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Chapter 36- Inflammatory and Structural Heart disorders

 Infective Endocarditis
o Infection of the endocardial layer of the heart
 The innermost layer and the valves
o Antibiotic therapy has improved the prognosis of this disease
o Classification
 Subacute
 the clinical course over months
 those with pre-existing valve disease
 Acute
 manifest as a rapidly progressing illness
 Classified today based on the cause or site of involvement
o Etiology and pathophysiology
 Most common causative agent: Staphylococcus aureus and Streptococcus
viridians
 Bacterial
 May be caused by fungal or viruses as well
 Blood flow within the heart brings the organism to affect damaged valves
 Vegetation
o Primary lesion of IE
o Consist of fibrin, leukocytes, platelets, and microbes
o High propensity to form an emboli
 Left sided vegetation
 Moves to various organs and the extremities
 causing limb infarction
 Right sided vegetation
 Moves to the lungs
 Resulting in pulmonary embolism
 Main contributing factors
 Aging
 IVDA
 use of prosthetic valves
 use of intra vascular devices
o resulting in healthcare associated infections
 Renal dialysis
o Clinical manifestations
 Nonspecific
 Involved multiple organ systems
 Common symptoms include
 fever, chills, weakness, malaise, fatigue, and anorexia
 Vascular signs of IE include
 splinter hemorrhages
o Black longitudinal streaks in the nail bed
 Petechiae
 Osler’s nodes
o Pea size lesions on toes and fingertips
 Janeway’s lesions
o Flat, painless, small red sports
 Roth’s spots
o Hemorrhagic retinal lesions
 Onset of new or worsening systolic murmur
 Aortic and mitral valves are most often effective
 Clinical signs secondary to embolization
 Spleen
o Sharp left upper quadrant pain
o Local tenderness
o Abdominal rigidity
 Kidney
o Flank pain
o Hematuria
o Renal Failure
o Diagnostic studies
 Ask about any recent dental, urologic, surgical, or gynecologic procedures
 Within past three to six months
 Blood cultures
 Three different cultures drawn over one hour from three sites
 Major Criteria
 Must met two of the following
o 2 positive blood cultures 12 hours apart
o non valvular regurgitation
o intracardiac mass or vegetation noted on echocardiography
 Echocardiography is critical in diagnosis
 Chest x-ray
 Detects cardiomegaly, degree of AV block
 Heart Catheterization
 Assesses valve function
o Interprofessional Care
 Usually consists of prophylactic antibiotic treatment
o Drug therapy
 Requires accurate identification of the causative Organism
 long term treatment is necessary
 to kill dormant bacteria
 Generally, requires 4-6 weeks of antibiotic therapy
o Nursing management
 Nursing diagnosis
 Decreased cardiac output related to altered heart rhythm, valvular
insufficiency, and fluid overload
 Activity intolerance related to generalized weakness, arthralgia,
alteration in O2 transportation secondary to valvular dysfunction
 Planning
 Overall goals include
o Normal or baseline heart function
o Performance of activities of daily living without fatigue
o Knowledge of the therapeutic regime to prevent
reoccurrence
 Acute Pericarditis
o Inflammation of the pericardial sac
 Normally contains 10-15 mL of fluid to help with friction
o Etiology and Pathophysiology
 Most causes are idiopathic
 Suspected viral cause
 Coxsackievirus B is most identified virus
 May be caused by infections, hypersensitivity, or noninfectious means
 Two distinct syndromes
 Acute pericarditis
o Occurs within 48-72 hours after MI
o Inflammation response is common sign
 Dressler syndrome
o 4-6 weeks after an MI
o Clinical manifestations
 Progressive frequent severe sharp chest pain
 Worse with deep inspiration and when lying flat
 relieved by sitting up and leaning forward
 pain may radiate to neck arms or left shoulder
 Main distinction from Angina
 Pain is focused on the trapezius muscle
 Hallmark finding
 Pericardial friction rub
o Best heard with stethoscope on lower left sternal border
o Have patient hold breath
 If you still hear the rub when pt breath is held it is
Cardiac
o Complications
 Two major complications
 Pericardial effusion
 Cardiac tamponade
 Pericardial effusion
 The buildup of fluid in the pericardium
 May occur rapidly or slowly
o compresses nearby structures
o causing cough, dyspnea, this tachypnea
 Phrenic nerve may also be compressed
o leading to hiccups
