Acid/Base Disorders

What is an acid?

A substance that donates protons (H+).

What is a base?

A substance that accepts protons (H+).

What is buffering?

The ability of a weak acid and its corresponding base to resist changes in pH.

What is the normal arterial blood pH?

7.35–7.45, with an average of 7.40.

How are pH and hydrogen ion concentration related?

Inversely; increased H+ decreases pH.

What three processes regulate acid-base homeostasis?

Extracellular buffering, respiratory CO2 elimination, and renal H+ and bicarbonate regulation.

What is the main extracellular buffering system?

Bicarbonate/carbonic acid.

What are the intracellular buffering systems?

Proteins and phosphates.

Which component of the bicarbonate buffer system is respiratory?

Carbonic acid, which is proportional to PaCO2.

Which component of the bicarbonate buffer system is metabolic?

Bicarbonate (HCO3-), regulated by the kidneys.

How quickly does respiratory compensation occur?

Within minutes.

How quickly does renal compensation occur?

It can take days.

What do medullary chemoreceptors detect?

Changes in pH and PCO2.

Where is bicarbonate primarily reabsorbed in the nephron?

The proximal tubule.

Where are hydrogen ions secreted in the nephron?

The distal tubule.

What is acidemia?

Arterial blood pH below 7.35.

What is alkalemia?

Arterial blood pH above 7.45.

What is acidosis?

A pathophysiologic process that causes acidemia.

What is alkalosis?

A pathophysiologic process that causes alkalemia.

What is the normal arterial PaCO2?

35–45 mmHg.

What is the normal arterial bicarbonate concentration?

22–26 mEq/L.

What is the normal arterial PaO2?

80–100 mmHg.

What is the normal mixed venous pH?

7.33–7.43.

What is the normal mixed venous PCO2?

45–51 mmHg.

What is the primary disturbance in respiratory acidosis?

Increased PaCO2, causing decreased pH.

What is the compensatory response to respiratory acidosis?

Increased bicarbonate (HCO3-).

What is the primary disturbance in metabolic acidosis?

Decreased bicarbonate (HCO3-), causing decreased pH.

What is the compensatory response to metabolic acidosis?

Decreased PaCO2 through increased ventilation.

What is the primary disturbance in respiratory alkalosis?

Decreased PaCO2, causing increased pH.

What is the compensatory response to respiratory alkalosis?

Decreased bicarbonate (HCO3-).

What is the primary disturbance in metabolic alkalosis?

Increased bicarbonate (HCO3-), causing increased pH.

What is the compensatory response to metabolic alkalosis?

Increased PaCO2 through hypoventilation.

ABG: pH 7.58, PaCO2 52, HCO3- 36. What is the primary disorder?

Metabolic alkalosis with respiratory compensation.

ABG: pH 7.31, PaCO2 51, HCO3- 29. What is the primary disorder?

Respiratory acidosis with elevated bicarbonate.

ABG: pH 7.22, PaCO2 24, HCO3- 11. What is the primary disorder?

Metabolic acidosis with respiratory compensation.

ABG: pH 7.53, PaCO2 26, HCO3- 19. What is the primary disorder?

Respiratory alkalosis with decreased bicarbonate.

What are common mechanisms causing metabolic acidosis?

Organic acid accumulation, reduced renal acid excretion, bicarbonate loss, exogenous acid buffering, and rapid administration of non-alkali IV fluids.

What are the two categories of metabolic acidosis based on anion gap?

Elevated anion gap and normal anion gap (hyperchloremic).

What is the anion gap formula?

AG = Na+ - (Cl- + HCO3-).

What is the normal anion gap according to the lecture?

8–12 mEq/L.

What does an anion gap greater than 20 mEq/L indicate?

Accumulation of unmeasured anions.

Calculate AG: Na 144, Cl 100, HCO3 23.

144 - (100 + 23) = 21 mEq/L.

What are causes of elevated anion gap metabolic acidosis?

