Valve disease and endocarditis Flashcards
Mitral stenosis - causes
Rheumatic, congenital, malignant carcinoid (rare) or prosthetic valve.
Mitral stenosis - clinical features
- Symptoms – usually occur when orifice is <2cm2 – dyspnoea, fatigue, chest pain, palpitations, systolic emboli, haemoptysis or a chronic bronchitis like picture.
- Signs – low volume pulse, AF is common, malar flush (decreased CO), tapping non-displaced apex beat and a rumbling mid-diastolic murmur best heard with patient on their left side.
Mitral stenosis - investigations
- ECG – look for AF, P-mitrale (P wave is M shaped) in sinus rhythm and signs of RVH.
- CXR – look for signs of RVH, pulmonary oedema and possibly mitral calcification.
- Echo is diagnostic – significant stenosis is a valve orifice of <1cm2/1m2 body SA.
Mitral stenosis - management
Treat AF if present and give diuretics to reduce preload and pulmonary venous congestion.
If this fails perform balloon or open valvuloplasty or a valve replacement.
Mitral stenosis - complications
Pulmonary hypertension, systemic emboli, LA enlargement can cause hoarseness (recurrent laryngeal nerve), dysphagia (oesophagus) or bronchial obstruction.
Mitral regurgitation - causes
Functional (LV dilatation), calcification (in elderly), rheumatic fever, infective endocarditis, ruptured chordae tendinae, papillary muscle dysfunction or rupture, connective tissue disorder (e.g. Ehlers-Danlos or Marfans), cardiomyopathy or congenital.
Mitral regurgitation - clinical features
- Symptoms – dyspnoea, fatigue, palpitations or infective endocarditis.
- Signs – AF is common, hyperdynamic displaced apex beat, LV heave, a quiet first heart sound and pansystolic murmur which is loudest at the axilla and radiates to the axilla.
Mitral regurgitation - investigations
- ECG – look for AF, P-mitrale if in sinus rhythm (LA enlargement) and LVH.
- CXR – enlarged LA and LV, mitral valve calcification and possibly pulmonary oedema.
- Echo – used to assess LV function and with doppler can be used to visualise regurge.
Mitral regurgitation - management
Treat AF if necessary and give diuretics to improve symptoms. Aim to repair or replace the valve before the left ventricle becomes irreversibly impaired.
Mitral prolapse - causes
Can occur alone or with ASD, patent ductus arteriosus, cardiomyopathy, Turners syndrome, Marfans syndrome, osteogenesis imperfect or Wollf Parkinson White syndrome.
Mitral prolapse - clinical features
- Symptoms – can be asymptomatic or can cause atypical chest pain or palpatations.
- Signs – a mid-systolic click and/or a late systolic murmur and occasionally mitral regurgitation.
- Complications – mitral regurgitation, cerebral emboli, arrhythmias or can cause sudden death.
Mitral prolapse - investigation and management
- Investigations – echocardiograph is diagnostic and ECG may show inferior T wave inversion.
- Management – β-blockers are used to relieve symptoms but if severe surgery will be required.
Aortic stenosis - causes
Senile calcification is the commonest cause, congenital disease (bicuspid valve or William’s syndrome – neurodegenerative disorder) or rheumatic heart disease.
Aortic stenosis - clinical features
- Presentation – the classic triad includes angina, syncope and heart failure usually after the age of 60 years. Can also cause dyspnoea, dizziness, faints, systemic emboli or sudden death.
- Signs – slow rising pulse with a narrow pulse pressure, heaving but non-displaced apex beat, left ventricular heave, aortic thrill, ejection systolic murmur (heard at the aortic area, left sternal edge and radiated to the carotids) and a quiet or inaudible A2 heart sound.
Aortic stenosis - investigations
- ECG – P mitrale, left ventricular hypertrophy, left axis deviation (due to left anterior hemiblock), poor R wave progression, left bundle branch block or complete AV block.
