Basic Approach to Acid-Base Disorders
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(I) Basic Formulae and Units used:
  
  HCO3- + H+ <===> H2O + CO2

  pKa=6.1;  pH= -log{[H+]}
		  [H+] in mole/l

  Henderson-Hasselbach Equation:
  pH= 6.1+log{[HCO3-]/(0.03*pCO2)}
	pCO2 (arterial) in mm Hg, 
	[HCO3-] in mEq/l

  Following directly from H-H eqn.:
     [H+]= 24*(pCO2/[HCO3-]) 
		   [H+] in units of nM

  [HCO3-]+15 ~ last 2 digits of pH

  Anion gap (AG)= [Na+]-[Cl-]-[HCO3-]
     -	AG and electrolytes in mEq/l
     -	AG decreases 2 mEq/l for every
          decrease of 1 g/dl of albumin
		___________________

(II) Determine if patient is
	acidemic: pH < 7.38 or 
	alkalemic: pH > 7.42

    Assess accuracy of ABG by comparing calculated [HCO3-] to measured [HCO3-] (clinical laboratory calculates bicarbonate from measured pH and pCO2). 

(III) Acidemia:
  (1) Assess primary cause:
	Respiratory: pCO2 > 40
	Metabolic: [HCO3-] < 24

  (2) Respiratory acidosis:
     •	In 1° respiratory acidosis:
		pCO2 increases
		pH decreases
		[HCO3-] increases
     •	often abnormal A-a gradient

     •  Expected renal compensation:
	acute changes in pH & [HCO3-]:
	   pH decrease ~0.008(pCO2-40) 
      [HCO3-] increase ~0.09(pCO2-40)

	chronic changes in pH & [HCO3-]:
	   pH decrease ~0.003(pCO2-40)
        [HCO3-] increase ~0.4(pCO2-40)

     •	pH > pH(expected) and/or 
	[HCO3-] > [HCO3-](expected):
	suggests 2° metabolic alkalosis

     •	pH < pH(expected) and/or
	[HCO3-] < [HCO3-](expected): 
	suggests 2° metabolic acidosis
	
  (3) Metabolic acidosis:
     •	In 1° metabolic acidosis:
		[HCO3-] decreases
		pH decreases
		pCO2 decreases
  	
     •	expected respiratory
	compensation:
		pCO2= [HCO3-]*1.54 + 8.36
	
     •	pCO2 < pCO2(expected): 
		2° respiratory alkalosis
     •	pCO2 > pCO2(expected): 
		2° respiratory acidosis

     •	Assess anion gap (AG)
		AG= [Na+]-[Cl-]-[HCO3-]
     •	In AG acidosis, AG >12
     •	In normal-AG or non-AG acidosis,
	AG<12:  hyperchloremic acidosis

     •	With AG acidosis, assess other
	concurrent factors using one
	of the two approaches below:

     (i) (AG-12)+[HCO3-]= 
			     corrected [HCO3-]

	22 < corrected [HCO3-] < 26
		-->1° AG metabolic acidosis
		(no appreciable 2° factors)
	corrected [HCO3-] > 26
		--> 	2° metabolic alkalosis
	    and/or 2° respiratory acidosis
	corrected [HCO3-] < 22
	  	--> 	2° nonAG acidosis
	   and/or 2° respiratory alkalosis

     (ii) DD= {AG-12}/{24-[HCO3-]}

         1 < DD < 2  --->
		1° AG metabolic acidosis
		(no appreciable 2° factors)
         DD < 1 --> 2° nonAG acidosis
	   and/or 2° respiratory alkalosis
         DD > 2 --> 2° metabolic alkalosis
	    and/or 2° respiratory acidosis

(III) Alkalemia:
  (1) Assess primary cause:
	Respiratory: pCO2 < 35
	Metabolic: [HCO3-] > 26

  (2) Respiratory alkalosis:
     •	In 1° respiratory alkalosis:
		pCO2 decreases
		pH increases
		[HCO3-] decreases
     •	HCO3- should never be < 10

     •	Expected renal compensation:
	acute changes in pH & [HCO3-]:
	    pH increase ~0.008(pCO2-40) 
    [HCO3-] decrease ~0.25(pCO2-40)

	chronic changes in pH & [HCO3-]:
	    pH increase ~0.003(pCO2-40)
       [HCO3-] decrease ~0.5(pCO2-40)

     •	pH > pH(expected) and/or 
	[HCO3-] > [HCO3-](expected):
	suggests 2° metabolic alkalosis

     •	pH < pH(expected) and/or
	[HCO3-] < [HCO3-](expected): 
	suggests 2° metabolic acidosis

  (3) Metabolic alkalosis:
     •	In 1° metabolic alkalosis:
		[HCO3-] increases
		pH increases
		pCO2 increases

