Hypoxemia

Cardiogenic/distributive/obstructive/hypovolemic shock, carbon monoxide poisoning, severe hypoxemia, severe anemia, and seizures... 

Treatment of severe acute asthma includes the use of oxygen for the rapid reversal of hypoxemia, a short-acting P2-agonist to reverse airway constriction, and a systemic corticosteroid to attenuate the inflammatory response.1 Close monitoring of objective measures such as FEVi or PEF is important to quantify the response to therapy. Because recovery from exacerbations is often gradual, intensified therapy should be continued for several days. 

Patients with an oxygen saturation less than 90% (less than 95% in children, pregnant women, and patients with co-existing heart disease) should receive oxygen with the dose adjusted to keep oxygen saturation above these levels.3,12,40 Hypoxemia usually results from a ventilation/perfusion mismatch, and low oxygen levels (less than 30% of the fraction of inspired air) administered by nasal cannula or facemask are sufficient to reverse hypoxemia in most patients. 

Monitor patients for hypoxemia. Oxygen saturation should be greater than 90% in adults and greater than 95% in children, pregnant women, and patients with co-existing cardiovascular disease. 

In advanced COPD, airflow obstruction, damaged bronchioles and alveoli, and pulmonary vascular abnormalities lead to impaired gas exchange. This results in hypoxemia and eventually hypercapnia. Hypoxemia is initially present only during exercise but occurs at rest as the disease progresses. Inequality in the ventilation/perfusion ratio (VAQ) is the major mechanism behind hypoxemia in COPD. 

Pulmonary hypertension develops late in the course of COPD, usually after the development of severe hypoxemia. It is the most common cardiovascular complication of COPD and can result in cor pulmonale, or right-sided heart failure. Hypoxemia plays the primary role in the development of pulmonary hypertension by causing vasoconstriction of the pulmonary arteries and by promoting vessel wall remodeling. Destruction of the pulmonary capillary bed by emphysema further contributes by increasing the pressure required to perfuse the pulmonary vascular bed. Cor pulmonale is associated with venous stasis and thrombosis that may result in pulmonary embolism. Another important systemic effect is the progressive loss of skeletal muscle mass, which contributes to exercise limitations and declining health status. 

In advanced COPD, signs of hypoxemia may include cyanosis and tachycardia. 

In advanced COPD, caution should be used since overly aggressive administration of oxygen to patients with chronic hypercapnia may result in respiratory depression and respiratory failure. In these patients, mild hypoxemia, rather than carbon dioxide accumulation, triggers their drive to breathe. 

Metabolic alkalosis is characterized by an increased arterial pH, a primary increase in the HCOf concentration, and a compensatory increase in the PaC02. Patients will always hypoventilate to compensate for metabolic alkalosis—even if it results in profound hypoxemia. For a metabolic alkalosis to persist there must concurrently be a process that elevates serum HC03 concentration (gastric or renal loss of acids) and another that impairs renal HC03 excretion (hypovolemia, hypokalemia, or mineralocorticoid excess). The etiologies of metabolic alkalosis are listed in Table 25-5. 

Respiratory acidosis is characterized by a reduced arterial pH, a primary increase in the arterial PaC02 and, when present for sufficient time, a compensatory rise in the HCOf concentration. Because increased C02 is a potent respiratory stimulus, respiratory acidosis represents ventilatory failure or impaired central control of ventilation as opposed to an increase in C02 production. As such, most patients will have hypoxemia in addition to hypercapnia. The most common etiologies of respiratory acidosis are listed in Table 25-6. 

Provide supportive measures that counter physiologic abnormalities such as hypoxemia, hypotension, and impaired tissue oxygenation. 

Patent ductus arteriosus Failure of the ductus arteriosus to close, resulting in neonatal hypoxemia. 

Hypoventilation is defined as a reduction in the rate and depth of breathing. Inadequate ventilation results in hypoxemia, or a decrease in the concentration of oxygen in the arterial blood. Hypoventilation may be induced inadvertently by various pharmacological agents, including opioid analgesics such as morphine. These medications cause hypoventilation by way of their effects on the respiratory centers in the brainstem. Doses of... 

Ventilation-perfusion mismatch leads to hypoxemia. Reduced ventilation caused by obstructed airflow or reduced perfusion caused by obstructed blood flow leads to impaired gas exchange. Interestingly, each of these conditions is minimized by local control mechanisms that attempt to match airflow and blood flow in a given lung unit. 

Chemoreceptor response to decreased arterial P02. Hypoxia has a direct depressant effect on central chemoreceptors as well as on the medullary respiratory center. In fact, hypoxia tends to inhibit activity in all regions of the brain. Therefore, the ventilatory response to hypoxemia is elicited only by the peripheral chemoreceptors. 

J.F. Martinez-Tica, R. Berbarie, P. Davenport, and M.H. Zornow, Monitoring brain p02, pC02, and pH during graded levels of hypoxemia in rabbits. J. Neurosurg. Anesthesiol. 11, 260-263 (1999). 

L. Padnick-Silver and R.A. Linsenmeier, Effect of hypoxemia and hyperglycemia on pH in the intact cat retina. Archives of Ophthalmol. 123, 1684-1690 (2005). 

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