Arterial Blood Gas

and Acid-Base
Analysis
Barry A. Mizock MD
Department of Medicine
Cook County Hospital
Approach to ABG and acid-
base analysis

Obtain required data base

Assess oxygenation status
Assess acid-base status
 Required data base
Routine ABGs (pH, P02, PC02, HC03)
HC03 is calculated from pH, PC02
HC03 should be 2-3meq/L < total C02
Knowledge of FI02 when ABG drawn
To assess shunt
Simultaneous serum electrolytes
To calculate the anion gap
To assess hyper- and hypochloremia
 Assessment of oxygenation
Room air vs. exogenous oxygen?
Prediction of normal P02 based on age
Causes of hypoxemia:
Hypoventilation
Drop in cardiac output
V/Q abnormalities
Shunts
 Room air?
If the patient was on RA when ABG drawn:
P02 + PC02 must be < 140mmHg
Therefore:
If P02 + PC02 is > 140mmHg:
The patient must have been on oxygen
However:
If P02 + PC02 is < 140mmHg:
The patient may or may not have been on oxygen
when the ABG was drawn
 Effect of age on P02
Predicted P02 = 107 0.43 x age
Caveat #1: P02 < 60mmHg is abnormal no
matter how old the patient
Caveat #2: The above formula may be
unreliable if the patient is hyperventilating
Alveolar-arterial oxygen gradient

A-a gradient = PAlv02 Part02

PAlv02 (on room air) = 150 1.25 x PartC02

(Normal A-a grad = <20-25mmHg)

Alveolar-arterial oxygen gradient
The A-a gradient should be calculated
on room air, not on exogenous oxygen
The A-a gradient is a index of gas
transfer from alveolus to pulmonary
capillary
An increased A-a gradient is seen in
many types of cardiopulmonary
disease (e.g. pneumonia, pulmonary
edema, asthma/copd, interstitial LD)
 Causes of hypoxemia
Hypoventilation
Hypoventilation in patients with normal
lungs (e.g., drug OD):
The PCO2 is elevated and A-a gradient is
normal
Hypoventilation in patients with
abnormal lungs (e.g., COPD)
The PCO2 is elevated and the A-a gradient is
increased
 Causes of hypoxemia
Low cardiac output
The venous return is more desaturated
with fall in CO:
Blood percolates more slowly through
nutrient beds, so more oxygen is extracted
Arterial P02 falls in the presence of
concomitant shunts (e.g., pulmonary
edema, atelectasis, pneumonia):
Difficult to document clinically unless CO
and 02 saturation are simultaneously
monitored
Ventilation-perfusion matching
 Causes of hypoxemia
VQ abnormality vs. shunt

Shunt
Alveoli completely flooded
or collapsed (pneumonia,
pulmonary edema)
Refractory to FIO2
May need ICU
VQ abnormality
Alveoli partially flooded or
collapsed, interstitial LD
Responsive to FIO2
Can be managed on ward
Diagnostic approach to hypoxemia
Assessment of acid-base status

Whats the pH?

Simple or mixed disorder?

 Whats the pH
Determines the major trend of the disorder
Normal pH range = 7.35 to 7.45
Acidemia/alkalemia
Acid or base is being generated with
corresponding in pH
Acidosis/alkalosis
Acid or base is being generated. pH may or
may not change if there is an accompanying
counterbalancing disorder
Utility of the anion gap
in diagnosis of acid-
base disorders
The normal anion gap
 Anion gap
AG = Na+ - (Cl- + HC03-)
AG is a tool used to assess the presence of
unmeasured anions in metabolic acidosis
AG in normal individuals 8meq/L
Albumin is the major determinant of AG in
normal individuals
AG with hypoalbuminemia so need to
correct:
For each gm/dl in albumin below 4, add 2.5meq
to the AG
For example: If measured AG = 8meq/L and
patients albumin is 2gm/dl add (2 X 2.5meq) to
AG = 13
Anion gap in metabolic acidosis
 Causes of anion gap metabolic
acidosis
Lactic acidosis (anion = lactate)
Ketoacidosis (anion = BOB, AcAc)
Renal failure (anion = phosphate, sulfate)
Certain toxic ingestions (e.g., formate w.
methanol poisoning)

