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MedSurg > Chapter 37: Inflammatory and Structural Heart Disorders > Flashcards

Chapter 37: Inflammatory and Structural Heart Disorders Flashcards

1
Q

Valve orifice is smaller. Forward blood flow is impeded. Pressure differences reflect the degree. Constriction/narrowing.

A

Stenosis

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2
Q

Incompetent/insufficient. Incomplete closure of valve leaflets. Results in backward blood flow. Floppy.

A

Regurgitation

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3
Q

Majority of adult cases result from rheumatic heart disease. Scarring of valve leaflets and chordae tendineae. Less common causes: congenital mitral stenosis, Rheumatoid arthritis, SLE.

A

Mitral valve stenosis

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4
Q

Results in decreased blood flow from left atrium to left ventricle. Increase in left atrial pressure and volume causes increase pressure in pulmonary vasculature. Risk for atrial fibrillation d/t overloaded left atrium.

A

Mitral valve stenosis

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5
Q

Exertional dyspnea. Loud S1. Diastolic murmur (rumbling at apex. Low-pitched). Fatigue. Palpitations. Hoarseness (atrial englagement pressing on the laryngeal nerve), hemoptysis (d/t pulmonary HTN). Chest pain (from decreased CO and coronary perfusion), seizures/stroke (from emboli- stagnant blood in atria more likely to clot).

A

Mitral valve stenosis

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6
Q

Most cases caused by MI, chronic rheumatic heart disease, mitral valve prolapse, ischemic papillary muscle dysfunction, and IE. A defect in mitral leaflets, mitral annulus, chord tendineae, or papillary muscles.

A

Mitral valve regurgitation.

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7
Q

Allows blood to flow backward from the LV to the LA because of incomplete valve closure during systole. LV and LA must work harder to preserve an adequate CO.

A

Mitral valve regurgitation

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8
Q

Sudden increase in pressure and volume transmits to the pulmonary bed. This results in pulmonary edema and if untreated cariogenic shock

A

Acute mitral valve regurgitation

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9
Q

Left atrial enlargement d/t additional volume, ventricular dilation and hypertrophy–> decrease in CO.

A

Chronic mitral valve regurgitation

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10
Q

Thready peripheral pulses and cool, clammy extremities.

A

Acute mitral valve regurgitation

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11
Q

May remain asymptomatic for many years. Initial sx of LVF may include weakness, fatigue, palpitations, and dyspnea that gradually progress to orthopnea, PNS and peripheral edema. Increased LV volume leads to an audible S3.

A

Chronic mitral valve regurgitation.

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12
Q

Abnormality of mitral valve leaflets and the papillary muscle or chordae tendineae. Leaflets prolapse back into left atrium during systole. Usually benign with valve closing effectively. Potential complications. Unknown cause but genetic link in some.

A

Mitral valve prolapse.

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13
Q

Most pts are asymptomatic and remain so for their entire lives. Only 10% present with sx. Murmur d/t regurgitation that is louder in systole. Confirmed with echocardiography. Dysrhythmias can cause palpitations, light-headedness, and dizziness. IE may occur in some. May of may not have chest pain- cause is not known (may be a result of abnormal tension on the papillary muscles), unresponsive to nitrates. Treat sx with beta blockers (control palpitations, chest pain). Valvular surgery.

A

Mitral valve prolapse

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14
Q

Patient education: Antibiotic prophylaxis if MR present. Take drugs as prescribed. Healthy diet; avoid caffeine and OTC stimulants. Exercise. Contact HCP or emergency medical services if sx develop or worse (ie. palpitations, fatigue, SOB, anxiety)

A

Mitral valve prolapse

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15
Q

Congenital stenosis usually discovered in childhood, adolescence, or young adulthood. Can also be degenerative or caused by rheumatic fever.

A

Aortic valve stenosis

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16
Q

Causes obstruction of flow from the left ventricle to the aorta during systole. The effect is LV hypertrophy and increase myocardial O2 consumption d/t increased myocardial mass. As the disease progresses and compensatory mechanisms fail, reduced CO leads to decreased tissue perfusion, pulmonary HTN, and HF.

