Monday, July 26, 2010

Bronchospastic Blood Pressure Badness

shared from http://lifeinthefastlane.com

July 26, 2010 By Chris Nickson

aka Pulmonary Puzzle 013
You arrive at work early and notice a considerable commotion in the resus area of the emergency department. A nurse spots you, and waves at you to come over. The medical team, at the end of their night shift, are stressed, sleep deprived and look worried.
A critically ill young man is now hypotensive following intubation. He was intubated for a severe asthma attack resulting in type 1 and 2 respiratory failure. The team leader asks you for help.

Questions

Q1. What are the most important things to check when there is a problem with a mechanically ventilated patient?

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.
Q2. What is the most important first step in managing the patient who is hypotensive soon after intubation?
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.
Q3. What are the likely causes of hypotension following intubation of the asthmatic?
In general, the causes of hypotension or shock are PRROVV:
  • Cardiogenic
      • Pump (e.g. imparied contractility, valve dysfunction)
      • Rate (fast or slow or absent)
      • Rhythm (regular or irregular)
  • Obstructive (e.g. tension pneumothorax, pericardial tamponade, PE, dynamic hyperinflation)
  • Vasodilation = distributive shock (e.g. sepsis, anaphlaxis, neurogenic, hepatic failure)
  • Volume depletion = hypovolemia (e.g. dehydration, hemorrhage, third spacing)
The most important causes to consider following the intubation of a patient with asthma are:
  • 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).
  • Dynamic hyperinflation (gas-trapping) due to excessive ventilation — especially in the patient with bronchospasm.
  • Tension pneumothorax due to positive-pressure ventilation.
Q4. What are the other early management priorities?
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 a way to avoid chest drain insertion here.
Q5. When should you intubate a patient with severe asthma?
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, and 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.
Q6. What are appropriate initial ventilator settings in the intubated asthmatic?
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.
Look for more on the pathophysiology and perils of dynamic hyperinflation in an upcoming post…

References

Posted by at

No comments:

Post a Comment

Subscribe to: Post Comments (Atom)