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Cardiac Muscle

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Cardiac Muscle Definition

Cardiac muscle, also known as heart muscle, is the layer of muscle tissue which lies between the endocardium and epicardium . These inner and outer layers of the heart, respectively, surround the cardiac muscle tissue and separate it from the blood and other organs. Cardiac muscle is made from sheets of cardiac muscle cells. These cells, unlike skeletal muscle cells, are typically unicellular and connect to one another through special intercalated discs . These specialized cell junction and the arrangement of muscle cells enables cardiac muscle to contract quickly and repeatedly, forcing blood throughout the body.

Cardiac Muscle Structure

Cardiac muscle exists only within the heart of animals. It is a specialized form of muscle evolved to continuously and repeatedly contract, providing circulation of blood throughout the body. The heart is a relatively simple organ. Through all the twists and turns and various chambers, there are only three layers. The outer layer, known as the epicardium or visceral pericardium , surround the cardiac muscle on the exterior. This helps protect it from contact with other organs. The parietal pericardium attaches to this outer layer creates a fluid-filled layer which helps lubricate the heart. The inner layer, or endocardium , separates the muscle from the blood it is pumping within the chambers of the heart. In between these two sheets lies the cardiac muscle. Cardiac muscle is sometimes referred to as myocardium . This can be seen in the image below.

When we look a bit closer at cardiac muscle, we can see that it is arranged in sheets of cells, which are connected to each other in a lattice-work fashion. Where two cells meet a specialized junction called an intercalated disc locks the two cells into place. While this region looks like a dark disc under the microscope, it is actually the interlocking of hundreds of finger-like projections from each cell. These projections have small holes in them, gap junctions , which can pass the impulse to contract to connected cells. Interlaced between and around these cells are nerves and blood vessels, which carry signals and oxygen to the cardiac muscle.

At the microscopic level, cardiac muscle is organized much like skeletal muscle. Both muscle tissues are striated , meaning they show dark and light bands when viewed under a microscope. These band are created by the highly organized sarcomeres . A sarcomere is a bundle of protein fibers which respond to a signal and contract. In both skeletal and cardiac muscle, these sarcomeres are made of actin and myosin and are supported by the same proteins. Tropomyosin is a protein which wraps actin and stops myosin from binding to it. Troponin is a protein which holds tropomyosin in place until a signal to contract has been received. These proteins are the same in both skeletal and cardiac muscle.

Function of Cardiac Muscle

As in skeletal muscle, the signal to contract is an action potential. However with skeletal muscle this signal usually comes from the somatic , or voluntary, nervous system. Cardiac muscle is controlled by the autonomous nervous system . Cells in your brain and cells embedded throughout your heart act to release well-timed nervous impulses which signal your heart cells to contract in the correct pattern. While the source of the signals is different, the reception of the signal and the rest of contraction are very similar.

The action potential , or nerve impulse, on the surface of the cell stimulates a specialized organelle to release calcium ions (Ca 2+ ). This organelle is called the sarcoplasmic reticulum , and is derived from the endoplasmic reticulum found in a general cell. The Ca 2+ ions released into the cytoplasm affect the protein troponin, causing it to release tropomyosin. Tropomyosin shifts position and myosin is allowed to attach to actin. Myosin then used the energy stored in ATP molecules to walk along the actin filaments and shorten the length of each sarcomere. When the impulse is gone, the Ca 2+ is reabsorbed quickly into the sarcoplasmic reticulum. Troponin reattaches to tropomyosin, and the cardiac muscle cells release. This general process happens every time your heart beats.

As all the muscle cells work in unison, a force can be exerted in the chambers of the heart. The sheets of cardiac muscle are laid so they run perpendicularly to one another. This creates the effect that when the heart contracts, it does so in multiple directions. The ventricles and atria of the heart shrink from top to bottom and from side to side as these multiple layers muscle fibers contract. This produces a strong pumping and twisting force in the ventricles, forcing blood throughout the body.

Lodish, H., Berk, A., Kaiser, C. A., Krieger, M., Scott, M. P., Bretscher, A., . . . Matsudaira, P. (2008). Molecular Cell Biology 6th. ed. New York: W.H. Freeman and Company. Reece, J. B., Urry, L. A., Cain, M. L., Wasserman, S. A., Minorsky, P. V., & Jackson, R. B. (2014). Campbell Biology, Tenth Edition (Vol. 1). Boston: Pearson Learning Solutions. Blausen.com staff (2014). “Medical gallery of Blausen Medical 2014”. WikiJournal of Medicine 1 (2). DOI:10.15347/wjm/2014.010. ISSN 2002-4436.

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cardiac muscle

Our editors will review what you’ve submitted and determine whether to revise the article.

• Healthline - How is Cardiac Muscle Tissue Different from Other Muscle Tissues?
• Innerbody - Cardiac Muscle Tissue
• The University of Hawaiʻi Pressbooks - Cardiac Muscle Tissue
• University of Hawaii Pressbooks - Anatomy and Physiology - Cardiac Muscle and Electrical Activity
• Verywell Health - Everything to know about Cardiac Muscle Tissue
• National Center for Biotechnology Information - Anatomy, Thorax, Cardiac Muscle

cardiac muscle , in vertebrates , one of three major muscle types, found only in the heart . Cardiac muscle is similar to skeletal muscle , another major muscle type, in that it possesses contractile units known as sarcomeres ; this feature, however, also distinguishes it from smooth muscle , the third muscle type. Cardiac muscle differs from skeletal muscle in that it exhibits rhythmic contractions and is not under voluntary control. The rhythmic contraction of cardiac muscle is regulated by the sinoatrial node of the heart, which serves as the heart’s pacemaker.

The heart consists mostly of cardiac muscle cells (or myocardium). The outstanding characteristics of the action of the heart are its contractility, which is the basis for its pumping action, and the rhythmicity of the contraction. The amount of blood pumped by the heart per minute (the cardiac output ) varies to meet the metabolic needs of peripheral tissues, particularly the skeletal muscles, kidneys , brain , skin , liver , heart, and gastrointestinal tract . The cardiac output is determined by the contractile force developed by the cardiac muscle cells, as well as by the frequency at which they are activated (rhythmicity). The factors affecting the frequency and force of heart muscle contraction are critical in determining the normal pumping performance of the heart and its response to changes in demand.

Cardiac muscle cells form a highly branched cellular network in the heart. They are connected end to end by intercalated disks and are organized into layers of myocardial tissue that are wrapped around the chambers of the heart. The contraction of individual cardiac muscle cells produces force and shortening in these bands of muscle, with a resultant decrease in the heart chamber size and the consequent ejection of the blood into the pulmonary and systemic vessels. Important components of each cardiac muscle cell involved in excitation and metabolic recovery processes are the plasma membrane and transverse tubules in registration with the Z lines, the longitudinal sarcoplasmic reticulum and terminal cisternae, and the mitochondria . The thick (myosin) and thin ( actin , troponin, and tropomyosin) protein filaments are arranged into contractile units, with the sarcomere extending from Z line to Z line, that have a characteristic cross-striated pattern similar to that seen in skeletal muscle.

The rate at which the heart contracts and the synchronization of atrial and ventricular contraction required for the efficient pumping of blood depend on the electrical properties of the cardiac muscle cells and on the conduction of electrical information from one region of the heart to another. The action potential (activation of the muscle) is divided into five phases. Each of the phases of the action potential is caused by time-dependent changes in the permeability of the plasma membrane to potassium ions (K + ), sodium ions (Na + ), and calcium ions (Ca 2+ ).

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Everything to Know About Cardiac Muscle Tissue

• Maintenance

Frequently Asked Questions

Cardiac muscle is found in the walls of the heart . It helps the heart perform its function of pumping blood throughout the body. Cardiac muscle tissue is located in the middle of three layers of the heart, called the myocardium . Problems in the myocardium can cause heart failure and arrhythmias or contribute to sudden cardiac death.

This article discusses the role of muscle tissue in the heart and ways to keep your heart's muscle tissue healthy.

manusapon kasosod / Getty Images

Heart Tissue Layers

The heart has three layers of tissue:

• Epicardium : The outermost layer of tissue
• Myocardium : The middle layer of tissue, made of muscle
• Endocardium : The tissue lining the inside of the heart and valves

The pericardium is the sac in which the heart sits.

Cardiac Muscle Tissue Function

The heart can be thought of as a pump. It is responsible for pumping blood throughout the body to provide oxygen and nutrients.

The heart's muscle is stimulated by the electrical system of the heart. Specialized pacemaker cells create an electrical signal that causes contraction, or shortening, of the muscle fibers. This muscle contraction is what causes the heart to squeeze and pump out blood.

At a cellular level, heart muscle tissue is made up of bundles or fibers of interconnected muscle cells, called cardiomyocytes . These cells are packed with units called sarcomeres that are made of proteins called actin and myosin . When stimulated, these two proteins slide against each other to result in contraction of the heart.

Types of Muscle Tissue

The body has three types of muscle tissue. All of them share the ability to contract and have important functions. The tissue types are:

• Skeletal muscle tissue provides the function of body movement. It is under voluntary control.
• Smooth muscle is found in the digestive tract and in the arteries. It is not under voluntary control.
• Cardiac muscle is only found in the heart. It is responsible for pumping blood out of the heart.

Conditions That Affect Cardiac Muscle Tissue

Heart muscle problems have many causes.

Cardiomyopathy , or heart muscle weakness, is a general term for problems with the heart muscle. It can be caused by:

• Genetic mutations
• Lack of blood flow
• Autoimmune or inflammatory conditions
• Vitamin deficiency
• Damage from toxins

Sometimes the cause is not determined, which is known as idiopathic cardiomyopathy.

Other conditions can affect cardiac muscle tissue. These can cause varying problems, from thickening of the heart muscle to heart failure, arrhythmias, and sudden cardiac death.

Most common causes:

• Ischemic heart disease from blocked coronary arteries
• Heart attack
• High blood pressure
• Valvular heart disease, such as aortic stenosis

High Blood Pressure and the Heart

Blood pressure is the force that the heart must pump against to eject blood. When blood pressure is high, the heart must work harder. Just like any other muscle, the heart muscle thickens in response to this increased work. This thickened (hypertrophied) heart muscle can lead to problems with heart filling and heart failure. High blood pressure is one of the more common causes of heart failure.

Other possible issues that could affect heart muscle include:

• Myocarditis (inflammation of the heart muscle)
• Toxins like alcohol, cocaine, amphetamines
• Medications, including certain cancer therapies
• Infiltrative disorders (accumulation of abnormal proteins or particles in the heart muscle), including cardiac amyloidosis , cardiac sarcoidosis , or hemochromatosis (iron overload)
• Genetic conditions, including left ventricular noncompaction , hypertrophic cardiomyopathy , arrhythmogenic right ventricular cardiomyopathy , glycogen storage disease, or muscular dystrophy
• Heart rhythm problems
• Congenital heart disease (heart defects present from birth)
• Endocrine disorders such as thyroid problems
• Extreme stress
• Vitamin B1 ( thiamine ) deficiency

When to See a Healthcare Provider

If you are concerned about cardiomyopathy, you should see a healthcare provider for evaluation. Seek medical attention for symptoms like shortness of breath, exercise intolerance, leg swelling, and fatigue, which are signs of heart failure. Even if you don't have any symptoms, if heart failure runs in your family, you should discuss this with your healthcare provider to determine whether screening or genetic testing is needed.

How to Keep Cardiac Muscle Tissue Healthy

While not all types of cardiomyopathy can be prevented, there are things you can do to help keep your heart muscle as healthy as possible.

Living a healthy lifestyle can help keep the heart's muscle tissue healthy by preventing coronary artery disease, high blood pressure, and diabetes. This includes eating a healthy diet , getting regular physical exercise, maintaining a healthy weight, and avoiding tobacco use.

In addition to living a healthy lifestyle, the following can be done to prevent cardiomyopathy:

• Controlling blood pressure
• Controlling cholesterol levels
• Treating coronary artery disease
• Avoiding toxins such as drugs and excess alcohol
• Controlling blood sugar (recent guidelines recommend sodium-glucose cotransporter-2 (SGLT2) inhibitors for those with diabetes and elevated risk of heart disease)

For those diagnosed with cardiomyopathy, several medications have been proven to prevent or reverse the abnormal remodeling that occurs due to heart disease. These include:

• Certain beta-blockers
• ACE ( angiotensin-converting enzyme ) inhibitors
• Angiotensin receptor blocker/ neprilysin inhibitor
• Aldosterone antagonists
• SGLT2 inhibitors

Cardiologists (doctors who specialize in heart disease) can prescribe and adjust these medications and provide an individualized treatment plan.

Cardiac muscle tissue is found in the middle of three layers of heart tissue. It enables the heart to pump blood and provide nutrients and oxygen throughout the body. Several things can cause problems with the heart muscle, including ischemic heart disease, heart attack, high blood pressure, and valvular heart disease.

The best ways to prevent cardiomyopathy are to live a healthy lifestyle, control blood pressure, cholesterol, and diabetes, and avoid substances that are known to be toxic to the heart. Those with cardiomyopathy can benefit from effective medications.

A Word From Verywell

The heart is arguably the most important muscle in the body. Keeping cardiac tissue healthy helps the heart function properly and decreases the risk of complications. Knowing your risk and controlling modifiable risk factors such as blood pressure, cholesterol, blood sugar, and smoking are important ways to lower your risk and protect your heart muscle.

Cardiac muscle tissue is a type of muscle tissue found only in the heart. It appears striated (striped) under a microscope due to the presence of sarcomere units that are responsible for its ability to contract. Heart muscle contracts in response to signals from specialized pacemaker cells located in the heart.

Cardiac muscle tissue is located in the middle of three layers of the heart, called the myocardium. It is the thickest of the three layers. On its outer surface, the myocardium is surrounded by a thin, protective layer called the pericardium. On its inner surface, it is lined by the endocardium.

The heart is made up of three layers of tissue. The epicardium is the outer, fibrous layer that lines and protects the heart. The myocardium is the thick muscular layer of tissue. The endocardium lines the inner surface of the heart. The heart also has four valves (aortic, mitral, tricuspid, and pulmonic).

National Heart, Lung, and Blood Institute. How the heart works .

American Heart Association. What is heart failure .

Vikhorev PG, Vikhoreva NN. Cardiomyopathies and related changes in contractility of human heart muscle .  International Journal of Molecular Sciences . 2018; 19(8):2234. doi:10.3390/ijms19082234

MedlinePlus. Types of muscle tissue .

Brieler J, Breeden MA, Tucker J.  Cardiomyopathy: an overview .  AFP . 2017;96(10):640-646.

Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA guideline for the management of heart failure: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines . Circulation . 2022;145:e895–e1032. doi:10.1161/CIR.0000000000001063

American Heart Association. How to help prevent heart disease at any age .

By Angela Ryan Lee, MD Dr. Lee is an Ohio-based board-certified physician specializing in cardiovascular diseases and internal medicine.

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Anatomy, thorax, cardiac muscle.

Anthony Saxton ; Muhammad Ali Tariq ; Bruno Bordoni .

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Last Update: August 8, 2023 .

• Introduction

Cardiac muscle (or myocardium) makes up the thick middle layer of the heart. It is one of three types of muscle in the body, along with skeletal and smooth muscle. The myocardium is surrounded by a thin outer layer called the epicardium (AKA visceral pericardium) and an inner endocardium. Coronary arteries supply to the cardiac muscle, and cardiac veins drain this blood. Cardiomyocytes are the individual cells that make up the cardiac muscle. The primary function of cardiomyocytes is to contract, which generates the pressure needed to pump blood through the circulatory system. [1]

• Structure and Function

Rapid, involuntary contraction and relaxation of the cardiac muscle are vital for pumping blood throughout the cardiovascular system. To accomplish this, the structure of cardiac muscle has distinct features that allow it to contract in a coordinated fashion and resist fatigue.

The individual cardiac muscle cell (cardiomyocyte) is a tubular structure composed of chains of myofibrils, which are rod-like units within the cell. The myofibrils consist of repeating sections of sarcomeres, which are the fundamental contractile units of the muscle cells. Sarcomeres are composed of long proteins that organize into thick and thin filaments, called myofilaments. Thin myofilaments contain the protein actin, and thick myofilaments contain the protein myosin. The myofilaments slide past each other as the muscle contracts and relaxes. This process activates from the release of calcium from the sarcoplasmic reticulum (SR) when delivering an action potential to the muscle, in a process called excitation-contraction coupling. The sliding of actin and myosin past each other produces the formation of “cross-bridges,” which causes contraction of the heart and generation of force.

Cardiomyocytes are rectangular, branching cells that typically contain only one centrally-located nucleus. [2] This arrangement contrasts with skeletal muscle cells, which often contain many nuclei. Cardiomyocytes contain many mitochondria to produce large amounts of adenosine triphosphate (ATP) and myoglobin to store oxygen to meet the demands of muscle contraction.  

Like skeletal muscle, the organization of thin and thick myofilaments overlapping within the sarcomere of the cell produces a striated appearance when viewed on microscopy. This characteristic appearance consists of thick dark-colored A-bands (mainly composed of myosin) with a relatively bright H-zone in the center, and lighter colored I-bands (mainly actin) with a dark central Z line (also known as Z disc) connecting the actin filaments.

The outside of the cardiomyocyte is surrounded by a plasma membrane called the sarcolemma that acts as a barrier between extracellular and intracellular contents. Invaginations of the sarcolemma into the cytoplasm of the cardiomyocyte are called T-tubules, and they contain numerous proteins like L-type calcium channels, sodium-calcium exchangers, calcium ATPases, and beta-adrenergic receptors that allow for the exchange of ions with extracellular fluid surrounding the cell. At the Z-line of the cardiomyocyte, T-tubules run adjacent to enlarged areas of the sarcoplasmic reticulum known as the terminal cisternae, and the combination of a single T-tubule with one terminal cisterna referred to as a diad. This configuration contrasts with skeletal muscle, which combines 2 terminal cisternae with 1 T-tubule to form “triads,” which appear at the A-I junction. [3]

Neighboring cardiomyocytes are joined together at their ends by intercalated disks to create a syncytium of cardiac cells. Within the intercalated disc, there are three different types of cell junctions: fascia adherens, desmosomes, and gap junctions. The transverse side of the intercalated discs runs perpendicular to the muscle fibers at the Z lines and provides a structural component via fascia adherens and desmosome connections. The lateral side of the discs contains gap junctions that permit intercellular communication by allowing ions from one cardiomyocyte to move to a neighboring cell without having to be excreted into the extracellular space first. The low resistance of the gap junctions allows depolarization to spread quickly throughout the syncytium, which facilitates the rapid transmission of action potentials to produce a synchronized contraction of the cardiomyocytes in unison. [4]

One other distinct feature of cardiac muscle fibers is that they have their own auto rhythmicity. Unlike smooth or skeletal muscle which require neural input for contraction, cardiac fibers have their own pacemaker cells like the sinoatrial (SA) node that spontaneously depolarizes. These depolarizations occur at a consistent pace, but the pacemaker cells can also receive input from the autonomic nervous system to decrease or increase the heart rate depending on the requirements of the body.

