By : Hamid Miyanaji

Student of MsCCN

Autumn 2014

Refrences :

Braunwald`s Heart Disease: A Textbook of Cardiovascular Medicine, 9th edition.

Cardiac nursing, [edited by] Susan L. Woods . . . [et al.], 6th edition.

Core Curriculum for Critical Care Nursing, JOANN GRIF ALSPACH,SIXTH EDITION.

Valvular heart disease accounts for 10% to 20% of all cardiac surgical procedures in the United States.

About two thirds of all heart valve operations are for aortic valve replacement (AVR), most often for aortic stenosis (AS).

Mitral valve surgery is most often performed for mitral regurgitation (MR) because most patients with mitral stenosis (MS) are treated by a percutaneous

approach.

Rheumatic Heart Disease

Infective Endocarditis

Miscellaneous Causes of Valvular Disease :

Degenerative changes of the tissue, such as myxomatousdegeneration, calcification, and changes associated with Marfan syndrome,

Trauma or infection,

Dilation of the ventricles caused by chronically elevated preloading,

Coronary heart disease (CHD) and myocardial infarction

Systemic diseases such as lupus erythematosus and scleroderma.

Based on :

oPatient history,

oPhysical assessment,

oDiagnostic testing :

Both TTE and TEE

Cause:

The predominant cause of mitral stenosis is rheumatic fever.

Left atrial myxoma,

Ball-valve left atrial thrombus,

Large left atrial endocarditis

Vegetations, or cor triatriatum (three atria).

The cross-sectional area of the mitral valve is reduced to2 cm2 or less, a pressure gradient between the leftatrium and left ventricle occurs ;

Left atrial hypertrophy Increased left atrialpressure and dilation pulmonaryhypertension and pulmonary congestion;

Symptoms of mitral stenosis are usually related toobstruction of the mitral valve rather than ventricular

dysfunction;

Rightsided heart failure may occur.

Mild dyspnea on exertion occurs as the most commonsymptom of mild mitral stenosis (valve area of 1.6 to 2.0

cm2) ;

As mitral stenosis becomes more severe (valve area of 1 to 1.5 cm2):

Dyspnea,

Fatigue,

Paroxysmal nocturnal dyspnea,

Atrial fibrillation

With advanced mitral stenosis:

pulmonary hypertension ;

symptoms of right-sided heart failure

Chest pain and hemoptysis.

In severe mitral stenosis, on auscultation, there arefour typical findings including:

I. An accentuated S1;

II. An opening diastolic snap;

III. A middiastolic rumble noted best at the apex(in sinus rhythm), followed by presystolicaccentuation;

IV. An increased pulmonic S2 intensity associated

with pulmonary hypertension.

Patients with mitral stenosis may exhibit malar blush (pink discoloration of the cheeks);

Weak pulses secondary to reduced cardiac output

A lower left parasternal lift or heave caused by right ventricular hypertrophy;

Cardiac rhythm is often irregularly irregular,

indicating atrial fibrillation.

Echocardiography

A TEE provides better detail of the mitral valve and better visualization of atrial thrombus than does TTE.

Cardiac catheterization

Is used less in diagnosis of mitral stenosis as

echocardiography techniques improve.

Electrocardiography

Is nonspecific and does not indicate the severity of mitral stenosis.

Chest radiography

correlates with the degree of mitral stenosis.

Is aimed at preventing the complications of systemicembolization and bacterial endocarditis as well as atrialfibrillation,

Patients who have asymptomatic mitral stenosis requireonly antibiotic prophylaxis.Patients with mild pulmonary congestion can bemanaged with diuretics alone. β -Blockers can be used toreduce heart rate and improve diastolic filling time.

When patients have atrial fibrillation, digoxin, β-blockers,or calcium channel blockers can be used for ventricularresponse rate control.

Patients with atrial fibrillation require anticoagulation to

prevent thrombus formation in the atrium.

Once the patient has symptoms of NYHA functional classIII or IV despite adequate medical management,mechanical correction of mitral stenosis by balloonvalvuloplasty or surgery should be performed.

Percutaneous Mitral Catheter Balloon ValvuloplastyPercutaneous mitral catheter balloon valvuloplasty is an

alternative, less invasive procedure than surgicaltreatment for mitral stenosis.

