Hemodynamic consequences of auto-PEEP.

Auto-positive end-expiratory pressure (PEEP) is a common but frequently unrecognized problem in critically ill patients. It has important physiologic consequences and can cause shock and cardiac arrest. Treatment consists of relieving expiratory airflow obstruction and reducing minute ventilation delivered by positive pressure ventilation. Sedation and fluid management are important adjunctive therapies. This analytic review discusses the prevalence, pathophysiology, and hemodynamic consequences of auto-PEEP and an approach to its treatment.

Trials of bilevel positive airway pressure - spontaneous in patients with complex sleep apnoea.

INTRODUCTION: Patients with complex sleep apnoea (CompSAS) have obstructive sleep apnoea and experience persistent central apnoeas when exposed to positive airway pressure. Elevated loop gain is one of the postulated mechanisms of CompSAS. We speculated that bilevel positive airway pressure - spontaneous (BPAP-S), by producing relative hyperventilation, may more readily produce CompSAS activity than continuous positive airway pressure (CPAP). If found to do so, a trial of BPAP-S might be a simple way of identifying patients with elevated loop gain who are at risk for CompSAS. MATERIALS AND METHODS: Thirty-nine patients with complex sleep apnoea were included in the study. Segments of NREM sleep on CPAP and BPAP-S matched for body position and expiratory airway pressure (comparison pressure) were retrospectively analysed. Correlations between clinical and demographic variables and polysomnographic response to CPAP and BPAP-S were sought. RESULTS: There was no difference in any of the polysomnographic indices on CPAP and BPAP-S. In 19 patients the use of CPAP was associated with lower AHI at the comparison pressure; in 20 patients the opposite was true. No clinical variables correlated to the differential response to CPAP vs. BPAP-S. CONCLUSIONS: BPAP-S was not more effective than CPAP in stimulating complex sleep apnoea activity.

Neural respiratory drive in obesity.

BACKGROUND: The load imposed on ventilation by increased body mass contributes to the respiratory symptoms caused by obesity. A study was conducted to quantify ventilatory load and respiratory drive in obesity in both the upright and supine postures. METHODS: Resting breathing when seated and supine was studied in 30 obese subjects (mean (SD) body mass index (BMI) 42.8 (8.6) kg/m(2)) and 30 normal subjects (mean (SD) BMI 23.6 (3.7) kg/m(2)), recording the electromyogram of the diaphragm (EMGdi, transoesophageal multipair electrode), gastric and oesophageal pressures. RESULTS: Ventilatory load and neural drive were higher in the obese group as judged by the EMGdi (21.9 (9.0) vs 8.4 (4.0)%max, p<0.001) and oesophageal pressure swings (9.6 (2.9) vs 5.3 (2.2) cm H(2)O, p<0.001). The supine posture caused an increase in oesophageal pressure swings to 16.0 (5.0) cm H(2)O in obese subjects (p<0.001) and to 6.9 (2.0) cm H(2)O in non-obese subjects (p<0.001). The EMGdi increased in the obese group to 24.7 (8.2)%max (p<0.001) but remained the same in non-obese subjects (7.0 (3.4)%max, p = NS). Obese subjects developed intrinsic positive end-expiratory pressure (PEEPi) of 5.3 (3.6) cm H(2)O when supine. Applying continuous positive airway pressure (CPAP) in a subgroup of obese subjects when supine reduced the EMGdi by 40%, inspiratory pressure swings by 25% and largely abolished PEEPi (4.1 (2.7) vs 0.8 (0.4) cm H(2)O, p = 0.009). CONCLUSION: Obese patients have substantially increased neural drive related to BMI and develop PEEPi when supine. CPAP abolishes PEEPi and reduces neural respiratory drive in these patients. These findings highlight the adverse respiratory consequences of obesity and have implications for the clinical management of patients, particularly where the supine posture is required.

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.

Auto-PEEP in respiratory failure.