The myocardial action potential occurs in five steps, beginning with rapid depolarization during Phase 0, followed by initial partial repolarization during Phase 1, a plateau period of Phase 2, then a rapid repolarization during Phase 3, leading to stabilization at the resting potential during Phase 4. Phase 2 plateau is a unique feature of the myocardial action potential that is not present in skeletal muscle. It is caused by balancing the effects of potassium efflux from the cell with an influx of calcium through voltage-gated L-type calcium channels (AKA dihydropyridine receptor) on the cell’s surface. This influx of calcium is relatively small and insufficient to cause contraction by itself. Still, it triggers the sarcoplasmic reticulum to release its stores of calcium into the myoplasm of the myocyte in a process called calcium-triggered-calcium-release. The calcium can then bind to troponin on the thin filament and begin the process of myocyte contraction seen with each heartbeat. [4]

The concentration of calcium in the myocyte is the critical factor that determines how much force is generated with each contraction. Cardiac muscle cells can increase contractility through beta-1 adrenergic receptors on the surface with a Gs G-protein. When stimulated by either the sympathetic nervous system or beta-1 agonist drugs, the Gs activate the enzyme adenylyl cyclase, which converts ATP to cAMP. Intracellular cAMP increases the activity of protein kinase A (PKA), which then phosphorylate calcium channels permitting more calcium to enter the cell, leading to increased contraction.

The cardiac muscle does not relax and prepare for the next heartbeat simply by ceasing contraction; it occurs in an active process called Lusitropy. During lusitropy, Sarco/endoplasmic reticulum Ca-ATPase (SERCA) pumps on the membrane of the sarcoplasmic reticulum use ATP hydrolysis to transfer calcium back into the sarcoplasmic reticulum ( SR) from the cytosol.

The regulatory protein phospholamban can control the rate at which the SERCA pumps calcium into the SR. Phospholamban reduces the transfer of calcium by the SERCA (sarcoplasmic reticulum Ca2+ ATPase) when bound together. Just as it can increase contractility, the sympathetic nervous system can also increase lusitropy through beta-1 adrenergic stimulation by phosphorylation of phospholamban with cAMP-dependent protein kinase (PKA). When phosphorylated, the phospholamban ceases inhibition of the SERCA, allowing it to increase the rate of calcium intake and relaxation of the cardiac muscle. [3]

The heart is one of the first organs to develop in utero. The visceral splanchnic mesoderm surrounding the heart tube gives rise to the cardiac muscle. Following gastrulation, mesodermal cells intercalate between the ectoderm and endoderm germ layers of the primitive streak, where signals from surrounding tissue promote cardiac progenitor cells to grow in the lateral plate mesoderm of the developing primitive streak. [5]  Cardiac development occurs between the second and seventh weeks of gestation.

• Blood Supply and Lymphatics

The process of contraction and relaxation requires a constant supply of oxygen and nutrients to meet the energy demands of cardiac muscle. Blood supply is delivered to the myocardium by coronary arteries, which are the first branches of the aortic root. Blood is drained away by the cardiac veins through the coronary sinus into the right atrium. There are left and right coronary arteries. The right coronary artery (RCA) arises from the right aortic sinus and supplies the right ventricle and the bundle of His. In 85% of the people (right dominance), it gives a branch known as the posterior descending artery (PDA), which supplies the AV node, posteromedial papillary muscle, and posterior portion of the interventricular septum and the ventricles. The left main coronary artery arises from the left aortic sinus. It branches off to give the left circumflex coronary artery (LCX) and the left anterior descending artery (LAD). The LCX supplies the lateral and posterior walls of the left ventricle, SA node, AV node, and anterolateral part of the papillary muscle. The LAD supplies the anterior part of the interventricular septum and anterior surface of the left ventricle.

Lymph drains via a myocardial plexus located within the myocardium. Along with a subendocardial plexus with lymphatics from the ventricles, the myocardial plexus drains into a subepicardial plexus, which gives rise to a right and left coronary trunk. [6] Lymph from the right side of the heart in the right coronary trunk travels to the brachiocephalic lymph nodes and then the thoracic duct. Lymph from the left side of the heart in the left coronary trunk travels to the inferior tracheobronchial lymph nodes and subsequently to the right lymphatic duct.

The autonomic nervous system (ANS) is a significant regulator of contractility, heart rate, stroke volume, and cardiac output. Parasympathetic innervation is provided from the right and left vagus nerves (CN X). Sympathetic innervation comes from fibers of the sympathetic trunk arising from the upper segments of the thoracic spinal cord. [7]  Afferent nerves also provide the central nervous system with feedback on blood pressure, blood chemistry, and to relay pain sensation from the heart.

Cardiac muscle makes up the thick middle layer of the heart and is surrounded by a thin outer layer called the epicardium or visceral pericardium and an inner endocardium.

• Physiologic Variants

Research has identified many genes responsible for the development of cardiomyopathies (diseases of the heart muscle) in the past two decades, including those encoding for sarcomere proteins in hypertrophic cardiomyopathy (HCM), cell-cell junction proteins in arrhythmogenic cardiomyopathy (AVC), cytoskeletal and sarcomere proteins in dilated cardiomyopathy (DCM), and sarcomere or Z-disk proteins with restrictive cardiomyopathy (RCM). [8]

• Surgical Considerations

Cardiopulmonary bypass is a technique used in cardiac surgery to suspend contractions of the cardiac muscle while maintaining perfusion of blood and oxygen to the organs and tissues of the body during an operation. Currently, the cardiac surgeon tries to use less invasive techniques. For example, replacing the median sternotomy with a lateral or inferior mini-thoracotomy. A cardiac surgery, due to induced hypothermia, can cause iatrogenic damage to the phrenic nerve (right and left), which passes under the pericardium. These lesions are transient, and only in a small percentage of patients, the damage will be permanent with an over-elevation of the diaphragmatic portion (especially on the left). [9]

• Clinical Significance

Diseases affecting cardiac muscle have a tremendous impact on health worldwide, with ischemic heart disease being the leading cause of morbidity and mortality in the world (as measured by disability-adjusted life-years, DALYs). [10] Ischemic heart disease characteristically demonstrates an imbalance between the supply and demand of oxygenated blood for cardiac tissue. This condition commonly occurs when the blood supply to the heart tissue is diminished, such as in coronary artery atherosclerosis, where an atherosclerotic plaque obstructs the lumen of a major epicardial artery and potentially a superimposed thrombosis. Ischemic syndromes include angina pectoris, acute myocardial infarction, and sudden cardiac death. Damage to the myocardium from ischemia leads to irreversible loss of cardiac function.

Damage to the heart muscle can also occur with a sufficient blood supply, such as in myocarditis (inflammation of the heart muscle), which is most commonly due to viral infection but can also have a bacterial infection etiology, or be due to certain medications, toxins, or autoimmune conditions.  Primary disorders of the heart muscle are collectively known as cardiomyopathies. These include dilated cardiomyopathy, which is characterized by an abnormally large heart, hypertrophic cardiomyopathy with abnormally thick walls of the heart, and restrictive cardiomyopathy with unusually stiff walls from causes such as amyloid deposition.

Any insult or injury to cardiac muscle can have grave consequences as cardiac muscle cells have minimal regeneration capabilities. However, ongoing research into the use of stem cells to grow cardiac muscle is an area of ongoing research. [5]

• Other Issues

Mutations in the gene that produces phospholamban are a cause of inherited human dilated cardiomyopathy with refractory congestive heart failure. [11]  Mutations in troponin are associated with hypertrophic, dilated, and restrictive cardiomyopathies. [12]  A mutation of the lamin A/C gene (LMNA) gene can cause cardiomyopathy. [13]

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Trans Sagittal Cross section of the Heart, Aorta, Left Auricula, Aortic Valve, Papillary muscles, Left Ventricle, Bicuspid Valve, Ventricular Septum, Inferior Vena Cava, Membranous septum, Musculi pectinati, Anterior Papillary Muscles, Tricuspid Valve (more...)

Disclosure: Anthony Saxton declares no relevant financial relationships with ineligible companies.

Disclosure: Muhammad Ali Tariq declares no relevant financial relationships with ineligible companies.

Disclosure: Bruno Bordoni declares no relevant financial relationships with ineligible companies.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

• Cite this Page Saxton A, Tariq MA, Bordoni B. Anatomy, Thorax, Cardiac Muscle. [Updated 2023 Aug 8]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

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4.4 Muscle Tissue

Learning objectives.

Describe the characteristics of muscle tissue and how these dictate muscle function.

By the end of this section, you will be able to:

• Identify the three types of muscle tissue
• Compare and contrast the functions of each muscle tissue type

Muscle tissue is characterized by properties that allow movement. Muscle cells are excitable; they respond to a stimulus. They are contractile, meaning they can shorten and generate a pulling force. When attached between two movable objects, such as two bones, contraction of the muscles cause the bones to move. Some muscle movement is voluntary, which means it is under conscious control. For example, a person decides to open a book and read a chapter on anatomy. Other movements are involuntary, meaning they are not under conscious control, such as the contraction of your pupil in bright light. Muscle tissue is classified into three types according to structure and function: skeletal, cardiac, and smooth ( Table 4.2 ).

Skeletal muscle is attached to bones and its contraction makes possible locomotion, facial expressions, posture, and other voluntary movements of the body. Forty percent of your body mass is made up of skeletal muscle. Skeletal muscles generate heat as a byproduct of their contraction and thus participate in thermal homeostasis. Shivering is an involuntary contraction of skeletal muscles in response to lower than normal body temperature. The muscle cell, or myocyte, develops from myoblasts derived from the mesoderm. Myocytes and their numbers remain relatively constant throughout life. Skeletal muscle tissue is arranged in bundles surrounded by connective tissue. Under the light microscope, muscle cells appear striated with many nuclei squeezed along the membranes. The striation is due to the regular alternation of the contractile proteins actin and myosin, along with the structural proteins that couple the contractile proteins to connective tissues. The cells are multinucleated as a result of the fusion of the many myoblasts that fuse to form each long muscle fiber.

Cardiac muscle forms the contractile walls of the heart. The cells of cardiac muscle, known as cardiomyocytes, also appear striated under the microscope. Unlike skeletal muscle fibers, cardiomyocytes are single cells with a single centrally located nucleus. A principal characteristic of cardiomyocytes is that they contract on their own intrinsic rhythm without external stimulation. Cardiomyocytes attach to one another with specialized cell junctions called intercalated discs. Intercalated discs have both anchoring junctions and gap junctions. Attached cells form long, branching cardiac muscle fibers that act as a syncytium, allowing the cells to synchronize their actions. The cardiac muscle pumps blood through the body and is under involuntary control.

Smooth muscle tissue contraction is responsible for involuntary movements in the internal organs. It forms the contractile component of the digestive, urinary, and reproductive systems as well as the airways and blood vessels. Each cell is spindle shaped with a single nucleus and no visible striations ( Figure 4.4.1 – Muscle Tissue).

External Website

Watch this video to learn more about muscle tissue. In looking through a microscope how could you distinguish skeletal muscle tissue from smooth muscle?

Chapter Review

The three types of muscle cells are skeletal, cardiac, and smooth. Their morphologies match their specific functions in the body. Skeletal muscle is voluntary and responds to conscious stimuli. The cells are striated and multinucleated appearing as long, unbranched cylinders. Cardiac muscle is involuntary and found only in the heart. Each cell is striated with a single nucleus and they attach to one another to form long fibers. Cells are attached to one another at intercalated disks. The cells are interconnected physically and electrochemically to act as a syncytium. Cardiac muscle cells contract autonomously and involuntarily. Smooth muscle is involuntary. Each cell is a spindle-shaped fiber and contains a single nucleus. No striations are evident because the actin and myosin filaments do not align in the cytoplasm.

Interactive Link Questions

Skeletal muscle cells are striated.

Review Questions

Critical thinking questions.

You are watching cells in a dish spontaneously contract. They are all contracting at different rates, some fast, some slow. After a while, several cells link up and they begin contracting in synchrony. Discuss what is going on and what type of cells you are looking at.

The cells in the dish are cardiomyocytes, cardiac muscle cells. They have an intrinsic ability to contract. When they link up, they form intercalating discs that allow the cells to communicate with each other and begin contracting in synchrony.

Why does skeletal muscle look striated?

Under the light microscope, cells appear striated due to the arrangement of the contractile proteins actin and myosin.

This work, Anatomy & Physiology, is adapted from Anatomy & Physiology by OpenStax , licensed under CC BY . This edition, with revised content and artwork, is licensed under CC BY-SA except where otherwise noted.

Images, from Anatomy & Physiology by OpenStax , are licensed under CC BY except where otherwise noted.

Access the original for free at https://openstax.org/books/anatomy-and-physiology/pages/1-introduction .

Anatomy & Physiology Copyright © 2019 by Lindsay M. Biga, Staci Bronson, Sierra Dawson, Amy Harwell, Robin Hopkins, Joel Kaufmann, Mike LeMaster, Philip Matern, Katie Morrison-Graham, Kristen Oja, Devon Quick, Jon Runyeon, OSU OERU, and OpenStax is licensed under a Creative Commons Attribution-ShareAlike 4.0 International License , except where otherwise noted.

19.1 Heart Anatomy

Learning objectives.

By the end of this section, you will be able to:

• Describe the location and position of the heart within the body cavity
• Describe the internal and external anatomy of the heart
• Identify the tissue layers of the heart
• Relate the structure of the heart to its function as a pump
• Compare systemic circulation to pulmonary circulation
• Identify the veins and arteries of the coronary circulation system
• Trace the pathway of oxygenated and deoxygenated blood thorough the chambers of the heart

The vital importance of the heart is obvious. If one assumes an average rate of contraction of 75 contractions per minute, a human heart would contract approximately 108,000 times in one day, more than 39 million times in one year, and nearly 3 billion times during a 75-year lifespan. Each of the major pumping chambers of the heart ejects approximately 70 mL blood per contraction in a resting adult. This would be equal to 5.25 liters of fluid per minute and approximately 14,000 liters per day. Over one year, that would equal 10,000,000 liters or 2.6 million gallons of blood sent through roughly 60,000 miles of vessels. In order to understand how that happens, it is necessary to understand the anatomy and physiology of the heart.

Location of the Heart

The human heart is located within the thoracic cavity, medially between the lungs in the space known as the mediastinum. Figure 19.2 shows the position of the heart within the thoracic cavity. Within the mediastinum, the heart is separated from the other mediastinal structures by a tough membrane known as the pericardium, or pericardial sac, and sits in its own space called the pericardial cavity . The dorsal surface of the heart lies near the bodies of the vertebrae, and its anterior surface sits deep to the sternum and costal cartilages. The great veins, the superior and inferior venae cavae, and the great arteries, the aorta and pulmonary trunk, are attached to the superior surface of the heart, called the base. The base of the heart is located at the level of the third costal cartilage, as seen in Figure 19.2 . The inferior tip of the heart, the apex, lies just to the left of the sternum between the junction of the fourth and fifth ribs near their articulation with the costal cartilages. The right side of the heart is deflected anteriorly, and the left side is deflected posteriorly. It is important to remember the position and orientation of the heart when placing a stethoscope on the chest of a patient and listening for heart sounds, and also when looking at images taken from a midsagittal perspective. The slight deviation of the apex to the left is reflected in a depression in the medial surface of the superior lobe of the left lung, called the cardiac notch .

Everyday Connection

The position of the heart in the torso between the vertebrae and sternum (see Figure 19.2 for the position of the heart within the thorax) allows for individuals to apply an emergency technique known as cardiopulmonary resuscitation (CPR) if the heart of a patient should stop. By applying pressure with the flat portion of one hand on the sternum in the area between the line at T4 and T9 ( Figure 19.3 ), it is possible to manually compress the blood within the heart enough to push some of the blood within it into the pulmonary and systemic circuits. This is particularly critical for the brain, as irreversible damage and death of neurons occur within minutes of loss of blood flow. Current standards call for compression of the chest at least 5 cm deep and at a rate of 100 compressions per minute, a rate equal to the beat in “Staying Alive,” recorded in 1977 by the Bee Gees. If you are unfamiliar with this song, a version is available on www.youtube.com. At this stage, the emphasis is on performing high-quality chest compressions, rather than providing artificial respiration. CPR is generally performed until the patient regains spontaneous contraction or is declared dead by an experienced healthcare professional.

When performed by untrained or overzealous individuals, CPR can result in broken ribs or a broken sternum, and can inflict additional severe damage on the patient. It is also possible, if the hands are placed too low on the sternum, to manually drive the xiphoid process into the liver, a consequence that may prove fatal for the patient. Proper training is essential. This proven life-sustaining technique is so valuable that virtually all medical personnel as well as concerned members of the public should be certified and routinely recertified in its application. CPR courses are offered at a variety of locations, including colleges, hospitals, the American Red Cross, and some commercial companies. They normally include practice of the compression technique on a mannequin.

Interactive Link

Visit the American Heart Association website to help locate a course near your home in the United States. There are also many other national and regional heart associations that offer the same service, depending upon the location.

