Functional Anatomy of Heart, Cardiac Muscle, Conducting System, and Cardiac Innervation

Introduction

The heart functions as an efficient muscular pump through the coordinated activity of specialized cardiac muscle fibers, an intrinsic conducting system, and autonomic innervation. This chapter explains how synchronized electrical activation, myocardial mechanics, and neural regulation work together to maintain effective cardiac output and a stable heart rate.

• The heart is a specialized muscular organ capable of generating rhythmic contractions throughout life.
• Although cardiac muscle resembles skeletal muscle structurally, it contracts independently of voluntary neural stimulation.
• Electrical impulses originate in the sinoatrial node, the normal cardiac pacemaker.
• Coordinated myocardial contraction pumps blood effectively through the circulation.
• Unique electrical, mechanical, and excitation–contraction coupling properties enable the heart to resist fatigue and prevent tetanic contraction, ensuring continuous cardiac function.

Functional Anatomy

• The heart is a hollow muscular organ approximately equal in size to an individual’s clenched fist.
• In adults, it weighs about 250–350 grams, depending on sex and body size.
• The heart is enclosed within the pericardium, which provides protection and support.
• It consists of four chambers: right and left atria, and right and left ventricles.
• The cardiac wall has three layers: endocardium, myocardium, and epicardium.
• The myocardium is thickest in the ventricles, especially the left ventricle, because of its greater pumping workload.

H3: Pericardium

• The pericardium is a double-layered sac that encloses, protects, and stabilizes the heart within the thoracic cavity.

H4: Fibrous Pericardium

• The fibrous pericardium is the outermost layer of the pericardial sac.
• It is composed of dense irregular connective tissue that provides mechanical strength and support.
• Its relatively inelastic nature limits excessive cardiac expansion and helps prevent acute overdistension of the heart.

Serous Pericardium

• The serous pericardium lies internal to the fibrous pericardium and consists of two layers.
• The parietal layer lines the inner surface of the fibrous pericardium.
• The visceral layer closely adheres to the external surface of the heart and is also known as the epicardium.

Pericardial Cavity

• The pericardial cavity is the potential space located between the parietal and visceral layers of the serous pericardium.
• This cavity normally contains about 15–50 milliliters of pericardial fluid.
• Pericardial fluid acts as a lubricant and reduces friction during cardiac contraction and relaxation.
• The fluid allows smooth movement of the heart within the pericardial sac throughout the cardiac cycle.
• Excess accumulation of fluid within the pericardial cavity is termed pericardial effusion.
• Pericardial effusion may occur in conditions such as pericardial inflammation, infection, malignancy, or trauma.
• Large or rapidly developing effusions can impair cardiac filling and compromise cardiac function.

Wall of Heart Chambers

• The wall of each heart chamber consists of three layers: epicardium, myocardium, and endocardium.

Epicardium

• The epicardium is the outermost layer and corresponds to the visceral layer of the serous pericardium.
• It is composed of mesothelium and supporting connective tissue that protects the heart surface.

Myocardium

• The myocardium is the middle and thickest layer of the cardiac wall.
• It consists of specialized cardiac muscle fibers responsible for the pumping action of the heart.
• The myocardium is most developed in the ventricles because they generate the force required to eject blood.
• Atrial walls are relatively thin, typically about 2–3 millimeters thick, because atrial contraction contributes only a small portion of ventricular filling.
• The right ventricular wall is approximately 3–5 millimeters thick and pumps blood into the low-pressure pulmonary circulation.
• The left ventricular wall is approximately 8–15 millimeters thick and generates the high pressure needed for systemic circulation.
• Ventricular muscle fibers are arranged in a complex spiral pattern.
• This spiral arrangement enhances the efficiency of ventricular contraction and promotes effective ejection of blood during systole.

Endocardium

• The endocardium lines the inner surface of the heart and consists of endothelium supported by thin connective tissue.
• It provides a smooth blood-contacting surface and is continuous with the endothelial lining of major blood vessels.

Cardiac Chambers

• The heart consists of four chambers: right and left atria, and right and left ventricles.
• The atria are thin-walled, low-pressure chambers that receive blood and act as temporary reservoirs.
• The ventricles have thicker muscular walls and generate the force required to pump blood into the pulmonary and systemic circulations.

