Porth's Essentials of Pathophysiology, 4e

200

Integrative Body Functions

U N I T 2

and severe metabolic alkalosis, they include mental confusion, hyperactive reflexes, tetany, and carpopedal spasm. Metabolic alkalosis also leads to a compensatory hypoventilation with development of various degrees of hypoxemia and respiratory acidosis. Significant mor- bidity occurs with severe metabolic alkalosis, including respiratory failure, arrhythmias, seizures, and coma. Treatment. The treatment of metabolic alkalosis usu- ally is directed toward correcting the cause of the condi- tion. A chloride deficit requires correction. Potassium chloride usually is the treatment of choice when there is an accompanying potassium deficit. When potassium chloride is used as a therapy, the Cl – anion replaces the HCO 3 – anion and the K + corrects the potassium deficit, allowing the kidneys to retain H + while eliminating K + . Fluid replacement is used in the treatment of volume contraction alkalosis. Respiratory Acidosis Respiratory acidosis represents a decrease in pH caused by an elevation in arterial PCO 2 , usually due to con- ditions that impair alveolar ventilation. It can present as an acute or chronic condition, and can occur as the result of decreased ventilatory drive, lung disease, or disorders of the chest wall or respiratory muscles. 72,73 Less commonly, it results from excess CO 2 production. Acute Disorders ofVentilation. Acute respiratory fail- ure is associated with a rapid rise in arterial PCO 2 along with a minimal increase in serum HCO 3 – and a large decrease in pH. It can be caused by impaired function of the respiratory center in the medulla (as in narcotic overdose), lung disease, chest injury, weakness of the respiratory muscles, or airway obstruction. Almost all persons with acute respiratory acidosis become hypox- emic when breathing room air. In many cases, signs of hypoxemia develop prior to those of respiratory acido- sis because CO 2 diffuses across the alveolar capillary membrane 20 times more rapidly than oxygen. 2,4 Chronic Disorders of Ventilation. Chronic respiratory acidosis is characterized by a sustained increase in arterial PCO 2 , resulting in renal adaptation with a more marked increase in serum HCO 3 – and a lesser decrease in pH. 72,73 It is a relatively common disturbance in persons with chronic obstructive pulmonary disease (COPD). In these persons, the persistent elevation of PCO 2 stimulates renal H + secretion and HCO 3 – reabsorption. The effectiveness of these compensatory mechanisms can often return the pH to near-normal values as long as oxygen levels are maintained within a range that does not unduly suppress chemoreceptor control of respirations. An acute episode of respiratory acidosis can develop in persons with chronic lung disease who receive oxy- gen therapy at a flow rate that raises their PO 2 to a level that produces a decrease in ventilation (see Chapter 23). In these persons, the medullary respiratory center has adapted to the elevated levels of CO 2 and no longer

Vomiting

K + depletion

Cl - depletion

Extracellular fluid depletion

Decreased GFR

HCO 3 - filtration

Renin release

Aldosterone secretion

HCO 3 - reabsorption

HCO 3 - reabsorption

HCO 3 - reabsorption

Alkalosis

ventilation, metabolic alkalosis may develop due to a rapid drop in PCO 2 , while serum HCO 3 – , which must be eliminated through the kidney, remains elevated. Maintenance of Metabolic Alkalosis. Maintenance of metabolic alkalosis resides within the kidney and its inability to rid the body of the excess HCO 3 – . Many of the conditions that accompany the development of met- abolic alkalosis, such as contraction of the ECF volume, hypochloremia, and hypokalemia, also increase reab- sorption of HCO 3 – by the kidney, thereby contributing to its maintenance. Manifestations. Metabolic alkalosis is characterized by a serum pH above 7.45, serum HCO 3 – above 29 mEq/L (29 mmol/L), and base excess above 3.0 mEq/L (3 mmol/L). Persons with metabolic alkalosis often are asymptomatic or have signs related to ECF volume depletion or hypokalemia. The manifestations of meta- bolic alkalosis are summarized in Table 8-10. Neurologic signs and symptoms (e.g., hyperexcitabil- ity) occur less frequently with metabolic alkalosis than with other acid–base disorders because HCO 3 – enters the cerebrospinal fluid (CSF) more slowly than CO 2 . When neurologic manifestations do occur, as in acute FIGURE 8-19. Renal mechanisms for bicarbonate (HCO 3 – ) reabsorption and maintenance of metabolic alkalosis following depletion of extracellular fluid volume, chloride (Cl – ), and potassium (K + ) due to vomiting. GFR, glomerular filtration rate.