Intrinsic positive end-expiratory pressure (auto-PEEP) is a common occurrence in patients with acute respiratory failure requiring mechanical ventilation. Auto-PEEP can cause severe respiratory and hemodynamic compromise. The presence of auto-PEEP should be suspected when airflow at end-exhalation is not zero. In patients receiving controlled mechanical ventilation, auto-PEEP can be estimated measuring the rise in airway pressure during an end-expiratory occlusion maneuver. In patients who trigger the ventilator or who are not connected to a ventilator, auto-PEEP can be estimated by simultaneous recordings of airflow and airway and esophageal pressure, respectively. The best technique to accurately measure auto-PEEP in patients who actively recruit their expiratory muscle remains controversial. Strategies that may reduce auto-PEEP include reduction of minute ventilation, use of small tidal volumes and prolongation of the time available for exhalation. In patients in whom auto-PEEP is caused by expiratory flow limitation, the application of low-levels of external PEEP can reduce dyspnea, reduce work of breathing, improve patient-ventilator interaction and cardiac function, all without worsening hyperinflation. Neurally adjusted ventilatory assist, a novel strategy of ventilatory assist, may improve patient-ventilator interaction in patients with auto-PEEP.

Cardiovascular collapse associated with extreme iatrogenic PEEPi in patients with obstructive airways disease.

Chronic obstructive pulmonary disease (COPD) is commonly associated with positive alveolar pressure at end-expiration (intrinsic PEEP or PEEPi) caused by a prolonged expiratory time constant. Positive pressure ventilation (PPV) with large tidal volumes and high ventilatory frequencies may cause pulmonary hyperinflation, with increases in intrathoracic pressure and cardiopulmonary effects. We report two cases, one of fatal pulseless electrical activity, the other of life-threatening hypotension, both during vigorous manual PPV, in patients with severe COPD. This phenomenon has been well-recognized by intensivists but is reported poorly more widely.

Static intrinsic PEEP in COPD patients during spontaneous breathing.

Intrinsic positive end-expiratory pressure (PEEPi) is routinely determined under static conditions by occluding the airway at end-expiration (PEEPi,st). This procedure may be difficult in patients with chronic obstructive pulmonary disease (COPD) during spontaneous breathing, as both expiratory muscle activity and increased respiratory frequency often occur. To overcome these problems, we tested the hypothesis that the difference between maximum airway opening (MIP) and maximum esophageal (Ppl max) pressures, obtained with a Mueller maneuver from the end-expiratory lung volume (EELV), can accurately measure PEEPi,st. Using this method, we found that, in eight ventilator-dependent tracheostomized COPD patients (age 71+/-7 yr), PEEPi,st averaged 13.0+/-2.9 cm H2O. That measurement was validated by comparison with a reference static PEEPi (PEEPi,st-Ref) taken at the same EELV adopted by patients during spontaneous breathing, and measured on the passive quasi-static pressure-volume (P/V) curve of the respiratory system, obtained during mechanical ventilation. PEEPi,st-Ref averaged 13.1+/-3.0 cm H2O, i.e., a value essentially equal to PEEPi,st measured by means of our technique. We conclude that PEEPi,st can be accurately assessed in spontaneous breathing COPD patients by the difference between MIP and Ppl max during the Mueller maneuver.

Intrinsic PEEP and cardiopulmonary interaction in patients with COPD and acute ventilatory failure.