Right Atrium

• The right atrium receives deoxygenated blood from the body through the superior and inferior venae cavae and the coronary sinus.
• Blood passes from the right atrium to the right ventricle through the tricuspid valve.
• Most ventricular filling occurs passively during ventricular relaxation.
• Atrial contraction contributes approximately 15–20% of ventricular filling under normal resting conditions.

Left Atrium

• The left atrium receives oxygenated blood from the lungs through four pulmonary veins.
• It delivers blood to the left ventricle through the mitral valve.

Right Ventricle

• The right ventricle pumps deoxygenated blood into the pulmonary circulation through the pulmonary valve.
• During systole, the right ventricle normally generates a peak pressure of approximately 25 millimeters of mercury.

Left Ventricle

• The left ventricle pumps oxygenated blood into the systemic circulation through the aortic valve.
• It generates a much higher peak systolic pressure, approximately 120 millimeters of mercury, to perfuse the entire body.

Cardiac Valves

• Cardiac valves are located between the cardiac chambers and at the ventricular outflow tracts.
• They ensure unidirectional blood flow through the heart and prevent backward movement of blood.
• Each valve is formed by thin fibrous leaflets covered by endothelium and attached to a fibrous valve ring.
• The opening and closing of valve leaflets occur in response to pressure changes within the heart.
• There are four cardiac valves: two atrioventricular valves and two semilunar valves.

Atrioventricular Valves

• Atrioventricular valves are situated between the atria and ventricles.
• The left atrioventricular valve is the mitral valve, which consists of two cusps.
• The right atrioventricular valve is the tricuspid valve, which consists of three cusps.
• The valve leaflets are larger than the corresponding atrioventricular openings.
• During valve closure, the leaflets overlap sufficiently to form a tight seal.
• This overlap effectively prevents regurgitation of blood from the ventricles into the atria during ventricular contraction.
• Chordae tendineae are strong fibrous cords attached to the free margins of the valve leaflets.
• These cords connect the valve leaflets to papillary muscles within the ventricles.
• Contraction of papillary muscles stabilizes the valve leaflets during ventricular systole.
• Chordae tendineae prevent prolapse or inversion of the valve leaflets into the atria.

Semilunar Valves

• Semilunar valves are located at the ventricular outflow openings.
• The pulmonary valve lies between the right ventricle and the pulmonary trunk.
• The aortic valve lies between the left ventricle and the aorta.
• Each semilunar valve is composed of three crescent-shaped cusps attached to a fibrous ring.
• At the start of ventricular systole, increased ventricular pressure opens these valves.
• Blood is then ejected into the pulmonary trunk and aorta.
• As ventricular relaxation begins, blood briefly tends to flow backward toward the ventricles.
• This reverse flow fills the cusps and causes them to close rapidly.
• Valve closure prevents regurgitation of blood into the ventricles and maintains efficient cardiac function.

Cardiac Muscle

• Cardiac muscle forms the myocardium and is classified as involuntary striated muscle.
• Individual cardiac muscle cells are enclosed by a cell membrane and usually contain one centrally located nucleus.
• The muscle fibers are short, cylindrical, and characteristically branched.
• Adjacent cardiac muscle cells are connected by specialized junctions called intercalated discs.
• Intercalated discs contain gap junctions and mechanical junctions that provide structural and electrical continuity.
• Gap junctions permit rapid passage of ions and electrical impulses between neighboring cells.
• As a result, depolarization spreads quickly throughout the myocardium.
• This coordinated electrical activity allows the heart to contract efficiently as a functional syncytium.
• Such synchronization is essential for effective pumping of blood.

Left Atrium

• The left atrium receives oxygenated blood from the lungs through four pulmonary veins.
• It delivers blood to the left ventricle through the mitral valve.

Right Ventricle

• The right ventricle pumps deoxygenated blood into the pulmonary circulation through the pulmonary valve.
• During systole, the right ventricle normally generates a peak pressure of approximately 25 millimeters of mercury.

Left Ventricle

• The left ventricle pumps oxygenated blood into the systemic circulation through the aortic valve.
• It generates a much higher peak systolic pressure, approximately 120 millimeters of mercury, to perfuse the entire body.

