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Acid Base Analysis

Hamza Y. Habib MD Student

Step 1

Look at pH

acidaemic
PH< 7.4
or alkalaemic
PH>7.4
note (acidemia not acidosis)

Step 2

Check PCO2
Is the primary disturbance respiratory or
metabolic disorder ?
R. As the PH increase
M. As the PH increase

the PCO2 decrease


theHCO3 increase

Step 3

Calculate the anion gap =


Na+- (HC03- + Cr).
If the primary disorder is M. Acidosis then we
know that its HAGMA
If the primary disorder is Not M. Acidosis then
we know that there is concurrent HAGMA

Step 4 R.

Acute or chronic? By change in pH

Step 5

The HCO3 correct !


If Metabolic:
AG = AG - 12
expected bicarbonate level = 24 AG
Compare the expected bicarbonate to the actual
bicarbonate.
Measured > Calculated M. Alkalosis
Measured < Calculated NAG M. Acidosis

Step 5

The HCO3 correct !


If Respiratory:

Step 6 - M

The P CO2 correct !


Metabolic acidosis: Pco2 = 1.5*(HCO3)
+ 8.
Metabolic alkalosis : Pco2 = 0.9*(HCO3)
+ 15.
Measured > Calculated R. Acidosis
Measured < Calculated R. Alkalosis


Ph =7.40 ,pco2 =40 ,Hco3 =24
Na =145, Cl =100


Ph=7.50 , pco2 =20 , Hco3 = 15
Na =145 , Cl = 100


Arterial blood gas results on room air from a
patient newly admitted to the intensive care
unit are as follows:
pH 7.42 Pa CO2 25 mm Hg
Pa02 100
mm Hg
Bicarbonate 14


32-year-old male with type 1 diabetes and
severe depression is brought to the emergency
department because of a 2-day history of
nausea and abdominal pain
Blood pH 7.31A
Pa02 90 mm Hg
PaC02
29 mmHg HCO3= 14
Blood glucose 450 mg/dL
Serum sodium
132
Serum potassium 5.0
Serum chloride 85
What is the acid base balance ?

A 17-year-old female is brought to the emergency


department by her parents, because she has become
lethargic and seems to have trouble breathing. They have
noticed that, over the last several weeks, she has been
going to the bathroom more frequently and appears to have
lost some weight.

She has always been a good student, but recently she has
felt poorly and has had difficulty completing her homework
assignments. For the last 2 days, she has completely lost
her appetite, has had nausea, and she vomited 57 times
during the day before she was brought in. She has no
previous medical history.
On physical examination, her blood pressure is 95/60, pulse
114 per minute, respirations 24, temperature afebrile. In
general, she is a thin and lethargic but arousable 17-yearold woman who is breathing deeply. Her skin turgor is
markedly decreased, and her neck veins are not visible. She
has a hyperdynamic precordium, but the examination is


Laboratory studies: sodium 124, potassium 5.9,
chloride 80, CO3 18, BUN 31, creatinine 1.4,
hemoglobin 15.1, hematocrit 47%.
Urinalysis: specific gravity 1.010, pH 5, 4+
glucose, 2+ ketones.
ABGs on room air: PO2 105,pH 7.25, PCO2 20,
bicarbonate 12.
The patient is immediately given 3 liters of .9 NS,
and an insulin drip is initiated with improvement
in her sensorium.


Which of the following acid-base
abnormalities does she have?
A. Metabolic acidosis, respiratory acidosis,
metabolic alkalosis
B. Respiratory acidosis, metabolic acidosis,
metabolic alkalosis
C. Metabolic acidosis, respiratory alkalosis,
metabolic alkalosis
D. Metabolic acidosis, respiratory alkalosis
E. Respiratory acidosis, metabolic alkalosis


A 45-year-old male is brought to the emergency
department in a stuporous state. His lab findings are as
follows:
Blood pH 7.21
Pa02 100 mmH
PaCO2 30 mmHg
HCO3= 13
Serum osm = 350 mosm/L
Blood glucose 90 mg/dl
Na+ 141 mEd/L
K+ 4.6 mEd/L
Cl- 100 mEq/L
BUN 28 mg/dL
Cr = 2.5
His urine shows the presence of rectangular, envelopeshaped crystals. His creatinine three months ago was
1.2 mg/dL.

Acid base
disterbances


HC03 + H2 <--> H2C03 <--> H2O +
CO2

This equation tells us that the body has only 2 ways to


control the serum pH:

1) Regulate the respiratory rate and tidal volume; thus,


control the P.C02.

