Acid Base
Acid Base
Na – (Cl + HCO3)
NaHCO3 + HCL NaCL + H2CO3
NaHCO3 + HX NaX+ H2CO3
Unmeasured cations: calcium,
magnesium, gamma globulins, potassium.
Unmeasured anions: albumin, phosphate,
sulfate, lactate.
Gap Acidosis
Methanol
Uremia
Diabetic ketoacidosis
Paraldehyde
INH
Lactic acidosis
Ethylene Glycol
Salicylate
Non Gap Acidosis
H: hyperalimentation
A: acetazolamide
R: RTA
D: diarrhea
U: rectosigmoidostomy
P: pancreatic fistula
Metabolic Acidosis
Respiratory compensation process takes 12-
24 hours to become fully active. Protons are
slow to diffuse across the blood brain barrier.
In the case of LA this will be faster because
LA is produced in the brain.
The degree of compensation can be
assessed by using Winter’s Formula. It is
INAPPROPRIATE to use this formula before
the acidosis has existed for 12-24 hours.
– PCO2 = 1.5 (HCO3) + 8 +/-2.
Decreased anion gap
Decrease in unmeasured anions
– Hypoalbuminemia
Increase in unmeasured cations
– Hypercalcemia
– Hypermagnesemia
– Hyperkalemia
– Multiple myeloma
– Lithium toxicity
Metabolic Alkalosis
Generation by gain of HCO3 and maintained by
abnormal renal HCO3 absorption.
This is almost always secondary to volume contraction
(low Cl in urine, responsive to NaCl, maintained at
proximal tubule)
– Vomiting: net loss of H+ and gain of HCO3.
– Diuretics: ECFV depletion
– Chronic diarrhea: ECFV depletion
– Profound hypokalemia
– Renal failure: if we cannot filter HCO3 we cannot excrete it.
Mineralocorticoid excess: increased H secretion,
hypokalemia (Na/K exchanger), saline resistant).
Respiratory Acidosis
Acute or Chronic: has the kidney had
enough time to partially compensate?
The source of the BUFFER (we need to
produce bicarb) is different in these states
and thus we need to make this distinction.
Respiratory Acidosis
Acute : H is titrated by non HCO3 organic tissue
buffers. Hb is an example. The kidney has little
involvement in this phase.
– 10 mm Hg increase in CO2 / pH should decrease by .08
Chronic: The mechanism here is the renal synthesis
and retention of bicarbonate. As HCO3 is added to
the blood we see that [Cl] will decrease to balance
charges.
– This is the hypochloremia of chronic metabolic acidosis.
– 10 mm H increase in CO2 / pH should decrease by .03
Respiratory Acidosis
Elevation of CO2 above normal with a drop in
extracellular pH.
This is a disorder of ventilation.
Rate of CO2 elimination is lower than the production
5 main categories:
– CNS depression
– Pleural disease
– Lung diseases such as COPD and ARDS
– Musculoskeletal disorders
– Compensatory mechanism for metabolic alkalosis
Respiratory Alkalosis
Initiated by a fall in the CO2 activate processes which
lower HCO3.
Associated with mild hypokalemia. Cl is retained to offset
the loss of HCO3 negative charge.
Acute response is independent of renal HCO3 wasting. The
chronic compensation is governed by renal HCO3 wasting.
Causes
– Intracerebral hemorrhage
– Drug use : salicylates and progesterone
– Decreased lung compliance Anxiety
– Liver cirrhosis
– Sepsis
Arterial Blood Gas (ABG) Analysis
ABG interpretation
Follow rules and you will always be right !!
1) determine PH
acidemia or alkalemia
2) calculate the anion gap
3) determine Co2 compensation (winters
formula)
4) calculate the delta gap (delta HCO3)
ABG analysis
Arterial Blood Gas (ABG) –interpretation
– Always evaluate PH first
Alkalosis – PH > 7.45
Acidosis – PH < 7.35
– Determine anion gap (AG) – AG = NA – (HCO3+ CL)
AG metabolic acidosis
Non AG acidosis – determined by delta gap
– Winters formula
Calculates expected PaCO2 for metabolic acidosis
PaCO2 = 1.5 x HCO3 + 8
ABG analysis
Delta gap
– Delta HCO3 = HCO3 (electrolytes) + change in AG
Delta gap < 24 = non AG acidosis
Delta gap > 24 = metabolic alkalosis