 Cardiac tamponade
 Develops as infusion increases in volume
 Causes compression of the heart
 May report chest pain
o Often confused anxious and restless
 Decrease cardiac output
 Muffled heart sounds
 Narrowed pulse pressure
o Tachypnea and tachycardia
 Neck veins may be distended
o Diagnostic studies
 EKG
 Most useful in diagnosis of acute pericarditis
 Shows a diffused ST segment elevation
 Laboratory findings
 Leukocytosis and elevation of CRP and ESR
 Troponin levels may also be elevated
o signifying heart damage
o Interprofessional care
 Aimed at identifying and treating the underlying problem and symptoms
 antibiotics to treat bacterial
 NSAIDs to control pain and inflammation
 Colchicine, an anti-inflammatory drug used for gout
o May be used in chronic recurrent cases
 Pericardiocentesis
 Needle is inserted into the pericardial space to remove fluid
 pericardial window
 A “window” or portion of the pericardium is cut to allow fluid to
drain continuously into the chest
o Nursing management
 Primary concern is management of the patient's pain and anxiety
 The acute pericarditis patient is at risk for cardiac tamponade and
decreased cardiac output
 Chronic constrictive pericarditis
o Etiology and pathophysiology
 Results from scarring of the pericardium
 Loss of elasticity
 Usually begins with the episode of acute pericarditis
 Fibrin is deposited involving fibrous scarring
 Thickening of the pericardium from calcium deposits
 Eventual destruction of the space
 Impairs the ability of the Atria and ventricles to stretch adequately
o Clinical manifestations and diagnostic studies
 Signs occur overtime and mimic those of heart failure and core pulmonal
 Decreased CO
 Peripheral Edema, ascites, fatigue
 Anorexia
 Weight loss
 Most prominent sign is JVD
 Chest x-ray may help with diagnostic procedure
o Nursing and interprofessional management
 Pericardiectomy
 Treatment of choice for chronic constriction
 Complete resection of the pericardium
 Improvement may be immediate or take weeks
o Depends on the patient
 Myocarditis
o Etiology and pathophysiology
 Focal or diffused inflammation of the myocardium
 causes include viral bacterial fungal radiation or pharmacological
 coxsackie A&B viruses are most common
o clinical manifestations
 Range from benign to severe heart involvement
 sudden cardiac death is possible
 Fever, fatigue, malaise, pharyngitis, dyspnea, nausea, and vomiting
 Early signs will appear 7 to 10 days after viral infection
 Late cardiac signs related to the development of heart failure
o Diagnostic studies in interprofessional care
 EKG
 changes are nonspecific
 laboratory findings
 Often inconclusive
 Virus is usually really present in tissue samples during the initial 8
to 10 days
 Endo myocardial biopsy
 Provides histological confirmation of Myocarditis
 Done within the first six weeks
 Treatment includes managing associated heart symptoms
 ACE inhibitors
 Beta blockers
 Diuretics
 Nitropress
 Digoxin
o use with caution due to increased sensitivity
o Nursing management
 Decreased Cardiac Output will be the ongoing problem
 Trying to decrease cardiac workload
 Put patient in semi fowlers position, space activity and rest periods,
and provide quiet environment
 Assess levels of anxiety
 Check for signs of infection when receiving immunosuppressive therapy
 Rheumatic fever and rheumatic heart disease
o Background
 Rheumatic fever is acute inflammatory disease
 involves all layers
 rheumatic heart disease has a chronic condition
 results from prolonged RF
 characterized by scarring and deformation of the heart valves
o Etiology and pathophysiology
 Occurs as a delayed result of Group A strep pharyngitis
 Cardiac lesions and valve deformities
 Rheumatic carditis is found mainly in the valves
o Swelling and erosion of the leaflets
 Vegetation forms from deposits of fibrin
o create a thickening of the leaflets
o which then become calcified resulting in stenosis
 Aschoff’s bodies
o Nodules formed by reaction to inflammation
 Extracardiac lesions
 Lesions of RF may include skin, joints, and CNS
o Clinical manifestations
 Basis for diagnosis requires two major criteria or one major and two minor
with evidence of group A
 Major criteria
o Carditis
 Consists of
 Heart murmur or mitral stenosis
 Heart enlargement and heart failure
 Pericarditis resulting in muffled heart
sounds, chest pain, pericardial friction rub,