Mitral balloon valvuloplasty is recommended in patientswith moderate-to-severe mitral stenosis that issymptomatic with favorable valve morphology.

Mitral balloon valvuloplasty may be used in women whoexperience hemodynamic decompensation duringpregnancy due to mitral stenosis as it offers less risk tothe fetus than mitral valve replacement and

cardiopulmonary bypass.

Surgical TreatmentSurgical replacement of the mitral valve is required whenthere is severe mitral regurgitation coexisting with mitralstenosis or if the mitral stenosis is not amenable topercutaneous balloon valvuloplasty.

For patients with coexistent tricuspid regurgitation,combined mitral valve surgery with tricuspid repair isrelated to better clinical outcomes than mitral balloonvalvuloplasty alone.

The usual prosthetic valve of choice in mitral stenosis is amechanical prosthesis, because patients already requirelife-long anticoagulation because of atrial fibrillation. Foryoung women who wish to become pregnant, abioprosthesis may be recommended.

Goals of care:I. Hemodynamics improve

II. Complications are treated and/or prevented

A. Anticipated patient trajectory: Patient with mitralstenosis will gradually develop limiting symptoms andheart failure with the likelihood of stroke and earlydeath.

I. Nutrition: Restricted sodium intake

II. Infection control: IE prophylactic therapy

III. Discharge planning: Patient education regarding thefollowing :

a) Activity limitations;

b) Medications;

c) Anticoagulation and follow-up requirements

A. …IV. Pharmacology:

a. Diuretics, nitrates: may lower CO

b. Digitals, β-blocker, CCB

c. β-blocking agent: Use carefully in patients withimpaired LV function

d. Anticoagulants: Goal is an INR of 2 to 3

e. Antibiotics: As a prophylaxis.

B. Potential complications:

i. Systemic or pulmonary emboli from atrial thrombus

a) CNS embolism: Symptoms of stroke;

b) Pulmonary embolism: Symptoms of tachycardia, tachypnea,hypoxia, dyspnea, cough, hemoptysis, elevated PAP,hypotension, chest pain, abnormal ABG values, cyanosis,positive lung scan results;

c) Renal embolism: Hematuria, oliguria, back pain, rising BUNlevel

d) Splenic embolism: LUQ pain with radiation to left shoulder;

e) Mesentric embolism: Pain in the lower abdomen, bloodydiarrhea, elevated leukocyte count and elevated ESR.

ii. Other complications include heart failure, infection

Cause:

Acute:

Endocarditis, myxomatous degeneration, rupture ofchordae tendineae, papillary muscle disorders,prosthetic valve failure, or trauma.

Chronic :

Rheumatic heart disease, injury after radiation,cardiomyopathies, infiltrative disease, ischemic damageto the subvalvular apparatus, infective endocarditis,myxomatous degeneration, hypertrophiccardiomyopathy, diet-drug-induced lesions, or markedleft ventricular dilation.

Mitral regurgitation occurs as the result of inadequateclosure of the mitral valve, allowing regurgitant flowback into the left atrium during each left ventricular

systole.

Regurgitant flow also increases left atrial pressure,causing left atrial dilation and pulmonary congestion.

During diastole, the regurgitant volume returns to theleft ventricle and increases its volume load.

In acute mitral regurgitation, neither the left atrium northe ventricle has had sufficient time to adjust to theincreased volume load.

In acute mitral regurgitation:

Symptoms are typically those of left ventricular failure;

Tachycardia to compensate for the reduced forward stroke volume;

Dyspnea secondary to pulmonary congestion and edema;

Orthopnea and PND and poor exercise tolerance;

Right-sided failure may occur secondary to pulmonary hypertension;

New-onset atrial fibrillation.

