ACID/BASE ABNORMALITY

 

  1. METABOLIC ACIDOSIS = pH and HCO3 change in same direction. Cl and HCO3 move in opposite directions. K+ is generally high . To differentiate between various forms of Met. Acidosis we use the following formula:  (Na) - [(Cl)+(HCO3)] =12+/-2. If the result is > 14 we talk about Met. Acidosis with Anion Gap (AG). If the result is less than 14 we talk about Met. Acidosis without gap.
     
    1. Metabolic Acidosis with AG:
       

Etiology:

      1. Methanol
      2. Ethylene glycol
      3. DKA
      4. AKA
      5. Starvation  KA
      6. Lactic Acidosis
      7. ASA
      8. Uremia
      9. INH
      10. Iron
      11. Cyanide
      12. CO

         
    1. Metabolic Acidosis without AG (hyperchloremic acidosis):

Etiology:

This is divided into:
Hyperkalemic

  • RTA IV
  • Hypoaldosteron (Addison) 
  • K-sparing diuretics
     

Hypokalemic

  • RTA I & II
  • Acetozolamide
  • Diarrhea
  • Ureterosigmoidostomy

     

S & S (of Met. Acidosis with or without AG):

  1. various CNS dysfunctions, dysrhythmias, symptoms related to precipitating cause.

DX (of Met. Acidosis with or without AG):

  1. On SMA ¯ in HCO3 and  increase in  K is generally evident. On ABG pH <7.35 (unless compensation occurred).
     
  2. (Na) - (Cl) + (HCO3) = 12+/-2; if K is included, normal =10-20mEq/L. If  the number is higher , Anion Gap Metabolic Acidosis is present.
     
  3. ABG helps to determine if there is any degree of compensation. In pure Met. Ac.  pCO2 = 1.5xHCO3 +8 (+/-2). Another simplified way to see if compensation has occurred is to look at two decimal  digits of pH, and if  this numerically equals  pCO2 then compensation is as expected. If pCO2 is higher/lower than  calculated, respiratory acidosis/alkalosis is present respectively.
     

Treatment:

    1. Underlying cause must be addressed
       
    2. NaHCO3 given only if pH is <7.1 otherwise alkaline overshoot occurs.
       
    3. HCO3 deficit = (Kg)x(0.4)x(desired HCO3-calculated HCO3).  Each ampoule of NaHCO3 contains 44.6 mEq of  HCO3. Generally 2-3 ampules are added into 1 L D5W and ½ of the calculated dose given over 4-5 hours.  HCO3 treatment has it's potential side effects:
       
      1. It creates alkaline milieu and shifts OxyHgb curve to L making the unloading of O2 more difficult.
      2. HCO3 does not cross the BBB while the CO2, the byproduct of HCO3 metabolism does and creates cerebral  acidosis.
    4. IVF
       
  1. METABOLIC  ALKALOSIS = >pH and >HCO3 change in same direction. Cl and HCO3 move in different directions. K is generally low .

Etiology:
This is divided into:

I. Chloride-Responsive ( urine Cl <15mEq)

  • Vomiting (pyloric stenosis)
  • Diuretics 
  • Diarrhea 
  • Dehydration ("contraction alkalosis")
  • Addition  of Citrate (PRBC transfusion)
  • Addition  of Lactate (large quantities of LR)
     

II. Chloride-Unresponsive (urine Cl > 15mEq)

  • Hyperaldosteronism
  • ¯K, ¯Mg,
  • Bartter's syndrome
  • Cushing
  • Renal artery stenosis
     

S & S: (both Chloride and Non-Chloride responsive)

    1.  hypotension, bradypnea, arrhythmias

    2.  decrease in ionized Ca leads to neuromuscular irritability,CNS changes,

    3.  hypoventilation leads to O2 availability and hypoxemia.

DX:

  1. >HCO3 & <K  on SMA and >pH > 7.45 (unless compensation occurred). In pure Met. Alk. the pCO2=0.7xHCO3 +20 (+/-1.5). If pCO2 is higher/lower respiratory acidosis/alkalosis is also present.
     
  2. Urinary Chloride  measurement
     

Treatment:

  1. Chloride-Responsive is treated with correction of hypokalemia and  NS solution
     
  2. Chloride-Resistant is treated with correction of hypokalemia and the underlying cause.
     
  3. RESPIRATORY  ACIDOSIS = <pH and >pCO2. The change is in the opposite direction

Etiology:

  1. Poor ventilation 2ry to COPD
  2. Pneumonia
  3. Edema
  4. Asthma
  5. FB obstruction
  6. PNTX
  7. Thoracic cage abnormality
  8. Diaphragmatic or accessory  muscles weakness
  9. Neuropathies ( Guillain-Barre, Cervical spine injury, ALS), Pickwick's disease
     

S & S:

  1. If acute, CNS symptoms predominate since CO2 penetrates lipids of  brain. Hypoxemia causes dysrythmias. Pt is diaphoretic and cyanotic. Narcolepsia and/or coma may be present.
     
