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How to take a set of Arterial Blood Gases

(ABGs)

Think lemon juice in a salted paper cut …..it does smart a little!
Part (a) – Skills practice
In order to perform the skills in this part of
the module – you will need to be in a
skills centre with access to :-
• The ‘blood gas’ manekin arm (you will
need someone else to pump the arterial
pulse!)
• A blood gas syringe
• A piece of clean gauze and an alcohol
wipe
Generic approach to all procedures
• Introduce yourself with name and role
• Check you have the correct patient by introduction and ID band (if in-patient)
• Explain procedure and gain verbal consent – ‘Is that alright / OK?’
• Check you have ALL the appropriate items to do the procedure and they are
in working order.
• Wash hands prior and after procedure
• Position the patient for ease of procedure and their comfort; Ensure they are
able to maintain this position for the duration of the procedure.
• Proceed explaining and reassuring as you carry out the procedure.
• Once completed thank the patient AND reposition them comfortably whilst
maintaining their dignity.
• CLEAR UP THE MESS! Place sharps and other similar items e.g. bloodied
items, into the sharps bin.
• Explain / Confirm to nursing staff what you have done and what if anything
you would like done as a result e.g. ‘I have re-sited a cannula in the left arm to
be used for IV antibiotics’; Indwelling catheter – ‘Please measure and record
hourly urine output’; Agree any observations that may need to be done and
other issues – NBM; Analgesia; Possible complications.
• Record procedure in the notes – include any difficulties and possible
complications. Accurately record any conversation with patient and relatives
around these problems.
Procedure – How to take ABGs
• Unfortunately taking ABGs hurt! Doing them badly means they really hurt.
• If they are done badly, patients (a) stop anyone else taking them (b) don’t come back to hospital
despite being unwell. Both of these can seriously affect their health!
• You should watch a few sets of gases being done before trying them yourself (here’s one we
prepared earlier ….)
http://www.etu.sgul.ac.uk/cso/video.php?skill=arterial_blood_gas
• Introduce yourself to the patient, gain verbal consent after explaining the procedure. (What are the
common complications of this procedure?)
• You will need to check you have all the correct equipment before proceeding
• Wash your hands and put on your gloves.
• Ask the patient to place their hand palm upwards comfortably supported on a surface e.g. the arm
of a chair
• Check there is a radial and ulnar pulse (Allen’s test) - note: rarely, if ever done in practice!
• The radial pulse is very superficial so you will need to bear this in mind when stabbing the patient
• Clean the area with an alcohol wipe
• Empty the syringe of the heparin solution so ‘heparinising’ the needle
• Place the index finger of your non-dominant hand over the radial pulse
• Insert the ABG needle at an angle of about 30 – 400 under your index finger.
• DO NOT use the ‘split finger’ technique where you place the needle vertically in between your
‘split’ index and middle fingers as you will end up doing a radial bone biopsy!
• Allow the appropriate amount of blood to fill the syringe (you may need to augment the action of
the needle if the patient has a very sluggish circulation (common in the sick patients that you will
be taking blood gasses from!))
• Remove the needle and press down hard over the puncture site with a piece of clean gauze for a
couple of minutes. If the patient is well enough you can ask them to do this for you.
• Thank the patient and ensure they are comfortable before leaving. You will invariably need to
return to act on the results of the ABGs
• Take the syringe immediately to the ABG machine for analysis. If there is any delay you will need
to ice the sample
How to interpret Arterial Blood Gases
(ABGs)

Feather’s less than scientific but near foolproof method


(the medi-sim is from Sante Fe!)
STEP (1) You need to know the normal values
7.35 – 7.45
pH
PaCO2 4.6 – 6.4KPa
PaO2 10.6 – 13.5 KPa
Oxygen saturation > 96%
Bicarbonate (HCO3-) 22 – 28mmol/l
Base excess (BXS) 0 +/- 2.0mmol/l
• The ranges may differ slightly from lab to lab.
• To understand what they are talking about on ‘ER’ multiply [KPa x 7.5] to
convert to mm Hg.
• Note – In respiratory failure the cut off to perform ABGs is sats of
<92%; DO NOT stab people for ABGs when they have normal
saturations! To obtain a pH and HCO3- you can use a venous
sample.
STEP (2) - There are two components
to ABGs
(1) The respiratory component i.e. how well
is this patient oxygenating / ventilating?

