Valvular Heart Disease - developinganaesthesia



VALVULAR HEART DISEASE

Drawing of the Heart and its Blood Vessels, from the Anatomical Notebooks, Leonardo da Vinci, Bibliotecha Ambrosiana, Milan, Italy, Late Fifteenth Century.

VALVULAR HEART DISEASE INDEX

1. Aortic Incompetence.

2. Aortic Stenosis.

3. Mitral Incompetence.

4. Mitral Stenosis.

5. Mitral Valve Prolapse

6. Pulmonary Incompetence.

7. Pulmonary Stenosis.

8. Tricuspid Incompetence.

9. Tricuspid Stenosis.

Appendix 1: Grading of the loudness of murmurs.

Appendix 2: Auscultatory regions of the heart.

Appendix 3: The JVP wave form.

VALVULAR HEART DISEASE AORTIC INCOMPETENCE

These guidelines are primarily based on the recommendations of The Task Force on the Management of Valvular Heart Disease of the European Society of Cardiology, 2007. 1

Introduction

Aortic incompetence (AI) may be the consequence of diverse aetiologies, the distribution of which has changed over time. The most frequent causes of AI are now those related to aortic root disease and bicuspid aortic valve.

Natural History

Patients with acute AI have a poor prognosis without surgical intervention.

There is little information in the literature on the progression from mild to severe AI.

Patients with severe AI and symptoms have a poor prognosis.

The natural history of aortic root aneurysm has been mainly studied in patients with Marfan’s syndrome. The strongest predictors of complication are the diameter of the aortic root at the level of the sinuses of Valsalva and the presence of a family history of cardiovascular events.

Causes

1. Valvular causes:

● Infective endocarditis, (acute onset)

● Rheumatic fever, (chronic onset)

2. Aortic root disruptions:

● Marfans

● Hypertension

● Stanford type A dissecting aortic aneurysm.

● Congential aortic root aneurysms.

● Aortitis, (tertiary syphilis, rheumatoid arthritis, sero-negative arthropathies)

Complications

1. Infective endocarditis.

● Note that aortic incompetence may also be caused by endocarditis, as well as predisposing to it.

2. Left heart failure:

● Left ventricular hypertrophy and eventually failure, the heart needs to work against a volume load. In relative terms this is not as great as working against a pressure load, (as for aortic stenosis).

3. Uncommonly angina pectoris, (possibly due to low diastolic pressures).

Clinical Features

In non acute cases:

Symptoms

1. Initially a patient may be asymptomatic for years.

2. Exertional dyspnea is generally the first symptom.

3. Occasionally angina pectoris.

4. Palpitations, related to a hyperdynamic circulation.

Signs

1. Pulse:

● Waterhammer, or “collapsing”.

● Prominent carotid pulsations, (“Corrigan’s sign”)

2. Blood pressure:

● Systolic pressure mildly increased

● Diastolic pressure significantly reduced.

● Increased pulse pressure.

3. Palpation:

Apex beat:

● Hyperkinetic.

● Somewhat displaced.

Thrill:

● Occasionally detected at the left sternal edge, on expiration.

4. Heart sounds:

● Soft 2nd heart sound (A2)

5. Murmur:

● Early decrescendo diastolic murmur.

● Maximal at the left sternal edge with valvular lesions, (right sternal edge with root lesions)

● Accentuated by sitting up and leaning forward with the breath held in expiration.

● May have an Austin Flint murmur, a diastolic murmur at the apex (sounds like M.S but no opening snap and S1 is soft. It is due to the regurgitant stream interfering with the anterior leaflet of the mitral valve during diastole).

Clinical Indicators of Severity

| | |

|SIGN |SEVERITY INDICATOR |

| | |

|Pulse |Collapsing nature and reflected in the blood pressure as a wide pulse pressure. |

| | |

|Heart sounds |S3 (left ventricle) and soft A2 |

| | |

|Murmur |Length of the murmur / presence of an Austin Flint murmur. |

| | |

|Heart failure |Left ventricular failure (late) |

Investigations

CXR

Check for:

● Cardiomegaly

● Signs of pulmonary congestion.

ECG

● Check for signs of LHV and strain.

