Nurse 405B: Valvular Heart Disease
Prophylactic Antibiotic Therapy
•Target Groups need prophylactic tx with abx •Prosthetic heart valve or prosthetic material for valve repair •Previous history of IE •Congenital heart disease •Heart transplant recipient with valvular disease •Conditions or Procedures •Oral •Dental manipulation of gums or roots & puncture of oral mucosa •Respiratory •Respiratory tract incisions (biopsy) or tonsillectomy & adenoidectomy •Surgery •Any procedure involving infected skin, skin structures, or MSK tissue Adults: amoxicillin 2 grams If allergic to PCN: cephalexin 2 grams, clindamycin 600 mg, or azithromycin (or clarithromycin) 500 mg Allergic to PCN and unable to take oral Rx: cefazolin or ceftriaxone 1 gram IM or IV, clindamycin 600 mg IM or IV, Vanco 15-20 mg/kg not to exceed 2 grams per dose Abx taken 30-60 minutes prior to procedure (except Vanco which should be given 120 minutes before)
Tricuspid & Pulmonic Valve Disease
•Uncommon •Stenosis more than regurgitation •Tricuspid stenosis •Caused by Rheumatic fever or IV drug use •RA enlargement & ↑ SVP •Pulmonic stenosis •Congenital •RV HTN & hypertrophy
Tricuspid & Pulmonic Valve Disease: Conservative Therapy- Percutaneous Transluminal Balloon Valvuloplasty
-Fused commissures split open -Mitral, tricuspid, & pulmonic stenosis (less often AS) -Done in cath lab: balloon tipped cath from femoral vein or artery to stenotic valve, inflate balloon to attempt separation of leaflets -Older adults & poor surgical candidates balloon put in to open stenosed valve
Surgical Interventions: Repair
-Lower operative mortality than replacement -Often used for mitral or tricuspid valves -May not restore total valve function a. mitral commissurotomy (valvulotomy) - pure mitral stenosis - open or closed - open requires bypass: remove thrombi & make commissure incision, fused chordae separated by splitting papillary muscle & debriding calcified valve b. Valvuloplasty (open surgical) - suture torn leaflets, chordae tendineae, or papillary muscles - mitral or tricuspid regurgitation c. minimally invasive valvuloplasty d. Annuloplasty - reconstruct annulus with or without prosthetic rings - mitral or tricuspid regurgitation
Nursing assessment: Subjective
-PMH: •RF, IE, congenital heart defects, MI, chest trauma, CMP, syphilis, Marfan's, streptococcal infections -Functional Health Patterns: •IV drug abuse, fatigue •Palpitations, generalized weakness, activity intolerance, dizziness, fainting, DOE, cough, hemoptysis, orthopnea •Paroxysmal nocturnal dyspnea •Angina or atypical chest pain
Tricuspid & Pulmonic Valve Disease: Conservative Therapy- Sapien Transcatheter Heart Valve
-Select patients with AS -Femoral artery to heart -Expand balloon at aortic valve -Patient eligible for surgery but high risk for complications (multiple comorbidities)
Surgical Interventions: Replacement
-mitral, aortic, tricuspid, and occ pulmonic -Wide range of valves available for use -Mechanical or biologic (Figure 36-10 in text) -Can also be done minimally invasive -Mechanical: -Metal alloys, pyrolytic carbon, Dacron -More durable & last longer -Increased risk of thromboembolism -Require long-term anticoagulation -Biologic:
Nursing assessment: Objective
Fever Diaphoresis, flushing, cyanosis, clubbing, peripheral edema Crackles, wheezes, hoarseness Abnormal heart sounds, murmurs, dysrhythmias, hypotension Ascites, hepatomegaly, unexplained weight gain
The nurse is caring for a 64-yr-old patient admitted with mitral valve regurgitation. Which information obtained by the nurse when assessing the patient should be communicated to the health care provider immediately? A. The patient has 4+ peripheral edema. B. The patient has diffuse bilateral crackles. C. The patient has a palpable thrill felt over the left anterior chest. D. The patient has a loud systolic murmur across the precordium.
