Role of proning and positive end-expiratory pressure in COVID-19

Table 1 Acute respiratory distress syndrome definition

ARDS definition
Onset	Within 1 wk of a known clinical insult or new or worsening respiratory symptoms
Chest imaging	Bilateral opacities – not fully explained by effusions, lobar/lung collapse, or nodules on either Chest X-ray or computed X-ray tomography scan
Origin of edema	Respiratory failure not fully explained by heart failure or fluid overload; Need objective assessment (e.g., echocardiogram) to exclude hydrostatic edema if no risk factors present
Oxygenation	PaO2/FiO2 ratio < 300 with PEEP > 5 cm/H2O

ARDS: Acute respiratory distress syndrome; PEEP: Positive end-expiratory pressure.

Table 2 Acute respiratory distress syndrome severity and associated mortality

PaO2/FiO2 ratio (with PEEP > 5 cm/H2O)	ARDS severity	Mortality (95%CI)
200-300	Mild	27% (24-30)
100-200	Moderate	32% (29-34)
< 100	Severe	45% (42-48)

PEEP: Positive end-expiratory pressure; ARDS: Acute respiratory distress syndrome; CI: Confidence interval.

Table 3 Histopathological features of 2009 H1N1, severe acute respiratory syndrome and severe acute respiratory syndrome coronavirus 2

Virus	Number of patients	Diffuse alveolar damage, n (%)	AFOP, n (%)	Organizing fibrosis, n (%)	End-stage fibrosis, n (%)	Superimposed pneumonia, n (%)	Microthrombi, n (%)	Pulmonary thrombosis, n (%)
2009 H1N1	287	90	0.30	40	3	30	24	6
SARS	64	98	9	47	6	31	58	28
SARS-CoV-2	171	88	4	52	1	32	57	15

AFOP: Acute fibrinous and organizing pneumonia; SARS: Severe acute respiratory syndrome; SARS-CoV-2: Severe acute respiratory syndrome coronavirus 2.

Table 4 Different views of Gattinoni et al[12] and Tobin et al[17]

Gattinoni et al[12]	Tobin et al[17]
Silent hypoxemia is caused by vasoplegia which increases the respiratory drive and increases the tidal volume, causing negative intrathoracic pressure. Dyspnea is not endorsed in the setting of near-normal respiratory compliance	Silent hypoxemia is caused by underlying physiologic mechanism such as fever causing right shift of oxygen dissociation curve, unreliability of pulse oximeter at SaO2 < 80% and decreased chemoreceptor response to PaO2 < 60 mmHg with normocapnia
Increased tidal volume causing progressive increase in negative intrathoracic pressure results in P-SILI	P-SILI needs further research and increase in tidal volume is not associated with requiring intubation, whereas, underlying critical condition leads to intubation
Esophageal manometric measurement of work of breathing is crucial to determine the inspiratory efforts of the patient. Esophageal pressure > 15 is associated with increased risk of lung injury and patient should be intubated as early as possible	No data available to support the arbitrary measurement of esophageal pressure as an indication of intubation. Also, insertion of esophageal balloon in dyspneic COVID-19 patients increases the risk for intubation
Early intubation is advised along with esophageal manometric measurement of work of breathing	Less liberal use of intubation and mechanical ventilation. Should be used when hypoxia is accompanied with increased work of breathing and severe respiratory distress
Spontaneous breathing trials should be implemented only at the end of the weaning process as strong spontaneous efforts raise oxygen demand, edema and P-SILI	Weaning and spontaneous breathing trial should be initiated as early as 24 h after initial intubation

P-SILI: Patient-self-induced lung injury; COVID-19: Coronavirus disease 2019.

Table 5 Studies on awake proning in coronavirus disease 2019

Ref.	Study sample	Percentage of patients prone, n (%)	Improvement in oxygenation amongst prone (percentage of patients), n (%)
Caputo et al[35]	50	100 (50)	76
Elharrar et al[36]	24	63 (15)	25
Sartini et al[37]	15	100 (15)	80
Xu et al[33]	10	100 (10)	100
Coppo et al[38]	56	84 (47)	100