Electrical Conduction and the Cardiac Cycle

Understanding Cardiac Anatomy and Physiology

This study guide reviews the physiology and electrophysiology of the heart’s electrical conduction system. It explains how electrical impulses travel through the heart, how these impulses correspond with the cardiac cycle, and the major factors that influence cardiac electrical and mechanical activity.

Main Topics

• Anatomy of the cardiac electrical conduction system
• Basic relationship between cardiac electrical activity and the ECG
• Phases of the cardiac cycle
• Cardiac output
• S1 and S2 heart sounds
• Special properties of cardiac muscle cells
• Effects of the parasympathetic nervous system on cardiac conduction

Cardiac Conduction Physiology

The heart contains two major functional types of cells. Some cells primarily perform a mechanical role, producing contraction, while others specialize in generating and transmitting electrical impulses.

The cardiac conduction system is a specialized network of electrical, or pacemaker, cells located within the heart muscle. These cells work together with the myocardial contractile cells to coordinate each heartbeat.

When the conduction system generates and transmits an electrical impulse, that stimulation causes the contractile elements within the myocardial cells to shorten. This produces the muscular contraction needed to pump blood.

Cardiac cells possess four important properties that distinguish them from many other cells in the body:

• Automaticity – The ability of pacemaker cells to spontaneously generate an electrical impulse without requiring outside stimulation.
• Excitability – The ability of cardiac cells to respond when they receive an appropriate stimulus.
• Conductivity – The ability of cardiac cells to receive an electrical impulse and transmit that impulse to neighboring cardiac cells.
• Contractility – The ability of myocardial cells to shorten and produce a contraction after receiving an electrical impulse.

Together, these characteristics allow the heart to generate its own electrical signals and respond to those signals by contracting.

Because cardiac pacemaker cells can independently produce electrical impulses, the heart is capable of continuing to beat for a period of time even when separated from the body, such as during heart transplantation.

Components of the Cardiac Conduction System

The cardiac conduction pathway includes six major structures:

• Sinoatrial (SA) node
• Atrioventricular (AV) node
• Bundle of His
• Right bundle branch
• Left bundle branch
• Purkinje fibers

Each structure has a specific function in transmitting the electrical impulse through the heart. Electrical activation of these structures corresponds with different stages of the cardiac cycle.

Sinoatrial Node

• The SA node is where the normal cardiac electrical impulse begins.
• The sinoatrial node is considered the heart’s natural pacemaker because it normally initiates each heartbeat.
• This specialized collection of pacemaker cells is located in the upper portion of the right atrium.
• Once an impulse is generated by the SA node, electrical activity spreads through the atria and causes atrial contraction.

Atrioventricular Node

• The AV node is located near the lower portion of the right atrium.
• Its major role is to briefly delay the electrical impulse as it passes from the atria toward the ventricles.
• This short delay is extremely important because it allows the atria to finish contracting and gives the ventricles enough time to fill with blood before ventricular contraction begins.
• After passing through the AV node, the electrical impulse enters the bundle of His, also called the atrioventricular bundle.
• Bundle of His: This structure is located within the interventricular septum below the atria.
• From this point, the impulse begins traveling deeper into the ventricular conduction system, leading toward ventricular contraction.

Right and Left Bundle Branches

• The bundle of His divides into the right bundle branch and left bundle branch.
• These pathways travel down the interventricular septum and conduct electrical impulses toward the right and left ventricles.
• Each bundle branch carries electrical activity toward the appropriate side of the heart.

Purkinje Fibers

• The Purkinje fibers form the final portion of the normal cardiac conduction pathway.
• These specialized fibers extend from the bundle branches throughout the ventricular myocardium.
• They rapidly distribute the electrical impulse through the ventricles, allowing the ventricular muscle to contract in a coordinated manner.

Sequence of Electrical Conduction

The normal conduction pathway follows an organized sequence:

1. The electrical impulse begins in the SA node.
2. The impulse travels through the atria toward the AV node.
3. The AV node briefly delays the impulse.
4. The impulse then travels through the bundle of His.
5. The bundle of His divides into the right and left bundle branches.
6. The impulse finally reaches the Purkinje fibers, which distribute electrical stimulation throughout the ventricles.

This organized electrical pathway allows the atria and ventricles to contract in the proper sequence.