In chronic mitral regurgitation:

Patients may be relatively asymptomatic for years;

Exertional dyspnea;

Orthopnea;

Paroxysmal nocturnal dyspnea;

Cough;

Palpitations;

New atrial fibrillation;

Lower extremity edema

The most easily noted characteristic of either chronic or acutemitral regurgitation is the holosystolic murmur, which is heard

best at the apex and radiates to the axilla;

Patients may have an S3 gallop in moderate-to-severeregurgitation;

In acute mitral regurgitation, an S4 gallop is common becausethe left atrium and ventricle are noncompliant;

Because of left ventricular dilation, patients with chronic mitralregurgitation have an easily palpated, left laterally displacedpoint of maximal impulse;

Patients with acute or decompensated chronic mitralregurgitation may be anxious and diaphoretic because of leftventricular failure;

Blood pressure may be normal to low and pulse pressure

may be narrowed;

Jugular venous pressure can be normal or elevated

Breath sounds can range from basilar crackles to dullnesssecondary to pleural effusion;

Symptoms of reight sided heart failure.

Echocardiography

TTE can identify the structural cause of the mitralregurgitation,

TEE is better than TTE for defining mitral valve anatomyand discriminating prosthetic valves and paravalvular leaks.

Cardiac catheterization

Is used to identify coexisting coronary artery disease and to grade the severity of mitral regurgitation.

Electrocardiography

In chronic mitral regurgitation may demonstrate leftventricular hypertrophy and left atrial enlargement or P

mitrale;

Atrial fibrillation may occur;

Patients may demonstrate ischemic changes and patientswith papillary muscle rupture can show acute inferior,posterior, or anterior myocardial infarction.

Left ventricular hypertrophy

Left atrial enlargement

Chest radiography

In chronic mitral regurgitation shows left ventricular

hypertrophy and left atrial enlargement;

Pulmonary vascular redistribution and pulmonary edemacan be observed.

Left ventricular hypertrophy

Left atrial enlargement

Pulmonary vascular redistribution

Pulmonary Edema

Medical therapy for mitral regurgitation is geared towardafterload reduction

Intravenous vasodilators such as nitroprusside;Intravenous diuretics are used to reduce volume overload;

In acutely ill patients refractory to medications, intra-aorticballoon counterpulsation;

In patients with chronic mitral regurgitation: other afterload-reducing agents, such as angiotensin-converting enzymeinhibitors, nitrates, or hydralazine, may be used.

The patient should be care-fully monitored, however, andreferred for mitral valve repair or replacement before significantleft ventricular dysfunction or pulmonary hypertension occurs.

In patients with chronic mitral regurgitation, mitralreplacement should occur before the patient has had

irreversible left ventricular dysfunction;

Mitral valve replacement involves implantation of aprosthetic valve, either mechanical or bioprosthetic;

Patients with NYHA class II symptoms should beconsidered for surgery.

These procedures consist of direct suture of the valvecusps, repair of the elongated or ruptured chordaetendineae (chordoplasty), or repair of the valve annulus(annuloplasty).

Annuloplasty

A. Anticipated patient trajectory: severe mitral regurgitationmust be corrected, or progressive LVF and early deathoccur.

I. Discharge planning:

i. Usual postoperative instruction for any heart surgery.

ii. If the valve is replaced, the importance of endocarditisprophylaxis and chronic anticoagulation is stressed.

II. Patient and family counseling about drugs, treatmentprocedures;

B. Control of potential complications.

Cause:

Aortic stenosis occurring from 1 to 30 years of age usuallyrepresents congenital aortic stenosis. Aortic stenosispresenting at the ages of 40 to 60 years is primarilyrheumatic in origin or secondary to calcific aortic stenosisin a congenitally bicuspid aortic valve. In patients past theage of 60 to 70 years, calcific degenerative stenosis is themost prevalent cause.

As the valve cusps become less mobile, the valve orificedecreases in size, resulting in an increasingly higher leftventricular systolic pressure necessary to eject bloodacross the stenosed valve.

Initially adaptive in aortic stenosis, left ventricularhypertrophy leads to decreased ventricular complianceand diastolic dysfunction.

As aorticstenosis becomes severe, left ventricular systolicfunction may also decline, resulting in CHF.

Myocardial oxygen demand is increased secondary toincreased left ventricular wall stress and muscle mass.Myocardial oxygen delivery is reduced as a result ofdecreased coronary perfusion pressure.

Syncope or near syncope

Orthostatic blood pressure changes may occur duringexertion

Development of atrial fibrillation with rapid ventricularresponse may produce light-headedness or syncope dueto loss of atrial kick and decline in cardiac output.

