In almost every year since 1900, cardiovascular disease (CVD) has been the number-one cause of death in the United States. Nearly 2300 Americans die of CVD each day, an average of one death every 38 seconds (American Heart Association [AHA], 2010b). The disease kills more people than the next four causes of death combined, including cancer, chronic lower respiratory diseases, accidents, and diabetes. Of particular concern is that CVD is the leading cause of death for women. In addition, the American Heart Association (AHA) estimates that more than one in three adults is living with some form of the disease. About 20% of people who experience a myocardial infarction will die within 1 year from the initial cardiac event (AHA, 2010b).

Anatomy and Physiology Review

Heart

Structure

The human heart is a fist-sized, muscular organ located in the mediastinum between the lungs (Fig. 35-1). Each beat of the heart pumps about 60 mL of blood, or 5 L/min. During strenuous physical activity, it can double the amount of blood pumped to meet the body’s increased oxygenation needs. The heart is protected by a covering called the pericardium. A muscular wall (septum) separates the heart into two halves: right and left. Each half has an atrium and a ventricle (Fig. 35-2).

FIG. 35-1 Surface anatomy of the heart.

FIG. 35-2 Blood flow through the heart.

The right atrium (RA) receives deoxygenated venous blood, which is returned from the body through the superior and inferior venae cavae. It also receives blood from the heart muscle through the coronary sinus. Most of this venous return flows passively from the RA, through the opened tricuspid valve, and to the right ventricle during ventricular diastole, or filling. The remaining venous return is actively propelled by the RA into the right ventricle during atrial systole, or contraction.

The right ventricle (RV) is a muscular pump located behind the sternum. It generates enough pressure to close the tricuspid valve, open the pulmonic valve, and propel blood into the pulmonary artery and the lungs.

After blood is reoxygenated in the lungs, it flows freely from the four pulmonary veins into the left atrium. Blood then flows through an opened mitral valve into the left ventricle during ventricular diastole. When the left ventricle is almost full, the left atrium (LA) contracts, pumping the remaining blood volume into the left ventricle. With systolic contraction, the left ventricle (LV) generates enough pressure to close the mitral valve and open the aortic valve. Blood is propelled into the aorta and into the systemic arterial circulation. Blood flow through the heart is shown in Fig. 35-2.

Blood moves from the aorta throughout the systemic circulation to the various tissues of the body. The pressure of blood in the aorta of a young adult averages about 100 to 120 mm Hg, whereas the pressure of blood in the RA averages about 0 to 5 mm Hg. These differences in pressure produce a pressure gradient, with blood flowing from an area of higher pressure to an area of lower pressure. The heart and vascular structures are responsible for maintaining these pressures.

The four cardiac valves are responsible for maintaining the forward flow of blood through the chambers of the heart (see Fig. 35-2). These valves open and close when pressure and volume change within the heart’s chambers. The cardiac valves are classified into two types: atrioventricular (AV) valves and semilunar valves.

The AV valves separate the atria from the ventricles. The tricuspid valve separates the RA from the RV. The mitral (bicuspid) valve separates the LA from the LV. During ventricular diastole, these valves act as funnels and help move the flow of blood from the atria to the ventricles. During systole, the valves close to prevent the backflow (regurgitation) of blood into the atria.

The semilunar valves are the pulmonic valve and the aortic valve that prevent blood from flowing back into the ventricles during diastole. The pulmonic valve separates the right ventricle from the pulmonary artery. The aortic valve separates the left ventricle from the aorta.

The heart muscle receives blood to meet its metabolic needs through the coronary arterial system (Fig. 35-3). The coronary arteries originate from an area on the aorta just beyond the aortic valve. All of the coronary arteries feeding the left heart originate from the left main coronary artery (LMCA). The right coronary artery (RCA) branches from the aorta to perfuse the right heart and inferior wall of the left heart.

FIG. 35-3 Coronary arterial system.