Intrinsic Pacemaker Rates

• The SA node normally acts as the dominant pacemaker of the heart.
• Under normal conditions, it produces electrical impulses at approximately 60–100 beats per minute, creating what is known as a normal sinus rhythm.
• If the SA node fails to generate impulses, another portion of the cardiac conduction system may take over as the pacemaker to maintain cardiac activity.
• However, structures located lower in the conduction pathway have progressively slower intrinsic firing rates.
• Typical intrinsic pacemaker rates include:
  • SA node: 60–100 beats per minute
  • AV junction: 40–60 beats per minute
  • Ventricles/Purkinje system: 20–40 beats per minute

Because the SA node has the fastest normal intrinsic rate, it ordinarily controls the rhythm of the heart.

The Cardiac Cycle

• As electrical impulses travel from the SA node through the conduction system and eventually reach the Purkinje fibers, they stimulate coordinated contractions of the heart muscle.
• These alternating periods of contraction and relaxation create the cardiac cycle, allowing the heart to continuously pump blood throughout the body.

Overview of the Cardiac Cycle

The cardiac cycle refers to the repeating sequence of events that occurs during each heartbeat.

It consists primarily of two phases:

• Systole
• Diastole

Systole is the phase in which a cardiac chamber contracts.

During ventricular systole, the ventricles contract and eject blood from the heart into the pulmonary and systemic circulations.

Diastole is the phase in which a cardiac chamber relaxes.

During this period, the chambers fill with blood in preparation for the next contraction.

The atria and ventricles alternate between contraction and relaxation so that blood continues moving efficiently through the heart.

At a normal resting heart rate, one complete cardiac cycle takes approximately 0.8 seconds. This cycle commonly repeats about 70–80 times per minute in a resting adult.

Blood Flow Through the Heart

The cardiac cycle depends on the continuous movement of blood through the heart’s chambers, valves, lungs, and systemic circulation.

• The cycle begins when deoxygenated blood returns to the heart and enters the right atrium through the superior and inferior vena cava.
• Atrial systole then occurs. During this phase, the atria contract and the atrioventricular (AV) valves—the tricuspid and mitral valves—are open, allowing blood to move into the ventricles.
• While the atria are in systole, the ventricles are in diastole.
  • During ventricular diastole, the ventricles remain relaxed and fill with blood.
• The atrioventricular valves then close. The atria enter diastole while the ventricles begin systole.
• During ventricular systole, the ventricles contract. This opens the semilunar valves—the pulmonary and aortic valves—and allows blood to be ejected from the ventricles.
  • The right ventricle sends blood toward the lungs.
  • The left ventricle sends blood into the systemic circulation.
• After ventricular ejection, the semilunar valves close.
• The atria refill with blood and eventually contract again, beginning another cardiac cycle.

Cardiac Pumping and Output

The amount of blood ejected from a ventricle during a single contraction is known as the stroke volume.

Stroke volume can be combined with the number of heartbeats occurring each minute to determine cardiac output.

Cardiac output = Heart rate × Stroke volume

Cardiac output refers to the total volume of blood the heart pumps into the circulation each minute.

A typical resting adult has a cardiac output of approximately 5–6 liters per minute.

The Frank-Starling Principle

One important factor that influences stroke volume is the Frank-Starling principle.

The Frank-Starling principle states that an increase in ventricular filling generally produces a stronger ventricular contraction, within normal physiological limits.

In simpler terms:

• A larger amount of blood entering the ventricle causes the ventricular muscle fibers to stretch more.
• Increased stretching of the myocardial fibers produces a stronger contraction.
• A stronger ventricular contraction can increase the amount of blood ejected from the heart.

Therefore, within normal limits, the more the ventricle fills before contraction, the greater the force with which it can contract.

Electrical Activity on the ECG

The electrical activity produced by the cardiac conduction system can be recorded using an electrocardiogram (ECG or EKG).

Different portions of the ECG tracing correspond with electrical activity occurring in specific regions of the heart.

Under normal conditions, this electrical activity leads to coordinated contraction and relaxation of the cardiac chambers.

