Cardiac Action Potential Properties of Cardiac Muscles PDF
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Jinnah Sindh Medical University
Dr. Padma Rathore
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Summary
This document provides an overview of the cardiac action potential and properties of cardiac muscles. It discusses the different phases of the action potential, the Frank Starling Law, and the excitation-contraction coupling process. The document also includes information on the heart's conductive system and its role in initiating and conducting electrical impulses. It's well-suited for undergraduate-level physiology courses.
Full Transcript
# Cardiac Action Potential Properties of Cardiac Muscles *Dr. Padma Rathore, Assistant Professor, Physiology* ## Learning Objectives * At the end of the lecture, the student will be able to define: * The properties of cardiac muscle * Frank Starling Law * The initiation of action pote...
# Cardiac Action Potential Properties of Cardiac Muscles *Dr. Padma Rathore, Assistant Professor, Physiology* ## Learning Objectives * At the end of the lecture, the student will be able to define: * The properties of cardiac muscle * Frank Starling Law * The initiation of action potential * Different phases of action potential ## Cardiovascular System - The heart consists of two separate pumps, right heart pumps the blood through the lungs and left heart pumps the blood to peripheral organs. - The two chambers: atria are the primer pump for the ventricle whereas the ventricles propel the blood in either pulmonary or peripheral circulation. ## Cardiac Muscle - It consists of contractile fibers (99%) which are atrial and ventricular muscles. - The specialized excitatory and conductive fibers necessary for the production of Action potential. ## Heart Function as Syncytium - When one cardiac cell undergoes an action potential, the electrical impulse spreads to all other cells that are joined by gap junctions so they become excited and contract as a single functional syncytium. - Atrial Syncytium and Ventricular Syncytium. ## Cardiac Muscles Act as a Syncytium Connected Through Gap Junctions and Desmosomes | Feature | Description | | ------------------------------------- | ---------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------- | | Desmosome | Provides greater strength between cells. | | Gap junction | For rapid communication between cells. | | Intercalated disc | Structure that connects cardiac muscle cells. Contains gap junctions and desmosomes. | | Plasma membrane | The outer layer of the cell. | | Gap Junction Channels | Allows electrical currents to flow between cells. | | Electrical Currents | The flow of electrical signals through gap junctions. | | Sarcomere | The basic unit of the muscle. | ## Properties of Cardiac Muscles 1. **Autorhythmicity:** The ability to initiate a heart beat continuously and regularly without external stimulation. 2. **Excitability:** The ability to respond to a stimulus. 3. **Conductivity:** The ability to conduct excitation through the cardiac tissue. 4. **Contractility:** The ability to contract in response to stimulation. ## Autorhythmicity - **Definition:** Ability of the cell to undergo depolarization spontaneously causing the production of electrical impulses at regular intervals (rhythmicity). - **Mechanism:** It is due to the specialized excitatory & conductive system of the heart. - **Functions:** 1. Act as a pacemaker (set the rhythm of electrical excitation) 2. Form the conductive system (network of specialized cardiac muscle fibers that provide a path for each cycle of cardiac excitation to progress through the heart) ### Mechanism of Auto Rhythmicity * **Autorhythmic cells do not have stable resting membrane potential (RMP)** * **Natural Leakiness to Na & Ca → spontaneous and gradual depolarization.** * **Unstable resting membrane potential (= pacemaker potential)** * **Gradual depolarization reaches threshold (-40 mv) → spontaneous AP generation.** ## Self excitation of SA Node * Because of high Sodium concentration in extracellular fluid and negative potential in resting sinus nodal fibers, the positive sodium ions tend to leak to the inside. * This inherent leakiness of sinus nodal fibers to sodium ions causes their self excitation. ## Resting Membrane Potential - In Sinoatrial Node: -55 to -60 mv - In Ventricular muscles: -85 to -90 mv - Threshold for excitation of SA node: -40 mv ## SA Node Action Potential - **RMP of SA node** : -55 to -60 mv in comparison of ventricular muscles' RMP (-85 to -95 mv). - **When memb.potential remains less negative than -60 mv**. The sodium channels closed. - **So only slow calcium-sodium channels become activated and cause AP.** - **Therefore the AP of SA node is slower to develop and also returns slowly to RMP as compared to ventricular muscle** ## SA Node (As Pacemaker) Action Potential - **Slow depolarization:** Pacemaker potential - **Fast Ca <sup>2+</sup> channels open.** - **Ca <sup>2+</sup> permeability** - **K<sup>+</sup> permeability accompanied by slow Na <sup>+</sup> entry** - **Action potential** - **Threshold** ## Action Potential in Cardiac Muscle | Phase | Description | | ------- | ------------------------------------- | | Phase 0 | Rapid Depolarization | | Phase 1 | Rapid Repolarization | | Phase 2 | Plateau | | Phase 3 | Final Repolarization | | Phase 4 | Resting membrane potential | ## Phases of the Action Potential * Specific sequence of events * Phases 0 through 4 * **Phase 0:** Depolarization * **Phase 1:** Initial repolarization * **Phase 2:** Plateau * **Phase 3:** Rapid repolarization * **Phase 4:** Resting membrane potential ## Rate of Generation of AP at Different Sites of the Heart | Site | Rate (Times/min) | | ---------------------------------------- | ----------------- | | SA node | 100 | | AV node | 40 – 60 | | AV bundle, bundle branches, & Purkinje fibres | 20 – 35 | - **SA node acts as heart pacemaker because it has the fastest rate of generating action potential** ## Excitability and Conductivity - **Definition:** The ability of cardiac muscle to respond to a stimulus of adequate strength & duration by generating an action potential (AP). - **AP initiated by SA node → travels along conductive pathway → excites atrial & ventricular muscle fibers** ## Conductivity - **Conductivity is the ability to propagate an impulse** - **Normally impulses are conducted in one direction** - **The velocity of conduction of action potential in atrial and ventricular muscle fibers**: 0.3 to 0.5 m/sec. This is about 1/250 the velocity in large nerve fibers; 1/10 the velocity in skeletal muscle fibers. - **The velocity of conduction in specialized Purkinje fibers:** 0.02 to 4 m/sec. ## Contractility - **Cardiac muscle contracts in response to the electrical impulse generated by the SA node**. - **Cardiac muscle begins to contract a few millisecond after the action potential begins and continues to contract until a few msec. after the AP ends.** - Values: - 0.2 sec in atrial muscle. - 0.3 sec in ventricular muscle. ## Refractory Period of Cardiac Muscle - **Cardiac muscle is refractory to restimulation during action potential**. - **It is the interval of time during which a normal cardiac impulse cannot reexcite an already excited area of cardiac muscle**. - **The normal refractory period of ventricles:** 0.25 to 0.30 sec. - **The refractory period of atrial muscles:** 0.15 sec ## Frank Starling Law - **The intrinsic ability of the heart to adapt to increasing volumes of inflowing blood is called the Frank Starling Mechanism of heart**. - **It means that the greater the heart muscle is stretched during filling the greater is the force of contraction and the greater the quantity of blood pumped into the aorta**. - **Within physiological limits, the heart pumps all the blood that returns to it by way of the veins.** ## Excitation Contraction Coupling - **It is the mechanism by which the action potential causes the myofibrils of muscle to contract.** - **The contraction is caused by the release of calcium ions from the sarcoplasmic reticulum and T-tubules.** - **Sarcoplasmic reticulum is much less developed in cardiac muscles as compared to skeletal muscles so the source of calcium in cardiac muscles is from extracellular calcium which then enters the t-tubules.**