A

Aortic valve stenosis

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17
Q

S/S: develop when the valve orifice becomes about 1/2 of its normal size. Classic triad of angina, syncope, and exertion dyspnea, reflecting LVF. Ausculatory findings: normal or soft S1, diminished or absent S2, systolic murmur, and a prominent S4.
Use nitroglycerin cautiously- reduces preload and BP; can worsen chest pain.

A

Aortic valve stenosis

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18
Q

May be the result of primary disease of the aortic valve leaflets, the aortic root, or both. Trauma, IE, or aortic dissection can cause acute, which constitutes a life-threatening emergency. Chronic is generally the result of rheumatic heart disease, a congenital bicuspid aortic valve, syphilis, or chronic rheumatic conditions such as ankylosing spondylitis or reactive arthritis

A

Aortic valve regurgitation.

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19
Q

Causes retrograde (backward) blood flow from the ascending aorta into the LV during diastole, resulting in volume overload. The LV initially compensates for chronic by dilation and hypertrophy. Myocardial contractility eventually declines, and BV in the LA and pulmonary bed increases. This leads to pulmonary HTN and RVF.

A

Aortic valve regurgitation

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20
Q

S/S: sudden manifestations of cardiovascular collapse. Severe dyspnea, chest pain, and hypotension indicating LVF and cardiogenic shock (a life-threatening emergency)

A

Acute aortic valve regurgitation

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21
Q

May be asymptomatic for years. Exertion dyspnea, orthopnea, and PND can develop only after considerable heart dysfunction has occurred. Can develop a water-hammer pulse (a strong, quick beat that collapses immediately). Heart sounds may include a soft or absent S1, S3, or S4; and a soft, high-pitched diastolic murmur.

A

Chronic aortic valve regurgitation

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22
Q

Uncommon. Occurs more frequently than regurgitation. Occurs in pts with RF and IVDA. Right atrial enlargement and increased systemic venous pressure. Manifestations: peripheral edema, ascites, hepatomegaly, murmur with increased intensity on inspiration.

A

Tricuspid valve stenosis.

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23
Q

Almost always congenital. Causes right ventricular HTN and hypertrophy. S/S: fatigue, loud murmur.

A

Pulmonic valve stenosis

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24
Q

Diagnostic studies for valvular heart disease

A

History and physical examination. CT scan of chest with contrast is the gold standard for evaluating aortic disorders. Echocardiogram reveals valve structure, function, and heart chamber size. Chest x-ray reveals the heart size, altered pulmonary circulation, and valve calcification. An ECG identifies heart rate, rhythm, and any ischemia or ventricular hypertrophy. Cardiac catheterization detects pressure changes in the cardiac chambers, records pressure differences across the valves, and measures the size of the valve openings.

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25
Q

Nonsurgical tx of valvular heart disease/conservative therapies

A

Prophylactic ABX to prevent recurrent RF and IE. Dependent of valve involved and severity. Prevent exacerbations of HF, pulmonary edema, thromboembolisms, and recurrent endocarditis. Anticoagulant therapy prevents and treats systemic or pulmonary emboli. Used prophylactically in pts with a-fib.

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26
Q

An alternative tx for some pts with valvular heart disease. Split open fused commissures. Use for mitral, tricuspid and pulmonic stenosis. Done in cardiac cath lab. Involves threading a balloon-tipped catheter from the femoral artery or vein the the stenotic valve. The balloon is inflated in an attempt to separate the valve leaflets.

A

Percutaneous transluminal balloon valvuloplasty

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27
Q

Drugs to treat/control HF

A

Vasodilators (eg. nitrates, ACE inhibitors). Positive inotropes (eg. digoxin- increase contractility). Diuretics (decrease fluid). Beta adrenergic blockers. Antidysrhythmia drugs

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28
Q

Type can be valve repair or valve replacement. The procedure that is used depends on the valves involved, the pathology and severity of the disease, and the pt’s clinical condition. All types are palliative, not narrative, and pts require lifelong health care.

A

Surgical therapy

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29
Q

Usually the surgery of choice. Lower operative mortality rate than valve replacement and is often used in mitral or tricuspid valvular heart disease. valvulotomy, valvuloplasty, annuloplasty

A

Valve repair

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30
Q

May be required for mitral, aortic, tricuspid, and occasionally pulmonic valve disease. Used esp. for combined aortic stenosis/regurgitation. Can have mechanical or biologic valves.