The major components of the ECG include:

• P wave – Represents atrial depolarization following initiation of the electrical impulse by the SA node. This electrical activity is followed by atrial contraction.
• PR segment – Represents the period during which the electrical impulse travels through the AV node and is briefly delayed before reaching the ventricular conduction system.
• QRS complex – Represents ventricular depolarization as the impulse travels through the bundle of His, right and left bundle branches, and Purkinje fibers. Ventricular contraction follows this electrical activation.
• ST segment – Represents the period when the ventricles remain depolarized and the early phase of ventricular repolarization begins. This period is associated largely with the ventricular absolute refractory period.
• T wave – Represents ventricular repolarization as the ventricles electrically recover in preparation for the next cardiac cycle. The later portion of this process is associated with the relative refractory period.

Normal Heart Sounds

Two major sounds are normally heard when auscultating the heart during the cardiac cycle.

These sounds are known as S1 and S2.

They are produced primarily by the closure of the heart valves and are commonly described as the familiar “lub-dub” sound.

First Heart Sound: S1

S1, commonly described as the “lub,” is the first major heart sound heard during the cardiac cycle.

It occurs when the atrioventricular valves close:

• Tricuspid valve
• Mitral valve

Closure of these valves occurs at the beginning of ventricular systole.

Therefore, S1 marks the beginning of ventricular contraction.

Second Heart Sound: S2

S2, commonly described as the “dub,” occurs later in the cardiac cycle.

It results from closure of the semilunar valves:

• Pulmonary valve
• Aortic valve

Closure of the semilunar valves occurs as ventricular systole ends and ventricular diastole begins.

Therefore, S2 marks the end of ventricular systole.

Autonomic Regulation of Cardiac Function

The autonomic nervous system (ANS) plays an important role in regulating cardiac activity.

Although the heart can generate its own electrical impulses through its intrinsic conduction system, the autonomic nervous system can modify how the heart functions.

The ANS can influence:

• Heart rate
• Conduction speed
• Strength of myocardial contraction

The autonomic nervous system does not normally initiate the heart’s electrical impulse. Instead, it modifies the activity of the heart’s natural pacemaker and conduction system.

The ANS is divided into two major branches:

• Sympathetic nervous system
• Parasympathetic nervous system

Sympathetic Nervous System

The sympathetic nervous system becomes especially active during the fight-or-flight response.

A major neurotransmitter associated with sympathetic activity at the heart is norepinephrine.

When sympathetic stimulation increases:

• Heart rate increases.
• Myocardial contractility increases.
• Cardiac output can increase.
• Blood is delivered more rapidly to tissues that require increased oxygen and nutrients.

Sympathetic stimulation can also promote vasoconstriction in certain blood vessels.

This helps redistribute blood away from less immediately essential areas, such as portions of the skin and gastrointestinal system, toward vital organs and active skeletal muscles.

Parasympathetic Nervous System

The parasympathetic nervous system is associated with the rest-and-digest response.

Its primary neurotransmitter is acetylcholine.

When parasympathetic activity increases:

• Heart rate decreases.
• Conduction through the AV node slows.
• Cardiac activity is reduced compared with sympathetic stimulation.

Acetylcholine also serves as the neurotransmitter at the neuromuscular junction, where it stimulates skeletal muscle fibers to contract.

After acetylcholine has transmitted its signal, it is broken down by the enzyme acetylcholinesterase. This helps terminate the signal and allows the muscle fiber to relax before another stimulation occurs.

Adrenergic Receptors

Adrenergic receptors respond to sympathetic neurotransmitters such as norepinephrine and epinephrine.

Two major categories are alpha and beta receptors.

• Alpha (α) receptors – Activation of certain alpha receptors, particularly α1 receptors in blood vessels, causes smooth muscle contraction and promotes vasoconstriction.
• Beta (β) receptors – Different beta receptor subtypes produce different effects. β1 receptors are especially important in the heart, while β2 receptors can cause relaxation of smooth muscle and vasodilation in certain vascular beds.

Many medications produce cardiovascular effects by either stimulating or blocking these receptors.

Factors That Modify Cardiac Activity

Several terms are used to describe factors that influence different aspects of heart function.

• Inotropic factors – Affect the strength or force of myocardial contraction.
  • Positive inotropic effects increase contractile force.
  • Negative inotropic effects decrease contractile force.
• Chronotropic factors – Affect heart rate.
  • Positive chronotropic effects increase heart rate.
  • Negative chronotropic effects decrease heart rate.
• Dromotropic factors – Affect the speed at which electrical impulses travel through the cardiac conduction system.
  • Positive dromotropic effects increase conduction velocity.
  • Negative dromotropic effects decrease conduction velocity.

