Properties of Cardiac Muscle

Introduction

The heart functions continuously throughout life because cardiac muscle possesses unique physiological properties that ensure efficient and rhythmic pumping. Features such as a prolonged refractory period, the all-or-none response, and force–frequency and length–tension relationships regulate cardiac performance and prevent sustained contraction.

• The heart is an essential organ that maintains continuous blood circulation throughout life.
• Prolonged cardiac arrest rapidly compromises tissue oxygen delivery and can be fatal.
• The myocardium possesses unique physiological properties that enable sustained, rhythmic contraction.
• Understanding these properties is fundamental for interpreting normal cardiovascular function and cardiac disorders.

Important Properties

• Cardiac muscle possesses specialized physiological properties that ensure effective and continuous pumping of blood.
• These properties include automaticity, rhythmicity, conductivity, excitability, contractility, and distensibility.
• Additional characteristics include a long refractory period, functional syncytium, extrasystole with compensatory pause, and the all-or-none response.
• Cardiac muscle also exhibits the staircase phenomenon, length–tension relationship, frequency–force relationship, and load–velocity relationship.
• The prolonged refractory period prevents tetanic contraction and allows adequate ventricular filling between successive heartbeats.
• Together, these properties coordinate electrical activity and mechanical performance of the heart.

Automaticity

• Automaticity is the intrinsic ability of the heart to generate electrical impulses without external neural stimulation.
• This property allows the heart to continue beating even when completely denervated, provided adequate oxygen and nutrient supply are maintained.
• Automaticity results from spontaneous depolarization of specialized pacemaker cells.
• The sinoatrial node is the primary pacemaker and normally initiates each heartbeat.
• Its pacemaker cells generate spontaneous electrical activity through the development of a pacemaker potential.
• Other components of the cardiac conduction system, including the atrioventricular node and the His–Purkinje system, also possess automaticity.
• These subsidiary pacemakers can generate impulses if the sinoatrial node fails.

Rhythmicity

• Rhythmicity is the ability of the heart to generate impulses at regular intervals and produce a coordinated rhythm.
• This property is also referred to as autorhythmicity.
• Rhythmic impulse generation ensures a consistent sequence of cardiac contractions.
• In a healthy heart, the intervals between successive beats remain relatively constant under resting conditions.
• The regular rhythm originates from the orderly discharge of the sinoatrial node.
• Therefore, heart rate depends primarily on the frequency of impulse generation by the sinoatrial node.
• The sinoatrial node is the dominant pacemaker because it has the highest intrinsic firing rate among cardiac pacemakers.
• Its normal discharge rate is approximately 60–100 beats per minute, which corresponds to the normal resting heart rate in adults.

Table 86.1: The rate of discharge of potential pacemakers of heart.

Cardiac Pacemaker	Intrinsic Rate (beats/minute)
Sinoatrial node	60–100
Atrioventricular node	40–60
His bundle and Purkinje fibers	25–40
Ventricular myocardium	15–30

Pacemaking Tissues in the Heart

• The heart contains specialized tissues capable of generating spontaneous electrical impulses.
• The principal intrinsic pacemakers are the sinoatrial node, atrioventricular node, and the His–Purkinje system.
• Under extreme conditions, ventricular myocardium can also exhibit pacemaker activity.
• Pacemaker activity refers to spontaneous, time-dependent depolarization that reaches threshold and initiates an action potential.
• All cardiac pacemakers can generate impulses independently, but they do so at different intrinsic rates.
• The pacemaker with the highest firing rate suppresses the activity of slower pacemakers through overdrive suppression.
• The sinoatrial node has the fastest intrinsic discharge rate and therefore acts as the primary pacemaker of the heart.
• As long as the sinoatrial node functions normally, cardiac rhythm remains under its control.
• If sinoatrial nodal activity fails, the atrioventricular node assumes pacemaker function.
• If both sinoatrial and atrioventricular nodal activity are lost, the His–Purkinje system can generate a slower escape rhythm.
• This orderly sequence is known as the hierarchy of cardiac pacemakers.

