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Metabolic acidosis:

1] Calculate the anion gap:

Anion gap = Na+ - [CL- + HCO3-]

Difference between calculated serum anions and

cations.

Based on the principle of electrical neutrality, theserum concentration of cations (positive ions) should

equal the serum concentration of anions (negative

ions).However, serum Na+ ion concentration is higher than

the sum of serum Cl- and HCO3- concentration.

Na+ = CL- + HCO3- + unmeasured anions (gap).

Normal anion gap: 12 mmol/L (10 - 14 mmol/L)

2] Based on the anion gap and patient history - review potential causes:

Normal anion gap (hyperchloremic) metabolic acidosis:

Normal anion gap acidosis: The most common causes of normal anion gap acidosisare GI or renal bicarbonate loss and impaired renal acid excretion. Normal anion gap

metabolic acidosis is also called hyperchloremic acidosis, because instead of

reabsorbing HCO3- with Na, the kidney reabsorbs Cl-. Many GI secretions are rich

in bicarbonate (eg, biliary, pancreatic, and intestinal fluids); loss from diarrhea, tubedrainage, or fistulas can cause acidosis. In ureterosigmoidostomy (insertion of ureters

into the sigmoid colon after obstruction or cystectomy), the colon secretes and losesbicarbonate in exchange for urinary Cl- and absorbs urinary ammonium, whichdissociates into NH3+ and H+.

Loss of HCO3 ions is accompanied by an increase in the serum Cl- concentration.The anion gap remains normal. Disease processes that can lead to normal anion gap

(hyperchloremic) acidosis. Useful mnemonic (DURHAM):

a) Diarrhea (HCO3- and water is lost).

b) Ureteral diversion: Urine from the ureter may be diverted to the sigmoid colon dueto disease (uretero-colonic fistula) or after bladder surgery. In such an event urinary

Cl- is absorbed by the colonic mucosa in exchange for HCO3-, thus increases the

gastrointestinal loss of HCO3-.c) Renal tubular acidosis: dysfunctional renal tubular cells causes an inappropriate

wastage of HCO3- and retention of Cl-.

d) Hyperalimentatione) Acetazolamide

f) Miscellaneous conditions: They include pancreatic fistula, cholestyramine, and

calcium chloride (CaCl) ingestion, all of which can increase the gastrointestinal

wastage of HCO3-.

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Increased anion gap metabolic acidosis

High anion gap acidosis: The most common causes of a high anion gap metabolicacidosis are ketoacidosis, lactic acidosis, renal failure, and toxic ingestions. Renal

failure causes anion gap acidosis by decreased acid excretion and decreased

bicarbonate reabsorption. Accumulation of sulfates, phosphates, urate, and hippurateaccounts for the high anion gap. Toxins may have acidic metabolites or trigger

lactic acidosis.

In increased anion gap metabolic acidosis, the nonvolatile acids are organic or other

inorganic acids (e.g., lactic acid, acetoacetic acid, formic acid, sulphuric acid). The

anions of these acids are not Cl- ions. The presence of these acid anions, which arenot measured, will cause an increase in the anion gap. Useful mnemonic (MUD

PILES):

Methanol poisoning: Methanol is metabolized by alcohol dehydrogenase in the liver

to formic acid.Uremia: In end-stage renal failure in which glomerular filtration rate falls below 10

20 ml/min, acids from protein metabolism are not excreted and accumulate inblood.

Diabetic ketoacidosis: incomplete oxidation of fatty acids causes a build up of beta-hydroxybutyric and acetoactic acids (ketoacids).

Paraldehyde poisoning.

Ischemia: causes lactic acidosis.

Lactic acidosis: Lactic acid is the end product of glucose breakdown if pyruvic acid,the end

product of anaerobic glycolysis, is not oxidized to CO2 and H2O via the

Tricarboxylic Acid Cycle. (Causes: hypoxia, ischemia, hypotension, sepsis).

Ethylene glycol poisoning: Ethylene is metabolized by alcohol dehydrogenase to

oxalic acid in the liver. Usually there is also a coexisting lactic acidosis.

Salicylate poisoning

Causes of common acid-base disturbances:

Metabolic acidosis (non-respiratory)High anion gap.

Ketoacidosis (diabetes, chronicalcoholism, malnutrition, fasting).

Lactic acidosis.

Renal HCO3- loss:

Tubulointerstitial renal disease.Renal tubular acidosis, types 1, 2, 4.

Hyperparathyroidism.

