Clinical Cases of Acid-base Balance

Case Scenario 1:

A 65-year-old man with a history of chronic obstructive pulmonary disease (COPD) visits the emergency department with shortness of breath and drowsiness. Arterial blood gas analysis reveals the following:

1. pH: 7.30
2. pCO₂: 60 mmHg
3. HCO₃⁻: 30 mmol/L
4. a. What is the most likely acid-base disorder?
   b. Describe the role of buffer systems in maintaining acid-base balance.
   c. Explain how the respiratory and renal systems contribute to acid-base regulation.

Answer:

a. Diagnosis:

• pH = 7.30 → indicates acidemia
• pCO₂ = 60 mmHg → increased → primary respiratory acidosis
• HCO₃⁻ = 30 mmol/L → increased → partial renal compensation

Conclusion:
The patient is suffering from respiratory acidosis with renal compensation, likely due to CO₂ retention from COPD.

b. Buffer Systems in Acid-Base Balance:

1. Bicarbonate Buffer System (HCO₃⁻/H₂CO₃):
   • Primary extracellular buffer
2. Phosphate Buffer System (HPO₄²⁻/H₂PO₄⁻):
   • Active in the kidneys and ICF
3. Protein Buffers (e.g., Hemoglobin, Plasma Proteins):
   • Act as amphoteric molecules (can accept or donate H⁺)
   • Important in both ICF and blood.
   • c. Role of Respiratory and Renal Systems:

1. Respiratory Regulation:
   • Lungs control CO₂ levels, which influence H⁺ concentration.
   • Increased ventilation removes CO₂ → ↓ H⁺ → corrects acidosis.
   • Decreased ventilation retains CO₂ → ↑ H⁺ → corrects alkalosis.
2. Renal Regulation:
   • Kidneys control H⁺ secretion and HCO₃⁻ reabsorption.
   • In acidosis:
     • ↑ H⁺ excretion
     • ↑ HCO₃⁻ generation
   • In alkalosis:
     • ↓ H⁺ secretion
     • ↓ HCO₃⁻ reabsorption

Case Scenario 2:

A 40-year-old man with uncontrolled diabetes mellitus is brought to the emergency department in a drowsy state. He has rapid, deep breathing (Kussmaul respiration) and a fruity odor to his breath. Arterial blood gas analysis reveals:

• pH: 7.20
• HCO₃⁻: 14 mmol/L
• pCO₂: 28 mmHg
• a. What is the acid-base disorder in this case? Explain the underlying cause.
  b. How do buffer systems act in this condition?
  c. Describe the compensatory roles of the respiratory and renal systems in metabolic acidosis.

Answer:

a. Diagnosis and Cause:

• pH = 7.20 → indicates acidemia
• HCO₃⁻ = 14 mmol/L (↓) → primary metabolic acidosis
• pCO₂ = 28 mmHg (↓) → partial respiratory compensation through hyperventilation

Likely cause:
Diabetic ketoacidosis (DKA) due to accumulation of ketone bodies (acidic), common in uncontrolled diabetes.

b. Role of Buffer Systems:

1. Bicarbonate Buffer System:
   • Immediate buffering of excess H⁺:
     H⁺ + HCO₃⁻ → H₂CO₃ → CO₂ + H₂O
   • Leads to bicarbonate depletion, as seen in low HCO₃⁻ levels
2. Phosphate and Protein Buffers:
   • Secondary intracellular and urinary buffering systems
   • Proteins (e.g., hemoglobin) accept excess H⁺ ion.
   • c. Compensatory Mechanisms:

1. Respiratory Compensation:
   • Hyperventilation (Kussmaul respiration) removes excess CO₂
   • ↓ CO₂ = ↓ H₂CO₃ = ↓ H⁺ → partially corrects acidosis
2. Renal Compensation:
   • Takes longer (hours to days) but crucial in chronic states
   • Kidneys:
     • ↑ H⁺ excretion (as titratable acid and ammonium)
     • ↑ HCO₃⁻ reabsorption and generation

Case Scenario 3:

A medical student volunteered a blood sample for a hematology experiment. During the procedure, the student became increasingly anxious and began to complain of tingling and numbness in the fingers and toes. Laboratory investigation revealed the following:

• Blood pH: 7.5
• Plasma HCO₃⁻: 24 mmol/L
• Arterial pCO₂: 25 mmHg
• a. What is the most likely acid-base disorder in this patient? Explain how the lab findings support your diagnosis.
  b. Describe the physiological mechanism by which anxiety could lead to this condition.
  c. What are the effects of this condition on calcium levels and neuromuscular excitability?

