Electrical and Mechanical Events of the Heart: Cardiac Conduction, ECG, and Cardiac Cycle

17.5 Electrical Events of the Heart

Overview of Cardiac Electrical Activity

The heart is capable of depolarizing and contracting independently of nervous system stimulation, although its rhythm can be modulated by the autonomic nervous system (ANS).

• Autorhythmicity: The heart's ability to generate its own electrical impulses.

• Autonomic Modulation: The ANS can alter heart rate and force of contraction.

Setting the Basic Rhythm: The Intrinsic Conduction System

Components and Function

The coordinated heartbeat is achieved through the presence of gap junctions and the intrinsic cardiac conduction system, a network of noncontractile (autorhythmic) cells that initiate and distribute impulses to coordinate depolarization and contraction.

• Gap Junctions: Allow direct electrical communication between cardiac cells.

• Intrinsic Cardiac Conduction System: Ensures the heart beats in a coordinated manner.

Action Potential Initiation by Pacemaker Cells

Cardiac pacemaker cells have unstable resting membrane potentials, known as pacemaker potentials or prepotentials. The action potential in these cells consists of three phases:

1. Pacemaker Potential: K+ channels close, slow Na+ channels open, causing the cell interior to become more positive.

2. Depolarization: Ca2+ channels open at around -40 mV, allowing a large influx of Ca2+ and initiating the rising phase of the action potential.

3. Repolarization: K+ channels open, allowing K+ efflux, making the cell interior more negative.

Example: Pacemaker Cell Action Potential

The following equation describes the change in membrane potential:

$ext{Membrane Potential} = f( ext{Na}^+, ext{K}^+, ext{Ca}^{2+})$

Sequence of Excitation in the Heart

Cardiac pacemaker cells transmit impulses in the following order, completing the process in approximately 0.22 seconds:

1. Sinoatrial (SA) node

2. Atrioventricular (AV) node

3. Atrioventricular (AV) bundle (Bundle of His)

4. Right and left bundle branches

5. Subendocardial conducting network (Purkinje fibers)

Key Structures of the Conduction System

• SA Node: Pacemaker located in the right atrial wall; depolarizes faster than other myocardium regions, generating impulses about 75 times per minute (sinus rhythm).

• AV Node: Located in the inferior interatrial septum; delays impulses by ~0.1 second, allowing atrial contraction before ventricular contraction. Inherent rate is 50 times per minute without SA node input.

• AV Bundle (Bundle of His): Only electrical connection between atria and ventricles, located in the superior interventricular septum.

• Right and Left Bundle Branches: Pathways in the interventricular septum carrying impulses toward the heart's apex.

• Purkinje Fibers: Complete the pathway through the interventricular septum into the apex and ventricular walls; more elaborate on the left side.

Clinical—Homeostatic Imbalance 17.4

Conduction System Defects

• Arrhythmias: Irregular heart rhythms due to conduction system defects.

• Fibrillation: Rapid, irregular contractions rendering the heart ineffective for pumping blood; may result in brain death. Treatment: Defibrillation resets the heart's electrical activity.

• Ectopic Focus: Abnormal pacemaker that takes over pacing, often due to defective SA node.

• Junctional Rhythm: AV node pacing the heart at 40–60 beats/min when SA node fails.

• Extrasystole: Premature contraction due to ectopic focus, often felt as a thud; can be triggered by caffeine or nicotine.

• Heart Block: Defective AV node prevents impulses from reaching ventricles, causing them to beat at their own rate, which is insufficient for proper circulation. Treatment: Artificial pacemaker.

Modifying the Basic Rhythm: Extrinsic Innervation of the Heart

Autonomic Nervous System (ANS) Regulation

• Cardioacceleratory Center: Sympathetic signals increase heart rate and force by stimulating SA and AV nodes, heart muscle, and coronary arteries.

• Cardioinhibitory Center: Parasympathetic signals via the vagus nerve decrease heart rate by inhibiting SA and AV nodes.

Action Potentials of Contractile Cardiac Muscle Cells

Phases of Action Potential

Contractile muscle fibers are responsible for the heart's pumping action and have a distinct action potential with a plateau phase.

1. Depolarization: Fast voltage-gated Na+ channels open, Na+ enters, causing the membrane potential to rise from -90 mV to +30 mV.

2. Plateau Phase: Slow Ca2+ channels open, prolonging depolarization as Ca2+ enters the cell.

3. Repolarization: Ca2+ channels close, K+ channels open, K+ exits, returning the cell to resting membrane potential.

Comparison Table: Skeletal vs. Cardiac Muscle Action Potentials

Feature	Skeletal Muscle	Cardiac Muscle
AP Duration	1–2 ms	200 ms
Contraction Duration	15–100 ms	200+ ms
Plateau Phase	Absent	Present

Benefits of Longer AP and Contraction

• Sustained contraction ensures efficient ejection of blood.

