Cardiovascular System: Electrical and Mechanical Events of the Heart

18.5 Electrical Events of the Heart

Heart Depolarization and Contraction

The heart is capable of depolarizing and contracting without direct stimulation from the nervous system, although its rhythm can be modified by the autonomic nervous system.

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

• Autonomic Nervous System (ANS): Can alter heart rate and force of contraction.

Setting the Basic Rhythm: The Intrinsic Conduction System

Components and Function

The intrinsic cardiac conduction system coordinates the heartbeat through a network of noncontractile (autorhythmic) cells. These cells initiate and distribute impulses to ensure synchronized depolarization and contraction of the heart.

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

• Pacemaker Cells: Specialized cells with unstable resting membrane potentials, generating spontaneous action potentials.

Action Potential Initiation by Pacemaker Cells

Pacemaker cells undergo three phases during an action potential:

1. Pacemaker Potential: Slow Na+ channels open, causing the membrane potential to become more positive.

2. Depolarization: Ca2+ channels open (around -40 mV), allowing rapid influx of Ca2+ and triggering the action potential.

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

Example: The sinoatrial (SA) node uses these phases to generate rhythmic impulses that set the pace for the heart.

Pacemaker and Action Potentials of Typical Cardiac Pacemaker Cells

Graphical Representation

The action potential of pacemaker cells is characterized by a gradual rise (pacemaker potential), a rapid spike (depolarization), and a return to baseline (repolarization).

• Threshold: The membrane potential at which Ca2+ channels open, initiating depolarization.

• Action Potential: The rapid change in membrane potential due to Ca2+ influx.

Sequence of Excitation in the Intrinsic Conduction System

Order of Impulse Transmission

Cardiac pacemaker cells transmit impulses in the following sequence, ensuring coordinated contraction:

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)

Details of Conduction System Components

• SA Node: Located in the right atrial wall; acts as the heart's pacemaker, generating impulses at about 75 times per minute (sinus rhythm).

• AV Node: Located in the inferior interatrial septum; delays impulses by ~0.1 seconds to allow atrial contraction before ventricular contraction.

• 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 apex of the heart.

• Subendocardial Conducting Network (Purkinje fibers): Completes the pathway through the septum into the ventricular walls; more elaborate on the left side; depolarizes at 30 times per minute in absence of SA node input.

Clinical – Homeostatic Imbalance 18.4

Conduction System Defects

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

• Fibrillation: Rapid, irregular contractions; heart cannot pump blood effectively, risking brain death. Treatment: Defibrillation interrupts chaotic twitching, restoring normal depolarizations.

• Heart Block: Defective AV node prevents impulses from reaching ventricles; may require artificial pacemaker.

Modifying the Basic Rhythm: Extrinsic Innervation of the Heart

Autonomic Nervous System Control

The heart rate is modulated by the ANS via cardiac centers in the medulla oblongata:

• 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.

Electrocardiography

ECG/EKG: Recording Electrical Activity

An electrocardiogram (ECG or EKG) is a graphic recording of the heart's electrical activity, representing all action potentials at a given time. Electrodes are placed at various body points to measure voltage differences; a 12-lead ECG is most typical.

• 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

Clinical – Homeostatic Imbalance 18.5

ECG Abnormalities

• Enlarged R waves: May indicate enlarged ventricles

• Elevated or depressed S-T segment: Indicates cardiac ischemia

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

18.6 Mechanical Events of Heart

Systole and Diastole

Systole is the period of heart contraction, while diastole is the period of heart relaxation. The cardiac cycle refers to the blood flow through the heart during one complete heartbeat, including both atrial and ventricular systole and diastole.

• Heart beats about 75 times per minute

• Cardiac cycle lasts about 0.8 seconds

• Atrial systole: ~0.1 seconds; Ventricular systole: ~0.3 seconds; Quiescent period: ~0.4 seconds

Phases of the Cardiac Cycle

1. Ventricular Filling (mid-to-late diastole):

   • Pressure is low; 80% of blood flows passively from atria to ventricles through open AV valves

   • Atrial depolarization triggers atrial systole (P wave), pushing remaining 20% of blood into ventricles

   • Depolarization spreads to ventricles (QRS wave)

2. Isovolumetric Contraction:

   • Atria relax; ventricles begin to contract

   • Rising ventricular pressure closes AV valves

   • When ventricular pressure exceeds pressure in arteries, SL valves are forced open

3. Isovolumetric Relaxation (early diastole):

   • Following ventricular repolarization (T wave), ventricles relax

   • Ventricular pressure drops, causing backflow of blood from aorta and pulmonary trunk, triggering closure of SL valves

   • Ventricles are completely closed chambers momentarily

Heart Sounds

Origin and Clinical Relevance

Two main heart sounds ("lub-dup") are associated with the closing of heart valves:

• First sound: Closing of AV valves at the beginning of ventricular systole

• Second sound: Closing of SL valves at the beginning of ventricular diastole

• Mitral valve closes slightly before tricuspid; aortic closes slightly before pulmonary

Example: Auscultation of heart sounds in different thoracic regions helps identify valve function.

