Clase 16 Fisiología Cardíaca 1 - Contracción-excitación y Potencial de acción (IG:@doctor.paiva)

Introduction to Cardiac Physiology

Overview of the Class

• The sixteenth class on physiology introduces topics related to cardiac muscle contraction, excitation, and action potentials.

• Key areas of focus include general characteristics of cardiac muscle, physiological anatomy, action potentials, refractory periods, and the coupling of excitation and contraction.

Importance of the Heart

• The heart is central to the circulatory system and indirectly supports metabolism by pumping oxygenated blood and nutrients throughout the body.

• It consists of four chambers: right atrium, left atrium, right ventricle, and left ventricle.

Cardiac Circulation Process

Blood Flow Dynamics

• The heart functions as two separate pumps: right for deoxygenated blood and left for oxygenated blood.

• Deoxygenated blood returns from the body via superior and inferior vena cavae into the right atrium before moving to the right ventricle.

Pulmonary Circulation

• Blood is then pumped from the right ventricle to the lungs through pulmonary arteries for gas exchange.

• Oxygen-rich blood returns to the heart via pulmonary veins into the left atrium before entering the left ventricle.

Muscle Types in Cardiac Function

Types of Cardiac Muscle

• The heart comprises three main types of muscle: atrial muscle, ventricular muscle, and specialized conduction fibers that contract weakly but generate electrical impulses.

• Histologically similar to skeletal muscle with actin and myosin arrangements; however, there are significant functional differences.

Functional Characteristics

• Cardiac muscle operates as a syncytium due to intercalated discs allowing ion diffusion between cells for coordinated contractions.

Electrical Activity in Cardiac Muscle

Pacemaker Mechanism

• The cardiac conduction system initiates impulses through natural pacemakers; primarily driven by the sinoatrial (SA) node.

• Action potentials propagate through intercalated discs leading to synchronized contractions across cardiac tissue.

Phases of Contraction

• Two key phases are identified: diastole (muscle relaxation filling ventricles with blood), and systole (muscle contraction ejecting blood).

Significance of Perfusion

Target Organs Dependent on Perfusion

• Vital organs such as heart, kidneys, and brain rely heavily on adequate perfusion for maintaining homeostasis. These are termed target organs due to their high perfusion needs.

Structural Division within Heart Functionality

Atrial vs. Ventricular Synchronization

• The heart's structure allows for sequential contraction—atria contract before ventricles—facilitating efficient blood flow which will be explored further in upcoming classes.

Cardiac Action Potential Phases

Overview of Cardiac Action Potential Phases

• The cardiac action potential begins with Phase 0, characterized by rapid depolarization due to sodium influx, shifting the intracellular voltage from -85mV to +20mV.

• In Phase 1, sodium channels inactivate, leading to a brief and rapid potassium efflux known as initial rapid repolarization. Chloride ions also enter the cell during this phase.

• Phase 2 involves the opening of slow calcium and sodium channels, prolonging the plateau phase before transitioning into Phase 3, where potassium channels open for rapid repolarization back to resting potential.

Mechanisms of Repolarization

• The process is regulated by the sodium-potassium pump, which extrudes three sodium ions while bringing in two potassium ions, essential for restoring ionic balance after action potentials.

• Two key phenomena contribute to prolonged action potentials: slow calcium-sodium channel activity extends the plateau duration, and decreased potassium permeability post-depolarization allows sustained calcium entry.

Conduction Velocity and Refractory Periods

• The conduction velocity of action potentials varies: atrial and ventricular fibers conduct at 0.3 to 0.5 m/s, while Purkinje fibers are faster at approximately 4 m/s.

• The cardiac muscle exhibits refractory periods; the absolute refractory period (0.25 - 0.30 seconds for ventricles) prevents any new action potential regardless of stimulus strength.

Relative Refractory Period Insights

• During the relative refractory period, a strong stimulus can induce another action potential since some sodium channels may be closed but not inactive.

• A notable example includes early extrasystoles occurring when a strong stimulus activates cells during their relative refractory period.

Histology and Functionality of Cardiac Muscle

Structural Characteristics

• Cardiac muscle shares histological similarities with skeletal muscle; it contains sarcolemma (cell membrane), mitochondria for ATP production, nuclei, and specialized endoplasmic reticulum called sarcoplasmic reticulum for calcium storage.

Myofibril Composition

• Myofibrils consist of repeating units called sarcomeres made up of actin (thin filaments) and myosin (thick filaments), crucial for contraction mechanisms.

Mechanism of Contraction

• Actin interacts with myosin heads during contraction; troponin binds calcium to expose active sites on actin allowing myosin attachment leading to muscle contraction.

Excitation-Contraction Coupling

Role of Calcium in Contraction

Physiology of Muscle Contraction

Mechanism of Muscle Contraction

• The contraction of myofibrils occurs when an action potential travels through the membrane and tubules, leading to the opening of voltage-dependent calcium channels in the cell membrane and sarcoplasmic reticulum.

• Calcium is released into the cytosol from the sarcoplasmic reticulum and enters from extracellular fluid, binding to troponin to initiate muscle contraction. This process involves a detailed mechanism previously discussed in skeletal muscle physiology.

• Calcium binds to troponin C, exposing active sites for myosin heads on actin filaments. Myosin then attaches to these active sites, with ATP being hydrolyzed by myosin ATPase during this interaction.

• The hydrolysis of ATP leads to a power stroke where the relaxed sarcomere contracts and shortens. Troponin inhibits active sites during relaxation when calcium is pumped back out.

Calcium Pumping Mechanisms

• Relaxation involves calcium pumping mechanisms that recapture calcium via the sarcoplasmic reticulum or sodium-calcium pumps, with lesser involvement from plasma membrane calcium pumps.

Adrenergic Receptors and Calcium Dynamics

• Adrenergic receptors (specifically beta 1 receptors) are stimulated by catecholamines like adrenaline, increasing intracellular calcium influx through phosphorylation of calcium channels via cyclic AMP signaling pathways.

• Cardiac glycosides increase intracellular calcium by inhibiting sodium-potassium pumps, leading to higher sodium levels which reduce sodium-calcium exchange efficiency, thus raising intracellular calcium concentrations.

Clinical Implications

• Increased intracellular calcium enhances contractile force; this effect is significant in treating heart conditions such as heart failure and arrhythmias due to its direct impact on cardiac function.

Conclusion