Our patient was admitted with severe COVID-19, and his condition worsened and he desaturated to 77% despite oxygen supplementation using NIV-CPAP. When a patient is intubated, a conventional mode of ventilation with an LTV strategy is usually used. However, we used the early APRV mode of ventilation , which outperformed the conventional method in terms of oxygenation, ventilator-free days, and length of stay in the intensive care unit (ICU).
APRV is one of the ventilation modes that was introduced in 1987. APRV is a pressure-controlled, intermittent mandatory ventilation, applied using inverse ratio ventilation. The mandatory breaths applied are time triggered, pressure targeted, and time cycled (depending on the ventilator, trigger and cycle events may be synchronized with patient breathing signals). Spontaneous breathing can occur both during and between mandatory breaths . The purpose of inverse ratio ventilation in APRV is to provide a shortened expiratory phase to permit an adequate tidal volume to escape without allowing alveoli to fall below their closing volume .
APRV is considered an “open lung approach” to mechanical ventilation . On the pressure–volume curve, the lower inflection point (LIP) represents the initial point at which alveoli are readily recruited, and below the LIP alveoli tend to collapse. The upper inflection point (UIP) represents the point at which alveoli become overdistented [10, 11]. In APRV, the amplitude of the time-triggered mandatory breath is called “P high” instead of inspiratory pressure, and the duration when pressure is applied is called “T high” instead of inspiratory time. The expiratory pressure is called “P low” and the release time, or expiratory time, is called “T low” .
The P high was set below the UIP and the P low was usually set at 0 cmH2O because of the development of auto-PEEP using APRV mode. This auto-PEEP maintains the airway pressure above the LIP on the pressure–volume curve. By keeping the P high and P low between the two inflection points, the tidal volume received by the patient is the most compliant portion of the curves. Because P high is set by the operator, the potential for ventilator-induced lung injury is minimized .
APRV improves alveolar recruitment by its long-term high and constant airway pressure, which maximizes alveolar recruitment and promotes collateral ventilation through the pores of Kohn . The ability to trigger spontaneous breathing in ARPV reduces asynchronization with the ventilator, thus improving patient comfort and reducing the need for sedation and neuromuscular blocking agents. Reduced sedation may reduce the incidence of constipation, cardiovascular depression, and cough reflex depression, all of which contribute to clearance and lower the risk of ventilator-associated pneumonia (VAP) . Using a neuromuscular blocking agent can cause polyneuropathy. Because of spontaneous breathing during APRV, diaphragm muscle atrophy caused by prolonged mechanical ventilation can be prevented . Greater hemodynamic performance can be seen in APRV because of spontaneous breathing. Decreased intrathoracic pressure during inspiration augments systemic venous return to the heart from the abdominal organs, hence improving cardiac output .
There have been multiple experiments in animal models in which APRV improves arterial oxygenation, increases ventilation in dependent areas of the lung, reduces inflammatory cytokine production, and can prevent the development of ARDS . In a porcine model with sepsis-induced and ischemia/reperfusion-induced lung injury, experiments compared the effectiveness of APRV in preventing ARDS with that of low tidal volume mechanical ventilation. APRV was applied to animals 1 hour after sepsis was induced, while LTV was applied to animals when the criteria for mild ARDS were met (P/F ratio of 300). The study found that APRV prevented clinical and histological lung injury by preserving alveolar epithelial integrity, reducing lung edema, preserving surfactant, and maintaining alveolar stability . In a rat model with pulmonary ARDS, APRV was compared with volume-controlled ventilation; alveolar overdistention was seen more in the volume-controlled ventilation group than in APRV. In the APRV group, there was less expression of amphiregulin, a gene that is expressed during times of alveolar stretch .
Nevertheless, using APRV mode does have its downside owing to its long T high, which can induce hypercapnia. More importantly, the degree of hypercapnia and respiratory acidosis tolerated by each patient varies. Some groups are not tolerant of hypercapnic conditions, such as those with coronary artery disease, arrhythmias, pulmonary hypertension, right ventricular dysfunction, and brain injury .
Until now, there have been no guidelines on the optimal APRV settings and titration strategy. However, there are two specific protocols proposed by Habashi and Zhou. In the Habashi protocol, P high was set at the desired plateau pressure, typically between 20–35 cmH2O, P low was set at 0 cmH2O, T high was set at 4–6 seconds, and T low was set at 0.2–0.8 seconds for restrictive lung disease and 0.8–1.5 seconds for obstructive lung disease. The PEEP was set at no more than 0 cmH2O because the airway resistance would create auto-PEEP . The weaning process begins if the FiO2 is 40% and the SpO2 is 95%. The P high was lowered and the T high was increased .While, according to the Zhou protocol, the P high was set at no more than 30 cmH2O, the P low was set at 5 cmH2O, and the T low was set at 1–1.5 times the expiratory time constant, and then adjusted to achieve termination of peak expiratory flow rate (PEFR) of more than 50% PEFR, the release frequency was 10–14 times per minute, and the T high was indirectly calculated based on the T low and release frequency .
As in our case report, the patient was treated with P high at 28 cmH2O, which if the P high was converted from the volume-cycled mode, is the plateau pressure or peak airway pressure in the pressure-cycled mode. The P-value was set at zero to allow end-expiratory or released lung volume to be controlled by time only. The inherent resistance of the artificial airway behaves as a flow resistor and, if coupled with a brief release time, can create auto-PEEP .
Zhout et al. compared the early use of APRV mode with low tidal volume mechanical ventilation in ARDS. APRV was found to improve oxygenation significantly on the third day, with a higher P/F ratio in the APRV group. In this case, our patient showed improved oxygenation and a higher P/F ratio on the first day after intubation . Based on the Carsetti et al. meta-analysis comparing APRV with conventional ventilation strategies in patients with acute hypoxemic failure, APRV has a higher number of ventilator-free days, at 28; a lower intensive care unit (ICU) length of stay; lower hospital mortality; and a higher mean arterial pressure than conventional ventilation .