Acid-Base Disorders

 

I. Measurement Considerations

A. some ABG machines measure only pH, pCO2, & pO2; HCO3 & O2% calculated
1. bicarbonate = 95% of total serum CO2
2. serum total CO2 measures bicarbonate, dissolved CO2, carbonate, carbamates
3. therefore, serum CO2 from electrolytes is usually about 2 mEq higher than the true bicarbonate level
B. adjust for patient temperature:
1. low pO2 & pCO2 and high pH are normal at increasingly low temperatures

II. Normal Physiology

A. CO2 + H2O = H2CO3 = HCO3- + H+
B. O2 carried almost entirely by hemoglobin; CO2 carried 75% by plasma
1. RBCs contain carbonic anhydrase to convert tissue CO2 into HCO3 for delivery to lung
2. CO2 20x more soluble than O2 in plasma
C. distribution space of HCO3 is 50% of total body weight

III. The Anion Gap

A. normally 10-14 depending on analyzer used (for some analyzers, normal is 6)
B. normal anions: albumin, lactate, pyruvate, sulfate, phosphate
C. alkalosis increases AG by uncovering anionic sites on albumin
D. causes of low anion gap: low albumin, low phosphorus, high calcium, high magnesium, high lithium, high cationic proteins (eg multiple myeloma), sodium salts of anionic antibiotics
E. increased AG + normal HCO3 = concurrent metabolic alkalosis
F. increased AG + disproportionately low HCO3 = concurrent hyperchloremic metabolic acidosis

IV. Normal Compensation:

A. buffers: hemoglobin, plasma proteins, bicarbonate, phosphate
1. occurs in minutes
B. ventilation:
1. occurs in minutes to hours
C. renal response:
1. may take up to 1 week

V. Effects of Acidemia

A. pulmonary effects:
1. increased pulmonary vascular resistance
2. decreased oxy-hemoglobin affinity
a) countered by 2,3 DPG in 12-36 hours (causing an increase in oxy-hemoglobin affinity
B. cardiac effects:
1. myocardial suppression (overcome by an increase in HR & catecholamines pH > 7.20)
a) respiratory acidosis affects heart more rapidly than metabolic acidosis because of more rapid entry of CO2 into the myocytes
2. severe acidosis causes bradycardia
3. re-entrant arrythmias and ventricular fibrillation
C. vascular effects:
1. venoconstriction - shifts blood to lungs worsening pulmonary edema but only occurs in severe acidemia
2. arterial dilation (counteracted by catecholamines at pH >7.20)
D. neuromuscular effects:
1. respiratory acidosis causes increased cerebral blood flow
2. rapid respiratory acidosis causes seizures and loss of consciousness
a) chronic respiratory acidosis is usually well tolerated by the brain, even with pCO2 levels as high as 150
3. acute respiratory acidosis causes impaired diaphram contractility
4. Kussmaul's breathing
E. metabolic effects
1. hyperkalemia
2. insulin resistance
F. cerebral effects:
1. coma

VI. Effects of Alkalemia

A. pulmonary effects:
1. if metabolic alkalosis causes compensatory hypoventilation and secondary atelectasis &V/Q mismatch
B. cardiac effects:
1. some increased contractility can occur in mild - moderate alkalemia
2. increased cardiac irritability + refractory arrhythmias
C. vascular effects:
1. vasodilation (maximal at pH = 7.65)
2. coronary artery spasm
D. neuromuscular effects:
1. acute respiratory alkalosis causes a decrease in cerebral blood flow
a) flow falls to 70% of baseline at a pCO2 = 30 mm
b) flow falls to 50% of baseline (maximum reduction) at a pCO2 = 20 mm
c) effect only lasts about 6 hours
2. seizures
E. metabolic effects:
1. causes lactate shift out of cells thus causing a 2-5 mEq rise in AG
2. increased lactate
3. decreased calcium
4. hypokalemia

