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Clinical Case 027: tachypnoea, tachycardia and tuckered out…

This was my night shift this week.  One of those situations where you know you have to do something quick – but what?  I am going to leave it open for comment at the crucial decision point and ask for your comments – then later this week I will tell you what I did and what happened!

The Ambos roll in with a 67 yo man in severe respiratory distress – sweating, tripod posture, gasping for air and looking a bit blue around the lips.  “Acute exacerbation of COPD” they handover – so off to the “ICU room”.  I did a quick exam – quiet chest, a few faint wheezes, nicotine-stained beard.  Radial pulse is thready – barely palpable, but the chap is able to answer questions with quick “yes” or “no” between gasps.  His skin looks mottled. He admits to ’emphysema’ and has been unwell for a few days. However tonight he became very SOB over the last few hours.  At this point I was happy with – exacerbation of COPD – as a diagnosis.

I ask for the BiPAP machine and we hook him up to the monitors.  I am a bit worried about his BP with NIV so I try and get a palp BP – no able, too weak at the radial… then the monitor goes on – obs are:  pulse rate =  215 /min, narrow complex rhythm, SpO2 unrecordable, BP unrecordable, RR = 45/min, T = 37.5.

This is not good.   A quick scan through his old chart reveals another surprise – his man has been followed by the Cardiologists for aortic stenosis – his last ECHO was 6 months ago and showed severe stenosis with a valve area of 1 cm2.  He was declined for valve repair on the basis of his severe lung disease.

A quick venous gas shows: pH = 7.08, pCO2 = 101, HCO3 = 28, Hb = 186 lactate = 5.7.  Not good…

So in summary:

  • 67 yo chap with acute-on-chronic COPD – currently severe hypercarbic respiratory failure
  • Supraventricular tachyarrythmia – probably AF @ 215/min.  That LV is getting a work out
  • Severe aortic stenosis
  • NO previously documented end-of-life discussion or NFR order etc
  • Currently tolerating BiPAP OK and appears alert though very scared

So here are my questions for you – and I am not sure there are ideal answers – so let me know:

  1. What differential diagnoses might you consider?  Any unifying thoughts
  2. What are you going to do bout his tachycardia?  What interventions will help, but not kill him in the process?
  3. Where and how would you discuss the role of intubation vs. palliation in this scenario?

OK, don’t be shy.  What would you do?

Comments

  1. DDx is pretty broad. COPD exacerbation, PNA, sepsis, pneumothorax, arrhythmia, critical AS, pulmonary embolism, tamponade, CHF, cardiogenic shock, lobar collapse, STEMI, NSTEMI, GI bleed (could keep going). PE, pneumonia, sepsis could all cause the arrhythmia and the vitals, the arrhythmia as a primary could cause it as well.

    I think you a few things: he’s preload dependent from the AS (but also cor pulmonale and some degree of pulmonary HTN), so you get 2 IVs and give him a bolus while you’re doing other things, including labs, a rectal temp, guiaic, blood cultures, fingerstick, EKG, airway equipment at the bedside. Pads on him or paddles near by. Broad spectrum antibiotic coverage for sepsis, a big slug of magnesium may help with his COPD and possible AF, IV steroids, continuous albuterol/atrovent. I think he also needs to be cardioverted; he’s unstable, that rate is too fast to be sinus tachycardia for him, and perhaps if he gets some of his atrial kick back, it’ll help his filling pressures and cardiac output, too. I think before you do that (the order of a lot of this stuff is happening in parallel, hopefully), you also do an ultrasound (if you have it). It’ll tell you a lot:

    1) IVC: big or small? Hypovolemia? Can I give them fluid without worrying too much?
    2) Cardiac: Tamponade? Massive RV like a PE?
    3) Lung: Pneumothorax, pleural effusions

    And you get a chest x-ray, you get a manual, palp blood pressure, try to get a sat, put him on some good BiPAP settings, and see where he goes.

    I think you try to get family on the phone or have some sort of discussion about intubation, but by his PCO2 and his respiratory status, I think it’s really hard to have a reasonable conversation with this guy about intubation and expect that he’s going to be able to mentate well enough to discuss this stuff. If this guy doesn’t fly on BiPAP despite all of your interventions, his intubation will be a mess since he’ll desat within seconds, has no reserve, and is already hypoxic and acidotic. Wouldn’t be surprised if he codes after. Ketamine and an awake intubation might not be a bad option in that case. Other issue is that he’ll probably never get extubated if he gets intubated.

  2. I think the first thing to recognize about this case is that even if management is optimal or perfect the patient may still die, what we are seeing is the physiological decompensation at the end of life due to multiple severe chronic diseases.