Coronary artery blood flow to the myocardium occurs primarily during diastole, when coronary vascular resistance is minimized. To maintain adequate blood flow through the coronary arteries, mean arterial pressure (MAP) must be at least 60 mm Hg. A MAP of between 60 and 70 mm Hg is necessary to maintain perfusion of major body organs, such as the kidneys and brain.

The left main artery divides into two branches: the left anterior descending (LAD) branch and the left circumflex (LCX) branch. The LAD branch descends toward the anterior wall and the apex of the left ventricle. It supplies blood to portions of the left ventricle, ventricular septum, chordae tendineae, papillary muscle, and, to a lesser extent, the right ventricle.

The LCX branch descends toward the lateral wall of the left ventricle and apex. It supplies blood to the left atrium, the lateral and posterior surfaces of the left ventricle, and sometimes portions of the interventricular septum. In about half of people, the LCX branch supplies the sinoatrial (SA) node. In a very small number of people, it supplies the AV node. Peripheral branches arise from the LAD and LCX branches and form an abundant network of vessels throughout the entire myocardium.

The right coronary artery (RCA) originates from the right sinus of Valsalva, encircles the heart, and descends toward the apex of the right ventricle. The RCA supplies the RA, RV, and inferior portion of the LV. In about half of people, the RCA supplies the SA node, and in almost everyone, it supplies the AV node.

Function

The electrophysiologic properties of heart muscle are responsible for regulating heart rate (HR) and rhythm. Cardiac muscle cells possess the characteristics of automaticity, excitability, conductivity, contractility, and refractoriness. Chapter 36 describes these properties and cardiac conduction in detail.

Sequence of Events During the Cardiac Cycle

The phases of the cardiac cycle are generally described in relation to changes in pressure and volume in the left ventricle during filling (diastole) and ventricular contraction (systole) (Fig. 35-4). Diastole, normally about two thirds of the cardiac cycle, consists of relaxation and filling of the atria and ventricles. Systole consists of the contraction and emptying of the atria and ventricles.

FIG. 35-4 Events of the cardiac cycle.

Myocardial contraction results from the release of large numbers of calcium ions from the sarcoplasmic reticulum and from the blood. These ions diffuse into the myofibril sarcomere (the basic contractile unit of the myocardial cell). Calcium ions promote the interaction of actin and myosin protein filaments, causing these filaments to link and overlap. Cross-bridges, or linkages, are formed as the protein filaments slide over or overlap each other. These cross-bridges act as force-generating sites. The sliding of these protein filaments shortens the sarcomeres, producing myocardial contraction.

Cardiac muscle relaxes when calcium ions are pumped back into the sarcoplasmic reticulum, causing a decrease in the number of calcium ions around the myofibrils. This reduced number of ions causes the protein filaments to disengage, the sarcomere to lengthen, and the muscle to relax.

Mechanical Properties of the Heart

The electrical and mechanical properties of cardiac muscle determine the function of the cardiovascular system. The healthy heart can adapt to various pathophysiologic conditions (e.g., stress, infections, hemorrhage) to maintain adequate blood flow to the various body tissues. Blood flow from the heart into the systemic arterial circulation is measured clinically as cardiac output (CO), the amount of blood pumped from the left ventricle each minute. CO depends on the relationship between heart rate (HR) and stroke volume (SV); it is the product of these two variables:

In adults, the CO ranges from 4 to 7 L/min. Because CO requirements vary according to body size, the cardiac index is calculated to adjust for differences in body size. The cardiac index can be determined by dividing the CO by the body surface area. The normal range is 2.7 to 3.2 L/min/m² of body surface area.

Heart rate (HR) refers to the number of times the ventricles contract each minute. The normal resting HR for an adult is between 60 and 100 beats/min. Increases in rate increase myocardial oxygen demand. The HR is extrinsically controlled by the autonomic nervous system (ANS), which adjusts rapidly when necessary to regulate cardiac output. The parasympathetic (vagus nerve) system slows the HR, whereas sympathetic stimulation increases the heart rate. An increase in circulating catecholamines (e.g., epinephrine and norepinephrine) usually causes an increase in HR and contractility. Many cardiovascular drugs, particularly beta blockers, block this sympathetic (fight or flight) pattern by decreasing the HR.

