![Cardiac Action Potential
• Five phases in cardiac muscle
• RMP of mucle cell is -90mV.
• Phase 0 – Rapid depolarisation ; Na+ channel
are triggered to open, transient inward
current resulting in depolarisation
• Phase 1 - Early rapid repolariastion .
Na+ channels are inactivated ; fast and slow
potassium channels are activated [Ito]](data:image/gif;base64,R0lGODlhAQABAIAAAAAAAP///yH5BAEAAAAALAAAAAABAAEAAAIBRAA7)
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Mechanism of arrythmia.pptx
- 1. SEMINAR
- 2. Cardiac Action Potential • Five phases in cardiac muscle • RMP of mucle cell is -90mV. • Phase 0 – Rapid depolarisation ; Na+ channel are triggered to open, transient inward current resulting in depolarisation • Phase 1 - Early rapid repolariastion . Na+ channels are inactivated ; fast and slow potassium channels are activated [Ito]
- 3. • Phase 2 – plateau phase calcium influx against potassium efflux. • Phase 3 – Rapid repolarisation ; result from inactivation of inward calcium channel and activation of delayed rectified potassium channels. • Phase 4 – Resting membrane potential
- 5. PACEMAKER POTENTIAL • 3 phases • Resting membrane potential -50 to- 60 mv
- 7. Action potentials recorded from different tissues in the heart
- 9. MECHANISM OF ARRHYTHMOGENESIS MECHANISM DISORDERS OF IMPULSE FORMATION TRIGGERED ACTIVITY DAD EAD ABNORMAL AUTOMATICITY BOTH COMBINED DISORDERS OF IMPULSE CONDUCTION BLOCK TACHYCARDIA DEPENDENT DECELERATION DEPENDENT RENTRY ANATOMICAL FUNCTIONAL
- 10. Normal Automaticity Membrane clock • HCN channels • If –funny current • Conduct both Na and K inward • Activated by repolarisation Calcium clock • Periodic sub membrane increases in Ca2+. • Activates NCX channel – inward current. • Intra cellular signals thus converted to membrane voltage signals
- 11. DISORDERS OF IMPULSE FORMATION • Inappropriate discharge rate of the normal pacemaker (too fast or too slow for physiologic needs of patient), • Discharge of an ectopic pacemaker either as escape rhythm or accelerated automaticity. • Pacemaker discharges from ectopic sites usually kept from reaching the level of threshold potential because of overdrive suppression by the more rapidly firing sinus node .
- 12. ABNORMAL AUTOMATICITY • Abnormal automaticity can arise from cells that have reduced maximum diastolic potentials [positive to −50 mV]. • Rhythms resulting from abnormal automaticity – slow atrial, junctional, or ventricular escape rhythms; – certain types of atrial tachycardias (ATs), accelerated junctional rhythms.
- 13. TRIGGERED ACTIVITY • Triggered activity is initiated by afterdepolarizations, which are depolarizing oscillations in membrane voltage. • termed Early afterdepolarizations [EAD]when they arise before full repolarization of the AP ; • Delayed afterdepolarizations (DAD) when they occur after completion of repolarization (phase 4).
- 14. Delayed Afterdepolarizations • DADs result from the activation of a calcium-sensitive inward current due to aberrant diastolic Ca2+ release. • The duration and amplitude of Ca2+ efflux from the SR are tightly controlled by the gating of RyR2 channels. – Increased catecholamine release due to adrenergic stimulation. – Reduced FKBP-12.6 [regulatory protein ] binding has been implicated in cardiac arrhythmogenesis associated with heart failure. – The IP3 receptor (IP3R) is another Ca2+-release channel in cardiomyocytes are upregulated in heart failure and AF.
- 16. • Calmodulin kinase type-II (CaMKII) is a key player in promoting DADs, via phosphorylation of multiple membrane proteins. • Intracellular Na+ is exchanged for Ca2+, drugs that reduce INa suppress Na+ load and, indirectly, Ca2+ load, NCX current, and DADs. • Overdrive pacing increase the amplitude and shorten the cycle length of DADs after cessation of pacing (overdrive acceleration), because they enhance cellular Ca2+ loading. • Hence DAD-triggered activity may not be suppressed easily or indeed may be precipitated by rapid rates.
