Cardiac Electrophysiology Anatomy

Aka: Cardiac Electrophysiology Anatomy, Cardiac Conduction System, Cardiac Action Potential, Heart Conduction Anatomy, Sinoatrial Node, SA Node, Atrioventricular Node, AV Node, Atrioventricular Bundle, AV Bundle, Bundle of His, Kent-His Bundle, Atrioventricular Fasciculus, Purkinje Fiber, Cardiac Cycle, Wiggers Diagram

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II. Anatomy: Images

  1. Cardiac Conduction
    1. cvHeartXsEkgGrayBB501.gifLewis (1918) Gray's Anatomy 20th ed (in public domain at Yahoo or BartleBy)
    2. heartElectrical.jpg
    3. CardiacActionPotential.png
    4. ekg.png
  2. Cardiac Cycle (Wiggers Diagram)
    1. cvCardiacCycleWiggers.png

III. Physiology: Nerve Impulse Transmission

  1. Nerve Impulse (Action Potential)
    1. See Nerve Impulse
    2. As with Neurons, specialized cardiac Muscle transmits electrical signals
      1. nerveActionPotential.png
    3. Vagus Nerve, SA Node and AV Node signals are relatively rapid (similar to Neurons)
      1. Prominent Voltage-Gated Sodium channel mediated depolarization
    4. Atrial Muscle, and especially Purkinje Fibers and Ventricular Muscle tend to have sustained impulses
      1. Prominent Voltage-Gated Calcium channel mediated depolarization
      2. Sustained impulse results in stronger atrial and ventricular contraction
      3. Also results in delayed repolarization (refractory period) protecting against rapid Heart Rates
  2. Sinoatrial Node (SA Node)
    1. Cluster of cells located at the junction of the superior vena cava and the right atrium
    2. The SA Node cell spontaneously generate an electrical signal, depolarizing in adults at 60-100/min
      1. SA Node assumes the Pacemaker function of the heart due to its intrinsic faster rate
      2. Other cardiac tissue also generate spontaneous signals, but at slower rates
    3. Electrical signals pass into the right and left atrial Muscles resulting in atrial contraction
      1. Atrial Muscle depolarization is detected on Electrocardiogram as P Wave
      2. Electrocardiogram does not detect the SA Node firing or atrial repolarization
    4. Signals then continue into the AV Node
    5. The SA Node is perfused by the right Coronary Artery in 50% (remainder by left circumflex artery)
  3. Atrioventricular Node (AV Node)
    1. Small cluster of specialized cardiac Muscle Cells in the interatrial septum near the coronary sinus
    2. AV Node slows electrical conduction, long enough to allow for ventricular filling after atrial contraction
    3. The AV Node depolarizes spontaneously at 40-60/min if the SA Node signal is absent
    4. Gives rise to the Atrioventricular Bundle which passes the electrical signal from the atria to the ventricles
    5. The AV Node is perfused by the right Coronary Artery in 90% (remainder by left circumflex artery)
  4. Purkinje Fibers
    1. Band of specialized cardiac Muscle fibers efficiently and rapidly transmit electrical signals to ventricles
    2. Atrioventricular Bundle (including the left and right bundles) are composed of Purkinje Fibers
  5. Atrioventricular Bundle (AV Bundle, Bundle of His, Kent-His Bundle, Atrioventricular Fasciculus)
    1. Purkinje Fibers transmit electrical signals from the AV Node to the Ventricles
    2. Electrical signals via the Atrioventricular Bundle resulting in Ventricular Contraction (systole)
    3. The ventricular Muscle depolarizes spontaneously at 20-40/min if the SA Node and AV Node signals are absent
    4. Atrioventricular Bundle divides into the left bundle (left ventricle) and right bundle (right ventricle)
      1. Rapid transmission of signals along the Purkinje Fibers ensures simultaneous ventricular contraction

IV. Physiology: Cardiac Action Potential

  1. See Action Potential
  2. Images
    1. CardiacActionPotential.png
  3. Background
    1. Cardiac Action Potential varies by location within the heart's electrical system
    2. Classic 4 phase Action Potential reflects ventricular depolarization
  4. Phase 0
    1. Voltage dependent Sodium channels open
    2. Rapid Sodium influx depolarizes cell
  5. Phase 1
    1. Repolarization begins with a brief rapid phase
    2. Inactivation of Sodium influx
    3. Transient activation of outward Potassium current
  6. Phase 2
    1. Plateau phase
    2. Low membrane conductance
    3. Activation of slow inward Calcium current
  7. Phase 3
    1. Outward Potassium current
    2. Results in repolarization to resting potential
  8. Phase 4
    1. Deactivation of outward Potassium current
    2. Inward Sodium channel current decreases transmembrane potential