Scenario 1: Suspected Acute Myocardial Infarction

Dispatch Information

You are dispatched to evaluate a 60-year-old female who is experiencing chest discomfort accompanied by lightheadedness and dizziness.

Scene Assessment

Upon arrival, you find the patient seated on a couch in her living room.

She appears pale, diaphoretic, and anxious, but she is alert and oriented to person, place, time, and event (AOx4).

There are no obvious signs of traumatic injury, significant neurological deficits, or external bleeding.

Patient History

The patient reports that she has felt generally unwell throughout the day.

Earlier that morning, she noticed a sensation of pressure in her chest. The discomfort gradually worsened as the day progressed and is now described as crushing substernal chest pain rated 8/10.

She has a previous history of chest pain and has been prescribed nitroglycerin for these episodes. However, she has not taken any nitroglycerin today.

The patient states that she takes a baby aspirin every morning. She denies any other significant medical conditions and reports no known allergies.

Initial Vital Signs

• Pulse: Strong and regular
• Heart rate: 114 beats per minute
• Blood pressure: 166/91 mmHg
• Respiratory rate: 22 breaths per minute with normal, equal chest rise and fall
• Blood glucose level: 111 mg/dL
• Temperature: 98.7°F
• GCS: 15
• SpO₂: 90%

Scenario 1: Continued

Assessment and Treatment

You obtain a 12-lead ECG, and the computerized interpretation indicates:

STEMI

Recognizing the need for immediate cardiac care, you transfer the patient onto the stretcher and begin emergency transport to the nearest cardiac-capable hospital.

During transport, you:

• Administer 324 mg of aspirin orally.
• Assist the patient with taking her prescribed nitroglycerin, provided no contraindications are present.
• Apply supplemental oxygen because of her low oxygen saturation.

Reassessment

After treatment, the patient’s vital signs are reassessed:

• Heart rate: 108 beats per minute, strong and regular
• Blood pressure: 142/89 mmHg
• Respiratory rate: 18 breaths per minute
• SpO₂: 95%
• GCS: 15

The patient remains stable during transport.

She is transported to the closest appropriate facility with cardiology services and the capability to manage a STEMI. Her condition remains stable, and no significant deterioration in her vital signs occurs during transport.

Key Clinical Takeaways

• This patient is experiencing a myocardial infarction (MI).
• A coronary artery has become obstructed, reducing blood flow and oxygen delivery to a portion of the heart muscle.
• Myocardial infarction commonly presents with chest discomfort described as pressure, heaviness, squeezing, or crushing pain.
• Compared with some other acute cardiovascular emergencies, such as aortic dissection, the discomfort associated with an MI may develop more gradually and worsen over time.
• The patient’s systolic blood pressure remains well above 100 mmHg, so assisting her with her prescribed nitroglycerin may be appropriate, provided there are no other contraindications.
• Nitroglycerin can help reduce myocardial oxygen demand and may relieve ischemic chest discomfort.
• Aspirin works as an antiplatelet medication by reducing platelet aggregation.
• In a suspected acute coronary syndrome, aspirin can help limit further growth of a coronary thrombus and reduce continued obstruction of blood flow.
• Because of its benefit in suspected MI, early administration of aspirin is an important part of prehospital treatment when no contraindications are present.

Recognition and Management of Cardiac Emergencies

Coronary Artery Disease: Recognition and Prehospital Management

Overview

• Coronary artery disease (CAD) occurs when blood flow to the heart muscle becomes limited, usually because the coronary arteries have narrowed.
• CAD is one of the most common forms of cardiovascular disease and is a major contributor to illness and death.
• CAD can create the conditions that lead to myocardial infarction and other forms of ischemic chest discomfort.

Key Concepts

• The myocardium, or heart muscle, requires its own blood supply because the heart wall is too thick to receive enough oxygen and nutrients directly from blood inside the heart chambers.
• The coronary arteries supply oxygenated blood to the myocardium.
• When coronary blood flow cannot meet the oxygen demands of the heart muscle, myocardial ischemia may occur.
  • Symptoms can include chest discomfort, shortness of breath, nausea, dizziness, weakness, or other nonspecific complaints.
• Atherosclerosis is a common underlying cause of CAD.
  • Atherosclerosis involves the buildup of fatty plaque within the inner walls of arteries.
  • This buildup restricts blood flow through the affected vessel.
• Stenosis refers to abnormal narrowing of a blood vessel.

