Acid Base Disturbances
Ian Chan MS4
Eliza Long R2
Dr. Abdul-Monim Batiha
ABG analysis
Why do we care ?
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Critical care requires a good understanding
Helps in the differential and final diagnosis
Helps in determining treatment plan
Treating acid/base disorders helps medications
work better (i.e. antibiotics, vasopressors, etc.)
– Helps in ventilator management
– Severe acid/base disorders may need dialysis
– Changes in electrolyte levels in acidosis
(increased K+ and Na+, and decreases in HCO3)
Acid buffering
The Anion Gap
Na – (Cl + HCO3)
NaHCO3 + HCL  NaCL + H2CO3
NaHCO3 + HX NaX+ H2CO3
Unmeasured
cations:
calcium,
magnesium, gamma globulins, potassium.
Unmeasured anions: albumin, phosphate,
sulfate, lactate.
Gap Acidosis
Methanol
Uremia
Diabetic ketoacidosis
Paraldehyde
INH
Lactic acidosis
Ethylene Glycol
Salicylate
Non Gap Acidosis
H: hyperalimentation
A: acetazolamide
R: RTA
D: diarrhea
U: rectosigmoidostomy
P: pancreatic fistula
Metabolic Acidosis
Respiratory compensation process takes 1224 hours to become fully active. Protons are
slow to diffuse across the blood brain barrier.
In the case of LA this will be faster because
LA is produced in the brain.
The degree of compensation can be
assessed by using Winter’s Formula. It is
INAPPROPRIATE to use this formula before
the acidosis has existed for 12-24 hours.
– PCO2 = 1.5 (HCO3) + 8 +/-2.
Decreased anion gap
Decrease in unmeasured anions
– Hypoalbuminemia
Increase in unmeasured cations
– Hypercalcemia
– Hypermagnesemia
– Hyperkalemia
– Multiple myeloma
– Lithium toxicity
Metabolic Alkalosis
Generation by gain of HCO3 and maintained
by abnormal renal HCO3 absorption.
This is almost always secondary to volume
contraction (low Cl in urine, responsive to
NaCl, maintained at proximal tubule)
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Vomiting: net loss of H+ and gain of HCO3.
Diuretics: ECFV depletion
Chronic diarrhea: ECFV depletion
Profound hypokalemia
Renal failure: if we cannot filter HCO3 we cannot
excrete it.
Mineralocorticoid excess: increased H
secretion, hypokalemia (Na/K exchanger),
saline resistant).
Respiratory Acidosis
Acute or Chronic: has the kidney had
enough time to partially compensate?
The source of the BUFFER (we need to
produce bicarb) is different in these states
and thus we need to make this distinction.
Respiratory Acidosis
Acute : H is titrated by non HCO3 organic tissue
buffers. Hb is an example. The kidney has little
involvement in this phase.
– 10 mm Hg increase in CO2 / pH should decrease by
.08
Chronic: The mechanism here is the renal
synthesis and retention of bicarbonate. As
HCO3 is added to the blood we see that [Cl] will
decrease to balance charges.
– This is the hypochloremia of chronic metabolic
acidosis.
– 10 mm H increase in CO2 / pH should decrease by
.03
Respiratory Acidosis
Elevation of CO2 above normal with a drop in
extracellular pH.
This is a disorder of ventilation.
Rate of CO2 elimination is lower than the
production
5 main categories:
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CNS depression
Pleural disease
Lung diseases such as COPD and ARDS
Musculoskeletal disorders
Compensatory mechanism for metabolic alkalosis
Respiratory Alkalosis
Initiated by a fall in the CO2  activate
processes which lower HCO3.
Associated with mild hypokalemia. Cl is
retained to offset the loss of HCO3 negative
charge.
Acute response is independent of renal
HCO3 wasting. The chronic compensation is
governed by renal HCO3 wasting.
Causes
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Intracerebral hemorrhage
Drug use : salicylates and progesterone
Decreased lung compliance Anxiety
Liver cirrhosis
Sepsis
Arterial Blood Gas (ABG) Analysis
ABG interpretation
Follow rules and you will always be right !!