Areas of the Thoracic Surface Where Valve Sounds are Heard Most Clearly

Valve	Location
Aortic valve	2nd intercostal space at right sternal margin
Pulmonary valve	2nd intercostal space at left sternal margin
Mitral valve	5th intercostal space in line with middle of clavicle
Tricuspid valve	5th intercostal space at right sternal margin

Clinical – Homeostatic Imbalance 18.6

Heart Murmurs and Valve Problems

• Heart murmurs: Abnormal heart sounds due to blood hitting obstructions, usually indicating valve problems.

• Incompetent (insufficient) valve: Fails to close completely, allowing backflow of blood; causes swishing sound.

• Stenotic valve: Fails to open completely, restricting blood flow; causes high-pitched sound or clicking.

18.7 Regulation of Pumping

Cardiac Output and Stroke Volume

Cardiac output (CO) is the amount of blood pumped out by each ventricle in one minute. It is calculated as:

• Formula: $CO = HR \times SV$

• At rest: $CO = 75 \text{ beats/min} \times 70 \text{ ml/beat} = 5.25 \text{ L/min}$

• Stroke volume (SV): Volume of blood pumped out by one ventricle with each beat; correlates with force of contraction.

• Cardiac reserve: Difference between resting and maximal CO.

Factors Affecting Cardiac Output

• Regulation of stroke volume

• Regulation of heart rate

Factors Involved in Determining Cardiac Output

Influences on Cardiac Output

• Exercise, emotional stress, and body temperature can increase heart rate and stroke volume.

• Venous return and contractility affect end-diastolic volume (EDV) and end-systolic volume (ESV).

• Autonomic nervous system and hormones modulate heart rate.

Regulation of Heart Rate

Mechanisms of Heart Rate Control

If stroke volume decreases due to decreased blood volume or weakened heart, cardiac output can be maintained by increasing heart rate and contractility.

• Positive chronotropic factors: Increase heart rate

• Negative chronotropic factors: Decrease heart rate

Heart rate can be regulated by:

• Autonomic nervous system

• Chemicals

• Other factors

Autonomic Nervous System Regulation

• Sympathetic stimulation: Norepinephrine increases heart rate and contractility.

• Parasympathetic stimulation: Acetylcholine hyperpolarizes pacemaker cells, slowing heart rate.

• Vagal tone: Parasympathetic influence keeps resting heart rate lower.

Chemical Regulation

• Hormones: Epinephrine and thyroxine increase heart rate and contractility.

• Ions: Proper concentrations of Ca2+ and K+ are essential for normal heart function; imbalances are dangerous.

Other Factors Influencing Heart Rate

• Age: Fetus has fastest heart rate; declines with age.

• Gender: Females generally have faster heart rates than males.

• Exercise: Increases heart rate; trained athletes may have slower heart rates.

• Body temperature: Heart rate increases with increased body temperature.

Clinical – Homeostatic Imbalance 18.8

Abnormal Heart Rates

• Tachycardia: Abnormally fast heart rate (>100 beats/min); may lead to fibrillation if persistent.

• Bradycardia: Heart rate slower than 60 beats/min; may result in inadequate blood circulation in nonathletes, but can be desirable in endurance training.

Homeostatic Imbalance of Cardiac Output

Congestive Heart Failure (CHF)

CHF is a progressive condition where cardiac output is too low to meet tissue needs, often due to weakened myocardium.

• Coronary atherosclerosis: Clogged arteries impair oxygen delivery.

• Persistent high blood pressure: Increases workload and weakens myocardium.

• Multiple myocardial infarcts: Heart cells replaced by scar tissue.

• Dilated cardiomyopathy (DCM): Ventricles stretch and become flabby.

CHF: Sidedness and Progression

• Left-sided failure: Pulmonary congestion; blood backs up in lungs.

• Right-sided failure: Peripheral congestion; blood pools in organs, causing edema.

• Failure of one side weakens the other, leading to decompensated heart.

• Treatment: Removal of fluid, drugs to reduce afterload and increase contractility.