ABGs and Acid-Base

1
ABGs and Acid-Base

• Deborah Cappell, MD

2
ABG

• The ABG contains pH, PCO2, PO2 as analyzed by
  three electrodes at 37C
• The presence of air bubbles can falsely can alter
  PO2 and PCO2 closer to RA. Ice keeps the gases
  from escaping from the solution.
• Leukocyte larceny can cause a false decrement in
  PO2 due to WBC consumption of oxygen.

3
ABG question 1

• A 72 yo male, 50 pk-yr smoker, p/w dyspnea and sx
  c/w chronic bronchitis. His SpO2 via pulse
  oximeter is 95. However, an ABG via co-oximeter
  reveals PCO2 54, PO2 65, SpO2 86. According to a
  standard Hgb dissociation curve the SpO2 should
  be gt90. Which explains the discrepancy btwn his
  PO2 and SpO2?
• A. He has significant leukocytosis
• B. He has carboxyhemoglobinemia
• C. He has respiratory alkalosis
• D. He has 2,3,-diphosphoglycerate deficiency
• E. He is hypothermic

4
ABG question 1

• A 72 yo male, 50 pk-yr smoker, p/w dyspnea and sx
  c/w chronic bronchitis. His SpO2 via pulse
  oximeter is 95. However, an ABG via co-oximeter
  reveals PCO2 54, PO2 65, SpO2 86. According to a
  standard Hgb dissociation curve the SpO2 should
  be gt90. Which explains the discrepancy btwn his
  PO2 and SpO2?
• A. He has significant leukocytosis
• B. He has carboxyhemoglobinemia
• C. He has respiratory alkalosis
• D. He has 2,3,-diphosphoglycerate deficiency
• E. He is hypothermic

5
Explanation of ABG question 1

• Pulse oxymeter does not distinguish oxygenated
  Hgb from carboxy or met hemoglobin.
• However, the co-oximeter can differentiate hgb,
  carboxy-hgb and met-hgb. The carboxy-hgb was
  10.7 in this pt likely from smoking.
• Hence using only standard oximetery in the
  setting of smoke inhalation can give a false
  sense of security. An ABG by co-oximetry to r/o
  carboxy-hgb is necessary.

6
Explanation of ABG question 1

• Leukocyte larceny will falsely reduce PO2 and
  SpO2.
• Resp Alkalosis will shift the Hgb dissociation
  curve to the left and give a higher SpO2 for the
  same PO2.
• 2,3 diphosphoglycerate deficiency shifts the Hgb
  dissociation curve to the left as well.
• Only the measured SpO2 would be less than then
  PO2 not the calculated SpO2 less than PO2.
• As the temperature decreases, pH increases.
• When blood flows to the cool periphery the pH
  increases as PCO2 and H falls, so SpO2 rises
  with cooling and the PO2 decreases.

7
Question

• A 23 yo male admitted to ICU with resp failure
  from diffuse PNA. PMH IVDU and HIV. He is Rx with
  IV Bactrim and prednisone for presumptive PCP.
  His initial PaO2 was 55.
• Within 24 hours he is intubated for hypoxemic
  resp failure. Initial post-intubation ABG on 100
  was 7.45/32/82 94. CXR diffuse infiltrates. The
  following day on 70 his ABG is 7.45/30/121 SpO2
  of 97. He is bronched and the BAL is positive
  for PCP.
• On day 5 he is on 40 and a weaning trial is
  begun.

8
Question

• After 60 min of CPAP with PS of 5 and 40 oxygen
  his ABG is 7.43/35/90 SPO2 77.
• What is the most appropriate next step in this
  patient's management?
• A. Repeat the ABG
• B. Extubate to nonrebreather
• C. Administer amyl nitrate by inhalation then
  sodium thiosulfate IV
• D. Switch the patients Abx from Bactrim to
  pentamidine and administer IV methylene blue

9
Question

• After 60 min of CPAP with PS of 5 and 40 oxygen
  his ABG is 7.43/35/90 SPO2 77.
• What is the most appropriate next step in this
  patient's management?
• A. Repeat the ABG
• B. Extubate to nonrebreather
• C. Administer amyl nitrate by inhalation then
  sodium thiosulfate IV
• D. Switch the patients Abx from Bactrim to
  pentamidine and administer IV methylene blue

10
Answer Explained

• This pt has clinically improved, however his SpO2
  has declined despite an adequate PaO2.
• A recognized complication of sulfonomides is
  methemoglobinemia. (Then Hgb cannot bind oxygen
  because of oxidation of fe.)
• Also can happen with nitrites, nitrates,
  phenacetin, aniline dyes, and lidocaine
• Rx methylene blue IV by reducing the Fe.