• If an atherosclerotic plaque ruptures:
  • Platelets and clotting factors may rapidly form a thrombus.
  • The clot can further reduce or completely block coronary blood flow.
  • Prolonged loss of blood flow may cause myocardial tissue injury or death.

Important Terms

• Ischemia
  • Refers to inadequate blood flow and oxygen delivery to body tissue.
• Angina or angina pectoris
  • Describes chest discomfort caused by myocardial ischemia.
• Myocardial infarction
  • Refers to death of heart muscle caused by prolonged inadequate blood flow.
  • Commonly called a heart attack.
• Myocardium
  • The muscular layer of the heart.
• Thrombus
  • A blood clot that forms within a blood vessel.
  • In CAD, thrombus formation may occur after an atherosclerotic plaque ruptures.
• Atherosclerosis
  • The buildup of fatty plaque within arterial walls that can reduce blood flow.
• Coronary arteries
  • Blood vessels located on the surface of the heart that supply oxygen and nutrients to the myocardium.

Recognizing Coronary Artery Disease

• Chest discomfort is one of the most common symptoms associated with CAD.
  • Pain or discomfort may radiate to the:
    • Arms.
    • Neck.
    • Jaw.
    • Back.
    • Upper abdomen.
  • Symptoms may become more noticeable during exertion or increased cardiac demand.
• Some patients may have an atypical presentation.
  • This may be more common in:
    • Older adults.
    • Patients with diabetes.
    • Women.
  • Instead of obvious chest pain, the patient may primarily report:
    • Nausea.
    • Anxiety.
    • Shortness of breath.
    • Weakness.
    • Fatigue.
    • Other unusual discomfort.

Associated Heart Failure Findings

• CAD may occur with signs and symptoms of heart failure.
• Left-sided heart failure
  • May produce respiratory distress.
  • Cardiogenic pulmonary edema may develop.
  • Crackles or other signs of fluid in the lungs may be present.
• Right-sided heart failure
  • May cause:
    • Peripheral swelling.
    • Pitting edema.
    • Jugular venous distention.
• Poor circulation may also produce:
  • Pale skin.
  • Cool skin.
  • Diaphoresis.

Patterns of Ischemic Chest Discomfort

• Patients with ischemic chest symptoms may present with either relatively stable symptoms or acute coronary syndrome.
• Stable Ischemic Heart Disease
  • Symptoms commonly occur during exertion, emotional stress, or increased cardiac workload.
  • Symptoms often improve when cardiac demand decreases.
  • Stable angina
    • Chest discomfort that typically follows a predictable pattern.
    • Usually improves with rest or prescribed nitroglycerin.
• Acute Coronary Syndrome (ACS)
  • Represents a sudden reduction in coronary blood flow.
  • Symptoms may begin unexpectedly and may not improve with rest.
  • ACS includes:
    • Unstable angina
      • Ischemic chest discomfort that may occur at rest or with less exertion than usual.
    • NSTEMI
      • A myocardial infarction without the classic ST-segment elevation pattern.
    • STEMI
      • A myocardial infarction associated with ST-segment elevation or equivalent ECG findings requiring rapid reperfusion evaluation.

Assessment and Initial Management

• Begin by identifying and treating immediate life threats involving:
  • Airway.
  • Breathing.
  • Circulation.
• Consider whether the patient requires:
  • Supplemental oxygen.
  • Assisted ventilation.
  • Positive-pressure ventilatory support.
• Position the patient in a way that supports breathing and circulation.
• Obtain baseline vital signs.
• Reassess frequently for changes in:
  • Blood pressure.
  • Heart rate.
  • Respiratory status.
  • Mental status.
  • Oxygen saturation.

ECG Evaluation

• Obtain a 12-lead ECG as early as possible when indicated.
• Even if an EMT is not authorized to interpret the ECG, obtaining it can allow trained providers or the receiving hospital to review the tracing.
• In EMS systems that permit it, transmit the ECG to the receiving facility.
• Consider ECG evaluation for:
  • Chest pain.
  • Shortness of breath suspicious for cardiac disease.
  • Upper abdominal or other symptoms that may represent an atypical cardiac presentation.

