6.1 cardiac arrhythmia drugs Flashcards
what are cardiac arrhythmias?
heart conditions where rate/timing of contractions are insufficient to maintain normal cardiac output
how is - Na - K - Ca distributed across a cell membrane?
Na conc is higher outside the cell
K conc is higher inside the cell
Ca conc higher outside the cell
what is the effect of class 1 drugs on the cardiac action potential? give 2 examples.
how will it affect an ECG?
Na channel blockers e.g Lidocaine and Flecainide
they block sodium channels so the upstroke of the AP is shifted = slower conduction throughout tissue
no effect in normal ECG but In a fast beating or ischaemic ECG, they will increase the length of the QRS complex
what is the effect of class 2 drugs on the cardiac action potential? name an example.
B blockers e.g Bisoprolol
block influx of Ca into myocyte
therefore increase refractory period = takes longer for depolarisation to occur and for another AP to start
what is the effect of class 3 drugs on the cardiac action potential? name two examples.
K channel blockers e.g amiodarone, sotalol
increase the length of the refractory period in AV node and myocyte and the duration of the action potential aka prolong depolarisation and AV conduction
also increase threshold potential
what is the effect of class 4 drugs on the cardiac action potential? give two examples.
Ca channel blockers e.g verapamil, diltiazem
decrease inward Ca currents, resulting in a decrease of spontaneous depolarisation and increased refractory period in the sa NODE
how do Ca channel blockers affect the action potential in the AV node?
they increase the length of the refractory period
also takes longer for the cell to depolarise = slower conduction velocity (due to longer slope)
how does adenosine affect the action potential in the AV node?
adenosine
binds to A1 receptors= activated K currents in AV and DS note = decreases action potential duration and HR = slows AV condctipm
good for convert re entrant supraventricular arrhythmias and diagnosis of coronary artery disease
how do B agonists affect the action potential in the AV node?
they increase the amount of Na and K entering the cell = decreases the length of the funny potential
what is an ectopic focus arrhythmia?
AP rises from sites other than the SA node
what is the difference between delayed after depolarisation and early afterdepolarisation?
delayed after depolarisation
- get depolarisation arising from the resting potential
early after depolarisation
- arises from the plateau which is prolonged
what s a conduction block?
when the impulse is not conducted from the atria to the ventricle
what is re-entry conduction?
1) a pathway is blocked
2) so, impulse from this pathway has to loop round and go backwards
3) so the cells here will be re-excited
what is wolf Parkinson white syndrome?
there is an accessory pathway in the heart called the bundle of Kent in some people, presents in only small populations
get heart arrhythmia’s
why do arrhythmia’s occur?
- automatic or triggered activity
- reentry due to scar, anatomy of AV node slow and fast pathway/ Wolf Parksinson White