A

Valve replacement

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31
Q

Made from bovine, porcine, and human cadaver tissue with some mad-made materials. Less durable, cause early calcification, tissue breakdown and leaflet stiffening. Do NOT require anticoagulation therapy. Not aortic valves b/c pressure is too high.

A

Biologic (tissue) valves

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32
Q

More durable, last longer. Increased risk of thromboembolism- requires long-term anticoagulation therapy. Cx: bleeding, valve leakage, endocarditis. May hear “click”.

A

Mechanical valves

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33
Q

Subjective data for valvular disease

A

Past medical hx. IVDA; fatigue; palpitations, weakness, activity intolerance, dizziness, fainting. DOE, cough, hemoptysis, orthopnea, PNS. Angolan or atypical chest pain.

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34
Q

Objective data for valvular disease

A

Fever, diaphoresis, flushing, cyanosis, clubbing, peripheral edema. Crackles, wheezes, hoarseness. S3 and S4. Dysrhythmias. Increase or decrease in pulse pressure; hypotension. Thready peripheral pulses. Hepatomegaly, ascites. Weight gain.

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35
Q

Nursing implementation

A

Individualize rest and exercise. Avoid strenuous activity. Discourage tobacco use. Ongoing cardiac assessments to monitor drugs effectiveness. Monitor INR.

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36
Q

The nurse is caring for a pt with aortic stenosis. For what should the nurse assess the pt?

a) systolic murmur
b) Pericardial friction rub
c) Diminished or absent S4
d) Low-pitched diastolic murmur

A

a) systolic murmur

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37
Q

infection of the inner layer of the heart including the cardiac valves. Improved prognosis with ABX.

A

Infective endocarditis (IE)

38
Q

Typically affects those with preexisting valve disease and has a clinical course that may extend over months.

A

Subacute IE

39
Q

Typically affects those with healthy valves and manifests as a rapidly progressive illness.

A

Acute IE

40
Q

Can be classified based on the cause (IV drug abuse, fungal) or site of involvement (prosthetic valve)

A

IE

41
Q

Causative organisms of IE

A

Bacterial most common (streptococcus viridians; staphylococcus aureus). Viruses. Fungi.

42
Q

Occurs when blood turbulence within the heart allows the causative organism to infect previously damaged valves or other endothelial surfaces.

A

IE

43
Q

Risk factors for IE

A

cardiac, noncardiac, procedural. Age (more than 50% of older people have aortic stenosis); IVDA; prosthetic valves; use of CVADs; renal dialysis

44
Q

The primary lesions of IE. Consist of fibrin, leukocytes, platelets, and microbes that stick to the valve surface or endocardium. The loss of parts of these into the circulation results in emboli. Left-sided lesions move to various organs and to the extremities, causing infarction. Right-sided lesions move to the lungs, resulting in pulmonary emboli.

A

Vegetations

45
Q

Clinical manifestations

A

Nonspecific; low-grade fever occurs in 90% of pts; chills; weakness; malaise; fatigue; anorexia. Onset of a new or changing murmur. HF occurs in up to 80% of pts with aortic valve IE and in approximately 50% of pts with mitral valve IE.

46
Q

S/S of subacute IE

A

Arthralgia’s; myalgia; back pain; abdominal discomfort; weight loss; headache; clubbing of the fingers.

47
Q

Vascular manifestations of IE

A

splinter hemorrhages in nailbeds. Petechiae. Osler’s nodes on fingers or toes (painful, tender, red or purple, pea-size lesions); Janeway’s lesions on palms or soles (flat, painless, small, red spots); Roth’s spots (hemorrhagic retinal lesions seen through fundoscopic exam).

48
Q

Manifestations secondary to embolism

A

Spleen (sharp LUQ pain, splenomegaly, local tenderness)
Kidneys (flank pain, hematuria, renal failure)
Limbs (ischemia and gangrene)
Brain (neurologic damage resulting in hemiplegia, ataxia, aphasia, visual changes, change in LOC)
PE (dyspnea, chest pain, hemoptysis, respiratory arrest)

49
Q

Diagnostic studies for IE

A

Hx. Any recent (w/i past 3-6 months) dental, urologic, surgical, or gynecologic procedures; IVDA; heart disease; recent cardiac cath; cardiac surgery; IV device placement; renal dialysis; infections.
Lab tests: blood cultures; CBC; ESR; C-reactive protein
Echocardiography; Chest X-ray; ECG; cardiac cath