11
SEEK

• A 33 yo female with p/w lower abdominal pain for
  1 day, assoc with nausea and decreased appetite.
  PE VS anl, abd soft with lower abd diffuse
  tenderness and the patient vomited twice during
  the exam. Pelvic showed b/l adnexal tenderness.
  WBC 19K, with 90 PMN.
• She received Metronidazole, Cipro, Morphine and
  metoclopramide and was sent for CT abd/pelvis.

12
SEEK

• 2 hours later she had acute onset SOB and feeling
  of impending doom. She was cyanotic despite 100
  Oxygen by NRB. HR 132, BP 160/100, RR 28, SpO2
  85 and the ABG 7.36/35/240. Naloxone was given
  but cyanosis and dyspnea continued, and she
  became lethargic.
• What is the best Rx for the disorder that caused
  the acute decompensation?

13
SEEK

• What is the best Rx for the disorder that caused
  the acute decompensation?
• High dose corticosteroids
• Broad spectrum Abx
• Surgery
• Sodium nitrite and sodium thiosulfate
• Methylene Blue

14
SEEK

• What is the best Rx for the disorder that caused
  the acute decompensation?
• High dose corticosteroids
• Broad spectrum Abx
• Surgery
• Sodium nitrite and sodium thiosulfate
• Methylene Blue

15
SEEK

• The pt has methemoglobinemia due to
  administration of metoclopramide and Rx with
  Methylene blue will reduce the seum ferric iron.
  Metoclopramide is an oxidizing agent which can
  convert ferrous () iron in hgb to the ferric
  form (). When given in excessive doses or to
  pt with enzyme deficiencies to convert methgb to
  hgb toxic levels may develop.
• MetHgb has a higher Oxygen affinity and reduces
  blood oxygen content shifting the curve to the
  left. Cyanosis develops at 15, sx at 30 and
  Change in MS at 50. Level gt70 are usually
  fatal.

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SEEK

• Many drugs are oxidants and cause this
  chloroquine, dapsone, local anesthetics
  (benzocaine, nitrates (nitroglycerin,
  nitroprusside, NO), and sulfonamides.
• High levels of MetHgb turn blood brown and does
  not turn red when exposed to air. SpO2 is
  inaccurate. The SpO2 not correlating with abg is
  a clue that co-oximetry is needed.

17
SEEK

• Rx for MetHgb gt30 with methylene blue which is a
  cofactor for NADP-metHb reductase and increases
  that enzymes capacity to reduce ferric iron. Dose
  is 1-2 mg/kg over gt5 minutes.
• Higher doses may increase MetHgb levels in doses
  gt15mg/kg and in pt with G6PD.
• This pt has PID and abx are useful.
• Sodium nitrite and sodium thiosulfate are used as
  antidotes to cyanide poisoning and work by
  increasing metHgb levels to facilitate transport
  of cyanide as cyanomethemoglobin from
  mitochondrial cytochromes to hepatocytes.

18
ABG

• Interpreting an ABG requires first an
  appreciation for the alveolar gas equation.
• Alveolar-arterial oxygen gradient
• Aa PAO2- PaO2
• FIO2(PB-PH20)-PaCO2/R -PaO2
• Where FIO2 0.21 PB760 PH2O 47
• A normal Aa gradient is dependent on age, body
  position, and nutritional status.
• (It is increased with age, obesity, fasting,
  supine position, heavy exercise and fasting)

19
ABG

• An increased Aa gradient can be caused by
• A. Hypoventilation
• B. Hyperventilation
• C. Pulmonary embolus
• D. A and C
• E. B and C

20
ABG
C. Pulmonary embolus

• An increased Aa gradient can be caused by
• A. Hypoventilation
• B. Hyperventilation
• C. Pulmonary embolus
• D. A and C
• E. B and C
• Hypoventilation will increase PCO2 and decrease
  PaO2 proportionally.
• Hyperventilation will decrease PCO2 and increase
  PaO2 proportionally.
• VQ mismatch will increase the Alveolar-arterial
  gradient.

