Chapter 23: Alterations of Cardiovascular Function

Key Points

Did You Understand?
Diseases of the Veins and Arteries
1. Varicosities are areas of veins in which blood has pooled, usually in the saphenous
veins. Varicosities may be caused by damaged valves as a result of trauma to the
valve or by chronic venous distention involving gravity and venous constriction.
2. Chronic venous insufficiency is inadequate venous return over a long period of time
that causes pathologic ischemic changes in the vasculature, skin, and supporting
tissues.
3. Venous stasis ulcers follow the development of chronic venous insufficiency and
probably develop as a result of the borderline metabolic state of the cells in the
affected extremities.
4. Deep venous thrombosis results from stasis of blood flow, endothelial damage or
hypercoagulability. The most serious complication of deep venous thrombosis is
pulmonary embolism.
5. Superior vena cava syndrome is a progressive occlusion of the superior vena cava that
leads to venous distention in the upper extremities and head. Because this syndrome
is usually caused by bronchogenic cancer, it is generally considered an oncologic
emergency rather than a vascular emergency.
6. Hypertension is the elevation of systemic arterial blood pressure resulting from
increases in cardiac output (such as an increase in blood volume), total peripheral
resistance, or both.
7. Hypertension can be primary, without a known cause, or secondary, caused by an
underlying disease.
8. The risk factors for hypertension include a positive family history; male gender;
advancing age; black race; obesity; high sodium intake; low magnesium, potassium or
calcium intake; diabetes mellitus; cigarette smoking; and heavy alcohol consumption.
9. The exact cause of primary hypertension is unknown, although several hypotheses are
proposed, including overactivity of the sympathetic nervous system; overactivity of
the renin-angiotensin-aldosterone system; sodium and water retention by the kidneys;
hormonal inhibition of sodium-potassium transport across cell walls; and complex
interactions involving insulin resistance, inflammation, and endothelial function.
10. Clinical manifestations of hypertension result from damage of organs and tissues
outside the vascular system. These include retinal changes, heart disease, renal
disease, and central nervous system problems, such as stroke and dementia.
11. Hypertension is managed with both pharmacologic and nonpharmacologic methods
that lower the blood volume and the total peripheral resistance.
12. Orthostatic hypotension is a drop in blood pressure that occurs on standing. The
compensatory vasoconstriction response to standing is replaced by a marked
vasodilation and blood pooling in the muscle vasculature.

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Huether and McCance: Understanding Pathophysiology, 5
th
Edition
Key Points 23-2
13. The clinical manifestations of orthostatic hypotension include fainting and may
involve cardiovascular symptoms, as well as impotence and bowel and bladder
dysfunction.
14. An aneurysm is a localized dilation of a vessel wall, to which the aorta is particularly
susceptible.
15. A thrombus is a clot that remains attached to a vascular wall. An embolus is a mobile
aggregate of a variety of substances that occludes the vasculature. Sources of emboli
include clots, air, amniotic fluid, bacteria, fat, and foreign matter. These emboli cause
ischemia and necrosis when a vessel is totally blocked.
16. The most common source of arterial thrombotic emboli is the heart as a result of
mitral and aortic valvular disease and atrial fibrillation, followed by myxomas.
Tissues affected include the lower extremities, the brain, and the heart.
17. Emboli to the central organs cause tissue death in lungs, kidneys, and mesentery.
18. Peripheral vascular diseases include Buerger disease and Raynaud disease, involving
arterioles of the extremities.
19. Atherosclerosis is a form of arteriosclerosis and is the leading contributor to coronary
artery disease (abbreviated CAD) and cerebrovascular disease (abbreviated CVD).
20. Atherosclerosis is an inflammatory disease that begins with endothelial injury.
21. Important steps in atherogenesis include vasoconstriction, adherence of macrophages,
release of inflammatory mediators, oxidation of low density lipoproteins, formation
of foam cells and fatty streaks, and fibrous plaque formation.
22. Once a plaque has formed, it can rupture, resulting in clot formation and instability
and vasoconstriction leading to obstruction of the lumen and inadequate oxygen
delivery to tissues.
23. Peripheral artery disease is the result of atherosclerotic plaque formation in the
arteries that supply the extremities, and it causes pain and ischemic changes in the
nerves, muscles, and skin of the limb.
24. Coronary artery disease (abbreviated CAD) is the result of an atherosclerotic plaque
that gradually narrows the coronary arteries or that ruptures and causes sudden
thrombus formation.
25. Many risk factors contribute to the onset and escalation of coronary artery disease,
including traditional risk factors such as dyslipidemia, smoking, hypertension,
diabetes mellitus (related to insulin resistance), obesity or sedentary lifestyle, and
nontraditional risk factors such as elevated C-reactive protein,
hyperhomocysteinemia, and changes in adipokines.
26. Ischemic heart disease is most commonly the result of coronary artery disease and the
resultant decrease in myocardial blood supply.
27. Atherosclerotic plaque progression can be gradual, causing stable angina pectoris
which is predictable chest pain caused by myocardial ischemia in response to
increased oxygen demand (such as from exercise) without infarction.
28. Prinzmetal angina results from coronary artery vasospasm.
29. Myocardial ischemia may be asymptomatic, which is called silent ischemia, and is a
risk factor for the development of the acute coronary syndromes.
30. Sudden coronary obstruction due to thrombus formation causes the acute coronary
syndromes. These include unstable angina, non ST-elevation myocardial infarction
(known as a nonSTEMI) and ST elevation myocardial infarction (abbreviated STEMI).
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Key Points 23-3
31. Unstable angina results in reversible myocardial ischemia.
32. Myocardial infarction is caused by prolonged, unrelieved ischemia that interrupts
blood supply to the myocardium. After about 20 minutes of myocardial ischemia,
irreversible hypoxic injury causes cellular death and tissue necrosis.
33. Myocardial infarction is clinically classified as non-ST elevation myocardial
infarction or ST elevation myocardial infarction based on electrocardiographic
findings that suggest the extent of myocardial damage (identifying subendocardial
versus transmural).
34. An increase in plasma enzyme levels is used to diagnose the occurrence of
myocardial infarction and indicate its severity. Elevations of the isoenzymes creatine
kinase, troponins, and lactic dehydrogenase are most predictive of a myocardial
infarction.
35. Treatment of a myocardial infarction includes revascularization (through the use of
thrombolytics or percutaneous coronary intervention), antithrombotics, angiotensin-
converting enzyme inhibitors, and beta-blockers. Pain relief and fluid management
also are key components of care. Dysrhythmias and cardiac failure are the most
common complications of acute myocardial infarction.

