Instructor: Dr. Christopher Potter
Published by: Pearson Education, Inc., 2018
Focus: Understanding the action potentials within heart cells, highlighting the differences between cardiac pacemaker cells and contractile cells.
Introduces the heart and its significance, setting the stage for detailed discussions related to action potentials in cardiac physiology.
Membrane Potential: It changes in response to stimuli, moving from resting potential (-70 mV) through depolarization to action potential (+50 mV).
Phases:
Depolarization: Rapid rise in potential.
Repolarization: Return to resting potential.
Refractory Periods: Following the action potential, preventing further stimulation during this phase.
Graded Depolarization: The membrane potential reaches the threshold (-60 mV).
Rapid Depolarization: Sodium channels open, causing sodium influx.
Repolarization Process: Inactivation of sodium channels and activation of potassium channels returning the cell to resting state.
Refractory Periods:
Absolute Refractory Period: No response to stimulus.
Relative Refractory Period: Increased stimulus needed for response.
Pacemaker Potential: Slow depolarization initiated by HCN channels; this is essential for heart rhythm.
Depolarization Phase: Triggered by the influx of calcium ions.
Repolarization Phase: Resumed by potassium efflux, resetting the cycle for the next action potential.
Duration: SA node action potentials span approximately 800 ms and there’s no true resting potential.
Major channels include:
HCN Channels: Responsible for pacemaker potential.
Calcium Channels: Crucial for further depolarization.
Potassium Channels: Involved in repolarization.
The "Funny Current" arises from the sodium influx through HCN channels, integral to maintaining heart rhythm.
Conducting Cells: Relay impulses but do not contract.
Pacemaker (Nodal) Cells: Auto-rhythmic, including cells in the SA and AV nodes.
Contractile Cells: Do not initiate impulses themselves; rely on conducting cells.
Resting Membrane Potential: ~-90 mV.
Dynamic: Involves ion channels of Na+, Ca2+, and K+; however, lacks HCN channels.
Stimuli: Induced by depolarization from neighboring cells around them.
AP Duration: 250-300 msec in contractile cells, significantly longer than in skeletal muscle (preventing tetany).
Phases of AP: Rapid depolarization, plateau, and repolarization.
Na+ Channels: Key for rapid depolarization; both absolute and relative refractory periods are critical for preventing abnormal heart rhythms.
Competition between potassium efflux and calcium influx leads to a plateau in the membrane potential, stabilizing it before repolarization begins.
Following the plateau, K+ efflux predominates while Ca2+ channels close.
The action potential triggers contraction in muscle fibers; calcium ions are fundamental for muscle contraction.
Calcium Sources: A portion is supplied by the plateau phase, which triggers further release from the SR.
Contractile cells are interconnected via gap junctions, ensuring coordinated contraction across the heart muscle.
Represents the summation of electrical activity among various cardiac cells, including pacemaker and contractile action potentials.
Video link to further illustrate differences between nodal and contractile action potentials.
Components: P wave, QRS complex, T wave - correspond to stages of atrial and ventricular depolarization and repolarization.
Arrhythmias: Explains various conditions like PACs, PVCs, Atrial Fibrillation, and Ventricular Tachycardia, detailing their impact on heart rhythm and function.
Detailed descriptions match arrhythmias with their ECG signature, facilitating assessment and recognition of abnormal heart rhythms.