CCU October 2014: BIPAP STAT!

Home / Journal Club / CCU October 2014: BIPAP STAT!

CCU presentation

Rafael Caban, MD

“Call Respiratory, He needs Bipap!”



61 y/o male with a past medical history of DM, HTN, CVA, CKD, prostate CA arriving via EMS as a medical notification complaining of dyspnea.  In the initial resuscitation the patient was noted to have BP 216/112,  116 BPM,  RR40,  T 97F, 88% in room air. Patient was anxious appearing, using accessory muscles for breathing. Not speaking in full sentences. Prominent rales were noted, with lower extremity edema.  IV access was established. Patient received 2 sublingual nitro tabs, nitro gtt was begun at 60 mc/min, Lasix 40 mg IVP was given. Non-invasive pressure ventilation was initiated as part of the resuscitation.



ECG was normal sinus rhythm, no ischemic changes note




 acute PE CXR


Example chest x-ray: courtesy of google images from

CXR: bilateral pleural effusions, enlarged cardiac silhouette

Labs: Trop: 0.233, CK 482

The patient was subsequently admitted to the CCU. He was weaned from non-invasive ventilation to O2 supplementation via nasal cannula. The patient was kept on the nitro drip in conjunction with aggressive diuresis with furosemide and gradually transitioned to oral antihypertensives. An echocardiogram  showed normal systolic function with an EF of 56 %, RV function was also normal. The troponemia trended down and was determined to be secondary to demand ischemia.  Acute pulmonary edema was likely due to hypertensive emergency with fluid overload secondary renal failure.



The patient arrived to the ED in significant respiratory distress presumed to be secondary to acute pulmonary edema. Below will be a discussion of the use of non-invasive positive pressure ventilation (NPPV) in the management of patients with acute pulmonary edema. Evidence behind the use of this intervention will also be discussed.

During acute pulmonary edema there is an elevated LV end-diastolic pressure which forces plasma across pulmonary capillaries into the pulmonary interstitium. This fluid shift “floods” the alveoli and causes impaired ventilation and oxygenation (3).When oxygenation and ventilation are severely impaired, the need for ventilator support becomes imminent. A subset of patients with severe respiratory compromise who are not agonal can benefit from non-invasive positive pressure ventilation (3). NPPV involves delivering high pressures of air via a face mask. During acute pulmonary edema, NPPV decreases the work of breathing, prevents alveolar collapse, improves oxygenation, improves ventilation while also decreasing preload and afterload (3, 9). These physiological parameters are improved without exposing the patient to the increased morbidity associated with invasive ventilation.

There are two different strategies for NPPV in the adult population, continuous positive airway pressure (CPAP), and bi-level positive airway pressure (BiPAP). CPAP delivers a constant pressure of air throughout the respiratory cycle. BiPAP delivers different pressures during inspiration and expiration. CPAP pressures usually range from 5-15 cm of water. BiPAP settings are usually set for 8-10 cm of water during inspiration (IPAP) and 3-4 cm of water during expiration (EPAP) (8). Both methods are currently considered appropriate NPPV interventions in the patients with acute pulmonary edema. (8). Interestingly one of the earlier trials comparing CPAP to BiPAP for cardiogenic pulmonary edema found an increased rate of myocardial infarctions for the BiPAP group (4). The trial had to be stopped prematurely. Nevertheless these results failed to be replicated in multiple other trials comparing CPAP and BiPAP, and thus far no significant differences in efficacy have been found (1,5,6).

The use of NPPV in cases of acute pulmonary edema makes sense from a theoretical perspective in relation to the pathophysiology of this disease. Anecdotally it has also been linked to decrease need for endotracheal intubations. There have been multiple studies comparing non-invasive ventilation with standard oxygen therapy. Various meta-analyses  have found a decrease in mortality and decrease in the need for endotracheal intubations (1, 7,9).  Nevertheless those studies were derived from trials that included a small number of patients.  A randomized trial from Gray et al which included over 1000 patients, compared NPPV with standard oxygen therapy. They found no mortality differences, but found improvements in patient reported dyspnea, and resolution of metabolic acidosis in the NPPV arm of the study(2).  Although there is some paucity in the data showing benefits in mortality and intubation rates when using NPPV, the overall trend is that there is benefit over standard therapy.



1-Collins SP, Mielniczuk LM, Whittingham HA, et al. The use of noninvasive ventilation in emergency department patients with acute cardiogenic pulmonary edema: a systematic review. Ann Emerg Med. 2006 Sep;48(3):260-9, 269.e1-4.

2-Gray A, Goodacre S, Newby DE, et al. Noninvasive ventilation in acute cardiogenic pulmonary edema. N Engl J Med. 2008 Jul 10;359(2):142-51.

3-Marx J, Hockberger RS and Walls, R. Rosen’s emergency medicine : concepts and clinical practice Philadelphia: Elsevier Saunders. Accessed via Clinical Key.

4-Mehta S, Jay GD, Woolard RH et al. Randomized, prospective trial of bilevel versus continuous positive airway pressure in acute pulmonary edema, Crit Care Med. 1997 Apr;25(4):620-8.

5-Moritz F, Brousse B, Gellée B, et al.Continuous positive airway pressure versus bilevel noninvasive ventilation in acute cardiogenic pulmonary edema: a randomized multicenter trial,  Ann Emerg Med 2007 Dec;50(6):666-75, 675.

6-Park M, Sangean MC, Volpe Mde S, et al. Randomized, prospective trial of oxygen, continuous positive airway pressure, and bilevel positive airway pressure by face mask in acute cardiogenic pulmonary edema, Crit Care Med. 2004 Dec;32(12):2407-15.

7-Peter JV, Moran JL, Phillips-Hughes J, et al. Effect of non-invasive positive pressure ventilation (NIPPV) on mortality in patients with acute cardiogenic pulmonary oedema: a meta-analysis. Lancet. 2006 Apr 8;367(9517):1155-63.

8-Tintinalli J, Stapczynski S, Ma J, Et al.  Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7e. McGraw-Hill Companies. Accessed via access medicine. www.

9-Vital FM, Ladeira MT, Atallah AN. Non-invasive positive pressure ventilation (CPAP or bilevel NPPV) for cardiogenic pulmonary oedema. Cochrane Database Syst Rev. 2013 May 31;5:CD005351. doi: 10.1002/14651858.CD005351.pub3.

Leave a Reply