Shape and Size of the Heart

The shape of the heart is similar to a pinecone, rather broad at the superior surface and tapering to the apex (see Figure 19.2 ). A typical heart is approximately the size of your fist: 12 cm (5 in) in length, 8 cm (3.5 in) wide, and 6 cm (2.5 in) in thickness. Given the size difference between most members of the sexes, the weight of a female heart is approximately 250–300 grams (9 to 11 ounces), and the weight of a male heart is approximately 300–350 grams (11 to 12 ounces). The heart of a well-trained athlete, especially one specializing in aerobic sports, can be considerably larger than this. Cardiac muscle responds to exercise in a manner similar to that of skeletal muscle. That is, exercise results in the addition of protein myofilaments that increase the size of the individual cells without increasing their numbers, a concept called hypertrophy. Hearts of athletes can pump blood more effectively at lower rates than those of nonathletes. Enlarged hearts are not always a result of exercise; they can result from pathologies, such as hypertrophic cardiomyopathy . The cause of an abnormally enlarged heart muscle is unknown, but the condition is often undiagnosed and can cause sudden death in apparently otherwise healthy young people.

Chambers and Circulation through the Heart

The human heart consists of four chambers: The left side and the right side each have one atrium and one ventricle . Each of the upper chambers, the right atrium (plural = atria) and the left atrium, acts as a receiving chamber and contracts to push blood into the lower chambers, the right ventricle and the left ventricle. The ventricles serve as the primary pumping chambers of the heart, propelling blood to the lungs or to the rest of the body.

There are two distinct but linked circuits in the human circulation called the pulmonary and systemic circuits. Although both circuits transport blood and everything it carries, we can initially view the circuits from the point of view of gases. The pulmonary circuit transports blood to and from the lungs, where it picks up oxygen and delivers carbon dioxide for exhalation. The systemic circuit transports oxygenated blood to virtually all of the tissues of the body and returns relatively deoxygenated blood and carbon dioxide to the heart to be sent back to the pulmonary circulation.

The right ventricle pumps deoxygenated blood into the pulmonary trunk , which leads toward the lungs and bifurcates into the left and right pulmonary arteries . These vessels in turn branch many times before reaching the pulmonary capillaries , where gas exchange occurs: Carbon dioxide exits the blood and oxygen enters. The pulmonary trunk arteries and their branches are the only arteries in the post-natal body that carry relatively deoxygenated blood. Highly oxygenated blood returning from the pulmonary capillaries in the lungs passes through a series of vessels that join together to form the pulmonary veins —the only post-natal veins in the body that carry highly oxygenated blood. The pulmonary veins conduct blood into the left atrium, which pumps the blood into the left ventricle, which in turn pumps oxygenated blood into the aorta and on to the many branches of the systemic circuit. Eventually, these vessels will lead to the systemic capillaries, where exchange with the tissue fluid and cells of the body occurs. In this case, oxygen and nutrients exit the systemic capillaries to be used by the cells in their metabolic processes, and carbon dioxide and waste products will enter the blood.

The blood exiting the systemic capillaries is lower in oxygen concentration than when it entered. The capillaries will ultimately unite to form venules, joining to form ever-larger veins, eventually flowing into the two major systemic veins, the superior vena cava and the inferior vena cava , which return blood to the right atrium. The blood in the superior and inferior venae cavae flows into the right atrium, which pumps blood into the right ventricle. This process of blood circulation continues as long as the individual remains alive. Understanding the flow of blood through the pulmonary and systemic circuits is critical to all health professions ( Figure 19.4 ).

Membranes, Surface Features, and Layers

Our exploration of more in-depth heart structures begins by examining the membrane that surrounds the heart, the prominent surface features of the heart, and the layers that form the wall of the heart. Each of these components plays its own unique role in terms of function.

The membrane that directly surrounds the heart and defines the pericardial cavity is called the pericardium or pericardial sac . It also surrounds the “roots” of the major vessels, or the areas of closest proximity to the heart. The pericardium, which literally translates as “around the heart,” consists of two distinct sublayers: the sturdy outer fibrous pericardium and the inner serous pericardium. The fibrous pericardium is made of tough, dense connective tissue that protects the heart and maintains its position in the thorax. The more delicate serous pericardium consists of two layers: the parietal pericardium, which is fused to the fibrous pericardium, and an inner visceral pericardium, or epicardium , which is fused to the heart and is part of the heart wall. The pericardial cavity, filled with lubricating serous fluid, lies between the epicardium and the pericardium.

In most organs within the body, visceral serous membranes such as the epicardium are microscopic. However, in the case of the heart, it is not a microscopic layer but rather a macroscopic layer, consisting of a simple squamous epithelium called a mesothelium , reinforced with loose, irregular, or areolar connective tissue that attaches to the pericardium. This mesothelium secretes the lubricating serous fluid that fills the pericardial cavity and reduces friction as the heart contracts. Figure 19.5 illustrates the pericardial membrane and the layers of the heart.

Disorders of the...

Heart: cardiac tamponade.

If excess fluid builds within the pericardial space, it can lead to a condition called cardiac tamponade, or pericardial tamponade. With each contraction of the heart, more fluid—in most instances, blood—accumulates within the pericardial cavity. In order to fill with blood for the next contraction, the heart must relax. However, the excess fluid in the pericardial cavity puts pressure on the heart and prevents full relaxation, so the chambers within the heart contain slightly less blood as they begin each heart cycle. Over time, less and less blood is ejected from the heart. If the fluid builds up slowly, as in hypothyroidism, the pericardial cavity may be able to expand gradually to accommodate this extra volume. Some cases of fluid in excess of one liter within the pericardial cavity have been reported. Rapid accumulation of as little as 100 mL of fluid following trauma may trigger cardiac tamponade. Other common causes include myocardial rupture, pericarditis, cancer, or even cardiac surgery. Removal of this excess fluid requires insertion of drainage tubes into the pericardial cavity. Premature removal of these drainage tubes, for example, following cardiac surgery, or clot formation within these tubes are causes of this condition. Untreated, cardiac tamponade can lead to death.

Surface Features of the Heart

Inside the pericardium, the surface features of the heart are visible, including the four chambers. There is a superficial leaf-like extension of the atria near the superior surface of the heart, one on each side, called an auricle —a name that means “ear like”—because its shape resembles the external ear of a human ( Figure 19.6 ). Auricles are relatively thin-walled structures that can fill with blood and empty into the atria or upper chambers of the heart. You may also hear them referred to as atrial appendages. Also prominent is a series of fat-filled grooves, each of which is known as a sulcus (plural = sulci), along the superior surfaces of the heart. Major coronary blood vessels are located in these sulci. The deep coronary sulcus is located between the atria and ventricles. Located between the left and right ventricles are two additional sulci that are not as deep as the coronary sulcus. The anterior interventricular sulcus is visible on the anterior surface of the heart, whereas the posterior interventricular sulcus is visible on the posterior surface of the heart. Figure 19.6 illustrates anterior and posterior views of the surface of the heart.

The wall of the heart is composed of three layers of unequal thickness. From superficial to deep, these are the epicardium, the myocardium, and the endocardium (see Figure 19.5 ). The outermost layer of the wall of the heart is also the innermost layer of the pericardium, the epicardium, or the visceral pericardium discussed earlier.

The middle and thickest layer is the myocardium , made largely of cardiac muscle cells. It is built upon a framework of collagenous fibers, plus the blood vessels that supply the myocardium and the nerve fibers that help regulate the heart. It is the contraction of the myocardium that pumps blood through the heart and into the major arteries. The muscle pattern is elegant and complex, as the muscle cells swirl and spiral around the chambers of the heart. They form a figure 8 pattern around the atria and around the bases of the great vessels. Deeper ventricular muscles also form a figure 8 around the two ventricles and proceed toward the apex. More superficial layers of ventricular muscle wrap around both ventricles. This complex swirling pattern allows the heart to pump blood more effectively than a simple linear pattern would. Figure 19.7 illustrates the arrangement of muscle cells.

Although the ventricles on the right and left sides pump the same amount of blood per contraction, the muscle of the left ventricle is much thicker and better developed than that of the right ventricle. In order to overcome the high resistance required to pump blood into the long systemic circuit, the left ventricle must generate a great amount of pressure. The right ventricle does not need to generate as much pressure, since the pulmonary circuit is shorter and provides less resistance. Figure 19.8 illustrates the differences in muscular thickness needed for each of the ventricles.

The innermost layer of the heart wall, the endocardium , is joined to the myocardium with a thin layer of connective tissue. The endocardium lines the chambers where the blood circulates and covers the heart valves. It is made of simple squamous epithelium called endothelium , which is continuous with the endothelial lining of the blood vessels (see Figure 19.5 ).

Once regarded as a simple lining layer, recent evidence indicates that the endothelium of the endocardium and the coronary capillaries may play active roles in regulating the contraction of the muscle within the myocardium. The endothelium may also regulate the growth patterns of the cardiac muscle cells throughout life, and the endothelins it secretes create an environment in the surrounding tissue fluids that regulates ionic concentrations and states of contractility. Endothelins are potent vasoconstrictors and, in a normal individual, establish a homeostatic balance with other vasoconstrictors and vasodilators.

Internal Structure of the Heart

Recall that the heart’s contraction cycle follows a dual pattern of circulation—the pulmonary and systemic circuits—because of the pairs of chambers that pump blood into the circulation. In order to develop a more precise understanding of cardiac function, it is first necessary to explore the internal anatomical structures in more detail.

Septa of the Heart

The word septum is derived from the Latin for “something that encloses;” in this case, a septum (plural = septa) refers to a wall or partition that divides the heart into chambers. The septa are physical extensions of the myocardium lined with endocardium. Located between the two atria is the interatrial septum . Normally in an adult heart, the interatrial septum bears an oval-shaped depression known as the fossa ovalis , a remnant of an opening in the fetal heart known as the foramen ovale . The foramen ovale allowed blood in the fetal heart to pass directly from the right atrium to the left atrium, allowing some blood to bypass the pulmonary circuit. Within seconds after birth, a flap of tissue known as the septum primum that previously acted as a valve closes the foramen ovale and establishes the typical cardiac circulation pattern.

Between the two ventricles is a second septum known as the interventricular septum . Unlike the interatrial septum, the interventricular septum is normally intact after its formation during fetal development. It is substantially thicker than the interatrial septum, since the ventricles generate far greater pressure when they contract.

The septum between the atria and ventricles is known as the atrioventricular septum . It is marked by the presence of four openings that allow blood to move from the atria into the ventricles and from the ventricles into the pulmonary trunk and aorta. Located in each of these openings between the atria and ventricles is a valve , a specialized structure that ensures one-way flow of blood. The valves between the atria and ventricles are known generically as atrioventricular valves . The valves at the openings that lead to the pulmonary trunk and aorta are known generically as semilunar valves . The interventricular septum is visible in Figure 19.9 . In this figure, the atrioventricular septum has been removed to better show the bicuspid and tricuspid valves; the interatrial septum is not visible, since its location is covered by the aorta and pulmonary trunk. Since these openings and valves structurally weaken the atrioventricular septum, the remaining tissue is heavily reinforced with dense connective tissue called the cardiac skeleton , or skeleton of the heart. It includes four rings that surround the openings between the atria and ventricles, and the openings to the pulmonary trunk and aorta, and serve as the point of attachment for the heart valves. The cardiac skeleton also provides an important boundary in the heart electrical conduction system.

Heart: Heart Defects

One very common form of interatrial septum pathology is patent foramen ovale, which occurs when the septum primum does not close at birth, and the fossa ovalis is unable to fuse. The word patent is from the Latin root patens for “open.” It may be benign or asymptomatic, perhaps never being diagnosed, or in extreme cases, it may require surgical repair to close the opening permanently. As much as 20–25 percent of the general population may have a patent foramen ovale, but fortunately, most have the benign, asymptomatic version. Patent foramen ovale is normally detected by auscultation of a heart murmur (an abnormal heart sound) and confirmed by imaging with an echocardiogram. Despite its prevalence in the general population, the causes of patent ovale are unknown, and there are no known risk factors. In nonlife-threatening cases, it is better to monitor the condition than to risk heart surgery to repair and seal the opening.

Coarctation of the aorta is a congenital abnormal narrowing of the aorta that is normally located at the insertion of the ligamentum arteriosum, the remnant of the fetal shunt called the ductus arteriosus. If severe, this condition drastically restricts blood flow through the primary systemic artery, which is life threatening. In some individuals, the condition may be fairly benign and not detected until later in life. Detectable symptoms in an infant include difficulty breathing, poor appetite, trouble feeding, or failure to thrive. In older individuals, symptoms include dizziness, fainting, shortness of breath, chest pain, fatigue, headache, and nosebleeds. Treatment involves surgery to resect (remove) the affected region or angioplasty to open the abnormally narrow passageway. Studies have shown that the earlier the surgery is performed, the better the chance of survival.

A patent ductus arteriosus is a congenital condition in which the ductus arteriosus fails to close. The condition may range from severe to benign. Failure of the ductus arteriosus to close results in blood flowing from the higher pressure aorta into the lower pressure pulmonary trunk. This additional fluid moving toward the lungs increases pulmonary pressure and makes respiration difficult. Symptoms include shortness of breath (dyspnea), tachycardia, enlarged heart, a widened pulse pressure, and poor weight gain in infants. Treatments include surgical closure (ligation), manual closure using platinum coils or specialized mesh inserted via the femoral artery or vein, or nonsteroidal anti-inflammatory drugs to block the synthesis of prostaglandin E2, which maintains the vessel in an open position. If untreated, the condition can result in congestive heart failure.

Septal defects are not uncommon in individuals and may be congenital or caused by various disease processes. Tetralogy of Fallot is a congenital condition that may also occur from exposure to unknown environmental factors; it occurs when there is an opening in the interventricular septum caused by blockage of the pulmonary trunk, normally at the pulmonary semilunar valve. This allows blood that is relatively low in oxygen from the right ventricle to flow into the left ventricle and mix with the blood that is relatively high in oxygen. Symptoms include a distinct heart murmur, low blood oxygen percent saturation, dyspnea or difficulty in breathing, polycythemia, broadening (clubbing) of the fingers and toes, and in children, difficulty in feeding or failure to grow and develop. It is the most common cause of cyanosis following birth. The term “tetralogy” is derived from the four components of the condition, although only three may be present in an individual patient: pulmonary infundibular stenosis (rigidity of the pulmonary valve), overriding aorta (the aorta is shifted above both ventricles), ventricular septal defect (opening), and right ventricular hypertrophy (enlargement of the right ventricle). Other heart defects may also accompany this condition, which is typically confirmed by echocardiography imaging. Tetralogy of Fallot occurs in approximately 400 out of one million live births. Normal treatment involves extensive surgical repair, including the use of stents to redirect blood flow and replacement of valves and patches to repair the septal defect, but the condition has a relatively high mortality. Survival rates are currently 75 percent during the first year of life; 60 percent by 4 years of age; 30 percent by 10 years; and 5 percent by 40 years.

In the case of severe septal defects, including both tetralogy of Fallot and patent foramen ovale, failure of the heart to develop properly can lead to a condition commonly known as a “blue baby.” Regardless of normal skin pigmentation, individuals with this condition have an insufficient supply of oxygenated blood, which leads to cyanosis, a blue or purple coloration of the skin, especially when active.

Septal defects are commonly first detected through auscultation, listening to the chest using a stethoscope. In this case, instead of hearing normal heart sounds attributed to the flow of blood and closing of heart valves, unusual heart sounds may be detected. This is often followed by medical imaging to confirm or rule out a diagnosis. In many cases, treatment may not be needed. Some common congenital heart defects are illustrated in Figure 19.10 .

Right Atrium

The right atrium serves as the receiving chamber for blood returning to the heart from the systemic circulation. The two major systemic veins, the superior and inferior venae cavae, and the large coronary vein called the coronary sinus that drains the heart myocardium empty into the right atrium. The superior vena cava drains blood from regions superior to the diaphragm: the head, neck, upper limbs, and the thoracic region. It empties into the superior and posterior portions of the right atrium. The inferior vena cava drains blood from areas inferior to the diaphragm: the lower limbs and abdominopelvic region of the body. It, too, empties into the posterior portion of the atria, but inferior to the opening of the superior vena cava. Immediately superior and slightly medial to the opening of the inferior vena cava on the posterior surface of the atrium is the opening of the coronary sinus. This thin-walled vessel drains most of the coronary veins that return systemic blood from the heart. The majority of the internal heart structures discussed in this and subsequent sections are illustrated in Figure 19.9 .

While the bulk of the internal surface of the right atrium is smooth, the depression of the fossa ovalis is medial, and the anterior surface demonstrates prominent ridges of muscle called the pectinate muscles . The right auricle also has pectinate muscles. The left atrium does not have pectinate muscles except in the auricle.

The atria receive venous blood on a nearly continuous basis, preventing venous flow from stopping while the ventricles are contracting. While most ventricular filling occurs while the atria are relaxed, they do demonstrate a contractile phase and actively pump blood into the ventricles just prior to ventricular contraction. The opening between the atrium and ventricle is guarded by the tricuspid valve.

Right Ventricle

The right ventricle receives blood from the right atrium through the tricuspid valve. Each flap of the valve is attached to strong strands of connective tissue, the chordae tendineae , literally “tendinous cords,” or sometimes more poetically referred to as “heart strings.” There are several chordae tendineae associated with each of the flaps. They are composed of approximately 80 percent collagenous fibers with the remainder consisting of elastic fibers and endothelium. They connect each of the flaps to a papillary muscle that extends from the inferior ventricular surface. There are three papillary muscles in the right ventricle, called the anterior, posterior, and septal muscles, which correspond to the three sections of the valves.

When the myocardium of the ventricle contracts, pressure within the ventricular chamber rises. Blood, like any fluid, flows from higher pressure to lower pressure areas, in this case, toward the pulmonary trunk and the atrium. To prevent any potential backflow, the papillary muscles also contract, generating tension on the chordae tendineae. This prevents the flaps of the valves from being forced into the atria and regurgitation of the blood back into the atria during ventricular contraction. Figure 19.11 shows papillary muscles and chordae tendineae attached to the tricuspid valve.

The walls of the ventricle are lined with trabeculae carneae , ridges of cardiac muscle covered by endocardium. In addition to these muscular ridges, a band of cardiac muscle, also covered by endocardium, known as the moderator band (see Figure 19.9 ) reinforces the thin walls of the right ventricle and plays a crucial role in cardiac conduction. It arises from the inferior portion of the interventricular septum and crosses the interior space of the right ventricle to connect with the inferior papillary muscle.