(2) pH component – remembered by the


simplified Henderson – Hasselbach [H-H]
equation (That’s Henderson Hasselbach Brother of Jimmy
Floyd)

pH HCO3-
PaCO2
STEP (3) You must consider each component
separately.
• Start with the
respiratory
component, or
• Start with the pH
component
• Don’t mix them up!
• To do so leads to
heartache and
confusion!
Jimmy Floyd Hasselbaink
Step 3(a) Let’s start with the pH
component
Consider pH HCO3- [M]
PaCO2 [R]
• The HCO3- should be considered as
the Metabolic [M] component of the
equation

• The PaCO2 the respiratory [R]


component
By Henderson-Hasselbach
(Draw out the equation – you know you want to!)

ACIDOSIS – ALKALOSIS
pH < 7.35 pH> 7.45
• Metabolic Acidosis • Metabolic Alkalosis
Low pH – Low HCO3- HIGH pH – HIGH HCO3-

• Respiratory Acidosis • Respiratory Alkalosis


Low pH – High PaCO
2 High pH – Low PaCO
2
If this has confused you – see the next few slides …
For the terminally confused …

Metabolic Acidosis Respiratory Acidosis


pH is caused by HCO3- pH is caused by PaCO2

• By H-H equation the pH • By H-H equation the pH


is proportional to the is inversely proportional
Bicarbonate. to the PaCO2
• If there is a metabolic • If there is a respiratory
acidosis present, the acidosis present, the
lowering of the pH must be lowering of the pH must
due to a similar and be due to a similar and
proportional REDUCTION inversely proportional
of the Bicarbonate. INCREASE of the PaCO2
Therefore for an alkalosis…

Metabolic Alkalosis Respiratory Alkalosis


pH is caused by HCO3- pH is caused by PaCO2

• By H-H equation the pH • By H-H equation the pH


is proportional to the is inversely proportional
Bicarbonate. to the PaCO2
• If there is a metabolic • If there is a respiratory
alkalosis present, the alkalosis present, the
increase of the pH must increase of the pH must
be due to a similar and be due to a similar and
proportional INCREASE of inversely proportional
the Bicarbonate. REDUCTION of the PaCO2
Metabolic Acidosis - Causes
There were many great things about the
retired Professor of Medicine at The
London Hospital, Professor Bob Cohen.
However as a medical student in the late
1980s the most difficult was he was the
man that co-wrote (and still writes) the
chapter on acid - base in the Oxford
textbook of medicine. [That’s the huge
tome that we all assiduously disregard in
the library not the ‘Cheese and Onion’!]
According to him to discuss
causes of metabolic acidosis without
discussing the anion gap would be, and
probably still is, a heinous crime
punishable by death.
So in a homage to the great man
and in recognition of the number of times Prof Cohen knew this was one
that I was unable to tell him the patient’s SHO who was never going to
chloride (therefore admitting that I had not
worked out their anion gap) here is a brief forget the chloride again!
discussion on the subject ….
Metabolic acidosis - I
• We know from the H-H equation that arterial pH is
regulated and maintained by strict control of the arterial
HCO3- and the PaCO2.

• In turn H+ production in the body comes from 3 principal


sources
(a) Cellular respiration CO2
production; this is eliminated by the lungs.

