ELECTRICAL CONDUCTION OF THE HEART

ELECTRICAL CONDUCTION OF THE HEART

MYOCARDIUM DEPOLARIZATION

• Phase 0: Initial upswing of action potential.
  • Na⁺ Channels open until threshold is reached.
• Phase 1: The potential may repolarize slightly before starting the plateau phase.
  • Na⁺ Channels are inactivated.
  • Outward Rectifier K⁺ Channels open transiently, causing slight repolarization.
  • Membrane potential remains near zero.
  
  
  
• Phase 2: Plateau Phase -- This stage is responsible for prolonging the cardiac action potential, making it longer than a nerve action potential.
  • Ca⁺² Channels open, to keep the cells depolarized.
• Phase 3: Repolarization
  • Ca⁺² Channels close.
  • Delayed Rectifier K⁺ Channels open to effect normal repolarization.
• Phase 4: Diastolic membrane potential.
  • Inward Rectifier K⁺ Channels (different than the ones above) are open, to maintain resting potential.
    • They are open at highly negative membrane potentials (i.e. hyperpolarization-activated).

• Depolarization results from influx of Ca⁺² rather than Na⁺
• There is no plateau phase (no Phase 1 and 2).
• Automaticity: Hyperpolarization-activated cation current is activated at low potentials, resulting in automaticity of the SA-Node.
  • Epinephrine increases the rate of rise and acetylcholine decreases the rate of rise of Phase-4 depolarization.

REFRACTORY PERIOD: Cardiac muscle cells have prolonged refractory periods, to prevent tetany of cardiac muscle.

AUTONOMIC REGULATION of HEARTBEAT:

• Acetylcholine slows heart rate by increasing K⁺ permeability.
• Norepinephrine speeds heart rate by increasing the rate of rise of the cardiac action potential during phase 0.

PROPAGATION of ACTION POTENTIAL:

• ATRIAL CONTRACTION: It takes about 70 msec to get from the SA-Node ------> depolarize the atria ------> to the AV-Node.
• AV-NODAL DELAY: There is a delay in depolarization of about 90msec, once the impulse reaches the AV-Node.
  • The function of this delay is to separate the contraction of the atria (i.e. atrial systole) from that of the ventricles (ventricular systole), so that more blood has a chance to fill into the ventricles.
  • The AV-Node depends on slow-conducting Ca⁺² Channels for depolarization, which helps to explain its slow rate of depolarization.
  • A smaller cell-size also helps to explain the slow rate of conductance.
• BUNDLE OF HIS
• BUNDLE-BRANCHES: Two continuing branches of the Bundle of His.
  • Left Bundle Branch: It depolarizes first. Depolarization goes from the left side of the ventricular septum to the right side, accounting for the Q-Wave.
  • Right Bundle Branch: It depolarizes after the left side.
• PURKINJE SYSTEM: Very fast conduction.
• VENTRICULAR MUSCLE
  • As depolarization proceeds in the ventricles, it moves from endocardium ------> epicardium.

EKG LIMB LEADS:

• Depolarization occurs toward the positive side (the positive sides are labelled to the right, and the respective negative sides are unlabeled).
• HEXAXIAL SYSTEM: The positive end of each limb lead is as follows:
  • I: 0
  • II: +60
  • III: +120: In a normal ECG, Lead III should have a net-zero QRS-Complex, as it is perpendicular to aVR.
  • aVR: -150: In a normal ECG, the aVR lead should have a completely negative QRS Complex.
  • aVL: -30
  • aVF: +90
• DIRECTION OF ECG DEFLECTION: A positive deflection on an ECG represents a depolarization that is traveling toward the positive side of a particular lead.
  • Maximal Positive Deflection: Occurs when depolarization vector is in the exact same direction as the limb lead.
  • Zero net deflection: Occurs when depolarization vector is exactly perpendicular to limb lead.
  • Maximal Negative Deflection: Occurs when depolarization vector is in the exact opposite direction as the limb lead (i.e. in the direction of the negative end).

