Diseases and Conditions of the Circulatory System
CHAPTER 10
Diseases and Conditions of the Circulatory System
Key Terms
 agglutination (ah-glue-tih-NAY-shun)
 aggregation (ag-reh-GAY-shun)
 angioplasty (AN-jee-oh-plas-tee)
 arteriosclerosis (ar-tee-ree-oh-skleh-ROW-sis)
 asystole (a-SIS-toh-lee)
 atherosclerosis (ath-er-oh-skleh-ROW-sis)
 bradycardia (brady-KAR-dee-ah)
 bruit (BREW-ee)
 cardiomegaly (car-dee-oh-MEG-ah-lee)
 cardiomyopathy (car-dee-oh-my-OP-ah-thee)
 cellulitis (sell-u-LIE-tis)
 dyscrasia (dis-CRAY-zee-ah)
 ecchymosis (ech-ih-MO-sis)
 embolism (EM-boh-lizm)
 hematopoiesis (hem-ah-toh-poy-EE-sis)
 hemolytic (hem-oh-LIT-ik)
 hypovolemia (high-poh-voh-LEE-mee-ah)
 hypoxia (high-POX-see-ah)
 ischemia (is-KEY-mee-ah)
 orthopnea (or–THOP-nee-ah)
 perfusion (per-FYOU-zhun)
 petechiae (pee-TEE-kee-ee)
 phlebotomy (phleh-BOT-oh-mee)
 plaque (PLACK)
 purpura (PUR-pu-rah)
 syncope (SIN-ko-pee)
 tachycardia (tack-ee-CAR-dee-ah)
 tamponade (tam-pon-ADE)
 thrombus (THROM-bus)
Orderly Function of the Circulatory System
 Circulation of blood to the organs and tissues of the body is the primary function of
the circulatory system. The heart is at the center of the circulatory system.

Its steady beating pumps about 5 quarts of blood through a complete vascular
circuit of the body every minute in an adult; this is called the cardiac cycle. This circuit
comprises a network of vessels: the arteries, veins, and capillaries.
The heart and great vessels, anterior view. (From Patton KT, Thibodeau GA: Anatomy and physiology, ed 7, St Louis,
2011, Mosby.)
The heart and great vessels, posterior view. (From Patton KT, Thibodeau GA: Anatomy and physiology, ed 7, St Louis,
2011, Mosby.)
Circulation through the body.
 The heart consists of two side-by-side pumps, each divided into two chambers: two
upper chambers called atria, and two lower chambers called ventricles. As venous
blood returns to the heart from the body, it enters the right atrium, passes through
the tricuspid valve, and with atrial contraction, enters the right ventricle.
 Heart valves prevent the blood from flowing backward. From the right ventricle,
blood is pumped through the pulmonary valve and, with ventricular contraction, into
the pulmonary arteries and on to the lungs. In the lungs, carbon dioxide is removed,
and oxygen is added to the blood. Freshly oxygenated blood then returns to the
heart via the pulmonary veins.
 It enters the left atrium, moves through the mitral (bicuspid) valve with atrial
contraction, and enters the left ventricle. As the left ventricle contracts, the blood is
forced through the aortic valve, into the aorta, and on to the rest of the body. This
process is called the cardiac cycle
Circulation through the heart.
Cardiac cycle. AV, Atrioventricular valves (both tricuspid and mitral). (From Gould B:
Pathophysiology for the health professions, ed 3, Philadelphia, 2006, Saunders.)
 The heart is enclosed by the double-layered pericardium, which is composed of an
inner serous layer (visceral pericardium or epicardium) and an outer fibrous layer
(parietal pericardium). Between these layers in the pericardial cavity is a small
amount of serous fluid that reduces friction during cardiac movements.
 Cardiac muscle tissue or myocardium is composed of striated muscle cells that can
contract rhythmically on their own and characteristically are both voluntary and
involuntary responses. Inside the cavities of the heart is a smooth serous lining called
the endocardium (Figure 10-6).
 The conduction system of the heart coordinates the contraction and relaxation
(cardiac cycle) of the heart by initiating impulses and distributing the impulses
throughout the myocardium.

Coronary arteries and a network of vessels continuously supply cardiac muscle tissue
with oxygen.
Layers of the heart wall. (From Applegate EJ: The anatomy and physiology learning system,
ed 4, Philadelphia, 2011, Saunders.)
Coronary arteries.
Cardiovascular Diseases

There are many and varied disorders of the heart and circulatory system. In some
disorders, the rhythm of the heartbeat becomes irregular, may
enter tachycardia (become abnormally fast), or may enter bradycardia (become
abnormally slow).