VII. Metabolic Acidosis

A. compensations:
1. H+ immediately buffered
2. hyperventilation occurs in minutes
3. H+ combines with carbonate from bone to form carbonic acid (takes a long time)
4. renal H+ excretion & HCO3 resorption in hours to days
B. increased anion gap acidosis:
1. uremia
2. ketoacidosis
a) BHBA:AcAc normally 4:1 but in hypoxia, ratio higher
b) in alcoholic ketoacidosis, BHBA:AcAc very high and nitroprusside reaction may be totally normal
3. lactic acidosis
a) usually defined as a lactate > 5 mmol/L
b) change in lactate = change in AG = change in HCO3
c) causes:
(1) increased oxygen consumption
(2) decreased oxygen delivery
(3) altered cellular metabolism
(4) toxins & drugs
(5) congenital
(6) diminished lactate clearance
(7) increased D-lactate
d) treatment:
(1) correct the underlying cause
(2) bicarbonate administration is controversial
4. salicylate toxicity
a) treat with D5W + 2-3 amps HCO3
b) keep pH 7.45-7.49
c) watch for hypokalemia
5. methanol toxicity
a) clue is increased osmolar gap
(1) Osm = 2(sodium) + glucose/18 + BUN/2.8 + ethanol/4.6
(2) normally the measured Osm - calculated Osm < 10
b) treatment:
(1) fomepizole (NEJM 2001; 344:424-9)
i) 15 mg/kg IV bolus
ii) 10 mg/kg IV bolus Q12 hours
iii) after 48 hours, increase to 15 mg/kg bolus
iv) continue until serum methanol is less than 20 mg/dl
(2) ethanol + dialysis; keep ethanol level > 100 mg/dL
6. ethylene glycol toxicity
a) clue is increased osmolar gap
b) oxalaturia
c) treatment:
(1) fomepizole (NEJM 1999; 340: 832-8)
i) 15 mg/kg IV bolus
ii) 10 mg/kg IV bolus Q12 hours
iii) after 48 hours, increase to 15 mg/kg bolus
iv) continue until serum ethylene glycole is less than 20 mg/dl
(2) ethanol + dialysis; keep ethanol level > 100 mg/dL
7. paraldehyde toxicity
C. normal anion gap acidosis:
1. GI bicarbonate losses (eg. diarrhea)
2. renal insufficiency
3. hyperalimentation
4. ureteroenterostomy
5. rapid IV hydration
6. small bowel, pancreatic, biliary drainage
7. hyperparathyroidism
8. renal tubular acidosis
a) type I (distal)
(1) distal acid secretion defect
(2) unable to decrease pH below 5.5
(3) stones frequent
(4) causes:
(a) obstructive uropathy
(b) nephrocalcinosis
(c) pyelonephritis
(d) cirrhosis
(e) multiple myeloma
(f) sickle cell
(g) amyloidosis
(h) SLE
(i) amphotericin
(j) analgesic abuse
(k) lithium
(5) treat with low dose bicarbonate
b) type II (proximal)
(1) proximal acid secretion defect
(2) can acidify urine
(3) osteomalacia occurs
(4) causes:
(a) nephrotic syndrome
(b) amyloidosis
(c) multiple myeloma
(d) SLE
(e) acetazolamide
(5) treat with high dose bicarbonate & potassium
c) type III (combination of type I & type II)
d) type IV
(1) decreased aldosterone or decreased response to aldosterone
(2) causes:
(a) obstructive uropathy
(b) hyporeninemia
(c) diabetes
(d) Addison's disease
(e) sickle cell
(f) spironolactone
(g) triamterene
(h) amiloride
(3) unlike other RTAs, accompanied by high serum potassium level

VIII. Metabolic Alkalosis

A. chloride responsive (urine chloride < 10 mM/L)
1. diuretic therapy
2. vomiting
3. NG drainage
4. chloride-wasting diarrhea
5. villous adenoma
6. penicillins
7. blood transfusion (citrate)
8. bicarbonate ingestion
9. hypoproteinemia
a) 1 g/dl fall in albumin causes 3.4 rise in HCO3
b) decreases anion gap
(1) therefore normal bicarbonate in hypoproteinemia means there is concurrent metabolic acidosis
c) treat with chloride containing solutions to prevent respiratory acidosis and carbon dioxide retention
B. chloride unresponsive (urine chloride > 20 mM/L)
1. hyperaldosteronism
2. Cushing's syndrome
3. exogenous steroids
4. Bartter syndrome
C. treatment:
1. hydrocholoric acid
a) 0.1 - 0.2 N (100 - 200 mmol hydrogen/liter)
b) can be added to TPN or D5
c) 0.2 mmol/kg/hr
d) requires a central line for administration
2. acetazolamide
3. gastric acid inhibition for GI losses

