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Cardiac problems (Valvular Heart Disease (Mitral valve prolapse (Patho:…
Cardiac problems
Valvular Heart Disease
Mitral valve prolapse
Patho: Occurs because the valvular leaflets enlarge and prolapse into the left atrium during systole. Usually benign but may progess to pronounced mitral regurgitation; etiology is variable but associated with conditions such as Marfans syndrome.
CM
Usually asymptomatic; normal HR & BP; Some may report
- Atypical chest pain
- Dizziness, syncope
- Palpitations
- Atrial tachycardia
- Ventricular tachycardia
- systolic click
Aortic stenosis
Patho: most common valve dysfunction; aortic valve orifice narrows and obstructs left ventricular outflow during systole. Increased resistance to ejection or afterload results in ventricular hypertrophy. As stenosis worsens, CO becomes fixed and cannot increase to meet the demands of the body during exertion. Eventually LV fails, blood backs up into the LA, and the pulmonary system becomes congested.
when the SA of the valve becomes 1cm or <, stat surgery is indicated
- CM**
- dyspnea
- angina
- syncope on exertion
- fatigue
- orthopnea
- paraxysmal nocturnal dyspnea
- narrowed pulse pressure
harsh, systolic crescendo-decrescendo murmur
At risk for significant reductions of CO after valve replacement surgery; carefully monitor CO and assess for indications of HF. Report any manifestations to the surgeon immediately.
Mitral regurgitation
Patho :primary cause infective endocarditis; fibrotic and calcific changes occurring in mitral regurgitation prevent the mitral valve from closing completely during systole. Incomplete closure allows backflow of blood into the left atrium. During diastole regurgitant output again flows from the LA to the LV along with normal blood flow. The inc volume must be ejected during the next systole. To compensate for inc volume and pressure, the LA and LV dilate and hypertrophy.
CM
- Fatigue
- Dyspnea on exertion
- Orthopnea
- Palpitations
- A fib
- JVD
- Pitting edema
- High pitched holosystolic murmur
Pt's often have pulmonary htn an stiff lungs. Monitor respiratory status closely during weaning from ventilator (after valve replacement).
Aortic regurgitation
Patho: usually results from nonrheymatic conditions such as infective endocarditis, congential anatomic aortic valvular abnormalities, HTN, marfan syndrome;
the aortic valve leaflets do not close properly during diastole and the annulus (valve ring that attaches to the leaflets) may be dilated, loose, or deformed. Allows flow of blood from the aorta back into the left ventricle during diastole. The LV eventually dilates and hypertrophies attempting to accommodate the greater blood volume
CM
Asymptomatic for several years
"Bounding" arterial pulse on palpation. Widened PP w/ elevated systolic and diminished diastolic
- palpitations
- dyspnea
- orthopnea
- paroxysmal nocturnal dyspnea
- fatigue
- nocturnal angina
- sinus tachycardia
- blowing, decrescendo diastolic murmur
Mitral stenosis
Patho: usually results from rheumatic carditis which causes valve thickening by fibrosis and calcification; the valve leaflets fuse and become stiff and the chordae tendineae contract and shorten. The valve opening narrows, preventing normal blood flow from LA to LV. Left atrial pressure rises, the left atrium dilates, pulmonary artery pressure increases, and the right ventricle hypertrophies.
CM:
Pulmonary congestion and right sided heart failure occur first. Later when the left ventricle receives insufficient blood volume, preload is decreased and CO falls.
- Fatigue
- Dyspnea on exertion
- Orthopnea
- Paroxysmal nocturnal dyspnea
- Hemoptysis
- Hepamegaly
- JVD
- Pitting edema
- A fib
- Rumbling, apical diastolic murmur
Reparative procedures
Balloon valvuloplasty: invasive nonsurgical procedure; initial treatment of choice for people with noncalcified, mobile mitral valves.
