONS: After admission, volume-pressure curves were measured and bronchoalveolar lavage and blood samples were obtained. Patients were randomized to either the control group (n = 19): tidal volume to obtain normal values of arterial carbon dioxide tension (35-40 mm Hg) and positive end-expiratory pressure (PEEP) producing the greatest improvement in arterial oxygen saturation without worsening hemodynamics; or the lung-protective strategy group (n = 18): tidal volume and PEEP based on the volume-pressure curve. Measurements were repeated 24 to 30 and 36 to 40 hours after randomization. MAIN OUTCOME MEASURES: Pulmonary and systemic concentrations of inflammatory mediators approximately 36 hours after randomization. RESULTS: Physiological characteristics and cytokine concentrations were similar in both groups at randomization. There were significant differences (mean [SD]) between the control and lung-protective strategy groups in tidal volume (11.1 [1.3] vs 7.6 [1.1] mL/kg), end-inspiratory plateau pressures (31.0 [4.5] vs 24.6 [2.4] cm H2O), and PEEP (6.5 [1.7] vs 14.8 [2.7] cm H2O) (P<.001). Patients in the control group had an increase in bronchoalveolar lavage concentrations of interleukin (IL) 1beta, IL-6, and IL-1 receptor agonist and in both bronchoalveolar lavage and plasma concentrations of tumor necrosis factor (TNF) alpha, IL-6, and TNF-alpha, receptors over 36 hours (P<.05 for all). Patients in the lung-protective strategy group had a reduction in bronchoalveolar lavage concentrations of polymorphonuclear cells, TNF-alpha, IL-1beta, soluble TNF-alpha receptor 55, and IL-8, and in plasma and bronchoalveolar lavage concentrations of IL-6, soluble TNF-alpha receptor 75, and IL-1 receptor antagonist (P<.05). The concentration of the inflammatory mediators 36 hours after randomization was significantly lower in the lung-protective strategy group than in the control group (P<.05). CONCLUSIONS: Mechanical ventilation can induce a cytokine response that may be attenuated by a strategy to minimize overdistention and recruitment/derecruitment of the lung. Whether these physiological improvements are associated with improvements in clinical end points should be determined in future studies.

Effects of intramuscular injection of alpha-tocopheryl acetate on fatty acid profile in lamb liver.

The effects of intramuscularly administrated vitamin E on total lipids, fatty acid profile, and lipid stability to oxidation was investigated in lamb liver. Twenty-four 5-day-old lambs were allotted to 4 groups of 6 each and given respectively 0 (control), 125, 200, 300 mg dl-alpha-tocopheryl acetate weekly from day 5 to 33. alpha-Tocopherol stored in lamb liver at the end of experiment showed linear correlation with the level of injected vitamin E. No effect on total lipids was found. A decrease in the level of liver thiobarbituric-acid reactive substances (TBARS), significantly correlated with liver alpha-tocopherol content, was found in vitamin E groups. The amount of linoleic and linolenic acids significantly increased in the vitamin E groups as compared to control group, and were correlated with the liver alpha-tocopherol content. TBARS were negatively correlated with the concentration of unsaturated fatty acids. Finally, in the liver of the treated groups, vitamin E concentrations in the range 30-50 micrograms/g showed adequate for an efficient protection from peroxidation of membrane lipids, and determined an increase in the unsaturated to saturated fatty acid ratio.

Impairment of lung and chest wall mechanics in patients with acute respiratory distress syndrome: role of abdominal distension.

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.

Liver inflammation and acute respiratory distress syndrome in a patient receiving hepatitis B vaccine: a possible relationship?

We describe a patient in whom clinical evidence of liver and lung dysfunction developed after he received the second dose of recombinant hepatitis B vaccine, despite no serologic evidence of viral hepatitis. However, liver biopsy specimens demonstrated both surface antigens and core antigens, possibly indicating silent hepatitis B virus infection. A search for an infective etiology for the patient's subsequent clinical deterioration in lung function did not yield pathogens: postmortem examination revealed evidence of immune complex-mediated organ injury in the liver, lungs, and kidneys.

Effects of proportional assist ventilation on inspiratory muscle effort in patients with chronic obstructive pulmonary disease and acute respiratory failure.

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.

Effects of positive end-expiratory pressure on right ventricular function in COPD patients during acute ventilatory failure.

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.

Right ventricular myocardial function in ARF patients. PEEP as a challenge for the right heart.