Disorders of the Heart Wall
1. Inflammation of the pericardium, or pericarditis, may result from several sources
(such as infection, drug therapy or tumors). Pericarditis presents with symptoms that
are physically troublesome, but in and of themselves they are not life-threatening.
2. Fluid may collect within the pericardial sac (known as pericardial effusion). Cardiac
function may be severely impaired if the accumulation of fluid occurs rapidly and
involves a large volume.
3. Cardiomyopathies are a diverse group of primary myocardial disorders that are
usually the result of remodeling, neurohumoral responses, and hypertension. The
cardiomyopathies are categorized as dilated (or congestive), restrictive (or rigid and
noncompliant), and hypertrophic (or asymmetric). The size of the cardiac muscle
walls and chambers may increase or decrease depending on the type of
cardiomyopathy, thereby altering contractile activity.
4. The hemodynamic integrity of the cardiovascular system depends to a great extent on
properly functioning cardiac valves. Congenital or acquired disorders that result in
stenosis, regurgitation, or both can structurally alter the valves.
5. Characteristic heart sounds, cardiac murmurs, and systemic complaints assist in
determining which valve is abnormal. If severely compromised function exists, a
prosthetic heart valve may be surgically implanted to replace the faulty one.
6. Mitral valve prolapse describes the condition in which the mitral valve leaflets do not
position themselves properly during systole. Mitral valve prolapse may be a
completely asymptomatic condition or can result in unpredictable symptoms.
Afflicted valves are at greater risk for developing infective endocarditis.
7. Rheumatic fever is an inflammatory disease that results from a delayed immune
response to a streptococcal infection in genetically predisposed individuals. The
disorder usually resolves without sequelae if treated early.
8. Severe or untreated cases of rheumatic fever may progress to rheumatic heart disease,
a potentially disabling cardiovascular disorder.
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Key Points 23-4
9. Infective endocarditis is a general term for infection and inflammation of the
endocardium, especially the cardiac valves. In the mildest cases, valvular function
may be slightly impaired by vegetations that collect on the valve leaflets. If left
unchecked, severe valve abnormalities, chronic bacteremia, and systemic emboli may
occur as vegetations break off the valve surface and travel through the bloodstream.
Antibiotic therapy can limit the extension of this disease.
10. Human immunodeficiency virus (abbreviated HIV) infection and autoimmune
deficiency syndrome are associated with cardiac abnormalities, including
myocarditis, endocarditis, pericarditis, and cardiomyopathy.