After the procedure:observe the pt for bleeding from the catheter insertion site and institute post-angiogram precautions. Assess for signs of a regurgitant valve by monitoring heart sounds, CO, and rhythm. Oserve for any indications of systemic emboli
Direct (open) commissurotomy: cardiopulonary bypass during open heart. The surgeon visualizes the valve, removes thrombi from the atria, incises the fused commissures, and debrides calcium from the leaflets, widening the orifice.
Mitral valve annuloplasty: procedure of choice for pts with acquired mitral insufficiency. To make the annulus smaller, the surgeon may suture the leaflets to an annuloplasty ring. Leaflet repair is performed at the same time.
Heart Valve replacements
- prosthetic valve: last longer and are more durable
- biologic valve: made with tissue;
-may be xenograft (from another species- must be replaced every 7-10 years). Calcium breaks down the valves.
-pulmonary autographs- relocation of pt's own pulmonary valve to the aortic (Ross procedure)
Nursing responsibilities
- Inform about postop pain, incision care, and strategies to prevent respiratory complications
- Teach pts on anticoagulants to stop taking them at least 72 hours before
- Teach pts the importance of maintaining lifetime prophylactic anticoagulation therapy and how to manage their therapy successfully including nutritional considerations (K-warfarin) and the prevention of bleeding.
- Teach to avoid heavy lifting and dental procedures after surgery for 3-6 months
- Remind pts to obtain a med alert bracelet or card to indicate valve replacement and anticoagulants
- Teach to report changes in cardiovascular status, such as dyspnea, syncope, dizziness, edema, and palpitations
Pericarditis
inflammation of the pericardium (sac that encloses the heart). Problem may be fibrous, serous, hemorrhagic, purulent, neoplastic.
Acute pericarditis is associated with
- Infective organism (bacteria, virus, fungus); usually respiratory
- Post- MI syndrome (Dressler's syndrome)
- Post-pericardiotomy syndrome
- Acute exacerbations of systemic connective tissue disease
Clinical Manifestations
- substernal precodial pain that readiates to the left side of the neck, shoulder, or back
- Pain in aggravated by breathing (inspiration), coughing and swallowing
- Pain is worse when pt is supine & may be relieved by sitting and leaning forward
- Pericardial friction rub (scratchy high pitched sound) may be heard with diaphragm at left lower sternal border (ask pt to hold their breath)
- Elevated white blood cell count
- Fever
- EKG shows ST-T spiking
- A-fib is common
Interventions
- NSAIDs for pain as prescribed
- corticosteroid therapy
- Assist the pt to comfortable positions
- Notify the PCP if pain is not relieved within 24-48 hrs (explain to pt pain will usually be decreased w/in 48 hours)
- antibiotics and pericardial drainage
- hemodialysis (for uremic pericarditis)
- Monitor for pericardial effusion (space between the parietal and visceral layers of the pericardium fills w/ fluid); puts pt at risk for cardiac tamponade
- avoid aspirin and anticoagulants as they inc. risk for tamponade
-Auscultate BP carefully to detect
Diagnostic Studies
- EKG (diffused ST segment elevation)
- Echo
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Chronic constrictive pericarditis (inflammation causes fibrous thickening) is cause by
- tuberculosis
- radiation therapy
- trauma
- renal failure
- metastatic cancer
*pericardium becomes rigid, preventing adequate filling of the ventricles and eventually resulting in cardiac failure
Clinical Manifestations
- Signs of right sided heart failure
- elevated venous pressure
- JVD
- hepatic engorgement
- dependent edema
- exertional fatigue and duspnea
-Thickening of the pericardium is seen on echo or CT
Interventions
- NSAIDs for pain
- corticosteroid therapy
- Assist the pt to comfortable positions
- Notify the PCP if pain is not relieved within 24-48 hrs
- radiation or chemotherapy
- Surgical excision of the pericardium
- Monitor for pericardial effusion (space between the parietal and visceral layers of the pericardium fills w/ fluid); puts pt at risk for cardiac tamponade
Infective Endocarditis
