The ins & outs of blood gas interpretation

Guest post by Dr Jono Holme, ACCS trainee

This is a tour through the real basics of blood gas analysis before quickly moving on to cover some more advanced concepts such as Anion Gap, A-a gradient and even Lactic acidosis.

ACID-BASE DISTURBANCES = H2O+CO↔H2CO↔HCO3+H+

Hydrogen ions are the product of Bloodgas1normal cellular metabolism. The body must continually dispose of acid to keep the arterial pH within a narrow range so that cellular metabolism, such as enzyme activity, is not disrupted. The pH is maintained in the body by several buffering systems, the main one being the carbonic acid-bicarbonate system above

Carbonic acid (H2CO3) links the respiratory and metabolic systems. The components can be varied independently of each other. So if the respiratory system falters, the metabolic system can attempt to compensate, and vice versa.

As Hydrogen ions are lost from the body, pH goes up. As they are maintained, pH goes down. This is the principle behind acid base balance


Respiratory

Bloodgas2The respiratory system controls carbon dioxide. If breathing is rapid or deep, more carbon dioxide will be “blown off.” Carbon dioxide is acidic, so as it is removed the blood becomes less acidic and the pH increases.

Equally, if breathing is ineffective, slow, or shallow, carbon dioxide is retained and the blood becomes more acidic and pH decreases.

Respiratory changes have a rapid effect on the pH.

Metabolic

Bloodgas3The kidneys are the metabolic system organ in the context of blood gas measurements, controlling the level of serum bicarbonate.

Bicarbonate is a base and an important buffer of hydrogen ions (H+) in the blood. The kidneys can regulate the amount of bicarbonate in the blood through increased production or reabsorption of these ions.

Metabolic changes are slower and may take several days to reach full effect.


Blood gas interpretation – key principles

Step 1: Is there an acid-base abnormality—that is, is the pH outside the normal range?

Blood gas normal range
  • pH = 7.35-7.45
  • PaO2 = >10.6 kPa
  • PaCO2 = 4.7-6 kPa
  • HCO3 = 24-30 kPa
  • Base excess = -2 to +2 mmol/l

Step 2: Is the respiratory (PaCO2) or the metabolic (HCO3 -) component abnormal? Is it the primary cause of the acid-base abnormality?

Bloodgas4

Step 3: Is there compensation? Look at the other compensating system—for example, if it is a respiratory problem then the metabolic system should try to compensate and vice versa

Bloodgas5

Step 4: What does the PaO2 tell you? Remember that the PaO2 does not affect the acid-base balance, but it is important to review. Type I respiratory failure is when the patient has hypoxaemia in the absence of hypercapnia. Type II respiratory failure occurs when the patient has both hypoxaemia and hypercapnia, indicating hypoventilation.


Case 1

A 60 year old man with a history of chronic obstructive pulmonary disease presents to the emergency department with increasing shortness of breath, pyrexia, and a cough productive of yellow-green sputum. He is unable to speak in full sentences. His wife says he has been unwell for two days.

On examination, a wheeze can be heard with crackles in the lower lobes; he has a tachycardia and a bounding pulse.

ABG on air
pH 7.2, PaCO2 9.3, PaO2 7.9, BE- 27, HCO3 26, K 3.2, Lactate 2.1
What type of acid base disturbance is this?
RESPIRATORY ACIDOSIS

This patient has respiratory (PaCO2 9.3) acidosis (pH 7.2) with no clear compensation (HCO3 26).

He is in acute type II respiratory failure as he is both hyperaemic (PaO2 7.9) and hypercapnic (PaCO2 9.3), and it is acute as there is no compensation.

Any condition leading to inadequate ventilation and consequent retention of carbon dioxide will lead to respiratory acidosis.

Causes include:

  • Airways disorders—life threatening asthma, acute exacerbation of chronic obstructive pulmonary disease
  • Drugs—opioids, sedatives, muscle relaxants causing hypoventilation
  • Central nervous system disorders—brain stem stroke, status epilepticus
  • Neuromuscular disorders—myasthenia gravis, causing hypoventilation

This patient meets criteria for BIPAP ventilation: pH < 7.30, pCO2 > 6.0, dyspnoea. He will require BIPAP if he does not improve quickly with medical management


Case 2

A six-year-old boy is taken to the emergency department with vomiting and a decreased level of consciousness. His breathing is rapid and deep (Kussmaul breathing), and he is lethargic and irritable in response to stimulation.

He appears to be dehydrated—his eyes are sunken and mucous membranes are dry—and he has a two-week history of polydipsia, polyuria, and weight loss.

VBG on 15L O2
pH 7.18, PaO2 13.3, PaCO2 3.3, HCO3 10, Na 126, K 5.0, Cl 95, Glucose 33.6
What type of acid base disturbance is this?
METABOLIC ACIDOSIS

These results show that he has metabolic (HCO3 10) acidosis (pH 7.18) with respiratory compensation (PaCO2 3.3). The glucose is 33.0. If blood ketones are raised, this will be diabetic ketoacidosis.

