Hāʻaleʻale i ka puʻuwai.

A heart full to the brim [with love].

ʻŌlelo Noʻeau, compiled by Mary Kawena Pukui #392

Introduction

Figure 19.1: The Heart Computer Generated Cross Section 3d Model of Heart. Source: https://commons.wikimedia.org/wiki/User:DrJanaOfficial

Creative Commons Attribution-Share Alike 4.0

In this chapter, you will learn about the cardiovascular system. This system is composed of the heart and blood vessels. The heart is a pump that propels the blood into the vessels. The contraction of the heart develops the pressure that ejects blood into the major vessels: the aorta and pulmonary trunk. From these vessels, the blood is distributed to the remainder of the body. In addition to the heart, the cardiovascular system has three categories of blood vessels. These are: arteries that take blood away from the heart towards other parts of the body; veins that bring blood towards the heart and; capillaries, which are areas where gas, nutrient, and waste exchange occurs.

Function of the Cardiovascular System

The main function of the cardiovascular system is to circulate blood throughout the body to meet the demands of body cells. To keep the homeostasis of our bodies, we need to have a constant delivery of nutrients and oxygen to our cells and at the same time, the removal of wastes, such as carbon dioxide, from our cells. If one assumes an average rate of contraction of 75 contractions per minute, a human heart will 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 of 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.

19.1 Anatomy of the Heart

Mediastinum

The human heart is located within the thoracic cavity, medially between the lungs in an area 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 called 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 lies below 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. This area localized in the superior surface of the heart is called the base. The base of the heart is located at the level of the third costal cartilage, as seen in Figure X. The inferior conical end of the heart, known as 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 located more anteriorly, and the left side is deflected posteriorly. 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. 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.

Figure 19.2 Position of the Heart in the Thorax: The heart is located within the thoracic cavity, medially between the lungs in the mediastinum. It is about the size of a fist, is broad at the top, and tapers toward the base. OpenStax A&P Textbook (Heart)

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. 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.

CPR

CPR or cardiopulmonary resuscitation is an emergency procedure that is applied when a person’s heart stops beating. This procedure consists of chest compressions with the flat portion of one hand on the sternum in the area between the line from vertebrae T4 and T9 [Figure 19.3]. This technique allows manual compression of the heart enough to push some of the blood within it into the pulmonary and systemic circuits. This technique aids in the maintenance of brain function. It is important to become familiar with the location of the hands because if they are placed too low on the sternum, the xiphoid process of the sternum could be pushed into the liver, and this could be fatal.

Figure 19.3 CPR Technique: If the heart should stop, CPR can maintain the flow of blood until the heart resumes beating. By applying pressure to the sternum, the blood within the heart will be squeezed out of the heart and into the circulation. Proper positioning of the hands on the sternum to perform CPR would be between the lines at T4 and T9. OpenStax A&P Textbook (Heart)

Components of the Pericardium

The heart is the center of the cardiovascular system [Figure 19.3]. The heart is enclosed in three layers, known as the pericardium. From the outermost to the innermost, these layers are:

The fibrous pericardium is made up of dense irregular connective tissue that encloses and protects the heart. This layer is attached to the diaphragm inferiorly and the pulmonary trunk and aorta superiorly.

The parietal layer of the serous pericardium is composed of simple squamous epithelium and areolar connective tissue that fuses to the fibrous pericardium. Forming a bag around the heart is the pericardial sac, which is composed of the fibrous pericardium and the parietal layer of the serous pericardium. This sac helps secure the heart within the thoracic cavity.

The visceral layer of the serous pericardium, which is also called the epicardium, is composed of simple squamous epithelium and areolar connective tissue. This layer is fused to the heart. The parietal and visceral layers are continuous to one another and separated by the pericardial cavity that is filled with lubricating serous fluid. This oily fluid helps diminish friction as the heart contracts and expands. The Figure below illustrates the layers of the heart.

Figure 19.4 Pericardial Membranes and Layers of the Heart Wall: The pericardial membrane that surrounds the heart consists of three layers and the pericardial cavity. The heart wall also consists of three layers. The pericardial membrane and the heart wall share the epicardium. OpenStax A&P Textbook (Heart)

Layers of the Heart Wall

The wall of the heart is composed of three layers of unequal thickness. From the outermost to the innermost, these layers are:

The epicardium or visceral layer of the serous pericardium is composed of simple squamous epithelium and areolar connective tissue.

The myocardium is the middle layer of the wall of the heart. This is the thickest layer and the contraction of this layer pumps blood through the heart and into the major arteries.

The endocardium covers the internal surface of the heart and the external surfaces of the heart valves. It is formed by simple squamous epithelium and areolar connective tissue, and it is continued with the endothelium that lines the blood vessels. The Figure above illustrates these layers of the heart.

Heart and Circulation

The heart pumps blood throughout the body. It is an organ with four chambers and it has two sides. The right side of the heart receives blood poor in oxygen and rich in carbon dioxide from the body and pumps it to the lungs. The left side of the heart receives blood rich in oxygen and poor in carbon dioxide from the lungs and pumps it to the rest of the body. The heart has four chambers. The smaller chamber, the atrium, receives blood and the larger chamber known as the ventricle, pumps blood. On the right side of the heart, there is the right atrium and the right ventricle and on the left side of the heart, we have the left atrium and left ventricle. There are two large trunks (also called arteries) attached to the superior region of the ventricles. These arteries are the pulmonary trunk which transports blood from the right ventricle away from the heart and the aorta which transports blood from the left ventricle away from the heart. Veins return blood to the atria of the heart. These veins are the superior vena cava which drains blood from the head, neck, and upper limbs, and the inferior vena cava which drains blood from the lower limbs and inferior portions of the trunk. Both vena cavae drain blood to the right atrium. The veins that drain blood from the lungs to the left atrium are called pulmonary veins. Note that the pulmonary veins carry blood that is rich in oxygen and poor in carbon dioxide.

There are valves within the heart. The right atrioventricular valve, also called the tricuspid, is found in between the right atrium and the right ventricle. The left atrioventricular valve, also called the bicuspid or mitral valve, is found in between the left atrium and the left ventricle. The pulmonary semilunar valve is localized in between the right ventricle and the pulmonary trunk. The aortic semilunar valve is found in between the left ventricle and the aorta. All these valves keep the blood moving in only one direction and then they close to prevent the backflow of blood. The Figure below illustrates the structures mentioned above.

Pulmonary circulation is the movement of blood from the right side of the heart to the lungs, and back to the left side of the heart. Blood rich in carbon dioxide and poor in oxygen is transported from the right side of the heart to the lungs where gas exchange occurs. Oxygen moves from the alveoli in the lungs into the blood, and carbon dioxide goes from the blood to the alveoli. Blood rich in oxygen is returned to the left side of the heart.

Systemic circulation is the movement of blood from the left side of the heart to the systemic cells of the body and then back to the right side of the heart. Blood rich in oxygen is moved from the left side of the heart to the systemic cells in different organs. Oxygen then moves from the blood to the systemic cells and carbon dioxide moves from the systemic cells into the blood. Blood rich in carbon dioxide and poor in oxygen is returned to the right side of the heart. The blood vessels are the conduit for the transportation of blood in both circulations. Please keep in mind that coronary circulation is part of the systemic circulation, and we will be taking a closer look at it. [Figure 19.4] shows the path of the blood in the pulmonary and systemic circulations.

Figure 19.5 Dual System of the Human Blood Circulation: Blood flows from the right atrium to the right ventricle, where it is pumped into the pulmonary circuit. The blood in the pulmonary artery branches is low in oxygen but relatively high in carbon dioxide. Gas exchange occurs in the pulmonary capillaries (oxygen into the blood, carbon dioxide out), and blood high in oxygen and low in carbon dioxide is returned to the left atrium. From here, blood enters the left ventricle, which pumps it into the systemic circuit. Following exchange in the systemic capillaries (oxygen and nutrients out of the capillaries and carbon dioxide and wastes in), blood returns to the right atrium and the cycle is repeated.OpenStax A&P Textbook (Heart)

Superficial Features of the Heart

Anterior View

In this view, we can see the following structures:

• Right atrium
• Left ventricle
• A flaplike extension on the surface of the right atrium called the right auricle
• Left auricle on the surface of the left atrium
• Left ventricle
• Pulmonary trunk
• Right and left pulmonary arteries (pulmonary trunk splits into these arteries)
• Aorta
• Ascending aorta (extending superiorly from the heart)
• Aortic arch
• Descending aorta (extending inferiorly)

Posterior View

In this view, we can see the following structures:

• Left atrium
• Left ventricle
• Superior vena cava
• Inferior vena cava
• Pulmonary veins

Surface Features of the Heart

The coronary sulcus is a groove that separates the atria from the ventricles and it can be viewed in the anterior and posterior views of the heart. The groove between the ventricles is known as the interventricular sulcus. The anterior interventricular sulcus is found on the anterior side of the heart and the posterior interventricular sulcus is found on the posterior side of the heart. Coronary vessels are localized within these sulci and they supply blood to the heart wall and therefore are part of the systemic circulation. Please see [Figure 19.6] with all the structures for the anterior and posterior views of the heart.

Figure 19.6 External Anatomy of the Heart: Inside the pericardium, the surface features of the heart are visible. OpenStax A&P Textbook (Heart)

Heart Chambers

The right and left atrial chambers are divided by the interatrial septum, and the right and left ventricles are separated by the interventricular septum. [Figure 19.7] shows the internal structures of the heart.

