It is mid afternoon in your busy regional ED when the triage nurse calls for help. A 57 year old woman who drove herself to hospital managed to tell her that she has been having awful pain in her chest when she collapsed, collecting her forehead on the windowsill on the way down. You poke your head through the triage window to see her looking up at you from the floor, clearly not well.
By the time you unstick your head from the triage window the patient has been moved onto a gurney. She is awake but with a clouded conscious state (confused mumbling, eyes open but not fixing and focusing, localising to pain) and his vitals are HR 40, BP 60/-, RR 26 with end of the bed wheeze, SpO2 not readable, afebrile. She is bathed in sweat and pale.
This is her 12 lead ECG
What to do? Read on and see what you think.
Granted, it is not much of an ECG but the nurse who took it is now expertly slipping a 16 gauge cannula into her left antecubital fossa so rather than interrupt him to demand another trace, what do you see on this one?
Rhythm: I think it is sinus rhythm however there are some P-like waves that do not produce a QRS (after the second T wave for example) but as these are not consistently occurring and are different morphology from the other P waves I am inclined to call them atrial ectopy without conduction.
ST segments: Obviously, regardless of the rhythm, this ECG shows a big proximal anterior STEMI with significant elevation of avL and 1 (high lateral), and V2-4 (anterior septum) backed up by reciprocal inferior lead depression. The lesion is likely to be in the proximal LAD.
Oh, and being a regional hospital, your cath lab does not have a primary PCI capability.
There are a lot of competing priorities in this patient. First up, do you-
a) Secure the airway and optimise ventilation and oxygenation?
c) Try to arrange urgent retrieval out to a place with a hot plasty service?
d) Perform a neurological examination?
e) Try to improve the haemodynamics with some inotrope/vasopressor?
Securing the airway doesn’t seem the thing to do right now. While the patient has a depressed conscious state she seems to be awake enough to ventilate and protect her airway for now and sedative drugs and positive pressure ventilation might just be enough to finish off this woman’s fragile haemodynamics. However, this patient is in for a stormy hour or two and in a more austere environment (pre-hospital, or retiriving the man from a small rural clinic) I might be tempted to intervene with the airway sooner just to take airway and breathing (not to mention confusion and agitation) out of the equation.
Thrombolysis we will come to in a bit.
Retrieval out should certainly be initiated early but retrieving a patient like this to a cath lab from a regional referral hospital in Australia is unlikely to be completed in a meaningful timeframe. Too many of our hospitals have no heli-pad and distances often make rotary wing retrieval too slow anyway. If your hospital can’t do primary PCI but is 10 minutes from somewhere that can then you will calculate this equation differently from someone in a place where it will be 4 hours at best before you can have someone in a lab if you decide to transfer for PCI.
Performing a neurological exam is not as crazy as it might have looked. This woman collapsed (and hit her head) and is now confused and drowsy. Presence or absence of localising signs will be important when deciding whether or not to use fibrinolytics for his heart.
Attacking the shock first up with vasopressor and inotrope may well improve coronary perfusion enough to overcome some of the coronary flow issues however it must be remembered that you are improving the coronary perfusion by increasing cardiac workload. If I am going to treat cardiogenic shock in the ED I will generally use adrenaline as my first line agent as balancing dobutamine and noradrenaline is going to be too complicated and no one has ever convinced me that there is any real advantage in doing so anyway. I was gratified at SMACC to hear John Myburgh’s lecture on catecholamines which I choose to interpret as supporting my approach (listen to the lecture and then to Scott Weingart defending dobutamine here <http://emcrit.org/wee/myburgh-on-catecholamines/> at emcrit.org and decide for yourself)
You decide to try some push-dose adrenaline and after 50mcg this is her ECG:
The BP is now 110/50 and the patient is looking less pale. A fluid bolus is started and aspirin given.
Without further adrenaline, 10 minutes later it looks like this:
Is this still a STEMI ECG?
The first of these two is still pretty ugly with very widespread ST depression,suggesting widespread subendocardial ischaemia. The elevation in avR goes with that (here is a nice article from Dr Smith’s ECG Blog on the topic http://hqmeded-ecg.blogspot.com.au/2011/04/st-elevation-in-avr-with-widespread-st.html) . The elevation in aVL looks very significant but there is no contiguous lead with elevation. With primary PCI available this would still be a no-brainer but does this justify fibrinolytics with all their attendant risks? The second ECG 15 mintues later looks better still but the elevation in aVL persists.
