Overview of Cardiovascular System (CVS) Physiology

Objectives of CVS Physiology

Understand the special characteristics of the heart, including its unique functions and mechanisms.

Explore the cardiac conduction system, which is essential for heart rhythm and function.

Analyze cardiac output, which is the volume of blood the heart pumps per minute, and its significance in overall health.

Study the cardiac cycle, which describes the sequence of events in one heartbeat, including contraction and relaxation phases.

Examine vascular physiology, focusing on blood vessels' structure and function, and their role in circulation.

Investigate blood pressure regulation mechanisms, including neural and hormonal influences.

Key Characteristics of the Heart

Automaticity: The heart's ability to generate its own electrical impulses without external stimuli, primarily through the SA node.

Excitability: The capacity of cardiac cells to respond to electrical stimuli, leading to contraction.

Conductivity: The ability of cardiac tissue to conduct electrical impulses rapidly, ensuring synchronized heartbeats.

Contractility: The strength of the heart's contraction, influenced by various factors including calcium levels and neural input.

Cardiac Conduction System

Anatomy of the Cardiac Conduction System

The cardiac conduction system is composed of specialized cardiac muscle cells that facilitate electrical impulses.

Key components include the SA node, AV node, Bundle of His, and Purkinje Fibres, which are crucial for heart rhythm.

The SA node, known as the heart's pacemaker, initiates each heartbeat and regulates heart rate.

The conduction system is non-contractile, meaning it does not contribute to the heart's pumping action but rather coordinates it.

Function of the SA Node

The SA node generates action potentials at a rate of approximately 100 beats per minute in the absence of external influences.

It is influenced by the autonomic nervous system: sympathetic stimulation increases heart rate, while parasympathetic stimulation decreases it.

The electrical impulse from the SA node spreads through the atria, causing simultaneous contraction of both atria.

Role of the AV Node

The AV node serves as a critical relay point for electrical impulses from the atria to the ventricles.

It introduces a delay (AV nodal delay) to allow the atria to fully contract and fill the ventricles with blood before ventricular contraction.

The AV node ensures one-way conduction, preventing backflow of impulses from the ventricles to the atria.

Electrical Activity of the Heart

Impulse Conduction Pathway

The SA node generates an action potential, which spreads through the atria, causing depolarization and contraction.

The AV node is the only pathway for impulses to travel from the atria to the ventricles due to the fibrous barrier separating them.

After the AV node, the impulse travels rapidly down the Bundle of His and into the right and left bundle branches.

The impulse spreads through the Purkinje fibres, ensuring rapid contraction of the ventricles.

Action Potential Formation in the SA Node

The SA node exhibits a prepotential phase due to sodium ion leakiness, leading to spontaneous depolarization.

When the membrane potential reaches approximately -40 mV, voltage-gated calcium channels open, causing rapid depolarization.

Repolarization occurs as potassium channels open, allowing potassium to exit the cell, returning the membrane potential to resting levels.

Differences in Atrial and Ventricular Muscle Action Potentials

Unlike nodal tissues, atrial and ventricular muscles do not generate their own action potentials under normal conditions.

The resting membrane potential (RMP) of ventricular muscle is stable at -90 mV, remaining unchanged until stimulated by the SA node.

Atrial and ventricular muscles rely on the conduction system for excitation and contraction.

Action Potentials in Cardiac Muscle

Phases of Action Potential

Phase 0 (Depolarization): Initiated by the SA node, this phase involves the rapid influx of sodium ions through fast voltage-gated sodium channels, leading to a significant depolarization of the membrane potential.

Phase 1 (Brief Repolarization): Sodium channels inactivate quickly, resulting in a transient repolarization as the membrane potential begins to decrease.

Phase 2 (Plateau Phase): Characterized by a sustained increase in calcium permeability due to the opening of voltage-gated calcium channels, which remain open longer than sodium channels, creating a plateau in the action potential.

Phase 3 (Repolarization): Calcium channels close and potassium channels open, leading to an efflux of potassium ions and a return towards the resting membrane potential.

Phase 4 (Resting Membrane Potential): The membrane returns to its resting state with the restoration of sodium, potassium, and calcium permeabilities, preparing for the next action potential.

Comparison of Action Potentials

The action potential duration in cardiac muscle (200-250 ms) is significantly longer than in nerve or skeletal muscle (2-15 ms), allowing for effective contraction and relaxation cycles.

The absolute refractory period (ARP) in cardiac muscle lasts nearly the entire duration of the action potential, preventing summation of contractions and allowing for proper filling of the ventricles.