Right Atrium

The wall of the right atrium has muscular ridges called pectinate muscles. The fossa ovalis is an oval depression that replaces the former location of the foramen ovale, a hole responsible for shunting blood from the right atrium to the left atrium, bypassing the lungs in the fetus. Inferiorly to the fossa ovalis is the coronary sinus that drains blood poor in oxygen from coronary circulation. The openings for the superior and inferior vena cavae can be seen as well. The right atrioventricular valve separates the right atrium from the right ventricle. Blood poor in oxygen flows from the right atrium to the right ventricle when the valve is open.

Figure 19.8 Internal Structures of the Heart: This anterior view of the heart shows the four chambers, the major vessels and their early branches, as well as the valves. The presence of the pulmonary trunk and aorta covers the interatrial septum, and the atrioventricular septum is cut away to show the atrioventricular valves. OpenStax A&P Textbook (Heart)

Right Ventricle

Within the surface wall of the right ventricle, we can see smooth muscular ridges, known as trabeculae carneae. Muscular projections with a shape of a cone, called papillary muscles, anchor strands of fibers called tendinous cords or chordae tendineae. These strands are made up of collagen fibers and attach to the three cusps of the right atrioventricular valve preventing them from prolapsing backward when the valve closes. The pulmonary semilunar valve is found in between the right ventricle and the pulmonary trunk. Blood poor in oxygen is pumped from the right ventricle to the pulmonary trunk via the pulmonary semilunar valve. From there, blood flows to the lungs for gas exchange and comes back to the left atrium via the pulmonary veins.

Left Atrium

Pectinate muscles are also found in the auricle of the left atrium. The openings for the pulmonary veins can also be seen here. The left atrioventricular valve is found in between the left atrium and left ventricle. Blood rich in oxygen moves from the left atrium into the left ventricle when the valve is open.

Left Ventricle

On the surface wall of the left ventricle, we can see smooth muscular ridges, known as trabeculae carneae. Muscular projections with a shape of a cone, called papillary muscles, anchor strands of fibers called tendinous cords or chordae tendineae that anchor the two cusps of the left AV valve. We can see the aorta at the superior region of the left ventricle. The aortic semilunar valve can be found in between the left ventricle and the ascending aorta. Blood rich in oxygen is pumped from the left ventricle to the aorta via the aortic semilunar valve.

The wall of the left ventricle is much thicker than the wall of the right ventricle. The reason for that is that the left ventricle must generate a lot more pressure to pump the blood through the systemic circulation. In comparison, the right ventricle only has to pump blood to the neighboring lungs and there is much less resistance to blood flow through the pulmonary circuit. This is a good example of how form (anatomy) meets function (physiology). [Figure 19.9] shows the differences in muscular thickness needed for each of the ventricles.

Figure 19.9 Differences in Ventricular Muscle Thickness: The myocardium in the left ventricle is significantly thicker than that of the right ventricle. Both ventricles pump the same amount of blood, but the left ventricle must generate a much greater pressure to overcome greater resistance in the systemic circuit. The ventricles are shown in both relaxed and contracting states. Note the differences in the relative size of the lumens, the region inside each ventricle where the blood is contained. OpenStax A&P Textbook (Heart)

Heart Valves

The heart valves are the atrioventricular valves and the semilunar valves. These valves ensure a one-way direction of the flow of the blood [Figure 19.10].

Atrioventricular Valves

Localized in between the right atrium and the right ventricle is the right atrioventricular valve. This valve has three cusps and is therefore called the tricuspid valve. Localized in between the left atrium and the left ventricle is the left atrioventricular valve. This valve has two cusps and is therefore called the bicuspid valve. Due to a resemblance to the headdress of bishops, this valve is also named the mitral valve. When the valves are open, their cusps extend into the ventricles, allowing blood to flow from the atria to the ventricles. With the contraction of the ventricles, the pressure increases, and the blood is forced back, resulting in the closure of the atrioventricular valves, which prevents the backflow of blood into the atria. The papillary muscles help secure the chordae tendineae attaching to each of the cusps of the atrioventricular valves to prevent prolapse of the valves back into the atria which would allow regurgitation of blood backward into the atria.

Semilunar Valves

Located between the right ventricle and the pulmonary trunk is the pulmonary semilunar valve. Another valve, the aortic semilunar is found in between the left ventricle and the ascending aorta. Each of the semilunar valves has three cups with a shape of a half-moon. These valves do not have tendinous cords or papillary muscles. These valves open when the ventricles contract and the increased pressure forces the blood to the semilunar valves, resulting in their opening. Blood flows into the arterial trunks. When the ventricles relax, the valves close, and the pressure within the ventricles becomes less when compared to the pressure in the arterial trunks. At this moment, blood in the arteries flows back towards the ventricles and gets held in the cusps of the semilunar valves forcing the valves to close thus preventing regurgitation backward into the ventricles. [Figure 19.10] shows that with the atria and major vessels removed, all four valves are visible, although it is difficult to distinguish the three separate cusps of the tricuspid valve.

Figure 19.10 Heart Valves: With the atria and major vessels removed, all four valves are clearly visible, although it is difficult to distinguish the three separate cusps of the tricuspid valve. OpenStax A&P Textbook (Heart)

Fibrous Skeleton

The fibrous skeleton supports the heart and is made up of dense irregular connective tissue. The functions of this skeleton are:

• Give support to the limits between the atria and the ventricles
• Help to support and anchor the heart valves
• Work as an electric insulator, preventing action potentials from going from the atria to the ventricles, in a direct way. As a result, the ventricles do not contract at the same time as the atria.

[Figure 19.11] shows the arrangement of the muscle cells that form spiral bundles around the chambers of the heart that attach to the fibrous skeleton. The muscle cells form a figure 8 pattern around the atria and the bases of the great vessels. Deeper ventricular muscles also form a figure 8 around the two ventricles and proceed toward the apex. This swirling pattern of the fibers allows the heart to pump blood more effectively. When the ventricles contract, the action starts at the apex of the heart and moves superiorly, pushing the blood into the great arteries.

Figure 19.11 Heart Musculature: The swirling pattern of cardiac muscle tissue contributes significantly to the heart’s ability to pump blood effectively. OpenStax A&P Textbook (Heart)

Coronary Circulation

The coronary circulation ensures that the heart receives the needed nutrients and oxygen to keep pumping blood through its chambers [Figure 19.12]. The reason that the heart has this complex circulation is that the heart wall is too thick and does not allow the diffusion of oxygen and nutrients to the heart. Coronary circulation is not continuous though. This is because the coronary vessels are open when the heart muscle is relaxing and the flow of blood occurs. When the heart contracts, the coronary vessels are compressed, which momentarily stops the flow of blood. The coronary arteries transport blood rich in oxygen to the muscle of the heart. The coronary veins transport blood poor in oxygen away from the muscle of the heart. Please see the Figure below to see the coronary circulation. Within the coronary sulcus, we have the right and left coronary arteries that branch directly off the base of the aorta. The right coronary artery branches into the right marginal artery that supplies the lateral wall of the right ventricle. The other branch of the right coronary artery is the posterior interventricular artery which supplies the posterior wall of both ventricles. This artery is also known as the posterior descending (PD) artery. One of the branches of the left coronary artery is the circumflex artery which supplies the lateral wall of the left ventricle. The other branch is the anterior interventricular artery, also called the left anterior descending (LAD) artery which supplies the anterior area of the left ventricle. This artery is known as the widowmaker because if this artery is blocked, there is a high risk of a deadly heart attack.

The LAD 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 be effectively delivered to a region even if there may be a partial blockage in another branch. However, the anastomoses in the heart are very small to efficiently shunt blood. As a result, a sudden coronary artery blockage often leads to the death of the cells (myocardial infarction) supplied by the particular vessel. However, if the blockage builds up slowly the small anastomoses have time to expand sufficiently to take over blood flow. Usually, it takes several blockages to trigger a heart attack unless the blockage occurs suddenly.

Amongst the cardiac veins, we have the great cardiac vein that runs with the LAD; the middle cardiac vein that runs with the PD; the small cardiac vein that runs with the right marginal artery. All these veins drain into the coronary sinus, which is a large vein found within the posterior coronary sulcus. Blood rich in carbon dioxide and poor in oxygen flows back to the right atrium via the coronary sinus.

Figure 19.12 Coronary Circulation: The anterior view of the heart shows the prominent coronary surface vessels. The posterior view of the heart shows the prominent coronary surface vessels. OpenStax A&P Textbook (Heart)

19.2 Cardiac Muscle

When you are running the Honolulu Marathon or the ironman in Kona or your neighborhood, you can feel that your heart is beating fast when you exercise. Have you ever wondered why your heart can beat on its own? When compared to skeletal and smooth muscles, the cardiac muscle has some unique characteristics of its own. One of them is the ability of the cardiac muscle to initiate an electrical potential that spreads rapidly from cell to cell to trigger the contractile mechanism. This property is known as autorhythmicity. Neither smooth nor skeletal muscle has autorhythmicity. However, even though cardiac muscle has autorhythmicity, heart rate is still modulated by the endocrine and nervous systems.