Meanwhile the patient goes through the CT for a look at the head. Here is a slice:
There is no bleed (on this or any other slice) but the VP shunt is a surprise. The patient says it was placed years ago but she can’t tell you what for.
How does prior neurosurgery fit in to the cardiac thrombolysis decision-making pathway? Or a bump on the head from fainting at triage for that matter?
Neurosurgery is not listed as a specific contraindication to cardiac thrombolysis although the relative contraindications “or known intracranial abnormality not covered in absolute contraindications” could be seen to encompass it. “Major surgery in the last 3 weeks” clearly does not apply in this case.
Cardiac thrombolysis after head injury is very difficult to find data on. A medline search using, for example, the terms thrombolysis OR thrombolytic AND head injury returns no results. The Australian Therapeutic Guidelines publication (1) lists “significant head or facial trauma within the last 3 weeks” as a contraindication but does not specify what constitutes significant head or facial trauma.
Both these factors should only be considered relative contraindications to lysis and should be weighed against the evidence that a true STEMI is occurring and the likely consequences of that STEMI.
While you are surfing pubmed trying to find data on thrombolysis after head strike your patient has a VF arrest. After a short resuscitation and some amiodarone loading her blood pressure is 80/40 despite adrenaline infusion and her ECG now looks like this:
Which brings us to our next question. Is fibrinolysis really good in STEMI complicated by cardiogenic shock or is it really useless?
This is harder to answer than you might think. We do know (from the many many patients that were studied in RCTs of cardiac thrombolysis leading up to its adoption as standard of care in the 1990s) that the bigger and nastier the infarct the more benefit is gained by fibrinolysis.
However, thrombolysis in cardiogenic shock has not been examined specifically in RCTs. A 1994 review (2) of the RCTs of cardiac thrombolysis up to that date found that most trials excluded cardiogenic shock patients and that of those that included them only 3 offered any subgroup data on their outcomes (one of these was a comparison of tPA and streptokinase and so offered no useful information for this case) and 2 more reported on outcomes of all hypotensive patients without separating out cardiogenic shock cases from other hypotensive patients (for example complete heart block with bradycardia or right ventricular infarction likely to respond to simple volume expansion). Data from these studies is conflicting- the two studies reporting on cardiogenic shock showed no benefit from thrombolysis, those reporting on all hypotensive patients showed enormous benefits (more than with any other subgroup of AMI patient). A metanalysis of all cardiac thrombolysis RCTs found strongly in favour of thrombolysis in hypotensive STEMI patients.(3)
Since the 1990s the papers offering any information on the role of thrombolysis in cardiogenic shock are limited to comparisons of thrombolysis, intra-aortic ballooin pump, both or neither. Unfortunately these studies are not randomized and are so confounded as to be unable to offer anything but misleading information on the topic.(4,5)
When weighing all this up it is very important to remember that the mortality of cardiogenic shock without reperfusion is 70-100%. It is hard to get deader than dead so if you are not within striking distance of a primary PCI service my recommendation would be to use thrombolysis in a cardiogenic shock STEMI patient as part of a package of care that might also include fluid loading, vasopressor/inotrope support, and early transfer for PCI/CABG and to not be swayed by relative contraindications.
Once upon a time that package of care might also have included the technophysiologically elegant IABP but no longer.
- Group CE. ST elevation myocardial infarction : reperfusion therapy. eTG Complete. Melbourne: Therapeutic Guidelines Limited; 2012.
- Col NF, Gurwitz JH, Alpert JS, Goldberg RJ. Frequency of inclusion of patients with cardiogenic shock in trials of thrombolytic therapy. The American Journal Of Cardiology. 1994;73(2):149-57.
- Indications for fibrinolytic therapy in suspected acute myocardial infarction: collaborative overview of early mortality and major morbidity results from all randomised trials of more than 1000 patients. Fibrinolytic Therapy Trialists’ (FTT) Collaborative Group. Lancet. 1994;343(8893):311-22.
- Drakos SG, Anastasiou-Nana MI, Terrovitis JV, Tsagalou EP, Kanakakis J, Ntalianis A, et al. Intra-aortic balloon counterpulsation and delayed revascularization for myocardial infarction and shock in the absence of primary angioplasty: a treatment strategy with or without thrombolysis? Coronary Artery Disease. 2008;19(7):521-6.
- Sanborn TA, Sleeper LA, Bates ER, Jacobs AK, Boland J, French JK, et al. Impact of thrombolysis, intra-aortic balloon pump counterpulsation, and their combination in cardiogenic shock complicating acute myocardial infarction: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK? Journal Of The American College Of Cardiology. 2000;36(3 Suppl A):1123-9.