Answer:

a. Diagnosis and Interpretation:

• The most likely diagnosis is acute respiratory alkalosis.
• Justification from lab values:
  • pH = 7.5 → indicates alkalosis.
  • pCO₂ = 25 mmHg (normal: ~40 mmHg) → decreased, suggesting CO₂ loss.
  • HCO₃⁻ = 24 mmol/L (normal) → shows no renal compensation yet (acute condition).
  • b. Mechanism:

• The patient likely experienced hyperventilation due to anxiety.
• Hyperventilation → excessive CO₂ exhalation → decreased pCO₂.
• CO₂ reacts with water to form carbonic acid (H₂CO₃), so CO₂ loss → ↓ H⁺ concentration → increased pH (alkalosis).
• c. Effect on Calcium and Neuromuscular System:

• Alkalosis increases calcium binding to albumin, reducing free (ionized) calcium in plasma.
• Hypocalcemia → increased neuromuscular excitability → symptoms such as:
  • Tingling, numbness
  • Muscle cramps
  • Possible carpopedal spasm or tetany in severe cases

Case Scenario 4:

A 50-year-old man was admitted to the hospital with a complaint of persistent vomiting for the past few days. On clinical examination, he was dehydrated. His laboratory investigations are as follows:

• Blood pH: 7.7
• Plasma HCO₃⁻: 45 mmol/L
• pCO₂: 60 mmHg
• Na⁺: 140 mEq/L (normal: 136–145)
• K⁺: 2.5 mEq/L (normal: 3.5–5.0)
• a. Interpret the acid-base disorder based on the above data.
  b. What is the likely cause of this condition in this patient?
  c. Explain the mechanism leading to hypokalemia in this scenario.

Answer:

a. Interpretation of Acid-Base Status:

• pH = 7.7 → indicates alkalosis.
• HCO₃⁻ = 45 mmol/L → elevated bicarbonate indicates a metabolic origin.
• pCO₂ = 60 mmHg → elevated, suggesting compensatory respiratory hypoventilation.
• Diagnosis: Metabolic alkalosis with respiratory compensation.

 

b. Likely Cause:

• The persistent vomiting led to loss of gastric HCl (a source of H⁺ ions).
• Loss of H⁺ → alkaline shift in plasma → metabolic alkalosis.
• Vomiting also leads to volume depletion, which activates RAAS → bicarbonate retention and worsens alkalosis.
• c. Mechanism of Hypokalemia:

• Vomiting leads to loss of K⁺ in gastric fluids.
• Secondary hyperaldosteronism (due to dehydration) increases renal K⁺ excretion.
• In alkalosis, H⁺ ions move out of cells into plasma → K⁺ shifts into cells to maintain electrical neutrality → further drop in serum K⁺.

 

Case Scenario 5:

A 35-year-old woman with a history of Type 1 Diabetes Mellitus is admitted with nausea, vomiting, and deep, rapid breathing. On examination, she is drowsy and dehydrated. Her breath has a fruity odor. Arterial blood gas (ABG) and serum electrolyte values are as follows:

• pH: 7.18
• HCO₃⁻: 12 mmol/L
• pCO₂: 26 mmHg
• Na⁺: 138 mEq/L
• Cl⁻: 100 mEq/L
• a. What is the acid-base disorder? How does the lab data support your diagnosis?
  b. Calculate the anion gap and interpret its significance.
  c. List common causes of high anion gap and normal anion gap metabolic acidosis.

Answer:

a. Diagnosis:

• pH = 7.18 → indicates acidemia
• HCO₃⁻ = 12 mmol/L (↓) → primary metabolic acidosis
• pCO₂ = 26 mmHg (↓) → indicates respiratory compensation (hyperventilation)

Diagnosis: Metabolic acidosis with respiratory compensation, likely due to diabetic ketoacidosis (DKA).

b. Anion Gap Calculation & Interpretation:

Formula:
Anion Gap (AG) = Na⁺ – (Cl⁻ + HCO₃⁻)
= 138 – (100 + 12)
= 26 mEq/L

Normal AG: 8–12 mEq/L

Interpretation:

• The anion gap is elevated (26 mEq/L) → high anion gap metabolic acidosis
• Suggests the presence of unmeasured anions like ketone bodies, lactate, etc.
• c. Causes of Metabolic Acidosis Based on Anion Gap:

High Anion Gap Metabolic Acidosis (HAGMA):
Mnemonic – MUDPILES

• Methanol
• Uremia (renal failure)
• Diabetic ketoacidosis
• Propylene glycol
• Isoniazid/Iron overdose
• Lactic acidosis
• Ethylene glycol
• Salicylates (aspirin overdose)

Normal Anion Gap Metabolic Acidosis (NAGMA):

• Diarrhea
• Renal tubular acidosis
• Ureteral diversion
• Carbonic anhydrase inhibitors
• Addison’s disease