V. Physiology: Autonomic System Mediators

  1. See Regulation of Circulation
  2. Sympathetic Nervous System (increases Cardiac Output)
    1. Norepinephrine acts at cardiac cells beta-1 Adrenergic Receptors
    2. Increases myocardial contractility
      1. Increases Calcium influx with each Action Potential (resulting in stronger contraction)
    3. Increases Heart Rate
      1. Increases SA Node firing and Action Potential conduction velocity (via Sodium, Calcium influx)
    4. Positive Mediators
      1. Alpha 1 Adrenergic ReceptorAgonists
        1. Vasoconstriction and increased cardiac contractility
        2. Examples: Phenylephrine, Norepinephrine, Epinephrine
      2. Alpha 2 Adrenergic ReceptorAntagonistS
      3. Beta 1 Adrenergic ReceptorAgonists
        1. Increases myocardial contractility (inotrope) and Heart Rate (chronotrope)
        2. Examples: Norepinephrine, Epinephrine
      4. Beta 2 Adrenergic ReceptorAgonists
        1. Vasodilation and bronchodilation
        2. Examples: Albuterol
    5. Negative Mediators
      1. Alpha 1 Adrenergic ReceptorAntagonists
        1. Alpha Adrenergic Antagonist (e.g. Prazosin, Terazosin, Doxazosin)
        2. Antihypertensives that reduce Peripheral Vascular Resistance
      2. Alpha 2 Adrenergic ReceptorAgonistS
        1. Alpha Adrenergic Central Agonist (e.g. Clonidine, Methyldopa, Aldomet, Guanabenz, Wytensin)
        2. Antihypertensives that reduce Peripheral Vascular Resistance (also reduce contractility, Heart Rate)
      3. Beta 1 Adrenergic ReceptorAntagonists
        1. Selective Beta Blockers (e.g. Metoprolol, Bisoprolol, Atenolol)
        2. Decrease Heart Rate and cardiac contractility (as well as Cardiac Output)
        3. Slows AV Node conduction, suppresses SA Node rates, ectopic atrial foci
        4. Inhibit renin release from renal juxtaglomerular cells (hence lowering Blood Pressure)
        5. Decreases cardiac workload and therefore cardiac oxygen demand (Antianginal effect)
      4. Beta 2 Adrenergic ReceptorAntagonists
        1. Adverse effect of non-selective Beta Blockers (e.g. Propranolol) resulting in bronchospasm, vasospasm
      5. Peripheral Acting Adrenergic Antagonist
        1. Block Norepinephrine release from postganglionic nerve terminals
        2. Examples: Reserpine, Guanethidine, Guanadrel
  3. Parasympathetic Nervous System (decreases Heart Rate)
    1. Decreases Heart Rate
      1. Vagal Nerve released Acetylcholine acts at SA Node, AV Node and Atrial Muscle
        1. Acetylcholine increases SA Node permeability of Potassium
        2. Membrane resting potential hyperpolarized and less susceptible to depolarization
      2. Decreases SA Node firing and Heart Rate
      3. Decreases AV Node Action Potential conduction velocity
      4. Decreases Atrial Muscle Contractility
    2. Marginal effect on reducing myocardial contractility
      1. Sympathetic effect on contractility is dominant

VI. Physiology: Other Mediators

  1. Sodium-Potassium Pump Inhibitors
    1. sodiumPotassiumATPase.jpg
    2. Digoxin (Digitalis) is a Sodium-Potassium ATPase Inhibitor
    3. Agents that decrease Sodium-Potassium pump (Sodium efflux from cell) increase intracellular Sodium
      1. Delays AV Node conduction and prolongs AV Node refractory period
      2. Blunts Atrial Tachycardias
    4. Extracellular Calcium may exchange with intracellular Sodium to increase intracellular Calcium
      1. Increased intracellular Calcium increases myocardial contraction strength
  2. Calcium Channel Blockers
    1. Decrease Calcium influx into cell
    2. Dihydropiridine Calcium Channel Blockers (e.g. Nifedipine) primarily target peripheral vessels
      1. Vasodilates by reducing vascular smooth Muscle Contraction
    3. Non-Dihydropiridine Calcium Channel Blockers (e.g. Diltiazem) target both cardiac tissues and vessels
      1. Vasodilation as with Dihydropyridines
      2. Decreased cardiac contractility
      3. Slows Heart Rate by delaying SA and AV Node repolarization

VII. References

  1. Goldberg (2014) Clinical Physiology, Medmaster, Miami, p. 35-50
  2. Guyton and Hall (2006) Medical Physiology, Elsevier Saunders, Philadelphia, p. 103-30

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