Visual Representation of Action Potential Phases

Phase 0: Depolarization

Phase 1: Brief Repolarization

Phase 2: Plateau Phase

Phase 3: Repolarization

Phase 4: Resting Membrane Potential

Excitation-Contraction Coupling in Cardiac Muscle

Mechanism of Coupling

The process begins with an action potential traveling along the plasma membrane and T-tubules, leading to the opening of voltage-gated calcium channels in both the sarcoplasmic reticulum and the plasma membrane.

Calcium influx from the extracellular fluid (ECF) triggers further calcium release from the sarcoplasmic reticulum through calcium-induced calcium release mechanisms.

Calcium binds to troponin, causing a conformational change that shifts tropomyosin away from actin binding sites, allowing crossbridge cycling to occur.

Steps of Excitation-Contraction Coupling

Action potential spreads along the plasma membrane and T-tubules.

Voltage-gated Ca++ channels open in the sarcoplasmic reticulum and plasma membrane.

Increased calcium influx into the cytosol occurs.

Calcium binds to ligand-gated channels on the sarcoplasmic reticulum, promoting further calcium release.

Crossbridge cycling occurs, leading to muscle contraction.

Calcium is removed from the cytosol by various mechanisms, including Ca++ ATPase and Na+-Ca++ exchanger, leading to muscle relaxation.

Comparison with Skeletal Muscle

Cardiac muscle excitation-contraction coupling is similar to that of skeletal muscle, but the prolonged calcium influx during the plateau phase enhances crossbridge cycling and calcium release from the sarcoplasmic reticulum.

Autonomic Nervous System Effects on Cardiac Function

Parasympathetic Stimulation

Stimulation of parasympathetic nerves releases acetylcholine (ACh), which acts on muscarinic receptors, increasing potassium permeability and hyperpolarizing the SA nodal cells.

This results in a decreased heart rate (negative chronotropic effect) and prolonged AV nodal delay, reducing conduction speed from the atria to the ventricles.

Sympathetic Stimulation

Sympathetic stimulation releases noradrenaline, which binds to β1 receptors on SA nodal cells, increasing calcium permeability and depolarizing the membrane.

This leads to an increased heart rate (positive chronotropic effect) and a decrease in AV nodal delay, enhancing conduction speed.

Summary of ANS Effects

The balance between sympathetic and parasympathetic stimulation regulates heart rate and cardiac output, adapting to the body's needs during various activities.

Discussion questions1 of 6

What are the key characteristics of the cardiac conduction system, and how do they contribute to heart function?

Difficulty: Easy

How does the autonomic nervous system influence heart rate through the cardiac conduction system?

Difficulty: Medium

Discuss the significance of the AV node in the cardiac conduction system.

Difficulty: Medium

Explain the phases of action potential in the SA node and their physiological importance.

Difficulty: Hard

What is the role of calcium in the excitation-contraction coupling of cardiac muscle?

Difficulty: Hard

How do the refractory periods in cardiac muscle differ from those in skeletal muscle, and why are they important?

Difficulty: Hard

Show example answer

The cardiac conduction system is characterized by automaticity, excitability, conductivity, and contractility. These features enable the heart to generate and propagate electrical impulses efficiently, ensuring coordinated contractions and effective blood pumping.

The autonomic nervous system modulates heart rate by affecting the SA node; sympathetic stimulation increases heart rate by enhancing calcium influx, while parasympathetic stimulation decreases it by increasing potassium efflux. This balance allows the body to adapt heart function to varying physiological demands.

The AV node plays a crucial role by slowing down the electrical impulse from the atria to the ventricles, allowing sufficient time for the atria to contract and fill the ventricles with blood. This delay is essential for maintaining effective cardiac output and preventing arrhythmias.

The action potential in the SA node consists of a prepotential phase, rapid depolarization, and repolarization. This sequence is vital for initiating heartbeats and maintaining a rhythmic heart rate, as it allows the SA node to act as the primary pacemaker of the heart.

Calcium plays a pivotal role in excitation-contraction coupling by entering the cardiac muscle cells during the plateau phase of the action potential, which triggers further calcium release from the sarcoplasmic reticulum. This influx is essential for crossbridge cycling and muscle contraction, distinguishing cardiac muscle function from that of skeletal muscle.

Cardiac muscle has longer refractory periods compared to skeletal muscle, preventing summation of contractions and allowing the heart to relax and fill with blood between beats. This characteristic is crucial for maintaining a rhythmic heartbeat and preventing conditions such as tetany, which could compromise cardiac function.