Every morning our team discusses cases over coffee. Here is a useful snippet…
Patients with a severe high anion gap metabolic acidosis (e.g. from severe DKA, AKI, toxic ingestions, severe lactataemia from bleeding/sepsis/some other form of badness) have a markedly increased respiratory drive to achieve the high alveolar minute ventilation required for their compensatory respiratory alkalosis. This manifests as “air hunger” (Kussmaul breathing).
Loads of bad stuff happens when the pH gets below 7.1-7.2. Chiefly:
– Reduced myocardial contractility
– Risk of arrythmias
– Poor response to catecholamines
– CNS depression
– “Air hunger”
When hypocapnia is already present due to the compensatory respiratory alkalosis, escalating hyperventilation results in increasingly marginal decreases (and ultimately a plateau) in pCO2 (1). This results in profoundly acidaemic states despite the patient maximally compensating. Minute volumes can climb to over 30L/min.
This respiratory drive is very challenging (often impossible) to match with a mechanical ventilator. Therefore, spontaneous breathing should be maintained for as long as possible, whilst treating the underlying cause.
In the maximally compensating patient, even a brief apnoeic period can lead to a devastating drop in pH given the loss of the already inadequate respiratory compensation. Performing an RSI in the patient with a profound metabolic acidosis is, therefore, an exceptionally dangerous procedure.
We’ve all seen the sick ketoacidotic patients with extraordinarily abnormal blood gases who manage to turn a corner and avoid intubation after prompt initiation of volume resuscitation and an insulin infusion.
However, when these patients get tired and/or severely obtunded they become increasingly unable to maintain their respiratory drive, rapidly circle the drain, and we have no choice but to proceed with RSI.
Below are some key points to consider in this challenging situation.
Do we really need to intubate?
– These patients are extremely high risk of cardiac arrest intra- or post procedure for the reasons explained above.
– Can we wait a little longer for the treatment to take effect, and potentially avoid RSI?
Consider a trial of BiPAP
– If tolerated this might buy you time.
– The machine will also provide a useful estimate of the minute volume to try and match if/when mechanically ventilating.
– Bag valve mask ventilation with a two-person technique must be performed after induction drugs are pushed.
– Use your most experienced laryngoscopist – the tube needs to go down first pass, and as fast as possible.
Common pitfall – ventilating to normal pCO2
– This will precipitate a rapid deterioration in pH and cardiac arrest.
– The patient needs to be hyperventilated/hypocapnic.
– Delegate someone to keep a close eye on the ETCO2 pre/intra/post procedure (ensure it isn’t rising).
Use Winter’s Formula
– Winter’s Formula tells you what the pCO2 should be if the patient is maximally compensating for their metabolic acidosis.
– Get a blood gas pre-RSI and do the calculation:
Expected pCO2 = 1.5 x HCO3 + 8 (+/- 2)
– This will be your target pCO2 when the patient is on the vent.
– Post RSI, set the vent to achieve approximate a minute ventilation according to the below table (a rough starting point in adult patients) (2).
|Target pCO2||Minute Ventilation|
– Get another blood gas within 15 minutes post-RSI and adjust as needed.
– Don’t rely solely on ETCO2 (get a gas), it is not a perfect surrogate. In a patient with normal lung function the ETCO2 value is usually 2–5 mmHg lower than the pCO2 (5).
– This would be ideal as it would negate the need to paralyse the patient and, therefore, preserve the native respiratory drive.
– However, application of the topical anaesthesia can take time that we often don’t have with these patients. Furthermore, they are often not compliant enough in their state of extremis.
– As a therapy for HAGMA? don’t bother. No evidence that giving sodium bicarbonate of any therapeutic benefit.
– It is indicated in certain specific situations which may be accompanied by a metabolic acidosis: TCA OD, urinary alkinisation for salicylate poisoning, NAGMA due to bicarb loss from renal/GI tract, hyperkalaemia (3, 4).
– Bicarb ultimately generates CO2 which likely puts further strain on a maximally compensated patient.
Unrecognised metabolic acidosis?
– Prior to ANY RSI have a brief pause point and check the respiratory rate/breathing pattern:
– Is the patient moving a lot of air? If yes it could be Kussmaul breathing. If in doubt, get a blood gas.
1. Capone J, Gluncic V, Lukic A, Candido KD. Physiologically Difficult Airway in the Patient with Severe Hypotension and Metabolic Acidosis. Case Rep Anesthesiol. Sep 2020
2. Frank Lodeserto MD, “Simplifying Mechanical Ventilation – Part 3: Severe Metabolic Acidosis”, REBEL EM blog, June 18, 2018. Available at: https://rebelem.com/simplifying-mechanical-ventilation-part-3-severe-metabolic-acidosis/
3. Use of Bicarbonate in Metabolic Acidosis, Anaesthesiamcq.com https://www.anaesthesiamcq.com/AcidBaseBook/ab8_7.php
4. Sodium bicarbonate use, LITFL, https://litfl.com/sodium-bicarbonate-use/
5. High-Risk Airway Management in the Emergency Department. Part I: Diseases and Approaches. Lentz S, Grossman A, Koyfman A, Long B. J Emerg Med, 59(1):84-95, 12 May 2020
Ketamine only dissociative intubation is my choice. Hyperangulated VL my instrument to perform. Thanks for the great topic.