21
Question Acid-Base

• In a hemodynamically stable pt on RA with nl BP
  and CXR which of the following arterial and
  venous ABG come from the same pt?
• (pH/PCO2/PHCO3 arterialvenous)
• A. 7.4/40/24 7.4/40/24
• B. 7.25/23/10 7.29/20/9
• C. 7.3/55/28 7.2/65/33
• D. 7.39/44/23 7.35/50/24
• E. 7.4/24/24 7.37/30/26

22
Question Acid-Base

• In a hemodynamically stable pt on RA with nl BP
  and CXR which of the following arterial and
  venous ABG come from the same pt?
• (pH/PCO2/PHCO3 arterialvenous)
• A. 7.4/40/24 7.4/40/24
• B. 7.25/23/10 7.29/20/9
• C. 7.3/55/28 7.2/65/33
• D. 7.39/44/23 7.35/50/24
• E. 7.4/24/24 7.37/30/26

23
Answer, explained

• 7.39/44/23 and 7.35/50/24
• The mean difference btwn arterial and venous pH
  was 0.036, PCO2 6, HCO3 1.5
• Venous pH should be lower and PCO2 higher than
  arterial. Bicarb is slightly higher in venous
  than arterial blood.
• If only a trend is what is being followed, eg in
  DKA, venous blood gases are likely adequate.

24
Answer, explained

• (Option A has same values for venous and
  arterial, option B the direction of change art to
  venous is backward, option C the magnitude of
  change is too great, option E makes no
  physiologic sense.)

25
SEEK

• A pregnant asthmatic is in the ER. She is 22 yo
  with asthma since early child with rare
  medication use until her pregnancy. She is 34
  weeks pregnant and this is her 1st pregnancy. In
  her 2nd trimester she was seen in her OBs office
  and was Rx with IV corticosteroids and then
  started on inhaled corticosteroids and a
  long-acting beta agonist. She did well until the
  last 2 days when DOE progressed to dyspnea at
  rest and over the prior evening used her rescue
  beta agonist many times.

26
SEEK

• On PE she is in moderate distress, using
  accessory muscles to breath while sitting
  upright. She can speak only 2-3 words at a time
  and there is insp and exp wheezing with decreased
  air movement. ABG on RA is 7.36/38/78. In this
  patient the most likely acute acid-base
  disturbance is
• Metabolic Alkalosis
• Metabolic Acidosis
• Respiratory Acidosis
• Respiratoy Alkalosis
• No acute acid-base disturbance

27
SEEK

• On PE she is in moderate distress, using
  accessory muscles to breath while sitting
  upright. She can speak only 2-3 words at a time
  and there is insp and exp wheezing with decreased
  air movement. ABG on RA is 7.36/38/78. In this
  patient the most likely acute acid-base
  disturbance is
• Metabolic Alkalosis
• Metabolic Acidosis
• Respiratory Acidosis
• Respiratory Alkalosis
• No acute acid-base disturbance

28
SEEK explained

• This ABG is signaling ventilatory failure from
  acute asthma. There are changes in pregnancy
  which must be taken into account. During pg
  oxygen consumption rises to 40-100 above
  baseline. This is due to fetal/placental needs
  and increased CO and work of breathing. Increased
  oxygen consumption is associated with a 30-50
  increase in CO2 production by the 3rd trimester
  requiring an increase in minute ventilation that
  starts in the 1st trimester and peaks at 20-40
  above baseline at term.

29
SEEK explained

• Alveolar ventilation is increased above the level
  needed to eliminate the increased CO2 production
  and hence PCO2 falls to 27-32 mm Hg in most of
  pregnancy. The augmented ventilation is
  attributed to respiratory stimulation from
  increased progesterone and results in a 30-35
  increased in TV while RR remains the
  same/slightly increased. Renal compensation
  results in a pH of 7.4-7.45 and bicarb 18-21.

30
SEEK explained

• The patient has an increased Aa gradient likely
  related to VQ mismatch from asthma. The pregnancy
  with the acute respiratory distress make the
  sequence of chronic resp alkalosis from
  pregnancy, with renal compensation by chronic
  metabolic acidosis, now complicated by acute
  respiratory acidosis. This example underscores
  the clinical context importance in interpreting
  abg.