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Renal failure.

Toxins metabolized to acids:Methanol (formic acid)

Ethylene glycol (oxalate)

Paraldehyde (acetate, chloracetate)Salicylates

Toxins causing lactic acidosis

CO2

Cyanide

IronIsoniazid

Toluene (initially high gap,

subsequent excretion of metabolites

normalizes gap)

Rhabdomyolysis (rare)

Loss of base -

Normal anion gap (hyperchloremic

acidosis)

GI HCO3- loss (diarrhea, ileostomy,colostomy, enteric fistulas, use of ion-

exchange resins)

Ureterosigmoidostomy, ureteroilealconduit

Ingestions (acetazolamide, CaCl2, MgSO4)

Others

Hypoaldosteronism, Hyperkalemia

Parenteral infusion of arginine, lysine,NH4Cl.

Rapid NaCl infusion. Toluene (late).

Formulas (Compensation):

pCO2 decreases 1.2 for each mEq/L change

in HCO3 or

pCO2 = last two digits of pH

Compensation

Ventilation of the lungs increases through

stimulation of central chemoreceptors (H+ion receptors) in the medulla and peripheral

chemoreceptors in the carotid and aortic

bodies. Consequently PCO2 falls belownormal, and H+ ion concentration falls.

Respiratory compensation increases the

acidic pH towards normal. The respiratorysystem responds to metabolic acidosis

quickly and predictably by hyperventilation,

so much so that pure metabolic acidosis isseldom seen.

Respiratory Alkalosis:CNS disorders or lesions, hypoxia

[Hypoxia-causing conditions],

pulmonary receptor stimulation(asthma, pneumonia, pulmonary

edema, PE), Pulmonary vascular

disease, anxiety, fear, pain, drugs(ASA, theophylline), liver failure,

sepsis.

Formulas (Compensation):

- Acute: HCO3 decreases 0.22 forevery mmHg change in pCO2

- Chronic: HCO3 decreases 0.5 for

every mmHg change in pCO2

Compensation:

In the presence of respiratory alkalosis the

kidneys compensate for the increase in pHby retaining H+ ions and excreting HCO3 -

ions. As a result, pH falls towards normal

and HCO3 - concentration falls belownormal. Renal compensation to respiratory

alkalosis is a slow process and the pH doesnot completely return to normal.

Metabolic (non-resp)alkalosis:

Respiratory Acidosis:

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acute ventilation failurePaCO2:

HCO3:

BE:

56

24

-4

uncompensated metabolic

alkalosis

pH:

PaCO2:

HCO3:

BE:

7.5640

34

+11

Respiratory alkalosis (chronicalveolar hyperventilation)

pH:

PaCO2:

HCO3:

BE:

7.44

2618

-4

Respiratory acidosis.

Chronic ventilation failure

pH:

PaCO2:

HCO3:

BE:

7.40

5634

+7

Respiratory alkalosis.Chronic alveolar hyperventilation

pH:

PaCO2:

HCO3:

BE:

7.44

2016

-7

Uncompensated metabolicacidosis

pH:

PaCO2:

HCO3:

BE:

7.24

3614

-13

Respiratory alkalosis (acute

alveolar hyperventilation)

pH:

PaCO2:

HCO3:BE:

7.52

28

22+1

Acute Respiratory Acidosis

Dx - heroin overdose.

Breathing - shallow, slow.

ABGs:

pH: 7.30

PaCO2: 55 mm/Hg

HCO3-: 27 mEq/L

Chronic Respiratory Acidosis

Hx/Dx: 73yo, emphysema, laboredbreathing at rest.

ABGs:pH: 7.36PaCO2: 64 mmHg

HCO3-: 35 mEq/L

Acute Respiratory Alkalosis Hx/Dx: 77yo, anxiety,

psychosomatic origin. Rapidbreathing and slurred speech.

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ABGs:

pH: 7.57

PaCO2: 23 mmHg

HCO3-: 21 mEq/L

Compensated RespiratoryAlkalosis

Persistent bacterial pneumonia.

Mild cyanosis and labored

breathing.

ABGs:pH: 7.44

PaCO2: 26 mmHg

HCO3-: 17 mEq/LPaO2: 53 mmHg

Metabolic Alkalosis

80 yo with heart disease. RX:

diuretic

ABGs:

pH: 7.58PaCO2: 48 mmHg

HCO3-: 44 mEq/L

BE: + 19 mEq/LSerum CL- 95 mEq/L