Disorders of cardiac rhythm are called arrhythmias or dysrhythmias.

Almost one third of all deaths in Western countries are attributed to heart disease.
Most of these deaths are caused by coronary artery disease and hypertension.
Cardiovascular disorders, such as angina pectoris, myocardial infarction (MI),
congestive heart failure (CHF), cardiac arrest, shock, and cardiac tamponade also can
result in death. Other diseases of the cardiovascular system include rheumatic fever,
pericarditis, myocarditis, endocarditis, thromboangiitis obliterans (Buerger’s
disease), Raynaud’s disease, and vascular (blood vessel) diseases.

Important presenting symptoms that tend to recur in patients with cardiovascular disease
and need further investigation include:
• Chest pain
• Dyspnea (difficulty in breathing) on exertion
• Tachypnea (rapid breathing)
• Palpitations (rapid fluttering of the heart)
• Cyanosis (slight blue color)
• Edema
• Fatigue
• Syncope (fainting)
Lymphatic and Blood Disorders
See disorders under discussion of specific diseases.
Coronary Artery Disease
Description
 Coronary artery disease (CAD) is a condition involving the arteries supplying the
myocardium (heart muscle). The arteries become narrowed by atherosclerotic
deposits over time, causing temporary cardiac ischemia and eventually MI
(myocardial infarction, or heart attack).
Symptoms and Signs
 Patients are asymptomatic initially, with the first symptom being the pain of angina
pectoris. In advanced disease, the severe pain of MI is described as burning,
squeezing, crushing, and radiating to the arm, neck, or jaw and is due to diminished
blood flow and lower oxygen saturation. Nausea, vomiting, and weakness also can be
experienced.
 Changes in the electrocardiogram (ECG) are often but not always recognized. Many
patients may be asymptomatic up until an MI or sudden death event; therefore
noninvasive screening of high-risk patients is imperative.
Patient Screening
 Severe chest pain of sudden onset with or without previous diagnosis of angina is a
cardiac event and has the potential for being catastrophic; therefore, the patient
should immediately be entered into the emergency medical system.
Etiology
 Deposits of fat-containing substances called plaque in the lumen (opening) of the
coronary arteries result in atherosclerosis and subsequent narrowing of the lumen of
the arteries.
 The myocardium must have an adequate blood supply to function. The coronary
arteries supply the cardiac muscle with blood but become constricted by
atherosclerosis.
Development of an atheroma leading to arterial occlusion. (From Gould B: Pathophysiology
for the health professions, ed 3, Philadelphia, 2006, Saunders.)

Possible consequences of atherosclerosis. (From Gould B: Pathophysiology for the
health professions, ed 3, Philadelphia, 2006, Saunders.)
 Arteriosclerosis, commonly called “hardening of the arteries,” is associated with the
elderly and diabetics.
 The arteries eventually lose elasticity and become hard and narrow, resulting in
cardiac ischemia. The cells in the myocardium gradually weaken and die.
Replacement scar tissue forms, interfering with the heart’s ability to pump, resulting
in heart failure.
 People at higher risk for CAD are those who have a genetic predisposition to the
disease, those older than 40 years of age, men (slightly more than women),
postmenopausal women, and Caucasians.

Other factors contributing to increased risk of the disease include a history of
smoking; residence in an urban society; the presence of hypertension, diabetes, or
obesity; and a history of elevated serum cholesterol or reduced serum high-density
lipoprotein (HDL) levels. Lack of exercise (a sedentary lifestyle) and stress are
additional risk factors.
Diagnosis
 The patient usually does not experience chest pain from atherosclerosis until the
coronary arteries are about 75% occluded.
 Collateral circulation often develops to supply the tissue with needed oxygen and
nutrients (Figure 10-10). An ECG shows ischemia (caused by a lack of blood supply)
and possibly arrhythmias.