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How to approach an Acid-Base
Disorder Primary Problem pH Compensation
Met Acidosis Decreased bicarb Decreased Decreased PaCO2
Met Alkalosis Increased bicarb Increased Increased PaCo2
Resp Acidosis Increased PaCO2 Decreased Increased Bicarb
Resp Alkalosis Decreased PaCO2 Increased Decreased Bicarb
32
Acid Base

• 1.Determine if acidemia (pHlt7.36) or alkalemia is
  present (pHgt7.44). In mixed disorders the pH will
  be normal but the bicarb/pCO2/AG will be abnl.
• 2. Is the primary disturbance met or resp? Does
  the change in PCO2 account for the direction of
  pH change?
• 3. Is there appropriate compensation for the
  primary disturbance? (see table ahead)
• 4. Is the AG elevated? If so is there a ?gap?
  If so is there an additional non-gap acidosis or
  a metabolic alkalosis?

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Appropriate Compensation

• Met acidosis
• PCO2 1.5XHCO3 8 2
• Met Alkalosis
• PCO2 0.7XHCO3 21 1.5
• (If bicarb gt40 PCO20.75xHCO3)19 7.5)
• Resp Acidosis
• Acute HCO3 (PCO2-40)/10 24
• Chronic HCO3 (PCO2-40)/324
• Resp Alkalosis
• Acute HCO3 (40-PCO2)/524
• Chronic HCO3(40-PCO2)/224

34
SEEK

• A 60 yo female is admitted with 2 day of cough
  productive of purulent sputum. She has a history
  of severe COPD on home 2L Oxygen NC. On admission
  the HR is 120, BP 140/95, RR 28. Labs reveal Na
  135, K 3.5, Cl 92, Bicarb 33. ABG on RA is
  7.2/80/45. What is the acid-base disorder?
• Inconsistent and uninterpretable data
• Acute respiratory acidosis
• Chronic respiratory acidosis
• Acute on chronic respiratory acidosis
• Acute respiratory acidosis with anion gap
  metabolic acidosis

35
SEEK

• A 60 yo female is admitted with 2 day of cought
  productive of purulent sputum. She has a history
  of severe COPD on home 2L Oxygen NC. On admission
  the HR is 120, BP 140/95, RR 28. Labs reveal Na
  135, K 3.5, Cl 92, Bicarb 33. ABG on RA is
  7.2/80/45. What is the acid-base disorder?
• Inconsistent and uninterpretable data
• Acute respiratory acidosis
• Chronic respiratory acidosis
• Acute on chronic respiratory acidosis
• Acute respiratory acidosis with anion gap
  metabolic acidosis

36
SEEK

• The first step is to check the internal
  consistency with the Henderson-Hasselback
  equation. The H 24xPaCO2/HCO3 or each
  change in pH of 0.01 represents a 1meq decreased
  in H so that at a pH of 7.2 the H is around
  62. 62does not24X80/3358.

37
SEEK

• Respiratory acidosis is when pH is less the 7.4
  and CO2 is increased.
• In acute resp acidosis the Ph declines 0.08 for
  each 10 rise in CO2. So if the baseline CO2 was
  40, the CO2 of 80 should decrease pH by 0.32 to
  7.08.
• In chronic resp acidosis the pH decline 0.03 for
  each 10 increase in CO2. A patient with chronic
  resp acidosis with CO2 of 80 would have a pH of
  7.28.
• Rather a combination of acute respiratory
  acidosis superimposed on chronic resp acidosis
  with baseline CO2 of 60 is more consistent with
  these values.

38
SEEK

• Finally any acid base problem should include
  anion gap calculation. The ag in the case is 10
  and normal is 12/- 4 so this pt does not have an
  AG met acidosis.