OBJECTIVE: To examine the hemodynamic effects of external positive end-expiratory pressure (PEEP) on right ventricular (RV) function in acute respiratory failure (ARF) patients. DESIGN: Prospective, with retrospective analysis on the basis of RV volume response to PEEP. SETTING: General intensive care unit in a university teaching hospital. PATIENTS: 20 mechanically ventilated ARF patients (mean lung injury score = 2.6 +/- 0.45 SD). INTERVENTION: Incremental levels of PEEP (0-5-10-15 cmH2O) were applied and RV hemodynamics were studied by means of a Swan-Ganz catheter with a fast-response thermistor for right ventricular ejection fraction (RVEF) measurement. According to their response to PEEP 15, two groups of patients were defined: group A (9 patients) with unchanged or increased RV end-diastolic volume index (RVEDVI) and group B (11 patients) with decreased RVEDVI. MEASUREMENTS AND RESULTS: At zero PEEP (ZEEP) the hemodynamic parameters of the two groups did not differ. In group A, cardiac index (CI) and stroke volume index (SI) decreased at all PEEP levels (5, 10, and 15 cmH2O), while RVEF started to decrease only at a PEEP of 10 cmH2O (-10.8%), and RVES(systolic)VI increased only at PEEP 15 cmH2O (+21.5%). RVEDVI was not affected by PEEP. In group B, CI and SI decreased at all PEEP levels (5, 10, and 15 cmH2O). Similarly, RVEDVI started to decrease at PEEP 5 cmH2O, while RVESVI decreased only at PEEP 15 cmH2O (-21.4%). RVEF was not affected by PEEP in this group. In each patient the slope of the relationship between RVEDVI and right ventricular stroke work index (RVSWI), expressing RV myocardial performance, was studied. This relationship was significant (no change in RV contractility) in 8 of 11 patients in group B and in only 2 patients in group A. In 4 patients in group A, PEEP shifted the RVSWI/RVEDVI ratio rightward in the plot, indicating a decrease in RV myocardial performance in these patients. CONCLUSIONS: PEEP affects RV function in ARF patients. The decrease in cardiac output is more often associated with a preload decrease and no change in RV contractility. On the other hand, the finding of increased RV volumes with PEEP may be associated with a reduction in RV myocardial performance. Thus, these results suggest that assessment of RV function by PEEP and preload recruitable stroke work may disclose otherwise unpredictable alterations in RV function.

Patient-ventilator interaction during acute hypercapnia: pressure-support vs. proportional-assist ventilation.

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.

Chest wall and lung contribution to the elastic properties of the respiratory system in patients with chronic obstructive pulmonary disease.

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.

Inspiratory effort and measurement of dynamic intrinsic PEEP in COPD patients: effects of ventilator triggering systems.

OBJECTIVE: To investigate effects of ventilator triggering systems (pressure and flow triggering: PT and FT) on measurement of dynamic intrinsic PEEP (PEEPidyn) and patient-ventilator interaction in patients with chronic obstructive pulmonary disease during weaning from mechanical ventilation. DESIGN: Prospective study. SETTING: Medical/surgical intensive care unit of an academic hospital. PATIENTS AND PARTICIPANTS: 6 COPD patients with acute respiratory failure ready to wean. MEASUREMENTS: We measured flow, airway opening, esophageal and gastric pressures. Minute ventilation, breathing pattern and pressure time product (PTP) of the respiratory muscles and of the diaphragm were obtained during spontaneous ventilation through a mechanical ventilator (Puritan-Bennett 7200ae). Two triggering systems, namely PT and FT, were evaluated. RESULTS: The inspiratory muscles effort necessary to overcome the triggering system overestimated PEEPidyn measurement of an amount equal to 49 +/- 2 and 58 +/- 3% during respectively pressure and flow triggering. FT increased tidal volume and minute ventilation and decrease PTP/b and PTP/min of the respiratory muscles and diaphragm. CONCLUSIONS: To correctly measure PEEPidyn, the inspiratory effort produced to overcome PEEPi and to trigger the ventilator must be discriminated. Application of flow triggering requires less effort to initiate inspiration and provide a positive end-expiratory pressure level that is able to unload the respiratory muscles by reducing PEEPi. With flow triggering higher minute ventilation are obtained in COPD patients during the weaning phase.

Cardiorespiratory effects of positive end-expiratory pressure during progressive tidal volume reduction (permissive hypercapnia) in patients with acute respiratory distress syndrome.

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.

[Pseudoaneurysm of the left ventricle: a clinical case]. / Pseudoaneurisma del ventricolo sinistro: caso clinico.

A case of left ventricular pseudoaneurysm with a clinical onset of left ventricular failure, in absence of preceding signs or symptoms of coronary artery disease, is described. This case is particularly interesting because it shows how much time can pass (at least six months) from clinical onset without rupture of the pseudoaneurysm.

Physiologic effects of positive end-expiratory pressure in patients with chronic obstructive pulmonary disease during acute ventilatory failure and controlled mechanical ventilation.

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.