Treadmill testing, thallium or Cardiolite scan, CT scans, stress echocardiograms,
cardiac catheterization, E10-1, and angiograms are other tools of cardiac status
evaluation used to detect insufficient oxygen supply and to confirm the diagnosis.
Electron beam computerized testing, a noninvasive assessment identifying calcium
buildup in arteries, is another means of risk evaluation.
Collateral circulation of the heart. (From Gould B: Pathophysiology for the health
professions, ed 3, Philadelphia, 2006, Saunders.)
Treatment
 Treatment consists of measures to restore adequate blood flow to the myocardium.
Vasodilators and other types of medicines are prescribed.
 Angioplasty with a balloon or stenting is attempted in some instances to open the
constricted arteries (Figure 10-11).
 Claims of reduction of the plaque buildup with hypolipidemic drugs are being
confirmed in some cases. First line drug therapy for the prevention of CAD may
include angiotensin-converting enzyme inhibitors (ACE inhibitors), angiotensin
receptor blockers (ARBs), calcium channel blockers (CCBs), thiazide diuretics, or
vasodilators. Beta-blockers and anticoagulants are used to prevent blood clots from
breaking off and lodging in cerebral arteries.

When the blockage is severe or does not respond to drug therapy or angioplasty,
coronary artery bypass surgery may be indicated to restore circulation to the
affected myocardium.
FIGURE 10–11 Angioplasty.
Coronary artery bypass.
Experimental gene therapy uses injections of DNA directly into cardiac muscle to stimulate
new growth of blood vessels; this is still very preliminary.
Prognosis
 The prognosis varies and depends on the patient’s response to the treatment,
whether prescribed drug therapy, angioplasty, or coronary bypass surgery. An
additional factor affecting the prognosis of smokers is the effect of smoking on the
coronary arteries and whether they cease smoking.
Prevention
 Measures to prevent CAD include a diet that is low in salt, fat, and cholesterol,
combined with exercise. Patients are encouraged to reduce stress and, if they smoke,
to stop or reduce smoking.
Patient Teaching
 Give patients information about symptoms of impending myocardial infarction and
encourage them to seek immediate emergency medical care at the first sign of any
related symptoms. Offer printed information to all patients about the prevention or
control of CAD and emphasize the importance of a low-fat diet, weight
control, exercise, and cessation of smoking. Encourage follow-up cholesterol blood
tests.
Angina Pectoris
Description
 Angina pectoris, chest pain due to ischemia during or shortly after exertion, is the
result of reduced oxygen supply to the myocardium.
Symptoms and Signs
 The patient has a sudden onset of left-sided chest pain during or shortly after
exertion.
 The pain may radiate to the left arm or back. The patient also may experience
dyspnea.
 The pain usually is relieved by ceasing the strenuous activity and placing nitroglycerin
tablets sublingually or using nitroglycerin spray also sublingually (under the tongue).
 The blood pressure may increase during the attack, and arrhythmias may occur.
Common sites of pain in angina pectoris.
Patient Screening
 Patients experiencing symptoms of angina for the first time require immediate
assessment.
 The sudden onset of chest pain could represent a life-threatening condition, and
acute myocardial infarction must be ruled out.
 Those who have been diagnosed with angina pectoris, and in whom cessation of
activity and use of vasodilating medications does not provide relief from the pain
within 20 minutes, require immediate medical intervention through the emergency
medical system.
Etiology
 Atherosclerosis causes a narrowing of the coronary arteries, compromising the blood
flow to the myocardium.
 Exertion requires increased blood flow to supply more oxygen, but the vessels
cannot supply it. S
 spasms of the coronary arteries also may be a causative factor. Severe prolonged
tachycardia, anemias, and respiratory disease also can cause cardiac ischemia.
Diagnosis
 The patient history reveals a previous exertional chest pain. An ECG taken during the
anginal episode may show ischemia; it is important to realize that a normal ECG does
not preclude the diagnosis of angina. Other diagnostic measures, such as those
described for CAD, are performed.
Treatment
 Treatment consists of cessation of the strenuous activity and the placing of
nitroglycerin tablets under the tongue. Transdermal nitroglycerin helps in preventing
angina. When angina persists after treatment or for more than 20 minutes,
immediate medical attention is indicated.
Prognosis
 The prognosis varies and depends on the extent of the arterial involvement. When
patients can stop the pain by ceasing strenuous activities and using vasodilating
medications, the angina usually will diminish or disappear. The patient’s ability to
modify his or her lifestyle may improve the prognosis.
Prevention
 Prevention is similar to that recommended for coronary artery disease.
Recommendations focus on lifestyle modification, including appropriate exercise; a
diet low in fat, cholesterol, and salt; control of hypertension; weight loss; and
smoking cessation. Patients are encouraged to reduce stress.
Patient Teaching
 Patients and families should be given dietary information and suggestions for menu
planning within the appropriate diet. Emphasize the importance of compliance with
prescribed drug therapy. Help the patient and family locate and contact community
services and support groups.
 Patients should be instructed to always carry the nitroglycerin tablets with them.
Additionally, patients and their families should be instructed that the tablets should
not be exposed to light or air and therefore the tablets should be kept in the original
light-resistant bottle with a cap that can be tightened.
Myocardial Infarction
Description
 Myocardial infarction is death of myocardial tissue caused by the development of
ischemia.
Symptoms and Signs
 An occlusion of a coronary artery resulting in ischemia and infarct (death) of the
myocardium causes sudden, severe substernal or left-sided chest pain (Figure 10-14).
 The pain may be crushing, causing a feeling of massive constriction of the chest, may
be burning, or may just be a vague discomfort. This pain may radiate to the left or
right arm, back, or jaw and is not relieved by rest or the administration of
nitroglycerin.
 Irregular heartbeat, dyspnea, and diaphoresis often accompany the pain, and the
patient usually exhibits denial and experiences severe anxiety, sometimes with the
feeling of impending doom.
 MI occasionally is clinically silent, especially in diabetics.
Myocardial infarction.
Locations of pain from myocardial infarction. (From Mosby’s dictionary of medicine, nursing
and health professions, ed 7, St Louis, 2010, Mosby.)
Patient Screening
 Early and immediate intervention improves the chance for survival and minimizes
irreversible injury to the myocardium. Recent recommendations include calling 911 for
entrance into the emergency medical system and chewing one 5 grain/325 mg aspirin
tablet.
 Emergency intervention must be initiated immediately to control pain, stabilize heart
rhythm, and minimize damage to the heart muscle. Most deaths caused by an MI
result from primary ventricular fibrillation. Thus immediate ECG monitoring and
possible defibrillation are of primary concern.