ELECTROCARDIOGRAM:

• P-WAVE: Atrial depolarization. P-Wave duration is normally 80 msec.
  • PR-INTERVAL: The distance from the beginning of the P-Wave to the beginning of the Q-Wave.
    • PR-Interval is the period from beginning of atrial depolarization to the beginning of ventricular depolarization.
    • PR-Interval is normally 180-220 msec.
  • PR-SEGMENT: The distance from the end of the P-Wave and the beginning of the Q-Wave.
• QRS-COMPLEX: Ventricular Depolarization. QRS Duration is normally 30-100 msec.
  • Individual Components:
    • Q-WAVE: Depolarization of the septum. On most leads (except III and aVR) the Q-Wave points downward if it can be seen at all. Septum depolarization goes from the left side of the septum to the right side.
    • R-WAVE: Depolarization of the ventricles. Sharp upward turn.
    • S-WAVE: Return of volt-potential to zero, because all the ventricular muscle has depolarized and is therefore once again isoelectric.
      • Sharp downward turn back to isoelectric point. The S-Wave may go slightly negative before return back to isoelectric point.
  • QT-INTERVAL: From beginning of Q-Wave to end of T-Wave. QT-Interval is normally 260-490 msec. This is the period from beginning of ventricular depolarization to the end of repolarization.
  • ST-SEGMENT: Short segment from end of S-Wave to beginning of T-Wave.
  • ST-INTERVAL: From end of S-Wave to end of T-Wave.
  • RR-INTERVAL: Distance between QRS-Complexes, or the distance between heart beats in a normal sinus rhythm.
• T-WAVE: Repolarization of Ventricles. Atrial repolarization masked by QRS-Complex.
  • Repolarization occurs in the opposite direction as depolarization, but the vector still points in the same direction because the change in voltage also has an opposite sign.
  • In the ventricles, the first tissue to depolarize is the last tissue to repolarize.

READING THE ECG:

• Vertical Direction: 10 mm = 2 big boxes = 1 mV deflection.
• Horizontal Direction:
  • 1 mm = 40 msec.
  • At standard speed, there are 25 mm, or 5 big boxes, in each second.
• Speeds:
  • Standard Speed = 25 mm/sec
  • Extra-Sensitivity Speed = 50 msec, at which point all values above must be doubled.
• Calculating Heart Rate Shortcut:

At standard speed:

PRECORDIAL LEADS: V1 thru V6 are placed to specific places on the chest, for advanced ECG diagnostics. V1 is right-most, near the SA-Node, while V6 is leftmost, past the apex of the heart.

MEAN ELECTRICAL AXIS OF THE HEART:

• Two ways to graphically determine mean electrical axis:
  • SHORT WAY: This is only accurate when there is a net QRS-Deflection of virtually zero (i.e. the R deflection is equal and opposite to the S deflection).
    • Determine the lead that has a net zero QRS-Deflection.
    • On the hexaxial system, the mean electrical axis points in the direction that is perpendicular to that lead.
  • LONG WAY: This is longer but more accurate.
    • Consider any two of the six hexaxial leads. Determine again the Net QRS-Deflection for each lead.
    • Plot that deflection along the appropriate axis on a hexaxial chart.
    • Draw a dotted line perpendicular to each of the above plots, and extend the two lines until the intersect each other.
    • The Mean Electrical Axis is the vector that points from the center to the intersection of those two lines.
• LAB: Different physiological effects on the mean electrical axis:
  • INSPIRATION: The diaphragm moves down ------> It pulls the apex of the heart toward the right (i.e. in a more vertical direction) ------> the mean electrical axis is more positive (+ more degrees).
  • FORCED EXPIRATION: The exact opposite of above. The apex of the heart gets pushed upward and toward the left horizontal axis ------> the mean electrical axis is less positive or even negative.
  • PREGNANCY: The mean electrical axis would deviate to the left, within normal limits. The physical presence of the fetus would push up the diaphragm ------> heart leans toward left.
  • LEFT VENTRICULAR HYPERTROPHY: Mean axis deviation toward the left.
  • Pulmonary Valve Stenosis: If we assume that it leads to Right Ventricular Hypertrophy ------> Then we get (potentially severe) right axis deviation.
  • INFANCY: Right Axis Deviation, because the infant's right ventricle and left ventricle musculature are about the same size at birth. Left ventricle becomes larger within a couple months.
• NORMAL MEAN AXIS: Anywhere between -30 and +110.
  • Anything negative of -30 is left axis deviation, as occurs from left ventricular hypertrophy.
  • Anything positive of +110 is right axis deviation, as occurs from right ventricular hypertrophy.