- CXR – a calcified aortic valve and post-stenotic dilatation of the ascending aorta.
- Echo – is diagnostic and a doppler echo can be used to estimate the pressure gradient across the valve – gradient is >50 mmHg and valve area <0.5cm2 in severe stenosis.
- Cardiac catheter – to assess valve gradient, LV function and coronary artery disease.
Aortic stenosis - management
If symptomatic prognosis is poor without surgery – 2-3 years if angina or 1-2 years if heart failure. If moderate to severe stenosis and treated medically mortality rate can be as high as 50% at 2 years.
Therefore prompt valve replacement is usually recommended. If the patient is not medically fit for surgery percutaneous valvuloplasty or replacement may be done
Aortic sclerosis
Senile degeneration of the aortic valve – there is an ejection systolic murmur, no carotid radiation, a normal pulse (character and volume) and a normal second heart sound.
Aortic regurgitation - causes
- Acute – infective endocarditis, ascending aortic dissection or chest trauma.
- Chronic – congenital, connective tissue disorders (Ehlers-Danlos or Marfans), rheumatic fever, Takayasu’s arteritis, rheumatoid arthritis, SLE, seronegative arthritides (e.g. ankylosing spondylitis), hypertension, osteogenesis imperfecta or syphilitic aortitis.
Aortic regurgitation - clinical features
- Symptoms – exertional dyspnoea, orthopnoea or paroxysmal nocturnal dyspnoea. In addition patients may experience palpitations, angina, syncope or congestive cardiac failure.
- Signs – collapsing pulse, wide pulse pressure, displaced hyperdynamic apex beat and a high pitched early diastolic murmur best heart in expiration with patient sitting forward.
- Corrigan’s sign – carotid pulsation, de Musset’s sign – head nodding with each beat, Quinke’s sign – nail bed pulsations, Duroziez’s sign – femoral murmur or Traube’s sign – pistol shot femorals.
Aortic regurgitation - investigations
ECG shows LVH, CXR shows cardiomegaly, dilated ascending aorta and pulmonary oedema, echocardiography is diagnostic and cardiac catheterisation is used to assess severity of lesion, anatomy of aortic root, LV function and coronary artery disease.
Aortic regurgitation - management
- The main goal of medical therapy is to reduce systolic hypertension. Patients should be given an ACEi and monitored with an echo every 6-12 months.
- Indications for surgery – worsening symptoms, increasing cardiomegaly on CXR or echo, ECG deterioration (T wave inversion in lateral leads) or infective endocarditis that is refractory to treatment. The aim should be to replace the valve before significant left ventricular dysfunction occurs.
Tricuspid stenosis
- Causes – rheumatic fever (normally effects mitral or aortic), congenital, infective endocarditis.
- Symptoms – fatigue, ascites and oedema. Signs – giant a waves and a slow y descent on JVP, an opening snap, an early diastolic murmur heard at the left sternal edge on inspiration or AF.
- Diagnosis – made on echocardiography.
- Management – give diuretics or a surgical repair.
Tricuspid regurgitation
- Causes – functional (RV dilatation e.g. due to pulmonary hypertension induced by left ventricular failure), rheumatic fever, infective endocarditis (IV drug abusers) or congenital.
- Symptoms – fatigue, hepatic pain on exertion, ascites, oedema, dyspnoea and orthopnoea.
- Signs – giant V waves and prominent y descent, right ventricular heave, pansystolic murmur heard best at lower sternal edge in inspiration, pulsatile hepatomegaly, ascites and jaundice.
- Management – give diuretics, digoxin and ACE inhibitor and plan a valve replacement.
Pulmonary stenosis
- Causes – usually congenital (Turner’s, Noonan’s or William’s syndrome, Tetralogy of Fallot or rubella) but can be acquired – rheumatic fever or carcinoid syndrome.