B.The patient has diffuse bilateral crackles. As valve disorder progresses and there is back flow, we are worried about the lungs from the backward flow with acute exacerbation of HF
The nurse will plan discharge teaching about prophylactic antibiotics before dental procedures for which patient? A. Patient being discharged after an exacerbation of heart failure B. Patient admitted with a large acute myocardial infarction C. Patient who had a mitral valve replacement with a mechanical valve D. Patient being treated for rheumatic fever after a streptococcal infection
C. Patient who had a mitral valve replacement with a mechanical valve
A 21-yr-old woman is scheduled for percutaneous transluminal balloon valvuloplasty to treat mitral stenosis. Which information should the nurse include when explaining the advantages of valvuloplasty over valve replacement to the patient? A. Ongoing cardiac care by a health care provider is not necessary after valvuloplasty. B. Mechanical mitral valves need to be replaced sooner than biologic valves. C. Biologic valves will require immunosuppressive drugs after surgery. D. Lifelong anticoagulant therapy is needed after mechanical valve replacement.
D.Lifelong anticoagulant therapy is needed after mechanical valve replacement.
While caring for a 23-yr-old patient with mitral valve prolapse (MVP) without valvular regurgitation, the nurse determines that discharge teaching has been effective when the patient states that it will be necessary to A. take an aspirin a day to prevent clots from forming on the valve. B. limit physical activity to avoid stressing the heart. C. take antibiotics before any dental appointments. D. avoid over-the-counter (OTC) drugs that contain stimulants.
D.avoid over-the-counter (OTC) drugs that contain stimulants. Want to avoid caffeine and drugs like Sudafed
When caring for a patient with mitral valve stenosis, it is most important that the nurse assess for A. diastolic murmur. B. peripheral edema. C. right upper quadrant tenderness. D. shortness of breath on exertion.
D.shortness of breath on exertion.
MVP Diagnosis and Treatment
ECHO to confirm diagnosis Beta blockers to control palpitations and chest pain Patient education: stay hydrated, routine exercise, & avoid caffeine
The nurse is caring for a patient with mitral regurgitation. Referring to the figure below, where should the nurse listen to best hear a murmur typical of mitral regurgitation?
Listen in fifth intercostal space
Fourth Heart Sound
The fourth heart sound (S4), also known as the "atrial gallop," occurs just before S1 when the atria contract to force blood into the left ventricle. If the left ventricle is noncompliant, and atrial contraction forces blood through the atrioventricular valves, a S4 is produced by the blood striking the left ventricle. A S4 heart sound can be an important sign of diastolic heart failure or active ischemia and is rarely a normal finding. Like S3, the S4 sound is low pitched and best heard at the apex with the patient in the left lateral decubitus position.
Third Heart Sound
The third heart sound (S3), also known as the "ventricular gallop," occurs just after S2 when the mitral valve opens, allowing passive filling of the left ventricle. The S3 sound is actually produced by the large amount of blood striking a very compliant left ventricle. A S3 can be a normal finding in children, pregnant females and well-trained athletes; however, a S4 heart sound is almost always abnormal. Also, the S3 sound is heard best at the cardiac apex, whereas a split S2 is best heard at the pulmonic listening post (left upper sternal border). To best hear a S3, the patient should be in the left lateral decubitus position.