May see low-grade in AG (2-3meq) in

respiratory or metabolic alkalosis
 Critically-ill patient commonly
have an elevated AG secondary
to production of organic
anions of unknown etiology
 Normal anion gap (hyperchloremic)
metabolic acidosis
Causes:
Renal tubular acidosis
Gastrointestinal
Diarrhea
Small bowel/pancreatic drainage
Iatrogenic
Saline (contains excessive Cl- relative to plasma)
Parenteral nutrition
Anion exchange resins
Differential diagnosis - lab:
Measure urine anion gap (see slide 60)
 Causes of decreased anion gap
Hypoalbuminemia
Promotes compensatory in chloride
Increased unmeasured cations
Multiple myeloma (cationic IgG paraproteins)
Hypercalcemia, hypermagnesemia
Lithium overdose (not with therapeutic levels)
Overestimation of serum chloride
Bromine ingestion (may cause negative AG)
Pyridostigmine bromide for myesthenia
Each meq of Br may be measured as 2-3meq Cl
Marked hyperlipidemia
Causes spurious elevation in chloride (by flame photometry)
Not seen with newer ion-selective devices
Iodide intoxication
Iodide measured as chloride
Seen with KI ingestion, contrast (esp. in pts w. CRF)
The importance of chloride
in diagnosis of acid-base
disorders
 Chloride in acid-base balance
Causes of
hyperchloremia
Hyperchloremic
(normal AG)
metabolic acidosis
Chronic respiratory
alkalosis
Causes of
hypochloremia
Metabolic alkalosis
Chronic respiratory
acidosis
What is the normal
serum value for
chloride?
It depends on the
sodium concentration!
 Chloride:
The companion of
sodium
 Euchloremia
Chloride reflects hydration status
When [Na+] changes
due to hydration:
The [Cl-] will track [Na+]
to maintain a Na-Cl
difference of 30-40meq/L
(i.e., euchloremia)
Na Cl < 30 =
hyperchloremia
Na Cl > 40 =
hypochloremia
Examples:
If Na =190meq, Cl should
be 150-160meq/l
If Na=100meq, Cl should
be 60-70meq/l
 Calculating the Na-Cl
difference is useful to
assess euchloremia in the
setting of altered hydration

That is, with hyper-

or hyponatremia
A Na-Cl difference of <30 or >40 meq/L (loss
of euchloremia) reflects an underlying acid-
base disorder
 Classification of
acid-base disorders
Simple vs. mixed
Simple (compensated) acid-base
disorder
An acid-base disorder in which a
primary abnormality ( pCO2 in
respiratory, HCO3 in metabolic)

is accompanied by a compensatory
response which occurs within
predicted limits
 Simple (compensated) acid-base
disorders
Compensatory responses

Compensation for metabolic disorders

Hyper- or hypoventilation
Compensation for respiratory disorders
Acute: RBC or tissue buffering
Chronic: renal compensation
 How was normal
compensation defined?
 Compensatory responses to simple acid-
base disorders
Compensation defined:
What normal people do
in response to metabolic
or respiratory acid-base
disorders
Determined by:
Measuring ventilatory
response to H+ or
pC02 in normal people
Confidence bands
created for each disorder
Resultant pH:
Compensation does not
usually result in a normal
pH
 Simple acid-base disorders

In simple acid-base disorders the direction of the

primary disturbance and compensatory response is
in the same direction
In mixed disorders these entities move in the
opposite direction
 In general, compensatory
processes do not normalize pH,
since to do so would remove the
stimulus for compensation
 Differential diagnosis of normal pH

Normal acid-base status

Mixed counterbalancing acid-base
disorder
e.g. Metabolic acidosis + respiratory alkalosis
Chronic respiratory acidosis/alkalosis
(if mild)
Clue is slightly or pCO2
 Mixed (uncompensated) acid-base
disorder

Definition:
An acid-base
disorder in which
the compensatory
response to a
primary abnormality
fails to conform to
predicted values
A patient who has appropriate
compensation for a primary
abnormality has a simple or
compensated disorder
Do not use two terms to
express appropriate
compensation
For example, a simple
metabolic acidosis should not
be labeled metabolic acidosis
with compensating
respiratory alkalosis (implies 2
disorders)
 Limits of compensation for 1o acid-base
disorders

Compensation for acute respiratory disorders:

Is less efficient than for chronic (renal compensation has not had time to
occur)
Ventilatory compensation for metabolic acidosis:
May be limited by ventilatory reserve of the patient ( with elderly, COPD)
Hypoventilation in response to severe metabolic alkalosis:
Is opposed by associated hypoxemia that stimulates respiratory drive
 How do I know if the
respiratory disorder is acute
or chronic?
When compared to acute
respiratory disorders, chronic
disorders have a pH closer to
normal and a bicarbonate that
is more significantly or
Mixed acid-base disorders
and clues to diagnosis
 General categories of mixed
disturbances
Summating
Combined acidoses
or alkaloses
pH markedly
abnormal due to
combined effect
Counterbalancing
Acidosis
accompanied by
alkalosis
pH closer to normal
Metabolic acidosis + respiratory acidosis

A summating mixed disorder

HC03 ; pCO2
pH very low
Example: methanol poisoning
 Metabolic alkalosis + respiratory
alkalosis
A summating mixed disorder
HC03 ; pCO2
pH very high
May see mild in AG 2o to alkalosis
Hypokalemia common
Example: vomiting in pregnancy
 Respiratory acidosis + metabolic
alkalosis
A counterbalancing mixed disorder
pCO2 ; HC03
pH may be normal
Example: COPD on diuretics (see higher
than predicted pCO2 on the basis of
metabolic alkalosis alone)
 Metabolic acidosis + metabolic
alkalosis
A counterbalancing mixed disorder
See AG with less than expected in
HC03
pH may be , or normal; diagnosis be
missed if AG not calculated
See AG/HCO3 >2 ( delta gap)
Example: DKA with vomiting
 Metabolic acidosis + respiratory
alkalosis
A mixed counterbalancing disorder
HC03 (<15meq/l), pC02 , AG
pH may be normal or even alkalemic
Example: salicylate poisoning
 Hyperchloremic and high AG metabolic
acidosis
Two types of metabolic acidosis occurring
concurrently (AG & Cl- metab acidosis)
AG , chloride (chloride typically normal or
in pure AG acidosis)
See AG/HC03 <1 ( delta gap)
Examples:
Severe diarrhea with tissue hypoperfusion (lactic
acidosis)
The acidosis of renal failure is often both
hyperchloremic and high AG
 Triple acid-base disturbance