There are two types of cardiac muscle cells: conducting (nodal) cells and contractile cells (cardiac muscle). The nodal cells represent one percent of the cardiac muscle cells and they are the autorhythmic fibers that form the conduction system of the heart. Their function is similar in many respects to neurons, although they are specialized muscle cells. The nodal cells initiate and propagate the action potential (the electrical impulse) that travels throughout the heart. The contractile cells constitute the bulk (99 percent) of the cardiac muscle cells in the atria and ventricles. After receiving the electric signal from the nodal cells, the contractile cells conduct impulses and undergo contractions that pump blood through the body. In the next section, we will learn about how the nodal cells and the contractile cells in the heart conduct different nerve impulses or action potentials.

Structure of Cardiac Muscle

Cardiac muscle cells are considerably shorter with much smaller diameters when compared to the skeletal muscle. Like skeletal muscle, cardiac muscle also demonstrates striations which appear as an alternating pattern of dark A bands and light I bands attributed to the precise arrangement of the myofilaments of sarcomeres that make up the fibrils along the length of the cell  [Figure 19.13a]. The sarcoplasmic reticulum (SR) stores fewer calcium ions than skeletal muscle, so most of the calcium ions must come from outside the cardiac cells. The result is a slower onset of contraction. Typically, cardiac muscle cells have a single nucleus, but two or more nuclei may be found in some cells. Mitochondria are plentiful, providing the needed energy for cardiac contractions.

Cardiac muscle cells branch freely. A junction between two adjoining cells is marked by a critical structure called an intercalated disc, which helps support the synchronized contraction of the muscle [Figure 19.13b]. The sarcolemma, which is the plasma membrane of the cardiac muscle cells, binds the cardiac myocytes together at the intercalated discs, which contain many strong desmosomes and gap junctions that allow the passage of ions between the cells to help to synchronize the contraction [Figure 19.13c]. Intercellular connective tissue also helps to bind the cells together. The importance of strongly binding these cells together is necessitated by the forces exerted by contraction.

Figure 19.13 Cardiac Muscle: (a) Cardiac muscle cells have numerous mitochondria for energy and intercalated discs that are found at the junction of different cardiac muscle cells. (b) A photomicrograph of cardiac muscle cells shows the nuclei and intercalated discs. (c) An intercalated disc connects cardiac muscle cells and consists of desmosomes and gap junctions. LM × 1600. (Micrograph provided by the Regents of the University of Michigan Medical School © 2012) OpenStax A&P Textbook (Heart)

Conduction System of the Heart

The reason why the heart beats on its own is because of the cardiac conduction system. The conduction system includes the sinoatrial node, the atrioventricular node, the atrioventricular bundle, the atrioventricular bundle branches, and the Purkinje cells [Figure 19.13]. These nodal cells form a relay system to make sure that the cardiac chambers become stimulated to contract in a coordinated way. Without this coordination, the heart would not be able to pump blood effectively.

Figure 19.14 Conduction System of the Heart: Specialized nodal components of the heart include the sinoatrial node, the atrioventricular node, the atrioventricular bundle, the right and left bundle branches, and the Purkinje fibers. OpenStax A&P Textbook (Heart)

Sinoatrial (SA) Node

Cardiac rhythm is established by the sinoatrial (SA) node, a specialized clump of nodal cells located in the superior and posterior walls of the right atrium near the opening of the superior vena cava [see Figure 19.15]. The SA node is known as the natural pacemaker of the heart because it has the highest inherent rate of depolarization when compared to the other nodal cells. The SA node initiates a nerve impulse about every 0.6 seconds which is about 100 times per minute. It initiates the sinus rhythm or electrical pattern followed by the contraction of the heart. You may wonder why a normal heart at rest does not beat 100 times per minute and this will be discussed in the section on the regulation of heart rate.

This impulse spreads from its initiation in the SA node to the atria through specialized internodal pathways. These pathways lead the SA node to the atrioventricular node and the contractile cells of the atria [see Figure 19.15 steps 1 to 3]. The impulse takes approximately 50 ms (milliseconds) to travel between these two nodes. As the impulse reaches the atrioventricular septum, the connective tissue of the cardiac fibrous skeleton prevents the impulse from spreading into the myocardial cells in the ventricles, except at the atrioventricular node. What happens next is that the atria then begin contraction and efficiently pump blood into the ventricles.

Figure 19.15 Cardiac Conduction: (1) The sinoatrial (SA) node and the remainder of the conduction system are at rest. (2) The SA node initiates the action potential, which sweeps across the atria. (3) After reaching the atrioventricular node, there is a delay of approximately 100 ms that allows the atria to complete pumping blood before the impulse is transmitted to the atrioventricular bundle. (4) Following the delay, the impulse travels through the atrioventricular bundle and the bundle branches to the Purkinje fibers and reaches the right papillary muscle via the moderator band. (5) The impulse spreads to the contractile fibers of the ventricle. (6) Ventricular contraction begins. OpenStax A&P Textbook (Heart)

Atrioventricular (AV) Node

The atrioventricular (AV) node is the second set of specialized nodal cells, located in the inferior portion of the right atrium within the atrioventricular septum. The septum prevents the impulse from spreading directly to the ventricles without passing through the AV node. There is a critical pause before the AV node depolarizes and transmits the impulse to the atrioventricular bundle [see Figure 19.15, step 3]. This delay in transmission is partially attributable to the small diameter of the cells of the node, which slows the impulse. This pause is critical to heart function, as it allows the atrial cardiac muscle the time needed to complete the contraction that pumps blood into the ventricles before the impulse is transmitted to the cells of the ventricle itself.

Atrioventricular Bundle (Bundle of His), Bundle Branches, and Purkinje Fibers

Arising from the AV node, the atrioventricular bundle, or bundle of His, proceeds through the interventricular septum before dividing into two atrioventricular bundle branches, commonly called the left and right bundle branches. The left bundle branch supplies the left ventricle, and the right bundle branch the right ventricle. Since the left ventricle is much larger than the right, the left bundle branch is also considerably larger than the right. Both bundle branches descend and reach the apex of the heart where they connect with the Purkinje fibers [see Figure 19.15, step 4]. This passage takes approximately 25 ms.

The Purkinje fibers are additional nodal fibers that spread the impulse to the myocardial contractile cells (cardiac muscle) in the ventricles. They extend throughout the myocardium from the apex of the heart toward the atrioventricular septum and the base of the heart [see Figure 19.15, step 5]. Since the electrical stimulus begins at the apex, the contraction also begins at the apex and travels toward the base of the heart, similar to squeezing a tube of toothpaste from the bottom. This allows the blood to be pumped out of the ventricles and into the aorta and pulmonary trunk. The total time elapsed from the initiation of the impulse in the SA node until depolarization of the ventricles is approximately 225 ms.

Pacemaker potentials

Comparative Rates of Conduction System Firing

All of these nodal cells can start the nerve impulses; however, they differ in the number of impulses that they send out each minute. The SA node is the natural pacemaker where it initiates a heart impulse approximately 80–100 times per minute. After the SA node, the rate progressively slows as it proceeds to the Purkinje fibers. Without the SA node, the AV node would generate a heart rate of 40–60 beats per minute. If the AV node were blocked, the atrioventricular bundle would fire at a rate of approximately 30–40 impulses per minute. The bundle branches would have an inherent rate of 20–30 impulses per minute, and the Purkinje fibers would fire at 15–20 impulses per minute. Towards the end of the chapter, we will learn about the patients having irregular heartbeats which are known as arrhythmias. Sometimes, arrhythmias are related to a defect in the conduction system of the heart.

Action Potential of the Cardiac Nodal Cell and Contractile Cells (Cardiac Muscle)

Now that we learn about the conduction system of the heart. Let’s look at how the cardiac nodal cells start their action potential (nerve impulses). First, recall that a cell’s resting membrane potential refers to the relative difference in charge between the inside and the outside of the cell when unstimulated. A resting potential of -60 mV indicates that the inside of the cells is more negatively charged at rest when compared to the positively charged environment outside the cells. This sets up the different “poles” across the cell membrane. Note that the cardiac contractile cells (cardiac muscles) also conduct action potential and we will take a closer look at it in the next section. The action potentials are considerably different between cardiac nodal cells and cardiac contractile cells (cardiac muscle).

Action Potential of the Nodal Cells

Unlike skeletal muscles and neurons, cardiac nodal cells do not have a stable resting potential. The nodal cells contain a series of sodium ion channels that allow a normal and slow influx of sodium ions into the cells. When the positively charged sodium ions enter cells, the membrane potential rises slowly from an initial value of −60 mV up to about –40 mV [see Figure 19.16]. The resulting movement of sodium ions entering cells creates spontaneous depolarization. At this point, calcium ion channels open and Ca2+ enters the cell, further depolarizing it at a more rapid rate until it reaches a value of approximately +15 mV. At this point, the calcium ion channels close, and K+ channels open, allowing outflux of positively charged K+ and resulting in repolarization. When the membrane potential reaches approximately −60 mV, the K+ channels close and Na+ channels open, and the prepotential phase begins again. This phenomenon explains the autorhythmicity properties of cardiac muscle.

Figure 19.16 Action Potential at the SA Node: The prepotential is due to a slow influx of sodium ions until the threshold is reached followed by a rapid depolarization and repolarization. The prepotential accounts for the membrane reaching the threshold and initiates the spontaneous depolarization and contraction of the cell. Note the lack of resting potential. OpenStax A&P Textbook (Heart)

Action Potential of Cardiac Contractile Cells (Cardiac Muscle)

There is a distinctly different electrical pattern involving the cardiac contractile cells. The cardiac contractile cells do not initiate an action potential like the nodal cells. Instead, they wait for the nerve impulse from the nodal cells to reach them. Afterward, there is a rapid depolarization, followed by a plateau phase and then repolarization (see Figure 19.21). This phenomenon accounts for the long refractory periods required for the cardiac muscle to allow the sustained contraction necessary to pump blood effectively before they are capable of firing for a second time.