Syncope at rest may be due to transient ventricularfibrillation that spontaneously converts.

mild-to-moderate aortic stenosis are usuallyasymptomatic;

Severe:

Dyspnea on exertion;

Angina;

Near syncope or syncope;

CHF;

Less commonly sudden death.

Aortic stenosis is most readily detected by auscultation ofits classic mid-systolic (systolic ejection) murmur;

The murmur often radiates to one or both carotids;

The murmur may be diminished at the base of the heartand radiate to the apex, which may be incorrectlythought to be mitral regurgitation (Gallavardinphenomenon);

An S4 gallop is usually present;

Blood pressure is normal-to-hypertensive;

Diminished carotid upstrokes and late systolic peak(tardus) in severe or critical aortic stenosis.

Echocardiography:

Is the most important diagnostic imaging technique used to diagnose and follow aortic stenosis.

Cardiac catheterization:

Is performed in patients with aortic stenosis primarily to rule out concomitant CHD.

Electrocardiography

Often shows a pattern of left ventricular hypertrophy, ST-Twave changes typical of left ventricular strain, QRS voltagechanges in the precordial leads.

Exercise testing:

In patients with mild-to-moderate aortic stenosis withequivocal symptoms may be accomplished with caution inthe hands of a cardiologist and can provide relevantinformation regarding exercise tolerance.

Gated blood pool radionuclide scans:

Provide information regarding ventricular function similarto echocardiography

Chest radiography:

May be negative even in advanced disease.

Because aortic stenosis is a mechanical problem, there isno effective medical management;

Serial physical examinations and periodicechocardiography.

Percutaneous Aortic Catheter Balloon Valvuloplasty:

The balloon is inflated, fracturing calcified nodules andseparating the fused commissures.

The aortic valve ring is also stretched to increase the size ofthe aortic valve orifice.

Restenosis is a major problem in balloon aortic valvuloplastyin adults, occurring in approximately half of the patientswithin 6 months.

Aortic Valve Replacement:

Aortic valve replacement should be considered the treatmentof choice for severe aortic stenosis in spite of age.

…Aortic Valve Replacement:

Valve replacement with stented bioprosthetic mechanical valves or pulmonic autograft(Ross procedure).

Aortic Valve Replacement

A. Anticipated patient trajectory: Aortic stenosisthreatens the patient with limiting angina, HF anddeath.

i. Nutrition: Diet should be low sodium;

ii. Infection control: IE prophylaxis.

iii. Discharge planning:

a) Teach the patient about the symptoms;

b) Activity restrictions: Moderate aortic stenosis---- avoidcompetition sports. Sever aortic stenosis---low levelactivity only.

iv. Psychosocial issues: Patients goals and wishes areimportant because of the high risk of mortlity.

B. Control of potential complications:

i. Sudden cardiac death;

ii. LVF;

iii. Conduction defects;

iv. IE;

v. Emboli.

Cause:

Aortic regurgitation may be caused by either intrinsicabnormalities of the aortic valve leaflets or disease of theaortic root.

In rheumatic fever and endocarditis, the aortic leaflets aredirectly affected.

Aortic root dilation is seen in patients with Marfansyndrome, rheumatic arthritis, ankylosing spondylitis,annuloaortic ectasia (associated with hypertension andaging), aortic dissection, syphilitic aortitis, and collagenvascular disease.

Retrograde flow occurs during diastole when leftventricular pressure is low and aortic pressure is high.

In chronic aortic regurgitation:

The left ventricle develops mild concentric hypertrophy,may remain asymptomatic for years, until progressive leftventricular dilation and dysfunction result in CHF.

In acute aortic regurgitation:

Left ventricular and left atrial pressures rise sharply, causingacute CHF and pulmonary edema.

Patients with chronic aortic regurgitation are oftenasymptomatic for many years;

Common symptoms:

Fatigue and exertional dyspnea;

Palpitations, dizziness;

Sensation of a forceful heartbeat, especially when lying ontheir left side;

Orthopnea, paroxysmal nocturnal dyspnea, and cough;

With acute aortic regurgitation, symptoms of left-sidedheart failure develop rapidly.

The typical murmur of aortic regurgitation is a high-pitched, early diastolic decrescendo murmur with a blowing quality;

May have a physiologic murmur of mitral stenosis(Austin Flint murmur);

In chronic aortic regurgitation, the point of maximal impulse is displaced laterally.

