CVP:LEC 3

Lecture 3 Recording 10: Action Potentials in the Heart

Types of Action Potentials

  • Fast Action Potentials are observed in:

    • Atrial myocardium

    • Ventricular myocardium

    • Bundle of His, Bundle branches, and Purkinje fibers

  • Slow Action Potentials are observed in:

    • Sinoatrial (SA) node

    • Atrioventricular (AV) node

Phases of Cardiac Action Potential

  • The phases of the cardiac action potential correlate with changes in the permeability of the cell membrane to ions, predominantly:

    • Potassium ions (K+)

    • Calcium ions (Ca2+)

    • Sodium ions (Na+)

    • Key permeability changes include:

    • [K+] in the cell is greater than [K+] outside the cell

    • [Ca2+] outside the cell is greater than [Ca2+] inside

    • [Na+] outside the cell is greater than [Na+] inside

SA Node Action Potential

  • Pacemaker Potential:

    • Characterized by a slow depolarization towards threshold due to the spontaneous generation of action potentials.

  • Mechanism:

  • 1. Pacemaker potential initiates via

  • → K+ channels (iK)

  • →F-type channels (funny channels) open: influx of Na+ (iNa)

  • →T-type channels open: transient influx of Ca2+ (iCa)

  • 2. Depolarization occurs when L-type channels open, allowing Ca2+ influx.

  • 3. Repolarization occurs due to K+ channels opening, resulting in K+ efflux and closure of Ca2+ channels.

Pacemaker Phases

  • Membrane Potential Dynamics:

    • Time frame considered:

    • 0 sec - Pacemaker potential

    • ~0.15 sec - Depolarization, K+ exits, Na+ enters, Ca2+ starts to enter

    • ~0.30 sec - Cells return to resting state, completing the cycle in approximately 150 msec

Ventricular Muscle Cell Action Potential

  • Phases of Action Potential:

    • Depolarization: Opens fast voltage-gated Na+ channels upon reaching threshold.

    • Repolarization: K+ channels open while Ca2+ channels close.

    • Plateau phase: Ca2+ enters through L-type channels with a slow opening of K+ channels, stabilizing the cell phase before repolarization.

    • Resting Phase: Maintained by slow leakage of K+.

Comparison of Cardiac Action Potentials

  • Differences among various cells:

    • Sinoatrial Node: Short plateau, quicker depolarization

    • Atrioventricular Node: Longer time to reach threshold

    • Atrial and Ventricular Myocardium: Varied plateau durations and thresholds.

Lecture 3 Recording 11: The Electrocardiogram

Understanding the ECG

  • The ECG is a graphic representation of the electrical activity of the heart, which is detected on the skin surface as changes in voltage gradients, potentially reaching up to 100 mV internally but represented as small as 1 mV externally.

  • The ECG is pivotal for diagnosing various cardiac conduction system pathologies.

Placement of Electrodes in the 12 Lead ECG

  • Different electrode placements (e.g., Lead I, II, III, aVR, aVL, and aVF) create specific tracing patterns which help in analyzing the heart’s electrical activity from various angles.

Key Features of ECG Recording

  • P-wave: Indicates depolarization across the atria; atrial contraction occurs about 25 msec after initiation.

  • QRS complex: Represents the depolarization of the ventricles; simultaneous atrial repolarization happens.

  • T-wave: Corresponds to the repolarization of the ventricles.

Relationship: ECG and Action Potentials

  • Visual representation in the ECG shows connections to the action potentials in atrial and ventricular muscle cells, capturing their unique phases (P, Q, R, S, T) in context with the membrane potentials.

Normal and Abnormal ECG Patterns

  1. Normal ECG: The P-wave is consistently followed by QRS and T-waves.

  2. Partial AV Node Block: There is a missed QRS complex coinciding with every other P-wave.

  3. Complete AV Node Block: A complete dissociation occurs between atrial and ventricular electrical activities, causing a slower heart rhythm regulated by the Bundle of His.

Lecture 3 Recording 12: Excitation-Contraction Coupling in the Heart

Cardiac Myocytes

  • Definitions:

    • Sarcolemma: The muscle cell membrane.

    • Sarcoplasmic Reticulum (SR): Stores calcium ions (Ca2+) necessary for muscular contraction.

  • Structure: Cardiac myocytes include intercalated disks, branching fibers, and structural organelles like mitochondria and a nucleus.

  • striated

  • T-tubules→ invaginations of sarcolemma transmit depolarization of membrane into interior of muscle cell

Mechanism of Excitation-Contraction Coupling (ECC)

  • Calcium ions play a vital role in regulating cardiac muscle contraction:

    • Binding to ryanodine receptors releases additional Ca2+ from the sarcoplasmic reticulum, in a process known as calcium-induced calcium release (CICR).

  • The cytosolic calcium is primarily responsible for the initiating muscle contraction, reflecting that 95% of the calcium necessary for contraction derives from SR and external sources through specialized channels.

Cross-bridge Activation by Calcium

  • Troponin → contains binding sites for calcium and tropomyosin, and regulates access to myosin- binding sites on actin (when relaxed, low Ca)

  • Tropomyosin → partially cover the myosin-binding sites on actin at rest, preventing cross-bridges from making contact with actin (when activated, high Ca)

Cellular Mechanism of Contraction

  • The excitation impulse spreads through the sarcolemma and into the cell’s interior via T-tubules. During the plateau phase of the action potential, permeability to calcium rises, facilitating Ca2+ influx through L-type channels and subsequent Ca2+ release from SR.

Steps Involved During ECC

  1. Action potentials travel through T-tubules.

  2. L-type Ca2+ channels open, resulting in Ca2+ entering the cytosol.

  3. Ca2+ binds to ryanodine receptors on SR, triggering further Ca2+ release.

  4. Elevated cytosolic Ca2+ activates troponin, leading to muscle contraction through cross-bridging.

Lecture 3 Recording 13: Excitation-Contraction Coupling in the Heart: Relaxation

Mechanism for Relaxation of Cardiac Muscle

  • Calcium Dynamics During Relaxation:

    • Closure of L-type Ca2+ channels halts Ca2+ influx.

    • Sarcoplasmic reticulum is stimulated to uptake cytosolic Ca2+ through the Ca2+ -ATPase pump.

    • Extrusion of Ca2+ from the cell is facilitated by the Na+-Ca2+ exchanger, leading to a reduction in tropomyosin's coverage on actin's binding sites, hence blocking interactions with myosin, facilitating relaxation.

Summary of Calcium Uptake Pathways

  • Summary of mechanisms ensuring uptake and decrease of calcium concentrations, crucial for muscle relaxation and cessation of contraction activities associated with heartbeats.

Refractory period: Period of time in which a new action potential cannot be initiated

• Absolute Refractory Period: ~ 250 msec, No response to another stimulus, Inactivation of Na+ channels

• Prevents tetanus