or signs of effusion
o Arthritis
 Affects the synovial membranes
o Sydenham’s chorea
 CNS
 Involuntary movements, muscle weakness,
disturbances of speech and gait
o Erythema marginatum
 Map-like macular lesions on trunk and extremities
 Exacerbated by heat
o Subcutaneous nodules
 Usually found in the knees, wrists, or elbows
 Minor Criteria
o Monoarthralgia
o Fever
o Increased ESR and/or increased CRP
o EKG finding
 Prolonged PR interval
 Evidence of Group A infection
o Lab findings
o AO titer positive
o Complications
 Chronic rheumatic carditis
 Results from changes in the valvular structure that occurs over
months
o Diagnostic studies and interprofessional care
 No single test exists for RF
 Echocardiogram
 Shows valvular insufficiency and fluid or thickening
 Chest X-ray
 Shows enlarged heart if HF is present
 EKG
 Changes in delayed AV conduction
 Treatment
 Antibiotic therapy
o Does not change course of disease but will remove
organisms
 Salicylates, NSAIDs, and Corticosteroids are most widely used
o Nursing management
 Inspect the patient skin for subcutaneous nodule
 Use proper lighting to observe rashes which may be present
o Planning
 Goals include
 Normal or baseline heart function
 Resumption of daily activities without joint pain
 Verbalization of ability to manage the disease
o Nursing implementation
 RF is a preventable heart disease
 early detection and immediate treatment
 When managing RF goals are
 Control and removal of the infecting Organism
 Prevention of heart complications
 Relief of joint pain fever or other symptoms
 Valvular heart disease
o Background
 The heart has two AV valves
 Mitral and tricuspid
 And two semi lunar valves
 Aortic and pulmonic
 Valves control blood flow through the heart
 Pressure on either side of a open valve is usually equal
 Stenosis
 The construction or narrowing
 Regurgitation
 Incompetency or insufficiency due to incomplete closure
 Mitral valve stenosis
o Etiology and Pathophysiology
 Most cases result from rheumatic heart disease
 Mitral valve takes on a fish-mouth shape
 Due to the thickening and shortening of valve structures
 Blood flow is blocked and creates a pressure difference between
the left atrium and left ventricle during diastole
o Clinical manifestations
 Primary symptom is exertional dyspnea caused by reduced lung
compliance
 First heart sound will be loud
 Emboli can form in the left atrium and cause a stroke
 Fatigue and palpitations may also occur
 Mitral valve regurgitation
o Etiology and Pathophysiology
 Defect of leaflets or changes in structures related that cause blood to flow
backwards
 Most cases of regurgitation are caused by
 Mi, chronic rheumatic heart disease, mitral prolapse or IE
 Due to the backflow the left ventricle and left atrium must work harder to
preserve cardiac output
o Clinical manifestations
 Determined by nature of onset
 May remain asymptomatic for many years
 Early signs include weakness fatigue palpitations and dyspnea
 Which progress to orthopnea, paroxysmal nocturnal dyspnea, or
peripheral edema
 Mitral valve prolapse
o Background
 An abnormality it was a mitral valve leaflets or the papillary muscles
 allows the leaflets to prolapse or buckle
 Most common form of valvular disease in the United States
o Genetic link
 Increases with familial incident
 Any inherited genetic disease that affects the connective tissue
 Will affect the valve such as Marfan’s syndrome
o Clinical manifestations
 90% remain asymptomatic for their entire life
 Severe MR is uncommon
 Treatment is effective
 Aortic valve stenosis
o Etiology and Pathophysiology
 AS is generally found in childhood, adolescence, or young adulthood
 Leaflets stiffen and retract
 Causing the stenosis
 Obstructs blood flow from the left ventricle to the aorta during aorta
 Causes hypertrophy of LV and increased O2 consumption
o Clinical Manifestations
 Develops when the valve orifice is about 1/3 of normal size
 Includes angina, syncope, and exertional dyspnea
 Aortic valve regurgitation
o Causes a retrograde blood flow from ascending order into the left ventricle during
diastole
 Results in volume overload
o Clinical Manifestations
 Sudden signs of cardiovascular collapse
 The development of severe dyspnea chest pains and hypo tension
 Chronic
 Water hammer impulse
o A strong quick beat that collapses immediately
 Heart sounds may include absent S1, S3 or S4
