Bronchospastic BP Badness

You may remember this question from Pulmonary Puzzle 012 – Man versus Machine — it is repeated for a reason… It’s important!

First determine the severity of the problem — do you need to start immediate resuscitation?

Then assess MASH:

• Movement of the chest during ventilation —
  is it absent or is movement only on one side? Is the chest hyper-expanded?
• Arterial saturation (SpO2) and PaO2 —
  obtain an ABG sample
• Skin colour of the patient (is he turning blue or pinking up?) —
  the SpO2 monitor lags behind the true oxygen saturation of the patient.
• Hemodynamic stability.

Now you can attempt to diagnose the problem.

Disconnect the the endotracheal tube from the ventilator circuit.

In asthmatics, this may be life-saving. If the cause is dynamic hyperinflation (‘gas trapping’) blood pressure will rise over 10-30 seconds as the gas is released.

When considering the causes of hypotension or shock, think ‘are they PROVED?’:

• Cardiogenic
  — Pump (e.g. imparied contractility, valve dysfunction)
  — Rate (fast or slow or absent) or Rhythm (regular or irregular)
• Obstructive (e.g. tension pneumothorax, pericardial tamponade, pumonary embolus, dynamic hyperinflation)
• Volume depletion = hypovolemia (e.g. dehydration, hemorrhage, third spacing)
• Endocrine (e.g. adrenal insufficiency, hyperthyroidism, hypothyroidism)
• Distributive shock (e.g. sepsis, anaphylaxis, neurogenic, hepatic failure)
• ? (e.g. artefact, measurement error, drug adminstration error)

The most important causes to consider following the intubation of a patient with asthma are:

• ‘Stacking’ or dynamic hyperinflation (gas-trapping) due to excessive ventilation — especially in the patient with bronchospasm.
• Hypovolemia exacerbated by decreased venous return due to positive intrathoracic pressure.
• Vasodilation and myocardial depression due to the induction drugs used for rapid sequence intubation (e.g. thiopentone, propofol).
• Tension pneumothorax due to positive-pressure ventilation.

The patient has already been disconnected from the ventilator circuit.

Important management priorities include:

• Administer high-flow oxygen (FiO2) via a bag-valve-mask and manually ventilate (usually <10 breaths/min) following adequate disconnection to allow the release of trapped gas.
• Consider needle thoracostomy for tension pneumothorax — carefully consider whether there is time for confirmation by bedside ultrasound or chest x-ray (there often is), so that an unnecessary invasive procedure is not performed. If the chest is needled, formal intercostal catheter insertion is mandatory.
• Administer 10-20 mL/kg IV fluid boluses to overcome the cardiovascular effects of induction drugs and/or unmasked hypovolemia. Vasopressors (e.g. metaraminol 0.5-1mg IV boluses) may also need to be administered as a temporizing measure.

Scott Weingart talks about ‘finger thoracostomy‘ as an alternative to needle thoracostomy

Never intubate an asthmatic… unless you absolutely have to!

Intubation and ventilation may be life-saving, but carries significant risks. There are the usual risks such as failed intubation, airway trauma, aspiration, increased risk of stress ulceration and nosocomial pneumonia. But there are additional risks specific to the patient with reactive airways disease.

These include:

• inadvertent pulmonary hyperinflation.
  — hypotension
  — barotrauma and pneumothoraces
  — PEA arrest due to dynamic hyperinflation.

• aggravation of bronchospasm.
• longer term risk of myopathy from the combination of corticosteroids and neuromuscular blockade required to facilitate mechanical ventilation.

Absolute indications for intubation of a patient with severe asthma are:

• cardiac or respiratory arrest
• severe hypoxia (e.g. hypoxic seizure)
• rapidly deteriorating level of consciousness

Relative indications for intubation are:

• progressive patient fatigue
• hypercapnea

These relative indications need to be balanced against the risks of intubation. Hyperacute asthma may have hypercapnea due to mechanical limitation of ventilation rather than fatigue, and this may improve with aggressive treatment.

There is no clear evidence for the superiority of one ventilation mode over another (i.e. volume-controlled versus pressure-controlled).

Initial ventilator settings (volume-controlled ventilation):

• Tidal volume 6-8 mL/kg
• Slow respiratory rate (e.g 8-10/min)
• High inspiratory flow rate (e.g 80-100L/min) to allow longer expiratory times
• PEEP of 0 cmH2O (some experts like a bit of PEEP — more on that another time…)
• FiO2 titrated to keep SaO2 >93%.

Variations of these settings may be used as long as the main principle of avoiding dynamic hyperinflation (by using small tidal volumes, long expiratory times and a slow respiratory rate) is followed. To my knowledge there is no convincing scientific evidence that this ventilation strategy is more effective than any other.

Expect the following with these initial settings in a patient with asthma:

• high peak inspiratory pressures (PIP) — don’t worry this does not necessarily correlate with lung barotrauma.
• respiratory acidosis due to a low target minute ventilation — sedation and neuromuscular blockade may be required to suppress spontaneous ventilation.

• Brenner B, Corbridge T, Kazzi A. Intubation and mechanical ventilation of the asthmatic patient in respiratory failure. J Emerg Med. 2009 Aug;37(2 Suppl):S23-34. Review. PMID: 19683662.
• Gomersall C. ICU Web — Trouble-shooting mechanical ventilation
• Holley AD, Boots RJ. Review article: management of acute severe and near-fatal asthma. Emerg Med Australas. 2009 Aug;21(4):259-68. Review. PMID: 19682010.
• For more Pulmonary cases check out the LITFL Top 150 Chest X-Rays