Download Pericarditis

Chapter 19
Common Cardiovascular
Disorders
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Layers of the Heart
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Pericarditis
• Pericardium surrounds the external surface of the heart and the roots
of the great vessels.
• Two layers: outer tough fibrous pericardium; inner serous layer
• Serous pericardium has two layers:
–
The parietal layer lines the internal surface of the fibrous
membrane.
–
It extends to the great vessels, where it then folds over on itself
to form the inner visceral layer (epicardium).
• 10 to 50 mL of clear serous fluid lies between these layers and acts as
a lubricant.
• The pericardium helps restrain the heart and isolate it from infections
in the surrounding structures.
• Pericarditis is inflammation of the pericardium.
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Question
• Which of the following confirms the diagnosis of
pericarditis?
– A. Pain on inspiration
– B. Chest pain
– C. Pericardial friction rub
– D. Low-grade fever
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Answer
• C. Pericardial friction rub
• Rationale: There may also be general symptoms of an
infection, such as a low-grade fever, tachycardia, or
malaise. The presence of a pericardial friction rub
confirms the diagnosis; however, absence of a rub does
not rule out pericarditis. The classic friction rub produces
a rasping or scraping, high-pitched sound that varies
with the cardiac cycle. The rub may wax and wane and
may even transiently disappear during the course of the
illness. It is best heard with the diaphragm of the
stethoscope placed over the lower to middle left sternal
edge.
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Assessment—Pericarditis
• Thorough history and physical examination
• Chest pain is the primary symptom.
• Pain is worse with breathing deeply or lying supine;
relieved by sitting up, leaning forward, and taking
shallow breaths.
• S & S of infection
• Pericardial friction rub confirms the diagnosis.
• Friction rub produces a rasping or scraping, high-pitched
sound that varies with the cardiac cycle.
– Best heard over the lower to middle left sternal edge
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Assessment—Pericarditis (cont.)
• Diffuse ST-segment elevation with an upward concavity
and PR-segment depression
• Laboratory tests include
– CBC, cardiac enzyme levels, rheumatoid factors, and
antinuclear antibody titers
– Blood cultures may be indicated if there is evidence
of infection.
– Viral studies may be obtained if the rest of the
diagnostic workup is negative.
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Management—Pericarditis
• Relieve symptoms, eliminate any possible causative
agents, and monitor for complications.
• NSAIDs, such as aspirin or ibuprofen
• Steroids may be indicated in resistant cases.
• Anticoagulants must be avoided in the patient recovering
from MI.
• Abates over 2 to 6 weeks
• Rare to have recurrent episodes
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Question
• Which of the following is a cause of sudden death in
athletes?
– A. Pericarditis
– B. Myocarditis
– C. Endocarditis
– D. Cardiomyopathy
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Answer
• B. Myocarditis
• Rationale: Myocarditis can be a devastating illness that
evolves into a chronic, progressive disease with a poor
prognosis. The disorder may result in dysrhythmias,
congestive heart failure, or death. It is also recognized as
a cause of sudden death in young athletes.
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Myocarditis
• Inflammation of the myocardium
• Primary myocarditis is believed to be related to an acute
viral infection or an autoimmune response to the
infection.
• Secondary myocarditis is inflammation related to a
specific organism.
• May result in dysrhythmias, congestive heart failure, or
death
• Cause of sudden death in young athletes
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Assessment—Myocarditis
• With viral myocarditis, there is a delay before the onset of
cardiac symptoms, such as congestive heart failure or
dysrhythmias.
• S & S:
– Fatigue, dyspnea, palpitations, and precordial discomfort
– Slight rise in serum enzyme levels
– Nonspecific ST-T wave changes
• Definitive diagnosis requires a positive endomyocardial biopsy.
• Lack of a positive biopsy does not rule out myocarditis.
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Management—Myocarditis
• Treatment is supportive.
• Treatment with corticosteroids or immunosuppressive agents
has not been shown effective.
• Myocarditis may resolve without further sequelae.
• Subacute disease may develop with persistent laboratory
findings of inflammation.
• Athletes with myocarditis should withdraw from competitive
sports for a period of at least 6 months.
– Return to training and competition depends on
normalization of cardiac function and absence of any
significant clinical findings, such as dysrhythmias.
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Endocarditis
• Endocarditis is an infection of the endocardial surface
of the heart (IE), including the valves, caused by
bacterial, viral, or fungal agents.
• Children with congenital heart disease are at risk.