39
Respiratory Acidosis

• Ineffective alveolar respiration or increased CO2
  production
• Etiologies include airway obstruction, resp
  center depression, neuromuscular d/o, pulm d/o,
  high carb diet

40
Respiratory Alkalosis

• Hyperventilation
• Etiologies
• Hypoxemic drive (eg altitude, shunt),
  acute/chronic pulm dz, vent over-breathing,
  stimulation of resp center (eg pain, psychogenic,
  pregnancy)

41
Metabolic Alkalosis

• Etiologies
• Cl depletion (hypovolemic)
• Ucl lt20
• Saline responsive
• Cl expanded (Hypervolemic)
• Ucl gt20
• Saline resistant

42
Etiologies of metabolic alkalosis

• Hypovolemic/Cl depleted
• GI loss vomit, gastric suction, Cl rich
  diarrhea, villous adenoma
• Renal loss of H
• Diuretic
• Post-hypercapnia
• High dose carbenicillin

43
Etiologies of metabolic alkalosis

• Hypervolemic/Cl expanded
• Renal H loss primary hyperaldo, primary
  hypercortisolism, adrenocorticotropic hormone xs.
• Pharm xs steroids
• Renal A. stenosis with RV HTN
• Renin secreting tumor
• Hypokalemia
• Bicarb overdose
• Pharm
• Milk-alkali syndrome
• Massive blood transfusion

44
Metabolic Acidosis
?

• An increase in acid accumulation or decreased
  extracellular bicarb.
• Compensate with increased ventilation and
  decreased PaCo2 and increased renal H excretion.
• During prolonged acidosis the last two digits of
  pH PaCO2 as long as pHgt7.1 down to PaCO2 of 10.
• PaCo2 1.5xHCO3 8 2
• Or ? PaCO2 1.2 X ? bicarb

45
Etiologies of Metabolic Acidosis
?

• Increase in endogenous acid production
  (ketoacidosis), exogenous acid input (poisons),
  xs bicarb loss (diarrhea) or decreased renal
  excretion of endogenous acid (chronic renal
  failure).
• Divided into anion gap and non-anion gap acidosis.

46
Etiologies of Metabolic Acidosis
?

• AG Na -(ClHCO3) 10 4
• AG increases with decreased unmeasured cations or
  increased unmeasured anions.
• (Unmeasured anions proteins, phosphate, sulfates
  and organic acids vs unmeasured cations K,Ca, Mg)
• Hypoalbuminemia will decrease the normal AG to
  4-5. For every 1 decrease in Alb a decrease of
  2.5-3 in AG is expected. Similarly parproteinemia
  will decrease the normal anion gap.

47
Etiologies of Metabolic Acidosis
?

• Increased anion gap
• Methanol
• Uremia
• Diabetic ketoacidosis
• Paraldehyde
• INH/Iron
• Lactic acidosis (including metformin)
• Ethylene glycol, EtOH
• Salicylates, starvation ketosis
• (others CO, CN, Sulfur, theophylline, toluene)

48
Etiologies of Metabolic Acidosis
?

• Normal anion gap
• Bicarb loss (kidney/gut)
• diarrhea
• urinary diversion
• fistulas/drain from bile/small bowel etc
• RTA
• Acid addition (with Cl- as the anion)
• Hcl
• NH4Cl
• Arginine HCL
• Lysine HCL
• CaCl2/MgCL2 (oral)
• sulfur

49
The DELTA GAP

• If there is an abnormal AG you can look for
  triple disorders by checking for the delta gap
• In an uncomplicated AG met acidosis for every 1
  increase in AG the HCO3 should decrease by 1. If
  this is not the case there is likely a mixed d/o.
• ?gap(AG-12) (24-HCO3)
• The normal ?gap should be zero 6.
• A positive delta gap indicates either
  simultaneous metabolic alkalosis (eg vomitting)
  or resp acidosis.
• A negative delta gap indicates then a concomitant
  normal AG hyperchloremic acidosis (eg diarrhea)
  or chronic resp alkalosis is present.

50
Acid Base

• 1.Determine if acidemia (pHlt7.36) or alkalemia is
  present (pHgt7.44). In mixed disorders the pH will
  be normal but the bicarb/pCO2/AG will be abnl.
• 2. Is the primary disturbance met or resp? Does
  the change in PCO2 account for the direction of
  pH change?
• 3. Is there appropriate compensation for the
  primary disturbance?
• 4. Is the AG elevated? If so is there a ?gap?
  If so is there an additional non-gap acidosis or
  a metabolic alkalosis?

