Is this Brugada syndrome?

This is a case I managed recently. I am left with a number of questions, to which I am struggling to find the answers. I’d love to hear any comments you have on the case and my discussion.

The Case:

47 year old man, out of hospital cardiac arrest. Bystander CPR a few minutes after collapse. Asystole on initial paramedic assessment. More CPR and 1mg of adrenaline evoked VT/VF. Single 200J biphasic shock gave ROSC ~25 minutes post collapse. GCS remained 3. Intubated at scene and transported to ED requiring further adrenaline boluses to maintain a recordable BP.

This is his 12 lead ECG on arrival:

This ECG shows a pattern which meets the criteria for a Type 2 Brugada ECG, as tabled below, in addition to a borderline 1st degree AV block (also present in the majority of Brugada ECGs). [There is also some lateral ST depression here, but I am unclear from the literature as to whether this means true Brugada is less likely and ischaemia is more so]:

This ECG was dismissed by some involved as merely a sign of “irritable myocardium” – what do you think?

The interventional cardiologist was consulted for consideration of primary PCI in view of the possibility of STEMI leading to VF arrest. The decision was made to delay until neurological status was clear, especially given that bedside Echo showed no regional wall motion abnormalities and a structurally normal heart beating strongly.

ABG showed pH of 6.61, with a Lactate of 21, Na 127 and Cl 93, BSL 5.8. For what it is worth, initial troponin was <0.01. Meanwhile the patient was plumbed and cooled.

Some more history came to light from collateral:

Previous craniectomy for traumatic ICH with subsequent temporal lobe epilepsy. On carbemazepine. Seizure free for years. No history of IHD. Smoker. T2DM (“diet controlled”). ETOH use. Family history of sudden death explained as heart attacks (SCD?). His acid base status rapidly improved. He began to cough and was paralysed. Pupils remained fixed. CTB showed old frontoparietal gliosis and old craniectomy with no acute pathology. He was transferred to ICU for the requisite therapeutic hypothermia.

I am left with some questions:

  • Is this really Brugada Syndrome?
  • Was the precipitating event a seizure?
  • If this is sudden unexpected death in epilepsy (SUDEP), what are the mechanisms of SUDEP? Could Brugada syndrome be implicated?
  • What is the link between seizures and ventricular arrhythmias?
  • What influence (if any) does the interplay of mild hyponatraemia, a Na-channel blocker (carbemazepine) and a possible Na-channelopathy have?

Over the next few days, I will try and answer these questions, but please comment if you can shed any light on them with me!

Reference: (AHA consensus paper on Brugada diagnostic criteria)


About dreapadoir

Emergency Physician, author of Emergency Medicine blog, photographer at
This entry was posted in Cases, ECGs, Education, Medical Musings. Bookmark the permalink.

14 Responses to Is this Brugada syndrome?

  1. Andy Buck says:

    Great case. Always hard to interpret post reversion ECG’s. My first thought was “did he have an old ECG for comparison?” and “what did the angio show?”, but reading on, it seems a sensible resource-sparing decision was made to not cath.
    Did the ECG changes persist in the following days?
    I recently had a case of asystolic arrest in a young (early 40’s) “known epileptic”. Made me wonder if he had a true seizure, went hypoxic (eg from positional asphyxia) and then went into asystole, or if he had a primary cardiac event (no ROSC so we never found out), or if his previous “seizures” had been cardiac events.
    Re: Na+ blocker and Na+ channelopathy, according to it’s on the preferably avoid list, although the references are a but oblique…
    Be interested to hear what your findings are.

  2. Andy Buck says:

    Gee that is hot! I’ll wait patiently for the outcome.

  3. dreapadoir says:

    A few (eminent) comments appearing on Twitter in favour of CAD (horse) over Brugada (zebra – or is it?)
    Features supportive of CAD as the cause are:
    It is (we think) a more common cause of SCD.
    There are those lateral ST depressions on the ECG.
    Features against CAD:
    No akinesis/hypokinesis on Echo.
    No history of IHD (although of course that means little).
    The Brugada type 2 morphology
    Story was suggestive of primary syncope vs. chest pain then syncope (some details were slightly altered in my sketch of the history of presenting illness above to protect the patient – small place, here!)

