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Last Session Overview

  • Understood the differences in vertebrate heart structures and circulatory systems.

  • Reviewed basic human heart anatomy.

  • Identified three cell types in the human heart.

Gas Exchange / Hypoxia

Learning Goals

  • Understand and describe:

    • Cardiac action potentials.

    • The importance of the plateau phase.

    • Transmission of electrical excitation over the heart.

Action Potentials

  1. Definition: The signal used by neurons to send information along the axon.

  2. All-or-none events: Action potentials occur fully or not at all.

  3. Generation Elements:

    • Active transport produces asymmetric concentrations of ions.

    • Generates an electrochemical gradient, which provides energy.

    • This gradient drives ions across the membrane, causing a change in membrane potential (Vm).

Characteristics of Action Potentials

  1. Threshold Current:

    • Just enough to achieve threshold potential, usually ranging from -30 to -50 mV.

  2. Regenerative Nature:

    • Self-perpetuating; Vm becomes extremely positive (+10 to +50 mV).

  3. After-Hyperpolarization:

    • When Vm falls below resting potential (Vrest).

Refractory Periods

  1. Absolute Refractory Period:

    • A phase where no action potential can occur.

  2. Relative Refractory Period:

    • An action potential can occur only if the trigger is more intense (analogous to flushing a toilet).

Ionic Basis of the Action Potential

Membrane States

  • At Rest:

    • Membrane is permeable to K+ due to leak channels.

  • Rising Phase:

    • Voltage-gated Na+ channels open, allowing Na+ to flow into the cell.

  • After Na+ inactivation:

    • Membrane remains permeable to K+ briefly as voltage-gated K+ channels open.

Pacemaker Action Potentials

  • Definition: Cells exhibit a more negative internal environment.

  • Electrical Properties:

    • Pacemaker cells lack a stable resting potential.

    • Steady spontaneous depolarization occurs post-contraction, leading to a gradual rise in membrane potential.

    • K+ retention within cardiac cells increases positivity, bringing the membrane to threshold potential.

Modulation of Heart Rate

  • Parasympathetic Innervation: Acetylcholine from the vagus nerve decreases heart rate by slowing pacemaker potential.

  • Sympathetic Innervation: Epinephrine accelerates pacemaker potential, increasing heart rate.

  • Catecholamines: Norepinephrine causes rapid depolarization and raises heart rate.

Cardiac Action Potentials

  1. Rapid due to a significant increase in Na+ conductance (leading to positivity).

  2. Delayed Repolarization:

    • Prolongs action potential and contraction, ensuring full contraction of heart chambers before relaxation and refilling.

  3. Calcium Conductance:

    • Maintains a high Ca2+ influx, prolonging the plateau phase.

    • Delay in K+ conductance further contributes to this phase.

Calcium and the Sarcoplasmic Reticulum

  • In lower vertebrates, Ca2+ enters through the plasma membrane.

  • In birds and mammals, the larger cell volume limits sufficient Ca2+ entry, relying on the sarcoplasmic reticulum.

Termination of the Plateau Phase

  • Occurs due to a reduction in Ca2+ conductance and an increase in K+ conductance.

Transmission of Excitation Over the Heart

  1. Mechanism: Electrical activity passes between cardiac cells via gap junctions.

  2. Impulse Direction: Transmission is generally unidirectional, ensuring impulses spread from the pacemaker region outward.

Spread of Electrical Activity

  • Speed of excitation in the SA node and atria is about 0.8 m/s.

  • From atria to ventricles via AV node, speed slows to 0.05 m/s, allowing complete filling of ventricles.

  • Junctional fibers (0.1 m/s) connect to the Bundle of His, spreading excitation rapidly (4-5 m/s) through Purkinje Fibers for simultaneous ventricular contraction.

Functional Significance of Transmission

  • Generates separate, synchronous contractions of the atria followed by the ventricles.

  • Slowing through the AV node allows atrial contraction to complete, facilitating blood flow into ventricles.

Conducting System

Components

  • Sinoatrial (S-A) Node: Pacemaker of the heart.

  • Atrioventricular (A-V) Node: Delays impulse transmission to ventricles for optimal contraction timing.

  • Bundle of His: Transmits impulses from A-V node to ventricles quickly.

Heartbeat Initiation and Spread

  1. Depolarization begins at the S-A node, spreading quickly through atrial muscle.

  2. A-V node delay allows atria to contract before ventricle activation.

  3. Rapid spread through the ventricular myocardium leads to strong ventricular contraction.

Frank-Starling Mechanism

  • Definition: Stretching of cardiac muscle increases the force of subsequent contractions.

  • Importance: Allows the heart to match its output to its input, crucial for maintaining blood flow efficiency.

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