The heart is composed of two major types of cells:
Contractile cells: These cells contract to pump blood.
Conducti cells: These cells send signals to set the heart's rate and rhythm.
Key structures:
Apex and base of the heart
Atria and ventricles
SA Node (Sinoatrial Node) and AV Node (Atrioventricular Node): Part of the conducti system.
Types of Cells in the Heart
Contractile Cells (Myocardium/Myocytes):
Responsible for contraction when triggered by an action potential.
Protein filaments form cross-bridges to facilitate contraction.
Conducti Cells (Nodal Cells):
Includes SA and AV nodes, also known as pacemaker cells.
Sets the rhythm of the heart by spreading action potentials throughout the heart tissue.
Resting Membrane Potential
All cells have a charge difference across their membrane, crucial for excitable tissues (nervous, muscle, endocrine).
Charge difference is maintained by:
Sodium-Potassium Pump: Exchanges 3 Na+ out for 2 K+ in, leading to a more positive charge outside the cell.
Leaky Potassium Channels: Allow K+ to diffuse out, further increasing positive charge outside.
Action Potentials in Nodal (Conducti) Cells
Spontaneous Depolarization: Conducti cells do not have a resting membrane potential. They continually drift towards depolarization due to:
Funny Sodium Channels: Allow slow Na+ influx, progressively making the cell more positive.
Threshold at -40 mV: Once reached, voltage-gated calcium channels open, allowing Ca2+ influx.
Depolarization Phase: Na+ and Ca2+ influx depolarizes the cell.
Repolarization Phase:
At about +10 mV, potassium channels open, allowing K+ efflux, making the cell more negative again.
Action Potentials in Contractile Cells
Resting Membrane Potential: At -90 mV, contractile cells have a true resting potential.
Depolarization: Triggered when Na+ and Ca2+ from conducti cells cause the membrane to reach a threshold of -70 mV, opening fast Na+ channels.
Plateau Phase:
A balance between Ca2+ influx (slow) and K+ efflux creates a plateau maintaining depolarization.
Lasts ~200 milliseconds and is crucial for the timing of contraction.
Repolarization:
Ca2+ channels close, continued K+ efflux returns the cell to a polarized state.
Importance of Calcium
In Conducti Cells: Slower Ca2+ influx sets a stable rhythm by creating a slower depolarization.
In Contractile Cells: Ca2+ is critical for muscle contraction, as it triggers actin and myosin interactions within the cell.
Most Ca2+ for contraction comes from the sarcoplasmic reticulum, not extracellular sources.
Clinical Implications
Blocking Ca2+ in nodal cells can slow the heart rate by reducing the rate of depolarization.
Blocking Ca2+ in contractile cells reduces the force of contraction, impacting heart muscle function.
Summary
Understanding the differences between nodal and myocardial action potentials helps in comprehending how the heart sets its rhythm and contracts.
Note: The lecture also emphasizes the physiological mechanisms behind the intrinsic ability of the heart to spontaneously generate action potentials and how they are crucial in maintaining coordinated heart contractions.