The American Heart Association and the American Red Cross currently recommend
defibrillation training for all certified first responders. The latest technology in AEDs
affords auditory instructions to the rescuer, making the use safe for victim and
rescuer.
Etiology
 Myocardial infarction (MI) results from insufficient oxygen supply, such as occurs
when a coronary artery is occluded by atherosclerotic plaque, thrombus, or
myocardial muscle spasm.
 The pain is caused by ischemia, and if ischemia is not reversed within about 6 hours,
the cardiac muscle dies. Coronary thrombosis is the most common cause of MI.
Common locations of myocardial infarction. (From Lewis SM, Heitkemper MM, Dirksen SR:
Medical-surgical nursing: assessment and management of clinical problems, ed 6, St Louis,
2004, Mosby.)
Diagnosis
 The diagnosis includes a thorough history, electrocardiogram (ECG), chest
radiographic studies, and laboratory tests for cardiac enzyme levels.
 Changes in enzyme levels indicate the death of cardiac tissue and include (1) creatine
phosphokinase (CPK) and troponin, which are elevated in the first 6 to 24 hours after
MI; (2) lactic dehydrogenase (LDH), which peaks at 48 hours after MI; and (3)
aspartate aminotransferase (AST).
 When an elevation of these enzymes is detected, a study of cardiac isoenzymes is
ordered to confirm the diagnosis. ECG changes in the P–R and QRS complexes and in
the ST segment correspond to the ischemic areas. Diagnostic confirmation is assisted
by elevated cardiac enzyme levels and altered isoenzyme levels identified through
blood tests.
Treatment
 Oxygen is administered, and morphine is given for pain. Aspirin is given as soon as
possible to reduce the risk of additional damage to the heart and tissue by ischemia.
 Vasodilation is attempted by nitroglycerin drip. Lidocaine or amiodarone given by an
intravenous drip, after a loading bolus, helps to control arrhythmias. Thrombolytic
drugs, including tissue plasminogen activator (TPA), streptokinase, or alteplase
(Activase) may be administered as soon as possible after the diagnosis, unless there
are contraindications.
 Within the 6-hour window before permanent damage, an attempt may be made to
open the occlusion and to restore blood flow to the area by angioplasty (see Figure
10-11), the administration of thrombolytic drugs, or by coronary artery bypass surgery.
 Currently, the standard of care is to try to emergently open the artery with a stent,
preferably within 60 to 90 minutes of arrival; this has been demonstrated to more
effectively decrease heart damage than IV thrombolytic drugs. E10-2
Coronary bypass graft. (From Mosby’s dictionary of medicine, nursing and health
professions, ed 7, St Louis, 2010, Mosby.)
Coronary artery stent. (From Mosby’s dictionary of medicine, nursing and health
professions, ed 7, St Louis, 2010, Mosby.)
Prognosis
 About 65% of deaths caused by MI occur in the first hour. The prognosis is
determined by immediate defibrillation for ventricular fibrillation. Late mortality
depends on the extent of damage to the heart muscle and the occurrence of
complications. Most late cardiac death is sudden, caused by the onset of a fatal
arrhythmia.
Prevention
 The prevention is similar to that recommended for coronary artery disease.
Recommendations focus on lifestyle modification, including appropriate exercise; a
diet low in fat, cholesterol, and salt; control of hypertension; weight loss; and
smoking cessation. Patients are encouraged to reduce stress. Those surviving an MI
are urged to take a daily aspirin dose and a beta-blocker or ACE inhibitor for life.
Lipid-lowering medications are also recommended.
Patient Teaching
 Give patients and families dietary information and suggestions for menu planning
within the appropriate diet. Emphasize the importance of compliance with
prescribed drug therapy. Help the patient and family find and contact community
services and support groups.
Cardiac Arrest
Description
 Cardiac arrest is the sudden, unexpected cessation of cardiac activity.
Symptoms and Signs
 The patient is unresponsive, with no respiratory effort and no palpable pulse.
Patient Screening