Systolic hypertension and decreased diastolic pressure create a widened pulse pressure.

SPECIFIC PHYSICAL EXAMINATION FINDINGS IN AORTIC REGURGITATION

Hill’s sign Blood pressure higher in arms than legs

Quincke’s sign Pulsatile flushing/blanching of nail bed with application of gentle pressure.

de Musset’s sign Bobbing of head with each pulse

Corrigan’s pulse (waterhammer)

Sharp systolic upstroke and diastolic collapse of pulse

Muller’s sign Bobbing of uvula with each pulse

Traube’s sign “Pistol shot” sound auscultated over the femoral arteries

Duroziez’s sign Biphasic femoral bruit auscultated with mild pressure

Echocardiography:

Doppler echocardiography is the best noninvasive means todetect aortic regurgitation.

TEE is especially useful in imaging the ascending anddescending aorta in patients with suspected aorticdissection.

Cardiac catheterization:

Should be performed to visualize and quantify the extentof regurgitation before surgery.

However, physical findings and noninvasive tests aresufficient to establish the diagnosis of aortic insufficiency.

Radionuclide imaging

Exercise testing

Electrocardiography:

May be normal;

Patients with moderate-to-severe chronic regurgitationmay have left-axis deviation and a pattern of left ventricularstrain (Q waves in leads I, aVL, and V3 to V6, with small Rwave in V1).

Chest radiography:

May show CHF only in the patient with acute aorticregurgitation.

In chronic aortic regurgitation, the left ventricle enlarges ina leftward and inferior direction.

Patients who have asymptomatic aortic regurgitationshould have afterload reduction with vasodilators.

Diltiazem and verapamil are contraindicated in aorticregurgitation.

In addition to long-acting nifedipine and felodipine, ACEinhibitors may be used to reduce afterload.

Sodium nitroprusside reduces preload and afterload.

Acute aortic regurgitation requires urgent aortic valvereplacement.

It is desirable to treat patients with acute aorticregurgitation secondary to infective endocarditis with aminimum of 48 hours of appropriate intravenousantibiotics before implanting a prosthetic valve.

In patients with active endocarditis who arehemodynamically unstable, use of cadaveric human aortichomografts may minimize the risk of prosthetic valveendocarditis.

Aortic valve replacement is recommended for thesymptomatic patient when left ventricular ejectionfraction drops to 0.50 or less.

A. Anticipated patient trajectory: When severe, AR willaltimately result in irreversible heart failure and early death ifnot recognized and corrected with aortic valve replacementprior to LV dysfunction.

i. Positioning: Head of bed elevated, if signs of HF are present.

ii. Infection control: Prophylaxis for IE risk

iii. Discharge planning:

a) Teach the patient about the need for adherence to themedication regimen and follw-up evaluations

b) Patient should understand what types of procedures require

antibiotic prophylaxis.

Tricuspid regurgitation is primarily “functional” ratherthan structural and occurs secondary to dilation of theright ventricle and the annulus of the tricuspid valve.

frequently accompanies mitral stenosis and pulmonaryhypertension.

Symptoms include signs of right-sided heart failure .

Other causes of tricuspid regurgitation include trauma,infective endocarditis, right atrial tumor, and tricuspidvalve prolapse.

The murmur of tricuspid regurgitation is a holosystolicmurmur heard along the left sternal border and mayextend over the precordium, sounding like the murmursof mitral regurgitation and ventricular septal defect

Patients with mild tricuspid regurgitation normally do notrequire treatment.

Medical treatment is aimed at reducing pulmonary arterypressures and right heart afterload.

If tricuspid regurgitation in severe and symptomatic,tricuspid valve repair may be performed.

Acquired tricuspid stenosis is uncommon, recognized inapproximately 5% of patients with rheumatic heartdisease, and usually does not occur without involvementof the mitral valve.

The murmur of tricuspid stenosis is a diastolicdecrescendo murmur along the left sternal border.

Common symptoms of tricuspid stenosis include fatigue,minimal orthopnea, paroxysmal nocturnal dyspnea,hepatomegaly, and anasarca.

Any Question ?

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