Let's start with a problem representation:

A 20 y/o F presents w/ PMH of sz d/o on keppra s/p "seizure like" episode ▶️cardiac arrest with bystander CPR and developed ROSC w/ EMS found to have a tongue laceration on exam w/ labs ▶️ hypoK and ⏫ qTC & Torsades on event monitor
Cardiac arrest in a 20 y/o, drugs vs structural heart disease vs arrhythmias (congenital long QT, electrolytes)

"Ts” & “Hs” causes (hypoxia, hypokalaemia/hyperkalaemia, hypothermia/hyperthermia, hypovolaemia, tension pneumothorax, tamponade, thrombosis, toxins)
Also want to know what was she doing prior to arrest. IF she was working out think HOCM

Important to know the initial rhythm, VFib/VTach vs PEA/asystole. It is not only prognostic sign but treatments change

Fam hx important in 20 year olds - not 80 year olds
Channelopathies could certainly do it --> seizure + long QT

Long QT is classically associated with sudden startles

Seizure or syncope...that's the big question here

but channelopathies can be subcategorized by the type of channel is involved.
the K+ channels are more arrhythmogenic. Na+ channels cause more seizure (e.g. Dravet syndrome)

Post arrest need to start hypothermia/normothermia protocol is the most important 34-36C is the target

SUDEPS: It’s the leading cause of epilepsy related death.
SUDEPS: Sudden unexpected death in epilepsy is a sudden unexpected mortality in otherwise healthy patients w/ epilepsy w/or w/or evidence of a seizure & excluding documented status, in which postmortem examination does not reveal a cause of death. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5034868/
Postcardiac arrest myocardial dysfunction

Although the heart initially becomes hyperkinetic, likely due to circulating catecholamines, global hypokinesis often follows

Usually resolves within 72 hours

Systemic ischaemia/reperfusion response...
U can see ekg changes with cooling and also electrolyte abnormalities - most significantly hypokalemia

intracellular shift if she is being cooled

Prolonged QTC? sorry correct the QT** Bazet is less than ideal.

A #MedTweetorial by @DoctorVig https://twitter.com/DoctorVig/status/1265741266060546048
I wonder if it's 1) Seizure causing cardiac arrest 2) cardiac causing seizure-like episodes 3) underlying condition causing both seizure and cardiac or 4) seizure unrelated to current

if you have difficulty raising K, then empiric Mg will often help despite a normal Mg level
long qtc = hypok, hypoCa, Hypomagnesemia

The anion gap is likely transient secondary to the seizure and elevated lactic

Hyperventilation ▶️ transient hypoCa as the Protons jump off alb to keep pH normal and the subsequent negative charge on the albumin grabs the Ca from serum
The impact of hypothermia on serum potassium concentration: A systematic review. https://www.resuscitationjournal.com/article/S0300-9572(17)30284-8/fulltext

was checked for Russell sign?
Huge fan of albumin in all pts atleast so I know what to do with their possible gap or non-gap.

Low albumin in a pt can "mask" presence of unmeasured organic acids

usually QT prolonging meds are SSRI, antipsychotic, antifungals, floroquinolones, macrolides etc
People with LQTS often show a prolonged Q-T interval during exercise, intense emotion (such as fright, anger, or pain), or as a reaction to a loud or startling noise.

People with LQTS have usually had at least one episode of fainting by the time they are 10 years old.
There are tons of drugs inhibit the hERG channel —> drug-induced/acquired long QTS

in congenital long QT, give BB paradoxically as
long QT can be brought out by exercise

Just please make sure when your ECG says long qt, please calculate it on your own https://www.mdcalc.com/corrected-qt-interval-qtc
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