Arterial Blood Gases

Athar M Siddiqui

Consultant in Anaesthetics & Critical Care

Shaukat Khanum Memorial Cancer Hospital &

Research Centre, Lahore.

Aims & Objectives of this session

By the end of this session we will:

Be able to interpret simple arterial blood gas analyses

Have a systematic approach to arterial blood gas interpretation

Know the meaning of common terms used

in arterial blood gas interpretation

Know the normal ranges for arterial blood gas values

Know some of the common causes of arterial blood gas

abnormalities and what to do to correct them

Reasons to Sample Arterial Blood

To establish the severity of an oxygenation abnormality.

To evaluate hyper- or hypoventilation

To determine acid-base status, particularly in patients

with metabolic acidosis (e.g. diabetic ketoacidosis)

To track the application of mechanical ventilation in a

critically ill patient

ABGs analysis is usually performed in

critical care areas

• Intensive care units

• Accident and emergency departments

• Operation theatres

• in all those areas where critical care outreach

services are extended

The values are expressed as

• Partial Pressure of Arterial Oxygen (PaO2) mmHg/KpA

• Partial Pressure of Arterial Carbon dioxide (PCO2)

• Arterial pH

• Bicarbonate Ion (HCO3) mmol/L

• Arterial Haemoglobin Oxygen Saturation (SaO2)%

• Sodium (Na) mmol/L

• Potassium (K) mmol/L

• Calcium (Ca) mmol/L

• Lactate.

How is Arterial sample taken?

• From Radial artery in a single stab technique under complete asepsis.

• The syringe is Heparanised and bears a small 21 gauge needle.

• Allen’s test needs to be performed .

• The needle is inserted at an angle of 45 degree

• Hard cotton plug is firmly placed over the artery for more than 5 minutes

• If the sample is contaminated with room air it will result in abnormally

low carbon dioxide and possibly raised oxygen levels, and an in pH.

• It is advisable to carry the sample in a container carrying ice cubes.

• The needle is pushed into a cork to avoid the needle stick injury.

• The sample is usually taken from an arterial catheter in ICUs & can be

taken from Brachial and Femoral arteries as well.

Regulation of Acid-Base

Balance • Each day during normal activity we produce

14500000000 nmol of H ions.

• Regulatory mechanisms are very sensitive to

small changes in pH

– Buffers

– Respiratory System

– Renal System

Regulation of Acid-Base Status:

Buffers

• Immediately combine with excess acid to form

substances that do not greatly affect pH.

• Bicarbonate (HCO3-) Most important buffer

CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3-

Absorption, excretion, production regulated by kidney

• Other buffers: Intracellular: Phosphate,

Ammonium, and Haemoglobin

• Extracellular: Proteins

Regulation of Acid-Base Status

Respiratory System

• Increased CO2 or H+ levels => stimulates

respiratory => increased ventilation => blows off

(exhales) CO2=> eliminating excess acid. If

acidotic • Hyperventilation => CO2 eliminated => improvement in

acidotic state

• If alkalotic (low CO2 or H+): • hypoventilation => CO2 retained => improvement in alkalotic

state

• Quick response: within 1-2 min of pH imbalance

Regulation of Acid-Base Status

Renal System

• Kidneys conserve and/or eliminate H+ and HCO3- in

response to abnormal pH

– If acidotic => eliminate H+ (acid) and retain HCO3-

(base) in effort to normalize pH

– If alkalotic => Eliminate HCO3- (base) in effort to

normalize pH

• Response to abnormal pH is slow (hours to days)

Acid Base Imbalances

Respiratory Acidosis

• Acidosis is due to hypoventilation

• Causes: – COPD (Emphysema, bronchitis)

– failure of respiratory muscles (ALS, Guillain-Barre)

– airway obstruction (e.g., post-op)

• Metabolic compensation: Kidneys excrete H+/retain HCO3- (if problem lasts hours/days)

Acid Base Imbalances

Respiratory Alkalosis

• Alkalosis is due to hyperventilation

• Causes

– anxiety (Rx with paper bag)

– pneumonia

– pulmonary edema

• Metabolic compensation: Kidneys excrete HCO3-

(if problem lasts hours/days)

Acid Base Imbalances

Metabolic Acidosis

• Acidosis is due increase in metabolic acids and/or loss of HCO3-

• Increased acids due to – diabetic ketoacidosis

– renal failure (kidneys cannot excrete H+)

• Lost alkali (base) due to: – severe diarrhea

– intestinal malabsorption

• Respiratory compensation: hyperventilation (to blow off CO2)

Acid Base Imbalances

Metabolic Alkalosis

• Alkalosis is due to elevated HCO3- secondary to loss

of acid/H+ or excess alkali intake.