- Symptoms – dyspnoea, fatigue, oedema or ascites. Signs – dysmorphic facies (in congenital causes), prominent a wave, RV heave, ejection click, ejection systolic murmur and a split S2.
- Investigations – ECG – right axis deviation, P pulmonale, right ventricular hypertrophy or RBBB. CXR – prominent main, right and left pulmonary arteries due to post-stenotic dilatation.
- Management – pulmonary valvuloplasty (balloon catheter) or valvotomy (valve incision).
Pulmonary regurgitation
Caused by pulmonary hypertension - a decrescendo murmur in early diastole at left sternal edge – Graham Steel murmur if accompanied by mitral stenosis and pulmonary hypertension.
Infective endocarditis - definition
Fever + a new heart murmur = endocarditis until proven otherwise. Any fever lasting >1 weeks in patients known to be at risk should prompt blood cultures.
Infective endocarditis - classification
- Normal valves = acute endocarditis – patients present with acute heart failure or emboli. Entry is usually via the skin and risk factors include dermatitis, IV access or injections, renal failure, organ transplantation, diabetes mellitus or post-op wounds. Mortality rate is between 5-50%.
- Abnormal valves = subacute endocarditis – risk factors include aortic or mitral valve disease, IV drug use (affects tricuspid valve), coarctation, patent ductus arteriosus, VSD or prosthetic valves (endocarditis can be early – during surgery or late – due to haematogenous spread).
Infective endocarditis - causes
The most common bacterial cause is strep viridans (>35%) and other causes include staph epidermis or aureus. Fungal causes include candida and aspergillus. Other causes are SLE which causes Libman-Sacks endocarditis (atypical non-bacterial endocarditis) and malignancy.
Endocarditis - clinical features
- Septic signs – fever, rigors, night sweats, malaise, weight loss, splenomegaly and clubbing.
- Cardiac lesions – a new murmur or a change to an existing murmur – vegetation’s can cause valve destruction and severe regurgitation or obstruction. LVF is a common cause of death.
- Immune complex deposition – roth spots, splinter haemorrhages, Janeway lesions or Osler’s nodes. Vasculitis causes microscopic haematuria, glomerulonephritis and acute renal failure.
- Embolic phenomena – can cause an abscess in any organ e.g. brain, heart, spleen or kidney.
Endocarditis - Duke criteria
Need 2 major, 1 major ad 2 minor or all 5 minor criteria.
- Major – positive blood cultures (typical organism in 2 separate cultures or persistently positive blood cultures e.g. 3 >12 hours apart) or endocardium involved (positive echocardiogram – vegetation, abscess, dehiscence of prosthetic valve or new valvular regurgitation).
- Minor – predisposition (cardiac lesion or IV drug abuse), fever >38°C, vascular or immunological signs, positive blood cultures or positive echocardiogram that do not meet major criteria.
Endocarditis - investigations
- Blood cultures – do 3 sets at different times from different sites at the peak of the fever. Up to 85-90% are diagnosed from the 1st 2 sets of cultures but up to 10% are culture negative.
- Blood tests – normochromic, normocytic anaemia, neutrophilia and raised ESR or CRP.
- Urinalysis – check for microscopic haematuria.
- Echocardiogram – TTE may show vegetation’s but only if they are >2mm so TOE is more sensitive and better for visualising mitral lesions and the development of an aortic root abscess.
Endocarditis - management
Liaise early with a microbiologist and a cardiologist.
- Antibiotics – e.g. 1.2g IV benzylpenicillin QDS with 1mg/kg IV gentamicin TDS for 4 weeks. If endocarditis is acute add 2g IV flucloxacillin QDS to cover infection with staphylococci.
- Indications for surgery – heart failure, valve obstruction, repeated emboli, fungal endocarditis, persistent bacteraemia, myocardial abscess or an unstable infected prosthetic valve.
- Prevention – antibiotic prophylaxis to prevent infective endocarditis is not currently recommended.