    That being said if we are to try to resuscitate this patient the following are my thoughts:
    The patient likely has some primary problem that has tipped him into atrial fibrillation or another atrial tachycardia (MAT or SVT). Possibilities include: sepsis, PE, pneumonia, pneumothorax, severe COPD, tamponade, atelectasis, etc. but his immediate life threatening problem is now rapid atrial fibrillation (or SVT or MAT) in the setting of severe/critical aortic stenosis.

    If I thought the patient was in SVT or a fib the first thing I would do in this patient is push 200mcg of phenylepherine, hoping for both brief perfusion support and some element of reflex bradycardia and give a litre of fluid as a bolus. I would then cardiovert the patient with anterior posterior pads at maximum joules (200 biphasic on my machine), and with some IV fentanyl on board for pain control. When this failed (and it surely will fail) I would consider either an infusion of diltiazem at 2.5mg/minute to rate control, versus careful 100mg boluses of procainamide to rhythm control, either supported with bolus doses of phenylepherine. The dilemma here as G rightly states is that for the critical aortic stenosis patient the atrial kick is critical so even beautifully controlled rate may not be enough to adequately perfuse the patient.

    I too would ultrasound this patient early on, though I think it is important to recognize that the US may well be misleading in this patient. The ultrasound will rule in or out tamponade which will be helpful. Estimates of RV size, and IVC will be inaccurate to detect PE because of the expected pulmonary hypertension (likewise the BNP will be predictably up due to RV stretch and offer us limited information about failure in this scenario). Scanning lung fields for PE is equally problematic as this is the exact patient where we could be fooled into believing there is a pneumothorax, when what we are seeing is a large bullae (and subsequently killing the patient with a chest drain that ruptures said giant bullae). So I would do the ultrasound, but I would take everything except the question of tamponade with a grain of salt.

    The patient needs to be intubated and I would use etomidate as a relatively hemodynamically neutral agent (recognizing that the patient will be getting high dose steroid anyways for COPD) and rocuronium, suspecting hyperkalemia in this patient though the electrolytes are not yet back. I would premeditate as above with fluids, phenylepherine, and a thought to bicarb. The patients vent settings are a post in and of themselves and I will only mention that correcting the CO2 to normal is not an immediate priority.

    In terms of other treatment I would give the patient an inhaled beta agonist and anticholinergic (eg. salbutamol and ipratropium), magnesium 2g IV, broad spectrum antibiotics, intravenous steroid and IV fluids. A CT chest would help clarify the state of the lung pathology and guide the next phase of management.

    Those are my initial thoughts, look forward to hearing the next chapter…
    Aaron

    • Casey Parker says:

      Some great comments and action plans. I was going to respond to G, but Dr J got in first.
      – Yes, phenylepherine boluses came in to play
      – US / ECHO was basically impossible – no good windows to get a decent look
      – IVC scan only really validated for normal intra-thoracic pressure changes – so will give a positive no matter how much fluid you throw in.
      – We tried ++++ to get a BP manual / NIBP but no go, just too fast. ECG like wise, the dots just fell off the sweaty heaving chest
      – Pneumotx US is likely to be false + with bullae. As would RV size be chronically large.
      – We don’t have a lab after hours – so gases at the bedside are all you get!
      – I did get a portable CXR = consistent with hyperinflation / COPD, nothing focal, no pneumothorax.
      – A lot of useful drugs are contraindicated due to the combo of severe lung disease and AS.

      Any other takers? Casey

      • Minh Le Cong says:

        Hi Casey
        Challenging case! I had something similar a few years ago on a remote retrieval case. Hypotensive guy with rapid AF and COPD. BiPAP worked a treat as did IV digoxin load and a couple of doses of amiodarone. In fact worked so well I avoided giving any vasopressors. I would do the same strategy in this guy.

        Priorities here appear to be correction of hypoxia and control of heart rate/rhythm.

  3. A very poorly patient!

    That said the main problems are:
    Tachycardia in severe Ao stenosis
    T2 RF (the fact he is awake with PaCO2 of 101 tells us he is chronically hypercapnic (and bicarb is likely to be 35ish normally)

    He needs DC cardioversion, I would use a touch of ketamine eg 30mg with an art line in situ, and after fluid loading (though he will go into LVF fairly quickly with too much fluid.)

    (having prev tried this in another similar pt with fentanyl who virtually arrested on the end of my syringe, I think less is more when it comes to induction agents / sedation.)

    A quick cardioversion is this chaps only hope!

    This man has a very high risk of death!
    His long term prognosis is worse than a lot of cancers, and early thought must be to comfort care.