- 17. Early Afterdepolarizations • Conditions that cause delayed repolarisation. • Seen in the acquired and congenital forms of LQTS. • When the AP is excessively prolonged, the membrane potential remains at levels that allow recovery of enough steady-state Ca2+ (particularly during phase 2) or Na+ (during phase 3) current to depolarize the cell, producing an EAD. • Can initiate tachyarrhythmias either by the induction of unstable transmural reentry or via repetitive rapid EADs.
- 18. • Sympathetic stimulation can increase EAD amplitude to provoke ventricular tachyarrhythmias. • Acquired LQTS and torsades de pointes from class III antiarrhythmic and non-cardiac agents like cisapride, erythromycin, moxifloxacin, and psychoactive drugs, likely mediated by EADs. • EAD-associated APD prolongation increases Ca2+ influx and produces Ca2+ loading in the SR, thus increasing the likelihood of DAD generation. Thus, EADs and DADs may occur together with common initiating conditions
- 19. Disorders of Impulse Conduction • Conduction delay and block can result in bradyarrhythmias or tachyarrhythmias. • Bradyarrhythmias occur when the propagating impulse is blocked and is followed by asystole or a slower escape rhythm; • Tachyarrhythmias occur when the delay and block produce reentrant excitation .
- 20. • DECELERATION-DEPENDENT BLOCK – Reduced spontaneous diastolic depolarisation. – However, excitability and the speed of impulse propagation increase as the membrane depolarizes • TACHYCARDIA-DEPENDENT BLOCK – Impulses are blocked at rapid rates or short cycle lengths – Occur as a result of incomplete recovery of refractoriness – Post repolarization refractoriness. – functional bundle branch block.
- 21. REENTRY • various names— reentry, reentrant excitation, circus movement, reciprocal or echo beat, and reciprocating tachycardia.
- 22. Anatomical Reentry • Discrete anatomical barrier separating alternate conduction pathways. • In many, AV node behaves as if there are two functionally independent pathways • Typically, the pathway with the faster conduction has a longer RP.
- 23. • Alternative conducting pathways separated longitudinally but with connections at each end; • Different Refractory Periods of the alternate pathways . • The maintenance of anatomic reentry requires the existence of an “excitable gap,” • Anatomic reentry occurs in patients with Wolff- Parkinson-White (WPW) syndrome, in AV nodal reentry, in some atrial flutters, and some VTs.
- 25. Functional Reentry • Lacks confining anatomic boundaries • Functionally different electrophysiologic properties caused by local differences in transmembrane AP. • Failing heart or infarct border zone or acutely ischemic myocardium. • Spiral wave rotor
- 27. Specific Arrhythmias Atrial Flutter • Reentry • Counterclockwise in a caudocranial direction in the interatrial septum and in a craniocaudal direction in the right atrial free wall
- 28. Atrial Fibrillation • Multiple disorganized reentrant waves • EPS shown that both reentrant and non reentrant mechanisms (automaticity and triggered activity) may underlie initiation of AF from the PVs. • Familial AF - Mutations in subunits of the delayed rectifier potassium channel and the voltage-gated sodium channel
- 29. Brugada Syndrome • Congenital sudden death syndrome • m/c genetic abnormalities - LOF in SCN5A . • Brugada syndrome–associated gene defects cause a reduction or loss of sodium or calcium current in combination with altered functional properties of voltage-gated sodium channels
- 30. Catecholaminergic Polymorphic Ventricular Tachycardia • Inherited arrhythmogenic syndrome characterized by stress-induced, adrenergically mediated polymorphic VT occurring in structurally normal hearts . • Spontaneous diastolic Ca2+ leak from the SR via RyR2, leading to intracellular Ca2+ waves and triggered activity . • RyR2 mutations - 95% of cases. • Mutations in genes encoding calsequestrin, calmodulin, and triadin
- 31. Arrhythmogenic Right Ventricular Cardiomyopathy • Inherited myopathy , sustained monomorphic VT and sudden death • Mutations in the desmosomal proteins, intercalated disk proteins, nuclear envelope proteins, along with desmin, titin, phospholamban, channel proteins, and growth factors • 20% to 45% mutations - gene encoding plakophilin 2 . – Loss of PKP2 expression reduces the voltage-gated sodium current and connexin 43 expression at the intercalated disc and thus results in slowed AP propagation.
- 33. THANK YOU
- 41. • DECREMENTAL CONDUCTION – Phenomenon where an impulse loses activation effectiveness as it spreads anterogradely. – Seen in the AV node, in relation to the relatively small amplitude of phase 0 Ca2+ current in slow channel tissue, especially at fast rates and in the presence of disease. – Associated with increased risk of conduction block.