(b) Organic acids and Urea production


- Includes lactate, ketones, FFAs
- Urea production

(c) ‘Fixed acids’ – sulphuric and phosphoric


acids
Metabolic acidosis - II
• Production of CO2 accounts for the largest amount of H+
production (10x that of the next source); This is
controlled by the elimination of CO2 by the lungs.
• Production of Lactate, the other organic acids and urea
synthesis are the next largest source.
• The kidneys were previously thought to be the main
controller of the elimination of this group of acids through
the production of HCO3- and their excretion in the tubules.
However it has become increasingly recognised that the
liver plays a very important role in acid-base
homeostasis, particularly in this lactate group. Urea
production occurs in the liver and 50% of lactate is
eliminated via hepatic pathways.
• The ‘fixed acids’ account for a very small amount of H+
production and only in specific acid derangement do they
play any significant role.
Mind the ‘Anion’ Gap – [Na+ + K+] - [HCO3- + Cl-]
• The anion gap is the difference
between the most commonly measured
cations [Na+ and K+] and anions [HCO3-
and Cl-] in the blood.
• I.e. [Na+ + K+] - [HCO3- + Cl-]
• Normal range is 10 -18mmol/l
• It is ONLY of use in differentiating the
causes of metabolic acidosis and in
trying to impress Professors of
Medicine!
• However it is also a guaranteed way to
lose friends at dinner parties and is
never recommended to be included in
any chat up lines [unless of course you
are sitting next to or trying to chat up a
Professor of Medicine!]
Normal Anion Gap Metabolic Acidosis [NAGMA]
Principally due to
(a) HCO3- loss from
• GI tract – diarrhoea
• Renal – Renal tubular acidosis (RTA types I, II and IV)
• Other causes – pancreatic fistulae; ureteroenterostomy following bladder
resection

(b) HCl ingestion or production - More rarely a normal anion gap


acidosis may be seen with ingestion of acidic substances e.g. HCl or
substances that cause the production of H+ and Cl- e.g. ammonium
chloride

Mechanism
• By the equation Anion Gap = [Na+ + K+] - [HCO3- + Cl-]
• If HCO3- is lost this has to be, and is, balanced by retention of chloride
ions in the renal tubules
• Hence NAGMA is invariably accompanied by hyperchloraemia.
• With the ingestion of acidic compounds producing H+ and Cl- the net loss
of bicarbonate (in buffering the H+) is countered by the increase in
chloride.
High Anion Gap Metabolic Acidosis [HAGMA]
Principally due to
(a) Increased endogenous H+ (increased production or failure of
elimination)
If you think about the metabolism of endogenous acids –logically there are several sources of HAGMA
• Increased Lactic acid production I.e. lactic acidosis (severe sepsis, shock,
hypoxaemia, paracetamol overdose, biguanides).
• Increased Ketogenesis – DKA, starvation, alcohol induced
• Decreased excretion of acids from the kidneys – renal failure
• Decreased elimination of urea – liver and renal failure
• Decreased hepatic elimination of lactate – liver disease

(b) Ingestion of Acidic substances or substances leading to production of


acids
Salicylate overdose (acidotic phase)
Methanol
Ethylene glycol (found in antifreeze)
The Best of the Rest
Fortunately the other acid – base disturbances are not as complicated!

Metabolic Alkalosis - Principally caused by


(a) Excess loss of H+
- Gastric outflow tract obstruction – Congenital and acquired
Pyloric stenosis
- Self induced and other causes of chronic vomiting
- Secretion of inappropriately acidic urine – this occurs in K+ and
Cl- depletion which are often associated with hyperaldosteronism

(b) Ingestion or infusion of alkali


- Classically ‘Milk-Alkali’ syndrome seen in patients with upper GI
inflammation and dyspepsia
- Excess IV bicarbonate given in acidosis
- Sherbet overdose (apparently!)
Respiratory causes of Acid – Base derangement
Acidosis Alkalosis
•Associated with hypercapnia i.e. • Caused by hyperventilation i.e.
any cause of type II respiratory ‘blowing off’ CO2, hypocapnia
failure
•Commonest – COPD May be associated with
• ‘Inhibition’ of the CNS respiratory • Any cause of hypoxaemia in
centres – Brain stem stroke and type I respiratory failure e.g.
tumours, sedative drugs and The ‘Pink puffer’. (Not to be
toxins confused with that pink feline
•The other causes may be divided cartoon character!)
anatomically • Severe metabolic acidosis e.g.
– Skin – severe scarring (burns) DKA
– Fat - obesity • ‘Hysteria’ or psychological
– Skeletal – restrictive shock (diagnoses of exclusion)
abnormalities of the rib cage and • Stimulation of CNS respiratory
spine; Flailed chest centres – initial alkalotic phase
– Muscular – myopathies of salicylate overdose, Carbon
– Neuromuscular – Polio, monoxide poisoning.
Tetanus, Motor neurone disease,
Myasthenia gravis
What’s this compensation thang?
It’s the devil’s spawn as far as medics are concerned! The reason for much confusion and
much nonsense written in exams.