  4. Hello Casey. An interesting case with many possibilities.
    Lots of good thoughts in the replies so far. My ideas to throw into the mix:

    DDx – pneumothorax as cause for both dyspnoea and hypotension (to be excluded first). Obviously, the tachyarrhythmia may be contributing to the hypotension, but not sure to what degree. Sepsis is always a possibility, and I’d also consider overinflation due to COPD (although more likely if he was on positive pressure ventilation). PE – consider fleetingly but will be almost impossible to diagnose unless he’s got a peripheral DVT that you can find. Finally, given he has critical aortic stenosis – could this be acute pulmonary oedema (on the background of his severe COPD) due to progressive disease or exacerbated by ischaemia, or the arrhythmia?

    The tachycardia – possibly rapid AF with an AV node heavily stimulated by sympathetic output (and also salbutamol nebs), possibly MAT. AF usually won’t go that fast unless there’s an accessory pathway (except in kids) but rarely can with sympathetic stimulation. COPD sometimes does cause these unusual tachyarrhythmias. I would treat with amiodarone and magnesium. It seems to have gone out of favour (and never came into favour in many places) but I still think amiodarone effectively controls the rate in AF with less negative inotropic effect than anything else (I’m not a believer that digoxin works until at least many hours later). I’ve not used IV diltiazem so can’t compare this (commonly used in US). If he’s in chronic AF then he’s very unlikely to revert in the setting of his other problems and this ranks low on his current problem list, so I don’t see this as a reason not to use it when they’re this sick. I don’t think I’d try cardioversion unless I knew for sure he was usually in sinus rhythm. In that case ketamine would be my sedation agent of choice, but expecting that I’d have to ventilate him, it may well be unsuccessful (due to the underlying cardiac and lung disease) and that the extra positive pressure ventilation may well remove any remaining blood pressure that he had.

    I would use ultrasound as described to try and help assess his fluid status, noting all the well made points mentioned:
    – His intrathoracic pressure swings will be large and being on BiPAP makes interpretation of the IVC size & collapsibility difficult (if you can find it).
    – He will have RV strain, and trying to distinguish between chronic cor pulmonale and acute massive PE (e.g. McConnell’s sign, etc.) in an acute setting is very difficult and (in my opinion) unreliable for all but the most expert.
    – US for PTx is great when the patient is lying down, but difficult when they sit up as the window is the supraclavicular recess and the apex doesn’t move much normally. Bullae are always on the list of PTx mimics but so far I haven’t seen one that doesn’t slide (I’ve looked a few times but not enough to be authoratative). Worth remembering that sliding present excludes PTx, but absent sliding doesn’t mean PTx (you need to see the transition or “lung” point to rule in PTx). Can be useful to exclude large or tension PTx rapidly in the erect patient, but these pts can decompensate with small loculated PTx.
    – Not yet mentioned is using US to diagnose or exclude pulmonary oedema, which can be difficult to diagnose on CXR in those with severe COPD. Look for the ‘lung rockets’, and if they’re present I would avoid further fluid (and decide if inotropes are appropriate – acute pul oedema + hypotension = very poor prognosis, then add in the COPD and the untreatable aortic stenosis), if not, then give fluid bolus(es). I can’t tell you how well it works in the setting of severe bullous COPD as I’ve not got the experience, but finding it increasingly useful in the breathless ?cause patients (I’ve put an example in the image library on the ultrasound village website to show what they look like).

    Dropping afterload in patients with critical aortic stenosis is supposed to be a problem, but in reality, it’s what we do when they present with heart failure (using CPAP or GTN) despite the theory about coronary artery perfusion pressure (I do recall reading one cath lab study in the distant past that measured this and said the theory didn’t happen in practice). However, in this man, his lack of BP would prevent the use of afterload reduction, with the exception of cautious BiPAP possibly.

    Palliation v intubation – to me, this will depend very much on what underlying cause is found. If he has pulmonary oedema, then his outlook is dismal. If it’s sepsis, then I’d be much more inclined to intervene with inotropes and intubation. If it’s exac of CAL, then I’d try very hard to stick to the BiPAP.

    Interested to hear what actually happened.
    Cheers
    Adrian

  5. Doncha love these cases?

    I’d be going for aggressive control of his hypoxaemia (BiPAP) and rate control (Mg, amiodarone) as priorities. Consider cardioverting if appropriate.

    He’s decompensated and likely to die. If too knackered to tolerate BiPAP and no firm decision from him or family, then I guess you are shoehorned into RSI/ETT/IPPV…with likelihood he’ll crash. So cautious boluses of induction agent of choice (I’d be going ketamine), RSi with sux, with phenylephrine chaser.

    How did it all pan out?

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