High positive end-expiratory pressure: only a dam against oedema formation?

Introduction

Healthy piglets ventilated with no positive end-expiratory pressure (PEEP) and with tidal volume (V_T) close to inspiratory capacity (IC) develop fatal pulmonary oedema within 36 h. In contrast, those ventilated with high PEEP and low V_T, resulting in the same volume of gas inflated (close to IC), do not. If the real threat to the blood-gas barrier is lung overinflation, then a similar damage will occur with the two settings. If PEEP only hydrostatically counteracts fluid filtration, then its removal will lead to oedema formation, thus revealing the deleterious effects of overinflation.

Methods

Following baseline lung computed tomography (CT), five healthy piglets were ventilated with high PEEP (volume of gas around 75% of IC) and low V_T (25% of IC) for 36 h. PEEP was then suddenly zeroed and low V_T was maintained for 18 h. Oedema was diagnosed if final lung weight (measured on a balance following autopsy) exceeded the initial one (CT).

Results

Animals were ventilated with PEEP 18 ± 1 cmH₂O (volume of gas 875 ± 178 ml, 89 ± 7% of IC) and V_T 213 ± 10 ml (22 ± 5% of IC) for the first 36 h, and with no PEEP and V_T 213 ± 10 ml for the last 18 h. On average, final lung weight was not higher, and actually it was even lower, than the initial one (284 ± 62 vs. 347 ± 36 g; P = 0.01).

Conclusions

High PEEP (and low V_T) do not merely impede fluid extravasation but rather preserve the integrity of the blood-gas barrier in healthy lungs.     

Is positive end-expiratory pressure suitable for liver recipients with a rescue organ offer?

Purpose

Rescue organ offers may help to overcome the organ shortage. However, because of initial poor liver function, the recipient may develop a severe lung injury with the requirement for higher positive end-expiratory pressure (PEEP) levels to achieve adequate oxygenation. Positive end-expiratory pressure has been associated with perfusion impairment in the hepatosplanchnic area. We assessed the effects of increased PEEP levels on systemic hemodynamic and liver perfusion in liver transplantation (LT) patients with a rescue organ.

Methods

Twenty-four LT recipients of a rescue organ offer were enrolled. All patients were postoperatively mechanically ventilated with biphasic positive airway pressure, and 3 different PEEP levels (0, 5, 10 mbar) were randomly set within 4 hours after admission at the intensive care unit. Systemic hemodynamic parameters were recorded using a pulmonary artery catheter; and flow velocities of the hepatic artery, portal vein, and right hepatic vein were measured using Doppler.

Results

Positive end-expiratory pressure of 10 mbar did not impair the systemic hemodynamic. Flow velocities in the right hepatic vein, the portal vein, and the hepatic artery were not influenced by PEEP.

Conclusion

Our study demonstrates that PEEP up to 10 mbar did not impair the liver outflow in recipients with a rescue organ offer.     

Does alveolar recruitment occur with positive end-expiratory pressure in adult respiratory distress syndrome patients?

We studied the effects of positive end-expiratory pressure (PEEP) (2 to 14 cm H₂O) on alveolar recruitment (Vrec), static respiratory compliance, and end-expiratory lung volume (EELV) in nine sedated, paralyzed, mechanically ventilated adult respiratory distress syndrome patients. Positive end-expiratory pressure was applied in increasing and decreasing steps of 2 cm H₂O. Flow, tidal volume, and airway pressure were measured. We used the rapid airway occlusion technique to determine static end-inspiratory elastic recoil pressure of the respiratory system (Pst, rs) and intrinsic PEEP (PEEPi). The changes in EELV were measured with respiratory inductive plethysmography. Alveolar recruitment was estimated as the difference in lung volume between PEEP and zero end-expiratory pressure (ZEEP) for the same end-inspiratory Pst,rs (20 cm H₂O). We found that (1) Vrec with PEEP up to 14 cm H₂O was in general rather small and was absent in two patients; (2) all patients exhibited PEEN at ZEEP (5.6 ± 1.0 cm H₂O) and little change in EELV and Vrec was achieved until the external PEEP exceeded PEEPi; (3) if end-inspiratory Pst, rs is high at ZEEP, there is little or no alveolar recruitment with PEEP; and (4) Vrec and EELV were slightly higher during stepwise deflation than stepwise inflation with PEEP, except at ZEEP where EELV did not change after inflation-deflation runs with PEEP.     