• The body has two principal methods of compensating for an abnormal


pH
• Metabolic compensation which is renal and hepatic and Respiratory
compensation through the CNS respiratory centres and the lungs.
• The compensatory mechanisms will try to produce a return to a normal
pH; this is often impossible with severe derangement.
• By the H-H equation the compensation will occur in the same direction
as the primary abnormality.
• E.g. In a metabolic acidosis - there is a low bicarbonate leading to a low
pH.
• The compensatory mechanism is to ‘blow off’ and therefore reduce the
PaCO2 by hyperventilating (This is classically seen in Kussmaul’s
breathing of DKA)
• I.e. In this case the respiratory compensation follows the primary low
bicarbonate in an attempt to maintain the normal pH
Compensation in Acidosis
Respiratory acidosis LOW pH – HIGH PaCO2
• Compensation = Metabolic (Renal and Hepatic)
• Bicarbonate is retained to buffer the increase in acid
• i.e. The compensation for a respiratory acidosis is a metabolic
alkalosis.
• This is commonly seen in patients with chronic Type II respiratory
failure (chronic hypercapnia)
• Renal compensation takes several days to occur; It is not seen in
the patient with acute type II RF.

Metabolic Acidosis LOW pH – LOW Bicarbonate


• Compensation = Respiratory
• CO2 is ‘blown off’ by hyperventilating
• i.e. The compensation for a metabolic acidosis is a respiratory
alkalosis
• This is classically seen in Diabetic Keto-acidosis (DKA) (but also in
any other severe metabolic acidosis) and is known as Kussmaul’s
breathing
• This respiratory compensation is commonly seen in the acutely ill,
acidotic patient
Compensation in Alkalosis
Respiratory alkalosis HIGH pH – LOW PaCO2
• Compensation = Metabolic (Renal)
• Bicarbonate is lost through the tubules
• i.e. The compensation for a respiratory alkalosis is a metabolic acidosis.
• This is not common and will only occur over a long period of time i.e. this is a
chronic compensatory mechanism.
• In the acute setting it is much more likely that the patient has a primary
metabolic acidosis with compensating respiratory alkalosis.

Metabolic Alkalosis HIGH pH – HIGH Bicarbonate


• Compensation = Respiratory
• CO2 is retained by Hypoventilating
• i.e. The compensation for a metabolic acidosis is a respiratory alkalosis
• This is very uncommon and will only occur in chronic, severe metabolic
alkalosis i.e. you are very unlikely to see this in practice (or exams). It is much
more likely that this is primarily a respiratory acidosis with compensatory
metabolic alkalosis (as in the chronic hypercapnia of COPD).
• It’s common sense really - it is not really in the body’s interest to hypoventilate
and send itself in to hypercapnia!
But the pH isn’t normal …
• One can only say a system is COMPENSATED when the pH is
within normal limits
• If the pH remains high or low, there is said to be a
COMPENSATORY mechanism but the pH is NOT compensated.
• This often occurs in severe illness where despite the best efforts of
the compensatory mechanisms the primary problem is simply too
overwhelming.
• E.g. Consider these results
pH 7.12, PaCO2 2.1KPa, PaO2 13.9KPa, HCO3- 7.4mmol/l, Base
excess – 14.9mmol/l
• There is a metabolic acidosis with a compensatory respiratory
alkalosis; However the acidosis is so severe that despite the
attempted compensation there is still a severe acidosis.
• Therefore this IS NOT a compensated system but there is attempted
compensation.
Base Excess
(That noise on the backing track of all Garage, House and Drum and Base!)