50
Q

Major criteria to diagnose IE include at least two of the following:

A

positive blood cultures; new or changed heart murmur; intracardiac mass or vegetation noted on echocardiography

51
Q

Prophylactic ABX for pts having:

A

Certain dental procedures; respiratory tract incisions; tonsillectomy and adenoidectomy; GI wound infection; UTI

52
Q

Drug therapy for IE

A

Accurate identification of the infecting organism. Long-term tx is necessary to kill dormant bacteria within the valvular vegetations. Relapses are common. Initially, pts are hospitalized and IV ABX based on blood cultures is started. Effectiveness is assessed with subsequent blood cultures. Valve replacement for fungal and PVE. Fever may persist for several days after tx has been started- tx with ASA, tylenol, advil, fluids, and rest. Complete bed rest is not usually indicated unless the temp remains elevated or there are signs of HF

53
Q

Subjective data IE

A

Health hx (valvular, congenital, or syphilltic cardiac disease; previous IE; staph or strep infection). Drugs. Recent surgeries or procedures. IVDA; alcohol abuse. Weight changes. Chills. Hematuria. Exercise intolerance, weakness, fatigue. Cough, DOE, orthopnea, palpitations. Night sweats. Pain, headache, joint/muscle tenderness.

54
Q

Objective data IE

A

Fever. Osler’s nodes; splinter hemorrhages; Janeway’s lesions; petechiae, purpura. Peripheral edema, clubbing. Tachypnea, crackles. Dysrhythmia, tachycardia, murmurs, S3, S4. Retinal hemorrhage.

55
Q

Nursing implementation for ambulatory and home care for IE

A

ABX therapy for 4-6 weeks. Assess home setting. Monitor lab data, including blood cultures. Assess IV lines. Coping strategies. Adequate rest. Moderate activity. Compression stockings. ROM exercises. C&DB q 2 hrs.

56
Q

Patient teaching for IE

A

Monitor body temp. S/S of complications and infection. Nature of disease and reducing the risk of infection. Stress follow-up care, good nutrition, early tx of common infections. Need for prophylactic ABX. Good oral hygiene.

57
Q

The nurse obtains a health hx from a 65 y/o pt with a prosthetic mitral valve who has sx of IE. Which question by the nurse is most appropriate?

a) Do you have a history of a heart attack?
b) Is there a family hx of endocarditis?
c) Have you had any recent immunizations
d) Have you had dental work done recently?

A

d) Have you had dental work done recently?

58
Q

Condition caused by inflammation of the pericardial sac. Commonly idiopathic or viral. Also occurs after infection, MI, trauma.

A

Pericarditis

59
Q

Normally contains 10-15 mL of serous fluid. Serves an anchoring function, provides lubrication to decrease friction during systolic and diastolic heart movements, and assists in preventing excessive dilation of the heart during diastole.

A

Pericardium

60
Q

Occurs within the initial 48-72 hours after an MI.

A

Acute pericarditis

61
Q

Appears 4-6 weeks after an MI.

A

Dressler syndrome (late pericarditis)

62
Q

S/S: friction rub can be intermittent, timed with the pulse. May have fever. Progressive, frequently severe, sharp chest pain that is worsened with deep inspiration and when lying supine and relieved by sitting up and leaning forward. Pain may radiate to neck, arms, or left shoulder, making it difficult to differentiate from angina. (Pain from this can be referred to the trapezius muscle). Dyspnea r/t the pt’s need to breathe in rapid, shallow breaths to avoid chest pain

A

Pericarditis

63
Q

Diagnostic studies for pericarditis

A

ECG-diffuse ST segment elevations (must differentiate from MI)
Echocardiography to look for cx.
High WBC, CRP, ESR (inflammation)
May send pericardial fluid or tissue for analysis

64
Q

Buildup of fluid in the pericardium. Can occur rapidly (i.e. chest trauma) or slowly (i.e. tuberculosis pericarditis). Can compress nearby structures. Pulmonary tissue compression can cause cough, dyspnea, and tachypnea. Phrenic nerve compression can induce hiccups, and compression of the laryngeal nerve may result in hoarseness. Heart sounds are generally distant and muffled with normal BP

A

Pericardial effusion from pericarditis

65
Q

Develops as the pericardial effusion increases in volume. This results in compression of the heart. May report chest pain; is often confused, anxious, and restless. As compression increases, there is a decreased CO, muffled heart sounds, and narrowed pulse pressure. Tachypnea and tachycardia. JVD d/t increased jugular venous pressure. Pulsus paradoxus ( decrease in SBP during inspiration that is exaggerated).