Focused Patient Assessment

• Obtain a detailed medical history.
• Ask about:
  • Previous cardiac disease.
  • Previous myocardial infarction.
  • Angina.
  • Heart failure.
  • Respiratory disease.
  • Medications.
  • Allergies.
  • Similar previous episodes.
• Examine the chest as appropriate.
  • Inspect for abnormalities.
  • Palpate when indicated.
  • Assess respiratory effort.
• Auscultate lung sounds.
• Evaluate for both cardiac and respiratory causes of the patient’s symptoms.

Supplemental Oxygen

• Provide oxygen when clinically indicated, particularly when hypoxemia is present.
• Titrate oxygen according to:
  • Oxygen saturation.
  • Respiratory status.
  • Local protocol.
• Avoid unnecessary excessive oxygen administration when the patient is already adequately oxygenated.

Aspirin

• Aspirin may be given to eligible patients with suspected acute coronary syndrome according to local protocol.
• A commonly used EMS dose is approximately 162–325 mg of chewable aspirin.
• Aspirin helps by reducing platelet aggregation and slowing further clot formation.
• It is used for its antiplatelet effect rather than primarily for pain relief.
• Before administration, assess for contraindications such as:
  • Aspirin allergy.
  • Significant active bleeding.
  • Other protocol-specific restrictions.

Nitroglycerin

• EMS providers may assist appropriate patients with their prescribed nitroglycerin according to local protocol.
• A common form is a 0.4 mg sublingual tablet or spray.
• Nitroglycerin causes vasodilation and may:
  • Reduce cardiac workload.
  • Decrease myocardial oxygen demand.
  • Improve coronary blood flow in some situations.
• Important precautions and contraindications may include:
  • Hypotension.
  • Certain heart-rate abnormalities.
  • Recent use of phosphodiesterase-5 inhibitors for erectile dysfunction.
  • Other restrictions identified in local protocols.
• Reassess blood pressure and symptoms after administration.

Transport

• Transport the patient to an appropriate receiving facility according to local EMS guidelines.
• Patients with suspected ACS may benefit from transport to a hospital capable of:
  • Rapid ECG evaluation.
  • Cardiac catheterization.
  • Advanced cardiac care.
• Avoid unnecessary delays in transport, particularly when the patient has:
  • Persistent chest discomfort.
  • ECG abnormalities.
  • Hypotension.
  • Respiratory distress.
  • Altered mental status.
  • Signs of worsening perfusion.

Heart Failure: Anatomy, Physiology, Recognition, and Management

Overview

• Cardiovascular disease is frequently encountered in the prehospital environment.
  • As obesity and other cardiovascular risk factors continue to increase, heart disease remains an important concern for EMS providers.
  • This section focuses primarily on left-sided and right-sided heart failure.
• Key topics include:
  • Basic cardiovascular anatomy and physiology.
  • How heart failure develops.
  • Common signs and symptoms.
  • Assessment and treatment of heart failure.
  • Application of these concepts to patient scenarios.

Essential Anatomy and Concepts

• Heart Anatomy
  • The heart is a muscular organ located in the mediastinum, near the center of the chest.
  • It lies:
    • Behind the sternum.
    • In front of the spinal column.
• Layers of the Heart
  • From the innermost to the outermost layer, the heart consists of:
    • Endocardium
      • Forms the inner lining of the heart chambers.
      • Comes directly into contact with circulating blood.
    • Myocardium
      • Thick muscular middle layer of the heart.
      • Responsible for the heart’s pumping action.
      • Cardiac muscle cells have specialized electrical properties that allow impulses to spread rapidly and coordinate contraction.
    • Pericardium
      • Protective sac surrounding the heart.
      • Includes:
        • Visceral pericardium, also called the epicardium.
        • Parietal pericardium, the outer layer.
• Heart Chambers
  • The heart contains four chambers:
    • Right atrium.
    • Right ventricle.
    • Left atrium.
    • Left ventricle.
  • Atria
    • The upper chambers of the heart.
    • Primarily receive blood returning to the heart.
    • The right and left atria are separated by the interatrial septum.
  • Ventricles
    • The lower chambers of the heart.
    • Responsible for pumping blood out of the heart.
    • The right and left ventricles are separated by the interventricular septum.
  • The septa contain connective and muscular tissue that separate the right and left sides of the heart.
• Heart Valves
  • Heart valves maintain one-way blood flow and help prevent blood from moving backward.
  • Two major valve groups are present:
    • Atrioventricular valves
      • Regulate blood flow from the atria into the ventricles.
      • Include:
        • Tricuspid valve.
        • Mitral valve.
    • Semilunar valves
      • Control blood flow from the ventricles into the major arteries.
      • Include:
        • Pulmonary valve.
        • Aortic valve.
  • A useful sequence for remembering the valves as blood travels through the heart is:
    • Tricuspid.
    • Pulmonary.
    • Mitral.
    • Aortic.