Cardiac contractile cells demonstrate a more stable resting membrane potential than nodal cells at approximately −80 mV for cells in the atria and −90 mV for cells in the ventricles. Despite this initial difference, the other components of their action potentials are virtually identical to the nodal cells. In both cases, when stimulated by an action potential, voltage-gated sodium channels rapidly open, beginning the process of depolarization. This rapid influx of positively charged Na+ raises the membrane potential to approximately +30 mV, at which point the sodium channels close. The rapid depolarization period typically lasts 3–5 ms. Depolarization is followed by the plateau phase, in which membrane potential declines relatively slowly. This is due in large part to the opening of the slow Ca2+ channels, allowing positively charged Ca2+ to enter the cell while few K+ channels are open, allowing K+ to exit the cell. The relatively long plateau phase lasts approximately 175 ms. Once the membrane potential reaches approximately zero, the Ca2+ channels close, and K+ channels open, allowing K+ to exit the cell. The repolarization lasts approximately 75 ms. At this point, membrane potential drops as the positively charged K+ leaves the cells. The entire event lasts between 250 and 300 ms [Figure 19.17]. The overall idea is that the ventricles receive the nerve impulse from the nodal cells. Then, the ventricles undergo contractions to pump the blood into the aorta and the pulmonary trunk where it reaches the rest of the body and the lungs, respectively.

In the cardiac muscles, the refractory period is defined as the interval where the second contraction cannot be triggered. The absolute refractory period for cardiac contractile muscle lasts approximately 200 ms, and the relative refractory period lasts approximately 50 ms, for a total of 250 ms. This extended period is critical since the heart muscle must contract to pump blood and relax before the next contraction. Without extended refractory periods, premature contractions would occur in the heart and would not be compatible with life.

Figure 19.17 Action Potential in Cardiac Contractile Cells: (a) Note the long plateau phase due to the influx of calcium ions. The extended refractory period allows the cell to fully contract before another electrical event can occur. (b) The action potential for heart muscle is compared to that of skeletal muscle. OpenStax A&P Textbook (Heart)

Electrocardiogram (ECG)

Have you ever gone to your doctor and gotten an ECG done during a checkup? When action potentials travel through the heart, electrical signals are generated. Since our bodies are made up of a significant amount of water, electrical signals pass through them. By careful placement of surface electrodes on the skin, it is possible to record the complex electrical signals of the heart. This tracing of the electrical signal is the electrocardiogram (ECG), also commonly abbreviated EKG (K meaning kardiology, the German term for cardiology). You can think of the ECG as the overall electrical signal from the action potentials that initiate the cardiac contraction.

Careful analysis of the ECG reveals a detailed picture of heart function, and it is an important clinical diagnostic tool for identifying abnormal heart function. The standard electrocardiograph (the instrument that generates an ECG) uses 3, 5, or 12 leads. The greater the number of leads an electrocardiograph uses, the more information the ECG provides. For example, with a 3-lead ECG you can see the overall electrical pattern of the heart but with a 12-lead ECG you get the electrical information from specific regions of the heart. The 12-lead electrocardiograph uses 10 electrodes placed in standard locations on the patient’s skin [Figure 19.17]. The term “lead” may be used to refer to the cable from the electrode to the electrical recorder, but it typically describes the voltage difference between two of the electrodes. In continuous ambulatory (with the patient walking around freely) electrocardiographs, the patient wears a small, portable, battery-operated device known as a Holter monitor, that continuously monitors heart electrical activity, typically for 24 hours during the patient’s normal routine [Figure 19.18].

Standard Placement of ECG Leads In a 12-lead ECG	Holter Monitor

Figure 19.18 a) Standard Placement of ECG Leads In a 12-lead ECG (left). Six electrodes are placed on the chest, and four electrodes are placed on the limbs. (b) Holter Monitor from Wikimedia.

Normal ECG and Interpretation

In a normal ECG, there are three prominent waves: the P wave, the QRS complex, and the T wave. The P wave represents atrial depolarization where Na+ is entering the cells. Then the atria begin contracting which usually happens about 25 ms after the start of the P wave. The QRS complex represents ventricular depolarization, which generates a much stronger electrical signal due to the much larger size of the ventricles. Following the QRS complex is the contraction of the ventricles. Lastly, the T wave represents ventricular repolarization. You might wonder if the atria undergo repolarization, and the answer is yes. However, atrial repolarization occurs during the QRS complex, which masks it on an ECG.

When reading the ECG, the size of the waves, segments, and intervals can provide clues about one’s heart function. Segments are defined as the regions between two waves. Intervals include one segment plus one or more waves. For example, a larger P wave could indicate an enlargement of the atria as it takes longer for the atrial depolarization to occur whereas an enlarged R wave may indicate ventricular enlargement. The PR segment begins at the end of the P wave and ends at the start of the QRS complex. This is known as the baseline or reference line of the ECG. The PR interval starts at the beginning of the P wave and ends with the beginning of the QRS complex. The PR interval is more clinically relevant, as it measures the duration from the beginning of atrial depolarization (the P wave) to the initiation of the QRS complex. The PR interval value can indicate if the transmission from the atria to ventricles is normal. Should there be a delay in the passage of the impulse from the SA node to the AV node, it would be visible in the PR interval [Figure 19.19]. The QRS duration is the time duration from the start to the end of the QRS complex. A short QRS complex signals rapid depolarization of the ventricles which reflects a normal nodal system. A wider QRS complex may indicate that ventricular depolarization is slow and there are disturbances in the conduction system. The QT interval reflects the duration from the start of the QRS complex (ventricular depolarization) to the end of the T wave (ventricular repolarization). This may be lengthened if there are conduction abnormalities, myocardial damage, or myocardial ischemia (decrease blood flow) in the heart.

Figure 19.19 Electrocardiogram: A normal tracing shows the P wave, QRS complex, and T wave. Also indicated are the PR, QT, QRS, and ST intervals, plus the P-R and S-T segments. OpenStax A&P Textbook (Heart)

19.3 The Cardiac Cycle

In the previous sections, we learned about the heart chambers, the cardiac conduction system, and how an action potential is propagated. Now, look at all the events that occur in a single heartbeat.

Pressures and Flow

Fluids, whether gases or liquids, are materials that flow according to pressure gradients—that is, they move from regions that are higher in pressure to regions that are lower in pressure. Accordingly, when the heart chambers are relaxed (diastole), blood will flow into the atria from the veins, which are higher in pressure  [Ventricular and atrial diastole; Figure 19.20]. As blood flows into the atria, the pressure will rise, so the blood will initially move passively from the atria into the ventricles. When the action potential triggers the muscles in the atria to contract (atrial systole), the pressure within the atria rises further, pumping blood into the ventricles [Atrial systole; Figure 19.20]. During ventricular systole, pressure rises in the ventricles, pumping blood into the pulmonary trunk from the right ventricle and into the aorta from the left ventricle [Ventricular systole; Figure 19.20]. Again, as you consider this flow and relate it to the conduction pathway, the elegance of the system should become apparent.

Figure 19.20 Overview of the Cardiac Cycle: The cardiac cycle begins with atrial systole and progresses to ventricular systole, atrial diastole, and ventricular diastole, when the cycle begins again. Correlations to the ECG are highlighted. OpenStax A&P Textbook (Heart)

Phases of the Cardiac Cycle

The period that begins with contraction of the atria and ends with ventricular relaxation is known as the cardiac cycle [Figure 19.21]. The period of contraction that pumps blood into circulation is called systole. The period of relaxation that occurs as the chambers fill with blood is called diastole. The atria and ventricles each undergo systole and diastole which are coordinated to ensure blood is efficiently pumped to the body.

At the beginning of the cardiac cycle, both the atria and ventricles are relaxed (diastole) [Figure 19.21, step 1]. Blood is flowing into the right atrium from the coronary sinus and superior and inferior venae cavae. If you recall, fluids flow according to pressure gradients from regions of higher to lower pressures. When the heart chambers are relaxed (diastole), blood will flow from the veins into the atria following the pressure gradient. At this time the two atrioventricular valves (the tricuspid and mitral valves) are both open, so blood flows unimpeded from the atria into the ventricles. This is called the ventricular filling phase and approximately 70–80 percent of ventricular filling occurs this way. The two semilunar valves (the pulmonary and aortic valves) are closed during this period. Now, let’s take a closer look at the systolic and diastolic phases of the atria and ventricles.

Figure 19.21 ECG Tracing Correlated to the Cardiac Cycle: This diagram correlates an ECG tracing with the electrical and mechanical events of a heart contraction. Each segment of an ECG tracing corresponds to one event in the cardiac cycle. OpenStax A&P Textbook (Heart)

Atrial Systole and Diastole

The atrial systole (atrial contraction) phase follows atrial depolarization which is represented by the P wave of the ECG [Figure 19.21, step 2]. As the atrial muscles contract from the superior portion of the atria toward the atrioventricular septum, pressure rises within the atria, and blood is pumped into the ventricles through the open atrioventricular valves. Atrial contraction, also referred to as the “atrial kick,” contributes about 25 mL and completes ventricular filling [Figure 19.21, step 3]. Atrial systole lasts approximately 100 ms and ends before ventricular systole.