     •	expected respiratory
	compensation:
		pCO2= [HCO3-]*0.9 + 9

     •	pCO2 < pCO2(expected): 
		2° respiratory alkalosis
     •	pCO2 > pCO2(expected):
		2° respiratory acidosis

     •	pCO2 > 50: 
		2° respiratory acidosis
     •	pCO2 < 40: 
		2° respiratory alkalosis
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Abbreviations:
	1° = primary
	2° = secondary (i.e. underlying)
	AG = anion gap
	DD = delta-delta
	[chemical]= concentration of chemical
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Brief comment about [HCO3-]/CO2 equilibrium:

To understand how changes in pCO2 or [HCO3-] affect the other reagents in the chemical equation: 
	HCO3- + H+ <===> H2O + CO2
remember LeChβtelier's principle.  A chemical equilibrium that is disturbed (by adding or removing a reagent) will cause a shift so as to counteract the effect of this initial change, and thereby restore equilibrium.  For example, adding CO2 (increasing pCO2) will promote a shift of the chemical equation towards the left (as written above), conseqently increasing [HCO3-] and [H+] (which is more properly written in its hydrated state, [H3O+]).  Likewise, decreasing pCO2 will act to decrease [HCO3-] and [H+] (increasing pH) by causing a shift towards the right.  (Physiological changes in the 'concentration' of water are negligible.) LeChβtelier's principle dictates the immediate (primary) response to a change.  Compensatory physiologic responses (i.e. respiratory and renal compensation) as well as other physiological buffers also influence pH and the concentrations of carbon dioxide and bicarbonate.  LeChβtelier's principle "responds" to all of these changes, maintaining a chemical equilibrium; so the effect of compensatory mechanisms on the chemical equation can also be understood and appreciated.
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Differential Diagnosis:

  (I) Respiratory acidosis:
     • Respiratory system
	  - pneumonia
	  - atelectasis
	  - pulmonary edema
	  - broncospasm/laryngospasm
	  - COPD
	  - obstruction
	  - pleaural effusions
	  - pneumothorax
	  - shunts
     • Mechanical dysfunction
	  - neurologic
		spinal cord injury
		phrenic nerve palsy
       		Guillain-Barre
		myasthenia gravis
		paralytic agents
		botulism
	  - muscular
		myositis, myopathy
		muscular dystrophy
		fatigue  (hypoK+, 
			hypoPO4-, COPD)        
	  - restrictive lunq disease
		kyphoscoliosis
		flail chest
     • Central nervous system
	  - sedation 
		(i.e. anesthesia, opiates)
	  - respiratory center dysfunct.
	  - hypothyroidism

  (II) Non anion gap metabolic acidosis:
     •	Hypokalemic
	  - GI loss
		diarrhea
		pancreatic fistula
		ureteral fistula
	  - ileal loop
	  - acetazolamide
	  - hyperparathyroidism
	  - RTAs I, II (urine AG +)
	     type I (distal, classic)
		urine pH>5.3
	     type II (proximal)
		urine pH<5.3
     •	Normokalemic
	  - post hypocapnea
	  - hyperalimentation
	  - hypoaldosterone
	  - mineral acid injestion
     •	Hyperkalemic
	  - RTA IV (urine AG +)
	     type VI (Hypoaldo, hyporenin)
		urine pH<5.3

  (III) Anion gap metabolic acidosis:  
     •	methanol
     •	uremia (BUN >=40, AG~15-25)
     •	DKA (also alcoholic ketosis, 
		starvation ketosis)
     •	paraldehyde, toluene
     •	ischemia
     •	lactic
     •	ethanol
     •	salicylates
     •	MUDPILES

  (IV) Respiratory alkalosis:
     • Respiratory system
	  - hypoxemia
		hypoventilation
		R-L Shunt
		V/Q mismatch
		diffusion impairment
		low FiO2
	  - altitude
	  - restrictive lung diseases
	  - pulmonary embolism
	  - CHF
     • Systemic disease
	  - sepsis, fever
	  - salicylates
	  - hyperthyroidism
	  - liver failure
     • Central nervous system
	  - anxiety
	  - subarachnoid hemorrhage
	  - ischemia or infart
	  - tumor
	  - infection
	  - stimulatinq drugs
	  - progesterone excess 

  (V) Metabolic alkalosis:
     •	Urine Cl < 10 mEq/L
	  (saline responsive; 
	   alkaline urine)
	  - emesis/NG suction
	  - diuretics
	  - post-hypercapnea
     •	Urine Cl > 10 mEq/L
	  (saline resistant)
	  - Elevated BP:
		1° aldosteronism (Conn's)
		Cushing's syndrome
		renal artery stenosis
		Liddle's syndrome
	  - Normal BP:
		hypomagnesium
		hypokalemia
		Bartter's syndrome
		alkali (HCO3-) intake
		HCO3- precursors 
		   (lactate, citrate, acetate)
		licorice
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by Michael T. Milano, MD PhD
MTMilano@yahoo.com
www.geocities.com/MTMilano/palm/