UK EM Field Notes #4
When to start NIV in COPD, ABGs vs VBGs, IV morphine and the "RV Death Spiral"
When to start NIV in COPD patients
Start NIV on COPD patients who remain in type 2 respiratory failure (pH <7.35, pCO2 >6.5) despite 1 hour of maximal medical therapy (steroids, nebs) and controlled oxygen therapy (target sats 88-92%).
I think too often we delay starting NIV. The gas doesn’t need to be dramatic for it to be indicated.
In my place we have an excellent local guideline which outlines when and how to start NIV. I would imagine most UK EDs have similar.
ABG vs VBG
pH, HCO3, lactate and base excess correlate well between in ABG vs VBG.
pCO2 also correlates well in normocapnia. However, in hypercapnia and severe shock the pCO2 on VBG is inaccurate.
Obviously pO2 is always inaccurate in a VBG.
In most ED scenarios, a VBG is entirely sufficient.
Here is a useful LITFL blog post on this topic.
When do COPD patients need ABGs in the ED?
I think it’s pretty rare. As with all investigations, first consider what clinical question am I asking?
If the goal is purely to identify a COPD patient in T2RF (which is our main job with these patients in the ED) then a VBG is fine. We don’t need to know a precise pCO2.
Further along in a patient’s journey, we might need to see how a T2RF patient’s pCO2 is trending when they are established on NIV, and therefore ABGs are appropriate. In the current UK EM climate (ie. exit block, crowding) these patients stay in resus for longer than they used to, which means they are more likely to need ABGs whilst with us (though this should be the responsibility of the admitting team).
I would argue an ABG is never indicated as part of a (non-shocked) COPD patient’s “workup” (ie along with CXR, lab bloods etc).
In the severely shocked patient, an ABG is necessary for accurate pCO2 and pO2. If they are peripherally shutdown in might be challenging to get a reliable SpO2 which heightens the importance of the ABG. In these cases, an arterial line should be strongly considered.
If you do need to do an ABG, strongly consider using local anaesthetic. “Local anaesthesia should be used for ABG sampling if the patient finds the procedure painful or if repeated arterial punctures are likely to be necessary” (BTS Emergency Oxygen Guideline).
Intravenous morphine in frail COPD patients
If the adult patient in severe pain, IV morphine is the analgesic of choice unless there is a clear reason not to give it. RCEM recommends IV morphine 0.1-0.2mg/kg as the initial dose. Therefore, in a 70kg male give 7-14mg (RCEM Management of Acute Pain in Adults).
In frail, COPD patients (who often have CKD) we must be more cautious and give lower IV morphine doses or consider an alternative analgesic strategy altogether. Why?
Morphine is renally excreted and so patients with CKD have impaired clearance and potentially delayed opiate toxicity.
COPD patients live right on the edge of compensation. Even the tiniest bit of opiate toxicity-induced respiratory depression can tip them into decompensation.
Morphine reduces preload (it’s a vasodilator) which can cause hypotension. In pulmonary hypertension, even mild hypotension can lead to RV failure and sudden cardiovascular collapse (the “RV Death Spiral” – see below).
The “RV death spiral”
The RV often gets overlooked when compared to the LV. In severe COPD patients (which we see loads of), pulmonary hypertension is very likely… therefore, we must be mindful of the RV death spiral. Here is my attempt at an explainer:
In pulmonary hypertension, the RV hypertrophies (Cor pulmonale). In acute on chronic hypoxia, hypercapnia and acidosis, (e.g. from a IECOPD), the pulmonary vascular resistance increases (an acute on chronic rise).
The already dodgy RV can’t generate enough pressure against the higher afterload. This causes it to dilate (strain) which impairs its contractility and reduces RV output.
A reduced RV output reduces the LV preload (there is less blood returning to the LV). Also, the RV dilatation shifts the septum to the left, which impairs LV filling. Reduces LV preload drops cardiac output.
When the patient’s (already poor) ability compensate for the drop in cardiac output (by generating a tachycardia) is overwhelmed, hypotension results. Hypotension worsens coronary artery perfusion, most crucially to the right coronary artery, and this induces RV ischaemia. This further worsens RV contractility.
Poor RV output (RV failure) reduces perfusion to ventilated areas (V:Q mismatch), worsening hypoxia and hypercapnia… which feeds back into the spiral. The cycle accelerates as it goes round and round.
Key principles:
Be careful with fluids in these patients. They might need a little as the RV is preload dependent… but overloading them will dilate the RV and feed the spiral. Move early to vasoactive drugs.
Avoid hypoxia, hypercapnia, and acidosis as these acutely increase PVR. Optimise COPD medical management and start NIV early!
Avoid intubation wherever possible. An RSI can cause hypotension and hypoxia, feeding the death spiral, as can the PPV from mechanical ventilation.
Check out this awesome lecture on “Breaking the RV Death Spiral” from CriticalCareNow. It focuses on a massive PE case, but the principles are the same.
Cheers all,
Robbie
@robbielloyd.bsky.social