Recommendations for continuous oxygen therapy in chronic obstructive lung disease. Report of the Committee on Emphysema. American College of Chest Physicians.

Although expiratory air flow obstruction is the physiologic sine qua non of chronic obstructive lung disease, tissue hypoxia ultimately accounts for the bulk of systemic physiologic changes. Tissue hypoxia results not only from an inadequate pulmonary gas exchange resulting in decreased oxygenation of arterial blood leaving the lungs (hypoxemia), but also from reductions in hemoglobin concentration and thus oxygen-carrying capacity of the blood. Hypoxia is also caused by inadequate tissue perfusion due to low cardiac output, structurally altered or poorly regulated regional circulation and from an inability of cellular enzymes to utilize the oxygen presented. In addition to these factors which result in tissue hypoxia, oxygen transport is influenced by the hemoglobin-oxygen affinity described by the oxyhemoglobin-dissociation curve and by the body’s oxygen consumption influenced by such factors as temperature, pH and muscular activity. Oxygen therapy changes only the level of oxygen in the arterial blood. But to the extent that there is less hypoxemia, total oxygen transport increases and improved tissue oxygenation occurs. Because multiple factors influence the degree of tissue hypoxia, it is not possible to delineate precisely a value of arterial oxygen saturation or oxygen tension (Pao2), which will result in adequate oxygenation for all organs. Disregarding the precise level at which alterations occur the major immediate effects of hypoxia include altered physiology in the pulmonary vasculature, systemic circulation, central nervous system and kidneys.1 The predominant pulmonary response to hypoxemia is an increase in pulmonary vascular resistance while systemically there is increased cardiac output and decreased vascular resistance, sometimes associated with tachycardia and sometimes with small increases in mean arterial pressure. Acute hypoxemia may produce a variety of cardiac arrhythmias and persistent pulmonary hypertension results in right ventricular hypertrophy. The effects of hypoxia on cerebral function encompass a wide spectrum of deficits from the most subtle personality changes to headache, somnolence, convulsions and syncope. Altered renal physiology attributable to hypoxemia ranges from an increase in renal blood flow with mild degrees of hypoxemia to decreased blood flow and decreased excretion of salt and water with more severe hypoxemia. Systemic oxygen transport is the product of arterial blood oxygen content and the cardiac output. Some altered cardiovascular responses, particularly those related to increases in blood flow, may be considered compensatory mechanisms since oxygen transport is thereby improved. Through stimulation of erythropoietin, erythrocytosis follows hypoxemia. The magnitude of the bone marrow response is roughly proportional to the degree of hypoxemia and the increase in oxygen carried is proportional to the amount of circulating hemoglobin: Each gram of normal adult hemoglobin is capable of transporting 1.39 ml of oxygen when completely saturated.28 The amount of oxygen transported by hemoglobin in 100 ml of blood is equal to the hemoglobin concentration times 1.39 times the percent saturation per 100 (Hgb x 1.39 x sat 02). Thus, the presence of anemia may have an overriding influence upon the amount of oxygen delivered to tissues even when hypoxemia is corrected. The amount of oxygen carried by a molecule of hemoglobin is further dependent upon the physicochemical characteristics of the hemoglobin protein and the factors which affect the affinity of oxygen for hemoglobin. Red cell age, blood hydrogen ion concentration [H +] and Pco2, temperature, genetic type of hemoglobin and the quantity of 2,3 diphosphoglycerate (DPG) are known to influence oxygenhemoglobin affinity. Less affinity of hemoglobin for oxygen is seen with acidosis, hypercapnia, elevated