THE ABCS OF

AN ABG
27 th July 2017
Dr Pauline Chan
Contents
Components of an ABG
How to read an ABG?
Causes of
Metabolic acidosis
Metabolic alkalosis
Respiratory acidosis
Respiratory alkalosis
Clinical Cases: Practice Makes Perfect J
Components of an ABG
iSTAT
Orange = ME (microelectrolytes
+ gas)
Green = gas only

Base excess
Dose of acid to restore a litre of
blood to normal pH (7.40) under
standard conditions (37 deg C,
pCO2 40 mmHg)
Calculated value from blood
pH and pCO2
Normal: - 3 to + 3 mmol/L
How to read an ABG?
Step 1: Where is this sample taken from?

Arterial
ideal for assessing oxygenation

Capillary
generally good approximation for arterial sample if taken when peripheral
perfusion adequate

Venous
can be used if main concern is acid-base status
Should not be used to interpret oxygenation/CO2 status
How to read an ABG?
Step 2: What is the pH?

pH 7.35 7.45 = normal

pH < 7.35 = acidosis
pH > 7.45 = alkalosis

Note that a normal pH does NOT mean that there is NO abnormality

Compensated
2 opposite processes happening e.g.
metabolic acidosis with respiratory alkalosis
metabolic acidosis with metabolic alkalosis
How to read an ABG?
Step 3: Is the pCO2 normal?

35 45 mmHg = normal

< 35 mmHg = low (alkalotic)

Respiratory alkalosis
Respiratory compensation for underlying acidosis

> 45 = high (acidotic)

Respiratory acidosis
Respiratory compensation for underlying alkalosis
How to read an ABG?
Step 4: Is the HCO3 normal?

22 26 mmol/L = normal

< 22 mmol/L = low (acidotic)

Metabolic acidosis
Compensation for underlying alkalosis

> 26 mmol/L = high (alkalotic)

Metabolic alkalosis
Compensation for underlying acidosis
How to read an ABG?
Step 5: Match the pH, pCO2 and HCO3 together
to determine initial process

Is the abnormality in the pCO2 or HCO3 or both giving rise to the pH

abnormality?

pH pCO2 HCO3 What is the initial process?

/N Respiratory alkalosis
/N Metabolic alkalosis
/N Metabolic acidosis
/N Respiratory acidosis
How to read an ABG?
Step 6A: Is there an underlying compensation
happening?

pCO2 and HCO3 changing in same direction compensation

HCO3 high = alkalosis; pCO2 high = acidosis
HCO3 low = acidosis; pCO2 low = alkalosis

pCO2 and HCO3 changing in opposite directions 2 ongoing

processes
 How to read an ABG?
Step 6B: Is there compensation?
Primary Initial Compensatory Expected compensation
disorder Chemical Response
Change
Metabolic HCO3 pCO2 pCO2 = 1.2 x HCO3
Acidosis
Metabolic HCO3 pCO2 pCO2 = 0.6 x HCO3
Alkalosis
Respiratory pCO2 HCO3 Acute: HCO3 by 1 mmol/L for every
Acidosis 10 mmHg in pCO2
Chronic: HCO3 by 3.5 mmol/L for
every 10 mmHg in pCO2
Respiratory pCO2 HCO3 Acute: HCO3 by 2 mmol/L for every
Alkalosis 10 mmHg in pCO2
Chronic: HCO3 by 5 mmol/L for every
10 mmHg in pCO2
Important Principles
There can never be over-compensation.
pH can be normal but never be over-corrected
Degree of compensation more than that expected
think of a second process

