Richard Stretton Respiratory Registrar. Arterial Blood Gases Seen as complicated Misunderstood Important An easy way and a hard way.

Richard Stretton

Respiratory Registrar

Arterial Blood Gases

Seen as complicated Misunderstood Important An easy way and a hard way

Objectives Develop an organised system for

looking at blood gases

Be able to comment on the arterial pO2 in relation to the FiO2

Interpret acid base disturbance and it’s significance in the acutely unwell

What Are We Measuring? pH pO2

pCO2

HCO3

Base Excess

Acid Base Balance pH is carefully controlled

Enzymatic Function relies on pH control

Buffers

○ Haemoglobin

○BICARBONATE

○ Ammonium

○ Phosphate

Striking the BalanceStriking the Balance

H+ + HCO3- H2CO3 CO2 + H2O

When you’ve got too much H+, lungs blow

off CO2

When you can’t blow off CO2, kidneys try to

get rid of H+

5-step approach1. Assess Oxygenation

2. Determine Acid-Base Deficit

3. Determine the respiratory component4. Determine the metabolic component5. Which is primary and which is secondary





pO2 = 10 -13 kPa on air Is the patient hypoxic? Is there a significant A-a Gradient?

A-a Gradient is the difference in concentration of oxygen between the Alveolus (A) and the artery (a)

Normal <3

A-a Gradient = PAO2 – (PaO2 + PaCO2/0.8)

I shouldn’t say this but…

v.v.v.v. rough guide

Inspired O2 - (pO2 + pCO2)

Add together pO2 and pCO2 from your blood gas

Take this away from the concentration of Oxygen the patient is breathing

With an upper limit of normal of about 5




5-step approach2. Determine Acid-Base Deficit

pH>7.45 alkalaemia pH<7.35 acidaemia

Acidosis - a process causing excess acid to be present in the blood. Acidosis does not necessarily produce acidaemia

Alkalosis - a process causing excess base to be present in the blood. Alkalosis does not necessarily produce alkalaemia.



3. Determine the respiratory component4. Determine the metabolic component 5. Which is primary and which is secondary

5-step approach3. Determine the respiratory component

Does this explain the acid-base deficit?

PaCO2: >6.0 kPa - respiratory acidosis

<4.7kPa - respiratory alkalosis



3. Determine the respiratory component4. Determine the metabolic component 5. Which is primary and which is secondary

5-step approach4. Determine the metabolic component.

Does this explain the acid-base deficit?

HCO3 <22 mmols/l - metabolic acidosis>26 mmols/l - metabolic

alkalosis

Remember……Remember……

H+ + HCO3- H2CO3 CO2 + H2O

When you’ve got too much H+, lungs blow

off CO2

When you can’t blow off CO2, kidneys try to

get rid of H+




5-step approach5. Which is primary and which is

secondary?

Remember

Compensation doesn’t always completely restore pH to the normal range

A mixed picture may be present




Assumptions

CO2 changes are related to respiratory changes

HCO3 changes relate to metabolic changes

Overcompensation does not occur Respiratory compensation is rapid Metabolic compensation is slow

Respiratory Acidosis

Any cause of hypoventilationCNS depressionNeuromuscular diseaseAcute or chronic lung diseaseCardiac arrestVentilator malfunction

Respiratory Alkalosis

Any cause of hyperventilationHypoxiaAcute lung conditionsAnxietyFeverPregnancyHepatic failureSome central CNS lesions

Metabolic AcidosisAdded Acid Loss of Bicarbonate

• Renal failure• Ketoacidosis• Lactic acidosis• Salicylate/Tricyclic overdose

• Renal tubular acidosis• Diarrhoea• Carbonic anhydrase

inhibitors• Ureteral diversion• Chloride administration

Metabolic Alkalosis

Loss of acid or gaining alkaliVomitingDiarrhoeaDiuretics (and hypokalaemia generally)Ingestion of alkali

Reminder of normal values pH 7.35 – 7.45 (H+ = 35 -45) pO2 10 - 13 kPa on air

pCO2 4.6 - 6.0 kPa

HCO3 25 - 35 mmols/l

Base excess ± 2.0

Lets get going……..

Working out acidosis/alkalosis and compensation is usually the bit people struggle with

So…..

Outcome codes

Outcome Code Outcome Code

pH High Alkali Low Acid

pCO2 High Acid Low Alkali

HCO3 High Alkali Low Acid

Translate

Value Code Translate Opinion

pH 7.1 Low AcidAcidaemi

a

pCO2 5.3 Normal Normal Normal

HCO3 16 Low Acid Primary

Uncompensated Metabolic Acidosis

Translate


pH 7.1 Low AcidAcidaemi

a

pCO2 8.3 High Acid Primary

HCO3 26 Normal Normal Normal

Uncompensated Respiratory Acidosis

Translate


pH 7.56 High AlkaliAlkalaemi

a

pCO2 2.3 Low Alkali Primary

HCO3 25 Normal Normal Normal

Uncompensated Respiratory Alkalosis

Translate


pH 7.37 Normal Normal Normal

pCO2 2.1 Low Alkali ????

HCO3 14 Low Acid ????