Echocardiography

Indications of severe AI on echocardiography include: 1

● A central jet with ≥ 65% of the LV outflow tract.

● Moderate to severe LV enlargement in the absence of other aetiologies of LV enlargement.

● Regurgitant volume > 60 mls per beat.

● Regurgitant fraction ≥ 50%

● Effective regurgitant orifice area ≥ 0.3 cm2

Coronary angiography:

Coronary angiography is indicated in selected cases to detect associated coronary artery disease when surgery is planned. Knowledge of coronary anatomy improves risk-stratification and determines whether coronary revascularization is indicated in association with valvular surgery.

Management

1. Antibiotic prophylaxis for surgical procedures, (see latest edition of Antibiotic guidelines)

2. Medical Therapy:

● In patients with chronic severe AI and heart failure, ACE-inhibitors are the treatment of choice when surgery is contraindicated or in cases with persistent postoperative LV dysfunction.

● In patients with Marfan’s syndrome, beta-blockers slow the progression of the aortic dilatation and should also be given after operation. In patients with severe AI, the use of beta-blockers should be very cautious because the lengthening of diastole increases the regurgitant volume. However, they can be used in patients with severe LV dysfunction.

3. Surgical Therapy:

● The approach to the need for surgery can be summarized by the flow chart below.

4. Screening:

● In patients with Marfan’s syndrome or in young patients with aortic root aneurysm, the family needs to be screened to detect asymptomatic cases.

VALVULAR HEART DISEASE AORTIC STENOSIS

These guidelines are primarily based on the recommendations of The Task Force on the Management of Valvular Heart Disease of the European Society of Cardiology, 2007. 1

Introduction

Aortic stenosis (AS) has become the most frequent type of valvular heart disease in Europe and North America. It primarily presents as calcific AS in adults of advanced age.

The second most frequent etiology, which dominates in the younger age group, is congenital, whereas rheumatic AS has now become rare.

Natural History

Calcific AS is a chronic progressive disease. Patients typically remain asymptomatic during long latent periods.

Sudden cardiac death is a frequent cause of death in symptomatic patients but appears to be rare in the asymptomatic

As soon as symptoms occur, the prognosis is dismal and mortality has been reported to be quite significant even within months of symptom onset which is often not promptly reported by patients.

Causes

1. Degenerative calcific aortic valve, (most common cause in adults).

2. Calcified congenital bicuspid valve.

3. Rheumatic fever, (early adulthood)

Complications

1. Excertional syncope.

2. Angina pectoris.

3. Infective endocarditis.

4. LVF, (late).

5 Sudden death.

Clinical Features

Symptoms

1. Initially a patient may be asymptomatic for years as the cardiac output is maintained by left ventricular hypertrophy.

Once symptoms do occur, average life expectancy will be less than 5 years if untreated.

2. Exertional dyspnea is generally the first symptom.

3. Next symptoms to appear will be:

● Angina pectoris, (this is not related to coronary artery disease)

● Exertional syncope

● Sudden death.

4. Eventually signs of congestive cardiac failure, (this will indicate advanced disease with average survival time of less than 2 years)

Signs

1. Pulse (carotid)

● Slow rising, sustained (or “plateau”) and small volume.

2. Blood pressure:

● Reduced systolic pressure

● Reduced pulse pressure

3. Palpation:

Apex beat:

● Hyperdynamic, maybe slightly displaced.

Thrill:

● At the base of the heart, in the aortic area), if severe.

4. Heart sounds:

● S4

● Splitting of the second heart sound, (ie paradoxical splitting on expiration), if severe, (there is delayed left ventricular ejection and aortic valve closure)

● Soft or absent S2.

● Occasionally an early systolic ejection click, (just after the first heart sound). This will mean that the valve is mobile.

5. Murmur:

● Harsh mid-systolic ejection murmur.

● Maximal in the 2nd right intercostal space and radiates to the carotids arteries.

● Accentuated by sitting up and leaning forward with the breath held in expiration.

