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Acid Base

Here are the key steps to analyze each ABG example: 1) Evaluate the pH to determine if there is acidosis or alkalosis 2) Look at the pCO2 and HCO3 levels to determine if it is respiratory or metabolic disturbance 3) Calculate the anion gap and see if it is elevated to suggest a metabolic acidosis 4) Consider the clinical history and lab values to help determine the underlying etiology Let me know if you would like me to analyze any of the examples in more detail. The critical part is following a systematic approach of evaluating the pH, then pCO2/HCO3, anion gap, and integrating the clinical picture.

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Dexter Gabriel
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0% found this document useful (0 votes)
34 views28 pages

Acid Base

Here are the key steps to analyze each ABG example: 1) Evaluate the pH to determine if there is acidosis or alkalosis 2) Look at the pCO2 and HCO3 levels to determine if it is respiratory or metabolic disturbance 3) Calculate the anion gap and see if it is elevated to suggest a metabolic acidosis 4) Consider the clinical history and lab values to help determine the underlying etiology Let me know if you would like me to analyze any of the examples in more detail. The critical part is following a systematic approach of evaluating the pH, then pCO2/HCO3, anion gap, and integrating the clinical picture.

Uploaded by

Dexter Gabriel
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PPT, PDF, TXT or read online on Scribd
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Acid Base Disturbances

Ian Chan MS4


Eliza Long R2
10/30/06
ABG analysis
Why do we care ?
– 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 12-
24 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)
– 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:
– 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
– 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:
– 7.22/30/65/10/90% 139 110 20 120
PH(7.22) = acidemia 4.0 10 1.5
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

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