Cardiac Valves

• Cardiac valves are located between the cardiac chambers and at the ventricular outflow tracts.
• They ensure unidirectional blood flow through the heart and prevent backward movement of blood.
• Each valve is formed by thin fibrous leaflets covered by endothelium and attached to a fibrous valve ring.
• The opening and closing of valve leaflets occur in response to pressure changes within the heart.
• There are four cardiac valves: two atrioventricular valves and two semilunar valves.

Atrioventricular Valves

• Atrioventricular valves are situated between the atria and ventricles.
• The left atrioventricular valve is the mitral valve, which consists of two cusps.
• The right atrioventricular valve is the tricuspid valve, which consists of three cusps.
• The valve leaflets are larger than the corresponding atrioventricular openings.
• During valve closure, the leaflets overlap sufficiently to form a tight seal.
• This overlap effectively prevents regurgitation of blood from the ventricles into the atria during ventricular contraction.
• Chordae tendineae are strong fibrous cords attached to the free margins of the valve leaflets.
• These cords connect the valve leaflets to papillary muscles within the ventricles.
• Contraction of papillary muscles stabilizes the valve leaflets during ventricular systole.
• Chordae tendineae prevent prolapse or inversion of the valve leaflets into the atria.

Semilunar Valves

• Semilunar valves are located at the ventricular outflow openings.
• The pulmonary valve lies between the right ventricle and the pulmonary trunk.
• The aortic valve lies between the left ventricle and the aorta.
• Each semilunar valve is composed of three crescent-shaped cusps attached to a fibrous ring.
• At the start of ventricular systole, increased ventricular pressure opens these valves.
• Blood is then ejected into the pulmonary trunk and aorta.
• As ventricular relaxation begins, blood briefly tends to flow backward toward the ventricles.
• This reverse flow fills the cusps and causes them to close rapidly.
• Valve closure prevents regurgitation of blood into the ventricles and maintains efficient cardiac function.

Cardiac Muscle

• Cardiac muscle forms the myocardium and is classified as involuntary striated muscle.
• Individual cardiac muscle cells are enclosed by a cell membrane and usually contain one centrally located nucleus.
• The muscle fibers are short, cylindrical, and characteristically branched.
• Adjacent cardiac muscle cells are connected by specialized junctions called intercalated discs.
• Intercalated discs contain gap junctions and mechanical junctions that provide structural and electrical continuity.
• Gap junctions permit rapid passage of ions and electrical impulses between neighboring cells.
• As a result, depolarization spreads quickly throughout the myocardium.
• This coordinated electrical activity allows the heart to contract efficiently as a functional syncytium.
• Such synchronization is essential for effective pumping of blood.

Table 85.1: Difference between the sarcotubular system of cardiac and skeletal muscle.

Feature	Cardiac Muscle	Skeletal Muscle
Sarcomere arrangement	Less uniform organization	Highly regular organization
T-tubule location	At the Z line	At the A–I junction
T-tubule size	Larger diameter	Smaller diameter
Sarcoplasmic reticulum terminal cisternae	Narrow and less developed	Large and well developed
T-tubule–cisternae complex	Diad (one T-tubule + one terminal cisterna)	Triad (one T-tubule + two terminal cisternae)

Myocardial Contractile System

• The myocardial contractile system is responsible for generating the force required for cardiac contraction.
• Cardiac muscle cells contain repeating contractile units called sarcomeres.
• Each sarcomere is composed of thick myosin filaments and thin actin filaments.
• Cardiac muscle contraction occurs through the sliding filament mechanism, similar to skeletal muscle.
• During contraction, actin filaments slide over myosin filaments, causing sarcomere shortening.
• This process generates tension and produces myocardial contraction.
• Although the contractile mechanism resembles that of skeletal muscle, cardiac muscle has important structural adaptations.
• Cardiac muscle cells contain numerous mitochondria, often occupying about 30–40% of the cell volume.
• The high mitochondrial content supports continuous aerobic metabolism and efficient production of adenosine triphosphate.
• This adaptation enables the heart to sustain rhythmic contractions throughout life.

Sarcotubular System

·  The sarcotubular system consists of transverse tubules and the sarcoplasmic reticulum.

