Experiences Using Airway Pressure Release Ventilation for Pneumonia with Severe Hypercapnia or Postoperative Pulmonary Edema

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Acute Crit Care. 2017;32(1):83-87

Publication date (electronic) : 2017 February 28

doi : https://doi.org/10.4266/kjccm.2016.00906

Kyung Sook Hong¹, Young-Joo Lee^,2

¹Department of Surgery and Critical Care Medicine, Ewha Womans Univertisty School of Medicine, Seoul, Korea

²Department of Anesthesiology and Critical Care Medicine, Ewha Womans University Medical Center Mokdong Hospital, Seoul, Korea

Young-Joo Lee Department of Anesthesiology and Critical Care Medicine, Ewha Womans University Medical Center Mokdong Hospital, 1071 Anyangcheon-ro, Yangcheon-gu, Seoul 07985, Korea Tel: +82-2-2650-5366 Fax: +82-2-2650-5906 E-mail: sicuab@hotmail.com

Received 2016 November 01; Revised 2016 December 17; Accepted 2017 February 13.

Case 1

A 63-year-old female patient was diagnosed with advanced breast cancer with hepatic metastasis and was treated with palliative chemotherapy consisting of pertuzumab (Perjeta^®, F. Hoffmann-La Roche, Basel, Switzerland), trastuzumab (Herceptin^®, F. Hoffmann-La Roche), and docetaxel (Taxotere^®, Sanofi UK, Dagenham, UK). She was admitted for a third cycle of chemotherapy. However, her chemotherapy schedule did not proceed as planned because she developed pneumonia. In addition to delaying her chemotherapy, she was also transferred to an intensive care unit (ICU) while intubated due to aggravation of the pneumonia on hospital day (HD) #5. Although the condition of her lungs based on plain radiography of the chest seemed to have recovered with ventilator care, her pCO₂ levels on arterial blood gas analysis (ABGA) gradually increased from HD #16, even with careful ventilator management. On HD #19, her ABGA demonstrated a pCO₂ of 69.2 mmHg (Table 1). Additionally, afterwards, the patient became agitated and exhibited vigorous inspiratory efforts. We increased her respiratory rate from 20 per minute to 24 per minute by securing a sufficient gas-exchange interval and with the use of neuromuscular blockades. However, her pCO₂ level declined only to 60.5 mmHg. At that time, we decided to apply the APRV mode (P_high 22 cmH₂O, P_low 10 cmH₂O, T_high 1.2, T_low 0.8, FiO₂ 0.35, Table 1) for her, and the follow-up ABGA results showed a pCO₂ of 45.0 mmHg, pO₂ of 71.4 mmHg and SaO₂ of 93.8%. The next day, her pCO₂ level had decreased even more, to 37.8 mmHg (Table 1). On HD #21, neuromuscular blockades were discontinued and the ventilator mode was changed to the adaptive support ventilation mode (settings: minute volume 100%, FiO₂ 0.35, positive end expiratory pressure [PEEP] 10 cmH₂O). After changing the ventilation mode, ABGA demonstrated very tolerable results (Table 1).

Table 1.

Arterial blood gas analysis results using different ventilation modes in case 1

Case 2

A 63-year-old female patient, who was intubated, was referred to the intensive care unit with a diagnosis of panperitonitis due to colonic perforation after surgery. Her initial postoperative ABGA results showed a pH of 7.288, pCO₂ of 38.5, pO₂ of 118, HCO₃^- of 17.8, and SaO₂ of 98.9 with the controlled mandatory ventilation (CMV) mode (settings: tidal volume 470 mL, respiratory rate 10/minute, FiO₂ 0.7, PEEP 5 cmH₂O) (Figure 1A). Initially, septic shock was strongly suspected, therefore the patient was managed with empirical antibiotics (ceftriaxone and metronidazole), vasopressors (norepinephrine and vasopressin) and other supportive treatments, and even continuous renal replacement therapy (CRRT) for severe lactic acidosis (initial lactic acid level of 9.97 mmol/L; maximal lactic acid level of 10.49 mmol/L). With intensive treatments, the septic shock improved, such that all vasopressors were tapered and discontinued, and lactic acid levels normalized; however, the pneumonia did not improve (Figure 1B). Postoperative pulmonary edema was combined with the pneumonia, and her oxygen demand was increased (FiO₂ 0.7) (Table 2). Accordingly, APRV (P_high 34 cmH₂O, P_low 14 cmH₂O, T_high 2.0, T_low 1.0, FiO₂ 0.5, Table 2) was applied on postoperative day #6. Pulmonary edema was dramatically improved after just a few hours based on the results of plain chest radiography (Figure 1C, Table 2), and her work of breathing was also decreased. This APRV mode was continued for 7 days, and her follow-up chest radiographic images showed improvement (Figure 1D, Table 2).

Figure 1.

Serial plain radiographic images of the chest using different ventilation modes in case 2. (A) Plain chest radiograph on the day of operation. (B) On postoperative day #6, the pneumonia combined with postoperative edema was aggravated. (C) Pneumonia combined with edema improved on a follow-up plain radiograph taken just 6 hours after starting APRV. (D) On postoperative day #12, slightly improvement was noted on the plain chest radiographic image. APRV: airway pressure release ventilation.

Table 2.

Arterial blood gas analysis results using different ventilation modes in case 2

Hypercapnia can be avoided by changing ventilator settings, for example, adding pressure support or changing the ratio of inspiratory time to expiratory time (I:E ratio) in conventional ventilation modes, such as CMV [3,4]. In our first case, however, the patient did not improve even using neuromuscular blockades. The APRV settings were determined to facilitate CO₂ removal with an inverse I:E ratio and P_low was also kept at 10 mmHg to avoid patient lung collapse during T_low, just like in case 1.

In APRV, the lungs are ventilated with a lower airway pressure close to the lower inflection point, which reduces the over expansion of the alveoli. It promotes gas exchange and improves oxygenation by better lung recruitment [3].

Additionally, in our second case of postoperative pulmonary edema, APRV may have been the ideal ventilator mode. There has been no previous well-designed study on APRV for postoperative pulmonary edema, although some individual cases have been reported [6].

Increased mean alveolar pressure with short release time (T_low) promotes the recuitment of collapsed lung while preventing over-distention of ventilated alveoli. APRV aids in pulmonary dysfunction management by maximizing alveolar recruitment while limiting the transalveolar pressure gradient, thereby reducing the risk of barotrauma [6]. Additionally, in an animal experiment, it has been shown that APRV reduces lung water [7].

APRV increases the intrathoracic pressure to reduce the venous return and, therefore, to lower the blood pressure in some cases. In addition, it is difficult to apply APRV to the patients with obstructive airway disease such as asthma. The use of APRV, however, resulted in improved ventilation and oxygenation and increased mean alveolar pressure. Additionally, many studies have reported significant benefits of APRV on cardiopulmonary variables [2]. Moreover, in this ventilation mode, the stability of the lungs can be controlled independently from breathing to breathing, which is not possible with other modes of ventilation [2]. Hence, we suggest that APRV may be very helpful for patients with severe hypercapnia or hypoxemia related to postoperative pulmonary edema in ICU.

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