Transcript Slide 1

I- Electrophysiology of the heart
Normal heart rate: 60-90
beats  minute
Abnormal:
 60 beats  min Bradycardia
 90 beats  min Tachycardia
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Conducting System of the Heart:
SA node, AV node, Purkinj fibers
Contractile tissue of the heart
Atrial & Ventricular muscles
Impulse Propagation:
 SA node  AV-node 
Bundle of His  Purkinje fibers
 ventricle.
 SA node is the initial
pacemaker.
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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:
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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) .
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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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Ca++
Na+
K+
K+
Na+
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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.
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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 conductivity
 Re-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:
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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:
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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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1- first degree
2- second degree
- mobitz 1 ( wenckebach )
-Mobitz 2
3- third degree or complete
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
1- first degree
2- second degree
- mobitz 1 ( wenckebach )
-Mobitz 2
3- third degree or complete
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
Second degree—Mobitz I (Wenckebach)
Caused by intranodal or His bundle conduction defect, drug effects (βblockers, 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)
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
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
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 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 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, 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.
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
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
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
Treatment = anticoagulation; rate control via calcium channel blockers, βblockers, 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
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-toQRS; 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 cases
Complications = may degenerate into Afib
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
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
I. 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.