• Transverse tubules are deep invaginations of the cell membrane that extend into the interior of cardiac muscle cells.
• In cardiac muscle, transverse tubules are located at the Z line of the sarcomere.
• They conduct electrical impulses rapidly into the cell and help synchronize contraction.
• The lumen of transverse tubules is continuous with extracellular fluid, facilitating calcium ion movement.
• Transverse tubules are more prominent in ventricular muscle cells than in atrial muscle cells.
• Their diameter is considerably larger than that of transverse tubules in skeletal muscle.
• The sarcoplasmic reticulum lies closely adjacent to the transverse tubules.
• Together, one transverse tubule and one terminal cisterna form a diad.
• In contrast, skeletal muscle contains a triad composed of one transverse tubule and two terminal cisternae.
• This specialized arrangement contributes to efficient excitation–contraction coupling in the myocardium.

Length–Tension Relationship

• The length–tension relationship describes the effect of myocardial fiber length on the force of contraction.
• Cardiac muscle develops maximum active tension when sarcomeres operate near their optimal length.
• At this length, the overlap between actin and myosin filaments is ideal for cross-bridge formation.
• Optimal filament interaction allows the generation of maximal contractile force.
• Stretching cardiac muscle within physiological limits increases the force of contraction.
• Increased sarcomere length enhances the sensitivity of myofilaments to calcium ions.
• Stretch also increases the affinity of troponin C for calcium, improving activation of the contractile apparatus.
• These changes enable greater force production without a substantial increase in intracellular calcium concentration.
• When sarcomeres are stretched beyond the optimal range, active tension decreases.
• Excessive stretch reduces the overlap between thick and thin filaments and decreases cross-bridge formation.
• Consequently, the force of contraction declines.
• This relationship plays an important role in the regulation of normal cardiac performance.

Frank-Starling Law of the heart

• The Frank–Starling law states that, within physiological limits, the force of cardiac contraction increases with the initial length of myocardial fibers.
• Increased ventricular filling during diastole raises the end-diastolic volume, which stretches myocardial fibers.
• Greater fiber stretch results in stronger ventricular contraction during the subsequent systole.
• This mechanism helps match cardiac output to venous return and maintains circulatory balance.
• Increased end-diastolic volume enlarges ventricular chamber dimensions and increases sarcomere length.
• Improved overlap between actin and myosin filaments enhances force generation.
• Stretch of myocardial cells can activate mechanosensitive ion channels, contributing to increased calcium entry.
• Additional calcium influx promotes a rise in intracellular calcium concentration.
• Calcium entering the cell triggers further calcium release from the sarcoplasmic reticulum through calcium-induced calcium release.
• The resulting increase in cytosolic calcium strengthens myocardial contraction.
• Stretch also increases the sensitivity of contractile proteins to calcium and enhances calcium binding to troponin C.
• Through these mechanisms, ventricular performance increases as preload rises, provided physiological limits are not exceeded.

