3. Auto rhythmicity and excitability

Autorhythmicity

• Autorhythmicity is the property of cardiac muscle to spontaneously generate its own action potentials (automaticity) in a regular and rhythmic manner (rhythmicity).

• The Heart's Pacemakers:

• Sinoatrial (SA) node: The primary pacemaker, located in the right atrial wall. It has the fastest inherent rate (100-110 beats/min) and sets the heart's normal rhythm (sinus rhythm).

• Atrioventricular (AV) node: A secondary, or latent, pacemaker. It's located at the base of the right atrium and takes over if the SA node fails. Its intrinsic rate is slower (45-60 beats/min), resulting in a nodal rhythm.

• Purkinje fibers: Tertiary, or latent, pacemakers. They have the slowest rate (25-40 beats/min) and take over if both the SA and AV nodes fail, leading to an idioventricular rhythm.

• Overdrive Suppression:

• This is the phenomenon where the fastest pacemaker (the SA node) suppresses the activity of all other latent pacemakers by driving them at a faster rate.

• Factors Affecting Autorhythmicity: These are called chronotropic factors.

• Positive chronotropic factors: Increase heart rate (e.g., sympathetic stimulation, catecholamines).

• Negative chronotropic factors: Decrease heart rate (e.g., vagal stimulation, acetylcholine).

Excitability

• Excitability is the ability of the heart to respond to a stimulus by generating an action potential.

Cardiac Action Potentials

• Two types of action potentials:

• Slow-response fibers: Found in the SA and AV nodes. They have an unstable resting potential, a slow depolarization phase, and no plateau.

• Rapid-response fibers: Found in the atria, ventricles, and Purkinje fibers. They have a stable resting potential and a fast depolarization followed by a plateau phase.

Phases of a Rapid-Response Action Potential (for contractile cells):

• Phase 4 (Resting Potential): The cell is at rest at about -90 mV.

• Phase 0 (Upstroke/Depolarization): A stimulus opens fast voltage-gated sodium (Na+) channels, causing a rapid influx of Na+ into the cell. The membrane potential rises quickly.

• Phase 1 (Initial Repolarization): Na+ channels inactivate, and some potassium (K+) channels open, causing a small efflux of K+ and a slight drop in membrane potential.

• Phase 2 (Plateau): This is a unique and critical phase for cardiac muscle. Calcium (Ca++) channels open, allowing a slow influx of Ca++ into the cell. At the same time, some K+ channels are open, allowing a slow efflux of K+. The balance between the inward Ca++ current and the outward K+ current results in a prolonged period where the membrane potential stays near zero.

• Phase 3 (Repolarization): The Ca++ channels close, and more potassium (K+) channels open. A large efflux of K+ rapidly brings the membrane potential back down to its resting level.

• The prolonged plateau phase is crucial for ensuring a long refractory period, which prevents the heart from entering a tetanic contraction.

• Phase 4 (Resting Potential):

The cell is at rest at about -90 mV.

• Phase 0 (Upstroke/Depolarization):

A stimulus opens fast voltage-gated sodium (Na+) channels, causing a rapid influx of Na+ into the cell. The membrane potential rises quickly.

• Phase 1 (Initial Repolarization):

Na+ channels inactivate, and some potassium (K+) channels open, causing a small efflux of K+ and a slight drop in membrane potential.

• Phase 2 (Plateau):

This is a unique and critical phase for cardiac muscle. Calcium (Ca++) channels open, allowing a slow influx of Ca++ into the cell. At the same time, some K+ channels are open, allowing a slow efflux of K+. The balance between the inward Ca++ current and the outward K+ current results in a prolonged period where the membrane potential stays near zero.

• Phase 3 (Repolarization):

The Ca++ channels close, and more potassium (K+) channels open. A large efflux of K+ rapidly brings the membrane potential back down to its resting level.

• The prolonged plateau phase is crucial for ensuring a long refractory period, which prevents the heart from entering a tetanic contraction.

Phases of Excitability:

• Absolute Refractory Period (ARP): Extends from phase 0 to the middle of phase 3. During this time, the cell is completely unresponsive to any new stimulus, no matter how strong. This prevents re-excitation and a tetanic state.

• Relative Refractory Period (RRP): Occupies the remainder of phase 3. The cell can be excited by a very strong stimulus, but the response will be weaker than normal.

• Supernormal Phase: A brief period in phase 4 where a weaker than normal stimulus can elicit a response.

• Absolute Refractory Period (ARP):

• Extends from phase 0 to the middle of phase 3. During this time, the cell is completely unresponsive to any new stimulus, no matter how strong. This prevents re-excitation and a tetanic state.

• Relative Refractory Period (RRP):

• Occupies the remainder of phase 3. The cell can be excited by a very strong stimulus, but the response will be weaker than normal.

• Supernormal Phase:

• A brief period in phase 4 where a weaker than normal stimulus can elicit a response.

Factors Affecting the Absolute Refractory Period (ARP):

The duration of the ARP is directly proportional to the duration of the action potential, especially the plateau phase.

• Heart Rate: An increased heart rate shortens the action potential and thus the ARP.

• Temperature: Increased temperature shortens the ARP by increasing metabolism.

• Sympathetic Stimulation: Can prolong the plateau phase by delaying K+ efflux, thereby increasing the ARP.

• Drugs: Quinidine, beta-blockers, and calcium channel blockers can prolong the ARP, which is why they are used to treat arrhythmias like atrial flutter and fibrillation.

• Heart Rate:

• An increased heart rate shortens the action potential and thus the ARP.

• Temperature:

• Increased temperature shortens the ARP by increasing metabolism.

• Sympathetic Stimulation:

• Can prolong the plateau phase by delaying K+ efflux, thereby increasing the ARP.

• Drugs: Quinidine, beta-blockers, and calcium channel blockers

• can prolong the ARP, which is why they are used to treat arrhythmias like atrial flutter and fibrillation.

What is the definition of autorhythmicity and excitability in the heart, and what are the main phases of a cardiac action potential?

• Autorhythmicity & Excitability

• Autorhythmicity: The ability of the heart muscle to spontaneously generate its own electrical impulses in a regular, rhythmic manner. The main pacemaker is the SA node, but the AV node and Purkinje fibers can also take over if needed.

• Excitability: The ability of the heart muscle to respond to a stimulus by producing an action potential.

Phases of a Rapid-Response Action Potential (Contractile Cells)

• Phase 4 (Resting): The cell is at rest with a stable potential of about -90 mV.

• Phase 0 (Depolarization): Rapid influx of sodium (Na+) ions causes the membrane potential to rise sharply.

• Phase 1 (Initial Repolarization): Na+ channels inactivate, and some potassium (K+) ions leave the cell.

• Phase 2 (Plateau): A sustained period of depolarization due to a balance between slow inward calcium (Ca++) ions and outward potassium (K+) ions. This phase is crucial for preventing tetanus.

• Phase 3 (Repolarization): Potassium (K+) ions rapidly leave the cell, bringing the membrane potential back to its resting state.