1) determine PH
acidemia or alkalemia
2) calculate the anion gap
3) determine Co2 compensation (winters
formula)
4) calculate the delta gap (delta HCO3)
ABG analysis
Arterial Blood Gas (ABG) –interpretation
– Always evaluate PH first
Alkalosis – PH > 7.45
Acidosis – PH < 7.35
– Determine anion gap (AG) – AG = NA – (HCO3+ CL)
AG metabolic acidosis
Non AG acidosis – determined by delta gap
– Winters formula
Calculates expected PaCO2 for metabolic acidosis
PaCO2 = 1.5 x HCO3 + 8
ABG analysis
Delta gap
– Delta HCO3 = HCO3 (electrolytes) + change in AG
Delta gap < 24 = non AG acidosis
Delta gap > 24 = metabolic alkalosis
– Note: The key to ABG interpretation is
following the above steps in order.
ABG analysis
33 y/o with DKA presents with the
following:
– Na = 128, Cl = 90, HCO3 = 4, Glucose = 800
– 7.0/14/90/4/95%
– PH = acidemia
– AG = 128 – (90 + 4) = 34
– Winters formula – 1.5(4) + 8 = 14
– Delta gap = 4 + (34 – 12) = 26
ABG analysis
Answer
– AG acidosis with appropriate respiratory
compensation
– History c/w ketoacidosis secondary to DKA
with appropriate respiratory compensation
ABG analysis
56 y/o with COPD exacerbation and hypotension
and associated diarrhea x 7 days presents with
the following ABG:
139 110 20
– 7.22/30/65/10/90%
120
4.0 10 1.5
PH(7.22) = acidemia
AG = 139 – (10 + 110) = 19 (nl AG = 8-12)
Winters formula
– PaCO2 = 1.5 (HCO3) + 8 = 1.5 (10) + 8 = 23
Delta gap
– Delta gap = HC03 + change in the AG = 24
– Delta gap = 10 + (19 – 12) = 10 + 7 = 17
– Delta gap = 17
ABG - example
Triple disorder
– AG acidosis – Incomplete respiratory compensation
– Non AG acidosis
History would suggest AG acidosis is secondary to
hypotension with lactic acid build up and the patient is not
able to compensate with his COPD therefore there is no
respiratory compensation and the non AG acidosis is
secondary to diarrhea with associated HCO3 loss.
Look at the pH.
– pH < 7.35, acidosis
– pH > 7.45, alkalosis
Look at PCO2, HCO3• Main pathology will be the change correlates with
the pH.
• If alkalosis pCO2 will be low or Bicarb high
• If acidosis pCO2 will be high or Bicard low
• The other abnormal parameter is the compensator
response
Respiratory or Metabolic
• pCO2 - respiratory
• Bicarb - metabolic
Metabolic Acidosis? Anion Gap?
• >12 - ketoacidosis, uremia, lactic acidosis, or
toxins
• Delta ratio to check for gap and non gap
disorders , or metabolic alkalosis happening
simultaneously
• Normal anion gap - diarrhea OR unknown. If
unknown calculate urine anion gap, if positive
likely RTA, if neg liekly diarrhea
Metabolic Alkalosis
If urin Cl is > 20 it is chloride-resistant alkalosis
(increased mineralcorticoid activity
If <20 chloride responsive alkalosis (vomitting
or gastric loss)
Example # 1
44 yo M 2 weeks post-op from total
proctocolectomy for ulcerative colitis.
Na+ 134, K+ 2.9, Cl- 108, HCO3- 16, BUN
31, Cr 1.5
BG: 7.31/ 33 /93 / 16
Example #2
9 yo M presents with N/V.
Na 132 , K 6.0, Cl 93, HCO3- 11 glucose
650
BG: 7.27/23/96/11/-8
Example #3
70 yo M s/p lap chole, on the morning of
POD #1. Pt received 2L bolus of
crystalloid throughout pm for tachycardia.
Now with SOB.
7.24 / 60 / 52 / 27 /+3
Example #4
54 yo F s/p mult debridements for
necrotizing fasciitis, now on vassopressin
to maintain blood pressure
BG - 7.29/40/83/17/-6
Example #5
35 yo M involved in crush injury, boulder
vs body.
Na 135 , K 5.0, Cl 98, HCO3- 15 BUN 38,
Cr 1.7, CK 42,346
BG: 7.30/32/96/15/-4
Example #6
4 wks M with projectile emesis
Na: 140, K:2.9, Cl: 92
7.49/40/98/30/+6