Respiratory alkalosis, hyperventilation

Q5 Alkalosis can be caused by both metabolic and respiratory problems. Apart from hyperventilation, respiratory alkalosis can be produced by hypoxia, for example, when a person moves to high altitude with a reduced arterial P02, stimulation of respiration occurs via the peripheral chemoreceptors in the carotid and aortic bodies, which respond to the low arterial P02. Increased rate and depth of respiration causes an increased quantity of C02 to be lost from the body, and so pH rises. 

All patients developed a compensatory metabolic acidosis due to chronic hyperventilation. Respiratory alkalosis was thought to have developed because of capillary leak into the lungs producing borderline or frank pulmonary edema. After several days a superimposed normal anion gap acidosis developed from dilution by large volumes of saline fluid resuscitation. The authors found no defects in renal handling of calcium, phosphorous, or magnesium. There was no evidence of a renal acidification defect or renal tubular acidosis. 

Respiratory alkalosis is the rise in pH associated with excessive respiration. Hyperventilation, which can result from anxiety or high fever, is a common cause. The body may control blood pH during hyperventilation by fainting, which results in slower respiration. An intervention that may prevent fainting is to have a hyperventilating person breathe into a paper bag, which allows much of the respired CX)2 to be taken up again. 

Respiratory alkalosis is caused by hyperventilation resulting in a decreased arterial C02 concentration. The compensation for respiratory alkalosis (if present for prolonged periods) is a decrease in serum HCO . ... 

Respiratory alkalosis is characterized by an increased arterial pH, a primary decrease in the arterial PaC02 and, when present for sufficient time, a compensatory fall in the HCOf concentration. Respiratory alkalosis represents hyperventilation and is remarkably common. The most common etiologies of respiratory acidosis are listed in Table 25-7 and range from benign (anxiety) to life-threatening (pulmonary embolism). Some causes of hyperventilation and respiratory acidosis are remarkably common (hypoxemia or anemia). 

Septic patients may have an elevated, low, or normal temperature. The absence of fever is common in neonates and elderly patients. Hypothermia is associated with a poor prognosis. Hyperventilation may occur before fever and chills and may lead to respiratory alkalosis. Disorientation and confusion may develop early in septic patients, particularly in the elderly and patients with preexisting neurologic impairment. Disorientation and confusion may be related to the infection or due to sepsis signs and symptoms (e.g., hypoxia). 

Respiratory alkalosis Alkalosis caused by excessive loss of carbon dioxide due to a respiratory abnormality (e.g., hyperventilation). 

Respiratory alkalosis secondary to hyperventilation is usually observed secondary to CNS stimulation of ventilatory centers as a result of trauma, sepsis, or shock. Lung auscultation may reveal crackles (pulmonary edema) or absence of breath sounds (pneumothorax, hemothorax). Chest roentgenogram can confirm early suspicions or disclose an undetected abnormality such as pneumonia (pulmonary infiltrates). Continued insult to the lungs may result in adult respiratory distress syndrome. 

The first sign of salicylate toxicity is often hyperventilation and respiratory alkalosis due to medullary stimulation. 

On the other hand, primary respiratory alkalosis occurs as a result of alveolar hyperventilation. This condition is associated with a number of pulmonary diseases, bui also may appear during pregnancy, liver disease, and salicylate intoxication, among others. The sequence of events proceeds along these lines (I) Ventilation removes CO faster than the gas is produced by metabolism, causing a decrease tn pCO in the blood and body fluids, including a reduction of venous pCO . This reduces the gradient... 

Hypoventilation causes retention of C02 by the lungs, which can lead to a respiratory acidosis. Hyperventilation can cause a respiratory alkalosis. Metabolic acidosis can result from accumulation of metabolic acids (lactic acid or the ketone bodies p-hydroxybutyric acid and acetoacetic acid), or ingestion of acids or compounds that are metabolized to acids (methanol, ethylene glycol). Metabolic alkalosis is due to increased HC03, which is accompanied by an increased pH. Acid-base disturbances lead to compensatory responses that attempt to restore normal pH. For example, a metabolic acidosis causes hyperventilation and the release of C02, which tends to lower the pH. During metabolic acidosis, the kidneys excrete NH4+, which contains H+ buffered by ammonia. 

