manipulating of the cardiac action potential Flashcards
what is the cardiac action potential
The cardiac action potential (CAP) is a complex electrical impulse that travels through the heart muscle, triggering contraction. It is generated by the sinus node and propagated through the atrioventricular (AV) node, then to the bundle of His and the Purkinje fibers. The CAP consists of three major phases: depolarization, plateau, and repolarization
what is the cardiac action potential governed by
electrolytes
- Na
- Ca
- K
what are the phases of the cardiac action potential
Phase 0: rapid influx of Na+ ions causes rapid depolarisation
Phase 1: potassium channels open and potassium begins to leak out
Phase 2: calcium channels opena and calcium comes in while potassium. is still leaving simultaneously (reason for flattening of curve)
Phase 3: calcium channels close as suddenly as they opened. no more calcium coming in, potassium channels still open
Phase 4: potassium channels close, return to initial state
what is the purpose of the slow rate of repolarisation in the cardiac action potential
ideal to have refractory period in order to slow myocyte contraction down. if contraction happens too quickly there wont be any cardiac output and blood wont be able to circulate
what are pacemaker cells
- have a set rhythm to them
- located in SA node and AV node
- sponteanous depolarisation (initiate electrical impulse that causes heart to contract)
- slow Na channels, then Na channels spontaneously open once an action potential has finished at -65mV. K channels close and influx of Ca speeds approach to threshhold
- once threshold reached, action potential occurs
- have absolute refractory period (period of time where pacemaker cells cannot send any signals)
how is the action potential propogated throughout the heart
- SA node kicks out action potential once hits the threshold of depolarisation (has shortest refractory period)
- signals sent to AV node (delays the signal to ensure atria can empty before contraction stops and ventricles begin contraction)
- autorhythmic cells (can depolarize without influence of neighbouring cells) of the bundle of His and purkinje fibres carry signal to ventricles of heart (purkinje fibres provide rapid propogation throughout rest of heart)
this is what generates an ECG
what are the other roles of calcium in the heart
- released when neurotransmitter noradrenaline interacts with receptors
- influx of calcium also leads to release of calcium from sarcoplasmic reticulum (calcium induced calcium release)
- calcium is important for actin and myosin cross bridges and therefore muscle contraction force
- when you give adrenaline you manipulate calcium and INCREASE rate and force of contractions (because calcium channels open more and for longer = increase force and open earlier and reach threshold potential to reset quicker = HR increases)
what causes dysrythmias
anything changing the action potential propogation through the heart
- structural cardiac disease
- drugs (that effect Ca, Na, K, parasympathetic tone etc.)
- toxins
- metabolic diseases/electrolyte imbalances (i.e. potassium or calcium. eg renal disease) (high concentration of K inside and outside of cell = cant reset = cant contract again)
- systemic disease (sepsis, neoplasia)
- sympathetic tone (increase adrenaline release from pain or fear)
how would you treat sympathetically mediated arrythmia. what occurs in symptathetically mediated arrythmia
adrenoreceptors are in overdrive/being innapropriately stimulated leading to supraventricular tachycardia (normal pqrst wave but very fast and irregular indicating problem with SA node firing too much)
- must decrease SA node tone by blocking adrenaline
treat with beta blockers (antagonsists of adrenaline:
- propranolol
- esmolol
what is parasympathetic mediated arrythmia and how do we treat them
- acetyl choline mediated
- vagal tone inhibits HR (see sudden drop in QRS rhythm)
- blocks adenylyl cyclase and reduces cAMP
- reduces calcium effects
- allows potassium efflux (hyperpolarisation in phase 3)
- reduces automaticity, contraction and slows AV node conduction
- can be usefult in some cases (sleep)
treated by muscarinic agonsists
- atropine (reduces vagal/parasympathetic tone and increases HR)
what is adenosine
a specific receptor
- A1 receptor blocks adenylyl cycalase and increases potassium efflux (slowing HR and making repolarisation harder)
- when given has a negative chronotropic effect and reduced AV node propogation
- short acting (can be used diagnostically)
- treatment for SVT
when would you use a sodium ion channel blocker
if you want to reduce phase 0 rate of depolarisation
- raises depolarisation threshold and slows Na channels
- slows action potential generation
- treatment for VTach (when ventricles take over pacemaker and contract before SA node)
DRUG example: lidocaine
when would you use potassium channel blockers
to slow phase 3 of the action potential and therefore increase refractory period and duration of action potential as repolarisation takes longer to occur
- must be careful as do not want to slow too much (pt dies)
- treats ventricular tachycardia
drug example: amiodarone, sotalol
when would you use calcium channel blockers
- if you want to block voltage-dependent L-type calcium channels in cardiac muscle and vascular smooth muscle
- slows conduction reduces contraction force(makes heart floppier whihc can help if heart is cramped) and causes coronary vasodilation
- treatment for SVT and feline HCM
drug examples; verapamil and diltiazem
describe the classification system of anti-dysrhythmic agents
Vaughan william’s system
Class 1 sodium channel blockers
Class 2 b-adrenoreceptor antagonists
class 3 prolong action potential
class 4 block voltage sensitive calcium channels