A

Cardiac tamponade d/t pericardial effusion from pericarditis

66
Q

Treatment of pericarditis

A

ABX if bacterial. NSAIDs to control pain and inflammation. Corticosteroids if not responding to NSAIDs. Position upright leaning forward. Pericardiocentesis- for pericardial effusion with acute cardiac tamponade. Remove fluid from pericardial space for analysis and to relieve cardiac pressure.

67
Q

Nursing management of acute pericarditis

A

Management of pt’s pain and anxiety. Assess the pain to distinguish the pain of MI (angina) and pericarditis (precordium or left trapezius region). Sharp, pleuritic quality that increases with inspiration.

68
Q

Caused by scarring and loss of elasticity of the pericardial sac after acute pericarditis. S/S: JVD; dyspnea, peripheral edema, fatigue, NO pulsus paradoxus. Heart sounds- pericardial knock.

A

Chronic constrictive pericarditis

69
Q

Dx of chronic constrictive pericarditis

A

ECG changes are nonspecific.
CXR- enlarged heart
Confirmed by color M-mode echocardigram- wall thickening without pericardial effusion

70
Q

Treatment for chronic constrictive pericarditis

A

pericardial window or pericardiectomy, may take time to show improvement

71
Q

Inflammatory disease that occurs after group A strep infection. Can affect heart, joints, skin,and brain.

A

Rheumatic fever

72
Q

Chronic condition resulting from RF that is characterized by scarring and deformity of the heart valves. Can cause vegetations in the valves leading to valve regurgitation and Aschoff’s bodies (nodules on the myocardium) leading to pericarditis. Can have systemic sx.

A

Rheumatic heart disease

73
Q 
Carditis (murmur; heart enlargement and HF 2* to myocarditis; pericarditis resulting in muffled heart sounds, chest pain, pericardial friction rub, or signs of effusion; all layers of the heart are involved). 
Polyarthritis (larger joints most frequently affected). 
Sydenham's chorea (CNS manifestation. Often delayed sign. Involuntary movements, esp of face and limbs; muscle weakness; disturbances of speech and gait)
Erythema marginatum (less common. bright pink, nonpruritic, manlike macular lesions on trunk and proximal extremities. Exacerbated by heat) 
Subcutaneous nodules (1-4 cm, hard, painless, on body surfaces; assoc. with severe carditis)
A

S/S of rheumatic fever/rheumatic heart disease

74
Q

Results from changes in valvular structure that may occur months to years after an episode of RF. Can result in fibrous tissue growth in valve leaflets and chordae tendon with scarring and contractors. The mitral valve is most frequently involved.

A

Chronic rheumatic carditis. Cx of RF

75
Q

Treatment of RF

A

No need for ABX unless strep A is still present. Anti-inflammatories. Bedrest

76
Q

Nursing care of RF

A

RF is preventable with early detection and tx of Strep A pharyngitis
Bedrest
Prevent recurrence of RF with monthly IM penicillin sometimes for up to 10 years
Teach pts to water for sx of valve disease
Susceptible for recurrence (no immunity)

77
Q

A group of diseases that directly affect myocardial structure or function. Primary (idiopathic, ONLY affects heart muscle) or secondary (cause is known and 2* to another disease process). Three major types: dilated, hypertrophic, restrictive. Can lead to cardiomegaly, heart failure. Leading cause for heart transplant.

A

Cardiomyopathy

78
Q

Most common type of cardiomyopathy. Some genetic link. Often follows infectious myocarditis. Can be caused by alcohol abuse, pregnancy. Diffuse inflammation and rapid degeneration of myocardial fibers, resulting in ventricular dilation, impaired systolic function, atrial enlargement, and stasis of blood in the LV. SCD from ventricular dysrhythmias is the leading cause of death. No ventricular hypertrophy, but will have dilation.