A normal pH does not imply that there is no acid-

base disorder
How to read an ABG
Step 7: Analyse the pO2

Valid only with arterial blood gas

80 100 mmHg = normal

< 60 mmHg = Type 1 respiratory failure

Interpret with respect to the FiO2 patient is receiving - PF ratio

(PaO2/FiO2)
Lower = worse
PF ratio < 300 raises concern for ARDS
Exercise 1: ABG Interpretation
A. Boy with severe diarrhea:
pH 7.28
pCO2 24 mmHg
HCO3 10 mmol/L
Metabolic acidosis with respiratory compensation
B. Girl brought in by ambulance:
pH 7.52
pCO2 20 mmHg
HCO3 20 mmol/L
Respiratory alkalosis with acute metabolic compensation
C. Infant with vomiting:
pH 7.69
pCO2 48 mmHg
HCO3 57 mmol/L
Metabolic alkalosis with partial respiratory compensation
Summary
METABOLIC
ACIDOSIS
Metabolic Acidosis
pH with HCO3
2 types:
High anion gap (HAGMA)
Addition of another acid
Normal anion gap (NAGMA)
Lose HCO3
Unable to excrete H+
Anion gap = Na+ (Cl- + HCO3)
HA H+ + A-
Normal = 10 14
> 14: high anion gap
Anion gap must always be
determined in metabolic
acidosis
Causes of Metabolic Acidosis
HAGMA NAGMA
Ketoacidosis Diarrhea
Starvation ketosis Renal Tubular Acidosis
DKA Type 1 (distal): hypokalaemia
Lactic Acidosis Failure to excrete H+
Shock Unable to acidify urine
Hypoxia
Metabolic e.g. mitochondial Type 2 (proximal): hypokalaemia
disorders Loss of HCO3
Still able to acidify urine
Chronic Renal Failure
Toxins Type 4: hyperkalaemia
Paraldehydes
Hypoaldosteronism
Ethanol
Aldosterone = hormone that causes
Ethylene glycol retention of sodium/water, and
Methanol excretion of H+/K+
Salicylates
Osmolar Gap (good to know)
Can help in detecting presence of low molecular weight toxins
e.g. ethanol, methanol, ethylene glycol

Osmolar gap = Measured osm (lab) calculated osm

Calculated osm = 2 x Na+ + urea + glucose
> 10 = elevated osmolar gap
Abnormal solute present in significant amounts
Management
Correction of the underlying aetiology
Consider bicarbonate replacement only in severe acidosis (i.e.
HCO3 < 12 or pH 7.0)
Why?
Severe acidosis can decrease cardiac contractility fall in cardiac output/BP
Cardiac arrhythmias
Beware
Broken down into CO2 which can lead to paradoxical decrease in intracellular
pH (especially if patient cannot clear CO2 effectively)
Cerebral edema especially in DKA patients
METABOLIC
ALKALOSIS
Causes of Metabolic Alkalosis
Vomiting
Loss of gastric H+
Volume contraction aldosterone secretion H+ excretion
May have concomitant electrolyte derangements (e.g. hypokalaemia,
hypo-/hypernatremia)
Can have concomitant metabolic acidosis due to starvation ketosis
Bartter/Gitelmann Syndrome
Genetic abnormality of transporter in tubules
Hyperaldosteronism
Diuretics loop (frusemide), thiazide (hydrochlorothiazide)
Volume contraction alkalosis
Good to know
Mixed Acid-Base Disorders
(good to know)
When to suspect?
Expected compensatory response does not occur
Compensatory response occurs but level of compensation inadequate
or too extreme (remember, no overcompensation)
pCO2 and HCO3 abnormality in OPPOSITE direction
pH normal but pCO2 or HCO3 abnormal
In HAGMA, change in HCO3 not equivalent to change in AG
 HAGMA
HA H+ + A-
A- contributes to AG
AG by 1 mmol/L HCO3 by 1 mmol/L
As such, in pure HAGMA, AG = HCO3
Allow difference of up to 6
If AG > HCO3 there is a process
adding more HCO3 mixed metabolic
alkalosis and NAGMA
If AG < HCO3 there is a process
taking away more HCO3 mixed
HAGMA and NAGMA
RESPIRATORY
ACIDOSIS
Causes of Respiratory Acidosis
Hypoventilation
Poor respiratory drive e.g. obtunded patient, drug-induced (opiates,
sedatives)
Weak muscles e.g. Guillain Barre Syndrome, Spinal Muscular Atrophy

Airway obstruction
Asthma
Bronchiolitis
Obstructive Sleep Apnea
Management
Support breathing
BVM
Non-invasive ventilation
Intubation
Correct underlying aetiology
E.g. reversal of sedatives
RESPIRATORY
ALKALOSIS
Causes of Respiratory Alkalosis
Hyperventilation
Pneumonia/pulmonary embolism/early phase of asthma
Salicylate Poisoning
Urea cycle defect
Hyperammonaemia can drive respiratory centre
CLINICAL CASES
Time to put everything together!
Clinical Case 1
A 12 year old girl with a background of asthma on flixotide 100
mcg BD, presents to the Childrens Emergency with shortness of
breath.
Vitals at triage: T 37.3 deg C, BP 108/78 mmHg, HR 98 bpm, RR
28/min, SpO2 90% on RA
On examination, she appears drowsy and has severe respiratory
distress. On auscultation, poor breath sounds bilaterally with
bilateral soft rhonchi.
A capillary blood gas done with FiO2 40% showed this:
pH 7.28
pCO2 60 mmHg
HCO3 28 mmol/L
pO2 72 mmHg
Clinical Case 1
What is your interpretation of her capillary blood gas?

What is the cause for her blood gas derangement?

What will be your management?