Ventricular Systole

Ventricular systole or ventricular contraction follows the depolarization of the ventricles represented by the QRS complex in the ECG [Figure 19.21, step 4]. It lasts about 270 ms. At the end of atrial systole, before ventricular systole, the ventricles contain approximately 130 mL of blood. This volume is known as the end-diastolic volume (EDV) or preload.

Initially, as ventricle muscles contract, the pressure of the blood within the chamber rises. This increase in pressure causes the tricuspid and mitral valves to close. Blood is not being ejected from the ventricles at this early stage of systole and, therefore, the volume of blood within the chamber remains constant. Consequently, this phase of the ventricular systole is known as the isovolumetric contraction phase [Figure 19.21, step 5].

In the second phase of systole, the ventricular ejection phase, contraction causes chamber pressure to exceed the pressure in the pulmonary trunk and the aorta. This opens the pulmonary and aortic semilunar valves allowing the blood to be pushed out. The pressure generated by the left ventricle is much greater than the right ventricle. This is necessary for the left ventricle to overcome the existing pressure in the aorta. Nevertheless, both ventricles pump the same amount of blood. This quantity is referred to as stroke volume. Stroke volume will normally be in the range of 70–80 mL, which means there is 50–60 mL of blood remaining in each ventricle following contraction. This volume of blood is known as the end-systolic volume (ESV).

Ventricular Diastole

Ventricular relaxation, or ventricular diastole, follows the repolarization of the ventricles and is represented by the T wave of the ECG [Figure 19.21, step 6]. Ventricular relaxation is also divided into two distinct phases and lasts approximately 430 ms.

During the early phase of ventricular diastole, ventricular muscles relax and chamber pressure falls. When pressure within the ventricles drops below the pulmonary trunk and aorta, blood flows back toward the heart. This produces the dicrotic notch (small dip) seen in blood pressure tracings. The backflow of blood closes the semilunar valves which prevent backflow into the heart itself. Since the atrioventricular valves remain closed at this point, there is no change in the volume of blood in the ventricle, so the early phase of ventricular diastole is called the isovolumetric relaxation phase.

In the second phase of ventricular diastole, called late ventricular diastole, ventricular muscle continues to relax, and pressure drops even further. Eventually, the pressure is lower than in the atria. When this occurs, blood flows from the atria into the ventricles by pushing open the tricuspid and mitral valves. At this point, all chambers are in diastole and while the atrioventricular valves are open the semilunar valves remain closed. This is the return of the ventricular filling phase. One cardiac cycle lasts about 0.8 seconds and then it repeats as long as you live. The following figure illustrates the correlations between the cardiac cycle and the ECG, heart sounds, changes in pressure of the left atria and left ventricles, and changes in the left ventricle volume.

Heart Sounds

Do you remember the time when your doctor used a stethoscope to listen to your heart sounds during a health checkup? Auscultation is one of the simplest diagnostic techniques to assess the state of a patient’s heart. In a normal, healthy heart, there are only two audible heart sounds: S1 and S2. S1 is the sound created by the closing of the atrioventricular valves during ventricular contraction and is normally described as a “lub,” or the first heart sound. The second heart sound, S2, is the sound of the closing of the semilunar valves during ventricular diastole and is described as a “dub” [Figure 19.22]. In both cases, as the valves close and the openings shrink, blood flow becomes turbulent. Sometimes third and fourth heart sounds, S3 and S4, can be heard but are rarely heard in healthy individuals. S3 may be the sound of blood flowing into the atria, or blood sloshing back and forth in the ventricle, or even tensing of the chordae tendineae. If the sound is heard later in life, it may indicate congestive heart failure, warranting further tests. S4 is heard from the contraction of the atria pushing blood into a stiff or hypertrophic ventricle, indicating failure of the left ventricle.

Figure 19.22 Heart Sounds and the Cardiac Cycle: In this illustration, the x-axis reflects time with a recording of the heart sounds. The y-axis represents pressure. OpenStax A&P Textbook (Heart)

The term heart murmur is used to describe an unusual sound coming from the heart that is caused by the turbulent flow of blood. Murmurs are graded on a scale of 1 to 6, with 1 being the most common, the most difficult sound to detect, and the least serious. The most severe is a 6. During auscultation, it is common practice for the clinician to ask the patient to breathe deeply. This procedure not only allows for listening to airflow but may also amplify heart murmurs. Inhalation increases blood flow into the right side of the heart and may increase the amplitude of right-sided heart murmurs. Expiration partially restricts blood flow into the left side of the heart and may amplify left-sided heart murmurs.  [Figure 19.23] indicates the proper placement of the bell of the stethoscope to facilitate auscultation and assessment of each valve.

Figure 19.23 Stethoscope Placement for Auscultation: Proper placement of the bell of the stethoscope facilitates auscultation. At each of the four locations on the chest, a different valve can be heard. OpenStax A&P Textbook (Heart)

Arrhythmias

Arrhythmias refers to the unusual rhythm of heartbeats where the heart is beating too slowly, too quickly, or irregularly. The symptoms may include fainting, chest pains, shortness of breath, lightheadedness, and dizziness. Arrhythmias may be caused by stress, caffeine, drugs, diseases of the heart, or a combination of factors. Arrhythmias are named according to speed, rhythm, and location. In the following section, we will take a closer look at different types of arrhythmias.

Bradycardia, Ventricular Tachycardia, Heart Block, Atrial and Ventricular Fibrillation

Bradycardia

Bradycardia is the condition of having a heart rate (HR) below 50 beats per minute (bpm). You may find a few exceptionally trained aerobic athletes who demonstrate resting heart rates in the range of 30–40 beats per minute but otherwise, bradycardia is a symptom of concern. Depending upon the specific individual, as rates fall much below 50bpm, the heart is unable to maintain adequate flow of blood to vital tissues. Over time this results in decreasing loss of function across organ systems, unconsciousness, and ultimately death. Bradycardia may be caused by either inherent factors or external causes. Inherent causes include abnormalities in the SA or AV node. If the condition is serious, a pacemaker may be required. Other causes include ischemic heart muscle and diseases of the heart vessels or valves. External causes include metabolic disorders, pathologies of the endocrine system often involving the thyroid, electrolyte imbalances, neurological disorders including inappropriate autonomic responses, autoimmune pathologies, and over-prescription of beta-blocker drugs that reduce HR, recreational drug use, or even prolonged bed rest. Treatment relies upon establishing the underlying cause of the disorder and may necessitate supplemental oxygen.

Ventricular Tachycardia

Ventricular tachycardia (V-tach or VT) is defined as a heart rate above 100 bpm [see Figure 19.24 ©]. Elevated heart rates in an exercising individual are normal and expected. In addition, the resting heart rates of children are often above 100 bpm, but this is normal and not considered to be tachycardia. In VT, the rapid heartbeat prevents the heart chambers from properly filling. When the heart is not able to pump enough blood to the body, you may feel shortness of breath or lightheaded, or you may lose consciousness. There are two types of VT. The nonsustained VT may go away on its own within 30 seconds while the sustained VT lasts more than 30 seconds. Sustained VT can cause serious problems. Treatment depends upon the underlying cause but may include medications, implantable cardioverter defibrillators, ablation, or surgery.

Heart Block

A heart block refers to an interruption in the normal conduction pathway. There are different types, depending on which pathway is being blocked. SA nodal blocks occur within the SA node. AV nodal blocks occur within the atrioventricular (AV) node. Infra-Hisian blocks involve the bundle of His. Bundle branch blocks occur within either the left or right atrioventricular bundle branches.

Clinically, the AV nodal block is the most common type of heart block. AV blocks are often described by degrees. A first-degree (partial) block indicates a delay in conduction between the SA and AV nodes. This can be recognized on the ECG as an abnormally long PR interval since the conduction to the AV node is slower than normal. A second-degree (partial) block occurs when some impulses from the SA node don’t reach the AV node. As a result, the ECG would reveal some P waves not followed by a QRS complex, while others would appear normal [see Figure 19.24 (a)]. In the third-degree (complete) block, there is no correlation between atrial activity (the P wave) and ventricular activity (the QRS complex). Even in the event of a total SA block, the AV node will assume the role of pacemaker and continue initiating contractions at 40–60 contractions per minute, which is adequate to maintain consciousness as seen in Figure 19.24 (e).

Atrial Fibrillation

Atrial fibrillation (AF or Afib) is the most common arrhythmia that starts in the atria. Instead of the SA node directing the electrical rhythm, many different impulses rapidly fire at once and cause a very fast rhythm in the atria. These electrical impulses are so fast and chaotic, that the atria cannot contract and pump the blood effectively into the ventricles. The ECG of an AF patient will show no clearly defined P wave and irregularly spaced QRS complexes [see Figure 19.24 (b)]. Since the atria and ventricles do not beat in rhythm, the heartbeat is irregular. The danger of having AF relates to the formation of blood clots. If the blood clot travels to the brain, it may cause a stroke. The blood clot can also travel to other parts of the body and cause damage.

Ventricular Fibrillation

An arrhythmia that starts in the ventricle is called ventricular fibrillation (VF or V-fib). This occurs when the electrical signals cause your ventricles to quiver (fibrillate) instead of working in unison. The quivering means that the heart is not efficiently pumping blood out to your body. During V-fib, there are no defined P waves, QRS complexes, or T waves [see Figure 19.24 (d)]. A common cause of V-fib is insufficient blood flow to the heart during myocardial infarction, cardiovascular shock, or very low potassium levels. Ventricular fibrillation is the deadliest arrhythmia because sustained V-fib can lead to cardiac arrest and death. Patients who suffer from V-fib require immediate medical attention. Treatments for patients with V-fib include cardiopulmonary resuscitation (CPR) and defibrillation.

