ARRHYTHMIAS

1. ARRHYTHMIAS

2. I- Electrophysiology of the heart Normal heart rate:60-90 beats  minute Abnormal:  60 beats  min Bradycardia  90 beats  min Tachycardia

3. Conducting system vs contractile tissue of the heart Conducting System of the Heart: Contractile tissue of the heart SA node, AV node, Purkinj fibers Atrial & Ventricular muscles Impulse Propagation:  SA node  AV-node  Bundle ofHis Purkinje fibers ventricle.  SA node is the initial pacemaker.

4. Origin of ECG Waves and Intervals-P wave and PR Interval P wave = atrial depolarization The PR interval corresponds to the time lag from the onset of atrial depolarization to the onset of ventricular depolarization.

5. 1. Resting membrane potential (RMP) • In resting state: • Myocytes are permeable to K+ only. • RMP determined by K+ conc. (Ko & Ki). • Ki is 150 mmol/L and Ko 4 mmol/L. • Resting membrane potential ranges: • From – 80 to -90 mv in contractile cells • From -60 to -70 mv in pacemaker cells (SA node, AV node and His-Purkinj fibers) . • Phase 4 of AP represents RMP.

6. The ECG is recorded at a speed of 25 mm/sec, and the voltages are calibrated so that 1 mV = 10 mm in the vertical direction. Therefore, each small 1-mm square represents 0.04 sec (40 msec) in time and 0.1 mV in voltage. Because the recording speed is standardized, one can calculate the heart rate from the intervals between different waves.

7. P Wave •  P duration < 0.12 sec • P amplitude < 2.5 mm • The normal deflection of the P wave is upright (positive) in leads I, II, and aVf. • PR Interval: 0.12 - 0.20 sec QRS Complex • QRS Duration: 0.06 - 0.10 sec • QRS duration < 0.10 sec • T wave is always upright in leads I, II, V3-6, and always inverted in lead aVR.

8. 2. Cardiac Action Potential Ca++ Na+ K+ K+ Na+

9. Summary of Action Potential Phase O: Na+ enter the cells (fastly). Phase 1:Na+ levels equalize & transient efflux of K+. Phase 2:Ca++ enter the cells. Phase 3:K+ efflux from the cells. Phase 4: Spontaneous depolarization in SA node, AV node and His-Purkinj system) Na and Ca influx.

10. Potential Terms 1. Refractory Period (RP): Phases 1,2 & 3. • ERP (absolute refractory period): • Phases 1 & 2 represent ERP (no response to any stimuli). • RRP (Relative Refractory Period): • Phase 3 represents RRP (respone only to strong stimuli. 2. Action Potential Duration: Phases 1,2 & 3: - During APD, the heart in refractory state and no impulse propagation.

11. Definitions of Arrhythmias & antiarrhythmics • Arrhythmias or dysrhythmias: Disturbances in cardiac rhythm (rate and/or regularity) due to abnormality in impulse origination (ectopic beats) or abnormality in conductivity (reentry) or both. • Antidysrhythmic drugs: Drugs which suppress abnormalities of automaticity and/or conductivity by blocking specific ion channels (Na+, Ca++ and K+) or by altering autonomic functions.

12. Causes of Cardiac Arrhythmias • Electrolyte disturbances:hypokalemia, hyperkalemia). • Cardiac ischemia & MI:e.g., hypoxia   O2supply. • Structural damage:changing the conduction pathway. • Drug toxicity:: e.g., digitalis toxicity. • Autonomic changes: sympathetic or  vagal tone.

13. Mechanisms of Arrhythmias Genesis • Abnormal automaticity: • Altered normal automaticity. • Ectopic beats • Triggered automaticity. • Abnormal conductivity • Re-entry

14. 1) Abnormal Automaticitya) Alteration of Normal Automaticity • In pacemaker cells (SA, AV & H-P fibers. • Precipitated by: • Autonomic disturbance: •  Sympathetic activity  sinus & nodal tachycardia. •  vagal tone  sinus bradycardia. • Hypokalemia sinus tachycardia.