Clinical Case 2
An 8 year old boy was
brought in by paramedics
for drowsiness. They had
found him in a pool of
vomit. Hypocount done on
scene was 18 mmol/L.
Vitals on arrival: T 37.8 deg
C, BP 88/54, HR 135 bpm,
RR 30/min, SpO2 97% on RA
On examination, you
notice this
Clinical Case 2
An arterial blood gas done on room air showed the following:
pH 7.25
pCO2 28 mmHg
HCO3 12
pO2 92 mmHg
What else would you like to know?
RP1 extended:
Na+ 136 mmol/L
K+ 3.6 mmol/L
Cl- 101 mmol/L
CO2 11 mmol/L
U 5.6 mmol/L
Cr 65 mol/L
Glucose 20 mmol/L
Clinical Case 2
What is your interpretation of this boys acid-base disorder?

What do you think is the possible cause(s) for his acid base
disorder?
Clinical Case 3
A 16 year old girl was brought in by paramedics for acute onset
of chest tightness, giddiness and shortness of breath while in
school.
Her vitals are as follows: T 36.9 deg C, BP 132/92 mmHg, HR 99
bpm, SpO2 100% on RA.
On examination, she appeared anxious looking clutching her
chest and breathing heavily. Her cardiovascular and respiratory
examinations were otherwise normal.
A capillary blood gas done on room showed this:
pH 7.52
pCO2 24 mmHg
HCO3 21 mmol/L
pO2 86 mmHg
Clinical Case 3
What is your interpretation of her capillary blood gas?

What is the cause for her blood gas derangement?

What will be your management?

Clinical Case 4
A 2 month old infant was admitted from clinic for work-up of
worsening projectile vomiting over the last 2 weeks. The child vomits
after every feed but is still keen to feed despite vomiting.
Vitals: T 37.0 deg C, BP 78/52 mmHg, HR 135 bpm, RR 30/min, SpO2
99% on RA
On examination, the child appears to be moderately dehydrated
with otherwise intact perfusion. Head to toe examination seemed
unremarkable.
Venous blood investigations done showed:
pH 7.55
pCO2 44 mmHg
HCO3 31 mmol/L
pO2 45 mmHg
Na 132 mmol/L, K 3.2 mmol/L, Cl 90 mmol/L, HCO3 32 mmol/L, U 2.1
mmol/L, Cr 21 mol/L
Clinical Case 4
What is your interpretation of this infants blood gas?

What is the cause for his blood gas derangement?

Clinical Case 4
While feeding the child, you
noticed this:
What is your diagnosis?

The medical officer asks for a

urine dipstick to look for
paradoxical aciduria.
How does this come about?
Clinical Case 5
A 5 year old girl is brought to the Childrens Emergency by her
grandmother. She had vomited 6 times in the last two hours. Her
grandmother had found an empty Wintergreen Oil bottle beside
her.
Vitals: 37.5 deg C, BP 95/70, HR 128 bpm, RR 36 br/min, SpO2 98%
on RA. On examination, the child appeared tired but still
responsive. She had normal perfusion with mild dehydration.
There was mild epigastric tenderness.
A set of bloods during cannulation was sent:
pH 7.32
pCO2 28 mmHg
HCO3 18 mmol/L
pO2 40 mmHg
Na 145 mmol/L, K 3.5 mmol/L, Cl 109 mmol/L, CO2 19 mmol/L
Clinical Case 5
What is your interpretation of this childs blood gas?
BEWARE OF OVER COMPENSATION!

What is the cause for her blood gas derangement?

Clinical Case 6
3 year old girl presents with 2 days of profuse diarrhea with poor
oral intake. There are other family members with similar symptoms.
Vitals: T 37.5 deg C, BP 82/59 mmHg, HR 126 bpm, RR 20/min, SpO2
98% on RA. On examination, she looked tired with moderate
dehydration. Abdomen was otherwise soft and not tender.
IV cannulation was performed and a set of bloods sent:
pH 7.28
pCO2 32 mmHg
HCO3 14 mmol/L
pO2 45 mmHg
Na 140 mmol/L, K 3.3 mmol/L, Cl 110 mmol/L, CO2 14 mmol/L
 What is your interpretation of this childs blood gas?
AG = 4
HCO3 = 10
AG < HCO3 mixed HAGMA and NAGMA

What is the cause for her blood gas derangement?

SUMMARY
Remember
Stepwise interpretation of blood gas to derive primary and
associated acid-base issue
The body cannot over compensate (but can fail to compensate),
think of mixed processes if compensation extreme
Always correlate the patients clinical picture when interpreting a
blood gas
Aetiology depends on patients symptoms/signs
When metabolic acidosis is detected, always good to:
Calculate anion gap ( osmolar gap if toxin ingestion suspected)
Check AG and HCO3
Management often involves treatment of underlying aetiology
THANK
YOU J
Any questions?