ABGs and Acid-Base
Deborah Cappell, MD
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.
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 cooximeter reveals PCO2 54, PO2 65, SpO2 86%.
According to a standard Hgb dissociation curve
the SpO2 should be >90%. 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
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 cooximeter reveals PCO2 54, PO2 65, SpO2 86%.
According to a standard Hgb dissociation curve
the SpO2 should be >90%. 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
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.
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.
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.
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
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
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.
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.
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?
SEEK
What is the best Rx for the disorder that caused
the acute decompensation?
A. High dose corticosteroids
B. Broad spectrum Abx
C. Surgery
D. Sodium nitrite and sodium thiosulfate
E. Methylene Blue
SEEK
What is the best Rx for the disorder that caused
the acute decompensation?
A. High dose corticosteroids
B. Broad spectrum Abx
C. Surgery
D. Sodium nitrite and sodium thiosulfate
E. Methylene Blue
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 >70% are usually fatal.
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.
SEEK
Rx for MetHgb >30% 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 >5 minutes.
Higher doses may increase MetHgb levels in
doses >15mg/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.
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 PB=760 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)
ABG
An increased Aa gradient can be caused by
A. Hypoventilation
B. Hyperventilation
C. Pulmonary embolus
D. A and C
E. B and C
y embolus
ABG
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 Alveolararterial gradient.
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 arterial;venous)
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
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 arterial;venous)
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
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.
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.)
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 OB’s office
and was Rx with IV corticosteroids and then
started on inhaled corticosteroids and a longacting 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.
SEEK
A.
B.
C.
D.
E.
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
SEEK
A.
B.
C.
D.
E.
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
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.
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.
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.
How to approach an Acid-Base
Disorder Primary
Problem
Met
Decreased
Acidosis bicarb
pH
Met
Increased
Alkalosis bicarb
Increased
Resp
Acidosis
Decreased Increased
Bicarb
Increased
PaCO2
Resp
Decreased
Alkalosis PaCO2
Compensation
Decreased Decreased
PaCO2
Increased
Increased
PaCo2
Decreased
Bicarb
Acid Base
1.Determine if acidemia (pH<7.36) or alkalemia
is present (pH>7.44). 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 Δgap? If
so is there an additional non-gap acidosis or a
metabolic alkalosis?
Appropriate Compensation
Met acidosis:
PCO2 = 1.5XHCO3 +8 ±2
Met Alkalosis
PCO2 = 0.7XHCO3 +21 ±1.5
(If bicarb >40 PCO2=0.75xHCO3)+19 ±7.5)
Resp Acidosis
Acute HCO3 = [(PCO2-40)/10] +24
Chronic HCO3 = [(PCO2-40)/3]+24
Resp Alkalosis
Acute HCO3 = [(40-PCO2)/5]+24
Chronic HCO3=[(40-PCO2)/2]+24
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?
A. Inconsistent and uninterpretable data
B. Acute respiratory acidosis
C. Chronic respiratory acidosis
D. Acute on chronic respiratory acidosis
E. Acute respiratory acidosis with anion gap
metabolic acidosis
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?
A. Inconsistent and uninterpretable data
B. Acute respiratory acidosis
C. Chronic respiratory acidosis
D. Acute on chronic respiratory acidosis
E. Acute respiratory acidosis with anion gap
metabolic acidosis
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 not=24X80/33=58.
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.
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.
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
Respiratory Alkalosis
Hyperventilation
Etiologies:
Hypoxemic drive (eg altitude, shunt),
acute/chronic pulm dz, vent over-breathing,
stimulation of resp center (eg pain, psychogenic,
pregnancy)
Metabolic Alkalosis
Etiologies:
Cl depletion (hypovolemic)
Ucl <20
Saline responsive
Cl expanded (Hypervolemic)
Ucl >20
Saline resistant
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
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
Δ
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 pH>7.1 down to PaCO2
of 10.
PaCo2 = 1.5xHCO3 +8 ± 2
Or ;Δ PaCO2 = 1.2 X Δ bicarb
Δ
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.
Δ
Etiologies of Metabolic Acidosis
AG = Na -(Cl+HCO3) = 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.
Δ
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)
Δ
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
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.
Δgap=(AG-12) – (24-HCO3)
The normal Δgap 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.
Acid Base
1.Determine if acidemia (pH<7.36) or alkalemia
is present (pH>7.44). 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 Δgap? If
so is there an additional non-gap acidosis or a
metabolic alkalosis?
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
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
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.
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?
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.
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.
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(86+16)=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.
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.
Which of the following labs is most
consistent with her presentation?
Na
K
A
147
B
Cl
BUN
Cr
2.9 105
CO
2
18
Glu
35
1.5 355
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
Which of the following labs is most
consistent with her presentation?
Na
K
A
147
B
Cl
BUN
Cr
2.9 105
CO
2
18
Glu
35
1.5 355
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
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.
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.
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?
Question cont
A. Methanol ingestion
B. Toluene toxicity
C. Ethylene Glycol ingestion
D. Ethanol intoxication
E. Isopropanol ingestion
Question cont
A. Methanol ingestion
B. Toluene toxicity
C. Ethylene Glycol ingestion
D. Ethanol intoxication
E. Isopropanol ingestion
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.
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.
Causes of an osmolal gap >10
Anion gap metabolic
No metabolic acidosis
acidosis
Isopropyl alcohol
Ethylene glycol
Diethyl ether
Methanol
Mannitol
Formaldehyde
ESRD without HD
Osm gap =
Osm(measured)- Nax2 +
Paraldehyde
Glu/18 + BUN/2.8 +
Alcoholic ketoacidosis
EtOH/4.6
Acid Base: Take Home Message
1.Determine if acidemia (pH<7.36) or alkalemia
is present (pH>7.44). 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 Δgap? If
so, is there an additional non-gap acidosis or a
metabolic alkalosis?