Összefoglaló. Számos közlemény született arról, hogy a COVID–19-pneumoniás betegek jelentős hányadában az artériás parciális oxigéntenzió kifejezetten alacsony, mégsem jellemző a dyspnoe, és a pulzusoximetria sem mutat – a csökkent oxigéntenzióval arányos – súlyos hypoxaemiát. A jelenséget „happy hypoxaemia” néven említik. Ugyanakkor a légszomjról nem panaszkodó, de súlyos alveolocapillaris O2-felvételi zavarban szenvedő COVID–19-pneumoniás betegek a legkisebb fizikai megterhelést sem tűrik, és állapotuk gyorsan kritikussá válhat, tehát a hypoxaemia mértékének időben való felismerése kulcskérdés. A jelen közleményben egy ilyen eset rövid ismertetése után összefoglaljuk a súlyos, de tünetmentes hypoxaemia hátterében meghúzódó élettani okokat. Ezek között szerepel a hypocapnia (respiratoricus alkalosis) is, mely alacsony oxigéntenzió mellett is a hemoglobin viszonylag megtartott oxigénszaturációját eredményezi. Ezért a mindennapi COVID–19-ellátásban a megismételt artériásvérgáz-meghatározások jelentősége nem hangsúlyozható eléggé. Orv Hetil. 2021; 162(10): 362–365.
Summary. Many COVID-19 patients have very low arterial partial oxigen tension while severe dyspnoe does not develop. Pulse oxymetry indicates only moderate reduction of arterial O2 saturation in these patients. The phenomenon is named “happy hypoxaemia”. Lack of (severe) dyspnoe and only moderately decreased O2 saturation in severely impaired alveolo-capillary O2 uptake may partially be explained by an increased oxygen affinity of hemoglobin in the presence of low arterial partial pressure of CO2. The latter results from increased alveolar ventilation, while low partial pressure of O2 in COVID-19 patients reflects right-to-left shunting of pulmonary blood flow and ventilation-perfusion mismatch of the diseased lungs. While such patients may have mild complaints as related to the real impairment of alveolo-capillary oxygen exchange, severe hypoxaemia is a negative prognostic factor of outcome in this state where severe clinical deterioration may rapidly appear. The latter circumstance together with the unusual relationship of O2 partial pressure and O2 saturation of hemoglobin in COVID-19 emphasize the importance of repeated complete arterial blood gas analyses in these patients. Orv Hetil. 2021; 162(10): 362–365.
Wu Z, McGoogan JM. Characteristics of and important lessons from the coronavirus disease 2019 (COVID-19) outbreak in China: summary of a report of 72 314 cases from the Chinese Center for Disease Control and Prevention. JAMA 2020; 323: 1239–1242.
Xie J, Tong Z, Guan X, et al. Critical care crisis and some recommendations during the COVID-19 epidemic in China. Intensive Care Med. 2020; 46: 837–840.
Tobin MJ, Laghi F, Jubran A. Why COVID-19 silent hypoxemia is baffling to physicians. Am J Respir Crit Care Med. 2020; 2020: 356–360.
Wilkerson RG, Adler JD, Shah NG, et al. Silent hypoxia: a harbinger of clinical deterioration in patients with COVID-19. Am J Emerg Med. 2020; 38: 2243.e5–2243.e6.
Ottestad W, Seim M, Maehlen JO. COVID-19 with silent hypoxemia. Tidsskr Nor Laegeforen. 2020 Apr 11; 140(7). . [English, Norwegian]
Gattinoni L, Coppola S, Cressoni M, et al. COVID-19 does not lead to a “typical” acute respiratory distress syndrome. Am J Respir Crit Care Med. 2020; 201: 1299–1300.
Ottestad W, Søvik S. COVID-19 patients with respiratory failure: what can we learn from aviation medicine? Br J Anaesthesia 2020; 125: e280–e281.
Xie J, Covassin N, Fan Z, et al. Association between hypoxemia and mortality in patients with COVID-19. Mayo Clin Proc. 2020; 95: 1138–1147.
Vaporidi K, Akoumianaki E, Telias I, et al. Respiratory drive in critically ill patients. Pathophysiology and clinical implications. Am J Respir Crit Care Med. 2020; 201: 20–32.
Manning HL, Schwartzstein RM. Pathophysiology of dyspnea. N Engl J Med. 1995; 333: 1547–1553.
Easton PA, Slykerman LJ, Anthonisen NR. Ventilatory response to sustained hypoxia in normal adults. J Appl Physiol. 1986; 61: 906–911.
Weil JV, Byrne-Quinn E, Sodal IE, et al. Hypoxic ventilatory drive in normal man. J Clin Invest. 1970; 49: 1061–1072.
Gattinoni L, Chiumello D, Caironi P, et al. COVID-19 pneumonia: different respiratory treatments for different phenotypes. Intensive Care Med. 2020; 46: 1099–1102.
Guan WJ, Ni ZY, Hu Y, et al. Clinical characteristics of coronavirus disease 2019 in China. N Eng J Med. 2020; 382: 1708–1720.
Dhont S, Derom E, Van Braeckel E, et al. The pathophysiology of “happy” hypoxemia in COVID-19. Respir Res. 2020; 21: 198.
Ackermann M, Verleden SE, Kuehnel M, et al. Pulmonary vascular endothelialitis, thrombosis, and angiogenesis in COVID-19. N Engl J Med. 2020; 383: 120–128.
Kelman GR, Nunn JF. Nomograms for correction of blood PO2, PCO2, pH, and base excess for time and temperature. J Appl Physiol. 1966; 21: 1484–1490.
Woyke S, Rauch S, Ströhle M, et al. Modulation of Hb-O2 affinity to improve hypoxemia in COVID-19 patients. Clin Nutr. 2021; 40: 38–39.
Divani AA, Andalib S, Biller J, et al. Central nervous system manifestations associated with COVID-19. Curr Neurol Neurosci Rep. 2020; 20: 60.