Mitral Valve Prolapse (MVP)
•Abnormality of mitral valve leaflets & papillary muscles or chordae •Result is leaflet prolapse or buckle into the LA during systole •Most common valvular disease in US •Usually benign •Affects males & females equally •Familial incidence - autosomal dominant •Connective tissue defect (Marfan's)
Types of valves
•Atrioventricular (AV) •Mitral (Left side) •Tricuspid (Right side) •Semilunar •Aortic (Left side) •Pulmonic (Right side) Valvular Heart Disease (VHD) is defined by the valve(s) affected & the type of dysfunction
MVP Clinical Manifestations
•Broad range of severity •May be asymptomatic for life •10% of patients symptomatic •Murmur louder during systole •No alteration of S1 or S2 •Severe MR uncommon but serious complication MVP Dysrhythmias •PVC, PSVT, VT •Palpitations, light-headedness, syncope Chest pain sometimes - ? Etiology: not certain why they get chest pain •Along with dyspnea, palpitations, syncope •Does NOT respond to antianginals
Aortic regurgitation (AR)
•Causes •Primary disease of aortic valve leaflets, aortic root, or both •Acute AR caused by trauma, IE, or aortic dissection = LIFE TREATENING •Chronic AR caused by RHD, congenital bicuspid aortic valve, syphilis, or chronic rheumatoid disease •Backward blood flow from ascending aorta into LV during diastole •Volume overload •LV initial compensation = dilation & hypertrophy •Contractility declines over time which results in ↑ blood volume in LA & pulmonary bed Seen as pulmonary HTN & RV failure Aortic valve not closing completely Pressure builds up, and volume overload occurs When stressed to compensate the heart is going to dilate to get back to homeostasis, eventually compensation will fail
Acute Mitral Regurgitation
•Clinical Manifestations: •Thready, peripheral pulses •Cool & clammy •Decreased CO may mask new systolic murmur •Rapid onset of pulmonary edema & cardiogenic shock •Assessment & intervention critical •Cardiac cath & valve repair or replacement Need quick life-saving intervention, a lot of blood going back into left atrium Cardiac output is next to nothing
Aortic stenosis (AS)
•Congenital AS •Older adult AS •Obstruction of blood flow from LV to aorta during systole •Results in: •More chest pain due to demand ischemia •LV hypertrophy, ↑ myocardial oxygen consumption •Progression results in compensatory mechanism failure •↓ CO = ↓ tissue perfusion, pulmonary HTN, & HF •Untreated → 50% mortality at 1 year Congenital AS seen in children, adolescents, young adults Older adults with AS caused by either rheumatic fever or degeneration - rheumatic fever incidence decreasing but degenerative stenosis increasing 3% of older adults > 65 with AS
Causes of VHD
•Congenital in children & adolescents •Acquired •Degenerative disease (mechanical stress, CAD, HTN) •Rheumatic disease (fibrotic changes & calcification of cusps) •Infective endocarditis (infectious organism destroys the valve, strep common cause) •Heart disease in older adults •Aortic stenosis (AS) & Mitral regurgitation (MR) common •Other causes •AIDS •Antiparkinsonian drugs •dopamine agonists - ergot derivatives: cabergoline & pergolide •When given in high doses Ergot derivatives similar to serotonin & thought to produce valve disease by stimulation of serotonin receptors Serotonin stimulates fibroblast growth and fibrogenesis
Mitral Stenosis: Clinical Manifestations
•Exertional dyspnea (primary symptom) •Hemoptysis: cough up blood •Loud S1 with low pitched diastolic murmur heard best at apex •Hoarseness, hemoptysis, chest pain •Emboli with a-fib and possible CVA: due to increase of pressure in right atrium •Fatigue and palpitations from a-fib Exertional dyspnea secondary to decreased lung compliance - primary symptom
Tricuspid & Pulmonic Valve Disease: Diagnostics
•History & Physical Exam •CXR •Heart size, altered pulmonic circulation, & valve calcification •CBC •EKG •HR, rhythm, ischemia, ventricular hypertrophy •ECHO •Valve structure, function, chamber size Cardiac Catheterization Pressures in chambers, pressure difference across valves, size of valve openings CT chest with contrast Gold standard to evaluate aortic disorders TEE & color flow doppler transesophageal Diagnose and monitor Real-time 3-D ECHO Assess mitral valve and congenital heart disease
Expected outcomes
•Maintain adequate tissue & organ perfusion •Achieve fluid & electrolyte balance •Achieve optimal level of activity •Describe the disease process & appropriate measures to prevent complications
Chronic Mitral Regurgitation