Figure 19.24 Common ECG Abnormalities: (a) In a second-degree or partial block, one-half of the P waves are not followed by the QRS complex and T waves while the other half are. (b) In atrial fibrillation, the electrical pattern is abnormal prior to the QRS complex, and the frequency between the QRS complexes has increased. (c) In ventricular tachycardia, the shape of the QRS complex is abnormal. (d) In ventricular fibrillation, there is no normal electrical activity. (e) In a third-degree block, there is no correlation between atrial activity (the P wave) and ventricular activity (the QRS complex).. OpenStax A&P Textbook (Heart)

External Automated Defibrillators

If the electrical activity of the heart is severely disrupted, complete cessation of electrical activity or fibrillation may occur. In fibrillation, the heart beats in a wild, uncontrolled manner, which prevents it from being able to pump effectively. In a hospital setting, it is often described as “code blue.” If untreated, even for as little as a few minutes, ventricular fibrillation may lead to brain death. The most common treatment is defibrillation, which uses special paddles to apply an electric charge to the heart. A defibrillator [Figure 19.25] effectively stops heart conduction so that the SA node can trigger a normal cycle. Because of their effectiveness in reestablishing a normal sinus rhythm, external automated defibrillators (EADs) are being placed in areas frequented by large numbers of people, such as schools, restaurants, and airports. These devices contain simple and direct verbal instructions that can be followed by nonmedical personnel to save a life.

Patients who are at a high risk of suffering from arrhythmias can now receive an implantable cardioverter-defibrillator (ICD). ICD is a small battery-powered device placed in the chest to detect and stop irregular heartbeats. An ICD will continuously monitor the heartbeat and deliver electric shocks when needed. You might need an ICD if you have ventricular tachycardia or ventricular fibrillation.

Figure 19.25 Defibrillators: (a) An external automatic defibrillator can be used by nonmedical personnel to reestablish a normal sinus rhythm in a person with fibrillation. (b) Defibrillator paddles are more commonly used in hospital settings. (Credit b: “widerider107”/flickr.com) OpenStax A&P Textbook (Heart)

19.4 Physiology of the Heart

Cardiac output is a measure of how effective the cardiovascular system is in performing its function of moving blood throughout the body to deliver nutrients and remove wastes. In a healthy person, cardiac output increases with exercise to meet the demands for oxygen and nutrients and the removal of waste substances. Cardiac output may not increase in a person with heart problems which may limit the performance of the physical activity.

By definition, cardiac output is the amount of blood that is pumped by a single ventricle, (either left or right) in one minute and is expressed in liters per minute. Cardiac output is calculated by multiplying the heart rate with the stroke volume. Heart rate (HR) is the number of beats per minute (BPM) whereas stroke volume (SV) is the volume of blood ejected during one beat (written as milliliters per beat, ml/b).

Cardiac output:

HR X SV = CO

For instance, when someone has an HR of 75 beats per minute (at rest) and the SV is 70 mL per beat, the CO is 5250 mL/min or 5.25 L/min. Because the average blood volume in the body is about 5 L and the CO is around 5 L per minute, the total volume of blood is being pumped through the body every minute!

Smaller hearts produce smaller stroke volumes. To maintain a homeostatic level of cardiac output at rest, people with smaller hearts, such as women and children, show a higher heart rate. On the other hand, athletes have larger hearts and because of that, they have a higher stroke volume. Their heart rates are lower to maintain normal resting cardiac output.

When we have an increase in heart rate and stroke volume, we also have an increase in CO. When we exercise, the heart rate can increase to around 170 beats per minute. Stroke volume also can be increased to even more than 100 mL. The increased CO above resting levels is called cardiac reserve. The cardiac reserve gives us a measure of how much physical exercise a person can do and is much greater in those who regularly exercise.

Factors Affecting the Heart Rate

The factors that can affect the heart rate are:

• The sympathetic division of the autonomic nervous system
• The parasympathetic division of the autonomic nervous system
• Hormones
• Drugs

The factors that can change heart rate are collectively called chronotropic agents. Positive agents cause an increase in heart rate. Examples of positive agents are sympathetic nerve stimulation and thyroid hormones. These agents act on the SA node and the AV node. Sympathetic stimulation releases the neurotransmitter norepinephrine that acts on the SA nodal cells and the net physiological effect is an increase in heart rate. Thyroid hormones act by making nodal cells more responsive to norepinephrine. Drugs that also act as positive agents are caffeine, nicotine, and cocaine. In comparison, negative agents decrease heart rate. Parasympathetic release of acetylcholine is the main intrinsic negative agent reducing HR. The beta-blocker medications are negative agents commonly used to treat high blood pressure.

Innervation of the Heart

The autonomic nervous system regulates the heart rate and force of contraction. Baroreceptors and chemoreceptors send sensory input to the cardiac center, localized within the medulla oblongata. From the cardiac center, sympathetic and parasympathetic neurons send projections to the heart [Figure 19.25]. The cardiac center has a cardioacceleratory center and a cardioinhibitory center. The cardioinhibitory center sends parasympathetic signals via the vagus nerves. Parasympathetic innervation reduces heart rate, with no effect on the force of contraction. The cardioacceleratory center sends sympathetic signals to increase heart rate and force of contraction. Please see Figure 19.25 to see the autonomic innervation of the heart.

Figure 19.26 Autonomic Innervation of the Heart: Cardioaccelerator and cardioinhibitory areas are components of the paired cardiac centers located in the medulla oblongata of the brain. They innervate the heart via sympathetic cardiac nerves that increase cardiac activity and vagus (parasympathetic) nerves that slow cardiac activity. OpenStax A&P Textbook (Heart)

Reflexes

Autonomic reflexes regulate the ability of the autonomic nervous system to influence heart rate. The cardiac center receives sensory information from baroreceptors and chemoreceptors. The cardiac center then responds reflexively by changing nerve signals to modify heart rate and stroke volume to maintain homeostasis. A reflex, called the atrial reflex or Bainbridge reflex, is associated with varying rates of blood flow to the atria. Increased venous return stretches the walls of the atria where specialized baroreceptors are located. As the atrial baroreceptors are stimulated by increased pressure, they send signals to the cardiac center which responds by increasing sympathetic and inhibiting parasympathetic stimulation to increase HR. The opposite is also true. This reflex prevents the over or under-filling of the heart.

Stroke Volume

The amount of blood ejected per heartbeat is the stroke volume. The stroke volume depends upon the end-diastolic volume (EDV). At rest, the EDV is about 130 mL. Since not all blood is ejected from the heart during ventricular contraction, the remaining blood is known as end-systolic volume (ESV). The ESV is about 60 mL. Stroke volume is calculated as the difference between these two:

Stroke Volume:

EDV – ESV = SV.

For the average adult person:

130 mL – 60 mL = 70 mL

Venous Return

The volume of blood returned to the heart directly impacts stroke volume. Venous return determines the EDV, which is the amount of blood in the ventricle right before contraction also known as the preload. Preload stretches the heart wall right before muscle contraction. Venous return increases during exercise and decreases in situations of low blood volume (such as due to a hemorrhage).

The Frank-Starling Law explains the relationship between venous return and stroke volume. According to this law, the preload increases as the volume of blood entering the heart increases, and as a result, the stroke volume also increases. The stroke volume increases as a direct consequence of the generation of a more forceful contraction of the ventricle. This is due to a better overlap of the actin and myosin filaments within the sarcomeres that occurs with the stretching of the heart wall. For the same reason, preload decreases as the volume of blood entering the heart decreases. The stroke volume then decreases as a direct consequence of a less forceful contraction of the ventricle. This is due to there being less overlap of the actin and myosin filaments within the sarcomeres, which generates fewer crossbridges.

Stroke volume can also be influenced by other factors such as contractility. Factors that change stroke volume by affecting contractility are called inotropic agents. These agents typically alter the force of contraction by changing the calcium concentration, which in turn alters the number of crossbridges formed and therefore the force of contraction.

Examples of positive inotropic agents include norepinephrine released from sympathetic neurons, the adrenalines and thyroid hormone. In general, these agents increase the concentration of calcium and consequently there is an increase in the number of crossbridges formed.

On the contrary, a negative inotropic agent decreases the force of contraction by decreasing calcium concentration and as a result, fewer cross-bridges are formed. One example of a negative inotropic agent is a class of drugs that are calcium channel blockers. These drugs are used to treat high blood pressure due to their effect on decreasing cardiac output.

Arteries resist the ejection of blood by the ventricles due to backpressure. This is known as afterload. Any condition that increases resistance (such as atherosclerosis) generates a greater afterload which will then require more force to open the semilunar valves and pump the blood out. Damage to the valves, such as stenosis, makes them harder to open and will also increase afterload. [Figure 19.27] summarizes the factors affecting stroke volume.

In summary, the heart rate is influenced by the chronotropic agents and these agents affect the conduction system of the heart. The stroke volume is affected by preload (venous return), contractility, and afterload. Cardiac output is determined by heart rate and stroke volume. [Figure 19.28] summarizes the factors affecting cardiac output. When heart rate and stroke volume increase, cardiac output also increases. When heart rate and stroke volume decrease, cardiac output also decreases. In the following, you will see the figures that summarize the major factors influencing stroke volume and cardiac output.

