Porth's Essentials of Pathophysiology, 4e

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Disorders of Ventilation and Gas Exchange

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in ventilation and greater diffusion rate of carbon diox- ide. Hypoxemia resulting from impaired diffusion can be partially or completely corrected by the administra- tion of high concentrations of oxygen. In this case, the high concentration of oxygen serves to overcome the decrease in diffusion by establishing a larger alveolar-to- capillary diffusion gradient. Hypercapnic/Hypoxemic Respiratory Failure In the hypercapnic form of respiratory failure, patients are unable to maintain a level of alveolar ventilation sufficient to eliminate CO 2 and keep arterial O 2 levels within normal range. Because ventilation is determined by a sequence of events ranging from the generation of impulses in the CNS to movement of air through the con- ducting airways, there are several stages at which prob- lems can adversely affect the total minute ventilation. Hypoventilation or ventilatory failure occurs when the volume of “fresh” air moving into and out of the lung is significantly reduced. It is commonly caused by condi- tions outside the lung such as depression of the respira- tory center (e.g., drug overdose, brain injury), diseases of the nerves supplying the respiratory muscles (e.g., Guillain-Barré syndrome, spinal cord injury), disorders of the respiratory muscles (e.g., muscular dystrophy), exac- erbation of chronic lung disease (e.g., COPD), or thoracic cage disorders (e.g., severe scoliosis or crushed chest). Hypoventilation has two important effects on arterial blood gases. First, it almost always causes an increase in PCO 2 . The rise in PCO 2 is directly related to the level of ventilation; reducing the ventilation by one half causes a doubling of the PCO 2 . Thus, the PCO 2 level is a good diagnostic measure for hypoventilation. Second, it may cause hypoxemia, although the hypoxemia that is caused by hypoventilation can be readily abolished by the administration of supplemental oxygen. Clinical Features Acute respiratory failure is usually manifested by vary- ing degrees of hypoxemia and hypercapnia. There is no absolute definition of the levels of PO 2 and PCO 2 that indicate respiratory failure; however, it is convention- ally defined as an arterial PO 2 of less than 60 mm Hg, an arterial PCO 2 of more than 45 mm Hg, or both when prior blood values have been normal. 71 Again, these cut- off values are not rigid, but serve as a general guide in combination with history and physical assessment data. The signs and symptoms of acute respiratory fail- ure are those of the underlying disease combined with those of hypoxemia and hypercapnia. 72,73 Hypoxemia is accompanied by increased respiratory drive and increased sympathetic tone. Potential signs include cya- nosis, restlessness, confusion, anxiety, delirium, fatigue, tachypnea, hypertension, cardiac arrhythmias, and tremor. The initial cardiovascular effects are tachycardia with increased cardiac output and increased blood pres- sure. Serious cardiac arrhythmias may be triggered. The pulmonary vasculature constricts in response to low alveolar PO 2 . If severe, the pulmonary vasoconstriction may result in acute right ventricular failure with

manifestations such as jugular vein distention and dependent edema. Profound acute hypoxemia can cause convulsions, retinal hemorrhages, and permanent brain damage. Hypotension and bradycardia often are preter- minal events in persons with hypoxemic respiratory fail- ure, indicating the failure of compensatory mechanisms. Many of the adverse consequences of hypercapnia are the result of respiratory acidosis. Direct effects of acidosis include depression of cardiac contractility, decreased respiratory muscle contractility, and arte- rial vasodilation (see Chapter 8). Raised levels of PCO 2 greatly increase cerebral blood flow, which may result in headache, increased cerebrospinal fluid pressure, and sometimes papilledema (see Chapter 38, Fig. 38-9). The headache is due to dilation of the cerebral vessels. Additional indicators of hypercapnia are warm and flushed skin and hyperemic conjunctivae. Hypercapnia produces nervous system effects similar to those of an anesthetic—hence the term carbon dioxide narcosis. There is progressive somnolence, disorientation, and, if the condition is left untreated, coma. Mild to moderate increases in blood pressure are common. Air hunger and rapid breathing occur when alveolar PCO 2 levels rise to approximately 60 to 75 mm Hg; as PCO 2 levels reach 80 to 100 mm Hg, the person becomes lethargic and sometimes semicomatose. The treatment of respiratory failure focuses on cor- recting the problem causing impaired gas exchange when possible and on relieving the hypoxemia and hypercapnia. A number of treatment modalities are available, including the establishment of an airway, use of bronchodilating drugs, and antibiotics for respiratory infections. Controlled oxygen therapy and mechanical ventilation are used in treating blood gas abnormalities associated with respiratory failure. 75 When alveolar ventilation is inadequate to maintain PO 2 or PCO 2 levels because of respiratory or neuro- logic failure, mechanical ventilation may be lifesaving. Usually a nasotracheal, orotracheal, or tracheotomy tube is inserted into the trachea to provide the airway needed for mechanical ventilation. There has been recent interest in noninvasive forms of mechanical ven- tilation that use a face mask to deliver positive-pressure ventilation. 76

SUMMARY CONCEPTS

■■ The hallmark of acute lung injury and acute respiratory distress syndrome is a pronounced inflammatory response that affects the lung and may result in systemic organ failure.The acute inflammatory response results in damage and dysfunction of the alveolar–capillary membrane of the lung. Classically, there is interstitial edema of lung tissue, an increase in surface tension caused by inactivation of surfactant, collapse of alveolar structures, a stiff and noncompliant lung

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