One predictable feature of a novel disease is that initial guidelines for treatment may need to be revised, as medical understanding of the disease evolves.

Initially, patients with COVID-19 experiencing severe respiratory distress were supposed to be intubated and placed on ventilators early, and non-invasive ventilation procedures like CPAP, BiPAP, and high-flow nasal cannula were to be avoided because they might spread the disease.

Over the course of the pandemic, we’ve seen additional evidence that a population of COVID-19 patients can be treated effectively with CPAP/BiPAP, and may not even need to be invasively ventilated.

These patients are what’s informally called the “silent hypoxemic” – they have very low oxygen levels, but are otherwise surprisingly functional (they can talk, have minimal altered mental status, etc) and they do _not _have the noncompliant lungs typical of ARDS. Therefore, following typical ventilation procedures like ARDSNet, in which patients are intubated when their oxygen saturation drops below a certain point, and placed on mechanical ventilation with high pressures, is actually a _bad _idea. Excessive PEEP for compliant lungs can cause barotrauma; and intubation in general carries risks (of e.g. hospital-acquired infections, damage to the airway, and PTSD) so if a patient can recover with _non-invasive _respiratory support, it’s safer to avoid intubation.

This clinical picture was once purely anecdotal, but the data is starting to come in.

Helmet CPAP, in which a continuous positive pressure of oxygenated air is administered through a clear helmet that covers the patient’s whole head, has been extensively used for COVID-19 patients in Italy. The helmet is more comfortable than traditional CPAP masks, and has a tighter seal, to avoid spreading virus particles to healthcare workers. The RICU of the L. Sacco University hospital in Milan had 75% of their severe COVID-19 patients on helmet CPAP, and had an in-hospital mortality rate of only 25%, compared to Seattle ICUs, which had a 50% in-hospital mortality rate and had 100% of patients on invasive mechanical ventilation.[1]

Helmet CPAP is much less likely to disperse exhaled air than conventional CPAP, making the risks of infection to healthcare workers lower; a study found that air only dispersed 2.5 cm from the helmet.[6]

Italian intensive care physicians observed that 50% of the 150 severe COVID-19 patients in their ICU were the “silent hypoxemia” type, characterized by “severe hypoxemia often associated with near normal respiratory symptom compliance.” They describe COVID-19 pneumonia as belonging to two separate “phenotypes”, Type L and Type H.

Type L COVID-19 has low elastance (= normally compliant lungs), low lung recruitability (most lung tissue is receiving air), but extreme hypoxemia due to ventilation-perfusion mismatch. That is, the lung is receiving oxygen but not blood flow, so the blood doesn’t get properly oxygenated.

These Type L patients may improve or suddenly worsen. Increased inflammation and negative intrathoracic pressure can cause swelling and fluid buildup in the lungs. (High inspiratory pressures literally suck fluid from capillaries into lung tissue, which contributes to pulmonary edema.) Increased edema transitions the patient to the Type H phenotype: high elastance (= noncompliant lungs), high recruitability (= lots of non-aerated lung tissue), and atelectasis (= collapsed alveoli).

This clinical picture implies that Type L patients should be treated noninvasively with high concentrations of oxygen (through masks or, in dyspneic patients, high-flow nasal cannula, CPAP, or BiPAP). Patients at risk of transitioning to type H, as measured by high inspiratory pressures, should be intubated, and type H patients should be placed on standard invasive ventilation for severe ARDS.[2]

A case report from Norway illustrates a typical case of “silent hypoxemia” in COVID-19: a man in his sixties with an O2 saturation of 66% who nevertheless seemed calm, was “smiling bravely”, and breathing almost silently. Hypocapnia (low CO2) meant there was little or no sensation of breathlessness despite the extremely low oxygen saturation.[5]

Three ICU doctors at the University College London hospital argued in the _Lancet Respiratory Medicine _against early intubation for COVID-19, saying

“Early intubation of a patient with known or suspected COVID-19 with respiratory distress could result in the intubation and mechanical ventilation of patients who would have otherwise improved on CPAP or NIV”.[3]

They note that the highest incidence of disease transmission to healthcare workers was on general wards, not ICU, i.e. where healthcare staff were least likely to wear personal protective equipment, and that NIV did not increase the risk of disease transmission during the SARS epidemic.

