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Normal heart rate: 60-90 beats minute

60 beats min Bradycardia 90 beats min Tachycardia

Abnormal:

I- Electrophysiology of the heart

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Conducting System of the Heart:Conducting System of the Heart:

Impulse Propagation: Impulse Propagation: SA node AV-node Bundle of His Purkinje fibers ventricle.

SA node is the initial pacemaker.

SA node, AV node, Purkinj fibers Atrial & Ventricular muscles

Contractile tissue of the heartContractile tissue of the heart

P wave = atrial depolarization

The PR interval corresponds to the time lag

from the onset of atrial depolarization to the

onset of ventricular depolarization.

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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.

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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.

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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.

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Na+

Ca++

K+

Na+

K+

Phase OPhase O: Na+ enter the cells (fastly).

Phase 1Phase 1:: Na+ levels equalize & transient efflux of K+.

Phase 2Phase 2:: Ca++ enter the cells.

Phase 3Phase 3:: K+ efflux from the cells. Phase 4Phase 4: Spontaneous depolarization in SA node, AV node and

His-Purkinj system) Na and Ca influx.

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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.

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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.

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Electrolyte disturbances: hypokalemia, hyperkalemia).

Cardiac ischemia & MI: e.g., hypoxia O2 supply.

Structural damage: changing the conduction pathway.

Drug toxicity:: e.g., digitalis toxicity.

Autonomic changes: sympathetic or vagal tone.

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Abnormal automaticity:Altered normal automaticity.Ectopic beats Triggered automaticity.

Abnormal conductivityRe-entry

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In pacemaker cells (SA, AV & H-P fibers. Precipitated by:

Autonomic disturbance: Sympathetic activity sinus & nodal

tachycardia. vagal tone sinus bradycardia.

Hypokalemia sinus tachycardia.

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A) Supraventricular 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 ArrhythmiasB) 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.

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A. Heart blockImpaired 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 impairmentH/P = asymptomaticECG = PR >0.2 sec , regular PR prolongation without skipped QRSTreatment = none necessary

A. Heart blockImpaired 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 impairmentH/P = asymptomaticECG = PR >0.2 sec , regular PR prolongation without skipped QRSTreatment = none necessary

Second degree—Mobitz I (Wenckebach)

Caused by intranodal or His bundle conduction defect, drug effects (β-blockers, digoxin, calcium channel blockers), or increased vagal toneH/P = asymptomaticECG = progressive PR lengthening until skipped QRS; PR progression, then resets and begins againTreatment = adjust doses of medications associated with heart block; treatment usually not necessary unless symptomatic bradycardia is present (pacemaker indicated)

Second degree—Mobitz II

Caused by an infranodal conduction problem (bundle of His, Purkinje fibers)H/P = usually asymptomaticECG = randomly skipped QRS without changes in PR intervalTreatment = ventricular pacemakerComplications = can progress to third-degree heart block

Complete or third-degree heart block

Cause is absence of conduction between atria and ventriclesH/P = syncope, dizziness, hypotensionECG = no relationship between P waves and QRSTreatment = avoid medications affecting atrioventricular (AV) conduction; ventricular pacemaker

Mechanism of atrioventricular nodal reentry tachycardia. (A)Action potential reaches division in conduction pathway with both fast and slow fibers. (B)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.

Mechanism of atrioventricular reentry tachycardia as seen for Wolff-Parkinson-White syndrome. (A)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.

B. Paroxysmal supraventricular tachycardia (PSVT)

Tachycardia (HR >100 bpm) arising in atria or AV junctionOccurs mostly in young patients with healthy heartsCause frequently is reentry anomaly

AV nodal reentry—- presence of both slow and fast conduction pathways in AV 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

H/P = sudden tachycardia; possible chest pain, shortness of breath, palpitations, syncopeECG = P waves hidden in T waves; 150–250 bpm HR; normal QRSTreatment = 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.

C. Multifocal atrial tachycardia (MAT)

Caused by several ectopic foci in the atria that discharge automatic impulses (multiple pacemakers), resulting in tachycardiaH/P = usually asymptomaticECG = variable morphology of P waves; HR >100 bpm and PR intervals and the irregular ventricular rateTreatment = calcium channel blockers or β-blockers acutely; catheter ablation or surgery to eliminate abnormal pacemakers

D. Bradycardia

HR <50 bpmCaused by increased vagal tone or nodal diseaseRisk factors = elderly, history of CADH/P = frequently asymptomatic; possible weakness, syncopePredisposition to development of ectopic beatsTreatment = stop precipitating medications; pacemaker if severe

E. Atrial fibrillation (Afib)

Lack of coordinated atrial contractions with independent sporadic ventricular contractionsCaused by rapid, disorderly firing from a second atrial focusRisk factors = pulmonary disease, CAD, HTN, anemia, valvular disease, pericarditis, hyperthyroidism, rheumatic heart disease (RHD), sepsis, alcohol useH/P = possibly asymptomatic; shortness of breath, chest pain, palpitations, irregularly irregular pulseECG = no discernible P waves, irregular QRS rate

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 casesComplications = increased risk of MI, heart failure; poor atrial contraction causes blood stasis, which leads to mural thrombi formation and a risk of embolization

F. Atrial flutter (Aflutter)

Caused by rapid firing of an ectopic focus in the atriaRisk factors = CAD, congestive heart failure (CHF), chronic obstructive pulmonary disease (COPD), valvular disease, pericarditisH/P = possibly asymptomatic; palpitations, syncopeECG = regular tachycardia >150 bpm with occasionally set ratio of P waves-to-QRS; sawtooth pattern of P waves , preceding QRS.

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 casesComplications = may degenerate into Afib

G. Premature ventricular contraction (PVC)

Caused by ectopic beats from a ventricular originCommon, frequently benign; can also be caused by hypoxia, abnormal serum electrolyte levels, hyperthyroidism, caffeine useH/P = usually asymptomatic; possible palpitations, syncopeECG = 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 CADComplications = 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

H. Ventricular tachycardia (Vtach)

Series of 3+ PVCs with HR 160–240 bpmRisk factors = CAD, history of MIH/P = possibly asymptomatic if brief; palpitations, syncope, hypotensionECG = series of regular, wide QRS complexes independent of P wavesTreatment = 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

I. Ventricular fibrillation (Vfib)

Lack of ordered ventricular contraction leads to no CO and is rapidly fatalFrequently occurs after severe MI, post-VtachRisk factors = CAD, MIH/P = syncope, hypotension, pulselessnessECG = totally erratic tracing; no P waves or QRSTreatment = CPR, immediate electric (± chemical) cardioversionAmiodarone also functions as an Na channel blocker.