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• W2055716701 abstract "We agree with P M A Calverley's1Calverley PMA Oxygen-induced hypercapnia revisited.Lancet. 2000; 356: 1538-1539Summary Full Text Full Text PDF PubMed Scopus (19) Google Scholar interpretation of the available data on oxygen-induced hypercapnia. We wish to suggest potential additional mechanisms for hyperoxic hypercapnia in acute exacerbations of chronic to those discussed. Although rare, the occasional patient with acute exacerbations will develop severe acute on chronic respiratory acidosis (partial pressure of carbon dioxide [paCO2] >20 kPa) when given oxygen. We believe that there are five distinct mechanisms that could underlie hyperoxic hypercarbia (figure). First, the Haldane effect refers to the reduction in haemoglobin affinity for CO2 with the binding of oxygen to haemoglobin. The CO2 that is released from haemoglobin leads to a small increase in PaCO2. Second, the increase in oxygen tension in lung units with low ventilation/perfusion (V/Q) ratios can blunt hypoxic pulmonary vasoconstriction in these low V/Q lung units, thus diverting perfusion away from high V/Q lung units (effectively increasing dead space in these latter lung units, ie, worsening CO2 elimination).2 CO2-induced bronchodilation might contribute to this mechanism.2 Third, data on PCO2 recruitment threshold in intubated patients with chronic obstructive pulmonary disease (COPD) persuasively support a change in sensitivity of the central nervous system to CO2 during hyperoxia, compared with normoxia.3Dunn WF Nelson SB Hubmayr RD Oxygen-induced hypercapnia in obstructive pulmonary disease.Am Rev Respir Dis. 1991; 144: 526-530Crossref PubMed Google Scholar Fourth, we believe that some patients with acute exacerbations of COPD are especially susceptible to the development of severe hypercapnia due to sleep deprivation that is common in acute illness before clinical presentation. Patients with underlying obstructive sleep apnoea might be particularly susceptible since they are acutely and chronically sleep deprived.4Wylam M Hall JB Cardiopulmonary failure associated with sleep disordered breathing.in: Hall JB Schmidt GA Wood LDH McGraw-Hill, New York1998: 609-616Google Scholar In acute exacerbations of COPD, oxygen may have anxiolytic and antidyspnoeic effects that allow the onset of sleep in people with high sleep drive. Therefore, the observed hypoventilation could be secondary to a reduced hypercapnic ventilatory response (sleep deprivation5White DP Douglas NJ Pickett CK Zwillich CW Weil JV Sleep deprivation and the control of ventilation.Am Rev Respir Dis. 1983; 128: 984-986PubMed Google Scholar); the loss of the wakefulness drive to breathe at the time of sleep onset; and the elimination of hypoxic drive. Previous sleep deprivation also increases the subsequent arousal threshold. Therefore, the development of CO2 narcosis could, in fact, be triggered by the onset of sleep. Fifth, during non-invasive oxygen administration, the actual fractional oxygen concentration delivered is dependent on minute ventilation and inspiratory flow demand. Therefore, as patients undergo a gradual reduction in minute ventilation by the above mechanisms,2Robinson TD Freiberg DB Regnis JA Young IH The role of hypoventilation and ventilation-perfusion redistribution in oxygen-induced hypercapnia during acute exacerbations of chronic obstructive pulmonary disease.Am J Respir Crit Care Med. 2000; 161: 1524-1529Crossref PubMed Scopus (137) Google Scholar the actual fractional oxygen concentration delivered gradually increases, despite no change in the oxygen flow rate from the source. The result can be a vicious cycle of increasing fractional oxygen with worsening hypercapnia, leading to severe respiratory acidosis in some patients. We believe that all five of these mechanisms might be relevant to acute exacerbations of COPD. We agree with Calverley's recommendations to judiciously limit fractional oxygen concentration in COPD patients with acute or chronic respiratory acidosis. Although most patients experience a small increase in PaCO2 with oxygen administration, the occasional patient might enter one of the cycles we describe and develop life-threatening hypercapnia." @default.
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• W2055716701 title "Dementia and statins" @default.
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• W2055716701 doi "https://doi.org/10.1016/s0140-6736(05)71817-1" @default.
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