Metabolic acidosis has many causes, and the anion gap can be used to help differentiate between the causes. The anion gap is the difference in the measured cations (positively charged ions) and the measured anions (negatively charged ions)

The anion gap = (Na + K) – (Cl- + HCO3-)

In this case this is = (126 + 5) – (95 + 10) = 26.

A normal anion gap is < 14

The anion gap is the DIFFERENCE between the POSITIVE and NEGATIVE ions as a measure of positive ion excess. As this is an acidosis, there is an excess of positive hydrogen ions. This excess of positive ions reflects decreased acid excretion or decreased bicarbonate reabsorption.

The causes of a HIGH anion gap acidosis (>14) can be remembered with the mnemonic MUDPILES:
  • Methanol Uraemia
  • Diabetic ketoacidosis
  • Paraldehyde Infection
  • Lactic acidosis
  • Ethylene glycol
  • Salicylates
The causes of a NORMAL anion gap acidosis (<14) with the mnemonic RAGE:
  • Renal tubular acidosis / Respiratory acidosis
  • Acetazolamide, Ammonium chloride
  • GI (diarrhea, enteroenteric fistula, ureterosigmoidostomy)
  • Endocrine (Addisons, Cushings, Thyroid disease)

How do you get a metabolic alkalosis?
METABOLIC ALKALOSIS

Metabolic alkalosis is unusual as the kidneys are able to rapidly excrete excess bicarbonate. Two phases are normal required:

  • Initiation: normally either gain of HCO3- or loss of H+
  • Maintenance: normally though either chloride or potassium depletion.
Classification of Causes of Metabolic Alkalosis
  • Addition of Base to ECF
    • Milk-alkali syndrome
    • Excessive NaHCO3 intake
    • Recovery phase from organic acidosis (excess regeneration of HCO3)
    • Massive blood transfusion (due metabolism of citrate)
  • Chloride Depletion
    • Loss of acidic gastric juice
    • Diuretics
    • Post-hypercapnia
    • Excess faecal loss (eg villous adenoma)
  • Potassium Depletion
    • Primary hyperaldosteronism
    • Cushing’s syndrome
    • Secondary hyperaldosteronism
    • Some drugs (eg carbenoxolone)
    • Kaliuretic diuretics
    • Excessive licorice intake (glycyrrhizic acid)
    • Bartter’s syndrome
    • Severe potassium depletion
  • Other Disorders
    • Laxative abuse
    • Severe hypoalbuminaemia

Table from AnaesthesiaMCQ.com

Metabolic Alkalosis Based on Urinary Chloride

If you’re not sure what the problem is, the chloride can be measured in the urine to help differentiate the cause. This should be used in caution in those with recent diuretic use however.

  • Urine Cl- < 10 mmol/l 
    • Often associated with volume depletion (increased proximal tubular reabsorption of HCO3)
    • Respond to saline infusion (replaces chloride and volume)
    • Common causes: previous thiazide diuretic therapy, vomiting (90% of cases)
  • Urine Cl- > 20 mmol/l
    • Often associated with volume expansion and hypokalaemia
    • Resistant to therapy with saline infusion
    • Cause: Excess aldosterone, severe K+ deficiency
    • Other causes: diuretic therapy (current), Bartter’s syndrome

For more information follow this link


Case 3

A 75-year-old lady attends the ED 2 weeks after an NSTEMI. She is vomiting, diaphoretic and appears breathless.

She appears to be delirious, and you wonder if she may be septic given her tachypnoea and tachycardia, but she is afebrile with a normal WCC.

She can’t hear you properly because of some ringing in her ears which began recently….

ABG on air
pH 7.37, pCO2 2.5, pO2 8.9, HCO3 10, Na 126
What type of acid base disturbance is this?
Mixed Acid / Base Disorders

These results show she has a pretty ‘OK’ looking blood gas – no acidosis or alkalosis. She looks pretty unwell though, so you scrutinise the blood gas a little further…

The CO2 looks a little low at 2.5…. The bicarbonate also looks a little low at 10.

You calculate the anion gap, because, well . . . . now you know how! (126 + 3.2) – (10 + 99) = 20, which is HIGH….???? What is going on???

This blood gas demonstrates a MIXED pathology – two opposing pathologies which ‘cancel each other out’ on the blood gas resulting in a pH in the normal range.  This may be 2 problems ‘cancelling’ each other out or it may represent a respiratory or metabolic problem that has had time to be COMPENSATED. A metabolic acidosis can be compensated relatively quickly by breathing off some CO2 however if a patient tires (or gets intubated) this can decompensate rapidly. It takes a much longer time to compensate for a respiratory acidosis. These mixed pictures are why it is important to look at the whole of the blood gas and not just the headline pH.

So if we suspect a mixed acid-base disturbance, how do we find it other than with shrewd detective work? You could use a Delta Ratio if you have the time or inclination.

Or you could just look at the patient (and her TTA list). A mixed respiratory alkalosis & metabolic acidosis with tachypnoea, tachycardia and tinnitus . . . this is textbook salicylate poisoning which causes a respiratory alkalosis and a metabolic acidosis!