• Adults with mitral valve prolapse, rheumatic heart
disease, illicit intravenous drugs, and patients with
prosthetic valves or long-term indwelling devices
• Common infectious organisms include streptococci,
enterococci, and Staphylococcus aureus.
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Endocarditis (cont.)
• The development of IE is a complex process that requires the
occurrence of several critical elements:
– Endothelial damage exposes the basement membrane of
the valve to turbulent blood flow.
– This exposure leads to the development of a platelet and
fibrin clot on the valve leaflet. The clots, or vegetations, are
exposed to bacteria by way of the bloodstream, such as
occurs after dental manipulations or urological procedures.
– Bacterial proliferation takes place.
• The infected vegetation eventually damages the valve structure.
• The incompetent valves eventually lead to severe heart failure.
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Assessment—Endocarditis
• Symptoms of endocarditis usually occur within 2 weeks of the precipitating
bacteremia.
• Four underlying processes: bacteremia or fungemia, valvulitis, immunologic
response, and peripheral emboli
• S & S: nonspecific, general malaise, anorexia, fatigue, weight loss, and night
sweats
• Careful history focusing on risk factors for IE and a physical examination
• Fever and a new or changed heart murmur are present in almost all patients.
• Definitive diagnosis of IE includes persistent bacteremia and evidence of
myocardial involvement such as echocardiographic visualization of a vegetation
or new or worsening murmur (Duke criteria).
• Blood is usually drawn for three separate sets of cultures.
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Management—Endocarditis
• Early identification of complications is key to good patient
outcomes.
• Antibiotic therapy is based on the results and the clinical setting.
• Treatment should not be delayed while waiting for identification of
the specific organism.
• Immediate surgical intervention is indicated in the presence of
severe congestive heart failure secondary to valve dysfunction,
uncontrolled infections, and prosthetic valve dysfunction or
dehiscence.
• Usually requires a prolonged course of antibiotic therapy
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Cardiomyopathies
• Cardiomyopathies are diseases of the heart muscle that cause
cardiac dysfunction resulting in heart failure, dysrhythmias, or
sudden death.
• Current theories under investigation suggest that ischemic,
immune, mechanical, and neurohormonal effects on the
pericardium, myocardium, and endothelium lead to structural
changes that result in functional changes.
• Structural changes at the cellular level leads to stiffness of the
ventricles and smooth muscle layers in the arteries.
• Both stiffness and spherical remodeling may occur in the same
heart, leading to a compromised cardiac output from impaired
relaxation and impaired emptying.
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Dilated Cardiomyopathy
• Increased myocardial cavity size in the presence of normal or reduced left
ventricular wall thickness and impaired systolic function
• Ischemia, alcohol abuse, endocrine disorders, pregnancy, viral infections, and
valvular disease may cause a decrease in contractility.
• Decreased contractility (ejection fraction <40%) results in an increased endsystolic volume.
• Over time, the ventricle dilates to accommodate the increased intraventricular
volumes (preload).
• In the dilated heart, the increased volume leads to a decreased stroke volume.
• Mitral and tricuspid insufficiency develop as the valve leaflets are stretched
and separated.
• Dysrhythmias and conduction defects commonly occur.
• DCM is the third most common cause of heart failure and the most frequent
cause of heart transplantation.
• In most cases, the specific cause is unknown.
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Ischemic Cardiomyopathy
• Result of oxygen levels that are inadequate to meet the metabolic
demands of the myocardial cells
• Caused by obstruction in the coronary arteries; may be acute or
chronic
• Severe, persistent ischemia causes the muscle tissue to die (MI).
• Dead muscle is replaced with scar tissue. The larger the scar, the
greater the dysfunction.
• Decreased muscle mass leads to decreased energy for pumping blood
and decreased cardiac output.
• Cardiogenic shock results.
• Left ventricular end-diastolic pressure increases, pulmonary artery
pressures increase, and pulmonary edema results.
• End-organ damage occurs.
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Nonischemic Cardiomyopathy
• Several causes:
– Idiopathic cardiomyopathy: heart dilates, remodels,
and becomes ineffective to pump.
– Myocarditis
– May result from pregnancy, heavy alcohol use,
hypertension, and tachycardia
• May be acute or chronic
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Question
• Is the following statement true or false?
• In dilated cardiomyopathy, the presence of right-sided
heart failure is a poor prognosis.
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Answer
• True
• Rationale: The natural history of DCM is not well defined.
