Acid-Base Disorders

extracellular pH must be maintained within a narrow range (7.35 – 7.45) or else proteins and enzymes will not function correctly
large amounts of acid are produced endogenously as a result of metabolism of fats and carbohydrates to CO₂ and H₂0
these acids must be neutralized by several buffer systems and excreted by the lungs and kidneys

pH is defined by the ratio of bicarbonate to pCO₂ concentration and not the absolute value of either
accurate diagnosis of a particular acid-base disorder requires the simultaneous measurement of pH, pCO₂, and bicarbonate concentration

daily metabolism produces 15,000 mmol of CO₂, which combines with water to produce H₂CO₃
regulation of carbonic acid is achieved by respiratory control of CO₂
daily protein catabolism produces 50 to 100 mEq of sulfuric acids, which reduces the body’s reserve of bicarbonate
bicarbonate concentration is controlled by reabsorption and regeneration in the kidney

acid-base conjugate pairs that can absorb or donate protons
principal extracellular buffer is bicarbonate, with small contributions made by inorganic phosphates and proteins
principal intracellular buffers are proteins, phosphates, and hemoglobin within erythrocytes
bone is a large buffer reservoir

changes in hydrogen ion concentration are blunted by renal and pulmonary changes
these mechanisms will return the pH toward normal but never completely to normal
if there is no metabolic component, when the pCO₂ drops by 10 mm Hg, then the pH rises by 0.08
renal compensation in respiratory acidosis or alkalosis is a slower response and evolves over 3 – 5 days

refers to the amount of base required to titrate the pH back to normal (when the contribution of respiratory factors is taken out of the equation)
calculated value that represents the absolute deficit or excess of total body HCO₃
the bicarbonate space is ~ 1/3 of body weight (90 kg person has a bicarbonate space of 30 L)
a base deficit of 6 in this 90 kg person represents a bicarbonate deficit of 180 mEq
following the base deficit is one way to follow the efficacy of fluid resuscitation (in place of lactate)

↓ pH, ↓ HCO₃^-
results from the excess production of acids (lactic acidosis, diabetic ketoacidosis), reduced acid excretion (renal failure) or loss of bicarbonate (pancreatic, biliary, or small bowel fistula, diarrhea)
initial buffering is accomplished by bicarbonate, although progressively increasing contributions are made by intracellular buffers and bone
initial compensation is respiratory, with an increase in the rate and depth of breathing
increased renal absorption and regeneration of HCO3^- is a later compensation
causes can be divided into two groups by determining the anion gap:

normal anion gap is 8 to 12 mEq/L
normal anion gap is made up of unmeasured anions (albumin, phosphates, sulfates)

common causes include shock (↑ lactic acid), diabetes (↑ ketoacids), renal failure (retention of sulfuric and phosphoric acids), and ingestion of methanol, ethylene glycol, or aspirin
indicates the loss of HCO₃^- ions without a concurrent increase in Cl^- ions
treatment is primarily directed towards correcting the underlying disorder
hyperventilation and bicarbonate are used to keep the pH > 7.3
large doses of bicarbonate are associated with hypernatremia, fluid overload, and hypocalcemia

results primarily from intestinal loss of bicarbonate (pancreatic, small bowel fistulas; diarrhea)
less commonly, a renal cause is implicated (renal tubular acidosis, ureteroenterostomy, spironolactone)
urine pH is high if the kidney is responsible, and low if the intestine is responsible
extracellular volume deficit associated with these disorders results in renal conservation of sodium chloride
ultimately the chloride concentration rises and the bicarbonate concentration falls
treatment is to replace the fistula output with fluid with a similar bicarbonate concentration
massive resuscitation with NaCl is an iatrogenic cause of nongap acidosis

for every 1 mEq/L drop in serum HCO₃^-, the pCO₂ drops by 1.2 mm Hg
the inability to generate the expected respiratory response usually indicates significant underlying respiratory or neurologic disease

↑ pH, ↑ HCO₃^-
results from the loss of acid or the gain of bicarbonate
exacerbated by hypokalemia and intravascular volume depletion
respiratory compensation is minimal (decreased ventilation results in hypoxia)
causes may be divided into two groups, chloride responsive and chloride resistant

urine chloride < 10 to 20 mEq/L
common causes include vomiting, nasogastric suctioning, gastric outlet obstruction, pyloric stenosis, diuretics
associated with volume deficits
if there is a deficit of chloride, sodium will be reabsorbed in the distal tubule in exchange for potassium or hydrogen, depending on their relative availability
this process results in the generation of one bicarbonate ion for each sodium ion that is reabsorbed, which perpetuates the alkalosis
treatment consists of volume replacement with an adequate amount of chloride, which allows more sodium to be reabsorbed with chloride in the proximal tubule, decreasing the generation of bicarbonate in the distal tubule
potassium should be added to the fluids once the patient is making urine

associated with normal to increased volume status
most causes are secondary to high levels of steroid secretion (Cushing’s disease, exogenous steroids, primary hyperaldosteronism)
results from high maximum reabsorption of sodium and bicarbonate and excessive loss of chloride in the urine

for every 1 mEq/L rise in serum HCO₃^-, the pCO₂ rises by 0.7 mm Hg
since hypoventilation results in hypoxemia, the pCO₂ usually does not rise above 55 mm Hg

↓ pH, ↑ pCO₂
results from decreased minute ventilation, not increased carbon dioxide production
acute elevations of carbon dioxide are not well handled because renal compensation takes several days
numerous conditions may cause inadequate ventilation: airway obstruction, incisional pain, oversedation, incorrect ventilator settings
treatment involves restoration of minute ventilation and maintenance of oxygenation (may require mechanical ventilation)
it is especially important to avoid respiratory acidosis in head injury patients (hypercapnia causes cerebral vasodilation, worsening cerebral edema)

↑ pH, ↓ pCO₂
causes include hypoxemia, pain, apprehension, CNS injury, incorrect ventilator settings, sepsis
severe respiratory alkalosis may result in cardiac arrhythmias and cardiac arrest secondary to hypokalemia (potassium is driven intracellularly in exchange for hydrogen ions) or hypocalcemia
cerebral ischemia may be worsened due to cerebral vasoconstriction
attention must be given to the primary disorder causing the hyperventilation