51
Question

• 38 yo male with chronic renal failure p/w
  weakness, anorexia and nausea to ER. He has
  recently had increased n/v but had refused HD.
  PE bibasilar crackles, regular cardiac rhythm,
  and 2 edema. Labs Na 135, K 5.2 Cl 80 HCO3 24,
  BUN 100 Cr 12. ABG pH7.4 pCO2 37 HCO3 22.
• Which best describes the acid-base status
• A. No acid-base abnormality
• B. Met acidosis and respiratory alkalosis
• C. Metabolic acidosis and metabolic alkalosis
• D. Respiratory acidosis and respiratory alkalosis

52
Question

• 38 yo male with chronic renal failure p/w
  weakness, anorexia and nausea to ER. He has
  recently had increased n/v but had refused HD.
  PE bibasilar crackles, regular cardiac rhythm,
  and 2 edema. Labs Na 135, K 5.2 Cl 80 HCO3 24,
  BUN 100 Cr 12. ABG pH7.4 pCO2 37 HCO3 22.
• Which best describes the acid-base status
• A. No acid-base abnormality
• B. Met acidosis and respiratory alkalosis
• C. Metabolic acidosis and metabolic alkalosis
• D. Respiratory acidosis and respiratory alkalosis

53
Answer Explained

• Recognize a large AG with normal bicarb may
  indicate a mixed metabolic acidosis and metabolic
  alkalosis.
• Would expect AG acidosis from renal failure. His
  AG is 31. His bicarb should therefore be 5. For
  each increase in AG from 12 bicarb should
  decrease by the same 19
• Due to the n/v he also has a metabolic alkalosis
  which increased his bicarb back to 24 with
  decreased Cl.
• No evidence of resp alkalosis since the PCO2 is
  nl. Very rare if ever to see mixed resp alk and
  acidosis.

54
Question

• A 52 yo f with advanced pulm sarcoid on
  prednisone 30 qd for 2 yrs. Pt is admitted with 2
  days of fever, flank pain, dysuria and vomiting
  for 6 hours. On admit HR 120 BP 80/60 RR 28. UA
  is loaded with WBC and gram stain is loaded with
  gram negative bacilli. ABG on RA 7.44/24/68. Na
  135, K 3.5, Cl 86, HCO3 16. What is the acid-base
  disorder?

55
Question

• A. Inconsistent and un-interpretable data
• B. Chronic resp alkalosis
• C. Acute and chronic resp alkalosis
• D. Resp Alkalosis and anion gap metabolic
  acidosis
• E. Resp Alkalosis, anion gap metabolic acidosis,
  and metabolic alkalosis.

56
Question

• A. Inconsistent and un-interpretable data
• B. Chronic resp alkalosis
• C. Acute and chronic resp alkalosis
• D. Resp Alkalosis and anion gap metabolic
  acidosis
• E. Resp Alkalosis, anion gap metabolic acidosis,
  and metabolic alkalosis.

57
Answer explained

• PH is greater than 7.4 (alkalemia) and PaCO2 is
  reduced so the primary abnormality is respiratory
  alkalosis. (This is likely related to pain she is
  hyperventilating)
• Is there a metabolic component? The AG is
  135-(8616)33. Normal AG is 8-16. So there is
  an AG acidosis. If the bicarb is not increased
  for each increase in AG there is a mixed d/o.
• The delta gap (AG-12) (24-bicarb)
• (33-12)-(24-16) 13. (normal is zero /- 6)
• A positive delta gap implies simultaneous resp
  acidosis or metabolic alkalosis. Here chronic met
  alkalosis likely related to chronic steroid use
  and vomiting.

58
MKSAP Question

• A 75 yo female is BIBEMS after ingesting 50 tabs
  of enteric coated asa. She has chronic OA and DM
  type 2. She has refractory arthritis and periph
  neuropathy. On PE T 100, HR 135 RR 28 BP 105/65.