Figure 19.27 Major Factors Influencing Stroke Volume: Multiple factors impact preload, afterload, and contractility, and are the major considerations influencing SV.

Figure 19.28 Summary of Major Factors Influencing Cardiac Output: The primary factors influencing HR include autonomic innervation plus endocrine control. Not shown are environmental factors, such as electrolytes, metabolic products, and temperature. The primary factors controlling SV include preload, contractility, and afterload. Other factors such as electrolytes may be classified as either positive or negative inotropic agents.

Cardiac Muscle Metabolism

Up to now, we have learned a lot about the structures and functions of the heart. Have you ever wondered what fuel your heart needs to work properly? Normally, cardiac muscle metabolism is entirely aerobic and it uses aerobic respiration to generate cellular energy. In terms of oxygen, the heart cells can also store appreciable amounts of oxygen in myoglobin which has a higher affinity for oxygen than hemoglobin in red blood cells. Normally, oxygen bound to hemoglobin and oxygen bound to myoglobin can supply sufficient oxygen to the heart, even during peak performance.

Cardiac muscle primarily uses fuels such as lipids and carbohydrates. Fatty acids and glucose are further oxidized in the mitochondria through aerobic respiration to release more energy in the form of ATP. In addition, the cardiac muscles can store glucose in the form of glycogen and lipids within the cytoplasm. During situations such as starvation, the cardiac muscles can use ketone bodies as fuels. Similar to skeletal muscles, cardiac muscles use creatine kinases to form ATP from creatine phosphate and ADP. In a normal individual, the level of creatine kinases in the blood is low. However, a high level of cardiac creatine kinases is observed in patients who suffered from a heart attack. In a heart attack, the cardiac muscles become injured and the cardiac creatine kinases are released into the bloodstream. This is a diagnostic method to test if a patient has signs of a heart attack in addition to other tests, especially testing for cardiac troponin levels in the blood.

Exercising and the Heart (outdoor activities, such as surfing…)

Exercise and Maximum Cardiac Output

Since the heart is a muscle, exercising increases its efficiency and size as would happen in skeletal muscles. In healthy young individuals, heart rate may increase to 150 beats per minute (bpm) during exercise. Stroke volume (SV) can also increase from 70 to about 130 mL due to increased strength of contraction. This would increase cardiac output (CO) to approximately 19.5 L/min, four to five times the resting rate. As a result, we will see a difference between the maximum and resting CO which is known as the cardiac reserve. Top cardiovascular athletes can achieve even higher levels of stroke volume every minute as their hearts become efficient. As a result, the hearts of the highly trained athletes get a bit bigger. During long-term training, the heart adapts to the demand by enlargement through physiological cardiomegaly. It is different from pathological cardiomegaly which is related to heart problems. Now that we have learned about the anatomy and physiology of the heart, it will be vital for each of us to take good care of it!

Chapter Summary

Key Terms

afterload

force the ventricles must develop to effectively pump blood against the resistance in the vessels

anastomosis

(plural = anastomoses) area where vessels unite to allow blood to circulate even if there may be partial blockage in another branch

angioplasty

a procedure in which a blockage is mechanically widened with a balloon

anterior interventricular artery

(also, left anterior descending artery or LAD) major branch of the left coronary artery that follows the anterior interventricular sulcus

anterior interventricular sulcus

sulcus located between the left and right ventricles on the anterior surface of the heart

aorta

largest artery in the body, originating from the left ventricle and descending to the abdominal region where it bifurcates into the common iliac arteries at the level of the fourth lumbar vertebra; arteries originating from the aorta distribute blood to virtually all tissues of the body

aortic arch 

descends toward the inferior portions of the body and ends at the level of the intervertebral disk between the fourth and fifth thoracic vertebrae

aortic stenosis

most common condition resulting from stenosis and it can be heard during auscultation as a high-pitched hum due to the turbulence created as the blood is forced through the narrowed valve

aortic valve

(also, aortic semilunar valve) valve located at the base of the aorta

arrhythmias 

unusual rhythm of heartbeats where the heart is beating too slowly, too quickly, or irregularly

artery

blood vessel that conducts blood away from the heart; may be a conducting or distributing vessel

ascending aorta

initial portion of the aorta, rising from the left ventricle for a distance of approximately 5 cm

athlete’s heart

A type of benign hypertrophy that involves hypertrophy of primarily the myocardium of the left ventricular and not the interventricular septum

atrial fibrillation

most common arrhythmia that starts in the atria

atrial reflex

(also, called Bainbridge reflex) autonomic reflex that responds to stretch receptors in the atria that send impulses to the cardioaccelerator area to increase HR when venous flow into the atria increases

atrioventricular (AV) node

clump of myocardial cells located in the inferior portion of the right atrium within the atrioventricular septum; receives the impulse from the SA node, pauses, and then transmits it into specialized conducting cells within the interventricular septum

atrioventricular bundle

(also, bundle of His) group of specialized myocardial conductile cells that transmit the impulse from the AV node through the interventricular septum; form the left and right atrioventricular bundle branches

atrioventricular bundle branches

(also, left or right bundle branches) specialized myocardial conductile cells that arise from the bifurcation of the atrioventricular bundle and pass through the interventricular septum; lead to the Purkinje fibers and also to the right papillary muscle via the moderator band

atrioventricular septum

cardiac septum located between the atria and ventricles; atrioventricular valves are located here

atrial systole

atrial contraction phase follows atrial depolarization which is represented by the P wave of the ECG

atrioventricular valves

one-way valves located between the atria and ventricles; the valve on the right is called the tricuspid valve, and the one on the left is the mitral or bicuspid valve

atrium

(plural = atria) upper or receiving chamber of the heart that pumps blood into the lower chambers just prior to their contraction; the right atrium receives blood from the systemic circuit that flows into the right ventricle; the left atrium receives blood from the pulmonary circuit that flows into the left ventricle

auricle

extension of an atrium visible on the superior surface of the heart

autonomic reflexes

regulate the ability of the autonomic nervous system to influence heart rate

autorhythmicity

ability of cardiac muscle to initiate its own electrical impulse that triggers the mechanical contraction that pumps blood at a fixed pace without nervous or endocrine control

Bainbridge reflex

(also, called atrial reflex) autonomic reflex that responds to stretch receptors in the atria that send impulses to the cardioaccelerator area to increase HR when venous flow into the atria increases

bicuspid valve

(also, mitral valve or left atrioventricular valve) valve located between the left atrium and ventricle; consists of two flaps of tissue

bradycardia

condition of having a heart rate (HR) below 50 beats per minute (bpm)

bundle of His

(also, atrioventricular bundle) group of specialized myocardial conductile cells that transmit the impulse from the AV node through the interventricular septum; form the left and right atrioventricular bundle branches

capillary

smallest of blood vessels where physical exchange occurs between the blood and tissue cells surrounded by interstitial fluid

cardiac center

area within the medulla oblongata that regulates heart rate through the nervous and endocrine systems

cardiac cycle

period of time between the onset of atrial contraction (atrial systole) and ventricular relaxation (ventricular diastole)

cardiac notch

depression in the medial surface of the inferior lobe of the left lung where the apex of the heart is located

cardiac output (CO)

amount of blood pumped by each ventricle during one minute; equals HR multiplied by SV

cardiac reserve

difference between maximum and resting CO

cardiac tamponade

condition where the heart is not able to pump blood anymore

cardioacceleratory center

sends sympathetic signals to increase heart rate and force of contraction

cardioinhibitory center

sends parasympathetic signals via the vagus nerves

chordae tendineae

string-like extensions of tough connective tissue that extend from the flaps of the atrioventricular valves to the papillary muscles

chronotropic agents

factors that can change heart rate 

circumflex artery

branch of the left coronary artery that follows coronary sulcus

conducting (nodal) cells

cells that initiate and propagate the action potential (the electrical impulse) that travels throughout the heart

contractile cells

these cells conduct impulses and undergo contractions that pump blood through the body

coronary arteries

branches of the ascending aorta that supply blood to the heart; the left coronary artery feeds the left side of the heart, the left atrium and ventricle, and the interventricular septum; the right coronary artery feeds the right atrium, portions of both ventricles, and the heart conduction system

coronary artery disease

also known as coronary heart disease, is characterized by the buildup of plaque (atherosclerosis), which is a fatty material including cholesterol, within the coronary arteries

coronary circulation

circulation of blood in the blood vessels that supply the heart muscle

coronary sinus

large, thin-walled vein on the posterior surface of the heart that lies within the atrioventricular sulcus and drains the heart myocardium directly into the right atrium

coronary sulcus

sulcus that marks the boundary between the atria and ventricles

coronary veins

vessels that drain the heart and generally parallel the large surface arteries

defibrillation

treatment which uses special paddles to apply an electric charge to the heart

depolarization

change in a cell membrane potential from rest toward zero. It results from the movement of sodium ions entering the cells

descending aorta

portion of the aorta that continues downward past the end of the aortic arch; subdivided into the thoracic aorta and the abdominal aorta

diastole

period of time when the heart muscle is relaxed and the chambers fill with blood

dicrotic notch

It is seen in the ECG and produced by the tendency for blood to flow back into the atria from the major arteries as ventricular pressure drops, following ventricular repolarization, when the ventricles begin to relax (ventricular diastole), and pressure within the ventricles drops.

