Non-invasive mechanical ventilation (NIMV) is a first-line the treatment in the management of patients with acute and chronic exacerbated respiratory failure.1 Protocols and clinical guidelines recommend initial continual use until the patient's respiratory failure has stabilized, after which rest periods can be introduced to give the patient the opportunity to chat, get washed, eat, and give the skin a break from the pressure of the mask.2 During these periods, the patient receives oxygen therapy, usually by nasal prongs or a Venturi mask, regulating the flow of oxygen/FiO2 to maintain saturations of 88%–92%.3 In more severe or unstable patients, these rest periods are accompanied by significant dyspnea or desaturation that need to be corrected with high FiO2 levels of over 50%. These patients are usually reconnected to the respirator, depriving them of their periods of rest from NIMV. We report the case of a patient with acute respiratory failure who used high-flow nasal cannula (HFNC) as an alternative therapy during the periods of disconnection from NIMV.

This was an 83-year-old woman, with a diagnosis of hypoventilation-obesity syndrome, receiving night-time NIMV. She had a giant umbilical hernia that caused significant ventilatory compromise. She attended the emergency room due to dyspnea and a low level of consciousness, blood pressure: 158/86mmHg, heart rate: 86bpm; breathing rate: 32breaths/min; SatO2 86%, with O2 at 6bpm and a Glasgow score of 10. Physical examination was significant for peripheral cyanosis, tachypnea, and abdominal breathing. Pulmonary auscultation revealed bilateral crackles and rhonchi. Clinical laboratory tests were significant for BNP 241mg/dl and leukocytes: 10400 (neutrophils: 70.6%). PCR for influenza type A-H1 subtype was positive. Arterial blood gases showed a pH of 7.07; pO2: 38mmHg; pCO2: 107mmHg; HCO3: 31mg/dl. Chest X-ray revealed right basal opacity with blunting of the left costophrenic angle. The principal diagnosis was acute respiratory failure with severe respiratory acidosis due to viral pneumonia caused by type A-H1 influenza. NIMV began with a V60 respirator in ST mode, regulated with IPAP 21cm H2O, EPAP 10cm H2O, and a back-up breath rate of 16breaths/min. Clinical assessment carried out at 1h showed an improved level of consciousness (Glasgow 14), respiration (25breaths/min) and arterial blood gases (pH: 7.18mmHg; pCO2: 82mmHg; pO2: 65mmHg; HCO3: 30mg/dl; FiO2: 35%; alveolar arterial O2 gradient: 64.5). Arterial blood gas at 6h showed pH: 7.33 (2) 78mmHg; pCO2: 50mmHg; HCO3: 26.4; FiO2: 35%; alveolar arterial O2 gradient: 91.5. The patient was admitted to the respiratory observation area, and prescribed NIMV in shifts. During the first attempt at disconnection from NIMV using a Venturi mask at 35%, the patient developed significant work of breathing, respiratory rate 40breaths/min, and arterial O2 saturation (SpO2) 70%, so we decided to use HFNC at 60l/min with FiO2 of 50%. The patient improved and recovered the level of comfort she had experienced with NIMV; her respiration rate normalized and SpO2 stabilized at 93%. The patient continued to alternate between NIMV and HFNC during hospital admission until discharge 8 days later. Arterial blood gases at discharge were pH 7.45, pCO2 42mmHg, pO2 57mmHg, and HCO3 29.2mg/dl. Chest X-ray showed that the radiological infiltrate had disappeared. The patient continued to receive domiciliary NIMV at night and during the day after eating, as she had done before admission.

This was a patient with acute respiratory failure and severe respiratory acidosis due to viral pneumonia caused by influenza A-H1, in which the use of HFNC allowed the patient to take NIMV rest periods without undue stress. HFNC has proven to be useful in the treatment of patients with hypoxemic respiratory failure, and evidence is emerging to suggest its usefulness in hypercapnic respiratory failure.4 It has multiple mechanisms of action, of which the most important are its ability to increase alveolar recruitment, improve the ventilatory pattern, generate a positive expiratory pressure, and flush CO2 from the dead space.5 By supplying the gas at a temperature of 37°C and 100% humidity, HFNC is better tolerated and more comfortable for the patient.6 Numerous studies have demonstrated a significant reduction in respiratory rate, heart rate, dyspnea score, supraclavicular and thoracoabdominal retraction, and asynchrony, and a significant improvement in SpO2 in patients with acute hypoxemic respiratory failure treated with HFNC.7 In COPD patients with hypercapnia, HFNC improves the effectiveness of breathing, reduces pCO2, work of breathing, and rapid, shallow breathing index, as an indicator of respiratory work load.8

There are few publications on the outcomes of combined therapy with NFNC and NIMV. Frat et al.9 published a prospective observational study in which they alternated the use of NFNC and NIMV in subjects with acute hypoxemic respiratory failure, the majority of which met criteria for ARDS. Compared with conventional oxygen therapy, the use of HFNC improved oxygenation levels and symptoms of respiratory distress. Despite a lower impact on oxygenation compared with NIMV, HFNC was better tolerated. The study concluded that this technique can be used as a bridge between NIMV sessions. Spoletini et al.10 subsequently published a review of the mechanisms of action and the clinical implications of HFNC. Among the potential clinical applications, they highlighted its use during NIMV rest periods, thanks to the physiological and subjective benefits, and its advantages over conventional oxygen therapy.

HFNC and NIMV may be complementary techniques in the management of patients with acute respiratory failure. The combined use of NIMV and HFNC offers advantages over conventional NIMV oxygen therapy in more severe and unstable cases, as was the case in our patient. Studies are needed to address the role of NIMV-HFNC combination therapy in patients with acute respiratory failure.