Professional Documents
Culture Documents
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