Similarly, a statement by tropical disease experts about treating COVID-19 in low-resource areas argues

“It seems that in a significant proportion of relatively younger patients, hypoxemia, even less than 88%, is reasonably well tolerated and not accompanied by severe respiratory distress or exhaustion. With the current experience, the trigger for intubation should, within certain limits, probably not be based on hypoxemia alone but more on respiratory distress and fatigue….Invasive ventilation can save lives in patients with severe respiratory distress. However, it can also aggravate or even cause damage,including barotrauma (air leaks, caused by high ventilation pressures), volutrauma (pulmonary edema, due to large tidal volumes), atelectrauma (repetitive opening and closing of vulnerable lung parts with atelectasis), biotrauma (local inflammation with spill to the systemic circulation of inflammatory mediators, bacteria, or bacterial products), and oxytrauma (by free oxygen radicals).”

The authors recommend, when COVID-19 patients are intubated, using lower PEEP and lower tidal volume than would be typical for ARDS, to avoid ventilator-induced injury.[4]

Early awake self-proning in COVID-19 patients can be very beneficial for the “silent hypoxemic” or “type L” patient population. One emergency department in New York City found that in 50 patients, the median SpO2 was 80% at triage, 84% after supplemental oxygen, and 94% after patients were encouraged to lie on their stomachs (in the prone position.) [7]

“In New York City, during the early stages of the COVID-19 pandemic, patients presented en masse with moderate to severe hypoxia. Some of these patients were distressed, quickly deteriorated and required endotracheal intubation. COVID-19 produced another group of patients whose pathophysiology confounded existing disease patterns, however. These patients had low oxygen saturations (SpO2 <90%), but were not in significant respiratory distress and often appeared clinically well; this group has been informally referred to as happy hypoxemics.”

One of the authors of the above article, Richard Levitan, an emergency physician in New York City, wrote a New York Times op-ed [8] about this phenomenon. They were seeing COVID-19 pneumonia in nearly every patient who came into the emergency department, even those without respiratory symptoms.

“The patient stabbed in the shoulder, whom we X-rayed because we worried he had a collapsed lung, actually had Covid pneumonia. In patients on whom we did CT scans because they were injured in falls, we coincidentally found Covid pneumonia. Elderly patients who had passed out for unknown reasons and a number of diabetic patients were found to have it.

“And here is what really surprised us: These patients did not report any sensation of breathing problems, even though their chest X-rays showed diffuse pneumonia and their oxygen was below normal. How could this be?

“Patients compensate for the low oxygen in their blood by breathing faster and deeper — and this happens without their realizing it. This silent hypoxia, and the patient’s physiological response to it, causes even more inflammation and more air sacs to collapse, and the pneumonia worsens until oxygen levels plummet. In effect, patients are injuring their own lungs by breathing harder and harder. Twenty percent of Covid pneumonia patients then go on to a second and deadlier phase of lung injury. Fluid builds up and the lungs become stiff, carbon dioxide rises, and patients develop acute respiratory failure.”

Dr. Levitan recommends that healthy people, and people who test positive for COVID-19, get pulse oximeters – available over at the counter at the drugstore – to monitor their oxygen levels _before _they get sick enough to need a hospital. Silent hypoxemia doesn’t come with symptoms, so most infected patients don’t get supplemental oxygen until they’ve progressed to severe lung injury that requires ventilation. If they caught the problem earlier, they could get supplemental oxygen and recover without ever needing to be ventilated.


[1]Radovanovic, Dejan, et al. “Helmet CPAP to Treat Acute Hypoxemic Respiratory Failure in Patients with Covid-19: A Management Strategy Proposal.” Journal of Clinical Medicine 9.4 (2020): 1191.

[2]Gattinoni, Luciano, et al. “COVID-19 pneumonia: different respiratory treatments for different phenotypes?.” Intensive care medicine (2020): 1.

[3]Arulkumaran, Nishkantha, et al. “Use of non-invasive ventilation for patients with COVID-19: a cause for concern?.” The Lancet. Respiratory Medicine (2020).

[4]Dondorp, Arjen M., et al. “Respiratory Support in Novel Coronavirus Disease (COVID-19) Patients, with a Focus on Resource-Limited Settings.” The American Journal of Tropical Medicine and Hygiene (2020): tpmd200283.

[5]Ottestad, William, Mari Seim, and Jens Otto Mæhlen. “COVID-19 with silent hypoxemia.” Tidsskrift for Den norske legeforening (2020).

[6]Whittle, Jessica S., et al. “Respiratory Support for Adult Patients with COVID‐19.” Journal of the American College of Emergency Physicians Open (2020).

[7]Caputo, Nicholas D., Reuben J. Strayer, and Richard Levitan. “Early Self‐Proning in Awake, Non‐intubated Patients in the Emergency Department: A Single ED’s Experience during the COVID‐19 Pandemic.” Academic Emergency Medicine (2020).