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.
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: http://circ.ahajournals.org/content/106/19/2514.full.pdf+html (AHA consensus paper on Brugada diagnostic criteria)