Causes of respiratory alkalosis:
  • Head Injury
  • Stroke
  • Anxiety-hyperventilation syndrome (psychogenic)
  • Other ‘supra-tentorial’ causes (pain, fear, stress, voluntary)
  • Various drugs (eg analeptics, propanidid, salicylate intoxication)

Case 4

A 28 year old girl attends the ED with 8 hours chest pain on a background of 48 hours dyspnoea. She is breathless on exertion only. She has no other past medical history apart from 2 prior miscarriages. She is on no other regular medications than the oral contraceptive pill. Her Oxygen saturation is 92% on air so she was started on Oxygen in triage. You do a quick, painless arterial gas (using warm local anaesthetic) to be sure . . .

ABG on 40% Venturi mask
pH 7.40, pO2 11.2, pCO2 3.2
Is this blood gas normal?
A-a Gradient interpretation

The mysterious A-a gradient is useful for determining the source of hypoxaemia. A high A-a gradient suggests a high respiratory effort relative to the achieved level of oxygenation. In other words, it demonstrates a ventilation – perfusion mismatch.

Calculating A-a gradient

= The difference between alveolar VENTILATION & alveolar PERFUSION

=PAO2 – PaO2

= [FiO2 x (Atmospheric Pressure – H2O Pressure)] – (pCO2/0.8) – PaO2 from ABG

This equation is complicated but useful…… so use an app to do the hard work for you !

In this case the gradient is  22.7. A normal A–a gradient, for a young adult non-smoker breathing air, is between 1 and 1.5KPa or 5-10mmHg. However, the A–a gradient increases with age

This girl’s blood gas looked normal to the naked eye, but her A-a gradient shows a significant ventilation / perfusion mismatch.

This suggests an underlying lung problem. This likely represents a PE given the history, but bear in mind a high A-a gradient can be caused by anything affecting the perfusion OR ventilation of the lungs to cause a mismatch…..

Calculating the A-a gradient is a useful screening tool to see if there is a problem, but it doesn’t tell you what that problem is – that relies on clinical judgement.

5 causes of hyperaemia. Numbers 1-3 have an elevated A-a gradient:
  1. V/Q Mismatch (ex: LRTI, CHF, ARDS, atelectasis, etc)
  2. Shunt (ex: PFO, ASD, PE, pulmonary AVMs)
  3. Alveolar Hypoventilation (ex: interstitial lung disease, environmental lung disease, PCP Pneumonia)
  4. Hypoventilation (ex: COPD, CNS d/o, neuromuscular disease, etc)
  5. Low FiO2 (ex: high altitude)

Case 5

A 78-year-old insulin dependent diabetic with poor glycaemic control presents to the ED with confusion in the context of a recently treated UTI. You remember the sepsis 6 pathway, and wonder if this raised lactate might be indicative of some of that sepsis stuff….

VBG
pH 7.25, PaCO2 3.3, PaO2 6.9, BE- 10, HCO3 16, K 3.2, Lactate 4.2
What does this blood gas show?
METABOLIC ACIDOSIS WITH A RAISED LACTATE….

Lactate is used in sepsis as a marker of tissue hypoperfusion. It can be raised in many other circumstances

  • Type A lactic acidosisin which there is clinical evidence of inadequate tissue perfusion or oxygenation.
    • Anaerobic muscular activity (for example, exercising)
    • Tissue hypoperfusion (for example, septic shock)
    • Reduced tissue oxygen delivery or utilization (for example, severe anaemia),
  • Type B lactic acidosisin which there is no clinical evidence of poor tissue perfusion and this is further subdivided into:
    • B1 – Associated with underlying diseases (for example, ketoacidosis)
    • B2 – Associated with several classes of drugs and toxins (for example, biguanides, salicylates, isoniazid and alcohol)
    • B3 – Associated with inborn errors of metabolism (for example, pyruvate dehydrogenase deficiency)

In this case it might be raised because the patient is on metformin. Whenever you see a raised lactate on a VBG, always use the result in context with your history and clinical findings, think of a broad differential  and consider which differentials you need to investigate further or treat.

A raised lactate doesn’t always mean septic shock and septic shock doesn’t always give you a raised lactate!


And finally…

There is always more to learn about blood gases but it is important to get the basics right. Always remember to stop and look at the whole blood gas, that includes:

  • sodium (yes it is an impressive lactate but the sodium is the reason why they are having seizures)
  • potassium (your monitor is working, that is called a sine wave…)
  • carbon monoxide (no wonder they aren’t feeling so good)
  • met-haemoglobin (chocolate brown blood after a good dose of amyl nitrate?)
  • haemoglobin (is that 15g/dL or g/L….)

If you are interested in blood gas analysis then why not try AnaesthesiaMCQ or if you are feeling like a challenge listen to all five podcasts on acid-base from the EMCRIT podcast

Tom Mitchell
Author: Tom Mitchell

Emergency Medicine Consultant UK