Stroke volume (SV) is the amount of blood ejected by the left ventricle during each contraction. Several variables influence SV and, ultimately, CO. These variables include HR, preload, afterload, and contractility.

Preload refers to the degree of myocardial fiber stretch at the end of diastole and just before contraction. The stretch imposed on the muscle fibers results from the volume contained within the ventricle at the end of diastole. Preload is determined by the amount of blood returning to the heart from both the venous system (right heart) and the pulmonary system (left heart) (left ventricular end-diastolic [LVED] volume).

An increase in ventricular volume increases muscle-fiber length and tension, thereby enhancing contraction and improving stroke volume. This statement is derived from Starling’s law of the heart: The more the heart is filled during diastole (within limits), the more forcefully it contracts. Excessive filling of the ventricles results in excessive LVED volume and pressure, however, and may result in decreased cardiac output.

Another factor affecting stroke volume, afterload, is the pressure or resistance that the ventricles must overcome to eject blood through the semilunar valves and into the peripheral blood vessels. The amount of resistance is directly related to arterial blood pressure and the diameter of the blood vessels.

Impedance, the peripheral component of afterload, is the pressure that the heart must overcome to open the aortic valve. The amount of impedance depends on aortic compliance and total systemic vascular resistance, a combination of blood viscosity (thickness) and arteriolar constriction. A decrease in stroke volume can result from an increase in afterload without the benefit of compensatory mechanisms, thus leading to a decrease in cardiac output.

Myocardial contractility affects stroke volume and CO and is the force of cardiac contraction independent of preload. Contractility is increased by factors such as sympathetic stimulation, calcium release, and positive inotropic drugs. It is decreased by factors such as hypoxia and acidemia.

Vascular System

The vascular system serves several purposes:

• Provides a route for blood to travel from the heart to nourish the various tissues of the body

• Carries cellular wastes to the excretory organs

• Allows lymphatic flow to drain tissue fluid back into the circulation

• Returns blood to the heart for recirculation

The vascular system is divided into the arterial system and the venous system. In the arterial system, blood moves from the larger arteries to a network of smaller blood vessels, called arterioles, which meet the capillary bed. In the venous system, blood travels from the capillaries to the venules and to the larger system of veins, eventually returning in the vena cava to the heart for recirculation.

Arterial System

The primary function of the arterial system is to deliver oxygen and nutrients to various tissues in the body. Nutrients are carried through arteries to arterioles, then branch into smaller terminal arterioles and finally join with capillaries and venules to form a capillary network. Within this network, nutrients are exchanged across capillary membranes by three primary processes: osmosis, filtration, and diffusion. (See Chapter 13 for detailed discussions of these processes.)

The arterial system delivers blood to various tissues for oxygen and nourishment. At the tissue level, nutrients, chemicals, and body defense substances are distributed and exchanged for cellular waste products, depending on the needs of the particular tissue. The arteries transport the cellular wastes to the excretory organs (e.g., kidneys and lungs) to be reprocessed or removed. These vessels also contribute to temperature regulation in the tissues. Blood can be either directed toward the skin to promote heat loss or diverted away from the skin to conserve heat.

Blood pressure (BP) is the force of blood exerted against the vessel walls. Pressure in the larger arterial blood vessels is greater (about 80 to 100 mm Hg) and decreases as blood flow reaches the capillaries (about 25 mm Hg). By the time blood enters the right atrium, the BP is about 0 to 5 mm Hg. Volume, ventricular contraction, and vascular tone are necessary to maintain blood pressure.