When the right ventricle contracts, it ejects blood into the pulmonary trunk, which branches into the left and right pulmonary arteries that carry it to each lung. The superior surface of the right ventricle begins to taper as it approaches the pulmonary trunk. At the base of the pulmonary trunk is the pulmonary semilunar valve that prevents backflow from the pulmonary trunk.

Left Atrium

After exchange of gases in the pulmonary capillaries, blood returns to the left atrium high in oxygen via one of the four pulmonary veins. While the left atrium does not contain pectinate muscles, it does have an auricle that includes these pectinate ridges. Blood flows nearly continuously from the pulmonary veins back into the atrium, which acts as the receiving chamber, and from here through an opening into the left ventricle. Most blood flows passively into the heart while both the atria and ventricles are relaxed, but toward the end of the ventricular relaxation period, the left atrium will contract, pumping blood into the ventricle. This atrial contraction accounts for approximately 20 percent of ventricular filling. The opening between the left atrium and ventricle is guarded by the mitral valve.

Left Ventricle

Recall that, although both sides of the heart will pump the same amount of blood, the muscular layer is much thicker in the left ventricle compared to the right (see Figure 19.8 ). Like the right ventricle, the left also has trabeculae carneae, but there is no moderator band. The mitral valve is connected to papillary muscles via chordae tendineae. There are two papillary muscles on the left—the anterior and posterior—as opposed to three on the right.

The left ventricle is the major pumping chamber for the systemic circuit; it ejects blood into the aorta through the aortic semilunar valve.

Heart Valve Structure and Function

A transverse section through the heart slightly above the level of the atrioventricular septum reveals all four heart valves along the same plane ( Figure 19.12 ). The valves ensure unidirectional blood flow through the heart. Between the right atrium and the right ventricle is the right atrioventricular valve , or tricuspid valve . It typically consists of three flaps, or leaflets, made of endocardium reinforced with additional connective tissue. The flaps are connected by chordae tendineae to the papillary muscles, which control the opening and closing of the valves.

Emerging from the right ventricle at the base of the pulmonary trunk is the pulmonary semilunar valve, or the pulmonary valve ; it is also known as the pulmonic valve or the right semilunar valve. The pulmonary valve is comprised of three small flaps of endothelium reinforced with connective tissue. When the ventricle relaxes, the pressure differential causes blood to flow back into the ventricle from the pulmonary trunk. This flow of blood fills the pocket-like flaps of the pulmonary valve, causing the valve to close and producing an audible sound. Unlike the atrioventricular valves, there are no papillary muscles or chordae tendineae associated with the pulmonary valve.

Located at the opening between the left atrium and left ventricle is the mitral valve , also called the bicuspid valve or the left atrioventricular valve . Structurally, this valve consists of two cusps, compared to the three cusps of the tricuspid valve. In a clinical setting, the valve is referred to as the mitral valve, rather than the bicuspid valve. The two cusps of the mitral valve are attached by chordae tendineae to two papillary muscles that project from the wall of the ventricle.

At the base of the aorta is the aortic semilunar valve, or the aortic valve , which prevents backflow from the aorta. It normally is composed of three flaps. When the ventricle relaxes and blood attempts to flow back into the ventricle from the aorta, blood will fill the cusps of the valve, causing it to close and producing an audible sound.

In Figure 19.13 a , the two atrioventricular valves are open and the two semilunar valves are closed. This occurs when both atria and ventricles are relaxed and when the atria contract to pump blood into the ventricles. Figure 19.13 b shows a frontal view. Although only the left side of the heart is illustrated, the process is virtually identical on the right.

Figure 19.14 a shows the atrioventricular valves closed while the two semilunar valves are open. This occurs when the ventricles contract to eject blood into the pulmonary trunk and aorta. Closure of the two atrioventricular valves prevents blood from being forced back into the atria. This stage can be seen from a frontal view in Figure 19.14 b .

When the ventricles begin to contract, pressure within the ventricles rises and blood flows toward the area of lowest pressure, which is initially in the atria. This backflow causes the cusps of the tricuspid and mitral (bicuspid) valves to close. These valves are tied down to the papillary muscles by chordae tendineae. During the relaxation phase of the cardiac cycle, the papillary muscles are also relaxed and the tension on the chordae tendineae is slight (see Figure 19.13 b ). However, as the myocardium of the ventricle contracts, so do the papillary muscles. This creates tension on the chordae tendineae (see Figure 19.14 b ), helping to hold the cusps of the atrioventricular valves in place and preventing them from being blown back into the atria.

The aortic and pulmonary semilunar valves lack the chordae tendineae and papillary muscles associated with the atrioventricular valves. Instead, they consist of pocket-like folds of endocardium reinforced with additional connective tissue. When the ventricles relax and the change in pressure forces the blood toward the ventricles, the blood presses against these cusps and seals the openings.

Visit this site to observe an echocardiogram of actual heart valves opening and closing. Although much of the heart has been “removed” from this gif loop so the chordae tendineae are not visible, why is their presence more critical for the atrioventricular valves (tricuspid and mitral) than the semilunar (aortic and pulmonary) valves?

Heart Valves

When heart valves do not function properly, they are often described as incompetent and result in valvular heart disease, which can range from benign to lethal. Some of these conditions are congenital, that is, the individual was born with the defect, whereas others may be attributed to disease processes or trauma. Some malfunctions are treated with medications, others require surgery, and still others may be mild enough that the condition is merely monitored since treatment might trigger more serious consequences.

Valvular disorders are often caused by carditis, or inflammation of the heart. One common trigger for this inflammation is rheumatic fever, or scarlet fever, an autoimmune response to the presence of a bacterium, Streptococcus pyogenes , normally a disease of childhood.

While any of the heart valves may be involved in valve disorders, mitral regurgitation is the most common, detected in approximately 2 percent of the population, and the pulmonary semilunar valve is the least frequently involved. When a valve malfunctions, the flow of blood to a region will often be disrupted. The resulting inadequate flow of blood to this region will be described in general terms as an insufficiency. The specific type of insufficiency is named for the valve involved: aortic insufficiency, mitral insufficiency, tricuspid insufficiency, or pulmonary insufficiency.

If one of the cusps of the valve is forced backward by the force of the blood, the condition is referred to as a prolapsed valve. Prolapse may occur if the chordae tendineae are damaged or broken, causing the closure mechanism to fail. The failure of the valve to close properly disrupts the normal one-way flow of blood and results in regurgitation, when the blood flows backward from its normal path. Using a stethoscope, the disruption to the normal flow of blood produces a heart murmur.

Stenosis is a condition in which the heart valves become rigid and may calcify over time. The loss of flexibility of the valve interferes with normal function and may cause the heart to work harder to propel blood through the valve, which eventually weakens the heart. Aortic stenosis affects approximately 2 percent of the population over 65 years of age, and the percentage increases to approximately 4 percent in individuals over 85 years. Occasionally, one or more of the chordae tendineae will tear or the papillary muscle itself may die as a component of a myocardial infarction (heart attack). In this case, the patient’s condition will deteriorate dramatically and rapidly, and immediate surgical intervention may be required.

Auscultation, or listening to a patient’s heart sounds, is one of the most useful diagnostic tools, since it is proven, safe, and inexpensive. The term auscultation is derived from the Latin for “to listen,” and the technique has been used for diagnostic purposes as far back as the ancient Egyptians. Valve and septal disorders will trigger abnormal heart sounds. If a valvular disorder is detected or suspected, a test called an echocardiogram, or simply an “echo,” may be ordered. Echocardiograms are sonograms of the heart and can help in the diagnosis of valve disorders as well as a wide variety of heart pathologies.

Visit this site for audio examples of heart sounds.

Career Connection

Cardiologist.

Cardiologists are medical doctors that specialize in the diagnosis and treatment of diseases of the heart. After completing 4 years of medical school, cardiologists complete a three-year residency in internal medicine followed by an additional three or more years in cardiology. Following this 10-year period of medical training and clinical experience, they qualify for a rigorous two-day examination administered by the Board of Internal Medicine that tests their academic training and clinical abilities, including diagnostics and treatment. After successful completion of this examination, a physician becomes a board-certified cardiologist. Some board-certified cardiologists may be invited to become a Fellow of the American College of Cardiology (FACC). This professional recognition is awarded to outstanding physicians based upon merit, including outstanding credentials, achievements, and community contributions to cardiovascular medicine.

Visit this site to learn more about cardiologists.

Cardiovascular Technologist/Technician

Cardiovascular technologists/technicians are trained professionals who perform a variety of imaging techniques, such as sonograms or echocardiograms, used by physicians to diagnose and treat diseases of the heart. Nearly all of these positions require an associate degree. Growth within the field is fast, projected at 29 percent from 2010 to 2020.

There is a considerable overlap and complementary skills between cardiac technicians and vascular technicians, and so the term cardiovascular technician is often used. Special certifications within the field require documenting appropriate experience and completing additional and often expensive certification examinations. These subspecialties include Certified Rhythm Analysis Technician (CRAT), Certified Cardiographic Technician (CCT), Registered Congenital Cardiac Sonographer (RCCS), Registered Cardiac Electrophysiology Specialist (RCES), Registered Cardiovascular Invasive Specialist (RCIS), Registered Cardiac Sonographer (RCS), Registered Vascular Specialist (RVS), and Registered Phlebology Sonographer (RPhS).

Visit this site for more information on cardiovascular technologists/technicians.

Coronary Circulation

You will recall that the heart is a remarkable pump composed largely of cardiac muscle cells that are incredibly active throughout life. Like all other cells, a cardiomyocyte requires a reliable supply of oxygen and nutrients, and a way to remove wastes, so it needs a dedicated, complex, and extensive coronary circulation. And because of the critical and nearly ceaseless activity of the heart throughout life, this need for a blood supply is even greater than for a typical cell. However, coronary circulation is not continuous; rather, it cycles, reaching a peak when the heart muscle is relaxed and nearly ceasing while it is contracting.

Coronary Arteries

Coronary arteries supply blood to the myocardium and other components of the heart. The first portion of the aorta after it arises from the left ventricle gives rise to the coronary arteries. There are three dilations in the wall of the aorta just superior to the aortic semilunar valve. Two of these, the left posterior aortic sinus and anterior aortic sinus, give rise to the left and right coronary arteries, respectively. The third sinus, the right posterior aortic sinus, typically does not give rise to a vessel. Coronary vessel branches that remain on the surface of the artery and follow the sulci are called epicardial coronary arteries .

The left coronary artery distributes blood to the left side of the heart, the left atrium and ventricle, and the interventricular septum. The circumflex artery arises from the left coronary artery and follows the coronary sulcus to the left. Eventually, it will fuse with the small branches of the right coronary artery. The larger anterior interventricular artery , also known as the left anterior descending artery (LAD), is the second major branch arising from the left coronary artery. It follows the anterior interventricular sulcus around the pulmonary trunk. Along the way it gives rise to numerous smaller branches that interconnect with the branches of the posterior interventricular artery, forming anastomoses. An anastomosis is an area where vessels unite to form interconnections that normally allow blood to circulate to a region even if there may be partial blockage in another branch. The anastomoses in the heart are very small. Therefore, this ability is somewhat restricted in the heart so a coronary artery blockage often results in death of the cells (myocardial infarction) supplied by the particular vessel.

The right coronary artery proceeds along the coronary sulcus and distributes blood to the right atrium, portions of both ventricles, and the heart conduction system. Normally, one or more marginal arteries arise from the right coronary artery inferior to the right atrium. The marginal arteries supply blood to the superficial portions of the right ventricle. On the posterior surface of the heart, the right coronary artery gives rise to the posterior interventricular artery , also known as the posterior descending artery. It runs along the posterior portion of the interventricular sulcus toward the apex of the heart, giving rise to branches that supply the interventricular septum and portions of both ventricles. Figure 19.15 presents views of the coronary circulation from both the anterior and posterior views.

Diseases of the...

Heart: myocardial infarction.

Myocardial infarction (MI) is the formal term for what is commonly referred to as a heart attack. It normally results from a lack of blood flow (ischemia) and oxygen (hypoxia) to a region of the heart, resulting in death of the cardiac muscle cells. An MI often occurs when a coronary artery is blocked by the buildup of atherosclerotic plaque consisting of lipids, cholesterol and fatty acids, and white blood cells, primarily macrophages. It can also occur when a portion of an unstable atherosclerotic plaque travels through the coronary arterial system and lodges in one of the smaller vessels. The resulting blockage restricts the flow of blood and oxygen to the myocardium and causes death of the tissue. MIs may be triggered by excessive exercise, in which the partially occluded artery is no longer able to pump sufficient quantities of blood, or severe stress, which may induce spasm of the smooth muscle in the walls of the vessel.

In the case of acute MI, there is often sudden pain beneath the sternum (retrosternal pain) called angina pectoris, often radiating down the left arm in males but not in female patients. Until this anomaly between the sexes was discovered, many female patients suffering MIs were misdiagnosed and sent home. In addition, patients typically present with difficulty breathing and shortness of breath (dyspnea), irregular heartbeat (palpations), nausea and vomiting, sweating (diaphoresis), anxiety, and fainting (syncope), although not all of these symptoms may be present. Many of the symptoms are shared with other medical conditions, including anxiety attacks and simple indigestion, so differential diagnosis is critical. It is estimated that between 22 and 64 percent of MIs present without any symptoms.

An MI can be confirmed by examining the patient’s ECG, which frequently reveals alterations in the ST and Q components. Some classification schemes of MI are referred to as ST-elevated MI (STEMI) and non-elevated MI (non-STEMI). In addition, echocardiography or cardiac magnetic resonance imaging may be employed. Common blood tests indicating an MI include elevated levels of creatine kinase MB (an enzyme that catalyzes the conversion of creatine to phosphocreatine, consuming ATP) and cardiac troponin (the regulatory protein for muscle contraction), both of which are released by damaged cardiac muscle cells.

Immediate treatments for MI are essential and include administering supplemental oxygen, aspirin that helps to break up clots, and nitroglycerine administered sublingually (under the tongue) to facilitate its absorption. Despite its unquestioned success in treatments and use since the 1880s, the mechanism of nitroglycerine is still incompletely understood but is believed to involve the release of nitric oxide, a known vasodilator, and endothelium-derived releasing factor, which also relaxes the smooth muscle in the tunica media of coronary vessels. Longer-term treatments include injections of thrombolytic agents such as streptokinase that dissolve the clot, the anticoagulant heparin, balloon angioplasty and stents to open blocked vessels, and bypass surgery to allow blood to pass around the site of blockage. If the damage is extensive, coronary replacement with a donor heart or coronary assist device, a sophisticated mechanical device that supplements the pumping activity of the heart, may be employed. Despite the attention, development of artificial hearts to augment the severely limited supply of heart donors has proven less than satisfactory but will likely improve in the future.

MIs may trigger cardiac arrest, but the two are not synonymous. Important risk factors for MI include cardiovascular disease, age, smoking, high blood levels of the low-density lipoprotein (LDL, often referred to as “bad” cholesterol), low levels of high-density lipoprotein (HDL, or “good” cholesterol), hypertension, diabetes mellitus, obesity, lack of physical exercise, chronic kidney disease, excessive alcohol consumption, and use of illegal drugs.

Coronary Veins

Coronary veins drain the heart and generally parallel the large surface arteries (see Figure 19.15 ). The great cardiac vein can be seen initially on the surface of the heart following the interventricular sulcus, but it eventually flows along the coronary sulcus into the coronary sinus on the posterior surface. The great cardiac vein initially parallels the anterior interventricular artery and drains the areas supplied by this vessel. It receives several major branches, including the posterior cardiac vein, the middle cardiac vein, and the small cardiac vein. The posterior cardiac vein parallels and drains the areas supplied by the marginal artery branch of the circumflex artery. The middle cardiac vein parallels and drains the areas supplied by the posterior interventricular artery. The small cardiac vein parallels the right coronary artery and drains the blood from the posterior surfaces of the right atrium and ventricle. The coronary sinus is a large, thin-walled vein on the posterior surface of the heart lying within the atrioventricular sulcus and emptying directly into the right atrium. The anterior cardiac veins parallel the small cardiac arteries and drain the anterior surface of the right ventricle. Unlike these other cardiac veins, it bypasses the coronary sinus and drains directly into the right atrium.

Heart: Coronary Artery Disease

Coronary artery disease is the leading cause of death worldwide. It occurs when the buildup of plaque—a fatty material including cholesterol, connective tissue, white blood cells, and some smooth muscle cells—within the walls of the arteries obstructs the flow of blood and decreases the flexibility or compliance of the vessels. This condition is called atherosclerosis, a hardening of the arteries that involves the accumulation of plaque. As the coronary blood vessels become occluded, the flow of blood to the tissues will be restricted, a condition called ischemia that causes the cells to receive insufficient amounts of oxygen, called hypoxia. Figure 19.16 shows the blockage of coronary arteries highlighted by the injection of dye. Some individuals with coronary artery disease report pain radiating from the chest called angina pectoris, but others remain asymptomatic. If untreated, coronary artery disease can lead to MI or a heart attack.

The disease progresses slowly and often begins in children and can be seen as fatty “streaks” in the vessels. It then gradually progresses throughout life. Well-documented risk factors include smoking, family history, hypertension, obesity, diabetes, high alcohol consumption, lack of exercise, stress, and hyperlipidemia or high circulating levels of lipids in the blood. Treatments may include medication, changes to diet and exercise, angioplasty with a balloon catheter, insertion of a stent, or coronary bypass procedure.

Angioplasty is a procedure in which the occlusion is mechanically widened with a balloon. A specialized catheter with an expandable tip is inserted into a superficial vessel, normally in the leg, and then directed to the site of the occlusion. At this point, the balloon is inflated to compress the plaque material and to open the vessel to increase blood flow. Then, the balloon is deflated and retracted. A stent consisting of a specialized mesh is typically inserted at the site of occlusion to reinforce the weakened and damaged walls. Stent insertions have been routine in cardiology for more than 40 years.