2) Regulate the kidney's reabsorption of HC03 -.

Serum Anion Gap

AG = Na+- (HC03- + Cl-)


normally unmeasured ions that stay relatively constant
have been dropped, leaving only the major measured
ions.
Remember that any increase in unmeasured anions
always is 1:1 with the increase of H+-so highAG always
indicates metabolic acidosis.
Any change in this gap is due to added anions such as
ketones or lactate
albumin is the main contributor to the AG; therefore,
hypoalbuminemia lowers the "normal" AG (- 2.5 mEq/L
decrease in the AG for each I g/dL decrease in albumin).

Urine Anion Gap

UAG=Na +K - Cl
+

UAG=Na+ +K+ +(NH4+) - Cl- - (HCO3-)


estimate of the unmeasured ions in the urine, the most important
one being NH4
In the setting of metabolic acidosis due to extra-renal bicarbonate
losses, renal H+ excretion should be high, and H+ is excreted in the
form of NH4
Normal value of UAG is close to 0.
A positive UAG value suggests low urinary NH4 + (e.g., RTA Type
4).
A negative UAG value suggests high urinary NH4 + (e.g.,
diarrhea).

OSMOLAL GAP

Osm {calc} = 2[Na+] + (BUN/2.8) + (glucose/18)


OG = Osm {meas} Osm {calc}
normal OG is< 10.
The main use of OG is in the workup of a patient with
possible acid alcohol ingestion (e.g., ethylene glycol,
methanol, or propylene glycol). Especially consider
these possible poisonings if the OG > 25 mOsm/kg
Normal AG High OG ---------Isopropyl alcohol or ethanol
ingestion
High AG High OG
--------Methanol and ethylene glycol

METABOLIC ACIDOSIS

Etiology
Metabolic acidosis occurs with the following:
1. Overproduction of lactic acid or ketoacids
2. HC03- wasting (renal tubular acidosis [RTA] or
diarrhea)
3. Failure to excrete daily acid production (renal failure)
4. Ingestion of agents that are acids (salicylates) or are
metabolized to acids (methanol, ethylene glycol,
paraldehyde) or cause a lactic/ketoacidosis
(salicylates, isoniazid, and iron)

NAGMA
(hyperchloremic)

increase in Cl with the decrease in HC03maintain electrical neutrality


The 3 causes of NAGMA:
1) Usual: Loss of HC03- due to diarrhea or
proximal RTA
2) Increased organic acids (NH4 +; e.g., patients
on total parenteral nutrition)
3) Inability of the kidney to excrete endogenous
acids (renal failure or distal RTA)

NAGMA
(hyperchloremic)

NAGMA plus hyperkalemia, think Type 4 RTA


(hypoaldosteronism).
NAGMA plus hypokalemia is caused by:
GI loss (sometimes)
RTA Types 1 (distal) and 2 (proximal)
Calculate the UAG
UAG is positive with NAGMA due to RTA.
UAG is negative with NAGMA due to GI

HAGMA

No equivalent increase in Cl is observed. Because


the net charge in the serum is always neutral, there
must be an increase in the unmeasured anions.
The 4 common causes of HAGMA include:
1. Ketosis (diabetic, alcoholic, and starvation):
Check 13-hydroxybutyrate and urine ketones.
2. Uremia causes an accumulation of anions,
including sulfate, phosphate, and urate. (Check
BUN and creatinine.)
3. Lactic acidosis (check blood lactic acid level):

HAGMA

4. Toxins (salicylates, ethylene glycol [makes


glycolic and oxalic acid], methanol [makes
formic acid], and propylene glycol)
Salicylate overdose: initially causes the
respiratory alkalosis, then HAGMA.
Ethylene glycol: calcium oxalate crystals in the
urine.
Methanol: Key clue is visual symptoms.
Propylene glycol: intravenous lorazepam.
HAGMA with an osmolal gap.

METABOLIC ALKALOSIS

Metabolic alkalosis commonly results from volume contraction


caused by diuretics or vomiting/gastric suction.
With vomiting and NG suction, HCl is lost via gastric secretions.
With primary hyperaldosteronism, there is renal acid loss.
With diuretic-induced "contraction" alkalosis, there is renal loss
of bicarb-free fluid.
The 2 types of metabolic alkalosis, chloride responsive or
chloride resistant,
In cases of volume depletion, urinary Cl is < 10 mEq/L .
If urinary Cl is > 10, think of other causes of alkalosis.

Thank You

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