occurs primarily in pts who abuse IV drugs, have had valve replacements, have experienced systemic infection, or have structural cardiac defects; microbial infection of the endocardium; there is an eroded section where platelets and fibrin adhere, forming a vegetative lesion. Bacteria become trapped causing the lesion to grow; can cause valve destruction
Clinical Manifestations (occur w/in 2 weeks)
- Recurrent fevers from 99-103 w/ chills, night sweats, malaise, fatigue
- Anorexia and weight loss
- Murmurs(carefully auscultate the precodium)
- Development of heart failure
- evidence of systemic embolization (When performing assessment, note rebound tenderness on palpation- indicates splenic infarction, assess for flank pain and hematuria- renal infarction, changes in mental status
- petechiae (Examine the mucous membranes, palate, conjunctivae, and the skin above the clavicles)
- splinter hemorrhages (Assess the distal 3rd of the nail bed; appear as black longitudinal lines or small red streaks)
- Osler's nodes (painful (OUCH) on palms of hands and soles of feet)
- Janeway's lesions (painless flat red maculae on hands and feet)
- Positive blood cultures
Complications:
- Heart failure (assess for right and left sided heart failure); most common
- Arterial embolization
- splenic infarction (sudden abdominal pain and radiation to the left shoulder)
- renal infarction (flank pain that radiates to the groin & hematuria)
- neurologic changes (confusion, reduced concentration, aphasia, dysphasia)
- Pulmonary infarction (chest pain, dyspnea, cough)
Diagnostic Assessment
Positive blood cultures
New regurgitant murmur
Evidence of endocardial involvement by endocardiography
Possibly low H&H
Interventions and Management
- IV Antimicrobials: course lasts 4-6 weeks; ideal is one of the penicillans or cephalosporins
*anticoagulants are avoided unless required to prevent thrombus formation on a prosthetic valve
- Aseptic technique
- Encourage rest
- Continue to assess for HF and report significant changes
- Surgery may be needed to remove the infected valve, repair or remove congenital shunts, repair injured valves, or drain abscesses
- Patients may resume antibiotic therapy at home- teach the family how to administer the antibiotic and care for the infusion site while maintaining aseptic technique
- Encourage proper oral hygeine
- Advise the pt to use a soft toothbrush and to brush at least twice per day (no floss)
- Teach to clean any open skin areas and apply antibiotic ointment
- Teach pts to request prophylactic antibiotics for every invasive procedure (esp dental)
- Instruct to note any indications of returning endocarditis
- Remind them to monitor and record temps daily for up to 6 weeks.
- Teach to report fever, chills, malaise, weight loss, increased fatigue, sudden weight gain, or dyspnea
Cardiac tamponade
Occurs when small volumes (20-50 ml) of fluid accumulate rapidly in the pericardium and cause a sudden decrease in CO. (if fluid accumulates slowly, the pericardium may stretch to accomadate up to hundreds of ml of fluid)
Clinical Manifestations
- Jugular vein distention
- Paradoxical pulse (systolic BP 10 mm Hg or more higher on expiration than on inspiration)
- Decreased HR, dyspnea, and fatigue
- Muffled heart sounds
- Hypotension
Pericardiocentesis
Procedure to remove fluid and relieve the pressure on the heart. Under hemodynamic monitoring, the cardiologist inserts an 8 in 16 or 18 gauge needle into the pericardial space. Once positioned a catheter is inserted and all available fluid is withdrawn. A pericardial drain may be placed.
- Monitor the pulmonary artery pressure
- Monitor wedge pressure
- Monitor right atrial pressure
- Fluid specimens may be sent to lab for C&S
- Closely monitor the pt for recurrence of tamponade
- Be prepared to provide adequate fluid volumes to increase CO and to prepare the pt for an emergency sternotomy
Pericardial Window
Surgeon removes a paortion of the pericardium to permit excessive pericardial fluid to drain into the pleural space
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Drug Therapy
- Beta blockers
- dieretics
- digoxin
- oxygen
- prophylactic atb
- diltiazem
- amniodarone
- coumadin (for pt with chronic A fib
Rheumatic Carditis
sensitivity response that develops after an upper respiratory infection with group A beta-hemolytic streptococci.
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