• The Base excess is a calculated measure of


the metabolic derangement within the blood if
the respiratory component is ‘removed’. (See
the graph opposite log PaCO2 vs pH).

• This is achieved by standardising the PaCO2


to a normal of 40mmHg (5.3KPa). At this level
any derangement of the pH will be due to non-
respiratory causes i.e. the metabolic
components.

• It is not measured from the sample directly,


but is calculated using the plots opposite. It
can therefore be misleading and doesn’t
always reflect the clinical status of the patient.

• However I like to think of it is as a Early


Warning System [EWS] as it is often more
deranged than the other components of the
ABGs.

• Think ‘This is how bad the metabolic


derangement could get if you don’t hurry up
and correct the underlying problems!’ This is figure 2 from Siggaard-Andersen, O. and Engel, K.
"A New Acid-Base Nomogram", Scand.J.Clin.& Lab.Invest.
12, 177; 1960. Figure Copyright Radiometer, Copenhagen,
Denmark
But what does it really mean ..?
• Technically it is the quantity of strong acid which has to be added to
a litre of fully saturated blood at 37°C to bring its pH to 7.4 when
PCO2 is 5.3KPa (40mmHg). (Siggaard-Andersen, 1960)

• But that’s not really very helpful to most of us!


• Essentially it gives a measure of the metabolic ‘meltdown’ that is
occurring or will occur very soon!
• Normal value 0 + / - 2.0mmol/l
• The more NEGATIVE the Base excess = The worse the metabolic
component of the ACIDOSIS
• The more POSITIVE the Base excess = The worse the metabolic
component of the ALKALOSIS.

