cardiac disorder 2 Flashcards
Primarily affect the valves, inflammation of endocardium (lining of heart chambers) by streptococcus and staph aureus
Infective Endocarditis
Risk for Infective Endocarditis
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
Pathophysiology Infective Endocarditis
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
Complications Infective Endocarditis
Heart failure and embolization
s/s Infective Endocarditis
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
medical treatment Infective Endocarditits
Antimicrobials, rest, limitation of activities
Prophylactic anticoagulants
Surgery to replace an infected prosthetic valve
Assessment Infective Endocarditis
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
interventions Infective Endocarditis
Administer prescribed
antibiotics
Encourage adequate rest
Assess cardiac output &
monitor for complications
Teach patient about the medications prescribed and any restrictions imposedInflammation of the pericardium
May be primary disease or associated with another inflammatory process
pericarditis
caused by viruses, bacteria, fungi, chemotherapy, or Acute MI (Dressler’s syndrome)
Acute pericarditis
caused by tuberculosis, radiation, or metastases Pathophysiology
Chronic pericarditis
Acute pericarditis
inflammatory process increases amount of pericardial fluid and inflammation of the pericardial membranes
Chronic pericarditis
scarring of the pericardium fuses the visceral and parietal pericardia together
Loss of elasticity results from the scarring
Constrictive process prevents adequate ventricular filling
Complications pericarditis
Pericardial effusion or accumulation of fluid in the pericardial space. May lead to cardiac tamponade
Fluid accumulation in
the pericardial sac
Causes compression
Can’t fill properly
Cardiac Tamponade
Possible Causes ~
Cardiac Tamponade
Effusion Hemorrhage Trauma MI Uremia (A history of renal failure can lead to a consideration of uremia as the cause of pericardial effusion)
Signs and symptoms
Pericarditis
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
Medical treatment pericarditis
Analgesics, antipyretics, anti-inflammatory agents, and antibiotics
Surgical creation of a pericardial window for chronic pericarditis with effusion
assessment pericarditis
Assessment of heart sounds especially important
intervention pericarditis
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
Disease of the heart muscle which usually leads to heart failure
Cause often unknown; may be secondary to another disease process
Three types:
Cardiomyopathy
ventricles are too weak to pump out the blood that is in them
W/ risk factors
Dilated (congestive):
Cardiomyopathy
Risk factors: excessive use of alcohol, pregnancy, and infections
ventricles are unusually thick so there is not a normal amount of room for blood inside them W/ cause
Cardiomyopathy
Hypertrophic
Maybe genetic and more common in younger individuals(36% of deaths)
Often secondary to valvular heart disease or hypertension
ventricles too stiff to stretch, becomes rigid, & noncompliant
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
Cardiomyopathy s/s
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
Medical treatment
Dilated cardiomyopathy
positive inotropic drugs, diuretics, ACE inhibitors and vasodilators; heart transplant
Medical treatment
Hypertrophic cardiomyopathy
: antidysrhythmics, antibiotics, anticoagulants, calcium channel blockers, beta-blockers; surgical interventions; implantable cardioverter-defibrillator
Medical treatment
Restrictive cardiomyopathy
: antidysrhythmics, antibiotics, anticoagulants, calcium channel blockers, beta-blockers; surgical interventions; implantable cardioverter-defibrillator
Assessment
Cardiomyopathy
Primarily for heart failure
Be alert for dyspnea, cough, edema, dysrhythmias, and decreased cardiac output
Interventions
Cardiomyopathy
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
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
Mitral stenosis
Valvular Disease
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
Mitral regurgitation
Valvular Disease
one or both leaflets enlarges and protrudes into the LA during systole
Mitral valve prolapse
Valvular Disease
valve cusps become fibrotic and calcify, most often due to the aging process, genetic malformation, syphilis, or rheumatic fever
Aortic stenosis
Valvular Disease
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!)
Aortic regurgitation
Valvular Disease
3 types of mechanical disruption
stenosis, incomplete closure, prolapse
Cardiac transplantation back ground
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
Cardiac transplantation donor criteria
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
cardiac transplantation aftercare
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