15. Types of Cardiac Arrhythmias A) Supraventricular arrhythmias: • Sinus tachycardia  90 beats min. • Sinus bradycardia 60 beats  min. • Premature atrial contractions (PACs) • Atrial tachycardia (regular pulse; up to 200 beats  min). • Atrial flutter (regular pulse; 200-300 beats  min). • Atrial fibrillation (irregular pulse;  300 beats  min). • Nodal tachycardia (AV nodal reentry; a common type of [SVT]). B) Ventricular Arrhythmias: • Premature ventricular contractions (PVCs), • Ventricular tachycardia (VT), • Ventricular fibrillation (VF), • Bundle branch block, • Torsade de pointes. N.B. Ventricular arrhythmias are life-threatening arrhythmias.

16. A- heart block

17. A. Heart block • Impaired myocardial conduction that occurs when electrical impulses encounter tissue that is electronically inexcitable, resulting in an arrhythmia • First degree • Caused by increased vagal tone or functional conduction impairment • H/P = asymptomatic • ECG = PR >0.2 sec , regular PR prolongation without skipped QRS • Treatment = none necessary

18. A- heart block

19. A. Heart block • Impaired myocardial conduction that occurs when electrical impulses encounter tissue that is electronically inexcitable, resulting in an arrhythmia • First degree • Caused by increased vagal tone or functional conduction impairment • H/P = asymptomatic • ECG = PR >0.2 sec , regular PR prolongation without skipped QRS • Treatment = none necessary

20. Second degree—Mobitz I (Wenckebach) • Caused by intranodal or His bundle conduction defect, drug effects (β-blockers, digoxin, calcium channel blockers), or increased vagal tone • H/P = asymptomatic • ECG = progressive PR lengthening until skipped QRS; • PR progression, then resets and begins again • Treatment = adjust doses of medications associated with heart block; treatment usually not necessary unless symptomatic bradycardia is present (pacemaker indicated)

21. Second degree—Mobitz II • Caused by an infranodal conduction problem (bundle of His, Purkinje fibers) • H/P = usually asymptomatic • ECG = randomly skipped QRS without changes in PR interval • Treatment = ventricular pacemaker • Complications = can progress to third-degree heart block

22. Complete or third-degree heart block • Cause is absence of conduction between atria and ventricles • H/P = syncope, dizziness, hypotension • ECG = no relationship between P waves and QRS Treatment = avoid medications affecting atrioventricular (AV) conduction; ventricular pacemaker

23. Mechanism of atrioventricular nodal reentry tachycardia. • Action potential reaches division in conduction pathway with both fast and slow fibers. • Conduction proceeds quickly down fast pathway to reach distal fibers and also proceeds up slow pathway in retrograde fashion. • (C) Impulse returns to original division point after fibers have repolarized, allowing a reentry conduction loop and resultant tachycardia. AV, atrioventricular.

24. Mechanism of atrioventricular reentry tachycardia • as seen for Wolff-Parkinson-White syndrome. • Action potential passes through AV node and encounters accessory pathway during conduction to ventricles. • (B) Accessory pathway conducts action potential back to AV node. • (C) Return of secondary action potential to AV node completes reentry loop and results in tachycardia. AV, atrioventricular node; AP, accessory pathway.

25. B. Paroxysmal supraventricular tachycardia (PSVT) • Tachycardia (HR >100 bpm) arising in atria or AV junction • Occurs mostly in young patients with healthy hearts • Cause frequently is reentry anomaly • AV nodal reentry— • - presence of both slow and fast conduction pathways inAV node; • - conduction proceeds quickly through fast pathway and progresses up slow pathway in retrograde fashion; • - conduction loop is created, resulting in reentrant tachycardia • AV reentry as found in Wolff-Parkinson-White (WPW) syndrome— • similar to AV nodal reentry, but instead of fast and slow pathways existing in the AV node, a separate accessory conduction pathway exists between the atria and ventricles that returns a conduction impulse to the AV node to set up a reentry loop; • ECG shows a delta wave (i.e., slurred upstroke of the QRS) • and shortened PR

26. H/P = sudden tachycardia; possible chest pain, shortness of breath, palpitations, syncope ECG = P waves hidden in T waves; 150–250 bpm HR; normal QRS Treatment = carotid massage or Valsalva maneuver may halt an acute arrhythmia, but cardioversion or calcium channel blocker is required in cases of hemodynamic instability; pharmacologic therapy (e.g., β-blocker or calcium channel blocker for AV nodal reentrant tachycardia and type IA or IC antiarrhythmic for WPW syndrome) or catheter ablation of accessory conduction pathways is frequently used for long-term control in symptomatic patients Antiarrhythmics, other than class IA or IC, are contraindicated for WPW syndrome because they can speed up conduction through the accessory pathway.