Deviation of end-expiratory lung volume from the elastic equilibrium volume of the respiratory system is recognized as a cardinal feature in mechanically-ventilated patients with severe chronic obstructive pulmonary disease (COPD) and acute ventilatory failure (AVF). The presence of dynamic hyperinflation implies that alveolar pressure remains positive throughout expiration. At the end of the expiration, this positive pressure is named intrinsic positive end-expiratory pressure (PEEPi). Recent studies have suggested that, in COPD patients with expiratory flow limitation, the application of external PEEP during assisted mechanical ventilation, or the use of continuous positive airway pressure (CPAP) in spontaneously breathing patients, can counterbalance and reduce the inspiratory threshold load imposed by PEEPi, without causing further increase in lung volume and alveolar and intrathoracic pressures until a critical value of PEEP (Pcrit) is reached. Above this critical limit further hyperinflation is observed. A specific and characteristic role of PEEPi in compromising the heart function in COPD patients during AVF may be identified based on: 1) an increase in right ventricular impedance due to lung hyperinflation; 2) an increase in the venous return to the right ventricle and, consequently, a leftward shift of the septum caused by the large negative deflections in intrathoracic pressure due to the inspiratory threshold load; 3) a further increase in venous return to the right ventricle, with the eventual collapse of the vena cava caused by the expiratory recruitment of abdominal muscles; and 4) hypoxia and hypercapnia consequent to acute ventilatory failure, which may further increase right ventricular impedance and venous return to the right ventricle. All these phenomenon are directly correlated to the large negative intrathoracic pressure developed by the respiratory muscles to overcome the inspiratory threshold caused by intrinsic positive end-expiratory pressure (preload effect), and to the increase in lung volume (afterload effect). Application of positive end-expiratory pressure/continuous positive airway pressure in chronic obstructive pulmonary disease patients during acute ventilatory failure may, hence, unload the respiratory muscles as well as the heart.

Effects of helium-oxygen on intrinsic positive end-expiratory pressure in intubated and mechanically ventilated patients with severe chronic obstructive pulmonary disease.

OBJECTIVE: To test the hypothesis that replacing 70:30 nitrogen: oxygen (Air-O2) with 70:30 helium:oxygen (He-O2) can decrease dynamic hyperinflation ("intrinsic" positive end-expiratory pressure) in mechanically ventilated patients with chronic obstructive pulmonary disease (COPD), and to document the consequences of such an effect on arterial blood gases and hemodynamics. DESIGN: Prospective, interventional study. SETTING: Medical intensive care unit, university tertiary care center. PATIENTS: Twenty-three intubated, sedated, paralyzed, and mechanically ventilated patients with COPD enrolled within 36 hrs after intubation. INTERVENTIONS: Measurements were taken at the following time points, all with the same ventilator settings: a) baseline; b) after 45 mins with He-O2; c) 45 mins after return to Air-O2. The results were then compared to those obtained in a test lung model using the same ventilator settings. MAIN RESULTS (MEAN + SD): Trapped lung volume and intrinsic positive end-expiratory pressure decreased during He-O2 ventilation (215+/-125 mL vs. 99+/-15 mL and 9+/-2.5 cm H2O vs. 5+/-2.7 cm H2O, respectively; p < .05). Likewise, peak and mean airway pressures declined with He-O2 (30+/-5 cm H2O vs. 25+/-6 cm H2O and 8+/-2 cm H2O vs. 7+/-2 cm H2O, respectively; p < .05). These parameters all rose to their baseline values on return to Air-O2 (p < .05 vs. values during He-O2). These results were in accordance with those obtained in the test lung model. There was no modification of arterial blood gases, heart rate, or mean systemic arterial blood pressure. In 12/23 patients, a pulmonary artery catheter was in place, allowing hemodynamic measurements and venous admixture calculations. Switching to He-O2 and back to Air-O2 had no effect on pulmonary artery pressures, right and left ventricular filling pressures, cardiac output, pulmonary and systemic vascular resistance, or venous admixture. CONCLUSION: In mechanically ventilated COPD patients with intrinsic positive end-expiratory pressure, the use of He-O2 can markedly reduce trapped lung volume, intrinsic positive end-expiratory pressure, and peak and mean airway pressures. No effect was noted on hemodynamics or arterial blood gases. He-O2 might prove beneficial in this setting to reduce the risk of barotrauma, as well as to improve hemodynamics and gas exchange in patients with very high levels of intrinsic positive end-expiratory pressure.