• In other words don’t worry too much about it but


bear it in mind as the EWS of metabolic meltdown –
[At any point if I get too technical …. stop me!]
Try these for size …
Example (1) A 32yo Type 1 diabetic is admitted
unwell after being found at home semiconscious
by his wife. His capillary blood glucose in A&E is
‘High’[>48mmol/l]
ABGs on 15l/min are:
pH 7.01
PaCO2 2.9KPa
Pa02 36.6KPa
Sats 100%
HCO3- 7mmol/l
Base excess – 21.9mmol/l
1.What are the inferred diagnoses from the data?
2.List 2 further essential tests are?
Answers (1)
(a) pH 7.01 – Very LOW - ACIDOSIS
(b) PaCO2 2.9 KPa – LOW – Respiratory Alkalosis
(c) Pa02 36.6 KPa - HIGH
(d) Sats 100% - supersaturated
(e) HCO3- 7 mmol/l – Very LOW – Metabolic Acidosis
(f) Base excess – 21.9 mmol/l – Very negative – Severe
metabolic acidosis
Inferred diagnoses
• Severe Metabolic Acidosis
By Henderson Hasselbach • Compensatory Respiratory
pH α HCO3- Alkalosis (attempted compensation)
PaCO2 • Probable DKA – thus you need a
lab glucose and urinary ketones;
other tests – FBC, U+Es, blood and
urinary cultures. BP, pulse and
Temp.
Example (2)
A 78yo man attends A&E with a 3 month history of weight
loss and a sensation of ‘early fullness’ on eating. This is
now associated with a four day history of worsening
‘projectile’ vomiting.
His ABGs on room air
pH 7.62
PaCO2 4.8KPa
Pa02 12.6KPa
Sats 96%
HCO3- 54.8mmol/l
Base excess + 20.9mmol/l
1.What are the inferred diagnoses from the data?
2.List 2 further essential tests are?
Answer (2)
(a) pH 7.62 - VERY HIGH - ALKALOSIS
(b) PaCO2 4.8KPa - Normal
(c) Pa02 12.6KPa - Normal
(d) Sats 96% - Normal
(e) HCO3- 54.8mmol/l -VERY HIGH – Metabolic alkalosis
(f) Base excess + 20.9mmol/l – VERY POSITIVE –
Metabolic alkalosis
Inferred diagnosis - Metabolic alkalosis
The history suggests Pyloric stenosis
By Henderson Hasselbach or gastric outflow tract obstruction. In a
pH α HCO3- man of this age this is most likely due
to a large gastric carcinoma.
PaCO2 Other tests – OGD and biopsy; CT
abdomen, CXR, FBC, U+Es, LFTs and
Calcium
Example (3)
A 64yo lifelong smoker is seen in MOPD with a 2 year
history of worsening cough and exertional dyspnoea. ABGs
performed in the clinic on room air show:
pH 7.43
PaCO2 6.9KPa
Pa02 7.1KPa
Sats 89%
HCO3- 33mmol/l
Base excess + 8.9mmol/l
1.What are the inferred diagnoses from the data?
2.List 2 further essential tests are?
Answer (3)
(a) pH 7.43 - NORMAL
(b) PaCO2 6.9KPa – HIGH – Respiratory Acidosis
(c) Pa02 7.1KPa – LOW - HYPOXIA
(d) Sats 89% - LOW
(e) HCO3- 33mmol/l – HIGH – Metabolic Alkalosis
(f) Base excess + 8.9mmol/l – POSITIVE – Metabolic
alkalosis
This is a compensated system. The pH is
normal; there is a metabolic alkalosis and a
By Henderson - Hasselbach respiratory acidosis. If you put these
together with the history this man has COPD
Normal pH α HCO3- with chronic type II respiratory failure
(hypercapnia) with a compensating
PaCO2 metabolic alkalosis
Investigations – CXR, PEFR, Spirometry
with assessment of reversibility, ECG and
Echocardiogram.
Step 3(b) – The Respiratory component
• Nearly forgot … You need to understand the respiratory
component!
• First what is the definition of ‘organ or system failure’?
Any organ or system you care to think about ..
• By definition organ / system failure is when that organ /
system is no longer able to fulfil its metabolic function
within the body
• Thus my simple definition of respiratory failure is when
the respiratory system is unable to maintain normal
oxygenation of the tissues i.e. HYPOXIA or hypoxaemia
occurs.
• However in most textbooks Respiratory failure is defined
by PaO2 of 8.0KPa +/- PaCO2 > 6.4 KPa
• Hypoxaemia is defined as an PaO2 < 10.6KPa
• Why the difference – see next slide …
Where do all these
cut-offs come from?
If you look at the Oxygen dissociation
91
curve (ODC) opposite you will see that
the definition for the normal oxygen
saturation and PaO2 are defined by the
curve straightening to the horizontal
I.e. 96% and 10.6KPa (80mmHg)

The definition for respiratory failure


often used in major textbooks and the
cut-off for performing ABGs is derived at
the ‘asymptote’ of the curve – where it
begins or tends to the horizontal (In the
USA this point on the ODC is
sometimes known as the ‘ICU point’).
I.e. 91% (<92%) and 8.0KPa (60mmHg)
At this point there is large / marked
desaturations for small changes in
PaO2.
Thus this is the minimal saturation that
ICU teams allow for sick patients. i.e. 60
≥92%.

Borrowed from http://en.wikipedia.org/wiki/Hemoglobin


Step 3(b) Respiratory Failure = Hypoxaemia
• So, to define respiratory failure there must
be a PaO2 <10.6KPa
• Next, is the PaCO2 normal, high or low?
• Type I respiratory failure – the PaCO2 is
normal or low
• Type II respiratory failure – the PaCO2 is
high.
• To understand this a little better one must
go back to first principles …
Type I respiratory failure
• Type I RF occurs due to any process which
interrupts gaseous exchange between the
alveolae and the pulmonary capillary bed.

• There are six generic causes of Type I RF


Asthma (and COPD) – stop ventilation
of the alveolae
Pulmonary embolism (capillary bed)
Pneumonia (particularly ‘atypicals’)
Pulmonary oedema (LVF)
Pulmonary fibrosis
Pulmonary haemorrhage

• The patient’s respiratory drive is normal – I.e.


Hypercapnia causes increased respiratory
effort.

• Oxygen therapy – as much as you like!