BP is determined primarily by the quantity of blood flow or cardiac output (CO), as well as by the resistance in the arterioles:

Any factor that increases CO or total peripheral vascular resistance increases the BP. In general, BP is maintained at a relatively constant level. Therefore an increase or decrease in total peripheral vascular resistance is associated with a decrease or an increase in CO, respectively. Three mechanisms mediate and regulate BP:

• The autonomic nervous system (ANS), which excites or inhibits sympathetic nervous system activity in response to impulses from chemoreceptors and baroreceptors

• The kidneys, which sense a change in blood flow and activate the renin-angiotensin-aldosterone mechanism

• The endocrine system, which releases various hormones (e.g., catecholamine, kinins, serotonin, histamine) to stimulate the sympathetic nervous system at the tissue level

Systolic BP is the amount of pressure/force generated by the left ventricle to distribute blood into the aorta with each contraction of the heart. It is a measure of how effectively the heart pumps and is an indicator of vascular tone. Diastolic BP is the amount of pressure/force against the arterial walls during the relaxation phase of the heart.

BP is regulated by balancing the sympathetic and parasympathetic nervous systems of the autonomic nervous system. Changes in autonomic activity are responses to messages sent by the sensory receptors in the various tissues of the body. These receptors, including the baroreceptors, chemoreceptors, and stretch receptors, respond differently to the biochemical and physiologic changes of the body.

Baroreceptors in the arch of the aorta and at the origin of the internal carotid arteries are stimulated when the arterial walls are stretched by an increased BP. Impulses from these baroreceptors inhibit the vasomotor center, which is located in the pons and the medulla. Inhibition of this center results in a drop in BP.

Several 1- to 2-mm collections of tissue have been identified in the carotid arteries and along the aortic arch known as peripheral chemoreceptors. These receptors are sensitive primarily to hypoxemia (a decrease in the partial pressure of arterial oxygen [PaO₂]). When stimulated, these chemoreceptors send impulses along the vagus nerves to activate a vasoconstrictor response and raise BP.

The central chemoreceptors in the respiratory center of the brain are also stimulated by hypercapnia (an increase in partial pressure of arterial carbon dioxide [PaCO₂]) and acidosis. The direct effect of carbon dioxide on the central nervous system (CNS), however, is 10 times stronger than the effect of hypoxia on the peripheral chemoreceptors.

Stretch receptors in the vena cava and the right atrium are sensitive to pressure or volume changes. When a patient is hypovolemic, stretch receptors in the blood vessels sense a reduced volume or pressure and send fewer impulses to the CNS. This reaction stimulates the sympathetic nervous system to increase the heart rate (HR) and constrict the peripheral blood vessels.

The kidneys also help regulate cardiovascular activity. When renal blood flow or pressure decreases, the kidneys retain sodium and water. BP tends to rise because of fluid retention and activation of the renin-angiotensin-aldosterone mechanism (see Fig. 13-6 in Chapter 13). This mechanism results in vasoconstriction and sodium retention (and thus fluid retention). Vascular volume is also regulated by the release of antidiuretic hormone (vasopressin) from the posterior pituitary gland (see Chapter 13).

Other factors can also influence the activity of the cardiovascular system. Emotional behaviors (e.g., excitement, pain, anger) stimulate the sympathetic nervous system to increase blood pressure (BP) and heart rate (HR). Increased physical activity such as exercise also increases BP and HR during the activity. Body temperature can affect the metabolic needs of the tissues, thereby influencing the delivery of blood. In hypothermia, tissues require fewer nutrients and blood pressure falls. In hyperthermia, the metabolic requirement of the tissues is greater and BP and pulse rate rise.

Venous System

The primary function of the venous system is to complete the circulation of blood by returning blood from the capillaries to the right side of the heart. It is composed of a series of veins that are located next to the arterial system. A second superficial venous circulation runs parallel to the subcutaneous tissue of the extremity. These two venous systems are connected by communicating veins that provide a means for blood to travel from the superficial veins to the deep veins. Blood flow is directed toward the deep venous circulation.