My paper 20 years later: Effect of positive end-expiratory pressure on right ventricular function in humans

Introduction

In 1992, we published a report on the effect of positive end-expiratory pressure (PEEP) on right ventricular (RV) function in humans.

Results

We measured RV volumes and pressures and pericardial pressure (Ppc) as PEEP was increased from zero to 15 cm H20 in 12 patients after thoracotomy, using a pulmonary arterial catheter equipped with a rapid responding thermistor that allowed measurement of RV ejection fraction (RVef), while Ppc was measured via a pericardial balloon catheter. RV end-diastolic volume (EDV) was estimated as the ratio of stroke volume (SV) to RVef, whereas RV end-systolic volume (ESV) were estimated as RV EDV-SV. PEEP increased Ppc and Pra, but RVef unaltered. There was no relation between either RV filling pressure (Pra-Ppc) and EDV or the change in RV filling pressure and EDV, although EDV varied significantly with PEEP (p < 0.05). The relations between EDV and both SV and RVef were weak (r = 0.54 and 0.55, respectively). RVef varied inversely with ESV (r = ?0.77), although it showed no relation to transmural peak pulmonary artery pressure (r = 0.28). However, both absolute and relative changes in EDV corresponded closely with respective ESV values (r = 0.94). We concluded that EDV varies independently of changes in filling pressure and that changes in ESV occur independently of changes in ejection pressure. These data can be explained by assuming that the RV shape changes can dissociate changes in RV EDV from changes in RV wall stress (preload). Thus, changes in RV EDV may or may not alter SV but should proportionately change ESV to a degree dependent on election pressure and contractility.

Conclusions

Subsequent studies confirmed our findings which can be summarized as 1) RV filling is independent of Pra; thus central venous pressure cannot be used to estimate RV preload; and 2) for cardiac output to increase by the Starling mechanism the RV must dilate increasing RV ESV. Since the pericardium limits absolute biventricular volume, there is a finite limit to which cardiac output can increase by the Starling mechanism defined not by left ventricular contractility but by RV function. And 3) if fluid loading causes Pra to increase without increasing cardiac output, then resuscitation should stop as the patient is going into acute cor pulmonale. These truths help bedside clinicians understand the echocardiographic and hemodynamic signatures of both RV failure and volume responsiveness.     

Positive end-expiratory pressure in acute respiratory distress syndrome – an old yet mysterious tool

A recent study by Bruhn and colleagues, discussed here, confirms that even high levels of positive end-expiratory pressure (PEEP) - up to 20 cmH2O - may be applied in conditions of moderate acute respiratory distress syndrome. Such levels of PEEP were found to be safe in terms of their impact on cardiac output and adequacy of gastric mucosal perfusion once systemic haemodynamics were stabilized by adequate fluid replacement and catecholamine therapy. However, we strongly recommend that the reader does not oversimplify the conclusions of that study. PEEP therapy is not inherently safe with respect to haemodynamics and regional organ perfusion, but it may be used safely, even at high levels of up to 20 cmH2O, if haemodynamic therapy is appropriate.     

Can nasal continuous positive airway pressure decrease clinic blood pressure in patients with obstructive sleep apnea?