Some patients remain asymptomatic or have minimal
clinical findings. Symptoms usually develop gradually and
are typically related to left ventricular heart failure. The
presence of right-sided heart failure is associated with
poor prognosis.
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Assessment—DCM
• Some patients remain asymptomatic or have minimal clinical
findings.
• Symptoms develop gradually and are typically related to left
ventricular heart failure.
• The presence of right-sided heart failure is associated with poor
prognosis.
• Laboratory tests include screening for potentially reversible
causes, including human immunodeficiency virus.
• The echocardiogram differentiates the primary abnormality and
determines ejection fraction.
• Cardiac catheterization to rule out coronary artery disease
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Management—DCM
• Identify and eliminate potential causes of DCM.
• Myocardial damage related to ingesting alcohol is reversible if
detected early and the patient abstains from further drinking.
• Control of heart failure, dysrhythmias, or intracoronary thrombus
• Biventricular for severe symptomatic heart failure, prolonged QRS,
dilated left ventricle, and poor ejection fraction
• Implantable cardioverter–defibrillators (ICDs) to prevent sudden
death associated with lethal dysrhythmias
• Heart transplantation and some medical therapies have been
shown to prolong life.
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Hypertrophic Cardiomyopathy (HCM)
• Hypertrophied, nondilated left ventricle not related to any
obvious cause (ie, hypertension or aortic valve stenosis)
• Diastolic dysfunction is a characteristic feature.
• The heart can contract but cannot relax and remains
abnormally stiff in diastole.
• Septal wall hypertrophy may occur, leading to a left
ventricular outflow tract obstruction during systole.
• Sudden death, usually from a ventricular dysrhythmia, in
asymptomatic or mildly symptomatic people of any age
group
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Assessment—HCM
• Often found unexpectedly during investigation of heart
murmurs or family screening
• The most common symptom is dyspnea.
• Presyncope and syncope also frequently occur.
• Left ventricular hypertrophy (LVH) present on the
echocardiogram confirms the diagnosis.
• Borderline LVH may be a normal finding in competitive
athletes.
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Management—HCM
• Control symptoms.
• Prevent complications and reduce the risk for sudden
death.
• Genetic screening and counseling
• Most symptomatic patients can be medically managed.
• ICD
• Percutaneous ablation with ethanol or surgery to remove
a portion of the septum may be necessary.
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Peripheral Vascular Disease
• A group of distinct disorders involving the arteries, veins,
and lymphatic vessels of the peripheral circulation
• Noncardiac diseases that affect the circulation as a whole
– Peripheral arterial disease (PAD)
– Venous disease
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Peripheral Arterial Disease
• Processes that obstruct the blood supply of the lower or
upper extremities
• Symptomatic PAD is a disease of the elderly found more
commonly in men aged 70 years and older.
• Patients of any age with risk factors for atherosclerosis,
such as smoking or diabetes
• Other risk factors: hypertension, lipid disorders, family
history, postmenopausal state, and
hyperhomocysteinemia
• The disease develops in major bifurcations and areas of
acute angulations.
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Question
• Which of the following is a classic symptom of PAD?
– A. Intermittent claudication
– B. Hair loss on extremities
– C. Thick nails
– D. Dry skin
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Answer
•
A. Intermittent claudication
•
Rationale: The classic symptom of PAD is intermittent
claudication, experienced as a cramping, burning, or
aching pain in the legs or buttocks that is relieved with
rest.
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Assessment—PAD
• The classic symptom of PAD is intermittent claudication.
• Trophic changes, such as hair loss on the extremities,
thickening of the nails, and drying of the skin
• Sudden onset of extreme pain indicates acute arterial
obstruction.
• Careful vascular examination of the extremities and
assessment of all peripheral pulses
• ABI is the ratio of ankle to brachial systolic blood
pressure.
– Normal—1.0 or greater
– Critical limb ischemia—less than 0.518
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Management—PAD
• Modifying or eliminating risk factors
• Smoking cessation, aggressive treatment of
hypertension, diabetes, and lipid disorders
• Antiplatelets (aspirin or clopidogrel [Plavix]) to reduce
the risk for MI and stroke and cilostazol (Pletal) to
increase walking distance
• Peripheral balloon angioplasty
• Surgical bypass in severe obstruction
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Venous Disease
• Phlebitis is inflammation of the vessel wall occurring as
the result of direct injury to the vein or as a complication
of varicose veins.