Clinical Indicators of Severity

| | |

|SIGN |SEVERITY INDICATOR |

| | |

|Pulse |Plateau, also reflected in the BP, Reduced systolic and pulse pressures. |

| | |

|Heart sounds |S4, and paradoxical split of S2 |

| | |

|Murmur |Long and late peaking, +/- an associated thrill. |

| | |

|Heart failure |Left ventricular failure is a very late sign. |

Investigations

CXR

Check for:

● Cardiomegaly

● Signs of pulmonary congestion.

● Aortic valve calcification may be seen.

ECG

● Check for signs of LHV and strain.

Echocardiography

Indications of the severity of AS on echocardiography include: 1

● Severe: Valve area of < 1cm2 or < 0.6 cm2/ m2 BSA.

● Moderate: Valve area of 1.0-1.5 cm2 (0.6 cm2/m2 to 0.9 cm2/m2 BSA) or mean aortic gradient 30–50 mmHg in the presence of normal flow conditions.

● The combination of a markedly calcified valve (particularly without movement) with a rapid increase in peak aortic velocity of 0.3 m/s per year.

● AS with low flow gradients ( 55 mm

● Regurgitant volume > 60 mls per beat.

● Regurgitant fraction > 50%

● Effective regurgitant orifice area ≥ 0.4 cm2

Coronary angiography:

● Coronary angiography is indicated in selected cases to detect associated coronary artery disease when surgery is planned. Knowledge of coronary anatomy improves risk-stratification and determines whether coronary revascularization is indicated in association with valvular surgery.

Management

1. Antibiotic prophylaxis for surgical procedures, (see latest edition of Antibiotic guidelines)

2. Medical therapy (organic MI):

● In acute MI, reduction of filling pressures can be obtained with nitrates and diuretics.

● Nitroprusside reduces afterload and regurgitant fraction. Inotropic agents should be added in case of hypotension.

● Anticoagulant therapy, with a target international normalized ratio (INR) range between 2 and 3, should be given in patients with MR and permanent or paroxysmal AF or whenever there is a history of systemic embolism or evidence of left atrial thrombus and during the first 3 months following mitral valve repair.

● In severe MI, maintenance of sinus rhythm after cardioversion is unlikely unless the MI is treated surgically.

● If AF occurs, heart rate should be controlled.

● There is no evidence to support the use of vasodilators, including ACE-inhibitors, in chronic MI without heart failure and therefore they are not recommended in this group of patients.

● On the other hand, when heart failure has developed, ACE-inhibitors have a benefit and may be used in patients with advanced MR and severe symptoms who are not suitable for surgery or when there are still residual symptoms following the operation, usually as a result of impaired LV function.

● Beta-blockers and spironolactone should also be considered as appropriate.

3. Surgical therapy:

The general approach to surgery in patients with severe organic MI is summarized in the flow diagram below:

VALVULAR HEART DISEASE MITRAL STENOSIS

These guidelines are primarily based on the recommendations of The Task Force on the Management of Valvular Heart Disease of the European Society of Cardiology, 2007. 1

Introduction

Although the prevalence of rheumatic fever has greatly decreased in industrialized countries, mitral stenosis (MS) still results in significant morbidity and mortality worldwide.

Since its development 20 years ago, percutaneous mitral (balloon) commissurotomy (PMC) has impacted significantly upon the management of MS.

Natural History

Studies on natural history are old and non-controlled.

In asymptomatic patients, survival was good up to 10 years, progression being highly variable with sudden deterioration, precipitated by complications, such as atrial fibrillation or

embolism, in half of the patients.

Symptomatic patients have a poor prognosis.

Causes

1. Rheumatic heart disease, (nearly always the cause)

Complications

1. Infective endocarditis.

2. Atrial fibrillation is common with the attendant risk of thrombo-embolic disease.

3. Pulmonary edema.

4. Pulmonary hypertension with consequent right ventricular failure.

5. Recurrent chest infections.

Clinical Features

Symptoms

1. Initially none, symptoms develop slowly.

2. Essentially those of left heart failure, (although the left ventricle does not fail, rather it is secondary to the increased left atrial pressures.

Therefore:

● Exertional dyspnea.

● Orthopnea.

● Paroxysmal nocturnal dyspnea.

3. Chest:

● Recurrent chest infections

● Occasionally hemoptysis (ruptured bronchial veins)

4. Symptoms related to systemic emboli

Signs

1. Pulse

● Small volume

● AF is common.