Obstructive sleep apnea (OSA) is commonly associated with systemic hypertension and now recognized as an independent risk factor for daytime hypertension. We aimed to study the short- and long-term effect of nasal continuous positive airway pressure (CPAP) in hypertensive and normotensive patients with OSA. Forty-six patients with moderated to severe OSA were treated with nasal CPAP and followed after one year of treatment. Clinic blood pressure, heart rate, and body weight were taken before and followed up for one year after beginning nasal CPAP. In this study 25 patients with OSA were found to have hypertension (54.3%). The hypertensive group showed a significant reduction in clinic blood pressure after nasal CPAP, whereas the normotensive group showed no changes. The subgroup of hypertensive patients with OSA who had no anti-hypertensive medication revealed a decrease in clinic blood pressure comparable to those with anti-hypertensive drugs. The heart rate was not significantly changed in any patients. There was no significant correlation between the decrease in body weight and the reduction in blood pressure. These results suggest that nasal CPAP alone might have a substantial blood pressure lowering effect in hypertensive patients with OSA. This effect could decrease the morbidity and mortality related to cardiovascular complications in patients with OSA.     

Continuous positive airway pressure ventilation with helmet in infants under 1 year

Objective  

To report the feasibility of helmet use in infants between 1 and 12 months old with acute respiratory failure.     

Noninvasive positive pressure ventilation in acute respiratory failure: does it improve outcomes?

Studies have shown that noninvasive positive pressure ventilation (NPPV) is well tolerated and safe, and that it improves oxygenation in some patients with acute respiratory failure. By obviating the need for endotracheal intubation in certain conditions, it results in fewer complications, shorter hospital stays, and consequently, lower mortality rates and costs of care.     

Non-invasive ventilation and continuous positive pressure ventilation in emergency departments: where are we now?

A number of emergency departments have introduced non-invasive positive pressure ventilation (NIV) and continuous positive airway pressure (CPAP) for patients presenting with acute respiratory failure. It is thought that early non-invasive respiratory support will avoid the need for invasive ventilation in many cases. This literature review studied current knowledge of NIV and CPAP in the acute setting with the aim of creating simple guidelines for hospitals initiating early non-invasive ventilatory support in emergency departments. NIV is effective in reducing intubation and mortality rates in patients with acute exacerbations of chronic obstructive pulmonary disease (COPD) and CPAP is effective in reducing mortality in patients with cardiogenic pulmonary oedema, especially when implemented early. NIV and CPAP were also found to be effective in some other causes of acute respiratory failure. There is a role for non-invasive respiratory support in emergency departments.     

Does noninvasive positive pressure ventilation improve outcome in acute hypoxemic respiratory failure? A systematic review

CONTEXT: The results of studies on noninvasive positive pressure ventilation (NPPV) for acute hypoxemic respiratory failure unrelated to cardiogenic pulmonary edema have been inconsistent. OBJECTIVE: To assess the effect of NPPV on the rate of endotracheal intubation, intensive care unit and hospital length of stay, and mortality for patients with acute hypoxemic respiratory failure not due to cardiogenic pulmonary edema. DATA SOURCE: We searched the databases of MEDLINE (1980 to October 2003) and EMBASE (1990 to October 2003). Additional data sources included the Cochrane Library, personal files, abstract proceedings, reference lists of selected articles, and expert contact. STUDY SELECTION: We included studies if a) the design was a randomized controlled trial; b) patients had acute hypoxemic respiratory failure not due to cardiogenic pulmonary edema; c) the interventions compared noninvasive ventilation and standard therapy with standard therapy alone; and d) outcomes included need for endotracheal intubation, length of intensive care unit or hospital stay, or intensive care unit or hospital survival. DATA EXTRACTION: In duplicate and independently, we abstracted data to evaluate methodological quality and results. DATA SYNTHESIS: The addition of NPPV to standard care in the setting of acute hypoxemic respiratory failure reduced the rate of endotracheal intubation (absolute risk reduction 23%, 95% confidence interval 10-35%), ICU length of stay (absolute reduction 2 days, 95% confidence interval 1-3 days), and ICU mortality (absolute risk reduction 17%, 95% confidence interval 8-26%). However, trial results were significantly heterogeneous. CONCLUSION: Randomized trials suggest that patients with acute hypoxemic respiratory failure are less likely to require endotracheal intubation when NPPV is added to standard therapy. However, the effect on mortality is less clear, and the heterogeneity found among studies suggests that effectiveness varies among different populations. As a result, the literature does not support the routine use of NPPV in all patients with acute hypoxemic respiratory failure.