Veins have the ability to accommodate large shifts in volume with minimal changes in venous pressure. This flexibility allows the venous system to accommodate the administration of IV fluids and blood transfusions, as well as to maintain pressure during blood loss and dehydration. Veins in the superficial and deep venous systems (except the smallest and the largest veins) have valves that direct blood flow back to the heart and prevent backflow. Skeletal muscles in the extremities provide a force that helps push the venous blood forward. The superior vena cava and inferior vena cava are valveless and large enough to allow blood flow to return easily to the heart.

Gravity exerts an increase in hydrostatic pressure in the capillaries when the patient is in an upright position, delaying venous return. Hydrostatic pressure is decreased in dependent areas such as the legs when the patient is lying down, and thus there is less hindrance of venous return to the heart.

Cardiovascular Changes Associated with Aging

A number of physiologic changes in the cardiovascular system occur with advancing age (Chart 35-1). Many of these changes result in a loss of cardiac reserve. Thus these changes are usually not evident when the older adult is resting. They become apparent only when the person is physically or emotionally stressed and the heart cannot meet the increased metabolic demands of the body.

Chart 35-1 Nursing Focus on the Older Adult

Changes in the Cardiovascular System Related to Aging

CHANGE	NURSING INTERVENTIONS	RATIONALES
Cardiac Valves
Calcification and mucoid degeneration occur, especially in mitral and aortic valves.	Assess heart rate and rhythm and heart sounds for murmurs. Question patients about dyspnea.	Murmurs may be detected before other symptoms. Valvular abnormalities may result in rhythm changes.
Conduction System
Pacemaker cells decrease in number. Fibrous tissue and fat in the sinoatrial node increase. Few muscle fibers remain in the atrial myocardium and bundle of His. Conduction time increases.	Assess the electrocardiogram (ECG) and heart rhythm for dysrhythmias or a heart rate less than 60 beats/min.	The sinoatrial (SA) node may lose its inherent rhythm. Atrial dysrhythmias occur in many older adults; 80% of older adults experience premature ventricular contractions (PVCs).
Left Ventricle
The size of the left ventricle increases. The left ventricle becomes stiff and less distensible. Fibrotic changes in the left ventricle decrease the speed of early diastolic filling by about 50%.	Assess the ECG for a widening QRS complex and a longer QT interval.	Ventricular changes result in decreased stroke volume, ejection fraction, and cardiac output during exercise; the heart is less able to meet increased oxygen demands.
	Assess the heart rate at rest and with activity. Assess for activity intolerance.	Maximum heart rate with exercise is decreased. The heart is less able to meet increased oxygen demands.
Aorta and Other Large Arteries
The aorta and other large arteries thicken and become stiffer and less distensible. Systolic blood pressure increases to compensate for the stiff arteries. Systemic vascular resistance increases as a result of less distensible arteries; therefore the left ventricle pumps against greater resistance, contributing to left ventricular hypertrophy.	Assess blood pressure. Note increases in systolic, diastolic, and pulse pressures. Assess for activity intolerance and shortness of breath. Assess the peripheral pulses.	Hypertension may occur and must be treated to avoid target organ damage.
Baroreceptors
Baroreceptors become less sensitive.	Assess the patient’s blood pressure with the patient lying and then sitting or standing. Assess for dizziness when the patient changes from a lying to a sitting or standing position. Teach the patient to change positions slowly.	Orthostatic (postural) and postprandial changes occur because of ineffective baroreceptors. Changes may include blood pressure decreases of 10 mm Hg or more, dizziness, and fainting.

Assessment Methods

Patient History

The focus of the patient history is on obtaining information about risk factors and symptoms of cardiovascular disease (Chart 35-2). Assess nonmodifiable (uncontrollable) risk factors including the patient’s age, gender, ethnic origin, and family history of cardiovascular disease. Ask about any chronic disease or illness that the patient may have. The incidence of conditions such as coronary artery disease (CAD) and valvular disease increases with age. The incidence of CAD also varies with the patient’s gender. Men have a higher risk for CAD than women of all ages except in the oldest age-group of 80 years and older (AHA, 2010b).

Chart 35-2

Cardiovascular Assessment

Using Gordon’s Functional Health Patterns