CLINICAL CHEMISTRY Respiratory Acidosis Lecture 6 PDF

‫اكاديمية المواهب الطبية‬ CLINICAL CHEMISTRY RESPIRATORY ACIDOSIS LECTURE 6 DESIGNED BY : MJ-M6 Respiratory acidosis (raised pCO2, reduced pH) Respiratory acidosis is characterized by: increased pCO2 due to inadequate alveolar ventilation (hypoventilation and consequently reduced elimination of CO2...

‫اكاديمية المواهب الطبية‬ CLINICAL CHEMISTRY RESPIRATORY ACIDOSIS LECTURE 6 DESIGNED BY : MJ-M6 Respiratory acidosis (raised pCO2, reduced pH) Respiratory acidosis is characterized by: increased pCO2 due to inadequate alveolar ventilation (hypoventilation and consequently reduced elimination of CO2 from the blood. Respiratory diseases, such as: bronchopneumonia emphysema asthma and Chronic Obstructive Pulmonary Disease (COPD) may all be associated with hypoventilation sufficient to cause respiratory acidosis. Some drugs (e.g., morphine and barbiturates) can cause respiratory acidosis by depressing the respiratory center in the brain. Damage or trauma to the chest wall and the musculature involved in the mechanics of respiration may reduce the ventilation rate. This explains the respiratory acidosis that can complicate the course of diseases such as poliomyelitis and recovery from severe chest trauma. 1 Respiratory alkalosis (reduced pCO2, increased pH) By contrast, respiratory alkalosis is characterized by: decreased pCO2 due to excessive alveolar ventilation and resulting excessive elimination of CO2 from blood. Disease in which, due to reduced oxygen in the blood (hypoxemia), the respiratory center is stimulated can result in respiratory alkalosis. Examples here include: severe anemia, pulmonary embolism, and adult respiratory syndrome. Hyperventilation sufficient to cause respiratory alkalosis can be a feature of anxiety attacks and response to severe pain. One of these welcome properties of salicylate (aspirin) is its stimulatory effect on the respiratory centre. This effect accounts for the respiratory alkalosis that occurs following salicylate overdose. 2 Primary disturbances of pCO2 (respiratory acidosis and alkalosis) are compensated for by renal adjustments of hydrogen ion excretion which result in changes in [HCO3 ] that compensate appropriately for the primary change in pCO2. Thus, the renal compensation for respiratory acidosis (raised pCO2) involves involves : increased reabsorption of bicarbonate, and renal compensation for respiratory alkalosis (reduced pCO2) involves reduced bicarbonate reabsorption. Respiratory compensation for a primary metabolic disturbance occurs much more quickly than metabolic (renal) compensation for a primary respiratory disturbance. In the second case, compensation occurs over days rather than hours. If compensation results in the return of pH to normal then the patient is said to be fully compensated. But in many cases the compensation returns pH towards normal without actually achieving normality; in such cases, the patient is said to be partially compensated. For the reasons described above, metabolic alkalosis is very rarely fully compensated. 3 Metabolic acidosis (decreased HCO3 , decreased pH) Reduced bicarbonate is always a feature of metabolic acidosis. Consider the patient with metabolic acidosis whose PH is low because bicarbonate [HCO3 ] is low. To compensate for the low [HCO3 ] and restore the all-important ratio towards normal the patient must lower his pCO2. Chemoreceptors in the respiratory centre of the brain respond to a rising hydrogen ion concentration (low pH), causing increased ventilation (hyperventilation) and thereby increased elimination of carbon dioxide. the pCO2 falls, and the ratio [HCO3 ]: pCO2 returns towards normal. This occurs for one of two reasons: increased use of bicarbonate in buffering an abnormal acid load increased losses of bicarbonate from the body. Diabetic ketoacidosis and lactic acidosis are two conditions characterized by: the overproduction of metabolic acids and the consequent exhaustion of bicarbonate. 4 In the first case, abnormally high blood concentrations of keto-acids (b-hydroxybutyric acid and acetoacetic acid) reflect the severe metabolic derangements which result from insulin deficiency. All cells produce lactic acid if they are deficient in oxygen, so increased lactic acid production and resulting metabolic acidosis occur in any condition in which oxygen delivery to the tissues is severely compromised. Examples include cardiac arrest and any condition associated with hypovolemic shock (e.g., massive fluid loss). Failure to: regenerate bicarbonate and excrete hydrogen ions explains the metabolic acidosis that occurs in renal failure. 5 Metabolic alkalosis (increased HCO3 , increased pH) Bicarbonate is always raised in metabolic alkalosis. Compensation for metabolic alkalosis in which [HCO3 ] is high, by contrast, involves depression of respiration and thereby retention of carbon dioxide so that the pCO2 rises to match the increase in [HCO3 ]. However, depression of respiration has the unwelcome side effect of threatening adequate oxygenation of tissues. For this reason, respiratory compensation of metabolic alkalosis is limited. Rarely, excessive administration of bicarbonate or ingestion of bicarbonate in antacid preparation can cause metabolic alkalosis, but this is usually transient. Abnormal loss of hydrogen ions from the body can be the primary problem. 6 Bicarbonate which would otherwise be consumed in buffering these lost hydrogen ions consequently accumulates in the blood. Gastric juice is acidic and gastric aspiration or any disease process in which gastric contents are lost from the body represents a loss of hydrogen ions. The projectile vomiting of gastric juice, for example, explains the metabolic alkalosis that can occur in patients with pyloric stenosis. Severe potassium depletion can cause metabolic alkalosis due to the reciprocal relationship between hydrogen and potassium ions. 7