Channelopathies Flashcards
What is the normal k range in body
3.6-5.2 mmol/l
How are abnormal genes linked to cardiac arrhythmias and channelopathies
They encode for ion channels so if mutated this affect heart by arrhythmias or channelopathies
What is qt
Time between beginning of dep phase 1 to phase 3 repolarisation
Which 2 channel mutations are responsible for long qt syndrome
Mutation in kcnq1 k channel for repolarisation
Mutation in scn5a Na channel for depolarisation ie doesn’t inactivate properly
What abnormal impulse formation is seen with long qt syndrome
Early after depolarisation
What type of ventricular tachycardia occurs with lqt due to early after depolarisation
Torsades de pointes (high peaks on ecg)
Why does someone collapse after untreated lqt
Because ventricular tachycardia due to ead means lack of edv ventricles can’t fill fast so small cardiac output
What is it called when heart ends up having no rhythm due to ventricular tachycardia/torsades de pointes
Ventricular fibrillation (uncontrolled firing) causes death
When does lqt attacks usually occur
During exercise when increased heart rate
Explain the steps of early after depolarisation
Slow repolarisation phase 1 and 3 due to k channel abnormalities causes increased ap time and chance of depolarisation again
K can’t leave the cell fast enough so there is inward current potential via Na channels like scn5a (which can also be mutated)
These lead to further depolarisation and vt eventually vf
What is the extra qrs in ead called
R on T event (dep on rep event)
How is brugada different to lqt
Ventricular tachycardia occurs at rest
What ion channelopathies cause brugada
Mainly abnormality in scn5a Na channel
How is brugada detected on ecg
Coved ST elevated segment
Which gender is brugada seen in usually
Males - 75%