Coronary bypass surgery may also be performed. This surgical procedure grafts a replacement vessel obtained from another, less vital portion of the body to bypass the occluded area. This procedure is clearly effective in treating patients experiencing a MI, but overall does not increase longevity. Nor does it seem advisable in patients with stable although diminished cardiac capacity since frequently loss of mental acuity occurs following the procedure. Long-term changes to behavior, emphasizing diet and exercise plus a medicine regime tailored to lower blood pressure, lower cholesterol and lipids, and reduce clotting are equally as effective.

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Conduction system of the heart

Author: Lorenzo Crumbie, MBBS, BSc • Reviewer: Adrian Rad, BSc (Hons) Last reviewed: August 17, 2023 Reading time: 27 minutes

The cardiac conduction system is a network of specialized cardiac muscle cells that initiate and transmit the electrical impulses responsible for the coordinated contractions of each cardiac cycle . These special cells are able to generate an action potential on their own (self-excitation) and pass it on to other nearby cells (conduction), including cardiomyocytes .

The parts of the heart conduction system can be divided into those that generate action potentials (nodal tissue) and those that conduct them (conducting fibers). Although all parts have the ability to generate action potentials and thus heart contractions, the sinuatrial (SA) node is the primary impulse initiator and regulator in a healthy heart . This aspect makes the SA node the physiological pacemaker of the heart. Other parts sequentially receive and conduct the impulse originating from the SA node and then pass it to myocardial cells. Upon stimulation by the action potential, myocardial cells contract synchronously, resulting in a heartbeat. The propagation of electrical impulses and synchronous contraction of cardiomyocytes is facilitated by the presence of intercalated discs and gap junctions .

This article will discuss the anatomy of the cardiac conduction system and its different parts. Disorders of the conduction pathway and how they manifest clinically will also be discussed.

Internodal conduction pathway

Interatrial conduction pathway, bundle of his, right and left bundle branches, purkinje fibers, sinuatrial node, atrioventricular node, impulse generation and conduction, autonomic regulation, sick sinus syndrome, wolf-parkinson-white syndrome.

The sinuatrial node (SA node) is a flat, elliptical collection of specialized nodal tissue with dimensions of up to 25 millimeters (mm) in length. The node is nestled in the superior posterolateral wall of the right atrium near the opening of the superior vena cava which is indicated by the sulcus terminalis (the junction of the venous sinus and the right atrium proper). Here it lies in the subepicardiac layer of the heart, often covered by a relatively thin fat pad . 

Centrally, the SA node is populated with pale-staining cells known as cardiac pacemaker (P) cells . They are circumferentially arranged around the arterial supply of the node (the SA nodal branch of the coronary artery). Histologically, P cells contain a relatively large, central nucleus but a scant amount of other organelles (likely the cause of the pale staining ). Unlike the surrounding cardiomyocytes, P cells have very few cytoplasmic myofibrils and no sarcotubular apparatus. The population of P cells begins to decrease towards the periphery of the SA node, where other transition cells become more apparent. These slender, fusiform cells resemble a crossover between the aforementioned P cells and typical cardiomyocytes. These transition cells form bridges between P cells and surrounding atrial cells. 

The SA node receives its blood supply from the sinuatrial nodal branch of the coronary artery . In about 60% of individuals, this artery is a branch of the right coronary artery (therefore arising from the left coronary artery in the other 40%). There are numerous autonomic ganglion cells bordering the SA node anteriorly and posteriorly. However, none of these ganglia appear to terminate on the cardiac pacemaker cells. Instead, the P cells contain both cholinergic and adrenergic receptors to respond to the neurotransmitters released by the surrounding autonomic ganglion cells.

The internodal conduction pathways are a part of the intra-atrial conduction network initially described by Thomas N. James in 1963. Not only do these pathways travel within the right atrium, but they also form direct points of communication between the sinuatrial and atrioventricular nodes. The internodal conduction pathway is divided into anterior , middle and posterior branches .

The anterior internodal pathway originates from the anterior margin of the SA node. It continues anteriorly, coursing around the superior vena cava where it gives off Bachmann’s bundle . The anterior internodal band continues anteroinferiorly toward the atrioventricular (AV) node where it enters the node by way of its superior margin. 

The middle internodal pathway arises from the posterosuperior margin of the SA node. It continues behind the superior vena cava toward the border of the interatrial septum . The pathway turns caudally in the interatrial septum to enter the AV node through its superior margin.

Finally, the posterior internodal pathway emerges from the posterior margin of the sinus node. It takes a posterior course around the superior vena cava and continues across the crista terminalis toward the Eustachian ridge (valve of the inferior vena cava). The pathway then enters the interatrial septum (above the point of the coronary sinus ) where it enters the AV node through its posterior surface. 

These conduction pathways transmit the action potential slightly faster than the surrounding cardiomyocytes. They contain the Purkinje-like (myofibril-poor) cells, which ensures that the action potential arrives at the AV node at an appropriate time. The blood supply of these pathways is similar to the blood supply of the right atrium – the circumflex branch of the left coronary artery .

The interatrial conduction pathway, also called Bachmann’s bundle , refers to a preferential pathway of specialized cardiomyocytes that facilitate the conduction of impulses between the atria . The pathway branches from the anterior internodal pathway at the level of the superior vena cava. The Bachmann’s bundle crosses the interatrial groove (an external landmark of the interatrial septum) and passes over the limbus of the fossa ovalis . A pad of fatty tissue separates the Bachmann’s bundle from the limbus.

The pathway bifurcates into right and left branches that travel toward the right and left atrial auricles, respectively. The right branch can be further divided into superior and inferior arms. The superior arm originates at the external junction of the superior vena cava and the atrium (near the location of the SA node). The inferior arm emerges in the vestibule of the right atrium. The left branch provides some structural support to the anterior atrial wall and continues to wrap around the left atrial auricle. Proximally, the superior part of the left branch passes in front of the openings of the left pulmonary veins . The inferior part continues caudally to the vestibule of the left atrium.

From a histological perspective, the interatrial conduction pathway is a series of parallel strands of myocardium traveling in the subepicardiac layer . The myocytes within Bachmann’s bundle are encased in thin septa made of tightly packed collagen fibrils. This uninterrupted sheath also forms inter-septal connections (the function of which is not yet clear). There are five identified cell types found within the interatrial pathway. These are:

• Myofibril-rich cells – which are the same as regular cardiomyocytes.
• Myofibril-poor cells – resemble Purkinje cells; are numerous in the pathway.
• P cells – like those described in the sinuatrial node.
• Slender transitional cells – short and narrow.
• Broad transitional cells – longer and wider than slender transitional cells.

The presence of these specialized cells facilitates rapid conduction of the action potential across the left atrium, minimizing the delay in depolarization between the atria. Bachmann’s bundle receives its blood supply from the sinuatrial nodal branch of the coronary artery .

Have you gotten into that study groove? Keep pushing while you have the momentum and check out these articles, quizzes and video for added insight into heart anatomy, histology and function.

There is another specialized structure in the heart, similar to the SA node described earlier, which also helps with the conduction of impulses. It is known as the atrioventricular node (AV node) and is often called the secondary pacemaker of the heart. Under normal circumstances, it functions as a conduit of electrical activity from the SA node to the ventricles of the heart. It is the only pathway by which the action potential can cross from the atria to the ventricles; as the atrioventricular septum is made of a cartilaginous structure that is unable to conduct electrical impulses. The AV node is smaller than the SA node and is located in the posteroinferior part of the interatrial septum. Specifically, the node rests in the triangle of the atrioventricular node (triangle of Koch or Koch’s triangle). This triangle is limited by the coronary sinus (basally), the septal leaflet of the tricuspid valve (inferiorly) and the tendon of inferior pyramidal space (tendon of valve of inferior vena cava or tendon of Todaro) (superiorly).

The hemi-oval-shaped node occupies the subendocardiac layer within Koch’s triangle. The base of the node also extends into the atrial muscle. The apex of the node extends anteroinferiorly. It passes through the fibrous cardiac skeleton to form the initial part of the atrioventricular (AV) bundle (of His) . The histological make-up of the AV node is relatively similar to that in the SA node. The chief differences are that there are fewer P cells and more transition cells compared to what is observed in the SA node. 

The AV node receives arterial blood from the atrioventricular nodal branch . This arises from the inferior interventricular branch of the right coronary artery in 80% of individuals. In the remaining 20% of individuals, the atrioventricular nodal branch stems from the circumflex branch of the left coronary artery. There is also a notable amount of autonomic ganglion cells surrounding the AV node (as observed in the SA node). However, none of these actually form synapses with the AV node. Like the SA node cells, the AV node cells also have adrenergic and cholinergic receptors in order to respond to autonomic input.

The atrioventricular (AV) bundle (of His) is the initial segment of the AV node that penetrates through the fibrous trigone into the membranous part of the interventricular septum . On transverse section at the level of the fibrous body, the AV bundle may appear oval, quadrangular or triangular. A unique and important feature of the AV bundle is that it only allows the ‘forward’ movement of action potentials. Therefore, the retrograde transmission of electrical impulses from the ventricles to the atria is not allowed in a normal functioning heart. The AV bundle is supplied by the anterior and inferior interventricular branches of the coronary arteries .

As the node moves from the membranous to the muscular interventricular septum, it bifurcates into right and left bundles.

The crus dextrum, which is Latin for right bundle branch , emerges from the AV bundle in the membranous interventricular septum. It is a round group of narrow fascicles that travels in the myocardium before moving superficially to the subendocardiac layer space. It travels to the right side of the interventricular septum where it gives of branches to the ventricular walls before going on toward the ventricular apex . Here, it enters the septomarginal moderator band (septomarginal band) before reaching the anterior papillary muscles . The terminal arborization of the right branch supplies the papillary muscle and recurs to supply the rest of the ventricular wall. 

The left bundle branch or crus sinistrum (Latin) branches from the atrioventricular bundle at the start of the muscular interventricular septum. It is made up of numerous small fascicles that become flattened sheets. These fascicles occupy the left half of the muscular interventricular septum. The sheet moves to the subendocardiac space as it travels toward the ventricular apex. Here it trifurcates into posterior , septal and anterior divisions . The branches will go on to activate the anterior and posterior papillary muscles, interventricular septum and the walls of the left ventricle. 

The right and left bundles are populated with subendocardiac branches (Purkinje fibers) . These cells can be much larger than those of the surrounding heart muscles and they function quite differently than the preceding cells in the AV node. Subendocardiac branches are found throughout the entire length of both bundles in the subendocardiac layer. They extend toward the cardiac apex, then curve upward and backward through the walls of the ventricles. 

The fibers have far more gap junctions than the AV nodal cells and surrounding myocytes. As a result, they are able to transmit impulses 6 times faster than ventricular muscles and 150 times faster than the AV nodal fibers. The increased number of gap junctions allow more ions to pass from one cell to the next, thus increasing the rate of conduction. Furthermore, there are fewer myofibrils in Purkinje cells, resulting in little to contraction (therefore shorter to absent refractory periods ) within these cells. Consequently, the bundles can achieve almost instantaneous transmission of the action potential to the rest of the ventricle once it passes through the AV node. This compensates for the delay at the AV node and allows the ventricles to contract shortly after the atria. 

Note that the main branches of the atrioventricular bundle are insulated by sheaths of connective tissue. This prevents premature excitation of adjacent cardiac tissue. Therefore, the papillary muscles will depolarize first, followed by the ventricular apex, then walls. The pattern of depolarization also goes from endocardium to epicardium, since the fibers are in the subendocardiac layer.

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Now that you have covered the anatomy of the cardiac conduction system, ask yourself these important questions: how does the SA and AV nodes work? How do the impulses travel through the heart? The simple answer to both questions is an action potential . 

Cardiomyocytes have the special ability to stimulate themselves ( self-excitation or automaticity ). The initiation of the action potential is dependent on ion channels that allow passage of ions into and out of the cells. In the case of cardiomyocytes, they have fast-acting sodium ion (Na+), slow sodium-calcium ion (Na+-Ca2+) and slow/fast potassium ion (K+) channels (among other important channels that maintain ionic equilibrium).

This automaticity is particularly enhanced in P cells . They have a lower resting membrane potential than the surrounding cardiomyocytes and transition cells due to the following factors:

• There is a high concentration of extracellular Na+ outside the nodal fibers.
• A relatively large amount of Na+ channels are already open.
• There is a passive diffusion of Na+ into the P cells between heartbeats due to the ‘leaky’ sodium channels.
• The passive influx of Na+ causes a slow rise in the membrane potential of the cell, bringing it progressively closer to the generation threshold of an action potential.

Therefore, cardiac P cells of the SA node are more readily depolarized than other cardiac cells. The SA node is also intimately connected with the surrounding heart muscles via the internodal and interatrial conduction pathways. Consequently, the generated action potential can be rapidly transmitted to other cells. This enables the SA node to set the pace at which the heart cells will depolarize and subsequently contract, making it the pacemaker of the heart. On average, the SA node can fire between 60 to 100 beats per minute at rest.

Although the main role of the AV node is to facilitate passage of the depolarization wave to the ventricles, it also has additional functions. In the absence of a functioning SA node, the AV node has the ability to take over as the pacemaker of the heart. Recall that it also has P cells that are able to establish an (albeit slower) rhythm ( 40 to 60 beats per minute ). 

The AV node is also responsible for slowing down the passage of the electrical impulse traveling to the ventricles. This important phenomenon allows more time for the ventricles to remain quiescent and fill with blood coming from the contracting atria. But how does the AV node slow down conduction? 

One key feature of the transition cells and P cells in the AV node is that they have fewer gap junctions at the intercalated discs. Consequently, there is more resistance to conduction in this part of the conduction pathway than there is in other areas. 

Now let’s put all that information together and outline the cardiac conduction steps:

• The SA node generates the action potential.
• The action potential passes along the internodal and interatrial conduction pathways , causing atrial systole.
• The impulse arrives at the AV node and is slowed down to facilitate ventricular filling (ventricular diastole).
• The impulse then passes from the AV node to the AV bundle .

It is then rapidly dispersed through the bundle branches and subendocardiac tissue causing ventricular systole.

The entire cardiac conduction system is under the influence of the autonomic pathway. Sympathetic stimulation of the conductive tissue comes from the cardiac plexus , while parasympathetic influence arises from the vagus nerve (CN X) . 

Activation of the sympathetic nervous system results in the release of adrenaline (epinephrine) and other adrenergic neurochemicals. They bind to beta-1 and beta-2 receptors found in both the SA and AV nodes, as well as along the supporting conduction pathways. The overall impact of the sympathetic system is an increase in the depolarization rate of the SA node. Consequently, this elevates the overall heart rate ( increased chronotropy ). Since these adrenergic receptors are also present on cardiomyocytes, the sympathetic drive will act on these cells, increasing the contraction force ( increased inotropy ). Therefore, the overall cardiac output will be increased.

On the other hand, the parasympathetic activation of muscarinic receptors at the SA and AV nodes will have the opposite effect when compared to the sympathetic system. Parasympathetic stimulation slows down SA node activation, thus reducing the heart rate. It also reduces the contractility of the cardiomyocytes, effectively reducing the cardiac output. 

Test what you have learned about about the sympathetic and parasympathetic innervation of the heart in the quiz below! 

Clinical notes 

Any abnormality of the conducting pathway – whether congenital or acquired – can result in a rhythm abnormality or arrhythmia. An arrhythmia simply means that the heart is not beating in the correct timing as it should. These may take the form of the heart beating too fast (tachycardia) or too slow (bradycardia). There may also be abnormal sites generating an electrical impulse (ectopic beats). Arrhythmias, as well as physiological electrical flow across the heart, can be traced using an electrocardiogram (ECG or EKG). While some rhythm abnormalities are transient and may go unnoticed, others can cause life-threatening alteration in the cardiac output. 

Sick sinus syndrome is a collective term used in reference to disorders of the SA node. The umbrella term addresses disorders that result in abnormally fast heart rates ( tachycardia ) or abnormally slow heart rates ( bradycardia ). It also includes some disorders that can cause the heart rate to switch between tachycardic and bradycardic states ( bradycardia-tachycardia syndrome ). Sick sinus syndrome can also include pauses in SA node activity longer than 2 or 3 seconds. It is a relatively rare disorder that becomes more prevalent with increasing age.

In addition to aging, sick sinus syndrome may also be caused by drugs used to slow down the heart (beta-blockers, calcium channel blockers and digitalis), drugs used to lower blood pressure levels and abnormal electrolyte levels (hyperkalemia). Other causes of sick sinus syndrome include (but are not limited to) previous heart attack, hypothyroidism and amyloidosis (abnormal deposition of amyloid tissue throughout the body). 

Some patients living with sick sinus syndrome may experience palpitations, pre-syncopal or syncopal episodes, fatigue, weakness, acute onset of confusion and chest pain. The abnormal heart rate may also cause sleep disturbances as well. The formal diagnosis can be made using a continuous electrocardiogram (ECG) known as a Holter monitor . The ECG tracing can be collected over 24 to 48 hours and evaluated for any abnormality. Ultimately, these patients may require placement of an artificial pacemaker to help regulate the heart rate. 

Wolf-Parkinson-White (WPW) syndrome is a congenital abnormality involving abnormal conduction pathways between the atria and the ventricles. These aberrant circuits provide pathways for reentrant tachycardia impulses associated with supraventricular tachycardia.

The bundle of Kent is the most common bypass tract found in WPW syndrome. It is an accessory pathway that allows impulses to pass from the atria to the ventricles without passing through the AV node. Patient symptoms vary with age; so infants may present with irritability over the past day or two, poor feeding and tachycardia. Other patients will mention that they feel their heart racing (palpitations), chest pain, or difficulty breathing (shortness of breath).

The ECG tracing characteristically have a short PR interval (less than 0.12 s), delta waves, abnormal T waves and dominant R waves in leads V1 and V2. There may also be Q waves in the inferior leads. The ECG pattern can also help to determine the type of abnormal pathways that are present. 

The immediate management for patients with WPW syndrome would be to treat the arrhythmia and its possible cause. This may require vasovagal techniques or chemical cardioversion . If those techniques fail then mechanical cardioversion (synchronized shocking) can also be employed. In the long run, these patients will require radio-frequency ablation to destroy the abnormal pathways. 