Cardiac arrest is a true life-threatening emergency. Immediate intervention with
instantaneous initiation of CPR and defibrillation by means of an automated external
defibrillator (AED) may successfully restore contraction of the heart (Figure 10-19).
The American Heart Association or American Red Cross protocol for caregivers in the
field requires immediate contact of the emergency medical system by calling 911.
Inpatient facilities use the “Code, Dr. Blue” message to alert personnel.
Photo of an automated external defibrillator. (Courtesy David Frazier, 2011, in cooperation
with St Johns County Sheriff’s Office, St Augustine, Fla.)
Etiology
 Cardiac arrest results from anoxia (absence of oxygen to the tissue) or interruption
of the electrical stimuli to the heart. It can be caused by respiratory arrest,
arrhythmia, or MI. Electrocution, drowning, severe trauma, massive hemorrhage, or
drug overdose also can cause cardiac arrest.
Diagnosis
 The diagnosis is based on the absence of respiratory effort and lack of palpable pulse.
The ECG shows ventricular fibrillation or asystole.
Treatment
 Cardiopulmonary resuscitation (CPR) must be instituted within 4 to 6 minutes of the
cardiac arrest. Until recently, cardiac defibrillation was only attempted by trained,
advanced life-support personnel. AEDs are now available for use by anyone who
observes a cardiac arrest.
 The latest technology implemented in these devices talks the rescuer through the
defibrillation process (see Figure 10-19). T
 he rescuer should be familiar with the device he/she is attempting to use. Cardiac
drugs are administered, including epinephrine (Adrenalin) and isoproterenol (Isuprel)
or dobutamine to stimulate the heart. Antiarrhythmic drugs, including lidocaine and
amiodarone, also may be administered.
Prognosis
 The prognosis varies depending on the length of time the individual has been in
cardiac arrest. The earlier in the event that CPR and defibrillation are instituted, the
greater possibility there is for survival.
 Within 1 to 2 minutes after cessation of cardiac activity, respiratory efforts will cease.
At 4 to 6 minutes after the cessation of cardiac activity, brain cells will begin to die. At
10 minutes after the cardiac activity has ceased with no intervention, the brain will die
and death is inevitable. Many public venues and emergency vehicles now have
portable defibrillators to allow more rapid resumption of cardiac function.
 Successful resuscitation depends on immediate and complete intervention. Other
factors that affect the outcome of the event include the general health and age of
the patient and the cause of the arrest.
 Successful interventions in cold water near drowning and electrical shock have been
recorded.
Prevention
 Prevention of the catastrophic event of cardiac arrest is problematic. However, as in
CAD and myocardial infarction, the same lifestyle modifications can reduce risk. One
cannot predict near drowning or electrical shock accidents, but the prudent
individual will try to avoid situations that carry this risk.

Recently, in high-risk patients with a history of abnormal heart rhythms or weak
heart muscle, the implanting of defibrillators has been shown to decrease the risk of
sudden cardiac death.
Patient Teaching
 Encourage all possible candidates for CPR training to become certified. Help families
of patients who do not survive cardiac arrest to find and contact support groups in
the community. Emphasize safety guidelines to prevent drowning and electrical
shock.
 Encourage survivors of cardiac arrest to comply with the prescribed regimen of
activities and drug therapy. Survivors also may need help in finding and contacting
support groups for survivors of cardiac arrest.