MYOCARDIAL ACTION POTENTIAL
Phase 0 = Rapid upstroke and depolarization
- Voltage-gated Na+ channels open.
Phase 1 = Initial repolarization
- Inactivation of voltage-gated Na+ channels.
Voltage-gated K+ channels begin to open.
Phase 2 = Plateau
- Ca2+ influx through voltage gated Ca2+ channels balances K+ efflux.
- Ca2+ influx triggers Ca2+ release from sarcoplasmic reticulum & myocyte
contraction.
Phase 3 = Rapid repolarization
- Massive K+ efflux due to
Opening of voltage-gated slow K+ channels and
Closure of voltage-gated Ca2+ channels.
Phase 4 = Resting potential
- High K+ permeability through K+ channels.
Occurs in all cardiac myocytes except for those in the SA and AV nodes.
In contrast to skeletal muscle:
Cardiac muscle action potential has a plateau, due to Ca2+ influx and K+ efflux.
Cardiac muscle contraction requires Ca2+ influx from ECF
- to induce Ca2+ release from sarcoplasmic reticulum (Ca2+ induced Ca2+ release).
Cardiac myocytes are electrically coupled to each other by gap junctions.
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PACEMAKER ACTION POTENTIAL
Occurs in
SA node
AV node
Key differences from the ventricular action potential include:
Phase 0 = Upstroke
Opening of voltage-gated Ca2+ channels.
Fast voltage-gated Na+ channels are permanently inactivated because of the less negative
resting potential of these cells.
Results in a slow conduction velocity that is used by the AV node to prolong transmission
from the atria to ventricles.
Phases 1 = Absent
Phases 2 = Absent
Phase 3 = Repolarization
Inactivation of Ca2+ channels, activation of K+ channels K+ efflux.
Phase 4 = Slow spontaneous diastolic depolarization due to I-f (“funny current”).
I-f channels responsible for a slow, mixed Na+/K+ inward current;
different from INa in phase 0 of ventricular action potential.
Accounts for automaticity of SA, AV nodes.
The slope of phase 4 in the SA node determines HR.
ACh/Adenosine - the rate of diastolic depolarization and HR,
Catecholamines - depolarization and HR.
Sympathetic stimulation - the chance that I-f channels are open and thus HR.
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ELECTRO CARDIOGRAM (ECG)
CONDUCTION PATHWAY:
SA node Atria AV node Bundle of His
Rt Lt bundle branches Purkinje fibers ventricles
Left bundle branch divides into
Left anterior fascicle
Left posterior fascicle
SA NODE:
Location: Junction of RA and SVC;
“Pacemaker” inherent dominance with slow phase of upstroke.
AV NODE:
Location: posteroinferior part of interatrial septum.
Blood supply usually from RCA.
100-msec delay allows time for ventricular filling.
PACEMAKER RATES:
SA > AV > bundle of His/ Purkinje/ventricles.
SPEED OF CONDUCTION:
His - Purkinje > Atria > Ventricles > AV node.
He Parks At Ventura Avenue
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P wave
Atrial depolarization.
PR interval
Time from start of atrial depolarization to start of ventricular depolarization
Normally 120-200 msec
QRS complex
Ventricular depolarization
Normally < 100 msec
QT interval
Ventricular depolarization,
Mechanical contraction of the ventricles,
Ventricular repolarization.
T wave
Ventricular repolarization.
T-wave inversion may indicate ischemia or recent MI.
J point
Junction between end of QRS complex and start of ST segment.
ST segment
Isoelectric, ventricles depolarized.
U wave
Prominent in
Hypo Kalemia (hyp“U”kalemia),
Bradycardia.
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TORSADES DE POINTES
Polymorphic ventricular tachycardia,
Characterized by shifting sinusoidal waveforms on ECG;
Can progress to ventricular fibrillation (VF).
Long QT interval predisposes to torsades de pointes.
Caused by
Drugs
K+
Mg2+
Ca2+
Congenital abnormalities
Treatment: Magnesium sulfate
Drug-Induced long QT (ABCDE):
Anti Arrhythmics (class IA, III)
Anti Biotics (eg, macrolides)
Anti “C”ychotics (eg, haloperidol)
Anti Depressants (eg, TCAs)
Anti Emetics (eg, ondansetron)
Torsades de pointes = twisting of the points
CONGENITAL LONG QT SYNDROME
Inherited disorder of myocardial repolarization
Typically due to ion channel defects (most commonly loss-of-function mutations affecting K+
channels);
Risk of sudden cardiac death (SCD) due to torsades de pointes.
Includes:
RomaNO - Ward syndrome
Autosomal dominant
Pure cardiac phenotype (NO deafness).
Jervell and Lange-Nielsen syndrome
Autosomal recessive
Sensorineural deafness.
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BRUGADA SYNDROME
Autosomal dominant
MC - Asian males
ECG pattern of pseudo-right bundle branch block and ST elevations in V1-V3
Risk of ventricular tachy arrhythmias and SCD
Prevent SCD with implantable cardioverter-defibrillator (ICD)
WPW SYNDROME
MC - Type of ventricular preexcitation syndrome.
Abnormal fast accessory conduction pathway from atria to ventricle (bundle of Kent)
bypasses the rate-slowing AV node
Ventricles begin to partially depolarize earlier
Characteristic delta wave with
Widened QRS complex
Shortened PR interval on ECG
May result in re-entry circuit Supraventricular tachycardia.
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ECG TRACINGS
ATRIAL FIBRILLATION
Chaotic & erratic baseline with no discrete P waves in between irregularly spaced QRS
complexes.
Irregularly irregular heartbeat.
MC risk factors
HTN
Coronary artery disease (CAD)
Occasionally seen after binge drinking (“holiday heart syndrome”)
Can lead to thromboembolic events, particularly stroke.
Treatment:
Anticoagulation
Rate & Rhythm control, and/or
Cardioversion
ATRIAL FLUTTER
A rapid succession of identical, back-to-back atrial depolarization waves.
The identical appearance accounts for the “sawtooth” appearance of the flutter waves.
Treat like atrial fibrillation +/- catheter ablation.
VENTRICULAR FIBRILLATION
A completely erratic rhythm with no identifiable waves.
Fatal arrhythmia without immediate CPR and defibrillation.
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AV BLOCK
1ST DEGREE
The PR interval is prolonged (> 200 msec).
Benign and asymptomatic.
No treatment required.
2ND DEGREE
Mobitz type I (Wenckebach)
Progressive lengthening of PR interval until a beat is “dropped”
(a P wave not followed by a QRS complex).
Usually asymptomatic.
Variable RR interval with a pattern (regularly irregular).
Mobitz type II
Dropped beats that are not preceded by a change in the length of the PR interval (as in type
I).
May progress to 3rd-degree block.
Often treated with pacemaker.
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3RD DEGREE (Complete)
The atria and ventricles beat independently of each other.
P waves and QRS complexes not rhythmically associated.
Atrial rate > ventricular rate.
Usually treated with pacemaker.
Can be caused by LymE disease.
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