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Clinical Nursing Skills

24.1 Cardiovascular System

Clinical Nursing Skills24.1 Cardiovascular System

Learning Objectives

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

  • Discuss the structures of the cardiovascular system
  • Describe the functions of the cardiovascular system
  • Explain cardiovascular abnormalities related to the ECG

The cardiovascular system, a magnificent physiological organ system, serves as the life-sustaining force within the human body. This intricate network consisting of the heart and blood vessels, also known as the circulatory system, coordinates an intricate network of functions to ensure the continuous flow of blood, oxygen, and nutrients throughout the body. At the core of this system lies the heart, a tireless muscle that propels blood through a complex web of blood vessels, working in tandem with various organ systems to maintain homeostasis. Primary functions needed for homeostasis are carried out via the supporting blood vessel structures, the arteries and veins.

Beyond mechanical functions, the cardiovascular system is a regulatory powerhouse, capable of adapting to the body’s ever-changing demands. Hormones such as adrenaline and intricate neural signals influence heart rate and blood pressure, demonstrating the system’s responsiveness to internal and external stimuli.

A primary role of the nurse is to address dysfunction within the cardiovascular system that can manifest in various ways, significantly affecting an individual’s health and well-being. One prevalent example is hypertension (high blood pressure), which places increased stress on the heart and blood vessels. As a result, hypertension can lead to serious complications (e.g., heart disease, stroke, kidney damage). Nurses must be adept at monitoring blood pressure, educating patients on lifestyle modifications, and administering medications to manage hypertension and other cardiovascular diseases effectively.

Structures of the Cardiovascular System

The cardiovascular system is a sophisticated network of structures vital for sustaining life. It encompasses the heart, blood vessels, and blood, working collaboratively with other organ systems to facilitate the transportation of oxygen, nutrients, and waste to and from the body’s tissues. This intricately interconnected system functions in harmony with the respiratory, lymphatic, gastrointestinal, and urinary systems to maintain homeostasis.

The heart, as the primary organ within the cardiovascular system, tirelessly pumps blood to guarantee consistent oxygenation of cells, supply of nutrients to tissues, and removal of wastes from tissues. It is divided into four chambers—two atria and two ventricles—employing a specific cardiac cycle cadence to coordinate atrial and ventricular contractions, thereby effectively circulating blood throughout the body. Simultaneously, blood vessels play a crucial role by carrying oxygenated blood to the body via arteries and returning deoxygenated blood to the heart through veins.

Blood, a pivotal component in maintaining homeostasis, ensures that blood is oxygen-rich and nutrient-laden, circulating throughout the body to vital organs. Blood is composed of red and white blood cells, platelets, and plasma. It not only facilitates oxygenation but also combats infections and aids in clotting. For nurses, a comprehensive understanding of blood composition, clotting mechanisms, and the effect of blood type on patient care is essential.

The cardiovascular system operates under intricate regulatory mechanisms, adapting to varying physiological demands. Hormones (e.g., adrenaline, angiotensin) influence heart rate and blood pressure. Nurses must fully understand how these regulatory systems promptly identify signs of instability and intervene effectively, ensuring optimal cardiovascular function. Patients often are seen for conditions such as hypertension, coronary artery disease, heart failure, and arrhythmias. Acquiring a solid understanding of the structures and functions of the cardiovascular system equips nurses with the knowledge needed to recognize, prevent, and manage various cardiovascular conditions.

Heart Chambers and Valves

The heart is an intricately designed pump composed of four chambers and four valve structures. Understanding the anatomy and function of these chambers and valves is paramount for nursing professionals because they play a pivotal role in assessing and intervening when necessary to help the heart maintain the continuous circulation of blood throughout the body. Having a thorough understanding of the complexity of the chambers and valves will allow the nurse to create nursing care plans that provide comprehensive care to patients with disorders such as atrial fibrillation, ventricular tachycardia, and mitral stenosis.

The heart has four primary chambers, two on each side—the atria (upper chambers) and the ventricles (lower chambers) (Figure 24.2). Deoxygenated blood from the body flows into the right atrium through the superior and inferior vena cavae. The left atrium receives oxygenated blood from the lungs through the pulmonary veins. The atria serve as reservoirs, collecting blood and then contracting to propel it into the ventricles.

A diagram showing the different parts of the heart’s chambers.
Figure 24.2 The heart pumps blood through the chambers and valves to ensure that blood reaches all areas of the body. The four chambers work in tandem to create a cardiac cycle cadence that works smoothly, pumping blood in and out of the heart. (credit: modification of work from Anatomy and Physiology. attribution: Copyright Rice University, OpenStax, under CC BY 4.0 license)

The ventricles, on the other hand, are responsible for pumping blood out of the heart. The right ventricle propels deoxygenated blood to the lungs through the pulmonary artery, where it undergoes gas exchange of carbon dioxide with oxygen. Simultaneously, the left ventricle pumps oxygenated blood into the systemic circulation, delivering it to the rest of the body. This rhythmic sequence ensures a continuous flow of oxygenated blood to meet the metabolic demands of the tissues.

The heart is equipped with four vital valves that regulate blood flow and prevent backflow, ensuring unidirectional circulation. The atrioventricular (AV) valves, located between the atria and ventricles, include the tricuspid valve on the right side and the bicuspid (mitral) valve on the left. These valves open to allow blood to flow from the atria to the ventricles and close to prevent regurgitation (backward leakage) during ventricular contraction.

The semilunar valves (pulmonary valve on the right, aortic valve on the left) protect the exits of the ventricles. These valves open during ventricular contraction, enabling blood to be ejected into the pulmonary and systemic circulations, respectively. They then promptly close to prevent blood from regurgitating back into the ventricles during relaxation.

Understanding the dynamics of these chambers and valves is fundamental for nurses in assessing cardiac function, detecting murmurs or irregularities, and interpreting diagnostic findings found on echocardiograms and electrocardiograms. In summary, blood flowing through the heart can be described as deoxygenated blood from the body entering the right atrium which contracts to send the blood through the tricuspid valve to the right ventricle. From here, the blood must enter the lungs as it passes through the pulmonary valve. Once it is oxygenated, it returns to the left atrium of the heart where it prepares for its journey throughout the body. From the left atrium, it enters the left ventricle, passing through the bicuspid valve. From the left ventricle, it passes through the aortic valve and enters the aorta to perfuse the body. In clinical practice, nurses collaborate with healthcare team members to monitor and intervene effectively in various cardiac conditions, emphasizing the importance of maintaining the integrity of the heart’s chambers and valves for optimal cardiovascular health.

Walls of the Heart

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

The membrane that directly surrounds the heart and defines the pericardial cavity is called the pericardium (also known as the pericardial sac). It also surrounds the “roots” of the major vessels—the areas of closest proximity to the heart. The pericardium, which literally translates as “around the heart,” consists of two distinct sublayers: the sturdy outer fibrous pericardium and the inner serous pericardium (Figure 24.3). The fibrous pericardium is made of tough, dense connective tissue that protects the heart and maintains its position in the thorax. The more delicate serous pericardium consists of two layers: the parietal pericardium, which is fused to the fibrous pericardium, and an inner visceral pericardium (also called the epicardium). The pericardial cavity, filled with lubricating serous fluid, lies between the epicardium and the pericardium.

A diagram showing the heart’s layers.
Figure 24.3 The pericardium that surrounds the heart consists of two layers: fibrous pericardium and serous pericardium. The heart wall consists of three layers: epicardium, myocardium, and endocardium. The pericardial cavity filled with lubricating serous fluid lies between the pericardium and epicardium. (credit: modification of work from Anatomy and Physiology. attribution: Copyright Rice University, OpenStax, under CC BY 4.0 license)

The wall of the heart is composed of three layers of unequal thickness. From superficial to deep, these are the epicardium, myocardium, and endocardium. The outermost layer of the heart is the epicardium, which is fused to the heart and is part of the heart wall. The middle and thickest layer is the myocardium, made largely of cardiac muscle cells. It is built on a framework of collagenous fibers, plus the blood vessels that supply the myocardium and the nerve fibers that help regulate the heart. It is the contraction of the myocardium that pumps blood through the heart and into the major arteries. The innermost layer of the heart wall, the endocardium, is joined to the myocardium with a thin layer of connective tissue. The endocardium lines the chambers where the blood circulates and covers the heart valves. It is made of simple squamous epithelium called endothelium, which is continuous with the endothelial lining of the blood vessels.

The muscle pattern is elegant and complex, as the muscle cells swirl and spiral around the chambers of the heart (Figure 24.4). They form a figure-eight pattern around the atria and around the bases of the great vessels. Deeper ventricular muscles also form a figure eight around the two ventricles and proceed toward the apex. More superficial layers of ventricular muscle wrap around both ventricles. This complex swirling pattern allows the heart to pump blood more effectively than a simple linear pattern would.

A diagram showing the heart’s cardiac muscles.
Figure 24.4 The swirling pattern of cardiac muscle tissue contributes significantly to the heart’s ability to pump blood effectively. (credit: modification of work from Anatomy and Physiology. attribution: Copyright Rice University, OpenStax, under CC BY 4.0 license)

Although the right and left ventricles pump the same amount of blood per contraction, the muscle of the left ventricle is much thicker and better developed than that of the right ventricle. To overcome the high resistance required to pump blood into the long systemic circuit, the left ventricle must generate a great amount of pressure. The right ventricle does not need to generate as much pressure because the pulmonary circuit is shorter and provides less resistance. As a result, the muscle in the left ventricle is thicker than in the right ventricle (Figure 24.5).

A diagram showing the difference between relaxed and contracted ventricles.
Figure 24.5 The myocardium in the left ventricle is significantly thicker than that of the right ventricle. The ventricles are shown in both relaxed and contracted states. Note the differences in the relative size of the lumens (the region inside each ventricle) where the blood is contained. (credit: modification of work from Anatomy and Physiology. attribution: Copyright Rice University, OpenStax, under CC BY 4.0 license)


As you recall from anatomy and physiology, blood is a connective tissue made up of cellular elements and an extracellular matrix. The cellular elements, or formed elements, include red blood cells (RBCs), white blood cells (WBCs), and cell fragments called platelets. The extracellular matrix, called plasma, makes blood unique among connective tissues because it is fluid. This fluid is primarily water and continuously suspends the formed elements, enabling them to circulate throughout the body within the cardiovascular system. Fluids, whether gases or liquids, are materials that flow according to pressure gradients; they move from regions of higher pressure to regions of lower pressure.

Blood pumped by the heart flows through a series of vessels known as arteries, arterioles, capillaries, venules, and veins before returning to the heart. Arteries transport blood away from the heart and branch into smaller vessels, forming arterioles. Arterioles distribute blood to capillary beds, the sites of exchange with the body tissues. Capillaries lead back to small vessels known as venules that flow into the larger veins and eventually back to the heart.

Based on this concept, when the heart chambers are relaxed (diastole), blood flows into the atria from the veins, which are higher in pressure. As blood flows into the atria, the pressure rises, causing the blood to initially move passively from the atria into the ventricles. An action potential triggers the muscles in the atria to contract (atrial systole), causing the pressure within the atria to rise even further, pumping blood into the ventricles. 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.

Functions of the Cardiovascular System

The primary function of the cardiovascular system is to maintain homeostasis by providing adequate blood supply to tissues. To do this, blood flow must be redirected continuously to the tissues as they become more active. There is not enough blood flow to equally distribute blood to all tissues simultaneously. Therefore, the cardiovascular system engages in a form of resource allocation to ensure active tissues are fully supplied with the oxygen and nutrients needed. For example, blood is directed to the skeletal muscles, heart, and lungs during exercise. The brain, however, receives more of a constant supply of blood whether the body is active, resting, thinking, or engaged in any other activity. Transporting blood to tissues also aids in maintaining blood pH and water balance.

To provide the body with needed oxygen, nutrients, and hormones, the cardiovascular system functions as a transportation highway. Nutrients from foods eaten are absorbed in the digestive tract where the majority travel through the bloodstream to the liver for processing. After being processed, nutritional molecules are released into the bloodstream for delivery to body cells. Transportation of oxygen occurs when inhaled oxygen diffuses into the blood from the alveoli in the lungs to the heart. Oxygenated blood is then pumped out to the body through the aorta. Hormones are released by endocrine glands that are scattered throughout the body into the bloodstream and carried to target cells. To maintain homeostasis, blood picks up cellular wastes and by-products and transports them to designated organs for removal. For example, carbon dioxide, which the blood takes back to the lungs for gas exchange, is removed from the body through exhalation.

Another function of the cardiovascular system is to defend the body against invading pathogens and damage to blood vessels caused by trauma. WBCs protect the body from external threats, such as disease-causing bacteria that have entered the bloodstream. Certain types of WBCs seek out and destroy internal threats, such as mutated cells that could lead to cancer or cells infected with a virus. When there is damage to the vessels, the body protects against blood loss by triggering platelets and thrombin to form a fibrinous barrier, typically a clot or scab depending on the location and severity of the trauma.

Thermoregulation is also an important function of the cardiovascular system and is regulated by a negative-feedback loop. This also involves resource allocation as blood is sent to the areas in need of warmth. When the body’s core temperature is increased, blood is sent to the extremities, which are most often cooler. When blood moves through the vessels of the skin, heat is dissipated to the environment; therefore, blood that is returned to the body is cooler. In the same context, when the body is cooled, such as in cold weather, blood is diverted away from the skin to maintain a warmer body core. This leaves the skin of the extremities susceptible to frostbite in extreme circumstances.

Electrical Conduction of the Heart

If embryonic heart cells are separated into a Petri dish and kept alive, each is capable of generating its own electrical impulse followed by contraction. When two independently beating embryonic cardiac muscle cells are placed together, the cell with the higher inherent rate sets the pace, and the impulse spreads from the faster cell to the slower cell to trigger a contraction. As more cells are joined together, the fastest cell continues to assume control of the rate. A fully developed adult heart maintains the capability of generating its own electrical impulse, triggered by the fastest cells, as part of the cardiac conduction system. The components of the cardiac conduction system include the sinoatrial node, the atrioventricular node, the atrioventricular bundle, the atrioventricular bundle branches, and the Purkinje fibers (Figure 24.6).

A diagram showing the parts of the heart’s cardiac conduction system.
Figure 24.6 Specialized conduction components of the heart include the sinoatrial node, atrioventricular node, atrioventricular bundle, right and left bundle branches, and Purkinje fibers. (credit: modification of work from Anatomy and Physiology. attribution: Copyright Rice University, OpenStax, under CC BY 4.0 license)


Normal cardiac rhythm is established by the sinoatrial (SA) node, a specialized clump of myocardial conducting cells (or pacemaker cells) located in the superior and posterior walls of the right atrium near the orifice of the superior vena cava. The SA node has the highest inherent rate of depolarization and is known as the pacemaker of the heart. The SA node initiates sinus rhythm in which electrical stimuli are initiated in the SA node and are then conducted through the AV node, bundle of His, bundle branches, and Purkinje fibers. This normal electrical pattern is followed by contraction of the heart.

This electrical signal, called the depolarization wave, starts in the right atrium and moves across both atria. It then goes through the contractile cells, causing them to contract from the top to the bottom of the atria, effectively pushing blood into the ventricles.

The atrioventricular (AV) node, located in the lower part of the right atrium within the atrioventricular septum, is made up of special conductive cells. The septum prevents the signal from going directly to the ventricles without passing through the AV node. There is an important pause before the AV node sends the signal to the atrioventricular bundle. This pause allows the atrial cardiomyocytes to finish their contraction, pushing blood into the ventricles before the signal goes to the ventricular cells. The AV node can send signals maximally at 220 per minute with extreme stimulation by the SA node, setting the typical maximum heart rate in a healthy young person. Damaged hearts or those stimulated by drugs can beat at higher rates, but at those rates, the heart cannot pump blood effectively.

From the AV node, the atrioventricular bundle (also called the bundle of His) goes through the interventricular septum before splitting into two atrioventricular bundle branches, known as the left and right bundle branches. The left bundle branch stimulates the left ventricle, which is much larger than the right, making the left bundle branch larger too. The right bundle branch reaches the right ventricle and is connected to the moderator band and right papillary muscles. Each papillary muscle receives the signal at the same time, so they start to contract together just before the rest of the ventricular cells. Both bundle branches reach the heart’s apex and connect with the Purkinje fibers, taking about 25 milliseconds (ms).

The Purkinje fibers are additional conductive fibers that spread the signal to the ventricular contractile cells. They go from the apex toward the atrioventricular septum and base of the heart. The Purkinje fibers have a fast conduction rate, and the signal reaches all the ventricular muscle cells in about 75 ms. The signal starts at the apex, so the contraction also begins there and moves toward the base of the heart, similar to squeezing a tube of toothpaste from the bottom. This movement helps pump blood out of the ventricles and into the aorta and pulmonary trunk. The whole process, from the SA node starting the signal to the ventricles depolarizing, takes about 225 ms.

Life-Stage Context

Congenital Complete Heart Block

Congenital complete heart block (CCHB) is a rare diagnosis, seen in approximately 1:15,000 to 1:20,000 live births. Diagnosis is made during fetal development and approximately 69 percent of patients have a pacemaker implanted by the first birthday. An estimated 74 percent to 96 percent of patients diagnosed with CCHB in infancy or early childhood will undergo pacemaker implantation before 20 years of age.

Dilated cardiomyopathy (left ventricular [LV] dysfunction) has been described as developing both early and late in the developmental stage with early onset caused by in utero myocardial inflammation or bradycardia. This inflammation leads to inadequate cardiac output and extreme hydrops fetalis. Late onset has been attributed to various patient characteristics (e.g., fetal diagnosis, maternal autoantibodies SSA [anti-Ro] and/or SSB [anti-La]). Left ventricular dysfunction also increases the risk for heart failure and cardiac mortality; however, previous studies have not reached a consistent consensus on the most important risk factors.

Echocardiography remains the most widely used tool to evaluate myocardial dysfunction in the pediatric population. Lifelong cardiac pacing is most often the required treatment.

Electrical Activity

Action potentials are considerably different between cardiac conductive cells and cardiac contractile cells. Although Na+ and K+ play essential roles, Ca2+ is also critical for both types of cells. Unlike skeletal muscles and neurons that have a steady, full reserve of energy that is ready to send off a signal when needed (called the resting potential), cardiac conductive cells do not have a strong or stable resting potential. Conductive cells contain a series of sodium ion channels that allow a normal and slow influx of sodium ions that causes the membrane potential to rise slowly from an initial value of −60 mV up to about –40 mV. The resulting movement of sodium ions creates spontaneous depolarization (also, prepotential 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 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 auto-rhythmicity properties of cardiac muscle (Figure 24.7).

A diagram showing the prepotential phase.
Figure 24.7 The prepotential phase occurs as the influx of sodium ions slowly begins until the threshold is reached followed by a rapid depolarization and repolarization. Prepotential accounts for the membrane reaching threshold and initiates spontaneous depolarization and contraction of the cell. The image helps visualize the weaker resting potential, which is what allows the buildup in the prepotential phase. (credit: modification of work from Anatomy and Physiology. attribution: Copyright Rice University, OpenStax, under CC BY 4.0 license)

Electrical activity in the heart’s contractile cells follows a specific pattern. First, there’s a quick depolarization, then a plateau phase, and finally repolarization. This process ensures that the heart muscle cells have enough time to effectively pump blood before they can contract again.

Unlike some other cells, cardiac myocytes (cells in the heart) do not start their own electrical signals. Instead, they wait for an impulse to reach them. These cells have a more stable resting phase compared to other types of cells, typically at around −80 mV for cells in the atria and −90 mV for cells in the ventricles. Despite this initial difference, the rest of their action potentials are very similar.

When these cells are stimulated by an action potential, specific channels quickly open, starting the process of depolarization. This quick influx of positively charged ions raises the cell’s potential, reaching approximately +30 mV. At this point, the sodium channels close and the rapid depolarization phase lasts for about 3 to 5 ms. After depolarization, the plateau phase occurs, where the membrane potential decreases relatively slowly. This is because slow calcium channels open, letting calcium enter the cell, while only a few potassium channels are open, allowing potassium to exit. The relatively long plateau phase lasts about 175 ms.

When the membrane potential reaches approximately zero, calcium channels close, and potassium channels open again, letting potassium exit the cell. This repolarization lasts about 75 ms. The membrane potential then drops until it reaches resting levels, and the cycle repeats. This whole event takes between 250 and 300 ms.

The absolute refractory period for these heart muscle cells (a time when the cell cannot respond to another stimulus) is about 200 ms. The relative refractory period, a time when the cell can respond but needs a stronger stimulus, is about 50 ms. This extended period is crucial because the heart must contract effectively to pump blood, and this contraction must follow the electrical events. Without these longer refractory periods, the heart might contract prematurely, which would not be compatible with life (Figure 24.8).

The left diagram shows the long plateau phase caused by the influx of calcium ions. The right diagram shows the action potential of heart muscle compared to skeletal muscle.
Figure 24.8 (a) This illustration shows the long plateau phase caused by the influx of calcium ions. The extended refractory period allows the cell to fully contract before another electrical event can occur. (b) This illustration shows the action potential of heart muscle compared to that of skeletal muscle. (credit a and b: modification of work from Anatomy and Physiology. attribution: Copyright Rice University, OpenStax, under CC BY 4.0 license)

There are two important roles that calcium ions play in how the heart muscles work. First, calcium ions come in through special channels and help create a steady phase and a time when the heart cannot respond to signals. This helps the heart muscle work correctly. Second, calcium ions join in the troponin complex with another protein called tropomyosin. This complex removes a block that stops myosin (a type of protein) from connecting with actin, which is needed for the heart muscles to contract and pump blood. This process is quite similar to how muscles work in our body. About 20 percent of the calcium needed for the heart’s contraction comes from the influx of calcium during the steady phase. The rest of the calcium comes from storage in a part of the cell called the sarcoplasmic reticulum.

The heart’s pattern of prepotential, quick depolarization, and repolarization is controlled by the SA node and some other heart cells. The SA node is like the boss, and it becomes ready to send signals faster than any other part of the heart’s system. It starts the signals that go to the other cells.

The SA node can send signals on its own about 80 to 100 times in a minute, even without any control from nerves or hormones. Each part of the heart system can initiate its own signals, but the rate slows down as the signal moves from the SA node to the Purkinje fibers. Without the SA node, the AV node would initiate signals at a rate of 40 to 60 times per minute. If the AV node is blocked, the atrioventricular bundle takes over and initiates signals about 30 to 40 times per minute. The bundle branches have a rate of 20 to 30 signals per minute, and the Purkinje fibers have a rate of 15 to 20 signals per minute.

Some very well-trained athletes might have a resting heart rate of 30 to 40 beats per minute. However, a heart rate lower than 60 beats per minute could mean the patient is experiencing bradycardia. When rates fall below this level, the heart might not pump enough blood to important tissues, leading to problems such as loss of function, passing out, and, eventually, death. The immediate intervention for a patient with sudden bradycardia is stabilization with respiratory and cardiovascular support, such as initiating oxygen, addressing any bleeding, and monitoring the patient with telemetry. After the patient is stabilized, the underlying cause should be addressed, and the patient’s provider notified.

The Cardiac Cycle

The time during which the heart contracts and relaxes is called the cardiac cycle (Figure 24.9). When the heart pumps blood, this is called systole and diastole is when it fills with blood. Both the atria and ventricles go through systole and diastole. The body’s control and coordination of these actions must be efficient in pumping blood throughout the body. In the cardiac cycle, the heart goes through atrial systole, ventricular systole, atrial diastole, and ventricular diastole, and then the cycle starts again.

A diagram showing the cardiac cycle.
Figure 24.9 Initially, both the atria and ventricles are relaxed (diastole). The P wave represents depolarization of the atria and is followed by atrial contraction (systole). Atrial systole extends until the QRS complex, at which point, the atria relax. The QRS complex represents depolarization of the ventricles and is followed by ventricular contraction. The T wave represents the repolarization of the ventricles and marks the beginning of ventricular relaxation. (credit: modification of work from Anatomy and Physiology. attribution: Copyright Rice University, OpenStax, under CC BY 4.0 license)

Fluids, such as blood, flow based on pressure differences. When the heart chambers are relaxed (diastole), blood flows into the atria from the veins, where the pressure is higher. As blood flows into the atria, the pressure rises, causing it to move passively from the atria into the ventricles. When the muscles in the atria contract (atrial systole), the pressure increases, pumping blood into the ventricles. 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.

At the start of the cardiac cycle, both the atria and ventricles are relaxed (diastole). Blood flows into the right atrium from the superior and inferior vena cavae and the coronary sinus. Blood also flows into the left atrium from the four pulmonary veins. The atrioventricular valves (tricuspid and mitral valves) are open, allowing blood to flow from the atria into the ventricles. About 70 to 80 percent of ventricular filling occurs during this time (called preload). The semilunar valves (pulmonary and aortic valves) are closed, preventing blood from flowing back into the ventricles.

Atrial systole follows depolarization, shown by the P wave of the electrocardiogram (ECG). As the atrial muscles contract, pressure rises within the atria, and blood is pumped into the ventricles through the open atrioventricular valves. Atrial systole lasts about 100 ms and ends before ventricular systole begins, allowing blood to flow into the atria again.


As the heart pumps, ventricular systole occurs and is split into two phases. First, the heart’s electrical activity occurs as represented by the QRS complex. This is followed by the ventricles contracting. At this point, the blood pressure in the ventricles rises, although it is not high enough to push blood out yet. Instead, the blood flows back toward the atria, closing the valves between the atria and ventricles. At this phase, no blood has left the heart yet so volume in the heart does not change, which is referred to as isometric contraction.

In the second phase, ventricular ejection, the pressure in the ventricles is high enough to open valves by pushing blood out. This is called isovolumetric contraction. Ventricular ejection, which is the main measure of ventricular function, is measured as ejection fraction, the percentage of blood that the left ventricle pumps out with each contraction. Even though the left ventricle has to push against higher pressure in the aorta, both sides of the heart pump the same amount of blood. The amount of blood pumped out of the left ventricle is called stroke volume (SV), or afterload. Normally, this is about 70 to 80 mL of blood. After this contraction, there’s still about 50 to 60 mL of blood left in the ventricle, known as end-systolic volume.


After the heart pumps, it takes a break during a phase called ventricular relaxation (diastole). This relaxation is represented by the T wave of the ECG and has two parts, lasting about 430 ms.

In the first phase, as the heart muscles relax, the pressure on the remaining blood in the heart decreases. When this pressure becomes lower than the pressure in the pulmonary trunk and aorta, blood flows back into the heart, causing a small dip in blood pressure called the dicrotic notch in an arterial waveform. Some valves close to prevent the blood from going back into the heart (regurgitation). The isovolumetric relaxation is the time interval between aortic valve closure and mitral valve opening when the ventricular pressures falls below the aortic and pulmonary pressures. During this time, cardiac circulation itself happens.

In the second phase, as the heart muscles keep relaxing, the pressure on the blood in the heart decreases even more. Eventually, it becomes lower than the pressure in the atria. When this happens, blood flows from the atria into the ventricles, opening the tricuspid and mitral valves. As the pressure decreases further, blood comes from the veins into the relaxed atria and stimulates another round of the cardiac cycle.

Cardiovascular Abnormalities That May Be Heralded by ECG Abnormalities

Occasionally, an area of the heart other than the SA node will initiate an impulse that will be followed by a premature contraction. Such an area, which may actually be a component of the conduction system or some other contractile cells, is known as an ectopic focus or ectopic pacemaker. An ectopic focus may be stimulated by localized ischemia; exposure to certain drugs, including caffeine, digitalis, or acetylcholine; elevated stimulation by both sympathetic or parasympathetic divisions of the autonomic nervous system; or a number of disease or pathological conditions. Occasional occurrences are generally transitory and nonlife threatening. However, if the condition becomes chronic, it may lead to either an arrhythmia (a deviation from the normal pattern of impulse conduction and contraction) or to fibrillation (an uncoordinated beating of the heart).

Although interpretation of an ECG is extremely valuable, a full understanding of the complexities and intricacies generally requires advanced ECG interpretation classes and several years of experience. In general, the size of the electrical variations, the duration of the events, and detailed vector analysis provide the most comprehensive picture of cardiac function. Following are some examples of ECG abnormalities and the problems these abnormalities may indicate (Table 24.1).

ECG Abnormality Associated Condition
An amplified P wave May indicate enlargement of the atria or hypokalemia
A P wave with decreased amplitude May indicate hyperkalemia
Absence of the P wave or a totally irregular baseline May indicate atrial fibrillation
An enlarged Q wave May indicate a myocardial infarction (MI)
An enlarged suppressed or inverted Q wave Often indicates enlarged ventricles
T waves appear flatter May indicate that insufficient oxygen is being delivered to the myocardium
Elevation of the ST segment above baseline Often seen in patients with an acute MI
Depression of the ST segment below the baseline May indicate that hypoxia is occurring
Table 24.1 ECG Abnormalities and Their Associated Conditions

As useful as analyzing these electrical recordings may be, there are limitations. For example, not all areas of the heart suffering an MI may be obvious on the ECG. Additionally, it will not reveal the effectiveness of the pumping, which requires further testing, such as an echocardiogram or nuclear medicine imaging scan. It is also possible for there to be pulseless electrical activity, which shows an ECG tracing, although there is no corresponding pumping action. Common abnormalities that may be detected by the ECGs include second-degree block, atrial fibrillation, ventricular tachycardia, ventricular fibrillation, and third-degree block (Figure 24.10).

A diagram showing five different types of common abnormal ECG results.
Figure 24.10 (a) In a second-degree or partial block, half of the P waves are not followed by the QRS complex and T waves. (b) In atrial fibrillation, the electrical pattern is abnormal before 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 third-degree block, there is no correlation between atrial activity (the P wave) and ventricular activity (the QRS complex). (credit a-e: modification of work from Anatomy and Physiology. attribution: Copyright Rice University, OpenStax, under CC BY 4.0 license)

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