Pathophysiology of Dysrhythmias Lecture Notes PDF

Pathophysiology of Dysrhythmias Dr Amanda Fleet Overview • Clinical Classification • Underlying physiology – Heart block – Ectopic pacemaker activity – Delayed after-depolarisation – Circus re-entry • Treatment rationale (details of the drugs used will be covered by Prof Guild) Underlying Physi...

Pathophysiology of Dysrhythmias Dr Amanda Fleet Overview • Clinical Classification • Underlying physiology – Heart block – Ectopic pacemaker activity – Delayed after-depolarisation – Circus re-entry • Treatment rationale (details of the drugs used will be covered by Prof Guild) Underlying Physiology Dysrhythmia (arrhythmia) describes conditions where the co-ordinated sequence of electrical activity in the heart is disrupted This could be due to: • Changes in the heart cells • Changes in the conduction of the impulse through the heart • Combinations of these Classification Dysrhythmias (arrhythmias) are broadly classified as: • Atrial (supraventricular) • Junctional (associated with the AV node) • Ventricular • Tachycardias or bradycardias Site of the origin of the abnormality Dysrhythmias (arrhythmias) Common types of tachyarrhythmia: • Atrial fibrillation • Supraventricular tachycardia (SVT) Ectopic beats Sustained ventricular arrhythmias more serious (VT and VF) Atrial fibrillation SVT Ventricular ectopic General Classification Dysrhythmias (arrhythmias) arise from four broad categories of event: • Heart block • Ectopic pacemaker activity • Delayed after-depolarisations • Circus re-entry Basic Physiology - Conduction Basic Physiology – inherent rates • SAN – “pacemaker” as has fastest inherent rate: _____bpm • AVN – can take over if SAN fails. Its inherent rate is: _____bpm • Bundle of His: _____bpm • Purkinje fibres: _____bpm Heart Block • Results from damage (usually ischaemia) to a part of the conducting system • Often affects AVN • AVN is the only path for electrical conduction between atria and ventricles • Impulses can be slowed (but make it through), partially blocked (some make it through) or completely blocked (none make it through) First Degree Heart Block • AV node is only slightly affected and conduction is slowed • Abnormally long P-R interval • Otherwise every atrial depolarisation (P wave) is passed to the ventricles (QRS) [reminder…] Normal P-R interval represents: Normal length = _____ms Second Degree Heart Block • More serious damage to the AVN leads to partial AV block, where some, but not all of the atrial depolarisations (P waves) lead to ventricular depolarisation (QRS) • The diagram here shows three P waves to each QRS complex Second degree block - subtypes Mobitz (type 2) Most beats are conducted with a constant P-R interval, but occasionally there is an atrial depolarisation without a ventricular depolarisation Four normal P-QRS-T P wave with no QRS-T Three normal P-QRS-T Second degree block - subtypes 2:1 or 3:1 • This describes the ratio of P waves to QRS complexes • A 2:1 block has two P waves for each QRS • A 3:1 block has three P waves for each QRS Second degree block - subtypes Wenckebach Progressive lengthening of P-R interval until a P wave fails to produce a QRS complex The P-R interval then shortens and normal conduction occurs before the P-R interval starts to lengthen again In the image below, look at the P-R interval – it is getting longer until the 4th P wave which is then not followed by a QRS complex Third Degree Heart Block • The AV node is completely blocked and no electrical activity from the atria progresses to the ventricles • The atria depolarise (and beat) at their inherent rate • The ventricles depolarise (and beat) at pace set by Purkinje fibres Reminder – basic physiology The spontaneous electrical discharge of the SAN is from the combined effect of: • Decrease in K+ outflow • “funny” Na+ current • Slow inward Ca2+ current Ectopic Pacemakers Other areas of the heart can develop pacemaker activity: • If damaged (ischaemia, CHD, rheumatic heart disease, hypertension etc.) • Increased sympathetic activity (stress, exercise etc.) • Increased sensitivity to catecholamines (GA, caffeine, hyperthyroidism etc.) • Cardiac glycoside toxicity Ectopic Pacemakers • Ischaemic damage can cause cells to become leaky to Na+ (and develop a “funny” current) • Catecholamines, acting on b1 receptors, increase the rate of depolarisation and can cause pacemaker activity to arise from cells which are normally quiescent Reminder of basic physiology • Phase 0 – rapid depolarisation (Na+ open) • Phase 1 – partial repolarisation (Na+ close) • Phase 2 – plateau (inward Ca2+ current) • Phase 3 – repolarisation (Ca2+ close; K+ open) • Phase 4 – “stable” [pacemaker potential: nodal and conducting tissue only] Early after depolarisation Occur towards end of phase 2 Prolonged QT Triggered by fluctuating increases in Ca2+ permeability Can set off selfsustaining depolarisations Delayed after-depolarisations • Following every AP, some of the Ca2+ entering in phase 2 has to be removed back to ECF • Done via Ca2+/3Na+ exchange • Net influx of + and insignificant depolarisation (normally) • If [Ca2+]i rises (cardiac glycosides, increased HR, high levels of NA or ADR), the afterdepolarisations can get increasingly larger • Can become self-perpetuating (triggering AP) Delayed after-depolarisations Delayed after-depolarisations • Delayed repolarisation (prolonged QT interval) increases [Ca2+]i • Leads to increased after-depolarisations and can lead to dangerous ventricular dysrhythmias Circus Re-entry Movements (CRM) • This describes when a electrical impulse can re-stimulate (re-enter) a region of the heart after its refractory period has passed • Comes from an unusual direction and before the tissue would have been re-stimulated by the next normal impulse from the SAN Circus Re-Entry Movements Normal: • The impulse originates in the SAN and is transmitted to the branches • Each branch depolarises • When the impulses meet (at 3), there is extinction by collision Two branches of conducting fibres connected to a chain of contractile fibres and forming a loop Circus Re-Entry Movements This impulse dies out in this area. By the time impulse B arrives, the grey area is repolarised B A B The grey area is an area of damage with no full conduction in the orthodromic direction – cells unable to generate sufficient current to maintain the depolarisation to reach threshold at A The bigger current generation from the tissue on the other side of the block has enough strength to be transmitted through Sinus impulse extinguished Circus Re-Entry Movements • The circuits are short in length and so the frequency of impulses generated is high • Either a unidirectional block (as in the diagram) or a transient block – one that allows some impulses but not all through – can generate these circus re-entries Wolf-Parkinson-White Syndrome • Additional or “accessory” electrical connection between atria and ventricles • Usually on the left; no AV node in the accessory bundle, so no delay • Depolarisation reaches the ventricle early • PR interval is short; QRS has early upstroke (delta wave) • Second part of QRS normal as conduction via AVN “catches up” • Can cause paroxysmal tachycardia and re-entry circuit Image taken from: http://bestpractice.bmj.com/best-practice/monograph/400/resources/images/print/1.html Image taken from: http://www.mayoclinic.org/wolff-parkinson-white/enlargeimage2572.html Treatment rationale • Vaughn-Williams Classification • Old system for classifying anti-dysrhythmic drugs • Based on four main categories of mechanisms of action • Some drugs don’t fit the categories • Prof Guild will cover the drugs in more detail Vaughn-Williams Classification • Class I: block fast sodium channels – Class now subdivided in Ia, Ib and Ic • Class II: block b-adrenergic receptors • Class III: prolong the duration of action potential repolarisation • Class IV: block Ca2+ channels • Unclassified: 2 main drugs – adenosine and digoxin - don’t fit any of the other classes