Labs and Lytes 015
Author: Aik Hau Tan
Reviewer: Chris Nickson
A 65 year-old man presented with worsening shortness of breath on exertion and orthopnoea over 1 week. He is a current smoker of 50 pack years.
His arterial blood gas (ABG) on high flow supplemental oxygen of FiO2 0.5 shows:
- pH 7.28
- pCO2 96 mmHg
- pO2 135 mmHg
- BE 11
- HCO3 44 mmHg
Q1. Interpret the ABG
Chronic compensated respiratory acidosis with hypoxemic respiratory failure
- expected HCO3 if chronic compensated respiratory acidosis is a HCO3 rise of 4 mmol/L for every 10 mmHg increase in PaCO2. As the measured PaCO2 is 56 mmHg above the normal value (40 mmHg), the expected HCO3 is the normal value (24 mmol/L) + 4 x 5.6 = 46.4 mmol/L. This closely approximates the measured HCO3 value.
- The A-a gradient = (FiO2%/100) x (Patm – 47 mmHg) – (PaCO2/0.8) – PaO2. Patm (atmospheric pressure) at sea level is 760 mmHg. Using this equation the A-a gradient is 101.5 mmHg. A useful rule of thumb holds that the normal A-a gradient should be less than [age in years/4] + 4.
The patient had bilateral lung crepitations on auscultation and his chest X-ray showed bilateral interstitial infiltrates suggestive of pulmonary oedema. Diuretics were given with symptomatic improvement.
This is his next ABG, on nasal supplemental oxygen of Fi02 0.3:
- pH 7.28
- PCO2 102 mmHg
- pO2 72 mmHg
- BE 14
- HCO3 46 mmHg
Q2. What is your interpretation of this ABG?
There is still a chronic compensated respiratory acidosis, However, the calculated A-a gradient is now 14.4 mmHg, which is within normal limits for this patient.
By this time, lung auscultation did not reveal any added breath sounds. A follow up chest X-ray showed normal lungs.
Q3. What is the likely cause of hypoxemic respiratory failure based on the second ABG?
Broadly speaking, hypoventilation. There is a normal A-a gradient and hypercapnia.
Causes of hypoventilation (from top down) can include disease processes affecting the:
- Brainstem/respiratory centre (including drugs)
- Spinal cord
- Motor neurons of the spinal cord
- Nerves to the respiratory muscles
- Neuromuscular junction
- Respiratory muscles
- Chest wall abnormalities
These can be thought of as “extra-pulmonary” causes of respiratory failure.
Q4. What should you suspect if widespread fasciculations in this context are seen?
There are numerous causes of fasciculations, some of which also cause weakness and could lead to respiratory embarrassment (e.g. amyotrophic lateral sclerosis).
Important causes of fasciculations include:
- amyotrophic lateral sclerosis (motor neuron disease)
- pharmacological causes such as stimulants, benzodiazepine withdrawal and cholinesterase inhibitors such organophosphates
- magnesium deficiency
- lower motor neuron disorders such as rabies and poliomyelitis
- benign fasciculation syndrome
Q5. What are the other pathophysiological mechanisms that cause hypoxemic respiratory failure?
Normal A-a gradient:
- Low inspired partial pressure of oxygen
- Hypoventilation
Increased A-a gradient:
- diffusion defect (rare)
- ventilation-perfusion (V/Q) mismatch
- right-to-Left shunt (intrapulmonary or cardiac)
- increased O2 extraction (CaO2-CvO2)
Reference
- West J.B. Respiratory Physiology: The Essentials, 8th edition. Philadelphia: Lippincott Williams and Wilkins, 2008
Q2. Why is this not a hypercapnic respiratory failure? A-a gradient is normal.
As well, the ABG results for Q2 is a partially compensated respiratory acidosis with metabolic alkalosis compensation, no? I say partially compensated due to the fact the that pH is not between 7.35 to 7.45. So I don;t think it is fully compensated as you mention for Q1 and Q2
Re: Q2
There is hypercapnic respiratory failure – more specifically it is a chronically compensated respiratory acidosis.
We know it is chronically compensated because the PaCO2 is 56mmHg above normal, and the HCO3 should increase by 4 mmol/L for every 10mmHg increase in PaCO2. Thus 4 x 5.6 = 22.6. Add this to 24 (the normal value for HCO3) and you get 46.6 – very close to the measured value of 44 mmHg that is presented.
The terminology re: partial vs complete compensation is confusing. I think most sources would call “complete or full” compensation a return to pH 7.4, however this is typically not achieved acutely or chronically even in a patient with “maximal” metabolic compensation.
It might be better to call this “appropriate” or “maximal” chronic compensation for respiratory acidosis as the HCO3 is exactly what you would expect if the patient compensates normally. The pH is not expected to be “normal” with appropriate metabolic compensation. If the pH was 7.4, it would mean that there is an additional process involved – i.e. an additional metabolic alkalosis (HCO3 would be higher than seen in this case).
Kerry Brandis discusses compensation, and the difference between “maximal” and “full” compensation: https://www.anaesthesiamcq.com/AcidBaseBook/ab4_5.php#ref