Occurs when mixed metabolic acidosis +

metabolic alkalosis is complicated by a
respiratory disturbance (resp acidosis or
alkalosis)
Diagnosis generally made in patients with
metabolic alkalosis + respiratory acidosis
in whom the AG is
Example: Vomiting in salicylate poisoning
 Summary of approach to ABG analysis

Analyze oxygenation status:

Check p02 relative to age
If hypoxemic, is patient hypoventilating?
Calculate A-a gradient
Assess response to exogenous 02 (shunt?)
Assess acid-base status:
Step one: Whats the pH?
Step two: Simple or mixed? check direction of
pC02 and HC03
Step three: If mixed, is it summating or
counterbalancing?
Step four: Check AG and Cl- for additional clues
Acid-base map
Sample problems
Case 1
pH is mildly
alkalemic
Disorder appears
simple (HC03 , C02 )
AG is normal
Cl is
Diagnosis: chronic
respiratory alkalosis
Example: pregnancy
Case 2
pH is alkalemic
Disorder may be
simple (HC03 , pC02
nl)
Cl- is , AG nl
Diagnosis:
metabolic alkalosis
Example: vomiting
Urinary chloride & metabolic alkalosis
Case 3
pH is low
Disorder appears
simple(HCO3 , pCO2
)
AG , Cl- nl
Diagnosis: High AG
metabolic acidosis
Example: DKA
Case 4
pH is slightly low
Disorder appears
simple (HCO3,pCO2)
AG nl, Cl- sl
Diagnosis: chronic
respiratory acidosis
Example: COPD
Case 5
pH is low
Disorder appears
simple (HC03,pC02)
Cl- , AG nl
Diagnosis:
Hyperchloremic
metabolic acidosis
Example: RTA
Urine anion gap in differential diagnosis
of hyperchloremic metabolic acidosis
(Renal vs. GI vs. Iatrogenic)
Case 6
pH is low
Disorder appears
mixed (HC03,pCO2)
Summating acidosis
AG , Cl- nl
Diagnosis: respiratory +
metabolic acidosis
Example: methanol
poisoning
Case 7
pH is normal
pCO2 is normal
AG , HCO3 nl
suggested mixed
counterbalancing
Diagnosis:
metabolic acidosis +
metabolic alkalosis
Example: DKA w.
vomiting
 Delta gap (AG/HC03-)
Primary utility of gap:
In diagnosis of mixed metabolic acidosis/metabolic alkalosis
In diagnosis of mixed hyperchloremic and high AG metabolic
acidosis
Principles:
Each increase in AG above normal (8) should accompanied by
an equivalent decrease in serum HCO3- from normal (25meq/L)
AG >HC03- suggests metabolic acidosis + metabolic alk
AG <HC03- suggests hyperchlor + high AG met acidosis
Problems with delta gap:
AG requires correction with albumin
For each gm/dl in albumin below 4, add 2.5meq to the AG
AG/HC03- in metabolic acidosis is not always 1:1
It averages 1.6:1 due to effect of intracellular buffers
 Delta gap (AG/HC03-)
Diagnostic recommendations

AG/HC03- >2:
Suggests mixed metabolic acidosis/ metabolic
alkalosis
AG/HC03- <1:
Suggests combined high and normal AG
metabolic acidosis
Case 8
pH is alkalemic
HC03 , pCO2
AG , Cl-
Suggests mixed
counterbalancing
disorder
Diagnosis: respiratory
alkalosis + metabolic
acidosis
Example: salicylate
poisoning
Case 9
pH is low
Disorder appears
mixed (HC03, pC02)
Summating alkalosis
AG nl, Cl- nl
Diagnosis: metabolic
and respiratory
alkalosis
Example: vomiting in
pregnancy
Case 10
pH is low
Disorder appears
simple (HC03 , pCO2
)
AG , but Cl- also
Diagnosis:
hyperchloremic and
high AG metabolic
acidosis
Example: Severe
diarrhea with
hypovolemia producing
lactic acidosis
Case 11
pH is low
Disorder appears mixed
(HC03 , pC02 )
Summating alkalosis
AG , Cl-
Diagnosis: triple acid-
base disorder
(respiratory alkalosis,
metabolic alkalosis,
metabolic acidosis)
Example: salicylate
poisoning with vomiting
Whats the acid-base status?