ECG ABNORMALITIES:

• SINUS BRADYCARDIA: A heart rate slower than 60 SA-Nodal depolarizations per minute. "Sinus" indicates that the cardiac impulse is originating from the SA-Node as normal.
• SINUS TACHYCARDIA: Heart rate faster than 100 bpm, originating as normal from the SA-Node.
  • Tachycardia generally means you'll see a shorter RR-Interval (i.e. faster heart rate).
• SINUS ARREST: No SA-Node depolarization.
  • This can be artificially induced by carotid massage, which results in overstimulation of the Vagus ------> SA-Node hyperpolarized.
• ATRIAL PAROXYSMAL TACHYCARDIA: Faster heart rate resulting from an ectopic pacemaker in the atrial muscle.
  • In the example the P-Wave points downward because the atrial depolarization starts in the LA, because that is where the tissue is leaky.
• BUNDLE-BRANCH BLOCKS: There is some conduction block in the Bundle of His (Left or Right Bundle branches), with results as below:
  • 1 BLOCK: Partial block. The PR-Interval is longer than normal because it takes longer to conduct the impulse from SA-Node to AV-Node.
  • 2 BLOCK: A QRS-Complex occurs only after every other P-Wave. In other words, it takes two P-Waves to sufficiently excite the AV-Node to conduct the impulse to the ventricles.
  • 3 BLOCK: There is no temporal relationship between the P-Wave and QRS-Complex. Atrial and ventricular depolarizations are being controlled by their own independent pacemakers (the SA-Node and AV-Node respectively).
• AV-NODAL TACHYCARDIA: Tachycardia, plus the P-Wave is insignificant or absent.
  • This is tachycardia, where the impulse originates from the AV-Node. The inherent pacemaker of the AV-Node is faster than the SA-Node.
• PREMATURE VENTRICULAR CONTRACTION (PVC): A premature QRS-Complex, or one that occurs without being preceded by a P-Wave.
  • That means that the P-Wave didn't start the impulse, but it started somewhere else.
  • Ectopic Pacemaker: With PVC, the impulse originates in the ventricular muscle itself, due to leaky membranes in the muscle.
• VENTRICULAR FIBRILLATION: Waves of depolarization traveling in multiple directions all over the ventricular muscle. The pacemaker activity is lost.
• ATRIAL FIBRILLATION: Fibrillation in the atria is not serious in children, but it is serious in old people.
  • That's because in old people, atrial systole contributes a greater relative blood volume to cardiac output than in children.

CLINICAL LECTURE: WOLF-PARKINSON-WHITE SYNDROME

• Normally, the AV-Node is the only pathway for conduction of the impulse from the atria to the ventricles.
  • Bachman's Bundle: Normally conducts the impulse from Right Atrium to Left Atrium during atrial systole.
  • Moderator Band: Normally conducts the impulse from the right ventricular septal wall to the right free wall during ventricular systole.
• Lupus Erythematosus: Rare condition associated with pediatric bradycardia. Usually pediatric heart problems result in Tachycardia -- not bradycardia.
• PEDIATRIC TACHYCARDIAS: They are divided into two types
  • Supraventricular Tachycardia (SVT): One where the problem originates somewhere in the AV-System.
  • Ventricular Tachycardia (VT): Problem originates in the ventricular system.
• Wolf-Parkinson-White Syndrome: Extra conductive tissue in the myocardium, creating an accessory pathway for conduction from atria to ventricles.
  • This accessory pathway ultimately results in a Reentry Tachycardia, or a conduction loop between the normal and accessory pathways.
  • The Wolf-Parkinson-White ECG: Shorter PR-Interval due to rapid conduction of signal to ventricles through accessory pathway.
    • This is the ECG when the patient is healthy and no problems are going on.
    • The P-Wave and the QRS-Complex are scrunched together, creating the appearance of a delta-wave (hump right before QRS), and a longer overall QRS Complex.
• Reentry Tachycardia: You get it from a unidirectional block in one pathway, coupled with slowed conduction of an alternative pathway. This results in continuous impulse conduction, or circus dysrhythmia.
  • With WPW, the accessory pathway can get blocked because it hasn't had the time to repolarize, then the normal pathway provides a mean for retrograde conduction of depolarization.
  • This results in a conduction loop and severe tachycardia.
• TREATMENT: Slow down the conduction through one pathway or the other.
  • Use Ca⁺²-Channel Blockers (such as Verapamil)
  • Use Digoxin to increase AV-Nodal sensitivity to ACh.
  • Use beta-Blockers to block the normal NorE sympathetic receptors on the AV-Node and cardiac muscle.
  • In severe cases, surgically remove the conductive tissue from the myocardium.