Peripheral Circulation

• Arteries and veins contain three basic vessel-wall layers:
  • Tunica intima
    • Innermost layer.
    • Consists of a thin endothelial lining.
  • Tunica media
    • Middle layer containing smooth muscle and elastic tissue.
    • Allows blood vessels to change diameter and respond to changing pressure.
  • Tunica adventitia
    • Outermost layer.
    • Provides structural strength and support to the vessel.
• Arterial Circulation
  • Arteries carry blood away from the heart.
  • Arteries branch into smaller vessels called arterioles.
  • Arterioles help regulate how much blood reaches different tissues and organs.
  • Arterioles eventually lead into capillaries.
  • Capillaries have very thin walls that permit the exchange of:
    • Oxygen.
    • Carbon dioxide.
    • Nutrients.
    • Fluids.
    • Metabolic waste products.
• Venous Circulation
  • Veins return blood from peripheral tissues back toward the heart.

Normal Blood Flow Through the Heart

• The right atrium receives deoxygenated blood from:
  • Superior vena cava.
    • Returns blood from the head, neck, and upper extremities.
  • Inferior vena cava.
    • Returns blood from areas below the heart.
• Blood moves from the right atrium through the tricuspid valve into the right ventricle.
• The right ventricle pumps blood through the pulmonary valve into the pulmonary arteries.
• Pulmonary arteries carry deoxygenated blood toward the lungs.
• In the lungs:
  • Carbon dioxide moves from the blood into the alveoli.
  • Oxygen moves from the alveoli into the blood.
• Oxygenated blood returns through the pulmonary veins into the left atrium.
• Blood then passes through the mitral valve into the left ventricle.
• The left ventricle pumps oxygenated blood through the aortic valve and into the aorta.
• The aorta distributes blood throughout the systemic circulation.

The Cardiac Cycle

• The cardiac cycle is the sequence of events occurring from one heartbeat to the next.
• Diastole
  • The relaxation and filling phase.
  • The ventricles relax and fill with blood.
  • Blood moves through the atrioventricular valves into the ventricles.
  • The pulmonary and aortic valves remain closed during most of ventricular filling.
• Systole
  • The contraction and ejection phase.
  • The atria finish moving blood into the ventricles.
  • Ventricular pressure rises as the ventricles contract.
  • The atrioventricular valves close.
  • When ventricular pressure exceeds arterial pressure, the semilunar valves open.
  • Blood is then ejected into the pulmonary artery and aorta.
• Ejection Fraction
  • Refers to the percentage of blood within a ventricle that is pumped out during each contraction.
  • It is commonly used as one measure of left ventricular pumping performance.
• Stroke Volume
  • The amount of blood pumped from a ventricle with each contraction.
  • Stroke volume is influenced by:
    • Preload
      • Degree of ventricular filling and myocardial stretch before contraction.
      • Appropriate stretch can improve contraction, but excessive stretch may eventually weaken pumping efficiency.
    • Contractility
      • Strength of myocardial contraction.
    • Afterload
      • Resistance the ventricle must overcome to eject blood.
• Cardiac Output
  • The amount of blood pumped by the heart each minute.
  • Calculated as:
    • Cardiac Output = Stroke Volume × Heart Rate

Nervous System Control of the Heart

• The autonomic nervous system influences heart rate, conduction, vascular tone, and contractile strength.
• Sympathetic Nervous System
  • Associated with the “fight-or-flight” response.
  • Norepinephrine is an important sympathetic neurotransmitter.
  • Sympathetic stimulation can:
    • Increase heart rate.
    • Increase myocardial contractility.
    • Produce vasoconstriction in selected blood vessels.
  • Important adrenergic receptors include:
    • Alpha receptors.
      • Primarily associated with peripheral vasoconstriction.
    • Beta receptors.
      • Beta-1 receptors in the heart increase heart rate and contractile force.
• Parasympathetic Nervous System
  • Associated with “rest-and-digest” functions.
  • Primarily affects the heart through the vagus nerve.
  • Acetylcholine is the main parasympathetic neurotransmitter.
  • Parasympathetic stimulation can:
    • Slow heart rate.
    • Slow conduction through the atrioventricular node.