 Tricuspid and pulmonic valve disease
o Uncommon
 Stenosis more common than regurgitation
o Tricuspid stenosis
 Seen in patients that abuse IV drugs or RF
o Pulmonic stenosis
 Always congenital
 Diagnostic studies for valvular heart disease
o CT scan with contrast
 Golden standard
o Chest x-ray
 Shows heart size, altered circulation, and valve calcification
 Interprofessional care
o Percutaneous Transluminal Balloon Valvuloplasty
 Done in the heart catheterization lab
 A balloon tipped catheter is fed through the femoral artery to the stenotic
valve
 Balloon is inflated to separate the leaflets
 Popular technique due to its ease and few complications
o Surgical Therapy
 Valve repair
 Valvulotomy
o For pure mitral stenosis
 Closed
 Insertion of trans ventricular dilator through
apex of LV
 Open
 Use of cardiopulmonary bypass
 Involves repair of the valve by suturing
 Valve Replacement
 Two types
o Mechanical valves
 Manufactured
 More durable
 Increased risk of thromboembolism
o Life-long anticoagulation therapy
o Biological valves
 Made form bovine, porcine, and human heart tissue
 Decellular process
 Lowers risk of immune response but are less
durable
 Type depends on factors
o For patients over 65, durability is less important so is
almost always biological valves
 Planning for valvular disorders
o Overall goals include
 return to normal
 Improved activity tolerance
 An understanding of the disease process in health maintenance
o Conserve energy
 Cardiomyopathy
o Definition
 A group of diseases that directly affect myocardial structures or function
 May be classified as primary or secondary
 Primary
o Etiology is idiopathic
 Secondary
o Causes is known and is related to another disease process
 Three major types of CMP
 Dilated
 Hypertrophic
 Restricted
 The main reason why heart transplants are done
o Dilated Cardiomyopathy
 Etiology and Pathophysiology
 Most common type of CMP
o Characterized by diffuse inflammation and rapid
degeneration of heart fibers
 Result in ventricular dilation, impaired systolic function, atrial
enlargement, and stasis of blood
o Cardiomegaly
 Clinical manifestations
 Symptoms may develop acutely after infection or slowly
 Usually progress is to heart failure
 Diagnostic studies
 Heart catherization
o Used to confirm or rule out coronary artery disease
 Echocardiography
o Basis for diagnosis
 Chest x-ray
o Used to observe cardiomegaly
 Nursing and interprofessional management
 Focuses on controlling heart failure by enhancing heart
contractility
 Drug and nutritional therapy
o May help alleviate symptoms of HF and improve CO and
quality of life
 Dilated CMP does not respond well to therapy
o Non-drug therapy such as VAD may help the heart to rest
and recover
 Hypertrophic cardiomyopathy
o Etiology and Pathophysiology
 Asymmetrical left ventricle hypertrophy without ventricular dilation
 Half of cases have genetic linkage
 Early detection is vital
 Four main characteristics
 Massive ventricular hypertrophy
 Rapid, forceful contractions of the LV
 Impaired relaxation
 Obstructive aortic outflow
 Result = heart ventricle cannot relax and become noncompliant
o Clinical manifestations
 Asymptomatic or exertional dyspnea fatigue angina and syncope
 Most common symptom is dyspnea
o Due to elevated diastolic pressure in LV
 Fatigue occurs due to decrease in CO
 Syncope is due to increase in obstructions
o Diagnostic Studies
 Palpation of apical pulse
 Pulse location may be exaggerated and displaced to the left
 Echocardiogram is primary diagnostic tool
o Nursing and interprofessional management
 Goals of care are to improve ventricular filling
 By reducing ventricular contractility and relieving LV outflow
obstructions
 May be obtained by using beata blockers, CCB, or digitalis
 AV pacing may be useful
 Restrictive Cardiomyopathy
o Least common type
 Impairs diastolic filling and stretch
o Cause is unknown
 Ventricles are resistant to filling (thus requiring higher diastolic pressures)
o Clinical Manifestations
 Fatigue, exercise intolerance, and dyspnea
 Occur because heart cannot increase CO
 May also cause angina, orthopnea, syncope and palpitations
o Nursing and interprofessional management
 No specific treatment for restrictive CMP
 Interventions are focused on improving diastolic filling and treating
underlying disease processes

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