Compensated Metabolic Acidosis or Compensated Respiratory Alkalosis

Translate


pH 7.40 Normal Normal Normal

pCO2 8 High Acid ????

HCO3 35 HIgh Alkali ????

Compensated Respiratory Acidosis orCompensated Metabolic Alkalosis

Translate


pH 7.21 Low Acid Acidaemia

pCO2 12 High Acid Primary

HCO3 32 High Alkali Secondary

Decompensated Respiratory Acidosis

What Now? Now you can determine any acid base pattern

Convert the numbers into high/low/normal

Convert that into acid/alkali

What is primary, what is compensation?

Distinguish between uncompensated, compensated, and decompensated

Nomenclature Uncompensated Respiratory Acidosis

Acute Type 2 Respiratory Failure

Compensated Respiratory Acidosis

Chronic Type 2 Respiratory Failure

Decompensated Respiratory Acidosis

Acute on Chronic Type 2 Respiratory Failure

Case 1 Young female admitted with overdose of

unknown tablets and smelling of alcohol

pO2 12 kPa on airpH 7.24

PaCO2 2.5

HCO3 8 Metabolic Acidosis with respiratory

compensation

Case 2 Elderly male admitted from nursing home

with one week history of fever and vomiting

pO2 12 kPa on 4l by mask

pH 7.49

PaCO2 6.3

HCO3 35

Metabolic alkalosis with respiratory compensation

Case 3a

Middle aged man admitted with cough sputum and haemoptysis. Life-long smoker

pO2 4 on air

pH 7.19

PaCO2 9.7

HCO3 28

Acute respiratory acidosis with no time for metabolic compensation

Case 3b

Middle aged man admitted with cough sputum and haemoptysis. Life-long smoker

pO2 6 on air SpO2 92%

pH 7.32

PaCO2 10.0

HCO3 39

Acute respiratory acidosis with no time for metabolic compensation

Case 4 Middle aged man post cardiac arrest.

Breathing spontaneously on endotracheal tube

pO2 35 on 15l via reservoir mask

pH 6.9

PaCO2 8.9

HCO3 13 Mixed metabolic and respiratory acidosis

Case 5 Elderly lady with congestive cardiac failure

pO2 9 on 40% oxygenpH 7.64

PaCO2 3.5

HCO3 29

Respiratory alkalosis secondary to pulmonary oedema.

Acute as no metabolic compensation

Case 6 Young diabetic male admitted with chest

infection, vomiting and drowsiness

pO2 12 on air

pH 7.31

PaCO2 1.6

HCO3 6.0

Acute metabolic acidosis with respiratory compensation

Case 7 54 yr-old lady post MI. Acutely unwell,

cold, clammy, hypotensive and oliguric

pO2 10 on 60% oxygen

pH 6.99

PaCO2 7.8

HCO3 14

Mixed pattern of respiratory and metabolic acidosis

Case 8 50 yr-old man admitted with

exacerbation of long-standing bronchial asthma. Respiratory rate of 18

pO2 5.1 on 60% oxygenpH 7.39

PaCO2 5.8

HCO3 26 Severe type I respiratory failure

Questions

?

The 6th step…6. If an acidosis is present work out the

anion gap to help determine cause.

Anion Gap is the difference between the measured positive and negatively charged ions.

It gives an estimate of the unmeasured ions in the serum

Unmeasured – proteins, sulphates

Anion Gap

Anion Gap = [Na+K] –[CL+HCO3]

Normal anion gap 10-18

Metabolic Acidosis

Increased anion gap (added acid) Renal failure Ketoacidosis Lactic acidosis Salicylate/Tricyclic overdose

Metabolic Acidosis

Decreased anion gap (loss of bicarbonate) Renal tubular acidosis Diarrhoea Carbonic anhydrase inhibitors Ureteral diversion Chloride administration

High Anion Gap A

M

U

D

P

I

L

E

S

High Anion Gap Alcohol (Alcohol dissociates to become a week acid)

M

U

D

P

I

L

E

S


Methanol (See alcohol. Causes blindness)

U

D

P

I

L

E

S



Uraemia (Failure to reabsorb HCO3- and excrete H+)

D

P

I

L

E

S

High Anion Gap Alcohol (Alcohol dissociates to become a weak acid)



DKA (Ketones are dehydrogenated alcohols, and dissociate to acid)

P

I

L

E

S





Paraquat (Very nasty poison, universally lethal)

I

L

E

S






Infection (Commonest cause. Localised tissue hypoxia leads to...)

L

E

S







Lactic Acid (Product of anaerobic respiration, and tissue necrosis)

E

S








Ethylene Gylcol (Antifreeze. Quite a potent acid, no longer sold in UK)

S








Ethylene Gylcol (Antifreeze. Quite a potent acid, no longer sold in UK)

Salicylates (Aspirin causes resp alkalosis, then metabolic acidosis)

Normal Anion Gap

Addison’s Disease High Output Fistulas RTA I, II, IV Acetazolamide Therapy Diarrhoea

Any more Questions?

Richard Stretton Respiratory Registrar. Arterial Blood Gases Seen as complicated Misunderstood Important An easy way and a hard way.

Documents

secondary slide

slow slide

present slide

unwell slide

base excess slide

respiratory component

metabolic component

ingestion of alkali