2. Blood pressure

● May be reduced.

3. Palpation:

Apex beat

● Tapping, (reflects a loud and palpable S1) Note, the term “tapping” applies to MS, virtually by definition.

Thrill

● Diastolic thrill at the apex, (very rare)

4. Heart sounds:

● Loud S1

5. Murmur:

● A low pitched mid-diastolic “rumble”, best heard with the bell lightly held at the apex, with the patient leaning to the left side and breath held in expiration.

May be accentuated by exercise.

● Opening snap may precede the murmur (a sudden tensing of an incompetently opened valve)

● The murmur may continue on with a “pre-systolic accentuation”, due to forceful left atrial systole, provided the patient is not in AF)

Therefore: H1 → H2 → Opening snap → rumbling mid-diastolic murmur → pre-systolic accentuation → H1

6. Pulmonary hypertension, (late)

● Left parasternal heave

● Loud P2

● Increased normal splitting of S2, (on inspiration)

● Increased “a” wave of the JVP (if not in AF)

● Pulmonary systolic murmur if there is associated PI, (rare)

Clinical Indicators of Severity

| | |

|SIGN |SEVERITY INDICATOR |

| | |

|Pulse |Small pulse pressure |

| | |

|Heart sounds |Soft S1,( indicates immobile cusps, S1 is usually loud in MS) |

| | |

| |Early opening snap, (due to increased left atrial pressure) |

| | |

|Murmur |Long diastolic murmur, (persists as long as there is a gradient) |

| | |

|Heart failure |Signs of pulmonary hypertension. |

Investigations

CXR

Look for:

1. Signs of pulmonary venous congestion.

2. Signs of left atrial enlargement:

● Double shadow behind the heart.

● Widened carina (> 70 degrees)

● Straightening of the left heart border.

● On the lateral, posterior displacement of the esophagus.

● On the lateral, a calcified valve, (which lies below the line joining the carina to the xiphisternum)

ECG

Look for:

● AF is common.

● P mitrale, if in sinus rhythm.

● Right ventricular hypertrophy / strain.

Echocardiography

Indications of the severity of MS on echocardiography include: 1

● Valve area 5 mm Hg is considered indicative of clinically significant TS.

Coronary angiography:

● Coronary angiography is indicated in selected cases to detect associated coronary artery disease when surgery is planned. Knowledge of coronary anatomy improves risk-stratification and determines whether coronary revascularization is indicated in association with valvular surgery.

Management

1. Antibiotic prophylaxis for surgical procedures, (see latest edition of Antibiotic guidelines)

2. Medical therapy:

● In the presence of heart failure, diuretics are useful but of limited efficacy.

3. Surgical therapy:

● Percutaneous balloon tricuspid dilatation has been performed in a limited number of cases, either alone or alongside PMC, (for the mitral valve) but frequently induces significant regurgitation. Data on evaluation of long-term results are lacking.

● Intervention on the tricuspid valve is usually carried out at the time of intervention on the other valves in patients who are symptomatic despite medical therapy.

● Conservative surgery or valve replacement, according to anatomy and surgical expertise in valve repair, is preferred to balloon commissurotomy, which can only be considered as a first approach in the rare cases of isolated TS

Appendix 1

Grading of the loudness of murmurs:

Grade 1 Very soft, requires an experienced listener.

Grade 2 Soft.

Grade 3 Moderate and without a thrill

Grade 4 Loud with thrill just palpable.

Grade 5 Very loud and thrill easily palpable.

Grade 6 Very loud, may be heard without the aid of a stethoscope.

Appendix 2

Auscultatory regions of the heart:

Note, these regions show the optimal areas for listening to the heart valve indicated, they do not exactly correlate with surface anatomy of the anatomical location of the valve.

Appendix 3

The JVP wave form:

Components of the jugular venous pressure wave with relationships to the first and second heart sounds.

References

1. Guidelines on the Management of Valvular Heart Disease. The Task Force on the Management of Valvular Heart Disease of the European Society of Cardiology. European Heart Journal January 2007 28: 230-268.

2. Talley N.J, Clinical Examination 3rd ed 1996.

Dr. J.Hayes

4 October 2007

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