• Can lead to the formation of a thrombus (VTE)
• Factors that predispose a patient to thrombus formation
are vessel wall injury, stasis of blood, and increased
blood coagulability (Virchow’s triad).
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Assessment—Venous Disease
• DVT is characterized by pain, swelling, tenderness, and
increased temperature over the affected area.
• Positive Homans’ sign (pain in the calf with passive
dorsiflexion of the foot)
• Accurate diagnosis requires diagnostic testing such as
compression ultrasonography.
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Management—Venous Disease
• Relieve symptoms, increase blood flow, and prevent
complications.
• Patients with DVT are at high risk for pulmonary
embolism.
• Treatment:
– Anticoagulant, long-term warfarin
– Assess for bleeding.
– Patient education to decrease recurrence of DVT
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Aortic Disease
• Longest and strongest artery in the body
• Congenital, degenerative, hemodynamic, and mechanical
factors stress the vessel’s elasticity.
• Dilation of the aortic wall may lead to aortic dissection or
rupture.
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Abdominal Aortic Aneurysm
• More common than thoracic aortic aneurysms
• Men > women
• Risk factors: smoking, age, hypertension, lipid disorders,
atherosclerosis, genetic and environmental influences
• The major risk from AAAs is rupture, which is associated
with a high rate of mortality.
• Typically identified during health screening for another
problem.
• Abdominal or back pain is the most common complaint.
• Worsening of symptoms is usually related to expansion or
rupture of the aneurysm.
• Abdominal ultrasonography is the most practical method of
confirming the diagnosis.
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Management—AAA
• Control of hypertension and elimination of risk factors
• Follow with serial noninvasive tests, such as
ultrasonography.
• Treatment involves surgical repair (AAA>5.5 cm).
• Minimally invasive approach using an endovascular graft
has become the treatment of choice for high-risk
patients.
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Thoracic Aortic Aneurysm
• Occur infrequently and are classified by the involved segment
of the aorta (root, ascending, arch, or descending)
• Etiology, natural history, and treatment differ for each segment
involved.
• Most ascending thoracic aortic aneurysms are due to cystic
medial degeneration.
• Ascending thoracic aortic aneurysms are also associated with
connective tissue disorders, genetic disorders, bicuspid aortic
valve, infections, inflammatory diseases, chronic aortic
dissection, and trauma.
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Assessment—Thoracic Aortic Aneurysm
• Most are asymptomatic at the time of diagnosis.
• Symptoms are related to the size and location of the
aneurysm; these include aortic insufficiency and signs of
pericardial tamponade if the aneurysm involves the aortic
root.
• Rupture or acute dissection of a thoracic aneurysm can be
fatal.
• Fewer than half of patients with rupture survive until they
are hospitalized, and by 24 hours, mortality is almost 80%.
• Management:
– Surgical repair is indicated at a diameter of 5.5 cm or
more.
– Repair of descending thoracic aneurysms is
recommended when the diameter is 6 cm or more.
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Aortic Dissection
• Acute aortic dissection is the most common and the most
lethal process involving the aorta.
• Mortality rates are very high, approaching 1% per hour.
• Death usually occurs from rupture of the aorta.
• Pathophysiology
– Dissection involves a longitudinal separation of the
medial layers of the aorta by a column of blood.
– The dissection begins at a tear in the aortic wall,
usually at the proximal end of the dissection.
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Assessment—Aortic Dissection
• Sudden, intense chest pain; “ripping” or “tearing”
• Careful history and physical examination
• Assess for aortic regurgitation or alteration of peripheral
pulses.
• Widened mediastinum on CXR
• Ischemia, tamponade, elevated serum creatinine,
decreased urine output, severe hypertension
• Transesophageal echo or CT with contrast confirms
diagnosis.
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Management—Aortic Dissection
• Timely diagnosis
• Blood pressure control
• Pain management
• Surgery for dissection of ascending aorta
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Classification of Blood Pressure for Adults
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Hypertensive Crisis
• Pathophysiology
– Marked rapid increase in BP
– Compensatory intense vasoconstriction
– May lead to hypertensive encephalopathy
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Assessment—Hypertensive Crisis
• S & S: headache, visual disturbances, confusion, nausea,
vomiting
• Cotton-wool exudate and hemorrhages of eyes
• Chest pain
• Decreased urine output or azotemia
• Management
– Reduce BP by not more than 25% within 1 hour.
– Continuous monitoring
– Identify the cause.
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