References:

• Assadi, R., & Motabar, A. (2018). Conduction System of the Heart: Overview, Gross Anatomy, Natural Variants. Retrieved from https://emedicine.medscape.com/article/1922987-overview#a1
• Ellis, C. (2017). Wolff-Parkinson-White Syndrome: Practice Essentials, Background, Pathophysiology. Retrieved 24 July 2019, from https://emedicine.medscape.com/article/159222-overview
• Gregoratos, G. (2003). Sick Sinus Syndrome. Circulation, 108(20). doi: 10.1161/01.cir.0000102938.55119.ec
• Guyton, A., & Hall, J. (2007). Textbook of medical physiology (11th ed.). India: Elsevier Saunders.
• Moore, K., Agur, A., & Dalley, A. (2006). Clinically oriented anatomy (5th ed.). Philadelphia: LippincottWilliams&Wilkins.
• Standring, S., & Gray, H. (2008). Gray's anatomy (42nd ed.). Edinburgh: Churchill Livingstone/Elsevier.
• van Campenhout, M., Yaksh, A., Kik, C., de Jaegere, P., Ho, S., Allessie, M., & de Groot, N. (2013). Bachmann’s Bundle. Circulation: Arrhythmia And Electrophysiology, 6(5), 1041-1046. doi: 10.1161/circep.113.000758

Illustrators:

• Heart diagram showing the atria and ventricles - Yousun Koh
• Branch to sinuatrial node (anterior view) - Yousun Koh
• Action potential graph of heart muscle - Jana Vaskovic

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6.1 Heart Anatomy

Learning Objectives

By the end of this section, you will be able to:

• Describe the location and position of the heart within the body cavity
• Describe the internal and external anatomy of the heart
• Identify the tissue layers of the heart
• Relate the structure of the heart to its function as a pump
• Compare systemic circulation to pulmonary circulation
• Identify the veins and arteries of the coronary circulation system
• Trace the pathway of oxygenated and deoxygenated blood through the chambers of the heart

The vital importance of the heart is obvious. If one assumes an average rate of contraction of 75 contractions per minute, a human heart would contract approximately 108,000 times in one day, more than 39 million times in one year and nearly 3 billion times during a 75-year lifespan! Each of the major pumping chambers of the heart ejects approximately 70 mL blood per contraction in a resting adult. This would be equal to 5.25 litres of fluid per minute and approximately 14,000 litres per day. Over one year, that would equal 10,000,000 litres (2.6 million gallons) of blood sent through roughly 97,000 kilometres (60,000 miles) of vessels. In order to understand how that happens, it is necessary to understand the anatomy and physiology of the heart.

Location of the Heart

The human heart is located within the thoracic cavity, medially between the lungs in the space known as the mediastinum. Figure 6.1.1 shows the position of the heart within the thoracic cavity. Within the mediastinum, the heart is separated from the other mediastinal structures by a tough membrane known as the pericardium, or pericardial sac, and sits in its own space called the  pericardial cavity . The dorsal surface of the heart lies near the bodies of the vertebrae, and its anterior surface sits deep to the sternum and costal cartilages. The great veins, the superior and inferior venae cavae, and the great arteries, the aorta and pulmonary trunk, are attached to the superior surface of the heart, called the base. The base of the heart is located at the level of the third costal cartilage, as seen in Figure 6.1.1. The inferior tip of the heart, the apex, lies just to the left of the sternum between the junction of the fourth and fifth ribs near their articulation with the costal cartilages. The right side of the heart is deflected anteriorly, and the left side is deflected posteriorly. It is important to remember the position and orientation of the heart when placing a stethoscope on the chest of a patient and listening for heart sounds, and when looking at images taken from a midsagittal perspective. The slight deviation of the apex to the left is reflected in a depression in the medial surface of the inferior lobe of the left lung, called the  cardiac notch .

Everyday Connection

CPR The position of the heart in the torso between the vertebrae and sternum (see Figure 6.1.1 for the position of the heart within the thorax) allows for individuals to apply an emergency technique known as cardiopulmonary resuscitation (CPR) if the heart of a patient should stop. In adults, pressure is applied with the flat portion of one hand on the sternum in the area between the line at T4 and T9 (Figure 6.1.2), it is possible to manually compress the blood within the heart enough to push some of the blood within it into the pulmonary and systemic circuits. This is particularly critical for the brain, as irreversible damage and death of neurons occur within minutes of loss of blood flow. Current standards call for compression of the chest at least 5 cm deep and at a rate of 100-120 compressions per minute, a rate equal to the beat in “Staying Alive,” recorded in 1977 by the Bee Gees. If you are unfamiliar with this song, a version is available on www.youtube.com. At this stage, the emphasis is on performing high-quality chest compressions, rather than providing artificial respiration, but typically compression to ventilation ratio is 30:2. CPR is generally performed until the patient regains spontaneous contraction or is declared dead by an experienced healthcare professional.

When performed by untrained or overzealous individuals, CPR can result in broken ribs or a broken sternum and can inflict additional severe damage on the patient. It is also possible, if the hands are placed too low on the sternum, to manually drive the xiphoid process into the liver, a consequence that may prove fatal for the patient. Proper training is essential. This proven life-sustaining technique is so valuable that virtually all medical personnel as well as concerned members of the public should be certified and routinely recertified in its application. CPR courses are offered at a variety of locations, including colleges, hospitals, the Australian Red Cross and some commercial companies. They normally include practice of the compression technique on a mannequin.

Shape and Size of the Heart

The shape of the heart is similar to a pinecone, rather broad at the superior surface and tapering to the apex (see Figure 6.1.1). A typical heart is approximately the size of your fist: 12 cm (5 in) in length, 8 cm (3.5 in) wide, and 6 cm (2.5 in) in thickness. Given the size difference between most members of the sexes, the weight of a female heart is approximately 250–300 grams (9 to 11 ounces), and the weight of a male heart is approximately 300–350 grams (11 to 12 ounces). The heart of a well-trained athlete, especially one specialising in aerobic sports, can be considerably larger than this. Cardiac muscle responds to exercise in a manner like that of skeletal muscle. That is, exercise results in the addition of protein myofilaments that increase the size of the individual cells without increasing their numbers, a concept called hypertrophy. Hearts of athletes can pump blood more effectively at lower rates than those of nonathletes. Enlarged hearts are not always a result of exercise; they can result from pathologies, such as  hypertrophic cardiomyopathy . The cause of an abnormally enlarged heart muscle is unknown, but the condition is often undiagnosed and can cause sudden death in apparently otherwise healthy young people.

Chambers and Circulation Through the Heart

The human heart consists of four chambers: The left side and the right side each have one  atrium  and one  ventricle . Each of the upper chambers, the right atrium (plural = atria) and the left atrium, acts as a receiving chamber and contracts to push blood into the lower chambers, the right ventricle and the left ventricle. The ventricles serve as the primary pumping chambers of the heart, propelling blood to the lungs or to the rest of the body.

There are two distinct but linked circuits in the human circulation called the pulmonary and systemic circuits. Although both circuits transport blood and everything it carries, we can initially view the circuits from the point of view of gases. The  pulmonary circuit  transports blood to and from the lungs, where it picks up oxygen and delivers carbon dioxide for exhalation. The  systemic circuit  transports oxygenated blood to virtually all the tissues of the body and returns relatively deoxygenated blood and carbon dioxide to the heart to be sent back to the pulmonary circulation.

The right ventricle pumps deoxygenated blood into the  pulmonary trunk , which leads toward the lungs and bifurcates into the left and right  pulmonary arteries . These vessels in turn branch many times before reaching the  pulmonary capillaries , where gas exchange occurs: Carbon dioxide exits the blood and oxygen enters. The pulmonary trunk arteries and their branches are the only arteries in the post-natal body that carry relatively deoxygenated blood. Highly oxygenated blood returning from the pulmonary capillaries in the lungs passes through a series of vessels that join together to form the  pulmonary veins —the only post-natal veins in the body that carry highly oxygenated blood. The pulmonary veins conduct blood into the left atrium, which pumps the blood into the left ventricle, which in turn pumps oxygenated blood into the aorta and on to the many branches of the systemic circuit. Eventually, these vessels will lead to the systemic capillaries, where exchange with the tissue fluid and cells of the body occurs. In this case, oxygen and nutrients exit the systemic capillaries to be used by the cells in their metabolic processes, and carbon dioxide and waste products will enter the blood.

The blood exiting the systemic capillaries is lower in oxygen concentration than when it entered. The capillaries will ultimately unite to form venules, joining to form ever-larger veins, eventually flowing into the two major systemic veins, the  superior vena cava  and the  inferior vena cava , which return blood to the right atrium. The blood in the superior and inferior venae cavae flows into the right atrium, which pumps blood into the right ventricle. This process of blood circulation continues as long as the individual remains alive. Understanding the flow of blood through the pulmonary and systemic circuits is critical to all health professions (Figure 6.1.3).

Membranes, Surface Features and Layers

Our exploration of more in-depth heart structures begins by examining the membrane that surrounds the heart, the prominent surface features of the heart and the layers that form the wall of the heart. Each of these components plays its own unique role in terms of function.

The membrane that directly surrounds the heart and defines the pericardial cavity is called the  pericardium  or  pericardial sac . It also surrounds the “roots” of the major vessels, or the areas of closest proximity to the heart. The pericardium, which literally translates as “around the heart,” consists of two distinct sublayers: the sturdy outer fibrous pericardium and the inner serous pericardium. The fibrous pericardium is made of tough, dense connective tissue that protects the heart and maintains its position in the thorax. The more delicate serous pericardium consists of two layers: the parietal pericardium, which is fused to the fibrous pericardium, and an inner visceral pericardium, or  epicardium , which is fused to the heart and is part of the heart wall. The pericardial cavity, filled with lubricating serous fluid, lies between the epicardium and the pericardium.

In most organs within the body, visceral serous membranes such as the epicardium are microscopic. However, in the case of the heart, it is not a microscopic layer but rather a macroscopic layer, consisting of a simple squamous epithelium called a  mesothelium , reinforced with loose, irregular, or areolar connective tissue that attaches to the pericardium. This mesothelium secretes the lubricating serous fluid that fills the pericardial cavity and reduces friction as the heart contracts. Figure 6.1.4 illustrates the pericardial membranes and the layers of the heart.

Disorders of the Heart: Cardiac Tamponade

If excess fluid builds within the pericardial space, it can lead to a condition called cardiac tamponade, or pericardial tamponade. With each contraction of the heart, more fluid—in most instances, blood—accumulates within the pericardial cavity. In order to fill with blood for the next contraction, the heart must relax. However, the excess fluid in the pericardial cavity puts pressure on the heart and prevents full relaxation, so the chambers within the heart contain slightly less blood as they begin each heart cycle. Over time, less and less blood is ejected from the heart. If the fluid builds up slowly, as in hypothyroidism, the pericardial cavity may be able to expand gradually to accommodate this extra volume. Some cases of fluid in excess of one litre within the pericardial cavity have been reported. Rapid accumulation of as little as 100 mL of fluid following trauma may trigger cardiac tamponade. Other common causes include myocardial rupture, pericarditis, cancer, or even cardiac surgery. Removal of this excess fluid requires insertion of drainage tubes into the pericardial cavity. Premature removal of these drainage tubes, for example, following cardiac surgery, or clot formation within these tubes are causes of this condition. Untreated, cardiac tamponade can lead to death.

Surface Features of the Heart

Inside the pericardium, the surface features of the heart are visible, including the four chambers. There is a superficial leaf-like extension of the atria near the superior surface of the heart, one on each side, called an  auricle —a name that means “ear like”—because its shape resembles the external ear of a human (Figure 6.1.5). Auricles are relatively thin-walled structures that can fill with blood and empty into the atria or upper chambers of the heart. You may also hear them referred to as atrial appendages. Also prominent is a series of fat-filled grooves, each of which is known as a  sulcus  (plural = sulci), along the superior surfaces of the heart. Major coronary blood vessels are located in these sulci. The deep  coronary sulcus  is located between the atria and ventricles. Located between the left and right ventricles are two additional sulci that are not as deep as the coronary sulcus. The  anterior interventricular sulcus  is visible on the anterior surface of the heart, whereas the  posterior interventricular sulcus  is visible on the posterior surface of the heart. Figure 6.1.5 illustrates anterior and posterior views of the surface of the heart.

The wall of the heart is composed of three layers of unequal thickness. From superficial to deep, these are the epicardium, the myocardium and the endocardium (see Figure 6.1.4). The outermost layer of the wall of the heart is also the innermost layer of the pericardium, the epicardium, or the visceral pericardium discussed earlier.

The middle and thickest layer is the  myocardium , made largely of cardiac muscle cells. It is built upon a framework of collagenous fibres, plus the blood vessels that supply the myocardium and the nerve fibres that help regulate the heart. It is the contraction of the myocardium that pumps blood through the heart and into the major arteries. The muscle pattern is elegant and complex, as the muscle cells swirl and spiral around the chambers of the heart. They form a figure 8 pattern around the atria and around the bases of the great vessels. Deeper ventricular muscles also form a figure 8 around the two ventricles and proceed toward the apex. More superficial layers of ventricular muscle wrap around both ventricles. This complex swirling pattern allows the heart to pump blood more effectively than a simple linear pattern would. Figure 6.1.6 illustrates the arrangement of muscle cells.

Although the ventricles on the right and left sides pump the same amount of blood per contraction, the muscle of the left ventricle is much thicker and better developed than that of the right ventricle. In order to overcome the high resistance required to pump blood into the long systemic circuit, the left ventricle must generate a great amount of pressure. The right ventricle does not need to generate as much pressure, since the pulmonary circuit is shorter and provides less resistance. Figure 6.1.7 illustrates the differences in muscular thickness needed for each of the ventricles.

The innermost layer of the heart wall, the  endocardium , is joined to the myocardium with a thin layer of connective tissue. The endocardium lines the chambers where the blood circulates and covers the heart valves. It is made of simple squamous epithelium called  endothelium , which is continuous with the endothelial lining of the blood vessels (see Figure 6.1.4).

Once regarded as a simple lining layer, recent evidence indicates that the endothelium of the endocardium and the coronary capillaries may play active roles in regulating the contraction of the muscle within the myocardium. The endothelium may also regulate the growth patterns of the cardiac muscle cells throughout life, and the endothelins it secretes create an environment in the surrounding tissue fluids that regulates ionic concentrations and states of contractility. Endothelins are potent vasoconstrictors and, in a normal individual, establish a homeostatic balance with other vasoconstrictors and vasodilators.

Internal Structure of the Heart

Recall that the heart’s contraction cycle follows a dual pattern of circulation—the pulmonary and systemic circuits—because of the pairs of chambers that pump blood into the circulation. In order to develop a more precise understanding of cardiac function, it is first necessary to explore the internal anatomical structures in more detail.

Septa of the Heart

The word septum is derived from the Latin for “something that encloses;” in this case, a  septum  (plural = septa) refers to a wall or partition that divides the heart into chambers. The septa are physical extensions of the myocardium lined with endocardium. Located between the two atria is the  interatrial septum . Normally in an adult heart, the interatrial septum bears an oval-shaped depression known as the  fossa ovalis , a remnant of an opening in the foetal heart known as the  foramen ovale . The foramen ovale allowed blood in the foetal heart to pass directly from the right atrium to the left atrium, allowing some blood to bypass the pulmonary circuit. Within seconds after birth, a flap of tissue known as the  septum primum  that previously acted as a valve closes the foramen ovale and establishes the typical cardiac circulation pattern.

Between the two ventricles is a second septum known as the  interventricular septum . Unlike the interatrial septum, the interventricular septum is normally intact after its formation during foetal development. It is substantially thicker than the interatrial septum, since the ventricles generate far greater pressure when they contract.

The septum between the atria and ventricles is known as the  atrioventricular septum . It is marked by the presence of four openings that allow blood to move from the atria into the ventricles and from the ventricles into the pulmonary trunk and aorta. Located in each of these openings between the atria and ventricles is a  valve , a specialised structure that ensures one-way flow of blood. The valves between the atria and ventricles are known generically as  atrioventricular valves . The valves at the openings that lead to the pulmonary trunk and aorta are known generically as  semilunar valves . The interventricular septum is visible in Figure 6.1.8. In this figure, the atrioventricular septum has been removed to better show the bicuspid and tricuspid valves; the interatrial septum is not visible, since its location is covered by the aorta and pulmonary trunk. Since these openings and valves structurally weaken the atrioventricular septum, the remaining tissue is heavily reinforced with dense connective tissue called the  cardiac skeleton , or skeleton of the heart. It includes four rings that surround the openings between the atria and ventricles, and the openings to the pulmonary trunk and aorta, and serve as the point of attachment for the heart valves. The cardiac skeleton also provides an important boundary in the heart electrical conduction system.

Disorders of the Heart: Heart Defects

One very common form of interatrial septum pathology is patent foramen ovale, which occurs when the septum primum does not close at birth, and the fossa ovalis is unable to fuse. The word patent is from the Latin root patens for “open.” It may be benign or asymptomatic, perhaps never being diagnosed, or in extreme cases, it may require surgical repair to close the opening permanently. As much as 20–25 percent of the general population may have a patent foramen ovale, but fortunately, most have the benign, asymptomatic version. Patent foramen ovale is normally detected by auscultation of a heart murmur (an abnormal heart sound) and confirmed by imaging with an echocardiogram. Despite its prevalence in the general population, the causes of patent ovale are unknown, and there are no known risk factors. In nonlife-threatening cases, it is better to monitor the condition than to risk heart surgery to repair and seal the opening.

Coarctation of the aorta is a congenital abnormal narrowing of the aorta that is normally located at the insertion of the ligamentum arteriosum, the remnant of the foetal shunt called the ductus arteriosus. If severe, this condition drastically restricts blood flow through the primary systemic artery, which is life threatening. In some individuals, the condition may be benign and not detected until later in life. Detectable symptoms in an infant include difficulty breathing, poor appetite, trouble feeding, or failure to thrive. In older individuals, symptoms include dizziness, fainting, shortness of breath, chest pain, fatigue, headache, and nosebleeds. Treatment involves surgery to resect (remove) the affected region or angioplasty to open the abnormally narrow passageway. Studies have shown that the earlier the surgery is performed, the better the chance of survival.

