PH = 7.06, that is severe acidaemia
PCO2 is very high (>40), So we have respiratory acidosis.
Next we calculate compensation, for acute respiratory acidosis, we expect HCO3 to increase by 1 for every 10 PCO2 above 40. According to that, expected HCO3 should be around 29 mmol/L.
Since the HCO3 we have is 27 (<29) then we have an additional metabolic acidosis.
Because we have additional acidosis, then we need to calculate the anion gap. That is Na – (Cl + HCO3) = 5. So, we have an additional NAGMA.
For NAGMA, considering the USED CARP mnemonic,
S—Small bowel fistula
C—Carbonic anhydrase inhibitors
A—Adrenal insufficiency/ Addison’s disease
R—Renal tubular acidosis
This patient had mild hyperchloraemia, 107 mmol/L. that was the cause of the metabolic acidosis.
Other abnormal findings:
K = 6.5, moderate hyperkalaemia. However, in the presence of acidosis, extracellular K level is higher due to extracellular shift. Extracellular K level increases by 0.6 for every 0.1 PH above normal. Accordingly, corrected K level will be around 4.7 (within normal range).
It is a good practice to calculate the A-a (PAO2 – PaO2) gradient since we have an arterial blood gas.
PAO2 = PiO2 – PaCO2/0.8 = (760 – 47) x 0.85 – 99/0.8 = 483.
Accordingly A-a gradient will be 483 – 381 = 102.
Expected A–a gradient is < [age in years/4] + 4, Accordingly, normal A-a gradient for this patient is 21-22. So we have high A-a gradient.
Final conclusion, we have Severe acute respiratory acidosis with mild HAGMA, associated with high A-a gradient.
Severe acidosis and PCO2 of 99 are two indications for mechanical ventilation.
Indications for mechanical ventilation in COPD are:
- Severe dyspnoea (with use of accessory muscles)
- Severe acidosis (PH<7.25) or severe hypercapnoea (PaCO2>60)
- Respiratory rate > 35
- Severe hypoxia (PaO2 < 40 or PaO2/FiO2 < 200)
- NIPPV is contraindicated
- The presence of other complication (Pneumonia, Metabolic abnormalities, Massive PE, Massive pleural effusion, Barotrauma, sepsis…)
This patient has Physiologically Difficult Airway because of the severe acidosis. The 3 physiological killer of Pre-intubation/Peri-intubation are:
- Metabolic Acidosis
Maintaining spontaneous respirations is a vital action as maintenance of acid-base homeostasis is dependent on hyperventilation. Even a short apnoeic period may lead to worsening acidosis and this might cause cardiac dysrhythmias.
Once the patient is sedated, we need to maintain the respiratory rate using bag-valve mask ventilation. The intubation should be performed by the most experienced person available with minimal time required. Then commence ventilation ASAP.
Other Part of the management is the usual management of exacerbation of COPD. These are steroids, bronchodilators and treatment of the cause. (Antibiotics if the cause was infection).