Excitation-Contraction Coupling

• Excitation–contraction coupling is the process by which an electrical impulse triggers contraction of cardiac muscle.
• The basic mechanism resembles that of skeletal muscle, but cardiac contraction depends heavily on extracellular calcium ions.
• Proper concentrations of sodium, potassium, and calcium ions are essential for normal cardiac electrical and mechanical activity.
• These ions contribute to the generation of the resting membrane potential, action potentials, pacemaker activity, and myocardial contraction.
• Potassium ions play a major role in maintaining the resting membrane potential and cellular excitability.
• Sodium ions are important for rapid depolarization in working atrial and ventricular muscle cells.
• Calcium ions are essential for action potentials in certain cardiac tissues and for the development of contractile force.
• Reduced extracellular sodium concentration decreases the amplitude and rate of depolarization, thereby reducing excitability and conduction.
• Mild reductions in extracellular potassium generally have limited effects on excitability.
• Marked elevation of extracellular potassium causes membrane depolarization and impairs impulse generation and conduction.
• Severe hyperkalemia may lead to cardiac arrest in diastole.
• Increased extracellular calcium enhances myocardial contractility by increasing intracellular calcium availability.
• Excessively high calcium concentrations may produce sustained contraction and cardiac arrest in systole.
• Low extracellular calcium reduces contractile force and, in severe cases, may impair cardiac function significantly.
• When an action potential reaches the cardiac muscle cell membrane, it spreads into the cell through transverse tubules.
• Depolarization opens voltage-gated calcium channels located in the transverse tubule membrane.
• Calcium enters the cytoplasm from the extracellular fluid.
• This incoming calcium triggers additional calcium release from the sarcoplasmic reticulum through calcium-induced calcium release.
• The resulting increase in cytosolic calcium initiates contraction.
• Calcium binds to troponin C on the thin filament.
• This interaction shifts tropomyosin away from the active sites on actin filaments.
• Myosin heads can then bind to actin, allowing cross-bridge cycling and force generation.
• The magnitude of contraction depends largely on the amount of calcium available within the cytoplasm.
  • Any mechanism that increases intracellular calcium generally increases myocardial contractility.
  • Conversely, mechanisms that reduce intracellular calcium decrease contractile force.
  • Catecholamines such as epinephrine enhance contractility by increasing calcium entry and calcium availability within cardiac cells.
  • Cytosolic calcium can increase when extracellular calcium concentration rises.
  • Intracellular calcium also increases when the sodium gradient across the cell membrane decreases.
  • A reduced sodium gradient limits the activity of the sodium–calcium exchanger, decreasing calcium extrusion from the cell.
  • As a result, calcium accumulates within the cytoplasm and strengthens contraction.
  • Digoxin increases contractility by inhibiting sodium–potassium adenosine triphosphatase, raising intracellular sodium concentration.
  • The resulting reduction in sodium–calcium exchange promotes intracellular calcium accumulation and enhances myocardial force generation.

Contractility

• Contractility is the intrinsic ability of the myocardium to generate force at a given fiber length and ventricular filling volume.
• It reflects ventricular performance independent of preload.
• Increased contractility produces greater force development and a faster rate of myocardial contraction.

Capillary Density

• The myocardium has an exceptionally rich capillary network to support its high metabolic demand.
• Cardiac muscle contains approximately one capillary for each muscle fiber, providing an abundant blood supply.
• This capillary density is much greater than that of skeletal muscle.
• The short diffusion distance between capillaries and muscle cells facilitates efficient delivery of oxygen and nutrients.
• It also promotes rapid removal of carbon dioxide and metabolic waste products.

Conducting System of the Heart

• The conducting system of the heart generates and distributes electrical impulses that coordinate cardiac activity.
• It consists of the sinoatrial node, atrial conduction pathways, atrioventricular node, atrioventricular bundle, bundle branches, and Purkinje fibers.
• This specialized tissue ensures orderly activation of the atria and ventricles.

SA Node

• The sinoatrial node is the normal pacemaker of the heart.
• It is located in the upper part of the right atrial wall near the opening of the superior vena cava.
• The node is composed of specialized pacemaker cells and a small number of contractile elements.
• Pacemaker cells possess spontaneous electrical activity and generate rhythmic impulses without external stimulation.
• These impulses initiate each cardiac cycle and determine the normal heart rate.
• The action potentials of sinoatrial nodal cells are classified as slow-response action potentials.
• Electrical conduction within the sinoatrial node is relatively slow, with an approximate velocity of 0.05 meters per second.
• Under normal conditions, the sinoatrial node discharges at a higher rate than other pacemaker tissues and therefore dominates cardiac rhythm.

Internodal Pathways

• Electrical impulses spread rapidly through the atrial myocardium from the sinoatrial node.
• Specialized atrial conduction pathways facilitate transmission toward the atrioventricular node.
• Three major pathways are commonly described: anterior, middle, and posterior internodal pathways.
• Additional atrial conduction fibers may also contribute to impulse propagation.
• The anterior pathway gives rise to Bachmann bundle, the principal interatrial conduction tract.
• Bachmann bundle conducts impulses from the right atrium to the left atrium, promoting synchronized atrial contraction.
• Conduction velocity in these pathways is approximately 1 meter per second, allowing rapid atrial activation.
• The internodal pathways converge toward the atrioventricular node.

