2. Regulation of plasma HCO3
-
• Via kidneys:
1. Reabsorption of filtered HCO3
2. Formation of titratable acid
3. Excretion of NH4
+ in urine
3. Maintenance of blood pH
• Maintenance of the ratio of HCO3 to pCO2
via compensatory responses by the
kidneys and lungs
• Chemical buffering:
– includes HCO3, phosphates, proteins,
hemoglobin, bone carbamates
4. Determinants of AG
Unmeasured Anions Unmeasured Cations
Albumin (15mEq/L) Calcium (5 mEq/L)
Organic Acids (5 mEq/L) Potassium (4.5 mEq/L)
Phosphate (2 mEq/L) Magnesium (1.5 mEq/L)
Sulfate (1 mEq/L)
---------------------------- ---------------------------
Total UA (23 mEq/L) Total UC (11 mEq/L)
AG = UA – UC = 12 mEq/L
5. Metabolic Acidosis
May be due to:
– Increased endogenous acid production (e.g.
lactate and ketones)
– Loss of bicarbonate (e.g. diarrhea)
– Decreased excretion of endogenous acids
(e.g. renal failure)
6. Metabolic Acidosis
CLINICAL EFFECTS
• Kussmaul breathing, dyspnea
• Headache, nausea, vomiting, confusion, stupor,
coma
• Decreased myocardial contractility and response
to catecholamine; peripheral vasodilatation with
central vasoconstriction predisposing to
pulmonary edema; arrhythmia
7. Metabolic Alkalosis
PATHOGENESIS
• Due to net gain of HCO3 or loss of volatile acid
(usually HCl by vomiting)
• 2 stages:
– GENERATIVE STAGE: loss of acid
– MAINTENANCE STAGE: failure of kidneys to
compensation by excreting HCO3, because of volume
contraction, low GFR, or depleted K+ or Cl-
8. Metabolic Alkalosis
CLINICAL EFFECTS
• increases the affinity of hemoglobin for oxygen --
--- decrease tissue unloading
• Decreases ventilation
• Decreases ionized calcium ----- neuromuscular
hyperirritability
• Supraventricular and ventricular arrhythmias
9. Metabolic Alkalosis
MANAGEMENT
• Identify and correct the underlying stimulus for
HCO3 generation
• Remove the factors that sustain HCO3
reabsorption (e.g. ECF contraction or hypoK+)
• Acetazoleamide
• Dilute 0.1N HCl or NH4Cl
• Hemodialysis
10. Respiratory Acidosis
ETIOLOGY and PATHOGENESIS
• may be due to severe pulmonary disease
(e.g. advanced COPD), respiratory muscle
fatigue, or abnormalities in ventilatory
control (e.g. stroke)
11. Respiratory Acidosis
CLINICAL EFFECTS
• depends on severity and acuteness
• may be dyspneic or tachypneic
• Systemic vasodilation especially cerebral
vasodilation ----- increased ICP -----
pseudotumor cerebri
• Myoclonic jerks, asterixis, tremors, restlessness,
coma
12. Respiratory Acidosis
MANAGEMENT
• Depends on severity and rate of onset
• May be life-threatening
• Measures to reverse underlying cause
• Restoration of adequate alveolar
ventilation
• Avoid rapid correction of hypercapnea
13. Respiratory Alkalosis
ETIOLOGY and PARTHENOGENESIS
• Develops when a sufficiently strong ventilator y
stimulus causes CO2 output in the lungs to
exceed its metabolic production in the tissues
• May be due to stimulation of CNS (e.g. pain,
anxiety), peripheral chemo receptors (e.g.
hypooxemia to pneumonia), chest receptors .
15. Interpretation of Acid - Base
Disorders
• Determine if sample is arterial or venous.
• Compare HCO3 on ABG and electrolyte panel to
verify accuracy
• Determine if pH or pCO2 are normal or
abnormal.
• If any of above are abnormal determine primary
A-B disturbance
• Compute for expected compensation to
determine presence of mixed disorders.
