Porth's Essentials of Pathophysiology, 4e

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Respiratory Function

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the partial pressure (P) of the gases. Thus, oxygen moves from the alveoli, where the partial pressure of oxygen (PO 2 ) averages 104 mm Hg when breathing room air, to the blood in the pulmonary capillaries, where the aver- age PO 2 is only 40 mm Hg. 1 Carbon dioxide moves in the opposite direction, from the blood in the pulmonary capillaries, where the partial pressure of carbon dioxide (PCO 2 ) is 45 mm Hg, to the alveolar air, where the PCO 2 is 40 mm Hg. 1 These values vary with tissue metabolism and the oxygen content of the inspired air. Perfusion involves the movement of blood through the pulmonary circulation, including the pulmonary capillaries, where gas exchange takes place. Adequate oxygenation of the blood and removal of CO 2 depend on perfusion or movement of blood through the pul- monary blood vessels and appropriate contact between ventilated alveoli and perfused capillaries of the pulmo- nary circulation (ventilation and perfusion matching). Hypoxemia Hypoxemia refers to a reduction in the PO 2 of the arte- rial blood. It can result from an inadequate amount of O 2 in the air, disease of the respiratory system, dysfunction of the neurologic system, or alterations in circulatory function. The mechanisms whereby respiratory disorders lead to a significant reduction in PO 2 are hypoventila- tion, impaired diffusion of gases, inadequate circulation of blood through the pulmonary capillaries, and mis- matching of ventilation and perfusion 2,3 (see Chapter 21). Often, more than one mechanism contributes to hypox- emia in persons with respiratory or cardiac disease. Hypoxemia produces its effects through tissue hypoxia and the compensatory mechanisms that the body uses to adapt to the lowered oxygen level. Body tissues vary con- siderably in their vulnerability to hypoxia; those with the greatest need are the brain and heart. If the PO 2 in these organs falls belowa critical level, aerobicmetabolismceases and anaerobic metabolism takes over, with formation and release of lactic acid. This results in increased serum lactate of arterial blood produces few manifestations. Recruitment of sympathetic nervous system compensatory mechanisms produces an increase in heart rate, peripheral vasocon- striction, and a mild increase in blood pressure. 3 This is because hemoglobin saturation is still approximately 90% when the PO 2 is only 60 mm Hg (see Chapter 21, Fig. 21-22). More pronounced hypoxemia may produce personality changes, restlessness, uncoordinated muscle movements, euphoria, impaired judgment, delirium, and, eventually, stupor and coma. Cyanosis refers to the bluish discoloration of the skin and mucous membranes resulting from an excessive concentration of reduced or deoxygenated hemoglobin in the small blood vessels. It usually is most pronounced in the lips, nail beds, ears, and cheeks. The degree of cya- nosis is modified by the amount of cutaneous pigment, skin thickness, and the state of the cutaneous capillaries. Cyanosis is more difficult to distinguish in persons with levels and a metabolic acidosis (see Chapter 8). Mild hypoxemia or reduction in the PO 2

dark skin and in areas of the body with increased skin thickness. Although cyanosis may be evident in persons with respiratory failure, it often is a late sign. A deoxy- genated hemoglobin concentration of approximately 5 g/dL of deoxygenated hemoglobin is required in the circulating blood for cyanosis to occur. 1 The absolute quantity of reduced hemoglobin, rather than the relative quantity, is important in producing cyanosis. Persons with anemia are less likely to exhibit cyanosis because they have less hemoglobin to transport oxygen even though their cardiac output and lung function are nor- mal. A person with a high hemoglobin level because of polycythemia may be cyanotic in the absence of hypoxia. Cyanosis can be divided into two types: central and peripheral. Central cyanosis is evident in the tongue and lips. It is caused by an increased amount of deoxygen- ated hemoglobin in the arterial blood. Peripheral cyano- sis occurs in the extremities and on the tip of the nose or ears. It is caused by slowing of blood flow to an area of the body, with increased extraction of oxygen from the blood. It results from vasoconstriction and diminished peripheral blood flow, as occurs with cold exposure, shock, heart failure, or peripheral vascular disease. The manifestations of chronic hypoxemia may be insidious in onset and attributed to other causes, par- ticularly in persons with chronic lung disease. The body compensates for chronic hypoxemia with increased venti- lation, pulmonary vessel vasoconstriction, and increased production of red blood cells. Pulmonary vasoconstric- tion occurs as a local response to alveolar hypoxia; it increases pulmonary arterial pressure and improves the matching of ventilation and perfusion. Increased pro- duction of red blood cells results from the release of erythropoietin from the kidneys in response to hypoxia (see Chapter 13). Other adaptive mechanisms include a shift to the right in the oxygen dissociation curve, which increases O 2 release to the tissues (see Chapter 21). Diagnosis of hypoxemia is based on clinical observa- tion and diagnostic tests that measure PO 2 levels. The analysis of arterial blood gases provides a direct mea- sure of the O 2 content of the blood and is the best indi- cator of the ability of the lungs to oxygenate the blood. Mixed venous oxygen saturation (SvO 2 ; i.e., oxygen saturation of hemoglobin in venous blood) reflects the body’s extraction at the tissue levels. Venous blood sam- ples can be obtained either through a pulmonary artery catheter or central line. Noninvasive measurements of arterial O 2 saturation of hemoglobin can be obtained using pulse oximetry. 4,5 Reusable clip probes (finger, nasal, ear) and single-use adhesive probes (finger and forehead) are available. 5 Advantages of the reusable clip probe include the rapid- ity with which measurements can be obtained and cost- effectiveness. The adhesive probes allow for more secure placement and ability to monitor sites other than those used by the clip probes. Pulse oximetry uses light-emitting diodes and com- bines plethysmography (i.e., changes in light absor- bance and vasodilation) with spectrophotometry. 4,5 Spectrophotometry uses a red-wavelength light that passes through oxygenated hemoglobin and is absorbed by