Normally 40 – 60%
http://www.mhhe.com/biosci/ap/dynamich
uman2/content/respiratory/visuals.mhtml
Type II respiratory failure
• Type II RF is caused by any process
which interferes with the mechanism of
ventilation i.e. physically stops the person
taking a deep breath in and out.
• The commonest cause by far is COPD

• The other causes may be divided


anatomically from the outside – in …
Skin – severe scars e.g. burns, Ichthyosis
Fat – Obesity (Pickwickian syndrome)
Skeletal – Congenital deformities of the
chest wall, crush injuries, flailed chest
Neuromuscular – Guillain- Barré, Polio,
Tetanus, Muscular dystrophy, Myasthenia
Gravis
• Also depression of the CNS respiratory
centres – sedation - drugs and alcohol,
brain stem stroke or tumours

• All causes of type I RF CAN cause type II


RF. This is a very bad prognostic sign
http://anatquest.nlm.nih.gov/aq/ImageXml?xml=DRR100205076-xsl.xml
and should alert the clinician to the need
for possible intubation and ventilation.
Type II respiratory failure
• Respiratory drive – HYPOXIA; Due
to their chronic hypercapnia these
patients switch their respiratory
drive to hypoxia

• Oxygen therapy – Low (%)


i.e. 24 – 28%

• However rule (1) – Hypoxia kills!


Therefore give them enough
oxygen to correct their hypoxia. If
this causes further worsening of
their hypercapnia or acidosis this
is an indication for NIV or indeed
Intubation (if appropriate).

• DO NOT STOP THEIR OXYGEN


due to hypercapnia
By definition For respiratory failure to exist there must
be hypoxaemia. I.e. PaO2 < 10.6KPa
Type I Type II
Disruption of the alveolar / Disruption to chest
Mechanism capillary network ventilation

PaCO2 Normal or low HIGH

Respiratory drive Normal - Hypercapnia Hypoxia

Asthma, PE, LVF, COPD


Causes Pulmonary fibrosis, Chest wall – Skin, Fat,
Pneumonia (especially Skeletal and neuromuscular
‘atypicals’), Pulmonary abnormalities
haemorrhage CNS respiratory centre
depression

Oxygen therapy 40 - 60% 24 – 28%


Always give enough oxygen to reverse the hypoxia! Give
BUT oxygen, give lots of it and then change your therapy according
to the ABGs and clinical response.
ABG Exercises
For each of the following examples write out
1. The pH abnormalities – metabolic or
respiratory acidosis / alkalosis
[Remember to write out the H-H equation every time!]
1. The respiratory abnormalities i.e. type I or
type II respiratory failure
2. The inferred diagnoses from the history
and ABG data.
3. The management that you would
institute.
Patient 1 – Don’t get in a flap!
63 year old man is brought into A&E
confused and unwell. His initial ABGs on
60% Oxygen received in the ambulance
show
pH 7.11
PaCO2 12.9KPa
Pa02 6.6KPa
Sats 68%
HCO3- 14mmol/l
Base excess – 16.3
Answer (1)
• Sorry - this was a really nasty one to start!
By H-H pH α HCO3-
PaCO2

