Previous Notes :

https://mednotesbyrazaullah.blogspot.com/2026/08/chapter-10-rhythmical-excitation-of.html

Control of Excitation and Conduction 

The heart relies on a highly specialized electrical system to control its rhythm and ensure synchronized contractions. Electrical impulses originate in the sinus node and travel through designated pathways to reach all areas of the cardiac muscle. Understanding how these electrical signals are generated, conducted, and regulated by the autonomic nervous system is essential for mastering cardiac physiology.

When the normal electrical sequence is disrupted, the heart’s ability to pump blood efficiently can be compromised. Differences in intrinsic discharge rates, abnormal pacemaker sites, and neural influences from the sympathetic and parasympathetic nervous systems all play critical roles in maintaining or altering normal cardiac function and maintaining blood circulation.

Sinus Node as the Heart’s Pacemaker

• Impulse normally originates in sinus node.
• Sinus node intrinsic rate: 70–80 BPM.
• A-V node intrinsic rate: 40–60 BPM.
• Purkinje fibers intrinsic rate: 15–40 BPM.
• Sinus node discharges faster than other tissues.
• Impulses discharge A-V node and Purkinje membranes.
• Sinus node resets slower tissues before self-excitation.
• Rapid discharge rate makes sinus node pacemaker.

Ectopic Pacemakers

• Abnormal areas can discharge faster than sinus node.
• Shift can occur to A-V node or Purkinje.
• Atrial or ventricular muscle can become overly excitable.
• Pacemaker outside sinus node is called ectopic.
• Ectopic pacemakers cause abnormal contraction sequences.
• Ectopic rhythms reduce overall heart pumping efficiency.
• Impaired impulse transmission also shifts pacemaker location.
• Blockage causes new pacemaker in A-V node/bundle.

A-V Block and Stokes-Adams Syndrome

• A-V block stops impulse transmission to ventricles.
• Atria continue beating at normal sinus rate.
• New ventricular pacemaker develops in Purkinje system.
• Ventricles beat at 15–40 beats per minute.
• Purkinje system delay lasts 5 to 20 seconds.
• Prior rapid sinus impulses overdriven and suppressed Purkinje.
• Ventricles fail to pump blood during delay.
• Lack of brain blood flow causes fainting (4–5s).
• Delayed heartbeat pickup called Stokes-Adams syndrome.
• Prolonged delay periods can lead to death.

Purkinje System and Synchronous Contraction

• Impulse reaches ventricles in a short time.
• First and last fibers excited within 0.03–0.06s.
• All ventricular portions begin contracting almost simultaneously.
• Ventricular contraction continues for about 0.3 seconds.
• Synchronous contraction is essential for effective pumping.
• Slow transmission causes unsynchronized muscle contraction.
• Uncoordinated contraction depresses overall pumping effect.
• Cardiac debilities can decrease pumping effectiveness 20–30%.

Cardiac Nerves Control

• Heart supplied by sympathetic and parasympathetic nerves.
• Parasympathetic nerves (Vagal) supply S-A/A-V nodes.
• Vagal supply atrial muscle and minimal ventricular muscle.
• Sympathetic nerves supply all heart regions heavily.
• Sympathetic supply is particularly strong in ventricles.

Parasympathetic (Vagal) Effects

• Vagal stimulation releases acetylcholine at endings.
• Acetylcholine decreases sinus node discharge rate.
• Acetylcholine decreases excitability of A-V junction.
• Reduced excitability slows impulse transmission to ventricles.
• Weak-to-moderate vagal stimulation halves pumping rate.
• Strong vagal stimulation can completely stop sinus node.
• Strong vagal stimulation can block A-V conduction.
• Ventricles stop beating for 5 to 20 seconds.
• Septal Purkinje fibers develop intrinsic rhythm.
• Ventricular contraction resumes at 15–40 BPM.
• Resumed contraction phenomenon called ventricular escape.

Mechanism of Vagal Action

• Acetylcholine increases membrane permeability to potassium.
• Rapid potassium leakage occurs out of fibers.
• Increased intracellular negativity causes membrane hyperpolarization.
• Hyperpolarization reduces excitable tissue excitability.
• Sinus nodal resting potential drops to −65/−75mV.
• Normal sinus nodal potential is −55 to −60mV.
• Inward sodium-calcium leakage takes longer for threshold.
• Slower threshold attainment decreases sinus node rhythmicity.
• Strong stimulation can completely halt self-excitation.
• A-V hyperpolarization hinders excitation by atrial fibers.
• Reduced safety factor delays or blocks A-V conduction.

Sympathetic Effects

• Sympathetic stimulation causes opposite effects to vagal.
• Increases rate of sinus node discharge.
• Increases conduction rate in all heart parts.
• Increases excitability throughout all cardiac tissues.
• Greatly increases atrial and ventricular contractile force.
• Overall cardiac activity increases under sympathetic influence.
• Maximal stimulation can triple heartbeat frequency.
• Maximal stimulation can double contraction strength.

Mechanism of Sympathetic Action

• Sympathetic nerve endings release norepinephrine hormone.
• Norepinephrine stimulates beta-1 adrenergic receptors.
• Beta-1 stimulation increases sodium-calcium membrane permeability.
• Increased permeability creates more positive resting potential.
• Diastolic potential drifts faster toward threshold level.
• Accelerated self-excitation increases overall heart rate.
• Increased permeability reduces A-V conduction time.
• Calcium influx increases cardiac muscle contractile strength.
• Calcium ions directly excite myofibril contractile process.