A patent ductus arteriosus is a congenital condition in which the ductus arteriosus fails to close. The condition may range from severe to benign. Failure of the ductus arteriosus to close results in blood flowing from the higher-pressure aorta into the lower pressure pulmonary trunk. This additional fluid moving toward the lungs increases pulmonary pressure and makes respiration difficult. Symptoms include shortness of breath (dyspnoea), tachycardia, enlarged heart, a widened pulse pressure, and poor weight gain in infants. Treatments include surgical closure (ligation), manual closure using platinum coils or specialised mesh inserted via the femoral artery or vein, or nonsteroidal anti-inflammatory drugs to block the synthesis of prostaglandin E2, which maintains the vessel in an open position. If untreated, the condition can result in congestive heart failure.

Septal defects are not uncommon in individuals and may be congenital or caused by various disease processes. Tetralogy of Fallot is a congenital condition that may also occur from exposure to unknown environmental factors; it occurs when there is an opening in the interventricular septum caused by blockage of the pulmonary trunk, normally at the pulmonary semilunar valve. This allows blood that is relatively low in oxygen from the right ventricle to flow into the left ventricle and mix with the blood that is relatively high in oxygen. Symptoms include a distinct heart murmur, low blood oxygen percent saturation, dyspnoea or difficulty in breathing, polycythaemia, broadening (clubbing) of the fingers and toes, and in children, difficulty in feeding or failure to grow and develop. It is the most common cause of cyanosis following birth. The term “tetralogy” is derived from the four components of the condition, although only three may be present in an individual patient: pulmonary infundibular stenosis (rigidity of the pulmonary valve), overriding aorta (the aorta is shifted above both ventricles), ventricular septal defect (opening), and right ventricular hypertrophy (enlargement of the right ventricle). Other heart defects may also accompany this condition, which is typically confirmed by echocardiography imaging. Tetralogy of Fallot occurs in approximately 400 out of one million live births. Normal treatment involves extensive surgical repair, including the use of stents to redirect blood flow and replacement of valves and patches to repair the septal defect, but the condition has a relatively high mortality. Survival rates are currently 75 percent during the first year of life; 60 percent by four years of age; 30 percent by 10 years; and five percent by 40 years.

In the case of severe septal defects, including both tetralogy of Fallot and patent foramen ovale, failure of the heart to develop properly can lead to a condition commonly known as a “blue baby.” Regardless of normal skin pigmentation, individuals with this condition have an insufficient supply of oxygenated blood, which leads to cyanosis, a blue or purple coloration of the skin, especially when active.

Septal defects are commonly first detected through auscultation, listening to the chest using a stethoscope. In this case, instead of hearing normal heart sounds attributed to the flow of blood and closing of heart valves, unusual heart sounds may be detected. This is often followed by medical imaging to confirm or rule out a diagnosis. In many cases, treatment may not be needed. Some common congenital heart defects are illustrated in Figure 6.1.9.

Right Atrium

The right atrium serves as the receiving chamber for blood returning to the heart from the systemic circulation. The two major systemic veins, the superior and inferior venae cavae, and the large coronary vein called the  coronary sinus  that drains the heart myocardium empty into the right atrium. The superior vena cava drains blood from regions superior to the diaphragm: the head, neck, upper limbs, and the thoracic region. It empties into the superior and posterior portions of the right atrium. The inferior vena cava drains blood from areas inferior to the diaphragm: the lower limbs and abdominopelvic region of the body. It, too, empties into the posterior portion of the atria, but inferior to the opening of the superior vena cava. Immediately superior and slightly medial to the opening of the inferior vena cava on the posterior surface of the atrium is the opening of the coronary sinus. This thin-walled vessel drains most of the coronary veins that return systemic blood from the heart. The majority of the internal heart structures discussed in this and subsequent sections are illustrated in Figure 6.1.8.

While the bulk of the internal surface of the right atrium is smooth, the depression of the fossa ovalis is medial, and the anterior surface demonstrates prominent ridges of muscle called the  pectinate muscles . The right auricle also has pectinate muscles. The left atrium does not have pectinate muscles except in the auricle.

The atria receive venous blood on a nearly continuous basis, preventing venous flow from stopping while the ventricles are contracting. While most ventricular filling occurs while the atria are relaxed, they do demonstrate a contractile phase and actively pump blood into the ventricles just prior to ventricular contraction. The opening between the atrium and ventricle is guarded by the tricuspid valve.

Right Ventricle

The right ventricle receives blood from the right atrium through the tricuspid valve. Each flap of the valve is attached to strong strands of connective tissue, the  chordae tendineae , literally “tendinous cords,” or sometimes more poetically referred to as “heart strings.” There are several chordae tendineae associated with each of the flaps. They are composed of approximately 80 percent collagenous fibres with the remainder consisting of elastic fibres and endothelium. They connect each of the flaps to a  papillary muscle  that extends from the inferior ventricular surface. There are three papillary muscles in the right ventricle, called the anterior, posterior, and septal muscles, which correspond to the three sections of the valves.

When the myocardium of the ventricle contracts, pressure within the ventricular chamber rises. Blood, like any fluid, flows from higher pressure to lower pressure areas, in this case, toward the pulmonary trunk and the atrium. To prevent any potential backflow, the papillary muscles also contract, generating tension on the chordae tendineae. This prevents the flaps of the valves from being forced into the atria and regurgitation of the blood back into the atria during ventricular contraction. Figure 6.1.10 shows papillary muscles and chordae tendineae attached to the tricuspid valve.

The walls of the ventricle are lined with  trabeculae carneae , ridges of cardiac muscle covered by endocardium. In addition to these muscular ridges, a band of cardiac muscle, also covered by endocardium, known as the  moderator band  (see Figure 6.1.8) reinforces the thin walls of the right ventricle and plays a crucial role in cardiac conduction. It arises from the inferior portion of the interventricular septum and crosses the interior space of the right ventricle to connect with the inferior papillary muscle.

When the right ventricle contracts, it ejects blood into the pulmonary trunk, which branches into the left and right pulmonary arteries that carry it to each lung. The superior surface of the right ventricle begins to taper as it approaches the pulmonary trunk. At the base of the pulmonary trunk is the pulmonary semilunar valve that prevents backflow from the pulmonary trunk.

Left Atrium

After exchange of gases in the pulmonary capillaries, blood returns to the left atrium high in oxygen via one of the four pulmonary veins. While the left atrium does not contain pectinate muscles, it does have an auricle that includes these pectinate ridges. Blood flows nearly continuously from the pulmonary veins back into the atrium, which acts as the receiving chamber, and from here through an opening into the left ventricle. Most blood flows passively into the heart while both the atria and ventricles are relaxed, but toward the end of the ventricular relaxation period, the left atrium will contract, pumping blood into the ventricle. This atrial contraction accounts for approximately 20 percent of ventricular filling. The opening between the left atrium and ventricle is guarded by the mitral valve.

Left Ventricle

Recall that, although both sides of the heart will pump the same amount of blood, the muscular layer is much thicker in the left ventricle compared to the right (see Figure 6.1.7). Like the right ventricle, the left also has trabeculae carneae, but there is no moderator band. The mitral valve is connected to papillary muscles via chordae tendineae. There are two papillary muscles on the left—the anterior and posterior—as opposed to three on the right.

The left ventricle is the major pumping chamber for the systemic circuit; it ejects blood into the aorta through the aortic semilunar valve.

Heart Valve Structure and Function

A transverse section through the heart slightly above the level of the atrioventricular septum reveals all four heart valves along the same plane (Figure 6.1.11). The valves ensure unidirectional blood flow through the heart. Between the right atrium and the right ventricle is the  right atrioventricular valve , or  tricuspid valve . It typically consists of three flaps, or leaflets, made of endocardium reinforced with additional connective tissue. The flaps are connected by chordae tendineae to the papillary muscles, which control the opening and closing of the valves.

Emerging from the right ventricle at the base of the pulmonary trunk is the pulmonary semilunar valve, or the  pulmonary valve ; it is also known as the pulmonic valve or the right semilunar valve. The pulmonary valve is comprised of three small flaps of endothelium reinforced with connective tissue. When the ventricle relaxes, the pressure differential causes blood to flow back into the ventricle from the pulmonary trunk. This flow of blood fills the pocket-like flaps of the pulmonary valve, causing the valve to close and producing an audible sound. Unlike the atrioventricular valves, there are no papillary muscles or chordae tendineae associated with the pulmonary valve.

Located at the opening between the left atrium and left ventricle is the  mitral valve , also called the  bicuspid valve  or the  left atrioventricular valve . Structurally, this valve consists of two cusps, known as the anterior medial cusp and the posterior medial cusp, compared to the three cusps of the tricuspid valve. In a clinical setting, the valve is referred to as the mitral valve, rather than the bicuspid valve. The two cusps of the mitral valve are attached by chordae tendineae to two papillary muscles that project from the wall of the ventricle.

At the base of the aorta is the aortic semilunar valve, or the  aortic valve , which prevents backflow from the aorta. It normally is composed of three flaps. When the ventricle relaxes and blood attempts to flow back into the ventricle from the aorta, blood will fill the cusps of the valve, causing it to close and producing an audible sound.

In Figure 6.1.12a, the two atrioventricular valves are open and the two semilunar valves are closed. This occurs when both atria and ventricles are relaxed and when the atria contract to pump blood into the ventricles. Figure 6.1.12b shows a frontal view. Although only the left side of the heart is illustrated, the process is virtually identical on the right.

Figure 6.1.13a shows the atrioventricular valves closed while the two semilunar valves are open. This occurs when the ventricles contract to eject blood into the pulmonary trunk and aorta. Closure of the two atrioventricular valves prevents blood from being forced back into the atria. This stage can be seen from a frontal view in Figure 6.1.13b.

When the ventricles begin to contract, pressure within the ventricles rises and blood flows toward the area of lowest pressure, which is initially in the atria. This backflow causes the cusps of the tricuspid and mitral (bicuspid) valves to close. These valves are tied down to the papillary muscles by chordae tendineae. During the relaxation phase of the cardiac cycle, the papillary muscles are also relaxed and the tension on the chordae tendineae is slight (see Figure 6.1.12b). However, as the myocardium of the ventricle contracts, so do the papillary muscles. This creates tension on the chordae tendineae (see Figure 6.1.13b), helping to hold the cusps of the atrioventricular valves in place and preventing them from being blown back into the atria.

The aortic and pulmonary semilunar valves lack the chordae tendineae and papillary muscles associated with the atrioventricular valves. Instead, they consist of pocket-like folds of endocardium reinforced with additional connective tissue. When the ventricles relax and the change in pressure forces the blood toward the ventricles, the blood presses against these cusps and seals the openings.

Disorders of the Heart Valves

When heart valves do not function properly, they are often described as incompetent and result in valvular heart disease, which can range from benign to lethal. Some of these conditions are congenital, that is, the individual was born with the defect, whereas others may be attributed to disease processes or trauma. Some malfunctions are treated with medications, others require surgery, and still others may be mild enough that the condition is merely monitored since treatment might trigger more serious consequences.

Valvular disorders are often caused by carditis, or inflammation of the heart. One common trigger for this inflammation is rheumatic fever, or scarlet fever, an autoimmune response to the presence of a bacterium,  Streptococcus pyogenes , normally a disease of childhood.

While any of the heart valves may be involved in valve disorders, mitral regurgitation is the most common, detected in approximately 2 percent of the population, and the pulmonary semilunar valve is the least frequently involved. When a valve malfunctions, the flow of blood to a region will often be disrupted. The resulting inadequate flow of blood to this region will be described in general terms as an insufficiency. The specific type of insufficiency is named for the valve involved: aortic insufficiency, mitral insufficiency, tricuspid insufficiency, or pulmonary insufficiency.

If one of the cusps of the valve is forced backward by the force of the blood, the condition is referred to as a prolapsed valve. Prolapse may occur if the chordae tendineae are damaged or broken, causing the closure mechanism to fail. The failure of the valve to close properly disrupts the normal one-way flow of blood and results in regurgitation, when the blood flows backward from its normal path. Using a stethoscope, the disruption to the normal flow of blood produces a heart murmur.

Stenosis is a condition in which the heart valves become rigid and may calcify over time. The loss of flexibility of the valve interferes with normal function and may cause the heart to work harder to propel blood through the valve, which eventually weakens the heart. Aortic stenosis affects approximately two percent of the population over 65 years of age, and the percentage increases to approximately four percent in individuals over 85 years. Occasionally, one or more of the chordae tendineae will tear or the papillary muscle itself may die as a component of a myocardial infarction (heart attack). In this case, the patient’s condition will deteriorate dramatically and rapidly, and immediate surgical intervention may be required.

Auscultation, or listening to a patient’s heart sounds, is one of the most useful diagnostic tools, since it is proven, safe, and inexpensive. The term auscultation is derived from the Latin for “to listen,” and the technique has been used for diagnostic purposes as far back as the ancient Egyptians. Valve and septal disorders will trigger abnormal heart sounds. If a valvular disorder is detected or suspected, a test called an echocardiogram, or simply an “echo,” may be ordered. Echocardiograms are sonograms of the heart and can help in the diagnosis of valve disorders as well as a wide variety of heart pathologies.

Career Connection

Cardiologist

Cardiologists are medical doctors that specialise in the diagnosis and treatment of diseases of the heart. The pathway to become a certified cardiologist in Australia consists of four basic steps. Firstly, a completion of an undergraduate degree (3 years full time) in either a health science or biomedical science field with provisional entry into medicine. Second step is completing either a Bachelor of Medicine/Bachelor of Surgery or a Doctor of Medicine (MD) degree which generally takes four years full time. The third step is to complete an internship/residency in a public hospital system (two years). The final stage requires further vocational training and a Fellowship in a specialised training program (e.g. Fellowship of the Royal Australasian College of Physicians (FRACP) which takes approximately three to five years to complete. The annual salary of a Cardiologist in Australia can range between $60k up to $630k.

Cardiovascular Technologist/Technician

Cardiovascular technologists/technicians are trained professionals who perform a variety of imaging techniques, such as sonograms or echocardiograms, used by physicians to diagnose and treat diseases of the heart. Nearly all of these positions require an associate degree, and include, but are not limited to, Grade 1 Cardiac Technician (~$48k – $80k per annum), radiographer (~$55k – $104k per annum), cardiac sonographer (~$62k – $135k per annum).

Coronary Circulation

You will recall that the heart is a remarkable pump composed largely of cardiac muscle cells that are incredibly active throughout life. Like all other cells, a  cardiomyocyte  requires a reliable supply of oxygen and nutrients, and a way to remove wastes, so it needs a dedicated, complex, and extensive coronary circulation. And because of the critical and nearly ceaseless activity of the heart throughout life, this need for a blood supply is even greater than for a typical cell. However, coronary circulation is not continuous; rather, it cycles, reaching a peak when the heart muscle is relaxed and nearly ceasing while it is contracting.

Coronary Arteries

Coronary arteries  supply blood to the myocardium and other components of the heart. The first portion of the aorta after it arises from the left ventricle gives rise to the coronary arteries. There are three dilations in the wall of the aorta just superior to the aortic semilunar valve. Two of these, the left posterior aortic sinus and anterior aortic sinus, give rise to the left and right coronary arteries, respectively. The third sinus, the right posterior aortic sinus, typically does not give rise to a vessel. Coronary vessel branches that remain on the surface of the artery and follow the sulci are called  epicardial coronary arteries .

The left coronary artery distributes blood to the left side of the heart, the left atrium and ventricle, and the interventricular septum. The  circumflex artery  arises from the left coronary artery and follows the coronary sulcus to the left. Eventually, it will fuse with the small branches of the right coronary artery. The larger  anterior interventricular artery , also known as the left anterior descending artery (LAD), is the second major branch arising from the left coronary artery. It follows the anterior interventricular sulcus around the pulmonary trunk. Along the way it gives rise to numerous smaller branches that interconnect with the branches of the posterior interventricular artery, forming anastomoses. An  anastomosis  is an area where vessels unite to form interconnections that normally allow blood to circulate to a region even if there may be partial blockage in another branch. The anastomoses in the heart are very small. Therefore, this ability is somewhat restricted in the heart, so a coronary artery blockage often results in death of the cells (myocardial infarction) supplied by the particular vessel.

The right coronary artery proceeds along the coronary sulcus and distributes blood to the right atrium, portions of both ventricles, and the heart conduction system. Normally, one or more marginal arteries arise from the right coronary artery inferior to the right atrium. The  marginal arteries  supply blood to the superficial portions of the right ventricle. On the posterior surface of the heart, the right coronary artery gives rise to the  posterior interventricular artery , also known as the posterior descending artery. It runs along the posterior portion of the interventricular sulcus toward the apex of the heart, giving rise to branches that supply the interventricular septum and portions of both ventricles. Figure 6.1.14 presents views of the coronary circulation from both the anterior and posterior views.

Diseases of the Heart: Myocardial Infarction

Myocardial infarction (MI) is the formal term for what is commonly referred to as a heart attack. It normally results from a lack of blood flow (ischaemia) and oxygen (hypoxia) to a region of the heart, resulting in death of the cardiac muscle cells. An MI often occurs when a coronary artery is blocked by the build-up of atherosclerotic plaque consisting of lipids, cholesterol and fatty acids, and white blood cells, primarily macrophages. It can also occur when a portion of an unstable atherosclerotic plaque travels through the coronary arterial system and lodges in one of the smaller vessels. The resulting blockage restricts the flow of blood and oxygen to the myocardium and causes death of the tissue. MIs may be triggered by excessive exercise, in which the partially occluded artery is no longer able to pump sufficient quantities of blood, or severe stress, which may induce spasm of the smooth muscle in the walls of the vessel.

In the case of acute MI, there is often sudden pain beneath the sternum (retrosternal pain) called angina pectoris, often radiating down the left arm in males but not in female patients. Until this anomaly between the sexes was discovered, many female patients suffering MIs were misdiagnosed and sent home. In addition, patients typically present with difficulty breathing and shortness of breath (dyspnoea), irregular heartbeat (palpations), nausea and vomiting, sweating (diaphoresis), anxiety and fainting (syncope), although not all of these symptoms may be present. Many of the symptoms are shared with other medical conditions, including anxiety attacks and simple indigestion, so differential diagnosis is critical. It is estimated that between 22 and 64 percent of MIs present without any symptoms.

