Cardiology Flashcards
Clinical signs of Aortic Stenosis
- Slow rising, low volume pulse
- Narrow pulse pressure
- Apex beat is sustained in stenosis (HP: heaving pressure‐loaded)
- Thrill in aortic area (right sternal edge, second intercostal space)
- Auscultation:
A crescendo-decrescendo, ejection systolic murmur (ESM) loudest in the aortic area during expiration and radiating to the carotids.
Severity:
soft and delayed A2 due to immobile leaflets and prolonged LV emptying, delayed (not loud) ESM, fourth heart sound S4.
Auscultation in Aortic stenosis
A crescendo-decrescendo, ejection systolic murmur (ESM) loudest in the aortic area during expiration and radiating to the carotids.
Severity:
Soft and delayed A2 due to immobile leaflets and prolonged LV emptying, delayed (not loud) ESM, fourth heart sound S4
Evidence of complications in Aortic stenosis
- Endocarditis:
Splinters, Osler’s nodes (finger pulp), Janeway lesions (palms), Roth spots (retina), temperature, splenomegaly and haematuria - Left ventricular dysfunction:
Dyspnoea, displaced apex and bibasal crackles - Conduction problems:
–> acute, endocarditis;
–> chronic, calcified aortic valve node
Differential diagnosis of Aortic stenosis
- HOCM
- VSD
- Aortic sclerosis: normal pulse character and no radiation of murmur
- Aortic flow: high output clinical states e.g. pregnancy or anaemia
Causes of Aortic stenosis
- Congenital: bicuspid aortic valve
- Acquired:
- -> Age (senile degeneration and calcification);
- -> Streptococcal (rheumatic)
Associations of Aortic stenosis
- Coarctation
- Bicuspid aortic valve
- Angiodysplasia
Severity of Aortic stenosis
• Signs
* Auscultation features:
Soft and delayed A2 due to immobile leaflets and prolonged LV emptying, delayed (not loud) ESM, fourth heart sound S4
* Mortality risk:
- Angina 50% mortality at 5 years
- Syncope 50% mortality at 3 years
- Breathlessness 50% mortality at 2 years
* Biventricular failure (right ventricular failure is preterminal)
Investigations in Aortic stenosis
- ECG: LVH on voltage criteria, conduction defect (prolonged PR interval)
- CXR: often normal; calcified valve
- Echo: mean gradient: >40 mm Hg aortic (valve area <1.0 cm2) if severe
- Catheter: invasive transvalvular gradient and coronary angiography (coronary artery disease often coexists with aortic stenosis)
Management of Aortic Stenosis
- Asymptomatic
⚬⚬ None specific, good dental health
⚬⚬ Regular review: symptoms and echo to assess gradient and LV function - Symptomatic
A- ⚬⚬ Surgical
1- ⚬⚬ Aortic valve replacement +/− CABG
2- ⚬⚬ Operative mortality 3–5% depending on the patient’s EuroScore (www.euroscore.org/calc.html)
B- ⚬⚬ Percutaneous
1- ⚬⚬ Balloon aortic valvuloplasty (BAV)
2- ⚬⚬ Transcutaneous aortic valve implantation (TAVI)
a- ⚬⚬ Transfemoral (or transapical and transaortic)
b- ⚬⚬ Maybe recommended
–> if high surgical risk (logEuroscore >20%) or
–> inoperable cases (number needed to treat to prevent death at 1 year = 5)
Duke’s criteria for infective endocarditis
Major:
• Typical organism in two blood cultures
• Echo: abscess, large vegetation, dehiscence*
Minor:
• Pyrexia >38°C
• Echo suggestive
• Predisposed, e.g. prosthetic valve
• Vascular phenomenon, including major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhage, or Janeway lesions
• Immunologic/Vasculitic phenomenon such as glomerulonephritis, Osler nodes, Roth spots, and rheumatoid factor, (ESR↑, CRP↑)
• Atypical organism on blood culture
Diagnose if the patient has 2 major, 1 major and 2 minor, or 5 minor criteria.
(* plus heart failure/refractory to antibiotics/heart block are indicators for urgent surgery).
Indications for antibiotic prophylaxis for Infective Endocarditis
Antibiotic prophylaxis is now limited to those with
1- Prosthetic valves,
2- Previous endocarditis,
3- Cardiac transplants with valvulopathy and
4- Certain types of congenital heart disease.
