arrythmia Flashcards
what is the difference between the action potential of SA/AV node compared to myocytes
The difference between the action potential in an SA/AV node and in a cardiac muscle is that there is no resting potential; In the SA node, the depolarisation (phase 0) is driven by influx of Ca+ ions instead of Na+ ions in cardiac muscle
There is no plateau phase in SA action potential bc we need the SA node to fire repetitively and very quickly
In the SA / AV node there is a ifunnychannel which is turned on by hyperpolarization & turned off by depolarisation
describe the AP of ventricular / atria myocytes
- Phase 0 = rapid depolarisation due to the opening of Na+ channels, there influx of Na+ ions into the cardiac muscle
- Phase 1 = peak/ partial repolarization, Na+ channel becomes inactivated, and K+ channel opens to allows efflux of K+ out of the muscles
- Phase 2 = plateau phase resulting from the opening of L type Ca+ channels, causing influx of Ca+ into the cells which counter balance out the efflux of K+ ions
- Phase 3 = repolarization occurs, L type calcium channel inactivate, and K+ channel increases their permeability, meaning that we get more efflux of K+ ions out of the cells
- Phase 4 = resting state, no pacemaker potential bc there is no ifunny Ca2+ channel.
describe the AP of the SA/AV node
Phase 0: Slow depolarization (upstroke) due to inward Ca2+ current
No Phase 1 or Phase 2: as no Na* current is activated and no plateau potential is present
Phase 3: Repolarization - inward Caz+ current is rapidly counterbalanced by strong outward delayed rectifier K+ currents
Phase 4: The ‘pacemaker potential’ - slow spontaneous depolarization is due to activation of the hyperpolarization-activated- cAMP-dependent ‘funny current’ (1)-Na/K- dependent) and opening of T-type (transient) Ca2+ channels
Arrhythmia may arise bc of what 3 major underlying mechanisms
Abnormal (ectopic) pacemaker activity = another parts of the heart takes over as the pacemaker, causing single abnormal heartbeats
Impulse entry= this happens when impulses propagate by more than one pathway and at different conduction speed in different region of the heart tissue (e.g. an area that is damaged by heart attack, can alters its conduction speed) (most common type of arrhythmia)
Heart block = this is when the AV node fails to conduct an impulses generated from the SA node, this can be cause damage by infarction. If the block is partial then only 2nd or 3rd impulses is transmitted (2:1 or 3:1 block) - btw the atria beat 2-3 times as fast as the ventricle
explain what is AF
where you have a irregular rapid beat due to one area in the heart that is acting as the pacemaker, causing the heart to beat irregularly. If AF continuous for a long period of time it means the heart is not pumping blood properly, so can cause stagnation of blood in the heart, leading to blood clots. Blood clots can reach the systemic circulation and get stuck in other organs like the brain and the lungs
what are the two strategies are available for the long-term management of AF
rate and rhythm control
what is the difference between rate and rhythm control in the management of AF?
rate control: aims to reduce heart rate at rest and during exercise, but the patient remains in AF. β-Blockers (p. 486) or calcium antagonists (verapamil, diltiazem, p. 489) are the preferred treatment except in predominantly sedentary people where digoxin (p. 485) is used
Rhythm control: is generally appropriate in patients who are <65 years of age, highly symptomatic, patients with heart failure and individuals with recent-onset AF Conversion to sinus rhythm is achieved by electrical DC cardioversion and then administration of β-blockers to suppress the arrhythmia
why is anticoagulation important in patient with arrythmia?
AF is associated with an increased risk of thromboembolism, and anticoagulation should be given for at least 3 weeks before (with the exception of those who require emergency cardioversion or new-onset AF <48 h duration) and 4 weeks after cardioversion.
what two assessment is used to determine is a patient requires anticoagulant?
A CHA2 DS2-VASc score of 2 requires oral anticoagulation and a score of 1 merits consideration for oral anticoagulation or aspirin. A score of 0 should not require any antithrombotic prophylaxis
The potential benefits of oral anticoagulation must be balanced against the risk of haemorrhage. The HAS-BLED score is used. A score of ≥3 indicates a high risk of major bleeding
what class of antiarrhythmics is amiodarone & explain the MAO
Class III
if we blocks K+ channels, we will increases the time it takes for repolarisation to occurs, and this will increases the refractory period thereby prolonging the action potential. The longer the refractory period, the frequency of AP fired is reduced. This is useful bc the chance of a delayed AP being able to re excite the heart as it emerges from damaged tissue via re-entry mechanism is reduced. It is used to treat:
