18.2 Cardiovascular System

Heart

The human heart is located within the thoracic cavity, medially between the lungs in the space known as the mediastinum. The great veins, the superior and inferior venae cavae, and the great arteries, the aorta and pulmonary trunk, are attached to the superior surface of the heart, called the base. The base of the heart is located at the level of the third costal cartilage. The inferior tip of the heart, the apex, lies just to the left of the sternum between the junction of the fourth and fifth ribs. It is important to remember the position of the heart when placing a stethoscope on the chest of a patient and listening for heart sounds.

The heart consists of four chambers: two atria and two ventricles. The right atrium receives deoxygenated blood from systemic circulation, and the left atrium receives oxygenated blood from the lungs. The atria contract to push blood into the lower chambers, the right ventricle, and the left ventricle. The right ventricle contracts to push blood into the lungs, and the left ventricle is the primary pump that propels blood to the rest of the body.

The heart tends to be considered as the muscle it is, but its structure actually includes three layers of slightly different cellular makeup. The outer layer is composed of fat and connective tissue and is an extension of the serous pericardium, one of three layers of protective pericardial tissue that surrounds the heart. Endothelial cells make up the heart’s inner layer and envelop the valves; this tissue is the same as that of the inner layer of the nearby larger blood vessels. It is the midlayer of the heart that consists of muscle cells specific to the heart. The coronary arteries are the source of perfusion specifically to the heart muscle cells, or cardiomyocytes.

Cardiac cells are unique in a few ways. First, they are able to initiate spontaneous action potential, also called automaticity. Another distinctive property is the heart’s own circulation: coronary arteries perfuse the cardiac muscle itself, and this blood flow is primarily supplied during diastole. Cardiac perfusion is enhanced by vasodilation of coronary arteries in response to catecholamines, hormones that function as neurotransmitters.

Blood Vessels

After blood is pumped out of the ventricles, it is carried through the body via blood vessels. An artery is a blood vessel that carries blood away from the heart, where it branches into ever-smaller vessels and eventually into tiny capillaries where nutrients and wastes are exchanged at the cellular level (Figure 18.7). Capillaries combine with other small blood vessels that carry blood to a vein, a larger blood vessel that returns blood to the heart. Compared to arteries, veins are thin-walled, low-pressure vessels. Larger veins are also equipped with a valve that promote the unidirectional flow of blood toward the heart and prevent backflow caused by the inherent low blood pressure in veins as well as the pull of gravity (Figure 18.8).

Figure 18.7 The arteries in the circulatory system carry oxygenated blood from the heart throughout the body. (credit: “Arterial System” by “LadyofHats”/Mariana Ruiz Villarreal/Wikimedia Commons, Public Domain)

Figure 18.8 The veins in the body carry blood to the heart to be oxygenated. (credit: “Venous System” by “LadyofHats”/Mariana Ruiz Villarreal/Wikimedia Commons, Public Domain)

In addition to their primary function of returning blood to the heart, veins may be considered blood reservoirs because systemic veins contain approximately 64 percent of the blood volume at any given time. Approximately 21 percent of the venous blood is located in venous networks within the liver, bone marrow, and integument. This volume of blood is referred to as venous reserve. Through venoconstriction, this reserve volume of blood can get back to the heart more quickly for redistribution to other parts of the circulation.

The amount of fluid within the blood vessels, or intravascular volume, contributes to blood pressure as measured by pressure within the arteries. Other organs may contribute waste products from metabolic functions into the bloodstream to be transported for further metabolism, and ultimately for some waste excretion from the body. An example is water entering the body through oral intake, absorption through the gastrointestinal tract, delivery to cells in need of fluid, and excess being delivered to the renal system for processing and urinary excretion.

Circulation

There are two distinct but linked circuits in human circulation called the pulmonary and systemic circuits (Figure 18.9). The pulmonary circuit transports blood to and from the lungs, where it picks up oxygen and delivers carbon dioxide for exhalation. The systemic circuit transports oxygenated blood to virtually all of the tissues of the body and returns deoxygenated blood and carbon dioxide to the heart to be sent back to the pulmonary circulation.

Figure 18.9 Blood flows through the cardiopulmonary circuit and the heart. (credit: modification of work from Anatomy and Physiology 2e. attribution: Copyright Rice University, OpenStax, under CC BY 4.0 license)

There are potential physiological interruptions that lead to a body not being in a state of homeostasis. An example is arteriosclerosis, or stiffening of the arterial walls, and a subcategory, atherosclerosis, or buildup of plaque deposits within the artery walls. Arteriosclerosis lessens the elastic properties of blood vessels and, therefore, the ability for vasodilation, which increases the intravascular pressure. Atherosclerosis narrows the internal space of blood vessels, which also increases the pressure within the intravascular space. These two pathophysiological properties often occur together, and either can cause hypertension when renal arteries are impacted. While hypertension is a possible result, uncontrolled hypertension is also a risk factor for the development of arteriosclerosis (AHA, 2023; Poznyak et al., 2022). Other risk factors include dyslipidemia, diabetes mellitus (DM), and cigarette smoking. Hypertension contributes to the development of arteriosclerosis by thickening the walls of blood vessels, plaque development, and the potential for rupture of the blood vessel walls. It is not uncommon for patients with these diagnoses to also be hypervolemic, from either cardiac or renal (or a combination) dysfunction. In these cases, multiple pathologies are contributing to excessive vascular volume and pressure. Temporary increases in fluid and BP can be helpful compensatory mechanisms for the improvement of perfusion; however, with these diagnoses, there is little relief from the elevated pressures, little rest for the body system, and ultimately, a reduction in perfusion.

Another example of a lack of stable perfusion is hypovolemia or a lack of fluid in the vascular space. This can be from different issues, like blood loss from surgery or traumatic injury, or fluid loss from exertion or hot weather. The loss of volume means less fluid volume in the circulatory system, which is typified by a low BP, manifested by signs and symptoms of low perfusion, such as mental status changes ranging from slight confusion to, potentially, seizure, cool and clammy skin, low urine output, climbing creatinine, and other laboratory results illustrating a concentrated sample.

Stroke Volume

The amount of blood expelled from the left ventricle during a single systolic contraction is known as stroke volume (SV). Three primary factors that affect SV are preload, or the stretch on the ventricles prior to contraction; contractility, or the force or strength of the contraction itself; and afterload, the force the ventricles must generate to pump blood against the resistance in the vessels. The calculation for SV is EDV – ESV.

The ejection fraction (EF) is the percentage of blood within the ventricle that is expelled during a single systolic contraction. A low EF means that the heart is not creating an efficient contraction, and this is a sign of HF. HF can occur with intact EF, or it can be reduced. Normal EF is approximately 50 to 70 percent; it is therefore considered preserved if it is over 50 percent (Bruss & Raja, 2022). Reduced EF is indicated when there are clinical manifestations of HF and the EF is at or under 40 percent. The formula for EF is SV/EDV. Cardiologists use information about EF to explore cardiac-related diagnoses like hypertrophy and HF, as well as to confirm adequate perfusion and function.

Electrical Impulses

The human body includes an electrical system, which directly and indirectly affects all systems. Cardiac electrical impulses (Figure 18.10) lead to the mechanical (muscle) movement of the myocardium, which pumps and circulates blood through both systemic and pulmonary circuits, thereby (in normal circumstances) perfusing the entire system.

Figure 18.10 Normal electrical conduction through the heart travels from the sinoatrial node, to the internodal pathways, the atrioventricular node, the bundle of His, to the bundle branches (right and left), and to the Purkinje fibers. (credit: modification of work from Anatomy and Physiology 2e. attribution: Copyright Rice University, OpenStax, under CC BY 4.0 license)

Sinoatrial Node

Known as the pacemaker of the heart, the sinoatrial (SA) node has the highest rate of depolarization. It initiates the sinus rhythm or normal electrical pattern followed by contraction of the heart. Criteria for normal sinus rhythm include that the impulse begins at the SA node, travels from the SA node to the atrioventricular (AV) node in 0.12 seconds or less, and has a rate between 60 and 100 beats per minute. The firing of the SA node can be visualized by an electrocardiogram (ECG or EKG), which is a noninvasive test that involves attaching leads to a patient’s chest and limbs: the machine then obtains a visual interpretation of the electrical impulses involved in the cardiac cycle (Figure 18.11).

Figure 18.11 (a) Cardiac conduction from the SA node of the right atrium through the Purkinje fibers of the ventricles. (b) The associated rhythm as seen on an ECG is shown in the image. (credit: modification of work from Anatomy and Physiology 2e. attribution: Copyright Rice University, OpenStax, under CC BY 4.0 license)

Dysrhythmia

The word dysrhythmia refers to a rhythm abnormality; the term arrhythmia indicates a lack or absence of rhythm but is often used synonymously with dysrhythmia to mean an abnormal rhythm. Dysrhythmias can be minor or extreme and life threatening, depending on where the anomaly originates, what it causes, and how extensive it is. One of the indicators of the severity of dysrhythmia is the patient’s symptoms. Depending on a patient’s medical history, level of well-being, mental state, and potentially other factors including the specific abnormal rhythm, there may be compensatory changes supporting little or no symptoms, or the patient may feel any combination of symptoms, including dizziness, weakness, syncope, palpitations, chest pain, or cardiac arrest.

Dysrhythmias have a variety of causes. A few examples are provided in the following paragraphs. Sometimes, irritable spots (foci) develop in the cardiac muscle where the property of automaticity may become a hindrance. This can lead to electrical misfires, as the irritable focus generates an impulse that may cause the normal electrical system to be interrupted, or the pathway altered.

Injuries to the heart or to a particular group of cells may also cause the normal electrical pathway to be disrupted, and slight changes or delays can develop, which are visible on ECGs when waves, intervals, and complexes are assessed and measured. An example is a first-degree heart block, where there is a delay in the period of time the impulse travels from the SA node to the AV node. On an ECG, this is seen as a prolonged PR interval.

Certain infectious diseases like bacterial endocarditis can lead to damage to the heart, including vegetations on valves causing valvular malformation, or an inability to open and close properly. This can produce disturbances in normal forward blood flow, which may be heard by auscultation with a stethoscope as a murmur.

Atrial fibrillation (A-fib) is a common dysrhythmia that sometimes is intermittent, may resolve on its own, or may respond well to treatment with medications or cardioversion. Sometimes, when interventions have not been successful in converting the patient out of A-fib, the goal becomes to minimize complications from inefficient atrial movement and subsequent increased risk for blood clot development. Medications like anticoagulants are used in this situation to prevent clot formation.

Link to Learning

More information on dysrhythmias, defibrillation versus cardioversion, and potential complications is presented in this video.

Ventricular dysrhythmias are generally considered more dangerous than those originating in the atria, as the ventricles are integral in oxygenation and perfusion. These abnormal rhythms can be the result of a variety of influences, including illicit drugs like cocaine or methamphetamine, a traumatic injury such as being hit directly in the chest by a baseball, or as a consequence of a myocardial infarction (MI), where both electrical and mechanical tissue can be damaged.

Nurses are trained to respond to respiratory and cardiac emergencies, some of which are the result of dysrhythmias. This may include basic life support (BLS) training incorporating the combination of rescue breathing and chest compressions of cardiopulmonary resuscitation (CPR). BLS instruction also includes the use of an automated external defibrillator (AED), which is an easy-to-use portable device available in many settings that can analyze a cardiac rhythm and defibrillate, if appropriate, in order to reestablish an effective cardiac rhythm. It is noteworthy that AEDs identify heart rhythm but do not provide an option for the operator to view it; they are more designed for bystander CPR response.

On patient care units within acute care hospitals, manual defibrillators are more common and offer portable monitoring on a small screen where medical providers can view and assess the patient’s rhythm, as well as other features. Defibrillators provide shocks of the intensity to treat ventricular tachycardia or fibrillation but can also be set to deliver lower joules to attempt synchronized cardioversion for such dysrhythmias as A-fib. Additionally, the option to externally pace a patient is available on these devices. Newer manual defibrillators have an automatic AED option (Figure 18.12).

Figure 18.12 (a) A manual defibrillator provides various options for monitoring, recording, and interventions, and (b) an AED is used for automated responses. (credit a: modification of work “Manual external defibrillator monitor” by “Aededitor”/Wikimedia Commons, CC BY 3.0; credit b: modification of work "AED & Fire Extinguishers, both necessary" by "David Bruce Jr."/Flickr, CC BY 2.0)

In advanced cardiac life support (ACLS), extra training is involved, often for medical providers in prehospital and hospital settings, and this includes the addition of resuscitation and support cardiac medications. Commonly, these include drugs in the antidysrhythmic classification as well as those like catecholamines that increase BP—both of these classes of medicines are used in arrest circumstances to attempt to convert abnormal rhythms to normal, and/or enhance perfusion through other means.

Clinical Safety and Procedures (QSEN)

QSEN Competency: Safety: Defibrillation

A hospitalized patient who suffers a ventricular fibrillation (VF) arrest is treated by a system of assessments, actions, and interventions, coordinating members of an interdisciplinary healthcare team, with QSEN Competencies in mind (QSEN, 2022). Associated competencies for the intervention defibrillation include patient-centered care, teamwork and collaboration (T&C), and safety (S). Considering the interdisciplinary nature of treatment of cardiac arrest, let us explore the knowledge, skills, and attitudes within the T&C competency through an unfolding example (QSEN, 2022):

1. Knowledge: “Describe scopes of practice and roles of healthcare team members” (p. 3).
   Example: VF arrest – code called by bedside RN, who immediately begins CPR while awaiting arrival of code team and equipment. Upon arrival of the team, there are predetermined roles based on scope of practice for the different professions. Team leader is typically a physician or advanced practitioner. BLS-certified personnel can alternate chest compressions every one to two minutes.
   Skills: “Function independently within own scope of practice as a member of the healthcare team” (p. 3). Example: The bedside nurse identified the arrest situation, called the code, and began CPR—all within the RN scope of practice. Others function within their professional scope as personnel converge on the patient setting, for example, RT begins bagging the patient during chest compressions by other personnel, team leader clearly states orders for interventions based on VF/cardiac arrest algorithm, education, and other skills, pharmacist provides ordered medications from the code cart as ordered, for the RN-assigned medication administration.
   Attitudes: “Value the perspectives and experiences of all health team members” (p. 3).
   Example: The team members realize, understand, and practice their specific roles during an arrest situation. Collaboration between all members of the patient care/code team is respectful and values all members equally.
2. Knowledge: “Describe strategies for identifying and managing overlaps in team member roles and accountabilities” (p. 3).
   Example: Hospital personnel, through BLS and ACLS certification/recertification, are practiced at the roles and responsibilities during emergencies. RNs assume roles including the primary nurse (whose patient is involved in the emergency), medication RN, recording RN—once the particular role is assumed, each of these nurses tends to continue that particular role throughout the event. RT provides bagging with the Ambu bag, followed by assisting with intubation, CO₂ confirmation, and placement of the patient on a ventilator. Various team members serve as compressors, providing chest compressions for one to two minutes at a time in relay format.
   Skills: “Clarify roles and accountabilities under conditions of potential overlap in team member functioning” (p. 3).
   Example: The primary RN role is changeable, based on nurse-patient assignments; an experienced team may have predesignated selections based on preference and experience/skill level, so the recorder may be the nursing supervisor, and the charge RN may administer medications. The team leader is usually a physician—intensivist or ED physician is common. As various members of the team provide chest compressions for short periods, transition from one compressor to another should be anticipated and verbally planned and executed for minimal disruption.
   Attitudes: “Respect the unique attributes that members bring to a team, including variations in professional orientations and accountabilities” (p. 3).
   Example: Team leaders tend to be those with advance practice background and prescriptive authority. The primary RN is considered to have the best familiarity with the patient—history, status trends, medications, and so on, and therefore can provide a quick overview. Various team members may be able to serve in more than one capacity, and clear communication is critical throughout an emergency, and in any transitions.
3. Knowledge: “Describe examples of the impact of team functioning on safety and quality of care” (p. 4).
   Example: Treatment of a VF arrest includes early defibrillation. The prompt arrival of the code team, and the code cart with the defibrillator/monitor to confirm the rhythm, and subsequently treat it, are necessary. Placement of pads on the patient, activation of the machine, and its readiness for defibrillation when charged all must be clearly communicated throughout the event.
   Skills: “Assert own position/perspective in discussions about patient care” (p. 4).
   Example: Each team member’s role is a critical part of the total situation, and the contribution is important and should be shared at appropriate times. A nurse may be responsible for pulse checks when chest compressions are briefly halted, and that nurse’s input is vital at that time. Whether the patient has bilateral breath sounds after intubation is also key, and the RN or RT who auscultates the chest should distinctly state these findings.
   Attitudes: “Appreciate the risks associated with handoffs among providers and across transitions of care” (p. 4).
   Example: During an emergency circumstance like a cardiac arrest and code response, all members of the healthcare team should realize the importance of clear, concise communication among personnel. Whether this is to have a second physician join the team, or RT and an RN help with intubation and securing the endotracheal tube (ETT), or to change compressors after a minute or two of exhausting work, transitions should always maintain the central focus on the patient and clearly move from one situation or care provision to another.

Ischemia

A lack of O₂ delivery to a part of the body, especially the cardiac tissue, is termed ischemia. Angina pectoris is a rather common ischemic event whereby O₂ supply does not meet demand. Angina can be chronic and stable, in which case it is predictable, and patients are often able to treat it by discontinuing activity, resting, and administering sublingual nitroglycerin. If angina becomes unpredictable, it is described as unstable angina and is associated with acute coronary syndrome (ACS), which involves worsening coronary disease. Ischemia is reversible if adequate perfusion is reestablished promptly. Coronary artery disease (CAD) can progress along a continuum, beginning with a healthy coronary system, to a diagnosis of stable angina pectoris, and to unstable angina. If it worsens and perfusion is inadequate for too long, it can advance to a MI. Once the tissue is damaged, terminology changes to infarction. Infarcted tissue does not recover and leads to permanent repercussions; a common adverse outcome of CAD is HF.

Heart Failure

Inefficiency of the heart’s contractility characterizes HF. Ineffective contractility may arise from chronic hypertension, often associated with hypervolemia (fluid volume excess). According to Starling’s law, the heart is capable of stretching muscle fibers, which initially improves the strength of muscle contraction and is a desired effect, as it increases SV. However, if this is a chronic situation, there can be a limit to this ability to stretch, and if exceeded, the cardiac muscle can become either hypertrophied (excessively enlarged) or unable to rebound from being overstretched, in which case the muscular walls become weak and floppy. Either circumstance reduces cardiac contractility, which is seen as HF symptoms, as seen in Figure 18.13.

Figure 18.13 Right- and left-sided heart failure show different symptoms. (credit: modification of work “Blood Flow Through the Heart” by “BruceBlaus”/Blausen Medical Communication/Wikimedia Commons, CC BY 3.0)