Pathophysiology
Summary
Acid-base disorders are complex and multi-faceted, encompassing a range of clinical scenarios—presenting as either acidosis or alkalosis. Acidosis is defined as a blood pH < 7.35 and alkalosis is defined as a blood pH > 7.45. These disorders are further classified into metabolic or respiratory subtypes depending upon the underlying pathophysiological mechanisms.
Metabolic acidosis is associated with a low serum bicarbonate (< 21 mEq/L) and low PaCO2 (< 35 mmHg) as a compensatory response (respiratory alkalosis). This condition can arise from two main pathways: increased anion gap and normal anion gap (hyperchloremic). Increased anion gap metabolic acidosis is caused by the accumulation of unmeasured organic acids, commonly abbreviated as MUDPILES (Methanol, Uremia, Diabetic ketoacidosis, Propylene glycol, Iron, Lactic acid, Ethylene glycol, Salicylic acid). Non-anion gap metabolic acidosis is primarily due to the loss of bicarbonate, which leads to reabsorption of chloride ions and hyperchloremic metabolic acidosis, another name for non-anion gap metabolic acidosis. Causes include excessive diarrhea (loss of bicarbonate from pancreatic secretions) and renal tubular acidosis (RTA).
Respiratory acidosis results from the buildup of PaCO2 (> 45 mmHg), and increased bicarbonate (> 27 mEq/L) as a compensatory mechanism. Etiologies include COPD, obstructive sleep apnea, opioid use, and neurological and muscle disorders that impair ventilation.
Metabolic alkalosis is characterized by increased bicarbonate levels (> 27 mEq/L) and high PaCO2 (> 45 mmHg). It can result from vomiting, loop & thiazide diuretics, or mineralocorticoid excess. It can be chloride-sensitive or chloride-resistant based on its responsiveness to saline.
Respiratory alkalosis is characterized by low PaCO2 (< 35 mmHg) and low bicarbonate (< 21 mEq/L), and occurs in conditions that increase ventilation. Common causes include high altitude, panic attacks, asthma, and pulmonary embolism. Aspirin can also cause respiratory alkalosis by directly stimulating the respiratory center in the medulla.
Lesson Outline
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FAQs
Acid-base disorders are characterized by an imbalance in the blood's pH levels, resulting in either acidosis (pH < 7.35) or alkalosis (pH > 7.45). These disorders are broadly categorized into four primary types: metabolic acidosis, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis. Each type is defined by the underlying mechanism affecting blood pH, and can be further classified based on specific causes and compensatory responses.
Metabolic acidosis is a subtype of acid-base disorder where the blood becomes overly acidic, indicated by a decrease in serum bicarbonate levels (< 21 mEq/L) and often accompanied by a low PaCO2 (< 35 mmHg) due to compensatory respiratory alkalosis. This condition can arise from two main pathways: increased anion gap and normal anion gap (hyperchloremic). Increased anion gap metabolic acidosis is caused by the accumulation of unmeasured organic acids, commonly abbreviated as MUDPILES (Methanol, Uremia, Diabetic ketoacidosis, Propylene glycol, Iron, Lactic acid, Ethylene glycol, Salicylic acid). Non-anion gap metabolic acidosis is often due to conditions like excessive diarrhea or renal tubular acidosis, which result in the loss of bicarbonate.
Respiratory acidosis occurs when there is an accumulation of CO2 in the blood, leading to a decrease in blood pH (acidosis). This is often reflected by a high PaCO2 (> 45 mmHg) and a compensatory increase in serum bicarbonate (> 27 mEq/L). Respiratory acidosis typically occurs in disorders that impair normal respiratory function and gas exchange, such as chronic obstructive pulmonary disease (COPD), obstructive sleep apnea, and CNS depressants like opiods. Additionally, restrictive lung diseases, neurological disorders, and muscle disorders can also contribute to respiratory acidosis by affecting the diaphragm's ability to facilitate ventilation.
Metabolic alkalosis is an acid-base disorder characterized by an elevated blood pH due to increased serum bicarbonate levels (> 27 mEq/L). Common causes include vomiting (loss of HCl) and the use of diuretics like loop and thiazide diuretics, which promote the excretion of hydrogen ions. Mineralocorticoid excess, such as in hyperaldosteronism, can also lead to metabolic alkalosis. In cases of chloride-sensitive alkalosis, administering a bolus of normal saline can correct the condition by replenishing chloride levels.
Respiratory alkalosis is an acid-base disorder where a decrease in blood carbon dioxide levels (PaCO2 < 35 mmHg) leads to an elevated pH (alkalosis). This is often accompanied by a compensatory decrease in serum bicarbonate (< 21 mEq/L). Conditions that increase ventilation rates, such as high altitude, pulmonary embolism, panic attacks, and asthma, can lead to respiratory alkalosis by causing a loss of CO2. Certain medications like aspirin can also induce this condition by directly stimulating the respiratory centers, leading to increased ventilation and subsequent loss of CO2.