  4. bortolo martini says:

    this ecg in a patient resuscitated from a cardiac arrest is totally aspecific.
    PH was 6.6.
    The patient had initially asystole!! Why not consider ictal syncope??

    • dreapadoir says:

      Thanks for your comment.
      In response: The assumption that the ECG in post arrest patients is non-specific is one of the main reasons for this post. I am unconvinced of the truth of this statement. I can understand that there are of course going to be marked changes after cardiac arrest for a variety of reaons, but to dismiss the utility of the ECG entirely in this context seems a little glib to me – surely sometimes there must be clues? It is a bit like the assumption that once there is a LBBB rhythm or a paced rhythm on an ECG, I notice that many people deem that no further information can be gleaned from it as regards ischaemia/ST elevation, etc. There are of course a number of criteria (such as Sgarbossa, Smith, etc.) which refute this dismissal.
      Having said all of this, I can find little evidence in the literature to either support or refute the utility of the ECG in this context. It is worth noting that a Brugada type pattern can be “unmasked” as it were by patient factors such as fever, drugs (Na-channel blockers, probably including carbemazepine) and indeed as Dr Steve Smith states – it is frequently mistaken for STEMI []
      So, when some cardiologists are using the post-arrest ECG to decide whether or not a patient should go for a primary PCI, and there is in practice frequent confusion between the diagnosis of STEMI and Brugada based on ECG findings, and in fact there is widespread recognition that Brugada syndrome is responsible for as much as “4 to 12 % of unexpected sudden deaths, and for up to 50% of all sudden death in patients with an apparently normal heart” according to the website of the Brugada’s themselves [] I really don’t see how one can dismiss the ECG as merely being non-specific and due to “irritable myocardium,” a phrase frequently bandied about in these situations.
      I accept that profound acidosis as here could very well influence the ECG findings, however the acid-base disturbances corrected rapidly with good resuscitation, and the ECG remined abnormal in V1 and V2. I also accept that the profound acidosis and very high lactate support the diagnosis of a seizure being the precipitating event in this case, as it is not uncommon to see numbers like this in the post-ictal phase that rapidly correct even without intervention.
      As for the presence of asystole – it is the final common pathway for all dangerous arrhythmias, and does not exclude VF/VT as the primary rhythm disturbance. VF often degenerates to asystole by the time of ambulance attendance!

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  7. anandansps says:

    2 things are high on the differentials
    1) sudep- sudden unexpected death in epilepsy syndrome
    2) brugada- vf- asystole

    The acidosis and its rapid correction signifies that it is probably due Cardiac arrest and resuscitation. CAD is lower down on my list.

    • dreapadoir says:

      Many thanks for your comment. Great thoughts!

      SUDEP is certainly in the mix – in fact I wonder could it be that one of the mechanisms in SUDEP could be Brugada? In terms of autopsy findings in the heart after SUDEP, it has been found that “Nonfatal pathologic findings, including fibrosis of the conductive system, have been reported in 33-40% of patients” however this is a non-specific finding.

      I quote from emedicine on the subject:
      “Cardiac arrhythmias also may play an important role as an underlying mechanism of SUDEP. Fatal arrhythmias can occur during the ictal attack and interictally.

      Erickson systematically studied ictal ECG changes for the first time.[16] He reported tachycardia, cardiac arrhythmia, and T-wave flattening secondary to a right temporal lobe seizure. Initial bradycardia, followed by tachycardia, was documented in as many as 64% of petit mal and 100% of generalized tonic-clonic seizure attacks.

      Subsequent recent studies, documenting simultaneous electroencephalograms (EEGs) and echocardiograms (ECG), reported tachycardia in 74-92% of complex partial seizures. Persistent bradycardia was less common, being reported in 3-7% of complex partial seizures.

      Ictal cardiac rhythm and conduction abnormalities have been reported in 5-42% of patients with partial seizures.

      Arrhythmias preceding SUDEP have been postulated to be the underlying cause of death. Lathers documented the synchronization of ictal and interictal spikes with cardiac sympathetic activity”

      I am not so sure that the acidosis can only be directly due to the cardiac arrest. These numbers are frequently seen both in cardiac arrest and in post ictal periods after prolonged seizure. I agree that here CAD is lower down the list!

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