An MI can be confirmed by examining the patient’s ECG, which frequently reveals alterations in the ST and Q components. Some classification schemes of MI are referred to as ST-elevated MI (STEMI) and non-elevated MI (non-STEMI). In addition, echocardiography or cardiac magnetic resonance imaging may be employed. Common blood tests indicating an MI include elevated levels of creatine kinase MB (an enzyme that catalyses the conversion of creatine to phosphocreatine, consuming ATP) and cardiac troponin (the regulatory protein for muscle contraction), both of which are released by damaged cardiac muscle cells.

Immediate treatments for MI are essential and include administering supplemental oxygen, aspirin that helps to break up clots, and nitroglycerine administered sublingually (under the tongue) to facilitate its absorption. Despite its unquestioned success in treatments and use since the 1880s, the mechanism of nitroglycerine is still incompletely understood but is believed to involve the release of nitric oxide, a known vasodilator, and endothelium-derived releasing factor, which also relaxes the smooth muscle in the tunica media of coronary vessels. Longer-term treatments include injections of thrombolytic agents such as streptokinase that dissolve the clot, the anticoagulant heparin, balloon angioplasty and stents to open blocked vessels, and bypass surgery to allow blood to pass around the site of blockage. If the damage is extensive, coronary replacement with a donor heart or coronary assist device, a sophisticated mechanical device that supplements the pumping activity of the heart, may be employed. Despite the attention, development of artificial hearts to augment the severely limited supply of heart donors has proven less than satisfactory but will likely improve in the future.

MIs may trigger cardiac arrest, but the two are not synonymous. Important risk factors for MI include cardiovascular disease, age, smoking, high blood levels of the low-density lipoprotein (LDL, often referred to as “bad” cholesterol), low levels of high-density lipoprotein (HDL, or “good” cholesterol), hypertension, diabetes mellitus, obesity, lack of physical exercise, chronic kidney disease, excessive alcohol consumption, and use of illegal drugs.

Coronary Veins

Coronary veins  drain the heart and generally parallel the large surface arteries (see Figure 6.1.14). The  great cardiac vein  can be seen initially on the surface of the heart following the interventricular sulcus, but it eventually flows along the coronary sulcus into the coronary sinus on the posterior surface. The great cardiac vein initially parallels the anterior interventricular artery and drains the areas supplied by this vessel. It receives several major branches, including the posterior cardiac vein, the middle cardiac vein, and the small cardiac vein. The  posterior cardiac vein  parallels and drains the areas supplied by the marginal artery branch of the circumflex artery. The  middle cardiac vein  parallels and drains the areas supplied by the posterior interventricular artery. The  small cardiac vein  parallels the right coronary artery and drains the blood from the posterior surfaces of the right atrium and ventricle. The coronary sinus is a large, thin-walled vein on the posterior surface of the heart lying within the atrioventricular sulcus and emptying directly into the right atrium. The  anterior cardiac veins  parallel the small cardiac arteries and drain the anterior surface of the right ventricle. Unlike these other cardiac veins, it bypasses the coronary sinus and drains directly into the right atrium.

Diseases of the Heart: Coronary Artery Disease

Coronary artery disease is the leading cause of death worldwide. It occurs when the build-up of plaque—a fatty material including cholesterol, connective tissue, white blood cells, and some smooth muscle cells—within the walls of the arteries obstructs the flow of blood and decreases the flexibility or compliance of the vessels. This condition is called atherosclerosis, a hardening of the arteries that involves the accumulation of plaque. As the coronary blood vessels become occluded, the flow of blood to the tissues will be restricted, a condition called ischaemia that causes the cells to receive insufficient amounts of oxygen, called hypoxia. Figure 6.1.15 shows the blockage of coronary arteries highlighted by the injection of dye. Some individuals with coronary artery disease report pain radiating from the chest called angina pectoris, but others remain asymptomatic. If untreated, coronary artery disease can lead to MI or a heart attack.

The disease progresses slowly and often begins in children and can be seen as fatty “streaks” in the vessels. It then gradually progresses throughout life. Well-documented risk factors include smoking, family history, hypertension, obesity, diabetes, high alcohol consumption, lack of exercise, stress, and hyperlipidaemia or high circulating levels of lipids in the blood. Treatments may include medication, changes to diet and exercise, angioplasty with a balloon catheter, insertion of a stent, or coronary bypass procedure.

Angioplasty is a procedure in which the occlusion is mechanically widened with a balloon. A specialised catheter with an expandable tip is inserted into a superficial vessel, normally in the leg, and then directed to the site of the occlusion. At this point, the balloon is inflated to compress the plaque material and to open the vessel to increase blood flow. Then, the balloon is deflated and retracted. A stent consisting of a specialised mesh is typically inserted at the site of occlusion to reinforce the weakened and damaged walls. Stent insertions have been routine in cardiology for more than 40 years.

Coronary bypass surgery may also be performed. This surgical procedure grafts a replacement vessel obtained from another, less vital portion of the body to bypass the occluded area. This procedure is clearly effective in treating patients experiencing a MI, but overall does not increase longevity. Nor does it seem advisable in patients with stable although diminished cardiac capacity since frequently loss of mental acuity occurs following the procedure. Long-term changes to behaviour, emphasising diet and exercise plus a medicine regime tailored to lower blood pressure, lower cholesterol and lipids, and reduce clotting are equally as effective.

Section Review

The heart resides within the pericardial sac and is located in the mediastinal space within the thoracic cavity. The pericardial sac consists of two fused layers: an outer fibrous capsule and an inner parietal pericardium lined with a serous membrane. Between the pericardial sac and the heart is the pericardial cavity, which is filled with lubricating serous fluid. The walls of the heart are composed of an outer epicardium, a thick myocardium, and an inner lining layer of endocardium. The human heart consists of a pair of atria, which receive blood and pump it into a pair of ventricles, which pump blood into the vessels. The right atrium receives systemic blood relatively low in oxygen and pumps it into the right ventricle, which pumps it into the pulmonary circuit. Exchange of oxygen and carbon dioxide occurs in the lungs, and blood high in oxygen returns to the left atrium, which pumps blood into the left ventricle, which in turn pumps blood into the aorta and the remainder of the systemic circuit. The septa are the partitions that separate the chambers of the heart. They include the interatrial septum, the interventricular septum, and the atrioventricular septum. Two of these openings are guarded by the atrioventricular valves, the right tricuspid valve and the left mitral valve, which prevent the backflow of blood. Each is attached to chordae tendineae that extend to the papillary muscles, which are extensions of the myocardium, to prevent the valves from being blown back into the atria. The pulmonary valve is located at the base of the pulmonary trunk, and the left semilunar valve is located at the base of the aorta. The right and left coronary arteries are the first to branch off the aorta and arise from two of the three sinuses located near the base of the aorta and are generally located in the sulci. Cardiac veins parallel the small cardiac arteries and generally drain into the coronary sinus.

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Essay on Cardiac Cycle (With Diagram) | Heart | Human | Biology

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Essay on Cardiac Cycle

Changes that occur in the heart during one beat are repeated in the same order in the next beat. This cyclical repetition of the various changes in heart, from beat to beat, is called cardiac cycle.

Cardiac Cycle Time :

This is the time required for one complete cardiac cycle. With the normal heart rate of 75 per minute, this time will be 60/75 = 0.8 sec. It means that every event in the cycle will be repeated at the interval of 0.8 sec. It is obvious that the cardiac cycle time will be inversely proportional to the heart rate.

Interrelations of the Various Events in the Cardiac Cycle :

In the cardiac cycle there are four main events:

i. Atrial systole.

ii. Atrial diastole.

iii. Ventricular systole.

iv. Ventricular diastole.

All the other changes are subsidiary to them.

Atrial systole initiates the cycle, because the pacemaker S.A. node is situated in it. It lasts for 0.1 sec, and is followed by atrial diastole, last­ing for 0.7 sec. At the end of diastole, the atrial systole returns, and in this way, the atrial cycle goes on (total duration 0.8 sec.).

At the end of atrial systole, ventricular systo­le starts—duration 0.3 sec. This is immediately followed by ventricular diastole—duration 0.5 sec. At the end of diastole, ventricular systole repeats and thus the ventricular cycle goes on (total duration 0.8 sec.)

In order to follow the march of events during the cardiac cycle and their interrelations, the Fig. 7.43 should be carefully studied. In it, there are two concentric rings, divided into eight equal parts. The whole circle represents one complete cardiac cycle, so that each of its eight divisions represents 0.1 sec. The inner ring represents the atrial events, the outer ring ventricular events.

Let us Follow Inner Ring First:

The one shaded division in it denotes atrial systole (0.1 sec.). During this period the atria contract and expel their contents into the respective ventricles. The left atrium, being further away from the S.A. node, contracts a little after the right atrium. But practically their contractions are simultaneous. The force of contraction is stronger in the first half than in the second. Because during first half or at initial stage the intra-atrial pressure remains high and during last half the same is decreased due to expulsion of blood to the ventricle (Fig. 7.44).

After atrial systole, comes its diastole (0.7 sec.) being represented by seven un-shaded divisions in the ring. During this period the atria relax and receive blood from the great veins—the right atrium from the venae cavae, the left atrium from the pulmonary veins. At the end of this period, the atrial systole comes again and in this way, the atrial events go on.

Let us now follow the ventricular events in the outer ring. There are three shaded divisions on it, representing ventricular systole (0.3 sec.). It is followed by five un-shaded divisions, indicating ventricular diastole (0.5 sec.). On comparing the two rings, it would be found that ventricular systole commences at the end of atrial systole.

The reason for this is very clear. The impulse originating at the S. A. node will certainly overtake the atrium first, and then it will travel down the junctional tissues, enter the ventricles and stimulate their contraction. Naturally then, ventricular systole will always come after atrial systole.

From these interrelations we can deduce one fundamental rule of cardiac action that -the systoles of atrium and ventricle will never overlap. In other words, when one chamber is contracting, the other must be relaxing.

At the onset of ventricular systole, the first sound occurs. It is caused by the sudden closure of the A.V. valves due to sharp rise of intraventricular pressure. The semilunar valves open a little later, because, until the intraventricular pressure goes above that in the aorta and pulmonary artery, the semilunar valves will not open.

Thus, at the beginning of ventricular systole, there is a brief period during which both the valves are closed and the ventricles are contracting as closed cavities (Fig. 7.45). No blood passes out and therefore, no shortening of the cardiac muscle will occur. Hence, this period is called isometric contraction period (0.05 sec.). It is marked at the onset by the closure of the A.V. valves (e.g., the first sound) and at the termination by the opening of the semilunar valves.

At the end of this period, the semilunar valves open and the ejection period starts. (0.25 sec.). During this period, blood is expelled from the ventricles—from the left ventricle into the systemic aorta, from the right into the pulmonary trunk. In the first part of this period (0.11 sec.) the outflow is very rapid.

Hence, it is known as the maximum ejection period (Fig. 7.46). In the last part (0.14 sec.) the rate of outflow slows down.

Hence, it is called the reduced ejection period (Fig. 7.47). Here, the ventricular systole ends and diastole begins.

Let us Follow the Outer Ring Further:

It will be seen that after the three shaded divisions, come the five clear divisions—representing the duration of ventricular diastole (0.5 sec.). As soon as ventricles relax, the intraven­tricular pressure starts falling. The blood columns in the aorta and pulmonary trunk try to roll back towards ventricles but are stopped by the sharp closure of the semilunar valves. This produces the second sound of heart. Thus the onset of ventricular systole is marked by the first sound and its termination by the second sound (approximately).

On comparing the two rings, it will be seen that the last one division (0.1 sec.) of ventricular diastole is overlapped by atrial systole. In other words, when atria are contracting, the ventricles are still in diastole and are having the last part of their filling. It will be seen further that the first four divisions of ventricular diastole coincide with the corresponding four divisions of the atrial diastole.

From this we can come to another fundamental rule of cardiac action that—the diastole of the two chambers will always partly overlap. In the left half of the Fig. 7.43 un-shaded division will be found. In other words, both the chambers are in diastole here. This is called the diastole of the whole heart (0.4 sec.).

Let us again follow the ventricular diastole on the outer ring. As mentioned above, the second sound occurs at the end of ventricular systole. But this statement is not exact, because, till the falling of intraventricular pressure goes below the intra-aortic pressure, the semilunar valves will not close.

Consequently, there will be a short interval between the onset of diastole and the closure of the semilunar valves (i.e., the second sound). This period is called the protodiastolic period (0.04 sec.). From this it is clear that the second sound does not occur just at the end of ventricular systole but a little afterwards (i.e., after the protodiastolic period).

Although the semilunar valves have closed, yet the A.V. valves are still not open. Because, the falling intraventricular pressure takes a little time to go below that of the atria, so that the A.V. valves may open. Consequently, there will be a brief interval during which both the valves remain closed and ventricles are relaxing as closed cavities. Since no blood enters the ventricles there will be no lengthening of cardiac muscle fibres. Owing to this, it is called the isometric relaxation period (0.08 sec.—Fig. 7.48).

At the end of isometric relaxation period, the A.V. valves open. Blood rushes into the ventricles and ventricular filling begins. The first part of this period is known as the first rapid filling phase (0.113 sec.). Because, as soon as the A.V. valves open, blood accumulating so long in the atria, rushes in to the ventricles.

The steep fall of the intraventricular pressure during the isometric relaxation period, make the inflow all the more intense. Although the duration is brief yet the largest part of ventricular filling takes place during it. Due to rapid rush of blood a sound is produced, known as the third sound of heart (Fig. 7.49).

In the next phase of diastole, the rate of filling slows down. The ventricles are already full to a large extent and ventricular pressure slowly rises. Consequently, the rate of inflow from the atria will be gradually slower. This period is called diastasis or slow inflow phase (0.167 sec.).

Although this is the longest phase of ventricular diastole, yet the amount of filling during this period is minimum. If one looks into the heart (Fig. 7.50) during this time, one will find that, the whole atrioventricular canal contains a continuous column of blood, more or less stagnant, in which the cusps of the A.V. valves are passively floating. After this period comes the last part of ventricular diastole represented by the last un-shaded division on the outer ring.

It is obvious that this phase corresponds with atrial systole. Due to atrial contraction, blood rushes into the ventricles and ventricular filling again becomes rapid. This phase—the last rapid filling phase (0.1 sec.) is responsible for the last part of ventricular filling. Due to rapid rush of blood, again a sound is produced—known as the fourth sound of heart.

Thus the onset of filling period is marked by the third sound and its termination by the fourth sound. Here the ventricular diastole ends. They are completely filled up, the impulse from the S.A. node arrives in the meantime and the ventricles plunge into systole again. Thus the cycle goes on.

Summary of the Sequence of Events in Cardiac Cycle :

The atrial systole is the first event (0.1 sec.). It initiates the cardiac cycle, because the pacemaker S.A. node is situated here. Due to higher atrial pressure, the first half of atrial systole is stronger than that of the last half. After systole comes the atrial diastole (0.7 sec.). These two alternately follow each other and constitute the atrial cycle (0.8 sec.).

Just after the atrial systole, the ventricular systole (0.3 sec) begins and is immediately followed by its diastole (0.5 sec.). These two events repeat alternately and make up the ventricular cycle (0.8 sec.).

At the onset of ventricular systole, the A.V. valves close producing the first sound. The semilunar valves open a little later. The interval between the closing of the A.V. valves and opening of the semilunar valves is called the isometric contraction period (0.05 sec.). During this period ventricles contract as closed cavities and intraventricular pressure steeply rises.

After this phase, comes the ejection period—when blood is pumped out of the ventricles. The first part of this period, when the outflow is very rapid, is called the maximum ejection period (0.11 sec.). The second part, when the rate of flow slows down, is known as the reduced ejection period (0.14 sec.). Here, ventricular systole ends and diastole begins.

At the beginning of ventricular diastole, the semilunar valves close producing the second sound. There is a brief interval between the beginning of diastole and the closure of the semilunar valves—known as the protodiastolic period (0.04 sec.). So that, second sound occurs actually after this period.

The A.V. valves open a little after the closing of the semilunar valves. The interval between these two is called the isometric relaxation period (0.08 sec.). During this period ventricle relax as closed cavities and intraventricular pressure steeply falls. At the end of this period, the intraventricular pressure goes below that of the atria and the A.V. valves open. Atrial blood rushes into the ventricles—producing the third sound.

Here, ventricular filling begins. The first part of filling is very rapid, being known as the first rapid filling phase (0.113 sec.). The maximum filling takes place during this brief period. The intermediate part of filling is very slow and is known as diastasis or slow inflow phase. Although this is the longest phase (0.167 sec.), yet the amount of filling is minimum.

The last part of diastole corresponds with atrial systole. Due to active contraction of the atria, filling becomes very rapid. This last rapid filling phase (0.1 sec.), is responsible for the last part of ventricular filling. Due to rapid rush of blood, another sound is produced – the so-called fourth sound of heart. Here, ventricular diastole ends and systole commences again. In this way the cycle continues (Fig. 7.51).

Time Relations of the Various Events :

It has been noted that the cardiac cycle time is inversely proportional to heart rate. But all the phases of cardiac cycle do not proportionally vary. The duration of diastole varies much more than that of systole. For instance, with a rate of 120 per minute the cardiac cycle time will be 0.5 sec.

The systolic period will be reduced to 0.23 sec, and diastolic period to 0.27 sec. with a rate of 60 per minute the cycle time is 1 sec. Here, the systole will be 0.33 sec and diastole 0.67 sec. Thus when the rate rises from 60 to 120 per minute the systole diminishes only by 0.1 sec., whereas diastole diminishes by 0.4 sec. In other words, heart rate varies more at the expense of diastole than that of systole.

Summary of the Time Relations :

With 0.8 sec, as the cardiac cycle time (heart rate 75 per minute), the time relations of the various events are given in Table 7.2.

Related Articles:

• Cardiac Cycle: Meaning, Duration and Phases
• Pressure and Volume Changes in the Human Heart (With Diagram) | Biology

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