The Role of CPAP in Treating Respiratory Distress in Patients With COVID-19
On Dec. 31, 2019, the Municipal Health Commission of Wuhan, China, reported a cluster of cases of severe pneumonia of unknown etiology. On Jan. 12, China publicly shared the genetic sequence of the virus that caused the novel pneumonia. On Feb. 11, 2020, the World Health Organization announced the official name for the disease: coronavirus disease 2019, commonly shortened to COVID-19. Shortly thereafter, the International Committee on Taxonomy of Viruses officially named the virus causing COVID-19 as severe acute respiratory syndrome coronavirus (abbreviated SARS-CoV-2).
COVID-19 quickly became a global pandemic. Many patients with COVID-19 developed pneumonia and required ventilators to assist their breathing. The need for ventilators soon overwhelmed the supply of ventilators. With the shortage of ventilators caused by the COVID-19 pandemic, early reports that continuous positive airway pressure (CPAP) therapy prevented or delayed some patients with COVID-19 from progressing to needing a ventilator and reduced chances of death were encouraging. This news created an interest in developing CPAP devices that could provide noninvasive ventilation or using less familiar forms of CPAP such as helmet CPAP and the Boussignac CPAP to counter the ventilator crisis. At the year anniversary of the pandemic, scientists are now aware that CPAP treatment may not be appropriate for all patients with COVID-19.
SARS-CoV-2 belongs to the Coronaviridae family, which consists of enveloped viruses that use ribonucleic acid (RNA) as its genetic material. A viral envelope consists of a lipid bilayer that closely surrounds a capsid (i.e., a shell of proteins that surrounds the viral RNA strand). The SARS-CoV-2 virus’ envelope contains large club or petal-shaped projections, commonly called “spikes” (the scientific name is peplomer [pronounced “PEH-plohmer”]), which appears as a crown (i.e., corona from the Latin for “crown”) under a microscope.
When SARS-CoV-2 infects a cell, the virus’ spike protein interacts with surface receptors for angiotensin-converting enzyme 2 (ACE2) on the host cell’s surface. Through this interaction, the virus enters the host cell. The host cell replicates the virus and is destroyed in the process. In the process of cellular death, the host cell releases various chemicals, as well as new virus particles. Nearby macrophages detect these chemicals and respond by producing proinflammatory cytokines (i.e., proteins that mediate intercellular activity such as the immune response; some examples of cytokines are interleukin 1, interleukin 6 and tumor necrosis factor alpha). These proteins attract other immune cells (e.g., monocytes, macrophages and T cells) to the site of infection, which further promotes inflammation and establishes a proinflammatory feedback loop (a process called “cytokine storm”).
If a person’s immune response is impaired, these immune cells may accumulate in the lungs and overproduce proinflammatory cytokines, which ultimately damages lung tissues. In a person with a healthy immune response, the initial inflammation attracts virus-specific T cells to the site of infection, where they eliminate SARS-CoV-2-infected cells before the virus can spread. Antibodies against the virus are produced, and the virus is neutralized. In the lungs, alveolar macrophages recognize neutralized viruses and dead host cells and clear them by phagocytosis.
To learn more about the use of CPAP in treating COVID-19 patients, read the full article in the 2021 Q2 issue ofA2Zzz.