Lung Injury in COVID-19 vs. High-Altitude Pulmonary Edema

As medical providers around the world struggle to care for patients with acute respiratory failure, secondary to coronavirus, or COVID-19, extreme efforts have been made to compare the virus to other forms of acute respiratory failure observed prior to the current pandemic. Among a number of theories, one that's been made on social media is that COVID-19 lung injury is not like the typical acute respiratory distress syndrome (ARDS) and instead is similar to high altitude pulmonary edema (HAPE).

A group of physicians who have cared for patients with COVID-19 and have cared for patients with HAPE, as well as studied its pathophysiology and management, feel it's important to correct the misconception to adverse effects on management of these patients.

The research collected was conducted into a report published in High Altitude Medicine & Biology. 

Related: Cardiology Organizations Bracing For Major Revenue Drop Because of COVID-19

In the report, the researchers discuss the similarities between HAPE and ARDS, and also highlight the differences between them. ARDS in COVID-19 occurs as a result of an inflammatory response to the presence of the virus, where HAPE doesn't occur as a result of underlying inflammation, but as a result of excessive and uneven hypoxic pulmonary vasoconstriction. Understanding the different mechanisms of HAPE and ARDS is critical for patient management because the treatment for each will be different. Long-term supportive care including mechanical ventilation may be needed to overcome the underlying inflammation in COVID-19.

According to the CDC, HAPE can occur by itself or in conjunction with acute mountain sickness and high-altitude cerebral  edema; incidence is one per 10,000 skiers in Colorado and up to one per 100 climbers at more than 14,000 ft (4,270 m). Initial symptoms are increased breathlessness with exertion, and eventually increased breathlessness at rest, associated with weakness and cough. Oxygen or descent is lifesaving. HAPE can be more rapidly fatal than  HACE.

Erik R. Swenson, MD, editor-in-chief of High Altitude Medicine & Biology, has said it's important to not equate these two diseases because they share some similarities in their radiologic appearance and cause hypoxemia (low blood oxygen content). He added any perceived link of HAPE to COVID-19 lung injury could have deleterious consequences if the same medications useful in HAPE were tried in those with COVID-19 related respiratory failure.

Understanding the distinction between the pathophysiological mechanisms of these entities is critical for patient management, the report says. In most patients, HAPE can be treated with supplemental oxygen alone or descent to lower elevation when supplemental oxygen is not available. Raising the alveolar PO2, or partial oxygen level, decreases pulmonary artery pressure, leading to resolution of the alveolar and interstitial edema and complete recovery within hours to a few days. In contrast, supplemental oxygen may improve hypoxemia in COVID-19, but will not resolve the underlying inflammation or lung injury. Only good supportive care, including mechanical ventilation, allows some patients to survive until their disease resolves.

HAPE can also be prevented or treated with pulmonary vasodilators such as nifedipine or sildenafil which decrease pulmonary artery pressure and lower pulmonary capillary hydrostatic pressure. While use of such medications might decrease pulmonary artery pressure and improve right ventricular function, by releasing hypoxic pulmonary vasoconstriction and increasing perfusion to poorly and nonventilated regions of the lung, they have the potential to worsen ventilation–perfusion, which will worsen hypoxemia.

In addition, these agents may cause or worsen hypotension. Vasodilators such as epoprostenol and nitric oxide do have a role in some patients with severe ARDS due to COVID-19 but only when given the inhalational route which improves rather than impairs ventilation–perfusion matching.

COVID-19 mediated lung injury has proven to be a heterogeneous disease in which patients present with varying degrees of hypoxemia, alterations in lung compliance and other physiologic derangements. During this time, it's encouraged to identify the best means to care for these critically ill patients. That approach should be grounded in sound pulmonary physiology, clinical experience and. It's also encouraged propagation of erroneous theories and treatments with potentially deleterious consequences for patient care, must be avoided.