IX. Respiratory Acidosis

A. compensation
1. shift of Henderson equation; carbonic acid immediately buffered by plasma proteins & hemoglobin
2. ion shifts from bone & muscle (hours to days)
3. renal reabsorption and generation of HCO3 (working at 2 days and maximal at 5 days)
B. causes:
1. CNS depression
2. neuromuscular disorders
3. thoracic cage limitation
4. impaired lung motion
5. airway obstruction

X. Respiratory Alkalosis

A. compensation:
1. H+ moves out from intracellular stores & is replaced by K+
2. renal response follows
B. causes:
1. anxiety
2. CNS disorders
3. aspirin
4. sepsis
5. hyperthyroidism
6. hypoxia
7. pregnancy
8. liver disease
9. pulmonary edema
10. restrictive lung disease
11. PE
12. pneumonia

XI. HCO3 Replacement:

A. calculate the bicarbonate space to be 0.5 of body weight
B. CO2 diffuses better than HCO3 into CSF causing an immediate paradoxic acidosis inside of brain (and other cells)
C. HCO3 increases oxy-hemoglobin dissociation curve increasing hypoxia
D. HCO3 may directly suppress myocardial function
1. although HCO3 is often recommended in lactic acidosis when the pH is < 7.20 (in order to counteract the potentially deleterious cardiovascular effects of acidemia), some studies actually show no cardiovascular benefit to HCO3 administration, even if the pH is < 7.20. This lack of benefit may be due to the acute hypocalcemia (which can adversely affect cardiovascular status) that develops in response to HCO3 administration
E. HCO3 induces hyperosmolarity & arrhythmia-inducing electrolyte shifts
F. THAM (0.3 N tromethamine). A non-sodium containing alkalinization agent. not shown to be better than bicarbonate and has potential for additional side effects.

XII. Expected Compensations:

A. metabolic acidosis:
1. pCO2 = last 2 digits of pH
2. pCO2 = 1.5 x HCO3 + 8 ± 2
B. metabolic alkalosis:
1. variable; patients have different sensitivities to rising pCO2 and thus respond differently; pCO2 rarely will exceed 55 mm in compensation to a metablic alkalosis
2. for many patients:
a) 6 rise in pCO2 for every 10 rise in HCO3
b) pCO2 = (0.7 x HCO3) + 21 ± 1.5
C. respiratory acidosis:
1. acute:
a) HCO3 rises 1 for every 10 pCO2
b) HCO3 = [(pCO2 - 40)/10] + 24
2. chronic:
a) HCO3 rises 3.5 for every 10 pCO2
b) HCO3 = [(pCO2 - 40)/3] + 24
D. respiratory alkalosis:
1. acute:
a) HCO3 falls 2 for every 10 pCO2
b) HCO3 = 24 - [(40 - pCO2)/5]
2. chronic:
a) HCO3 falls 5 for every 10 pCO2
b) HCO3 = 24 - [(40 - pCO2)/2]
 
 Recent Reference: Adrogue, N. Engl. J. Med. 1998; 338: 26.

Acid-Base Disorder Problems:

Note: all ABGs given as: pH/pO2/pCO2/HCO3/O2%
 
1. 7.15/80/16/6/96%
• Na = 140
• K = 5.6
• Cl = 104
• CO2 = 6
2. 7.28/80/28/14/96%
• Na = 140
• K = 3.5
• Cl = 114
• CO2 = 16
3. 7.48/80/46/34/96%
• Na = 140
• K = 3.2
• Cl = 88
• CO2 = 37
4. 7.32/80/50/27/96%
• Na = 140
• K = 4.5
• Cl = 100
• CO2 = 28
5. 7.50/80/20/20/96%
• Na = 140
• K = 3.4
• Cl = 102
• CO2 = 22
6. 7.40/80/40/24/96%
• Na = 140
• K = 4.5
• Cl = 96
• CO2 = 24
7. 7.20/80/20/14/96%
• Na = 140
• K = 5.2
• Cl = 109
• CO2 = 16
8. 7.18/80/34/18/96%
• Na = 140
• K = 5.2
• Cl = 110
• CO2 = 20
 
last updated: February 14, 2002
 

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