A 56-year-old male diagnosed case of COPD for the past 2 years presented to the emergency department of our hospital with shortness of breath (Medical Research Council (MRC) Grade 3) and cough with expectoration for the last 3 days and decrease in level of consciousness for 1 day. There was no history of fever, chest pain, hemoptysis, orthopnea, pedal edema, and focal neurological deficit or seizure. He had no history of hypertension, diabetes, or pulmonary tuberculosis. There was no history of previous hospitalization, though he consulted his primary care physician for worsening of respiratory symptoms, two times in a preceding year. He was a reformed smoker with a smoking index of 450. He worked as a security guard in a hospital and left the job 2 years back due to his illness. Spirometry done 2 years ago showed evidence of moderately severe obstruction with no bronchodilator response. His medications included inhaled corticosteroids and long-acting beta agonist (ICS/LABA). He used to take alcohol on social occasions with no other illicit drug use. There was no significant family history of respiratory illness.
On examination, he was drowsy, but arousable and flapping tremors were present. He was using accessory muscles of respiration and had a respiratory rate of 34/min. Pulse oximetry showed an oxygen saturation of 84% on breathing in ambient air. Heart rate and blood pressure were 102/min (regular) and 130/80 mmHg, respectively. Respiratory system examination revealed barrel-shaped chest, bilaterally reduced chest wall movements, and hyper-resonant note on percussion with obliterated cardiac and liver dullness. On auscultation, the intensity of breath sounds was grossly reduced on both sides with presence of bilateral diffuse expiratory wheeze. There was no clinical evidence of heart failure or deep-venous thrombosis.
Arterial blood gas (ABG) analysis showed evidence of acute on chronic hypercapnic respiratory failure (pH = 7.251, PaCO2= 87.9 mmHg, and HCO3= 39 meq/dl). His blood counts and routine biochemistry were within normal limits. His chest radiography showed the presence of hyperinflated lung fields without consolidation or effusion. Electrocardiography showed right-axis deviation and P-pulmonale. Troponin-I and pro-b-type natriuretic peptide levels were within normal limits. Screening two-dimensional-echocardiography revealed mild dilatation of right ventricle and right atrium with moderate pulmonary arterial hypertension. Both ventricles were contracting normally. There were no features suggestive of pulmonary thrombosis. There was A-profile on lung ultrasound with no effusion or consolidation. Deep-venous systems of lower limbs were free from thrombus. For management of AHRF, the patient was started on standard medical care (bronchodilators, systemic steroids, and antibiotics) in addition to NIV. NIV was provided by NAVA ventilator with dedicated software (Servo-i Maquet, Sweden) after written informed consent was obtained from the next of kin. EdiA catheter was inserted through the nose, and its accurate position (to pick up diaphragmatic signals) was confirmed by characteristic waveforms on the ventilator screen. Proper fitting nonvented NIV face mask was used as interface to provide ventilation. Edi signals were used to select the initial NAVA level such that the estimated pressure curve (to provide a tidal volume of approximately 6-8 ml/kg of ideal body weight of 57 kg) overlapped with the pressure delivery curve. The NAVA level of 2.0 cm of H2O/muv was required for this patient to generate the target tidal volume of around 486 ml. The airway pressure limit of 25 cm of H2O, positive end-expiratory pressure of 6 cm of H2O, and the FiO2of 0.4 were set to achieve oxygen saturation of at least 92% with adequate respiratory rate and tidal volume. Baseline vital signs, ventilator parameters, and ABG parameters were recorded [Table 1]. Subsequent assessment of vital signs, ventilator parameters, and ABG parameters were recorded at prespecified time intervals (initial at 30 min and then 6 hourly). Various types of asynchronies from recorded waveforms were noted and asynchrony index (ASI) was calculated [Table 1]. Patient comfort was noted using visual analog scale (VAS). Patient reported no discomfort to ventilator, with mild discomfort to the presence of EdiA catheter that resolved within 24 h of ventilation. Analysis of patient-ventilator asynchrony revealed only few asynchronies, the most common being double triggering [Table 1]. Once EdiA peak reduced without decrease in tidal volume (suggested improvement in respiratory failure), NAVA level was reduced by steps of 0.1 cm of H2O/muv. Total duration of NIV use was 4 days and weaning was started on the 3rd day after respiratory failure improved. On discharge, his oxygen saturation was 93% on room air. ABG showed pH 7.445, PaCO248.5 mmHg, PaO267.5 mmHg, and HCO337.99 meq/dl. He was discharged home on ICS/LABA plus long-acting antimuscarinic agents.