• There is a metabolic AND respiratory acidosis i.e. a


mixed metabolic / respiratory acidosis
• The respiratory acidosis is caused by the severe
hypercapnia; The hypoxaemia leads to tissue hypoxia
and this in turn to a build up of lactic acid (hence the
metabolic component)
• There is hypoxia and hypercapnia – i.e. type II
respiratory failure
• The most likely cause in a 63yo man is an acute
exacerbation of COPD
• The management may well include NIV or even
intubation (if appropriate) – you should NOT be
managing such ill patients on your own!
Patient 2 – Are you mad?
A 23 year old woman is brought into A&E
hyperventilating and unwell. Her initial
ABGs on room air show
pH 7.34
PaCO2 1.6KPa
Pa02 7.3KPa
Sats 88%
HCO3- 19mmol/l
Base excess – 4.9
Answer (2)
• Did you note the words ‘unwell’? It is easy to dismiss the hyperventilating
patient as ‘hysterical’ – do so at your peril!
• Always make sure they are not diabetic [Kussmaul breathing] and that their
oxygen saturation is normal on room air.
• This patient has a very slight acidosis with a mildly reduced bicarbonate (a
mild metabolic acidosis); This is confirmed by the negative base excess
• The PaCO2 is low – respiratory alkalosis (secondary to hyperventilation i.e.
blowing off her CO2)
• She has hypoxia (PaO2 7.3KPa) with low PaCO2 thus she has type I RF
• The most likely cause for a young woman such as this is a PE (but other
causes of type I RF e.g. atypical pneumonia are just as likely)
• Aspirin overdose will also cause a metabolic acidosis and respiratory
alkalosis [which comes first in salicylate poisoning?] but is unlikely to cause
the respiratory failure
• The history and examination are particularly important in this case to
differentiate the likely causes.
• The patient should be placed on 40 -60% Oxygen and investigations and
management directed at elucidating the cause.
• In the absence of any other clues she should be treated as if she has had a
PE until proven otherwise.
• Whatever is wrong – hysteria is not one of the differentials!
Patient 3 – Incontinence pads to the fore!
A 23 year old asthmatic woman is brought
into A&E acutely dyspnoeic and unwell.
Her initial ABGs on 15litres /minute re-
breathing mask
pH 7.21
PaCO2 7.6KPa
Pa02 8.3KPa
Sats 85%
HCO3- 12mmol/l
Base excess – 14.9mmol/l
Answer (3)
• This patient is sick –very sick and you need to be calling
for help pretty sharpish (if not sooner)!
• As with patient (1) she has a mixed metabolic and
respiratory acidosis
• Despite being on 15l/min of oxygen she is severely
hypoxic and desaturated. She has type II respiratory
failure (hypoxia and hypercapnia) and is in urgent need
of assisted ventilation. An anaesthetist should be called
as soon as possible
• She should be given IV hydrocortisone and back to back
oxygen driven nebulisers.
• She will need to be examined (excluding underlying
pneumothorax, lobar collapse, pneumonia)
• Arrange initial investigations – including CXR (why do
you want a CXR?), Further ABGs and routine bloods
(what would you send?)
Arterial Blood Gases – The Sequel
The ABGs shown below are the only six variations on a theme that really exist. If you can do these you are just about there! You should all be
able to get the implied diagnoses, the causes are more difficult. I have not given the answers so you may use them as a tutorial with an SHO, SpR
or even a consultant.

The patients listed below have all presented with abnormalities of their arterial blood gases. You may assume the ABGs were all taken on room
air. Although in a clinical setting you would hope that many had been placed on oxygen therapy the moment they presented!
Implied diagnoses – e.g. Metabolic acidosis with type II respiratory failure
Cause: Lactic acidosis secondary to severe respiratory failure eg pulmonary oedema

Normals 1 2 3 4 5 6
pH 7.35 –7.45 7.21 7.61 7.05 7.36 7.48 7.51
PaCO2 (KPa) 4.6 – 6.4 7.30 4.9 2.7 6.8 2.7 2.8
HCO3- 22 - 28 14.6 48.7 7.1 31.3 20.3 25.9
(mmol/l)
PaO2 >10.6 5.9 13.6 13.5 8.2 8.1 14.0
(KPa)
Sats >96% 76% 99% 98% 86% 85% 100%
Base Excess 0+/-2 -7.9 +18 -21 +4.9 -4.1 +0.76
(mmol/l)
Implied Diagnoses

Causes
For more on ABGs
• http://www.acid-base.com/index.php
Another Old Londoner tries to teach medical students
ABGs!
• http://www.studentbmj.com/issues/04/03/educatio
n/105.php
Very good overview of ABGs; worth visiting just
for the questions at the end
• http://www.usyd.edu.au/su/anaes/lectures/a
cidbase_mjb/description.html
Excessively technified version of acid-base - fantastic
references and historical perspective! – someone,
somewhere will love it! Explains Base excess in lots of
detail!

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