How Heart Failure Develops

• Heart failure is a clinical syndrome in which the heart cannot pump enough blood to adequately meet the body’s metabolic needs or can do so only at abnormally high filling pressures.
• Heart failure may primarily involve:
  • Left-sided failure.
  • Right-sided failure.
  • Both sides of the heart.
• Potential contributing causes include:
  • Coronary artery disease.
  • Myocardial disease.
  • Heart valve disorders.
  • Chronic hypertension.
  • Myocardial infarction.
  • Pulmonary embolism.
  • Severe infection or sepsis.
  • Excessive alcohol or certain drug use.
  • Excessive sodium and fluid retention in susceptible patients.

Left-Sided Heart Failure

• Occurs when the left ventricle cannot effectively pump blood into systemic circulation.
• Blood and pressure begin to back up toward the lungs.
• Pressure rises within:
  • Left atrium.
  • Pulmonary veins.
  • Pulmonary capillaries.
• When pulmonary capillary pressure becomes sufficiently elevated:
  • Fluid can move into the lung interstitial tissue and alveoli.
  • Pulmonary edema may develop.
  • Oxygen diffusion becomes more difficult.
  • Hypoxemia and respiratory distress can result.

Right-Sided Heart Failure

• Occurs when the right ventricle cannot effectively pump blood into the pulmonary circulation.
• Blood backs up into the systemic venous circulation.
• Increased venous pressure can cause fluid accumulation in body tissues.
• Findings may include:
  • Peripheral edema.
  • Jugular venous distention.
  • Abdominal swelling or ascites.
• Left-sided heart failure is a common cause of chronic right-sided heart failure.

Recognizing Left-Sided Heart Failure

• Possible findings include:
  • Shortness of breath at rest or during exertion.
  • Orthopnea.
    • Difficulty breathing while lying flat.
  • Wheezing.
  • Crackles.
  • Tachypnea.
  • Cyanosis.
  • Chest discomfort or pain.
  • Cough.
  • Pink, frothy sputum in severe pulmonary edema.
  • Increased work of breathing.
  • Hypoxemia.

Recognizing Right-Sided Heart Failure

• Possible findings include:
  • Peripheral edema.
  • Swelling of the feet or lower legs.
  • Jugular venous distention.
  • Abdominal distention.
  • Ascites.
  • Weight gain caused by fluid retention.
  • Chest discomfort in some patients.

Prehospital Care of Heart Failure

Right-Sided Heart Failure

• Begin with assessment and stabilization of:
  • Airway.
  • Breathing.
  • Circulation.
• Obtain and trend vital signs.
• Assess:
  • Oxygenation.
  • Mental status.
  • Peripheral perfusion.
  • Degree of edema.
  • Jugular veins.
  • Lung sounds.
• Provide supportive treatment according to the patient’s presentation and local protocols.
• Transport to an appropriate receiving facility.
• Consider an ALS intercept when advanced assessment or treatment is required and it will not unnecessarily delay transport.

Left-Sided Heart Failure

• Assess and manage:
  • Airway.
  • Breathing.
  • Circulation.
• Obtain baseline and repeat vital signs.
• Place the patient in a position that makes breathing easier.
  • An upright or high-Fowler’s position is commonly preferred when blood pressure and clinical condition allow.
• Administer supplemental oxygen when hypoxemia is present or according to local protocol.
• Consider CPAP when:
  • The patient is alert enough to cooperate.
  • Significant respiratory distress or pulmonary edema is present.
  • Blood pressure and other clinical findings allow its safe use.
• CPAP may:
  • Improve oxygenation.
  • Reduce work of breathing.
  • Recruit alveoli.
  • Reduce venous return and cardiac workload in appropriate patients.
• Continually reassess:
  • SpO₂.
  • Respiratory rate.
  • Work of breathing.
  • Lung sounds.
  • Blood pressure.
  • Mental status.
  • Response to treatment.
• Transport promptly to an appropriate facility.
• Request or arrange ALS support when indicated without causing unnecessary delay.