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Why you shouldn’t handle COVID-19 ARDS like HAV

 


COVID-19 Do not treat Acute Respiratory Distress Syndrome (ARDS) as if it were High Alveolar Edema (HAPE).

Unusual observation The calmness of patients with hypoxia saturation in hospitalized COVID-19 patients (such as hypoxia without a significant reduction in lung compliance or increased work of breathing and attention) has led to confusion and speculation.

ARDS and HAPE share some clinical similarities, including hypoxemia, radiopacity, and altered lung compliance. Wrote in American Thoracic Society Annual Report.

However, “the pathophysiological mechanisms of COPE-19-induced HAPE and lung injury are fundamentally different, and entities cannot be equated,” the team wrote.

While HADS concentrates in the exaggerated, hypoxic pulmonary vasoconstriction across the lung, ARDS is typically from the virus that causes the COVID-19 coronavirus, SARS-C0V-2. It is caused by a strong host cytokine-mediated inflammatory response that applies to ARDS. . In the case of ARDS, elevated pulmonary arterial pressure is the result, not the cause.

HAPE treatments-systemically administered pulmonary vasodilators and acetazolamide-should not be used for COVID-19. This is because there is a risk of multiple adverse effects including poor ventilation-perfusion matching, poor carbon dioxide transport, systemic hypotension, and increased work. Breathing Hazard, ”Lux and Swenson warned.

Increasing oxygen helps in both conditions, but not in solving lung damage with COVID-19 as it does with HAPE. “Instead, time and proper supportive care often involve a long course of invasive mechanical ventilation and are needed to allow the lungs to heal,” Luks and Swenson write.

Pulmonary vasodilators such as nifedipine, sildenafil (Revatio), tadalafil (Adcirca) can be used for hypoxic pulmonary vasoconstriction and lowering pulmonary arterial pressure. However, these drugs actually exacerbate gas exchange and arterial oxygenation in hypoxic COVID-19 patients because lung injury patients rely on their vasoconstriction to maintain adequate ventilation and perfusion alignment That is expected, the authors said.

Other pulmonary vasodilators, such as epoprostenol and nitric oxide, may help some of the COVID-19 ARDS. Administered by inhalation, allowing preferential delivery to the ventilated area of ​​the lung. It can selectively vasodilate in these areas, and in non-ventilated areas it can improve the matching of ventilation and perfusion, resulting in improved oxygenation. “

Luks and Swenson warn that the respiratory stimulant acetazolamide is not a good idea because it can cause dyspnea, which can cause dyspnea and respiratory failure in patients with respiratory muscle fatigue. did. “In addition, existing metabolic acidosis is exacerbated if the patient is unable to increase ventilation adequately. High dose and / or renal dysfunction may lead to hypercapnic respiratory failure, as occurs in patients with severe COPD. Increases the risk of erythrocyte CA inhibition that can cause and limited respiratory reserve. “

Respiratory stimulant aluminthine, which is also being discussed on COVID-19’s social media, has been discontinued in some countries because it is not available in the United States and may cause polyneuropathy.

Luks and Swenson suggested that hypoxia, which did not significantly reduce COVID-19 compliance, may reflect acute symptoms. “By starting mechanical ventilation earlier than usual, we may only be observing the earliest stages of ARDS in some patients. But, as evidenced by other published reports, Many patients with COVID-19 lung injury have been reported in other ARDS studies. ”

Disclosure

Luks and Swenson do not disclose sources of support.

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