Lactic acidosis, ketoacidosis, toxic ingestions, and advanced kidney disease.

What does MUDPILES stand for?

Methanol, Uremia, Diabetic ketoacidosis, Paraldehyde, Isoniazid/Iron, Lactic acidosis, Ethanol/Ethylene glycol, Salicylates.

What are causes of normal anion gap metabolic acidosis?

GI bicarbonate loss, renal bicarbonate wasting, impaired renal acid excretion, and exogenous acid gain.

Which medication class can cause renal bicarbonate wasting?

Carbonic anhydrase inhibitors.

How does the body compensate for metabolic acidosis?

Increases respiratory rate to decrease PaCO2.

How much does PaCO2 decrease for every 1 mEq/L decrease in bicarbonate below 24?

Approximately 1–1.5 mmHg.

How is mild-to-moderate metabolic acidosis treated?

Gradual correction with oral alkali therapy, usually sodium bicarbonate, and treatment of the underlying cause.

What laboratory values characterize acute severe metabolic acidosis ?

HCO3- below 8 mEq/L and pH below 7.2.

What treatments may be required for acute severe metabolic acidosis?

Treatment of the underlying cause, possible IV sodium bicarbonate, or emergent hemodialysis.

What is the treatment goal for acute severe metabolic acidosis ?

pH approximately 7.2 and HCO3- approximately 8–10 mEq/L.

What causes metabolic alkalosis?

Increased plasma bicarbonate due to hydrogen ion loss, bicarbonate gain, or impaired renal bicarbonate excretion.

What are causes of sodium-chloride-responsive metabolic alkalosis?

Vomiting, diarrhea with chloride loss, and diuretic use.

What is a cause of sodium-chloride-resistant metabolic alkalosis?

Mineralocorticoid excess.

How does the respiratory system compensate for metabolic alkalosis?

Hypoventilation increases PaCO2.

How much does PaCO2 increase for every 10 mEq/L increase in bicarbonate during metabolic alkalosis?

Approximately 6–7 mmHg.

What is the first treatment approach for sodium-chloride-responsive metabolic alkalosis?

Expand intravascular volume and replace chloride using sodium and potassium chloride solutions.

What medication can treat chloride-responsive metabolic alkalosis when fluid loading is not tolerated?

Acetazolamide, which inhibits renal bicarbonate reabsorption.

What medications can treat mineralocorticoid-related metabolic alkalosis?

Spironolactone, amiloride, or triamterene.

What is the primary disturbance in respiratory acidosis?

Failure of the lungs to eliminate CO2, increasing PaCO2 and decreasing pH.

How much does bicarbonate increase in acute respiratory acidosis?

1 mEq/L for every 10 mmHg increase in PaCO2 above 40.

How much does bicarbonate increase in chronic respiratory acidosis?

4 mEq/L for every 10 mmHg increase in PaCO2 above 40.

What is the immediate treatment goal in acute respiratory acidosis?

Ensure adequate oxygenation and aggressively treat the underlying cause; mechanical ventilation may be required.

What is respiratory alkalosis?

Increased pH caused by decreased PaCO2 when CO2 excretion exceeds metabolic production.

What medications can cause respiratory alkalosis?

Nicotine, topiramate, catecholamines, caffeine, and theophylline.

What non-drug conditions can cause respiratory alkalosis?

Anxiety, pain, fever, pregnancy, CNS disorders, hypoxia, asthma, and thyrotoxicosis.

How much does bicarbonate decrease in acute respiratory alkalosis?

3 mEq/L for every 10 mmHg decrease in PaCO2.

How much does bicarbonate decrease in chronic respiratory alkalosis?

4 mEq/L for every 10 mmHg decrease in PaCO2.

What is the primary treatment for respiratory alkalosis?

Correct the underlying cause; oxygen may be needed for severe hypoxemia.

When can respiratory alkalosis become life-threatening?

Severe alkalosis with pH greater than 7.55.