Porth's Essentials of Pathophysiology, 4e

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Disorders of Ventilation and Gas Exchange

C h a p t e r 2 3

deoxygenated hemoglobin, and an infrared-wavelength light that is absorbed by oxygenated hemoglobin and passes through deoxygenated hemoglobin. The pulse oximeter cannot distinguish between oxygen–carrying hemoglobin and carbonmonoxide–carrying hemoglobin. In addition, the pulse oximeter cannot detect elevated levels of methemoglobin. Although pulse oximetry is not as accurate as arterial blood gas measurements, it pro- vides the means for noninvasive and continuous moni- toring of O 2 saturation, which is a useful indicator of respiratory and circulatory status. Treatment of hypoxemia is directed toward correct- ing the cause of the disorder and increasing the gradient for diffusion through the administration of supplemen- tal oxygen. Oxygen may be delivered by nasal cannula or mask or administered directly into an endotracheal or tracheostomy tube in persons who are mechanically ventilated. 3 A high-flow administration system is one in which the flow rate and reserve capacity are sufficient to provide all the inspired air. A low-flow administration system delivers less than the total inspired air. The con- centration of O 2 being administered (usually determined by the flow rate) is based on the PO 2 . Ahigh flow ratemust be carefully monitored in persons with chronic lung dis- ease because increases in alveolar oxygen concentration above the person’s baseline may suppress the hypoxia- induced ventilatory drive. Although oxygen is necessary and vital to life, there also is the danger of oxygen toxic- ity with concentrations above 60%. Continuous breath- ing of oxygen at high concentrations can lead to diffuse parenchymal lung injury due to oxygen free radicals. Persons with healthy lungs begin to experience respira- tory symptoms such as cough, sore throat, substernal distress, nasal congestion, and painful inspiration after breathing pure oxygen for 24 hours. 2 Hypercapnia Hypercapnia refers to an increase in the carbon diox- ide content of the arterial blood. 3,6 The PCO 2 is pro- portional to carbon dioxide production and inversely related to alveolar ventilation. The diagnosis of hyper- capnia is based on physiologic manifestations and arte- rial blood gas levels. Hypercapnia can occur in a number of disorders that cause hypoventilation or mismatching of ventilation and perfusion. 3,6 The diffusing capacity of carbon dioxide is 20 times that of oxygen; therefore, hypercapnia without hypoxemia is usually observed only in situations when supplemental oxygen is provided. In cases of ventilation– perfusion mismatching, hypercapnia is usually accom- panied by a decrease in arterial PO 2 levels. Conditions that increase carbon dioxide production, such as an increase in metabolic rate or a high-carbohydrate diet, can contribute to the degree of hypercapnia that occurs in persons with impaired respiratory function. Changes in the metabolic rate resulting from an increase in activ- ity, fever, or disease can have profound effects on carbon dioxide production. Alveolar ventilation usually rises proportionally with these changes, and hypercapnia

occurs only when this increase is inappropriate or a compensatory rise in alveolar ventilation is inadequate. Hypercapnia affects a number of body functions, including acid–base balance, as well as kidney, nervous system, and cardiovascular function. Elevated levels of PCO 2 produce respiratory acidosis (see Chapter 8). The body normally compensates for an increase in PCO 2 by increasing renal bicarbonate (HCO 3 – ) retention, which results in an increase in serum HCO 3 – and pH levels. As long as the pH is within normal range, the main complications of hypercapnia are those resulting from the accompanying hypoxia. Because the body adapts to chronic increases in blood levels of carbon dioxide, per- sons with chronic hypercapnia may not have symptoms until the PCO 2 becomes markedly elevated, causing respiratory depression and altered mental status. The treatment of hypercapnia is directed at decreasing the work of breathing and improving the ventilation– perfusion balance. The use of intermittent rest therapy, such as nocturnal negative-pressure ventilation, in per- sons with chronic obstructive pulmonary disease or chest wall disease may be effective in increasing the strength and endurance of the respiratory muscles and improving the PCO 2 . Respiratory muscle retraining aimed at improv- ing the respiratory muscles, their endurance, or both has been used to improve exercise tolerance and diminish the likelihood of respiratory fatigue. Mechanical ventilation may become necessary in situations of acute hypercapnia. ■■ The primary functions of the respiratory system are to remove appropriate amounts of carbon dioxide from the blood entering the pulmonary circulation and provide adequate amount of oxygen to blood leaving the pulmonary circulation. This is accomplished through the process of ventilation, in which air moves into and out of the lungs, and diffusion, in which gases move between the alveoli and the pulmonary capillaries. Although both affect gas exchange, oxygenation of the blood largely depends on diffusion, while removal oxygen levels that results in a decrease in tissue oxygenation. Hypoxemia can occur as the result of hypoventilation, diffusion impairment, shunt, and ventilation–perfusion abnormalities. Acute hypoxemia is manifested by increased respiratory effort (increased respiratory and heart rates), cyanosis, and impaired sensory and neurologic function.The body compensates for chronic hypoxemia by increased ventilation, pulmonary vasoconstriction, and increased production of red blood cells. SUMMARY CONCEPTS of carbon dioxide depends on ventilation. ■■ Hypoxemia refers to a decrease in blood

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