  2. Chronic Resp. Acidosis is better  tolerated and usually evolves over 3-5 days. Symptoms are not as prominent.

DX:

  1. On ABG pCO2 > 45mmHg and pH < 7.35.
     
  2. It is Acute, i.e. uncompensated if pH had decreased 0.008 for each 1mmHg increase of pCO2.
     
  3. It is Chronic, i.e. compensated if pH had decreased 0.003 for each 1mmHg increase of pCO2.
     
  4. If pH/pCO2 ratio is > 0.008 then also metabolic acidosis is present.
     
  5. If pH/pCO2 ratio is < 0.003 then metabolic alkalosis is present i.e. compensated
     
  6. If pH/pCO2 ratio is  between 0.003 to 0.008 then partial compensation is present.
     

Treatment:

    1. Improvement in  ventilation  and oxygenation, guided by pt's mental status, is the main goal. This, while may have to be corrected STAT in acute case, must proceed slowly in chronically  ill pt who depends on low pCO2 for respiratory center.
       
    2. Various modalities for acute and/or chronic resp. acidosis are Epi, Albuterol, High flow O2 (if not contraindicated), Intubation.
       
  1. RESPIRATORY  ALKALOSIS = >pH and <pCO2. The change is in opposite direction
     

Etiology:

1. Hyperventilation 2ry to hypoxemia:  PE, Asthma, Anemia,  Drugs (ASA, progesterone)

2.  CNS/Metabolic: Anxiety, CVA, Sepsis, Exercise, Pregnancy.
 

S & S:

  1. Lightheaded, tetany (2ry to decrease in ionized Ca), syncope, dysrythmias, perioral paresthesias, seizures.

DX:

  1. ABG shows < pCO2 and > pH.
     
  2. If Acute alkalosis, pH will increase by  0.008 for every 1mmHg decrease of pCO2
     
  3. If Chronic i.e. compensated, pH increases 0.002  for every 1mmHg decrease of pCO2
     
  4. If pH/pCO2 ratio is > 0.008 then met. alk. is also present
     
  5. If pH/pCO2 ratio is <0.002 then met. ac. is present i.e. compensated
     
  6. If pH/pCO2  ratio is between 0.002 to 0.008  then partial compensation is present.

Treatment:
- Correction of underlying cause.
- If anxiety  or exercise related apply paper bag
- If  pt suffered CVA and pH is >7.5 then re-breathing CO2 apparatus is used.

 As we see, various forms of AB abnormality are possible:
 

  1. Pure Met. Acidosis = <pH, <HCO3
     
  2. Pure Met. Alkalosis =>pH, >HCO3
     
  3. Pure Resp. Acidosis =<pH, >PaCO2
     
  4. Pure Resp. Alkalosis =>pH, <PaCO2
     
  5. Met. Ac /Resp. Alk. (compensated) = N pH, <HCO3, <PaCO2 (e.g. ASA toxicity)
     
  6. Met. Alk/Resp. Ac. (compensated) = N pH, >HCO3, >PaCO2 (Furosamide + COPD)
     
  7. Met. Ac/Resp. Ac =<<pH,  <HCO3, >PaCO2 (lactic acidosis + depressed respiratory drive)
     
  8. Met. Alk/Resp. Alk = >>pH,  >HCO3, <PaCO2 (vomiting + hyperventilating)
     
  9. Met. Ac + Met. Alk = N pH, N HCO3 (DKA + vomiting). In most cases of  this type of abnormality, despite normal pH and HCO3 there is > AG (DKA + Diuretic). Yet cases with normal AG exist, as in cases of  Diarrhea + Vomiting.  The latter is not possible to id on laboratory basis
     
  10. Triple AB abnormality:
     
    1. Met. Ac and  Met. Alk + Resp. Ac. =  <pH, >>PaCO2,>>HCO3, >AG. Seen in cases of combined COPD, DKA and Furosamide use
        
    2. Met. Ac. and  Met Alk  + Resp. Alk  = >pH, <PaCO2,  >HCO3,> AG . Seen in cases of combined Pregnancy, DKA and Vomiting

NOTE!! Resp. Ac + Resp. Alk together do not occur.

[BACK]