59
Which of the following labs is most consistent
with her presentation?
Na K Cl CO2 BUN Cr Glu
A 147 2.9 105 18 35 1.5 355
B 140 4.5 105 28 35 1.5 355
C 140 3.3 105 28 10 0.7 45
D 121 4.3 105 18 35 1.5 655
E 130 5.3 110 18 35 2.5 655
60
Which of the following labs is most consistent
with her presentation?
Na K Cl CO2 BUN Cr Glu
A 147 2.9 105 18 35 1.5 355
B 140 4.5 105 28 35 1.5 355
C 140 3.3 105 28 10 0.7 45
D 121 4.3 105 18 35 1.5 655
E 130 5.3 110 18 35 2.5 655
61
MKSAP explained

• Mixed anion gap metabolic acidosis with resp
  alkalosis and volume depletion characteristic of
  salicylism.
• Early salicylate OD central hypervent with resp
  alk then renal compensation
• Later metabolic acidosis due to uncoupled
  oxidative phophorylation and ketosis.
• Progressively salicylates enter cns causing
  change in Mental status and tinnitis. Volume loss
  can be worse by renal and vomit losses causing
  increased BUN/Cr.
• Stress can cause hyperglycemia.

62
MKSAP explained

• So the answer is mild hypernatremia due to renal
  free water loss, AG acidosis with low bicarb, and
  volume depletion with elevated BUN/Cr, with mild
  hyperglycemia.
• B normal AG, mild dehydration and hyperglycemia
  eg vomiting.
• C mild hypokalemia and hypoglycemia without
  volume depletion eg hypoglycemic episode
• D AG with hyperglycemia and hyponatremia likely
  with DKA and hyperkalemia
• E Hyperkalemia, hyperchloremia, low bicarb and
  normal AG eg RTA.

63
Question

• A 20 yo college student is BIB fraternity
  brothers to the ER because he is unarousable. No
  PMH until the party the previous night.
• BP 120/70 HR 118 RR 32 Sclera anicteric, pupils 8
  mm and poorly responsive. Fundoscopy reveals sl
  blurring of the disk margins b/l with decreased
  retinal sheen. PE otherwise unresponsive and
  unremarkable.
• Na 142, K 4.3 Cl 98 HCO3 10 Glu 108, BUN 14 Osm
  (measured 348) 7.22/24/108. Blood alcohol level
  is 45. UA is unremarkable. What is the etiology
  of his metabolic acidosis?

64
Question cont

• A. Methanol ingestion
• B. Toluene toxicity
• C. Ethylene Glycol ingestion
• D. Ethanol intoxication
• E. Isopropanol ingestion

65
Question cont

• A. Methanol ingestion
• B. Toluene toxicity
• C. Ethylene Glycol ingestion
• D. Ethanol intoxication
• E. Isopropanol ingestion

66
Answer explained

• This pt has a high AG and elevated osmolal gap.
• This suggests either methanol or ethylene glycol
  intoxication. Optic nerve dysfunction on exam
  makes methanol most likely.
• The osmolal gap is calc osmolality -osm measure
• 2XNa Glu/18 BUN/2.8- measured
• 295-358. or a gap of 63 ( part of which is
  explained by EtOH (EtOH/4.6 45/4.6 10)
• High AG met acidosis is usually methanol/ethylene
  glycol.

67
Answer explained

• Methanol causes optic n injury with blurred disc,
  retinal edema (increased sheen), loss of pupilary
  light reflex. Rx with EtOh or fomepizole to
  decrease formation of formaldehye.
• Ethylene Glycol also causes increased AG and
  osmolal gap met acidosis. It is associated with
  oxalate crytaluria and not optic n injury.
• Ethanol with ketolactic acidosis would not
  explain the optic findings.
• Isopropanolol is met to acetone and causes
  osmolal gap without AG acidosis
• Toluene (glue-sniffing) intoxication is not
  associated with osmolal gap only AG acidosis.

68
Causes of an osmolal gap gt10

• Anion gap metabolic acidosis
• Ethylene glycol
• Methanol
• Formaldehyde
• ESRD without HD
• Paraldehyde
• Alcoholic ketoacidosis

• No metabolic acidosis
• Isopropyl alcohol
• Diethyl ether
• Mannitol

Osm gap Osm(measured)- Nax2 Glu/18 BUN/2.8
EtOH/4.6
69
Acid Base Take Home Message

• 1.Determine if acidemia (pHlt7.36) or alkalemia is
  present (pHgt7.44). In mixed disorders the pH will
  be normal but the bicarb/pCO2/AG will be abnl.
• 2. Is the primary disturbance met or resp? Does
  the change in PCO2 account for the direction of
  pH change?
• 3. Is there appropriate compensation for the
  primary disturbance?
• 4. Is the AG elevated? If so is there a ?gap?
  If so, is there an additional non-gap acidosis or
  a metabolic alkalosis?