– Loss of acid

– Vomiting

– gastric suction

– diuretics

• Minimal respiratory compensation b/c hypoxemia will

result and stimulate respirations

5-Steps for ABGs interpretation

1. Assess oxygenation

Is the patient hypoxic?

Is there a significant alveolar-arterial gradient?

2. Determine status of the pH or H+ concentration

pH > 7.45 (H+ < 35 nmol l-1) – alkalaemia

< 7.35 (H+ > 45 nmol l-1) – acidaemia

3. Determine respiratory component

PaCO2 > 6.0 kPa (45 mmHg) – respiratory acidosis

< 4.7 kPa (35 mmHg) – respiratory alkalosis

4. Determine metabolic component

HCO3- < 22 mmol l-1 – metabolic acidosis

> 26 mmol l-1 – metabolic alkalosis

5. Combine the information from 2, 3 and 4:

- determine the primary disturbance

- is there any metabolic or respiratory compensation?

In the presence of a low pH (acidaemia):

- a high PaCO2 implies a primary respiratory acidosis

- a low PaCO2 implies respiratory compensation for a

primary metabolic acidosis.

In the presence of a high pH (alkalaemia):

- a low PaCO2 implies a primary respiratory alkalosis

- a high PaCO2 implies respiratory compensation for

a primary metabolic alkalosis.

5-Steps for ABGs interpretation (continued)

5. (continued)

It is also possible to have mixed acid base disorders, e.g.

a combination of a respiratory and a metabolic acidosis

creating an acidaemia, or a combination of a respiratory

and metabolic alkalosis creating an alkalaemia.

5-Steps for ABGs interpretation (continued)

HCO3- or base excess HCO3

- or base excess Metabolic

CO2 CO2 Respiratory

Alkalosis Acidosis

Evaluating Oxygenation

• Determine the A-a gradient

• The easiest way, let me explain

A-a Gradient = [(Patm - PH2O) x FiO2] - (PCO2/RQ) - PaO2

Patm = 760 mmHg, PH2O = 47 mmHg

FiO2 = 0.21, PCO2 is 40 mmHg

RQ can be assumed to be 1 (possible range from 0.7

to 1.0)

* If the compensation is virtually complete the pH may be in the normal range –

over compensation does not occur.

Those marked in bold are particularly common after cardiac arrest.

Summary of changes in pH, PaCO2 and HCO3-

in acid-base disorders

Acid-base disorder pH PaCO2 HCO3-

Respiratory acidosis N

Metabolic acidosis N

Respiratory alkalosis N

Metabolic alkalosis N

Respiratory acidosis with renal

compensation

*

Metabolic acidosis with

respiratory compensation

*

* If the compensation is virtually complete the pH may be in the normal range –

over compensation does not occur.

Those marked in bold are particularly common after cardiac arrest.

Summary of changes in pH, PaCO2 and HCO3-

in acid-base disorders (continued)

Acid-base disorder pH PaCO2 HCO3-

Respiratory alkalosis with renal

compensation

*

Metabolic alkalosis with respiratory

compensation

*

Mixed metabolic and respiratory

acidosis

Mixed metabolic and respiratory

alkalosis

Scenario 1

Initial Information

A 75 year old man presents to the emergency

department after a witnessed out-of-hospital VF cardiac

arrest.

The paramedics arrived after 10 minutes, during which

CPR had not been attempted. The paramedics had

successfully restored spontaneous circulation after 3

shocks.

On arrival:

comatose (GCS 3)

ventilated with 50% oxygen via tracheal tube

HR 120 min-1 BP 150/95 mmHg.

Scenario 1 (continued)

Arterial blood gas analysis reveals:

FiO2 0.5 (50%) Normal Values

pH 7.10 7.35 – 7.45

PaCO2 6.2 kPa (47 mmHg) 4.7 – 6.0 kPa (35–45 mmHg)

PaO2 7.5 kPa (56 mmHg) > 10 kPa (75 mmHg) on air

HCO3- 14 mmol l-1 22 – 26 mmol l-1

BE - 10 mmol l-1 +/- 2 mmol l-1

Scenario 2

Initial Information

A 65 year old man with severe COPD has just collapsed in the

medical unit.

On initial assessment by the ward nurse he is apnoeic but has

an easily palpable carotid pulse at 90 min-1.