electrocardiogram (ECG)

surface recording of the electrical activity of the heart that can be used for diagnosis of irregular heart function; also abbreviated as EKG

endocardium

innermost layer of the heart lining the heart chambers and heart valves; composed of endothelium reinforced with a thin layer of connective tissue that binds to the myocardium

endothelium

layer of smooth, simple squamous epithelium that lines the endocardium and blood vessels

epicardium

innermost layer of the serous pericardium and the outermost layer of the heart wall

fibrous pericardium

dense irregular connective tissue that encloses and protects the heart

fibrous skeleton

anchors the heart valves and works as an electric insulator

foramen ovale

opening in the fetal heart that allows blood to flow directly from the right atrium to the left atrium, bypassing the fetal pulmonary circuit

fossa ovalis

oval-shaped depression in the interatrial septum that marks the former location of the foramen ovale

Frank-Starling Law

relationship between ventricular stretch and contraction in which the force of heart contraction is directly proportional to the initial length of the muscle fiber

great cardiac vein

vessel that follows the interventricular sulcus on the anterior surface of the heart and flows along the coronary sulcus into the coronary sinus on the posterior surface; parallels the anterior interventricular artery and drains the areas supplied by this vessel

gap junctions

they allow the passage of ions between the cells to help to synchronize the heart contraction

heart block

interruption in the normal conduction pathway

heart rate (HR)

number of times the heart contracts (beats) per minute

heart sounds

sounds heard via auscultation with a stethoscope of the closing of the atrioventricular valves (“lub”) and semilunar valves (“dub”)

heart murmur

sound coming from the heart that is caused by the turbulent flow of blood

hypertrophic cardiomyopathy

pathological enlargement of the heart, generally for no known reason

inferior vena cava

large systemic vein that returns blood to the heart from the inferior portion of the body

inotropic agents

factors that change stroke volume by affecting contractility 

interatrial septum

cardiac septum located between the two atria; contains the fossa ovalis after birth

intercalated disc

physical junction between adjacent cardiac muscle cells; consisting of desmosomes, specialized linking proteoglycans, and gap junctions that allow passage of ions between the two cells

internodal pathways

specialized conductile cells within the atria that transmit the impulse from the SA node throughout the myocardial cells of the atrium and to the AV node

interventricular septum

cardiac septum located between the two ventricles

interventricular sulcus

groove between the ventricles

ischemia

a reduction in blood flow that results in hypoxia (insufficient delivery of oxygen to the cells and tissues of the body) 

left atrioventricular valve

(also, mitral valve or bicuspid valve) valve located between the left atrium and ventricle; consists of two flaps of tissue

left auricle

flaplike extension on the surface of the left atrium

mediastinum

area within the thoracic cavity that contains the lungs and the heart

middle cardiac vein

vessel that parallels and drains the areas supplied by the posterior interventricular artery; drains into the great cardiac vein

mitral valve

(also, left atrioventricular valve or bicuspid valve) valve located between the left atrium and ventricle; consists of two flaps of tissue

mitral valve prolapse

one of the cusps of the mitral valve is forced backward by the force of the blood

moderator band

band of myocardium covered by endocardium that arises from the inferior portion of the interventricular septum in the right ventricle and crosses to the anterior papillary muscle; contains conductile fibers that carry electrical signals followed by contraction of the heart

murmur

unusual heart sound detected by auscultation; typically related to septal or valve defects

conducting cells

specialized cells that transmit electrical impulses throughout the heart and trigger contraction by the myocardial contractile cells

myocardium

thickest layer of the heart composed of cardiac muscle cells built upon a framework of primarily collagenous fibers and blood vessels that supply it and the nervous fibers that help to regulate it

myocardial infarction

commonly known as a heart attack, results from a complete blockage of a coronary artery, or more likely several coronary arteries, resulting in the death of the cardiac muscle cells (necrosis)

P wave

component of the electrocardiogram that represents the depolarization of the atria

pacemaker

cluster of specialized myocardial cells known as the SA node that initiates the sinus rhythm

papillary muscle

extension of the myocardium in the ventricles to which the chordae tendineae attach

pectinate muscles

muscular ridges seen on the anterior surface of the right atrium

pericardial cavity

cavity surrounding the heart filled with a lubricating serous fluid that reduces friction as the heart contracts

pericardial sac

(also, pericardium) membrane that separates the heart from other mediastinal structures; consists of two distinct, fused sublayers: the fibrous pericardium and the parietal pericardium

pericarditis

inflammation of the pericardium

pericardium

(also, pericardial sac) membrane that separates the heart from other mediastinal structures; consists of two distinct, fused sublayers: the fibrous pericardium and the parietal pericardium

posterior interventricular artery

(also, posterior descending artery) branch of the right coronary artery that runs along the posterior portion of the interventricular sulcus toward the apex of the heart and gives rise to branches that supply the interventricular septum and portions of both ventricles

posterior interventricular sulcus

sulcus located between the left and right ventricles on the posterior surface of the heart

preload

(also, end diastolic volume) amount of blood in the ventricles at the end of atrial systole just prior to ventricular contraction

pulmonary arteries

left and right branches of the pulmonary trunk that carry deoxygenated blood from the heart to each of the lungs

pulmonary capillaries

capillaries surrounding the alveoli of the lungs where gas exchange occurs: carbon dioxide exits the blood and oxygen enters

pulmonary circulation 

movement of blood from the right side of the heart to the lungs, and back to the left side of the heart

pulmonary circuit

blood flow to and from the lungs

pulmonary trunk

large arterial vessel that carries blood ejected from the right ventricle; divides into the left and right pulmonary arteries

pulmonary veins

veins that carry highly oxygenated blood into the left atrium, which pumps the blood into the left ventricle, which in turn pumps oxygenated blood into the aorta and to the many branches of the systemic circuit

Purkinje fibers

specialized myocardial conduction fibers that arise from the bundle branches and spread the impulse to the myocardial contraction fibers of the ventricles

QRS complex

component of the electrocardiogram that represents the depolarization of the ventricles and includes, as a component, the repolarization of the atria

repolarization

it results from the outflux of positively charged K+ 

right atrioventricular valve

(also, tricuspid valve) valve located between the right atrium and ventricle; consists of three flaps of tissue

right marginal artery

a branch from the right coronary artery that supplies the lateral wall of the right ventricle

semilunar valves

valves located at the base of the pulmonary trunk and at the base of the aorta

septum

(plural = septa) walls or partitions that divide the heart into chambers

serous fluid

oily fluid helps diminish friction as the heart contracts and expands

sinoatrial (SA) node

known as the pacemaker, a specialized clump of myocardial conducting cells located in the superior portion of the right atrium that has the highest inherent rate of depolarization that then spreads throughout the heart

sinus rhythm

normal contractile pattern of the heart

small cardiac vein

parallels the right coronary artery and drains blood from the posterior surfaces of the right atrium and ventricle; drains into the coronary sinus, middle cardiac vein, or right atrium

spontaneous depolarization

(also, prepotential depolarization) the mechanism that accounts for the autorhythmic property of cardiac muscle; the membrane potential increases as sodium ions diffuse through the always-open sodium ion channels and causes the electrical potential to rise

stroke volume (SV)

amount of blood pumped by each ventricle per contraction; also, the difference between EDV and ESV

sulcus

(plural = sulci) fat-filled groove visible on the surface of the heart; coronary vessels are also located in these areas

superior vena cava

large systemic vein that returns blood to the heart from the superior portion of the body

systemic circulation 

movement of blood from the left side of the heart to the systemic cells of the body and then back to the right side of the heart

systemic circuit

blood flow to and from virtually all of the tissues of the body

systole

period of time when the heart muscle is contracting

T wave

component of the electrocardiogram that represents the repolarization of the ventricles

trabeculae carneae

ridges of muscle covered by endocardium located in the ventricles

tricuspid valve

term used most often in clinical settings for the right atrioventricular valve

valve

in the cardiovascular system, a specialized structure located within the heart or vessels that ensures one-way flow of blood

vein

blood vessel that conducts blood toward the heart

ventricle

one of the primary pumping chambers of the heart located in the lower portion of the heart; the left ventricle is the major pumping chamber on the lower left side of the heart that ejects blood into the systemic circuit via the aorta and receives blood from the left atrium; the right ventricle is the major pumping chamber on the lower right side of the heart that ejects blood into the pulmonary circuit via the pulmonary trunk and receives blood from the right atrium

ventricular ejection phase

second phase of ventricular systole during which blood is pumped from the ventricle

ventricular fibrillation

arrhythmia that starts in the ventricle 

ventricular relaxation 

also known as ventricular diastole, follows the repolarization of the ventricles and is represented by the T wave of the ECG

ventricular systole 

follows the depolarization of the ventricles represented by the QRS complex in the ECG

ventricular tachycardia

heart rate above 100 bpm

Attributions and Links:

1. OpenStax A&P Textbook: Heart
2. Wikipedia Commons: Holter monitor,
3. ECG Interpretation
4. Ventricular tachycardia: Mayo Clinic VT
5. Heart Blocks: Cleveland Clinic
6. Atrial fibrillation: Cleveland Clinic
7. Ventricular Fibrillation: Johns Hopkins Medicine
8. Implantable cardioverter-defibrillator: Mayo Clinic
9. Creatine kinases: University of Rochester Medical Center
10. Cardiomegaly: Cleveland Clinic