Nausea, vomiting, tinnitus, and hyperventilation are seen early in toxicity. As severity of toxicity increases, intractable vomiting, hyperthermia, hypotension, tachycardia, confusion, coma, seizures, pulmonary edema, acute renal failure, and death may occur. Hyperglycemia may be seen early, whereas hypoglycemia may occur later in toxicity. Acid-base disturbances such as respiratory alkalosis and/or metabolic acidosis may be noted. Signs and symptoms of salicylate toxicity may be noted as blood levels rise over 30mgdN. ... 

Fever accelerates lipid metabolism. The serum concentrations of cholesterol, nonesterified fatty acids, and the other lipids may decrease initially, but within a few days the free fatty acid concentration may increase. Fever is often associated with a respiratory alkalosis caused by hyperventilation. This pH increase causes a reduction of the plasma phosphate concentration, with an increased excretion of phosphate and other electrolytes. Serum iron and zinc concentrations decline with accumulation of both elements in the liver. The copper concentration increases because of increased production of ceruloplasmin by the liver. Some representative changes in serum composition induced by fever are listed in Table 17-12. 

Salicylates directly stimulate the central respiratory center and thereby cause hyperventilation and respiratory alkalosis. Moreover, salicylates cause uncoupling of oxidative phosphorylation. As a result, heat production (hyperthermia), oxygen consumption, and metabolic rate may be increased. In addition, salicylates enhance anaerobic glycolysis but inhibit Krebs cycle and transaminase enzymes, all of which lead to accumulation of organic acids and thus to metabolic acidosis. ... 

Respiratory alkalosis occurs when the respiratory rate increases abnormally (hyperventilation), leading to decrease in PCO2 and rise in blood pH. Hyperventilation... 

The answer is e. (Murray, pp 298-307. Scriver, pp 1471-1488. Sack, pp 217-218. Wilson, pp 361-384.) In the presence of insulin deficiency, a shift to fatty acid oxidation produces the ketones such as acetoacetate that cause metabolic acidosis. The pH and bicarbonate are low, and there is frequently some respiratory compensation (hyperventilation with deep breaths) to lower the PCO2, as in choice e. A low pH with high PCO2 would represent respiratory acidosis (choices a and b—the low-normal bicarbonate values in these choices indicate partial compensation). Choice d represents respiratory alkalosis as would occur with anxious hyperventilation (high pH and low Peep, partial compensation with high bicarbonate). Choice c illustrates normal values. 

CNS depression correlates more closely with spinal fluid pH than with blood pH. For this reason, neurologic symptoms tend to occur more frequently and to a greater degree in patients with respiratory acidosis, because the CO2 accumulated in the respiratory form readily crosses the blood-brain barrier to cause acidosis in the CNS. Because of the slow penetration of administered bicarbonate into the CNS, the CNS pH fails to normalize as rapidly as blood pH. Therefore patients continue to hyperventilate because of sustained CNS acidity, and severe respiratory alkalosis may occur. Sustained lowering of the PaC02 within 12 to 36 hours is to be anticipated during the correction of any metabolic acidosis. ... 

In severe respiratory alkalosis pH >7.60 Syncope and seizures Cardiac arrhythmias Hyperventilation... 

A decrease in PaC02 may occur in patients with cardiogenic, hypovolemic, or septic shock because oxygen delivery to the carotid and aortic chemoreceptors is reduced. This relative deficit in Pa02 stimulates an increase in ventilation. The hyperventilation in sepsis is also mediated via a central mechanism. Hyperventilation-induced respiratory alkalosis with an elevation in cardiac index and hypotension without peripheral vasoconstriction may therefore be an early sign of sepsis. 

The combination of respiratory and metabolic alkalosis is the most common mixed acid-base disorder. This mixed disorder occurs frequently in critically ill surgical patients with respiratory alkalosis caused by mechanical ventilation, hypoxia, sepsis, hypotension, neurologic damage, pain, or drugs, and with metabolic alkalosis caused by vomiting or nasogastric suctioning and massive blood transfusions. It may also occur in patients with hepatic cirrhosis who hyperventilate, receive diuretics, or vomit, as well as in patients with chronic respiratory acidosis and an elevated plasma bicarbonate concentration... 

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