The nurse is attempting to ventilate his lungs with a bag -mask

and supplemental oxygen (with reservoir) as the cardiac arrest

team arrive.

Scenario 2 (continued)

Arterial blood gas analysis reveals:

FiO2 0.85 (85%) estimated Normal Values

pH 7.10 7.35 – 7.45

PaCO2 18.0 kPa (135 mmHg) 4.7 – 6.0 kPa (35–45 mmHg)

PaO2 19.5 kPa (147 mmHg) > 10 kPa (75 mmHg) on air

HCO3- 36 mmol l-1 22 – 26 mmol l-1

BE + 12 mmol l-1 +/- 2 mmol l-1

Scenario 3

Initial Information

A 75 year old woman is admitted to the emergency

department following a VF cardiac arrest, which was

witnessed by the paramedics. This had been preceded

by 30 minutes of severe central chest pain.

A spontaneous circulation was restored after 2 shocks,

but the patient remained comatose and apnoeic. The

paramedics intubated her trachea, and on arrival in

hospital her lungs are being ventilated with an

automatic ventilator using a tidal volume of 900 ml and

a rate of 18 breaths min-1.

Scenario 3 (continued)

Arterial blood gas analysis reveals:

FiO2 1.00 (100%) Normal Values

pH 7.62 7.35 – 7.45

PaCO2 2.65 kPa (20 mmHg) 4.7 – 6.0 kPa (35–45 mmHg)

PaO2 25.4 kPa (192 mmHg) > 10 kPa (75 mmHg) on air

HCO3- 20 mmol l-1 22 – 26 mmol l-1

BE - 4 mmol l-1 +/- 2 mmol l-1

Scenario 4

Initial Information

An 18 year old insulin dependent diabetic is admitted to

the emergency department.

He has been vomiting for 48 hours and because he was

unable to eat, he has taken no insulin.

On arrival:

HR 130 min-1 BP 90/65 mmHg.

Spontaneous breathing, RR 35 min-1

Oxygen 4 l min-1 via Hudson mask

GCS 12 (E3, M5, V4)

Scenario 4 (continued)

Arterial blood gas analysis reveals:

FiO2 0.3 (30%) estimated Normal Values

pH 6.89 7.35 – 7.45

PaCO2 2.48 kPa (19 mmHg) 4.7 – 6.0 kPa (35–45 mmHg)

PaO2 17.0 kPa (129 mmHg) > 10 kPa (75 mmHg) on air

HCO3- 4.7 mmol l-1 22 – 26 mmol l-1

BE - 29.2 mmol l-1 +/- 2 mmol l-1

The blood glucose is 30 mmol l-1 and there are ketones+++

in the urine

Scenario 5

Initial Information

A 75 year old man is on the surgical ward 2 days after a

laparotomy for a perforated sigmoid colon secondary to

diverticular disease. He has become hypotensive over

the last 6 hours. His vital signs are:

HR 120 min-1 – sinus tachycardia –

warm peripheries

BP 70/40 mmHg

RR 35 min-1

SpO2 on oxygen 92%

Urine output 50 ml in the last 6 hours

GCS 13 (E3, M6, V4)

Scenario 5 (continued)

Arterial blood gas analysis reveals:

FiO2 0.4 (40%) approx Normal Values

pH 7.17 7.35 – 7.45

PaCO2 4.5 kPa (34 mmHg) 4.7 – 6.0 kPa (35–45 mmHg)

PaO2 8.2 kPa (62 mmHg) > 10 kPa (75 mmHg) on air

HCO3- 12 mmol l-1 22 – 26 mmol l-1

BE - 15 mmol l-1 +/- 2 mmol l-1

References

• Driscoll BR, Howard LS, Davison AG, BTS guidelines

for emergency Oxygen use in adult patients. Thorax

2008, 63 Suppl 6

• Driscoll P, Brown T, Gwinnatt C, Wardale T. A simple

guide to blood gas analysis. BMJ Publication Group

1997.

• Roger W. Stevens (Wikipedia),

http://en.wikipedia.org/wiki/File:Oximeter.jpg CC: BY-

SA

• http://creativecommons.org/licenses/by-sa/3.0/

• www.pemed.com/lab/labanalz/labanalz.htm

Now we are able to

• Interpret simple arterial blood gas analyses

• Know a systematic approach to arterial blood

gas interpretation

• Know the meaning of common terms used

in arterial blood gas interpretation

• Know the normal ranges for arterial blood

gas values

• Know some of the common causes of arterial

blood gas abnormalities and what to do to

correct them