A 55-yrs-old male presents with prolonged epigastric pain and, severe vomiting. Lab evaluation finds that his blood pH is 7.46, while his serum HCO3 is 30. PaC02 is 60. Most likely diagnosis?
* The uncomplicated acid-base disorders, which may be of metabolic or respiratory origin, are classified as being metabolic acidosis, metabolic alkalosis, respiratory acidosis, or respiratory alkalosis.The pH (normal 7.38 to 7.44) determines whether the primary process is an acidemia (pH < 7.38) or an alkalemia (PH > 7.44). (Note that compensation for an alkalosis is always acidosis, while compensation for acidosis is always alkalosis, but in either case, compensation does not bring the pH into the normal range.) * Bicarbonate levels in metabolic acidosis are <21 mM, while those in metabolic alkalosis are >28 mM. Similarly, with respiratory disorders, examine the Pac02 (normal PC02 is 35 to 40 mmHg aerial, 40 to 45 mmHg venous). in patient with respiratory alkalosis the Pac02 is <35, while with respiratory acidosis the Pac02 is >40. * Patients with metabolic alkalosis lose acid, and this causes an increase in the blood pH the body compensates for - this increased pH by decreasing the respiratory rate, which increases blood CO2 levels (hypercapnia) and increases the renal excretion of bicarbonate. Causes of metabolic alkalosis include vomiting (losing gastric acid), increased aldosterone secretion (which causes increased excretion by the kidneys), and ceain diuretics. * In contrast, metabolic acidosis increases serum acid (increased hydrogen ion concentration), which decreases serum pH and decreases serum bicarbonate concentration. The causes of metabolic acidosis are broken down clinically into two groups: those with a normal anion gap and those with an increased anion gap. (The serum anion gap is found by taking the serum sodium concentration and subtracting the concentration of two anions, namely chloride and bicarbonate. * Normally, the anion gap is between 10 and 16 meq/L.) Increased anion gaps result from increased unmeasured anions, such as may occur in the following clinical situations: ketoacidosis (increased beta- hydroxybutyric acid and acetoacetic acid, seen with diabetic ketoacidosis); lactic acidosis (hypoxic conditions); chronic renal failure (uremia); and ingestion of ceain substances such as salicylates, ethylene glycol, methanol, and formaldehyde. * A normal anion gap metabolic acidosis may result from either loss of bicarbonate (diarrhea) or loss of renal regeneration of bicarbonate, seen with renal tubular acidosis type 1 (decreased excretion of titratable acid, i.e., NH and renal tubular acidosis type 4. * In a patient with metabolic acidosis, the body tries to combat the decreased pH by increasing the respiratory rate (tachypnea), which helps to raise the pH by blowing off CO2 and decreasing the serum CO2 (hypocapnia). The body also compensates through renal mechanisms that increase H excretion and increase bicarbonate reabsorption.
Metabolic alkalosis with respiratory compensation
Mixed metabolic acidosis and metabolic alkalosis
Respiratory acidosis with renal compensation
Respiratory alkalosis with no compensation