Manifestations of Heart Disease
1. A dysrhythmia (also referred to as arrhythmia) is a disturbance of heart rhythm.
Dysrhythmias range in severity from occasional missed beats or rapid beats to
disturbances that impair myocardial contractility and are life-threatening.
2. Dysrhythmias can occur because of an abnormal rate of impulse generation or the
abnormal conduction of impulses.
3. Heart failure is an inability of the heart to supply the metabolism with adequate
circulatory volume and pressure.
4. Left heart failure (known as congestive heart failure) can be divided into systolic and
diastolic heart failure.
5. The most common causes of left ventricular failure are myocardial infarction and
hypertension.
6. Systolic heart failure is caused by increased preload, decreased contractility, or
increased afterload. These processes result in an increased left ventricular end-
diastolic volume and an increase in left ventricular end-diastolic pressure that results
in increased pulmonary venous pressures and pulmonary edema.
7. In addition to the hemodynamic changes of left ventricular failure, there is a
neuroendocrine response that tends to exacerbate and perpetuate the condition.
8. The neuroendocrine mediators of heart failure include the sympathetic nervous
system and the renin-angiotensin-aldosterone system; thus, diuretics, beta-blockers,
and angiotensin-converting enzyme (abbreviated ACE) inhibitors are important
components of the pharmacologic therapy.
9. Diastolic heart failure is a clinical syndrome characterized by the symptoms and signs
of heart failure, a preserved ejection fraction, and abnormal diastolic function.
10. Diastolic dysfunction means that the left ventricular end-diastolic pressure is
increased, even if volume and cardiac output are normal.
11. Right heart failure can result from left heart failure or pulmonary disease.

Shock
1. Shock is a widespread impairment of cellular metabolism involving positive feedback
loops that places the individual on a downward physiologic spiral leading to multiple
organ dysfunction syndrome.
2. Types of shock are cardiogenic, hypovolemic, neurogenic, anaphylactic, and septic.
Multiple organ dysfunction syndrome can develop from all types of shock.
3. The final common pathway in all types of shock is impaired cellular metabolism
cells switch from aerobic to anaerobic metabolism. Energy stores drop, and cellular
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Key Points 23-5
mechanisms relative to membrane permeability, action potentials, and lysozyme
release fail.
4. Anaerobic metabolism results in activation of the inflammatory response, decreased
circulatory volume, and decreasing pH.
5. Impaired cellular metabolism results in cellular inability to use glucose because of
impaired glucose delivery or impaired glucose intake, resulting in a shift to
glycogenolysis, gluconeogenesis, and lipolysis for fuel generation.
6. Glycogenolysis is effective for about ten hours. Gluconeogenesis results in the use of
proteins necessary for structure, function, repair, and replication that leads to more
impaired cellular metabolism.
7. Gluconeogenesis contributes to lactic acid, uric acid, and ammonia buildup,
interstitial edema, and impairment of the immune system, as well as general muscle
weakness leading to decreased respiratory function and cardiac output.
8. Cardiogenic shock is decreased cardiac output, tissue hypoxia, and the presence of
adequate intravascular volume.
9. Hypovolemic shock is caused by loss of blood or fluid in large amounts. The use of
compensatory mechanisms may be vigorous, but tissue perfusion ultimately decreases
and results in impaired cellular metabolism.
10. Neurogenic shock results from massive vasodilation, causing a relative hypovolemia
even though cardiac output may be high, and results in impaired cellular metabolism.
11. Anaphylactic shock is caused by physiologic recognition of a foreign substance. The
inflammatory response is triggered, and a massive vasodilation with fluid shift into
the interstitium follows. The relative hypovolemia leads to impaired cellular
metabolism.
12. Septic shock begins with impaired cellular metabolism caused by uncontrolled
septicemia. The infecting agent triggers the inflammatory and immune responses.
This inflammatory response is accompanied by widespread changes in tissue and
cellular function.
13. Multiple organ dysfunction syndrome (abbreviated MODS) is the progressive failure
of two or more organ systems after a severe illness or injury. It can be triggered by
chronic inflammation, necrotic tissue, severe trauma, burns, adult respiratory distress
syndrome, acute pancreatitis, and other severe injuries.
14. Multiple organ dysfunction syndrome involves the stress response; changes in the
vascular endothelium resulting in microvascular coagulation; release of complement,
coagulation, and kinin proteins; and numerous inflammatory processes.
Consequences of all these mediators are a maldistribution of blood flow,
hypermetabolism, hypoxic injury, and myocardial depression.
15. Clinical manifestations of multiple organ dysfunction syndrome include
inflammation, tissue hypoxia, and hypermetabolism. All organs can be affected
including the kidney, lung, liver, gastrointestinal tract, and central nervous system.

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