Demonstration of Hierarchy of Pacemakers

• The hierarchy of pacemakers has been demonstrated experimentally in amphibian hearts using Stannius ligatures.
• In the normal state, the dominant pacemaker generates the highest heart rate.
• Placement of the first ligature between the sinus venosus and atria isolates the primary pacemaker region.
• The atria then develop their own slower rhythm, indicating the presence of a secondary pacemaker.
• Placement of a second ligature between the atria and ventricles further isolates the ventricles.
• The ventricles subsequently generate an even slower intrinsic rhythm.
• These observations demonstrate that lower pacemakers possess automaticity but discharge at slower rates than higher pacemakers.
• The experiment illustrates the hierarchical organization of impulse generation within the heart.

Conductivity

• Conductivity is the ability of cardiac tissue to transmit electrical impulses from one region of the heart to another.
• Impulses generated in the sinoatrial node travel through the specialized cardiac conduction system to the ventricular myocardium.
• Rapid and coordinated impulse transmission ensures synchronized contraction of the atria and ventricles.
• Efficient conduction is essential for maintaining normal cardiac rhythm and effective pumping function.

Contractility

• Contractility is the ability of cardiac muscle to develop force and shorten in response to electrical stimulation.
• Under normal conditions, contraction is initiated by impulses arising from the sinoatrial node.
• Ventricular contraction generates the pressure required to eject blood into the pulmonary and systemic circulations.
• Increased contractility enhances stroke volume and cardiac output.
• Reduced contractility lowers cardiac output and may impair tissue perfusion.
• This property remains evident even in isolated, adequately perfused cardiac preparations.

Excitability

• Excitability is the ability of cardiac muscle cells to respond to an adequate stimulus by generating an action potential.
• Cardiac excitability is influenced by electrolyte concentrations, hormones, and autonomic nervous system activity.
• Sympathetic stimulation generally increases excitability, whereas parasympathetic stimulation reduces it.

Distensibility

• Distensibility is the ability of cardiac chambers to stretch during filling.
• This property depends largely on myocardial compliance.
• Adequate distensibility facilitates efficient filling of the atria and ventricles during diastole.
• Reduced ventricular distensibility decreases end-diastolic volume and may limit cardiac output.

Long Refractory Period

• The refractory period is the interval during which cardiac muscle cannot respond normally to a new stimulus.
• It consists of an absolute refractory period followed by a relative refractory period.
• In ventricular muscle, the absolute refractory period is approximately 200 milliseconds, and the relative refractory period is about 50 milliseconds.
• Cardiac muscle action potentials have a prolonged duration compared with those of skeletal muscle.
• The refractory period overlaps with most of the mechanical contraction of the ventricle.
• Therefore, a second action potential cannot initiate another effective contraction before the previous contraction has ended.
• As a result, individual cardiac contractions remain separate and do not summate.
• This property prevents tetanic contraction of the myocardium.
• Prevention of tetanus is essential because the heart must relax during diastole to allow ventricular filling.
• In contrast, skeletal muscle has a much shorter action potential and refractory period, permitting summation of contractions and tetanus under repeated stimulation.

Functional Syncytium

• Cardiac muscle functions as a functional syncytium because adjacent cells are interconnected by numerous gap junctions.
• These junctions allow rapid spread of electrical impulses from one cell to another.
• As a result, myocardial fibers contract in a coordinated and nearly simultaneous manner.
• This synchronization ensures efficient pumping of blood by the heart.

Extrasystole and Compensatory Pause

• An extrasystole is a premature cardiac contraction triggered by an impulse arising before the next expected normal beat.
• It commonly occurs when a sufficiently strong stimulus excites the myocardium during the relative refractory period.
• In clinical settings, extrasystoles often originate from ectopic foci within the atria or ventricles.
• Isolated extrasystoles may occur in healthy individuals and are not always associated with disease.
• Following an extrasystole, the next normal sinoatrial nodal impulse may fall within the refractory period of the prematurely activated myocardium.
• Consequently, the expected normal contraction is absent.
• This produces a prolonged interval known as a compensatory pause.
• During the compensatory pause, ventricular filling time increases.
• The resulting increase in end-diastolic volume enhances the force of the subsequent contraction through the Frank–Starling mechanism.
• The stronger contraction that follows an extrasystole is termed postextrasystolic potentiation.
• Postextrasystolic potentiation may also occur independently of increased ventricular filling.
• Accumulation of intracellular calcium during the pause can increase the strength of the subsequent contraction.
• Therefore, both enhanced ventricular filling and increased calcium availability may contribute to this phenomenon.
• Extrasystoles and compensatory pauses are important indicators of cardiac excitability and impulse generation.

