Noninvasive Pressure Support Ventilation with PEEP in Acute Pulmonary Edema
Noninvasive Pressure Support Ventilation with PEEP in Acute Pulmonary Edema
Abstract & Commentary
Synopsis: Noninvasive pressure support ventilation is a highly effective technique used to treat patients with severe cardiogenic pulmonary edema from rapidly reversible causes, particularly when they are hypercapnic.
Sources: Hoffmann B, Welte T. Intensive Care Med 1999;25:15-20; Rusterholtz T, et al. Intensive Care Med 1999;25:21-28.
Two studies have been recently carried out evaluating the use of noninvasive pressure support ventilation (NIPSV) for severe respiratory insufficiency due to acute cardiogenic pulmonary edema (ACPE). Both studies showed that NIPSV was generally well tolerated and that its application was followed by a rapid and significant improvement of pulse oximetry saturation (SpO2) with progressive normalization of heart rate and blood pressure.
Hoffmann and Welte enrolled 29 patients with confirmed ACPE. Underlying diseases were arterial hypertension (n = 8), myocardial infarction (MI) (n = 5), mitral valve insufficiency (n = 1), renal failure (n = 2), pneumonia (n = 1), and left ventricular failure (n = 13) without specification. All patients received oxygen, intravenous furosemide, continuous infusion of nitroglycerine if the systolic blood pressure was above 120 mmHg (n = 17), or continuous infusion of catecholamines if mean blood pressure was below 60 mmHg (n = 5). Inclusion criteria were respiratory rate greater than 25 breaths per min, use of accessory respiratory muscles and SpO2 below 85% with at least 5 L/min supplemental oxygen requirement or an observed decline in saturation of more than 10 percentage points during a 10-min period. NIPSV was applied via a tight-fitting face mask delivering between 13-24 cm H2O (mean, 16.6 cm H2O) inspiratory airway pressure and 2-8 cm H2O (mean, 5.5 cm H2O) expiratory airway pressure. Changes of the main respiratory and circulatory parameters within the first 30 min of NIPSV are shown in the table.
| Table | ||
| Effects of NIPSV in Acute Cardiogenic Pulmonary Edema | ||
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| Pulse oximetry saturation (%)
Venous pH Venous PCO2 (mmHg) Oxygen (L/min) Heart rate (b/min) Systolic blood pressure (mmHg) |
7.22 ± 0.1 62 ± 18.5 7.3 ± 3.7 123.7 ± 26.1 145.7 ± 36.7 |
7.29 ± 0.08** 48.1 ± 13.1** 5.1 ± 3.0* 110.2 ± 21.3* 126 ± 22.1* |
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*p < 0.01 **p < 0.05 ___________________________________________________________ |
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The mean duration of NIPSV in these patients was 6 h 9 min (range, 120 min to 16 h). Only one patient with both pulmonary edema and pneumonia had to be intubated because of an insufficient improvement of SpO2 with NIPSV.
In the second study, Rusterholtz and colleagues also enrolled patients with ACPE who had been treated conventionally with oxygen and diuretics without improvement. Twenty-six consecutive patients were studied. NIPSV was started with a pressure support of 20.5 ± 4.7 cm H2O and a PEEP of 3.5 ± 2.3 cm H2O. There was a rapid general improvement of SpO2 in addition to a reduction of respiratory rate and arterial blood pressure. However, five out of 26 patients (21%) required intubation between 1 h 30 min and 17 h after admission. These patients were intubated because of a subsequent decrease of SpO2 with exhaustion or associated with shock and/or a decrease in their level of consciousness. Rusterholtz et al compared the initial clinical parameters of the group of patients who improved with NIPSV (success group) with those who finally required intubation (failure group). The only differences between the patient groups were in the arterial PCO2 and the number of patients who had had an acute MI. Arterial PCO2 was significantly higher in the success group than in the failure group (54.2 ± 15 vs 32 ± 2.1 mmHg; P < 0.001), and the number of patients with acute MI was significantly lower in the success group than in the failure group (2/21 vs 4/5; P < 0.05). Rusterholtz et al also noted that all patients with acute MI in the failure group died.
COMMENT BY FRANCISCO BAIGORRI, MD, PhD
Acute cardiogenic pulmonary edema is a frequent cause of respiratory failure, and many patients with this condition require endotracheal intubation and mechanical ventilation. Mechanical ventilation can markedly improve cardiovascular status while decreasing global oxygen consumption, independent of any beneficial effects that mechanical ventilation may have on gas exchange. These effects of positive-pressure ventilation need not be confined to patients whose tracheas are intubated.
Continuous positive airway pressure (CPAP) has been shown to be a form of noninvasive ventilatory assistance useful as a method to improve oxygenation and to avoid mechanical ventilation in patients with ACPE (Bersten AD, et al. N Engl J Med 1991; 325:1825-1830; Lin M, et al. Chest 1995;107:1379-1386). The results of the two present studies suggest that NIPSV can also prevent endotracheal intubation in this kind of patient. Moreover, there are data showing that NIPSV may improve hemodynamic and physiological respiratory parameters more rapidly than CPAP in patients with ACPE (Mehta S, et al. Crit Care Med 1997;25:620-628). In practice, some ACPE patients may have underlying chronic respiratory diseases and in these patients NIPSV may be better than CPAP. Consequently, it is not a matter of what modality is best for use in ACPE patients. Actually, both modalities should be considered as complementary in clinical practice when we should treat patients with the clinical characteristics described by Hoffmann and Welte.
It would seem appropriate to start noninvasive ventilatory assistance with NIPSV, adjusting pressure levels to improve patient comfort, minimizing inspiratory efforts, and avoiding relevant leakage. In this manner, some patients can move from NIPSV to CPAP and others can move from CPAP to NIPSV when the clinical condition evolves. However, the intriguing observation of Rusterholtz et al regarding patients with acute MI raises an important doubt about the use of NIPSV in patients with ACPE due to MI. A previous study comparing NIPSV vs. CPAP in ACPE patients (Mehta S, et al. Crit Care Med 1997;25:620-628) also reported a high proportion of MIs in the NIPSV group (71%) compared to the CPAP group (31%). Unfortunately, there was no clear explanation of whether MI was present at admission or occurred during the study. Why NIPSV rather than CPAP might be harmful to patients with coronary heart disease is unclear to me.
Noninvasive pressure support ventilation in patients with acute cardiogenic pulmonary edema:
a. does not improve hemodynamic or physiological respiratory parameters.
b. causes a late improvement of physiological respiratory parameters but does not prevent endotracheal intubation.
c. causes a rapid improvement of hemodynamic and physiological respiratory parameters avoiding endotracheal intubation in most of these patients.
d. rapidly worsens hemodynamic and physiological respiratory parameters.
e. causes a rapid improvement of hemodynamic and physiological respiratory parameters but does not prevent endotracheal intubation.
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