28. C. Multifocal atrial tachycardia (MAT) Caused by several ectopic foci in the atria that discharge automatic impulses (multiple pacemakers), resulting in tachycardia H/P = usually asymptomatic ECG = variable morphology of P waves; HR >100 bpm and PR intervals and the irregular ventricular rate Treatment = calcium channel blockers or β-blockers acutely; catheter ablation or surgery to eliminate abnormal pacemakers

29. D. Bradycardia HR <50 bpm Caused by increased vagal tone or nodal disease Risk factors = elderly, history of CAD H/P = frequently asymptomatic; possible weakness, syncope Predisposition to development of ectopic beats Treatment = stop precipitating medications; pacemaker if severe

30. E. Atrial fibrillation (Afib) Lack of coordinated atrial contractions with independent sporadic ventricular contractions Caused by rapid, disorderly firing from a second atrial focus Risk factors = pulmonary disease, CAD, HTN, anemia, valvular disease, pericarditis, hyperthyroidism, rheumatic heart disease (RHD), sepsis, alcohol use H/P = possibly asymptomatic; shortness of breath, chest pain, palpitations, irregularly irregular pulse ECG = no discernible P waves, irregular QRS rate

31. Treatment = anticoagulation; rate control via calcium channel blockers, β-blockers, or digoxin; electric or chemical (i.e., class IA, IC, or III antiarrhythmics) cardioversion if presenting within initial 2 days; cardioversion can be performed in delayed presentation if absence of thrombi is confirmed by transesophageal echocardiogram; if presenting after 2 days or if thrombus is seen on ECG, then anticoagulate and wait 3–4 weeks before cardioversion; AV nodal ablation can be considered for recurrent cases Complications = increased risk of MI, heart failure; poor atrial contraction causes blood stasis, which leads to mural thrombi formation and a risk of embolization

34. F. Atrial flutter (Aflutter) Caused by rapid firing of an ectopic focus in the atria Risk factors = CAD, congestive heart failure (CHF), chronic obstructive pulmonary disease (COPD), valvular disease, pericarditis H/P = possibly asymptomatic; palpitations, syncope ECG = regular tachycardia >150 bpm with occasionally set ratio of P waves-to-QRS; sawtooth pattern of P waves , preceding QRS.

35. Treatment = rate control with calcium channel blockers, β-blockers; electrical or chemical (class IA, IC, or III antiarrhythmics) cardioversion if unable to be controlled with medication; catheter ablation to remove ectopic focus may be possible in some cases Complications = may degenerate into Afib

36. G. Premature ventricular contraction (PVC) Caused by ectopic beats from a ventricular origin Common, frequently benign; can also be caused by hypoxia, abnormal serum electrolyte levels, hyperthyroidism, caffeine use H/P = usually asymptomatic; possible palpitations, syncope ECG = early , and wide QRS without preceding P wave followed by brief pause in conduction , Treatment = none if patient is healthy; β-blockers in patients with CAD Complications = associated with increased risk of sudden death in patients with CAD , PVCs become concerning for the development of other ventricular arrhythmias if there are >3 PVCs/min

37. H. Ventricular tachycardia (Vtach) Series of 3+ PVCs with HR 160–240 bpm Risk factors = CAD, history of MI H/P = possibly asymptomatic if brief; palpitations, syncope, hypotension ECG = series of regular, wide QRS complexes independent of P waves Treatment = electrical cardioversion followed by antiarrhythmic medications (class IA, IB, II, or III); for recurrent Vtach, internal defibrillator may be necessary (senses ventricular arrhythmia and automatically releases electric pulse to restore normal rhythm) Complications = sustained Vtach can quickly deteriorate into Vfib if not corrected

39. Ventricular fibrillation (Vfib) • Lack of ordered ventricular contraction leads to no CO and is rapidly fatal • Frequently occurs after severe MI, post-Vtach • Risk factors = CAD, MI • H/P = syncope, hypotension, pulselessness • ECG = totally erratic tracing; no P waves or QRS • Treatment = CPR, immediate electric (± chemical) cardioversion • Amiodarone also functions as an Na channel blocker.