•May be asymptomatic for years - monitor •Early LV failure = weakness, fatigue, palpitations, dyspnea •Disease progression = orthopnea, paroxysmal nocturnal dyspnea, peripheral edema •Increased LV volume = S3 (even with normal LV function) •Loud holosystolic murmur at apex that radiates to left axilla •ECHO to make sure regurgitation is not progressing •Valve repair or replacement BEFORE significant LV failure or pulmonary HTN develop
Mitral Regurgitation
•Mitral valve function is dependent on intact: •Mitral leaflets, mitral annulus, chordae tendineae, papillary muscles, LA, & LV •A defect in ANY structure = regurgitation •Backward blood flow from LV to LA secondary to incomplete closure during systole •May be acute or chronic & causes include: •Myocardial infarction (MI) •Chronic RHD •Mitral valve prolapse (MVP) •Ischemic papillary muscle dysfunction •Infective endocarditis (IE)
Mitral Stenosis
•Most cases caused by rheumatic heart disease (RHD) •Infection creating scar tissue at any area in the valve, with scar tissue things aren't as flexible and unable to open as it used to •Opening gets smaller and smaller •Other causes: congenital, rheumatoid arthritis, lupus •In RHD: •Endocarditis causes scarring of valve leaflets & chordae tendineae •Contractures & adhesions develop between commissures •Stenotic mitral valve looks like a "fish mouth" •Deformities block blood flow •Pressure difference between LA and LV during diastole •Increased LA pressure & volume = increased pulmonary pressure •Increase risk of a-fib secondary to LA overload •Chronic: LA increased pressure causes increased pulmonary and RV pressure
Valvular dysfunction
•Normal •Pressure on either side of the valve is equal •Stenosis •Smaller valve opening •Forward flow impaired •Amount of stenosis is seen in the pressure difference: •the greater the difference, the greater the stenosis •Regurgitation •Incompetence or insufficiency •Incomplete valve closure •Backward flow of blood
Tricuspid & Pulmonic Valve Disease: Conservative Therapy
•Prevent recurrent rheumatic fever & infective endocarditis (IE) •Treatment dependent on valve involved & disease severity •Prevent HF exacerbations, acute pulmonary edema, thrombo-embolisms, & recurrent endocarditis •HF treatment: •Vasodilators, ➕ inotropes, beta-blockers, diuretics, & low sodium diet •Anticoagulant therapy •Prevent and/or treat systemic or pulmonary emboli •Prophylaxis in patients with a-fib •Atrial dysrhythmias common - antidysrhythmic therapy •CCB, beta-blocker, antidysrhythmics, or cardioversion + inotropes = digoxin, dobutamine, dopamine, epinephrine
Nursing Interventions
•Prophylactic antibiotic therapy Manage HF Appropriate exercise program & avoid strenuous activities Conserve energy, set priorities, & planned rest periods Medication teaching: Prophylactic antibiotic therapy Anticoagulation therapy with monitoring When to seek care: HF, infection, bleeding Make sure they go to CBC, PT/INR checks for whatever anticoag therapy they are receiving
Surgical Interventions
•Repair a)Mitral commissurotomy (valvulotomy) b)Valvuloplasty (open surgical) c)Minimally invasive valvuloplasty d)Annuloplasty Replacement a)Mitral: common b)Aortic: common c)Tricuspid d)Occasionally pulmonic
Surgical therapy
•Repair or replacement •Dependent on: 1.Valve 2.Pathology & severity of disease 3.Patient's clinical condition •Palliative, NOT curative •Lifelong healthcare required As we go in and replace valve, it's not a cure; they can continue to develop heart disease-->this procedure is more palliative care
Chronic AR Clinical Manifestations
•Severe: water-hammer pulse •Soft or absent S1 , S3 , or S4 •Soft, high-pitched diastolic murmur •Asymptomatic for years •Exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea •After considerable damage has occurred •Angina less frequently than with AS Bounding pulse
Acute AR Clinical Manifestations
•Sudden onset of CV collapse characterized by: •Severe dyspnea, chest pain, hypotension •LV failure & cardiogenic shock •Life-threatening will present already in shock
AS clinical manifestations
•Symptoms appear when orifice 1/3 normal size •Classic Triad of symptoms reflects LV failure: •Angina, syncope, & exertional dyspnea •Poor prognosis with symptoms and no treatment or repair •Caution NTG use - decreased preload = increased chest pain & hypotension •Normal or soft S1 with diminished or absent S2 , systolic murmur, prominent S4 •Be caution with nitrate use, more we decrease preload the more issues we have at the end