AV Node

• The atrioventricular node is located in the lower part of the right atrium near the interatrial septum.
• It lies close to the opening of the coronary sinus and above the fibrous atrioventricular skeleton.
• The atrioventricular node contains small-diameter cells and a complex branching arrangement.
• These structural features slow impulse conduction to approximately 0.05 meters per second.
• A physiological delay of about 0.1 second occurs within the atrioventricular node.
• This delay allows atrial contraction to be completed before ventricular contraction begins.
• Sympathetic stimulation shortens the nodal delay, whereas parasympathetic stimulation prolongs it.
• The node also exhibits decremental conduction, which limits transmission of excessively rapid atrial impulses to the ventricles.
• Like the sinoatrial node, it generates slow-response action potentials.
• The atrioventricular node contains latent pacemaker cells with an intrinsic firing rate lower than that of the sinoatrial node.
• If sinoatrial nodal activity fails, the atrioventricular node can assume the pacemaker function and maintain cardiac rhythm.

His Bundle

• The atrioventricular bundle (His bundle) is the only normal electrical connection between the atria and ventricles.
• It arises from the atrioventricular node and passes through the fibrous cardiac skeleton into the interventricular septum.
• The bundle is approximately 1 centimeter long before dividing into right and left bundle branches.
• It rapidly conducts impulses from the atrioventricular node to the ventricular conduction system.
• Cells within the His bundle possess latent pacemaker activity.
• If both the sinoatrial and atrioventricular nodes fail, the His bundle may generate escape rhythms at a slower rate.

Bundle Branches

• The His bundle divides into right and left bundle branches within the interventricular septum.
• These branches conduct electrical impulses to their respective ventricles.
• Distally, they give rise to Purkinje fibers, which distribute impulses throughout the ventricular myocardium.
• Bundle branch cells can also exhibit automaticity under pathological conditions.

Right Bundle Branch

• The right bundle branch is longer and thinner than the left bundle branch.
• It conducts impulses to the right ventricular myocardium and ensures coordinated right ventricular contraction.

Left Bundle Branch

• The left bundle branch is broader and divides into anterior and posterior fascicles.
• The anterior fascicle supplies the anterior and superior regions of the left ventricle.
• The posterior fascicle supplies the posterior and inferior regions of the left ventricle.
• This branching pattern promotes synchronized activation of the left ventricle.

Purkinje Fibers

• Purkinje fibers form a specialized network of conducting cells located mainly in the subendocardial regions of both ventricles.
• These cells are the largest specialized conducting cells in the heart.
• They contain numerous gap junctions, which provide low-resistance pathways for electrical impulse transmission.
• Their large cell diameter and extensive intercellular connections enable very rapid conduction.
• Purkinje fibers conduct impulses at approximately 2–4 meters per second, making them the fastest-conducting elements of the cardiac conduction system.
• This rapid conduction ensures nearly simultaneous activation of ventricular myocardium and promotes efficient ventricular contraction.
• Their action potentials are fast-response type and resemble those of ventricular muscle cells.

Cardiac Innervation

• The heart receives autonomic innervation from both the sympathetic and parasympathetic divisions of the nervous system.
• These systems continuously regulate heart rate, impulse conduction, and myocardial contractility.
• In general, sympathetic stimulation enhances cardiac activity, whereas parasympathetic stimulation suppresses it.
• The sinoatrial node is influenced continuously by both autonomic divisions.
• Under resting conditions, parasympathetic activity predominates, producing a lower resting heart rate than the intrinsic pacemaker rate.
• Therefore, normal resting heart rate is largely determined by vagal tone.
• Ventricular myocardium receives abundant sympathetic innervation but relatively sparse parasympathetic innervation.
• As a result, ventricular contractility and stroke volume are influenced mainly by sympathetic activity.

