cardiac disorder 2 Flashcards

1
Q

Primarily affect the valves, inflammation of endocardium (lining of heart chambers) by streptococcus and staph aureus

A

Infective Endocarditis

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2
Q

Risk for Infective Endocarditis

A

Incidence has decreased with the use of antibiotics, but there has been a resurgence of the problem in intravenous drug abusers
Dental work
Patients with valvular disease also at risk

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3
Q

Pathophysiology Infective Endocarditis

A

Pathogens, usually bacteria, enter the bloodstream resulting in positive blood cultures
The pathogen accumulates on the heart valves and/or the endocardium and forms vegetations – will calcify

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4
Q

Complications Infective Endocarditis

A

Heart failure and embolization

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5
Q

s/s Infective Endocarditis

A

Fever, chills, malaise, fatigue, and weight loss
Chest or abdominal pain; may indicate embolization
Petechiae inside the mouth and on the ankles, feet, and antecubital areas
Osler’s nodes (Pea-size, tender, reddish-purple lesions) on the patient’s fingertips or toes

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6
Q

medical treatment Infective Endocarditits

A

Antimicrobials, rest, limitation of activities
Prophylactic anticoagulants
Surgery to replace an infected prosthetic valve

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7
Q

Assessment Infective Endocarditis

A

Review patient’s history for risk factors, recent invasive procedures, pathologic cardiac conditions, and onset of symptoms
Assess for temperature elevation, heart murmur, evidence of HF (cough, peripheral edema), and emboli

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8
Q

interventions Infective Endocarditis

A
Administer prescribed 
    antibiotics 
Encourage adequate rest
Assess cardiac output &
    monitor for complications 
Teach patient about the medications prescribed and any restrictions imposed
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9
Q

Inflammation of the pericardium

May be primary disease or associated with another inflammatory process

A

pericarditis

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10
Q

caused by viruses, bacteria, fungi, chemotherapy, or Acute MI (Dressler’s syndrome)

A

Acute pericarditis

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11
Q

caused by tuberculosis, radiation, or metastases Pathophysiology

A

Chronic pericarditis

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12
Q

Acute pericarditis

A

inflammatory process increases amount of pericardial fluid and inflammation of the pericardial membranes

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13
Q

Chronic pericarditis

A

scarring of the pericardium fuses the visceral and parietal pericardia together
Loss of elasticity results from the scarring
Constrictive process prevents adequate ventricular filling

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14
Q

Complications pericarditis

A

Pericardial effusion or accumulation of fluid in the pericardial space. May lead to cardiac tamponade

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15
Q

Fluid accumulation in
the pericardial sac
Causes compression
Can’t fill properly

A

Cardiac Tamponade

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16
Q

Possible Causes ~

Cardiac Tamponade

A
Effusion
 Hemorrhage
Trauma
 MI
 Uremia (A history of renal failure can lead to a consideration of uremia as the cause of pericardial effusion)
17
Q

Signs and symptoms

Pericarditis

A

Chest pain
Most severe on inspiration
Sharp and stabbing but may be described as dull or burning
Relieved by sitting up and leaning forward
Dyspnea, chills, and fever

18
Q

Medical treatment pericarditis

A

Analgesics, antipyretics, anti-inflammatory agents, and antibiotics
Surgical creation of a pericardial window for chronic pericarditis with effusion

19
Q

assessment pericarditis

A

Assessment of heart sounds especially important

20
Q

intervention pericarditis

A

Rest and reduction of activity
Administer and teach patient about medications
Emotional support
Vital signs; auscultate for pericardial friction rub
Note pain characteristics and response to analgesics and anti-inflammatory agents
Monitor the ECG for dysrhythmias
Reduce anxiety
Assess respiratory system

21
Q

Disease of the heart muscle which usually leads to heart failure
Cause often unknown; may be secondary to another disease process
Three types:

A

Cardiomyopathy

22
Q

ventricles are too weak to pump out the blood that is in them
W/ risk factors

A

Dilated (congestive):
Cardiomyopathy
Risk factors: excessive use of alcohol, pregnancy, and infections

23
Q

ventricles are unusually thick so there is not a normal amount of room for blood inside them W/ cause