• Longer refractory period prevents tetanic contractions.

Electrocardiography (ECG/EKG)

Principles and Features

An electrocardiograph detects electrical currents generated by the heart. The ECG is a composite recording of all action potentials at a given time, measured by electrodes placed at various body points (typically 12 leads).

• P wave: Depolarization of SA node and atria.

• QRS complex: Ventricular depolarization and atrial repolarization.

• T wave: Ventricular repolarization.

• P-R interval: Beginning of atrial excitation to beginning of ventricular excitation.

• S-T segment: Entire ventricular myocardium depolarized.

• Q-T interval: Beginning of ventricular depolarization through ventricular repolarization.

Example: ECG Tracing

• Normal Sinus Rhythm: Regular P, QRS, and T waves.

• Junctional Rhythm: Absent P waves, slower rate.

• Second-degree Heart Block: More P waves than QRS waves.

• Ventricular Fibrillation: Chaotic, irregular ECG deflections.

Clinical Significance

• Enlarged R waves: May indicate enlarged ventricles.

• Elevated/Depressed S-T segment: Indicates cardiac ischemia.

• Prolonged Q-T interval: Indicates repolarization abnormality, increasing risk of ventricular arrhythmias.

17.6 Mechanical Events of the Heart

Cardiac Cycle

The cardiac cycle describes blood flow through the heart during one complete heartbeat, including both systole (contraction) and diastole (relaxation).

• Systole: Period of heart contraction.

• Diastole: Period of heart relaxation.

• Phases:

  1. Ventricular filling (mid-to-late diastole): 80% of blood flows passively from atria to ventricles; atrial systole pushes remaining 20%.

  2. Isovolumetric contraction: Ventricles contract, AV valves close, all valves shut briefly.

  3. Isovolumetric relaxation: Ventricles relax, SL valves close, all valves shut briefly.

• End Diastolic Volume (EDV): Volume of blood in each ventricle at end of diastole.

• End Systolic Volume (ESV): Volume of blood remaining after systole.

Heart Sounds

Normal and Abnormal Heart Sounds

• Lub-dup: Two sounds associated with valve closure.

  • Lub: Closing of AV valves at beginning of ventricular systole.

  • Dup: Closing of SL valves at beginning of ventricular diastole.

• Heart Murmurs: Abnormal sounds due to valve problems.

  • Incompetent Valve: Fails to close completely, causing backflow.

  • Stenotic Valve: Fails to open completely, restricting flow.

17.7 Regulation of Pumping

Cardiac Output (CO)

Cardiac output is the amount of blood pumped by each ventricle per minute.

• Formula: $CO = HR imes SV$ Where: $CO$ = Cardiac Output $HR$ = Heart Rate $SV$ = Stroke Volume

• Stroke Volume (SV): Volume of blood pumped by one ventricle per beat. $SV = EDV - ESV$

• Normal Values: $CO = 75 ext{ beats/min} imes 70 ext{ ml/beat} = 5250 ext{ ml/min} = 5.25 ext{ L/min}$

Regulation of Stroke Volume

• Preload: Degree of stretch of cardiac muscle before contraction; related to venous return.

• Contractility: Contractile strength at a given muscle length; increased by sympathetic stimulation and certain hormones.

• Afterload: Pressure ventricles must overcome to eject blood; increased by hypertension.

Regulation of Heart Rate

• Positive Chronotropic Factors: Increase heart rate (e.g., sympathetic stimulation, epinephrine).

• Negative Chronotropic Factors: Decrease heart rate (e.g., parasympathetic stimulation, acetylcholine).

• Other Influences: Age, gender, exercise, body temperature.

Clinical—Homeostatic Imbalance

• Tachycardia: Abnormally fast heart rate (>100 beats/min).

• Bradycardia: Abnormally slow heart rate (<60 beats/min).

• Congestive Heart Failure (CHF): Progressive condition where CO is too low to meet tissue needs; caused by coronary atherosclerosis, persistent high blood pressure, multiple myocardial infarcts, or dilated cardiomyopathy.

Example Table: Causes and Effects of CHF

Cause	Effect
Coronary atherosclerosis	Impaired oxygen delivery, hypoxic myocardium
High blood pressure	Increased afterload, myocardial hypertrophy
Myocardial infarcts	Scar tissue replaces contractile cells
Dilated cardiomyopathy	Flabby ventricles, weak myocardium

Additional info: These notes expand upon the original slides by providing definitions, equations, and clinical context for key cardiac physiology concepts, suitable for college-level Anatomy & Physiology students.