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| LETTER TO THE EDITOR |
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| Year : 2021 | Volume
: 12
| Issue : 3 | Page : 181-182 |
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COVID-19 happy hypoxemia and high-altitude pulmonary edema – Pathophysiological links?
Harsha Jain, Nitesh Gupta, Pranav Ish
Department of Pulmonary, Critical Care and Sleep Medicine, VMMC and Safdarjung Hospital, New Delhi, India
| Date of Submission | 17-Apr-2021 |
| Date of Decision | 07-May-2021 |
| Date of Acceptance | 07-May-2021 |
| Date of Web Publication | 09-Jul-2021 |
Correspondence Address:
Dr. Pranav Ish
Department of Pulmonary, Critical Care and Sleep Medicine, VMMC and Safdarjung Hospital, New Delhi
India
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/injms.injms_53_21
How to cite this article:
Jain H, Gupta N, Ish P. COVID-19 happy hypoxemia and high-altitude pulmonary edema – Pathophysiological links?. Indian J Med Spec 2021;12:181-2 |
How to cite this URL:
Jain H, Gupta N, Ish P. COVID-19 happy hypoxemia and high-altitude pulmonary edema – Pathophysiological links?. Indian J Med Spec [serial online] 2021 [cited 2023 Mar 31];12:181-2. Available from: http://www.ijms.in/text.asp?2021/12/3/181/321052 |
Dear Editor,
COVID-19 has been reported to be uncommon and mild at high altitudes. Activation of the renin–angiotensin system during the 1st hour of hypoxia at high altitude leads to a transient increase of angiotensin-converting enzyme (ACE2) receptors in the lung, thus offsetting the hypoxia-induced pulmonary vasoconstriction. Subsequently, the expression of ACE2 in the lung decreases after the accumulation of the hypoxia-inducible factor-1. This physiological mechanism of acclimatization to high-altitude hypoxia leading to reduced ACE2 may be the reason for the decrease in the severity of COVID-19 in high-altitude dwellers. Besides, environmental factors may also contribute to reduced incidence of COVID-19 at high altitudes. A study reported only 134 cases of COVID-19 among the nine million inhabitants in Tibet. The investigators identified certain environmental factors including temperature, dry air, and ultraviolet light radiation as possible natural sanitizers. It has also been postulated that due to the lower density of air and distance between molecules at high altitudes, the size of the airborne virus inoculum may be smaller.[1]
COVID-19 patients have been seen to display limited breathlessness, despite profound hypoxemia, referred to as “happy hypoxemia” or silent hypoxemia” (Gattinoni et al., 2020). The mechanism responsible for silent hypoxemia is multifactorial, namely preserved lung compliance (Type L phenotype) and hypoxic pulmonary vasoconstriction (HPV) leading to sizable intrapulmonary shunt and profound hypoxemia.[2] Lately, one more hypothesis is speculated, i.e. high-altitude pulmonary edema (HAPE) hypothesis similar to that seen in patients with acute high-altitude disease who have a chemoreceptor dysfunction.[3] According to this hypothesis, there is a malfunctioning of O2-sensing mechanisms including impaired carotid body function,[4] as shown in [Figure 1]. | Figure 1: Mechanism of silent hypoxemia in SARS-CoV-2 infection – The high-altitude pulmonary edema hypothesis
Click here to view |
Speculation of COVID-19 pathophysiology being similar to HAPE further led to the assumption that therapies used for HAPE can be efficacious in the treatment of COVID-19. But till date, this is unproven and can be harmful. Primary treatment of HAPE is descent to lower altitude, supplemental oxygen and pulmonary vasodilators such as the calcium channel blocker, nifedipine, or the phosphodiesterase-5 inhibitors (sildenafil and tadalafil). However, administration of these drugs in COVID-19 can lead to pulmonary vasodilation which mitigates HPV. This can worsen the already abnormal ventilation-perfusion mismatching in injured regions of the lung and leading to worsening of gas exchange and arterial oxygenation. The reason for this is that HAPE affects pulmonary vasculature characterized by exaggerated, regionally heterogeneous HPV which results in the increased pulmonary artery and capillary pressure leading to hydrostatic capillary damage and alveolar leak of blood and protein, whereas COVID-19 is a predominantly parenchymal disease due to viral inflammation.
To conclude, the pathogenesis of the two diseases (HAPE and COVID-19 pneumonia) is clearly different despite similarities in clinical features and a possible common mechanism for happy hypoxemia. Adoption of prevention and treatment strategies from HAPE for the treatment of patients with COVID-19 pneumonia is not advocated and warrants further studies and research.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | |  |
| 1. | Arias-Reyes C, Zubieta-DeUrioste N, Poma-Machicao L, Aliaga-Raduan F, Carvajal-Rodriguez F, Dutschmann M, et al. Does the pathogenesis of SARS-CoV-2 virus decrease at high-altitude? Respir Physiol Neurobiol 2020;277:103443.  |
| 2. | Gattinoni L, Chiumello D, Caironi P, Busana M, Romitti F, Brazzi L, et al. COVID-19 pneumonia: different respiratory treatments for different phenotypes? Intensive Care Med 2020;46:1099-102. |
| 3. | Hampl V, Herget J, Bííbová J, Baňňasová A, Husková Z, Vaňourková Z, et al. Intrapulmonary activation of the angiotensin-converting enzyme type 2/angiotensin 1-7/G-protein-coupled Mas receptor axis attenuates pulmonary hypertension in Ren-2 transgenic rats exposed to chronic hypoxia. Physiol Res 2015;64:25-38. |
| 4. | Soliz J, Schneider-Gasser EM, Arias-Reyes C, Aliaga-Raduan F, Poma-Machicao L, Zubieta-Calleja G, et al. Coping with hypoxemia: Could erythropoietin (EPO) be an adjuvant treatment of COVID-19? Respir Physiol Neurobiol 2020;279:103476. |
[Figure 1]
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