A

Cardiomyopathy
Hypertrophic
Maybe genetic and more common in younger individuals(36% of deaths)
Often secondary to valvular heart disease or hypertension

24
Q

ventricles too stiff to stretch, becomes rigid, & noncompliant

A

Cardiomyopathy
Restrictive:
Amyloidosis (metabolic disorder that deposits starch like protein in tissues), sarcoidosis (unknown eithiology, formation of grain like lesion in tissue) and other immunosuppressive disorders may predispose individuals to restrictive cardiomyopathy

25
Q

Cardiomyopathy s/s

A
Dilated cardiomyopathy (A): dyspnea, fatigue, left-sided heart failure, and moderate-to-severe cardiomegaly 
Hypertrophic cardiomyopathy (B): dyspnea, orthopnea, angina, fatigue, syncope, palpitations, ankle edema, and S4 sounds
Restrictive cardiomyopathy (C): dyspnea, fatigue, right-sided HF, S3 and S4 sounds, and mitral valve regurgitation
26
Q

Medical treatment

Dilated cardiomyopathy

A

positive inotropic drugs, diuretics, ACE inhibitors and vasodilators; heart transplant

27
Q

Medical treatment

Hypertrophic cardiomyopathy

A

: antidysrhythmics, antibiotics, anticoagulants, calcium channel blockers, beta-blockers; surgical interventions; implantable cardioverter-defibrillator

28
Q

Medical treatment

Restrictive cardiomyopathy

A

: antidysrhythmics, antibiotics, anticoagulants, calcium channel blockers, beta-blockers; surgical interventions; implantable cardioverter-defibrillator

29
Q

Assessment

Cardiomyopathy

A

Primarily for heart failure

Be alert for dyspnea, cough, edema, dysrhythmias, and decreased cardiac output

30
Q

Interventions

Cardiomyopathy

A

Similar to that of patients with HF
A hopeful atmosphere and careful explanation of care requirements
Encourage the family to support the patient
Guide the patient to make lifestyle changes
Encourage patient to make decisions and choices

31
Q

narrowing of the opening in the mitral valve that impedes blood flow from the LA into the LV. Symptoms similar to CHF.
Rheumatic fever leading cause

A

Mitral stenosis

Valvular Disease

32
Q

allows blood to flow back into the LA during diastole.
Left side of heart enlarges…LA due to back flow, LV due to compensation for decreased cardiac output….eventually have S/S HF

A

Mitral regurgitation

Valvular Disease

33
Q

one or both leaflets enlarges and protrudes into the LA during systole

A

Mitral valve prolapse

Valvular Disease

34
Q

valve cusps become fibrotic and calcify, most often due to the aging process, genetic malformation, syphilis, or rheumatic fever

A

Aortic stenosis

Valvular Disease

35
Q

fibrosis and thickening of the aortic cusps progress until the valve no longer maintains unidirectional blood flow. Secondary to rheumatic fever (infection by group A beta hemolytic Strep or throat infection!)

A

Aortic regurgitation

Valvular Disease

36
Q

3 types of mechanical disruption

A

stenosis, incomplete closure, prolapse

37
Q

Cardiac transplantation back ground

A

The first heart transplantation was performed in 1967 in South Africa by Dr. Christiaan Barnard
Today in the United States, approximately 2500 are done annually for end-stage heart disease
Donor must meet the criteria for brain death, have no malignancies outside the central nervous system, be free of infection, and not have experienced severe chest trauma

38
Q

Cardiac transplantation donor criteria

A

Donor and recipient organs carefully matched
Recipient must be free of infection at the time of transplantation
Patient prepped as any open-heart procedure
Cardiopulmonary bypass initiated; recipient’s heart is removed except for the posterior portions of the atria
Donor heart trimmed and anastomosed to the remaining native heart
Patient removed from bypass, heart restarted, and chest is closed

39
Q

cardiac transplantation aftercare

A

Aftercare similar to that of coronary artery bypass surgery
Hemodynamic monitoring, ventilation, cardiac assessment, care of chest tubes, and accurate intake and output measurements are vital
Modified protective isolation used
Patients and families taught sign/symptoms of infection, to avoid crowds and others with infections
Lifelong immunosuppression
Rejection monitored by endomyocardial biopsies