Parasympathetic Innervation

• Cardiac parasympathetic fibers travel through the right and left vagus nerves.
• Preganglionic neurons originate from autonomic centers in the medulla oblongata, including the dorsal motor nucleus of the vagus, nucleus ambiguus, and associated cardiovascular regulatory pathways.
• Most parasympathetic ganglia are located within or near the cardiac wall.
• Consequently, postganglionic fibers are short and distributed within the heart.
• The right vagus nerve predominantly supplies the sinoatrial node and much of the right atrium.
• Stimulation of the right vagus nerve produces a marked reduction in heart rate.
• The left vagus nerve mainly influences the atrioventricular node and adjacent conduction tissues.
• Increased activity of the left vagus nerve slows atrioventricular conduction and may produce atrioventricular block when stimulation is intense.
• Despite this functional predominance, considerable overlap exists between the distributions of the two vagus nerves.
• Therefore, stimulation of either nerve can affect both the sinoatrial and atrioventricular nodes.
• Parasympathetic stimulation decreases the rate of impulse generation and slows impulse conduction through the atrioventricular node.
• Because parasympathetic innervation of the ventricles is limited, its effect on ventricular contractile force is generally small.
• Overall, parasympathetic activity conserves cardiac work and helps maintain cardiovascular stability during resting conditions.

Table 85.2: Conduction velocity in cardiac tissues.

Cardiac Tissue	Conduction Velocity (m/s)
Purkinje fibers	4.0
Internodal pathways	1.0
His bundle	1.0
Ventricular muscle	1.0
Sinoatrial node	0.05
Atrioventricular node	0.05

Vagal Stimulation Results in:

• Vagal stimulation reduces cardiac activity through parasympathetic influence on the heart.
• It produces a negative chronotropic effect by decreasing heart rate.
• It produces a negative dromotropic effect by slowing impulse conduction, particularly through the atrioventricular node.
• It produces a negative bathmotropic effect by reducing cardiac excitability.
• It produces a mild negative inotropic effect, mainly affecting the atria because ventricular parasympathetic innervation is sparse.

Concept of Basal Heart Rate and Intrinsic Heart Rate

• Basal heart rate is the resting heart rate maintained under normal autonomic influence.
• It is largely determined by the resting discharge of the vagus nerve, known as vagal tone.
• Under normal conditions, parasympathetic influence exceeds sympathetic influence on the sinoatrial node.
• The intrinsic heart rate is the rate generated by the sinoatrial node in the absence of autonomic input.
• Complete autonomic blockade or cardiac denervation increases heart rate from about 70 beats per minute to approximately 100–110 beats per minute.
• This finding demonstrates the dominant role of vagal tone in regulating resting heart rate.

Sympathetic Innervation

• Sympathetic innervation of the heart arises from preganglionic neurons located in the intermediolateral cell column of the upper thoracic spinal cord, mainly from the first to fifth thoracic segments.
• Preganglionic fibers enter the sympathetic chain and synapse in the cervical and upper thoracic sympathetic ganglia.
• Postganglionic fibers originate primarily from the superior, middle, and inferior cervical ganglia.
• These fibers travel along the walls of major blood vessels to reach the heart.
• Sympathetic nerves supply the atria, sinoatrial node, atrioventricular node, conducting system, and ventricular myocardium.
• Ventricular sympathetic innervation is particularly extensive and strongly influences myocardial contractility.

Difference in Distribution of Left and Right Sympathetic Fibers

• The right and left cardiac sympathetic nerves show some functional differences in their distribution.
• The right sympathetic fibers predominantly influence the sinoatrial node, right atrium, and much of the right ventricle.
• The left sympathetic fibers have greater influence on the atrioventricular node, left atrium, and left ventricle.
• Stimulation of the right sympathetic pathway tends to produce a more pronounced increase in heart rate.
• Stimulation of the left sympathetic pathway has a greater effect on myocardial contractility.
• Despite these differences, substantial overlap exists between the two sides.
• Therefore, activation of either sympathetic pathway can influence both heart rate and contractile force.
• At rest, the heart receives continuous sympathetic activity, known as sympathetic tone.
• However, parasympathetic influence usually predominates at the sinoatrial node, making resting heart rate largely dependent on vagal tone.

Sympathetic Stimulation Results in:

• Sympathetic stimulation produces a positive chronotropic effect by increasing heart rate.
• It produces a positive inotropic effect by increasing myocardial contractility.
• It produces a positive dromotropic effect by accelerating impulse conduction through the cardiac conduction system.
• It produces a positive bathmotropic effect by increasing cardiac excitability.
• These effects collectively enhance cardiac output during exercise, stress, and other conditions requiring increased circulatory demand.