Question 10

College Answer

Severe acidemia due to a mixed severe respiratory and metabolic (lactate) acidosis. Apparently adequate oxygenation (very low A-a gradient). The elevation in lactate may have been due to tissue hypoxia but the PaO2 at present might appear adequate. She is likely to have received intravenous adrenaline and possibly salbutamol, both can cause lactic acidosis (due to inhibition of pyruvate dehydrogenase (Day NP et al Lancet 1996;348:219-223) and possibly other effects on glycolytic enzymes, accelerating glycolysis).
Measures to increase alveolar ventilation are urgently required. Evaluation of airway, breathing and circulation (ABC) is the first response. Urgent chest auscultation and observation should be performed. Capnography (+/- laryngoscopy) should be used to confirm intra-tracheal position of ETT. To achieve a PO2 of 90 with almost zero A-a gradient, the tube must be in the trachea; for the same reason, endobronchial intubation is unlikely but should be excluded. Consider pneumothorax
– as this might compromise alveolar ventilation. Any leak should be identified (if the endotracheal tube is un-cuffed it could be replaced with a larger tube or a cuffed tube). Check to make sure the ventilator tubing is not leaking/unattached. The tidal volume and respiratory rate must be checked together with the peak pressure limit (if the patient is being ventilated with a mechanical ventilator). The chest excursion should be observed to ensure that there is a rise during inhalation. If excursion appears inadequate it is appropriate to try an increase in the volume or pressure and observe
whether the ventilation improved. The extent of gas trapping needs to be evaluated. If there is significant gas trapping then a reduction of respiratory rate is required (to prolong the expiratory time), however given the current PaCO2 this may require an increase in tidal volume. An alternative strategy would be to plan for regular 30 second disconnections every 5 minutes or so (particularly if there was associated hypotension).

Discussion

This is not a pure ABG interpretation question; it required some thinking about the management of severe asthma.

But first, lets interpret the ABG.

1. The A-a gradient is normal:
   (0.5 x 713) - (212 x 1.25) = 91.5
   Thus, A-a = (91.5 -90) = 1.5mmHg
2. There is acidaemia
3. The PaCO₂ is contributing to the acidosis
4. The SBE is not given, but the bicarbonate is normal, suggesting that there is either no metabolic acidosis, or that the metabolic acidosis coexists with a metabolic alkalosis. The presence of a raised lactate (12mmol/L) suggests that the latter is correct. 
5. This question gives a history of asthma and cardiac arrest which suggests that the respiratory acidosis is acute. The expected HCO₃^- in this setting would be 41.2:
   bicarbonate compensation = (212-40)/10 multiplied by 1 = 17.2 mmol/L
   Thus, there is also a metabolic acidosis present here.

The lactate can be left to its own devices. Given that you would be using vast amounts of salbutamol here, it can be expected to persist for some time.

The PaCO₂ requires immediate attention.

The ventilation strategies in status asthmaticus are discussed elsewhere.

A systematic approach would resemble the following:

Airway:

• Ensure the ETT is not kinked or blocked with secretions, and is of a satisfactory internal diameter

Breathing:

• Assess the expiratory flow using ventilator waveforms and capnometry
• Adjust the I:E ratio to allow for prolonged expiration
• Adjust the repiratory rate to allow for prolonged expiration
• Consider using a low PEEP.

Circulation

• Assess the extent of dynamic hyperinflation
• Assess intravascular volume and aim for a higher CVP, to counteract the preload-limiting effects of dynamic hyperinflation
• Consider regular disconnections of the ETT, and/or manual decompression

Oh's Intensive Care manual: Chapter 35   (pp. 401) Acute  severe  asthma by David  V  Tuxen  and  Matthew  T  Naughton.