All or None Law

• Cardiac muscle exhibits the all-or-none law, meaning that once a threshold stimulus is reached, the response is maximal for that physiological state.
• A stimulus below threshold fails to produce an action potential or contraction.
• A threshold stimulus generates a full propagated action potential and an effective contraction.
• Increasing stimulus strength beyond threshold does not further increase the magnitude of contraction under identical conditions.
• This principle applies because cardiac action potentials are themselves all-or-none events.
• The functional syncytial organization of the myocardium also contributes to this response.
• Through extensive gap junctions, excitation spreads throughout interconnected cardiac muscle cells, allowing the myocardium to behave as a coordinated unit.
• The all-or-none law is valid only when physiological conditions remain unchanged.
• Alterations in autonomic activity, electrolyte concentrations, temperature, or pharmacological agents can modify cardiac contractility.
• For example, sympathetic stimulation increases intracellular calcium availability and enhances the force of contraction despite the all-or-none nature of excitation.

Staircase Phenomenon

• The staircase phenomenon refers to the progressive increase in the strength of several initial contractions when cardiac muscle is stimulated repeatedly after a period of rest.
• It is also known as the treppe phenomenon.
• The first few contractions gradually become stronger before reaching a steady level.
• This phenomenon does not violate the all-or-none law because each contraction alters the physiological state of the myocardium before the next stimulus occurs.
• The principal mechanism involves progressive accumulation of intracellular calcium.
• Calcium released during one contraction may not be completely removed before the next stimulus.
• Consequently, a greater amount of calcium becomes available to the contractile proteins during subsequent contractions.
• Increased calcium availability enhances actin–myosin interaction and increases contractile force.
• Repeated contractions also improve calcium handling by the sarcoplasmic reticulum, contributing to stronger contractions.
• A slight increase in myocardial temperature during repetitive activity may enhance enzymatic reactions involved in contraction and relaxation.
• Warming of the tissue can improve the efficiency of metabolic and contractile processes.
• Repeated contractions may also reduce internal mechanical resistance within muscle cells, facilitating force generation.
• The staircase phenomenon is most evident after a period of quiescence and during moderate rates of stimulation.
• It demonstrates that myocardial performance depends not only on electrical excitation but also on intracellular calcium dynamics and the recent contractile history of the heart.

Length-Tension Relationship

• The length–tension relationship describes the effect of initial myocardial fiber length on the force of contraction.
• Within physiological limits, increased fiber length produces a stronger contraction.
• Tension rises with increasing sarcomere length until an optimal length is reached.
• Beyond the optimal range, further stretching reduces force generation.
• The initial length of ventricular muscle fibers depends largely on preload, which is closely related to end-diastolic volume.
• Increased ventricular filling stretches myocardial fibers and enhances stroke volume.
• This mechanism enables the heart to adjust its output according to venous return.
• Such intrinsic regulation of cardiac output is termed heterometric autoregulation.

Frequency-Force Relationship

• The frequency–force relationship refers to an increase in myocardial contractile force as heart rate rises within a physiological range.
• Moderate increases in stimulation frequency enhance intracellular calcium availability.
• Increased calcium availability strengthens myocardial contraction and improves cardiac performance.
• Excessively high heart rates may reduce ventricular filling time and impair cardiac function.

Load-Velocity Relationship

• The load–velocity relationship describes the association between the velocity of myocardial shortening and the load opposing contraction.
• Velocity of shortening is inversely related to the applied load.
• As afterload increases, the speed of myocardial shortening decreases.
• Therefore, contraction occurs more rapidly against lower loads and more slowly against higher loads.
• Maximum shortening velocity is achieved when the opposing load is minimal.
• The velocity of shortening and the force of contraction are distinct physiological variables and should not be considered equivalent.