A

Dilated cardiomyopathy

79
Q

S/S of dilated cardiomyopathy

A

May be acute or slowly develop; fatigue; dyspnea; PND; orthopnea; HF sx; risk of emboli. Dry cough, palpitations, abdominal bloating, nausea, vomiting, anorexia. Abnormal S3 and/or S4, dysrhythmias, heart murmurs, pulmonary crackles, edema, weak peripheral pulses, pallor, hepatomegaly, and JVD.

80
Q

Diagnosis of dilated cardiomyopathy

A

Based on pt hx and ruling out other causes of HF. Cardiac cath. Echocardiography. Endomyocardial biopsies for infectious organisms.

81
Q

Tx of dilated cardiomyopathy and nursing care

A

Does not response well to therapy. Treat like HF. may need VAD and ultimately heart transplant.
Usually very ill with a poor prognosis. Caregivers must know CPR. Goal is to keep them at optimal functioning, keep them out of the hospital

82
Q

Asymmetric LV hypertrophy without ventricular dilation. Less common than dilated form. Usually diagnosed in young adulthood in active, athletic people. Most common cause of SCD in young people. Most commonly genetic or idiopathic. Massive ventricular hypertrophy. Rapid/forceful contraction of the LV. Impaired relaxation. Obstruction to aortic outflow. Causes decreased CO especially with exertion (nowhere for blood to go= decreased CO). S

A

Hypertrophic cardiomyopathy

83
Q

S/S and Dx of hypertrophic cardiomyopathy

A

S/S: may be asymptomatic or cause dyspnea (caused by an elevated LV diastolic pressure), fatigue(resultant decrease in CO and in exercise-induced flow obstruction) , syncope or angina(increased LV muscle mass or compression of the small coronary arteries by the hypertrophic ventricular myocardium).
Dx: apical impulse is exaggerated and displaced laterally (to the left). S4 and systolic murmur. ECG changes. Ventricular dysrhythmias. SCD may be the only sx.

84
Q

Treatment and nursing care for hypertrophic cardiomyopathy

A

Goals of care are to improve ventricular filling by reducing ventricular contractility and relieving the LV outflow obstruction.
Tx: Beta blockers; digoxin; calcium channel blockers; ICD if at risk for SCD; AV pacing; maybe surgery or ablation if pt has hypertrophied septum.
Nursing interventions: relieve sx; observing for and preventing cx; providing emotional support; avoid strenuous activity and dehydration; rest and elevation of the feet to improve venous return to the heart to manage chest pain; vasodilators (nitroglycerin) may worsen the chest pain by decreasing venous return

85
Q

Least common type of cardiomyopathy. Disease of the myocardium that impairs diastolic filling and stretch. Systolic function remains unchanged. Unknown cause. Ventricles are resistant to increasing pressure from filling. Stiff muscle heart.

A

Restrictive cardiomyopathy

86
Q

S/S, Dx, and Tx of restrictive cardiomyopathy

A

S/S: fatigue, exercise intolerance, dyspnea; occur because the heart cannot increase CO by increasing the HR without further compromising ventricular filling. Pt may have signs of HF (dyspnea, peripheral edema, weight gain, ascites, hepatomegaly, JVD).
Dx: CXR; Echo (LV normal size with thickened wall); ECG changes (mild tachy at rest; a-fib)
Tx: no specific tx. Try to improve diastolic filling. Treat like HF. Restrict exercise. May consider heart transplant.

87
Q

Pt education for Cardiomyopathies

A

Low Na+ diet. Maintain reasonable weight. Avoid stimulants. Balance activity and rest. Exercise guidelines. Stress reduction. Report s/s of HF. Caregivers need to know CPR

88
Q

Summary: common causes (risk factors)

A

Valve problems-
IE- prosthetic heart valves, recent dental care/tx
RF- recent strep throat

89
Q

Summary: common complications

A

Valve problems- heart failure, IE
IE- emboli, valve problems
RF- valve problems, recurrent infection

90
Q

Summary: treatment

A

IE- IV ABX for 4-6 weeks
RF- NO ABX, NSAIDs, rest
All need prophylactic ABX before dental and other procedures to prevent IE

91
Q

The nurse is caring for a pt with pericarditis. What finding correlates with this disorder?

a) Pericardial friction rub
b) Systolic murmur
c) Ventricular gallop
d) Paradoxical splitting

A

a) Pericardial friction rub

MedSurg (5 decks)

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