Porth's Essentials of Pathophysiology, 4e

201

Disorders of Fluid, Electrolyte, and Acid–Base Balance

C h a p t e r 8

responds to increases in PCO 2

. Instead, a decrease in

readily crosses the blood–brain barrier, exerting its effects by changing the pH of brain fluids. Elevated lev- els of CO 2 produce vasodilation of cerebral blood ves- sels, causing headache, blurred vision, irritability, muscle twitching, and psychological disturbances. If severe and prolonged, it can cause an increase in CSF pressure and papilledema. Impaired consciousness, ranging from lethargy to coma, develops as the PCO 2 rises to extreme levels. Paralysis of extremities may occur, and there may be respiratory depression. Treatment. The treatment of acute and chronic respira- tory acidosis is directed toward improving ventilation. In severe cases, mechanical ventilation may be neces- sary. The treatment of respiratory acidosis due to respi- ratory failure is discussed in Chapter 23. Respiratory Alkalosis Respiratory alkalosis is a systemic acid–base disorder characterized by a primary decrease in arterial PCO 2 , which produces an elevation in pH and a subsequent decrease in HCO 3 – . 72 It is caused by hyperventilation or a respiratory rate in excess of that needed to maintain normal PCO 2 levels. It may occur as the result of cen- tral stimulation of the medullary respiratory center or stimulation of peripheral (e.g., carotid chemoreceptor) pathways to the medullary respiratory center. Because respiratory alkalosis can occur suddenly, a compensa- tory decrease in bicarbonate level may not occur before respiratory correction has already taken place. Central stimulation of the medullary respiratory cen- ter occurs with anxiety, pain, pregnancy, febrile states, sepsis, encephalitis, and salicylate toxicity. One of the most common causes of respiratory alkalosis is

the PO 2 becomes the major stimulus for respiration. If oxygen is administered at a flow rate that is sufficient to suppress this stimulus, the rate and depth of res- piration decrease and PCO 2 increases. Thus, any per- son who is in need of additional oxygen should have it administered, but at a flow rate that does not depress the respiratory drive. Increased Carbon Dioxide Production. Carbon diox- ide is a product of the body’s metabolic processes, gener- ating a substantial amount of acid that must be excreted by the lungs or kidney to prevent acidosis. An increase in CO 2 production can result from numerous processes, including exercise, fever, sepsis, and burns. For example, CO 2 production increases by approximately 13% for each 1°C rise in temperature above normal. 72 Nutrition also affects the production of CO 2 . A carbohydrate-rich diet produces larger amounts of CO 2 than one contain- ing reasonable amounts of protein and fat. In healthy persons, the increase in CO 2 is usually matched by an increase in CO 2 elimination by the lungs, whereas per- sons with respiratory diseases may be unable to elimi- nate the excess CO 2 . Manifestations. Respiratory acidosis is associated with a serum pH below 7.35 and an arterial PCO 2 above 50 mm Hg. The signs and symptoms of respiratory aci- dosis depend on the rapidity of onset and whether the condition is acute or chronic (Table 8-11). Less severe forms of acidosis often are accompanied by warm and flushed skin, weakness, and tachycardia. Because respi- ratory acidosis often is accompanied by hypoxemia, the manifestations of respiratory acidosis often are inter- mixed with those of oxygen deficit. Carbon dioxide

TABLE 8-11 Manifestations of Respiratory Acidosis and Alkalosis Respiratory Acidosis Respiratory Alkalosis

LaboratoryTests pH decreased

LaboratoryTests

pH increased

PCO 2

(primary) increased

PCO 2

(primary) decreased

Bicarbonate (compensatory) increased

Bicarbonate (compensatory) decreased

Signs of Compensation

Signs of Compensation

Acid urine

Alkaline urine

Nervous System Effects Nervous System Effects Dilation of cerebral vessels and decreased neuronal activity Constriction of cerebral vessels and increased neuronal activity Headache Dizziness, panic, light-headedness Behavioral changes Tetany Confusion Numbness and tingling of fingers and toes Depression Seizures (severe respiratory alkalosis) Paranoia Hallucinations Weakness

Tremors Paralysis Stupor and coma

Skin

Cardiovascular Effects Cardiac arrhythmias

Warm and flushed