Clinical signs of Aortic Incompetence
- Collapsing pulse (water-hammer pulse) reflecting a wide pulse pressure, e.g. 180/45
- Apex beat is hyperkinetic and displaced laterally (TV: thrusting volume‐loaded)
- Thrill in the aortic area
- Auscultation:
- Early diastolic murmur (EDM) loudest at the lower left sternal edge with the patient sat forward in expiration.
- There may be an aortic flow murmur and a mid-diastolic murmur (MDM) (Austin–Flint) due to regurgitant flow impeding mitral opening.
- In severe AR there may be ‘free flow’ regurgitation and
the EDM may be silent. - Signs of severity:
collapsing pulse, third heart sound (S3) and pulmonary oedema - Eponymous signs
• Auscultation in Aortic Incompetence
- Early diastolic murmur (EDM) loudest at the lower left sternal edge with the patient sat forward in expiration.
- There may be an aortic flow murmur and a mid-diastolic murmur (MDM) (Austin–Flint) due to regurgitant flow impeding mitral opening.
- In severe AR there may be ‘free flow’ regurgitation and the EDM may be silent.
Eponymous signs in Aortic Incompetence
- Corrigan’s: visible vigorous neck pulsation
- Quincke’s: nail bed capillary pulsation
- De Musset’s: head nodding
- Duroziez’s: diastolic murmur proximal to femoral artery compression
- Traube’s: ‘pistol shot’ sound over the femoral arteries
Congenital Causes of Aortic Incompetence
- Bicuspid aortic valve;
2. Perimembranous VSD
Acquired Causes of Aortic Incompetence
** Valve leaflet:
(Acute) - Endocarditis,
(Chronic) 1- Rheumatic fever or 2- Drugs: pergolide, slimming agents
**Aortic root
(Acute): 1- Dissection (type A) 2- Trauma
(Chronic): 1- Dilatation: Marfan’s and hypertension, 2- Aortitis: syphilis, ankylosing spondylitis and vasculitis
Other causes of a collapsing pulse
- Pregnancy
- Patent ductus arteriosus
- Paget’s disease
- Anaemia
- Thyrotoxicosis
- AR
Investigation in Aortic Incompetence
- ECG: lateral T‐wave inversion
- CXR: cardiomegaly, widened mediastinum and pulmonary oedema
- TTE/TOE:
- Severity: LVEF and dimensions, root size, jet width
- Cause: intimal dissection flap or vegetation - Cardiac catheterization: grade severity aortogram and check coronary patency
Medical Management of Aortic Incompetence
- ACE inhibitors and ARBs (reducing afterload)
* Regular review: symptoms and echo: LVEF, LV size and degree of AR
Indications for Surgery in Aortic Incompetence
Acute:
1. Dissection
2. Aortic root abscess/endocarditis (homograft preferably)
Chronic:
Replace the aortic valve when:
• Symptomatic: dyspnoea and reduced exercise tolerance (NYHA > II) AND/OR
• The following criteria are met:
1. wide pulse pressure >100 mm Hg
2. ECG changes (on Exercise Tolerance Test)
3. Echo: LV enlargement >5.5 cm systolic diameter or EF <50%
Ideally replace the valve prior to significant LV dilatation and dysfunction.
Prognosis of Aortic Incompetence
Asymptomatic with EF > 50% – 1% mortality at 5 years.
Symptomatic and all three criteria present − 65% mortality at 3 years
Clinical signs of Mitral stenosis
- Malar flush
- Irregular pulse if AF is present
- Tapping apex (palpable first heart sound)
- Left parasternal heave if pulmonary hypertension is present or enlarged left atrium
- Auscultation
- Loud 1rst heart sound.
- Opening snap (OS) of mobile mitral leaflets opening
followed by a mid-diastolic murmur (MDM), which is best
heard at the apex, in the left lateral position in expiration with the bell.
- Presystolic accentuation of the MDM occurs if the patient is in sinus rhythm.
- If the mitral stenosis is severe then the OS occurs nearer A2 and the MDM is longer. - Haemodynamic significance
- Pulmonary hypertension: functional tricuspid regurgitation, right ventricular heave, loud P2.
- LVF: pulmonary oedema, RVF: sacral and pedal oedema. - Endocarditis
- Embolic complications: stroke risk is high if mitral stenosis + AF
Causes of Mitral stenosis
Congenital: (rare) Acquired 1. Rheumatic (commonest) 2. Senile degeneration 3. Large mitral leaflet vegetation from endocarditis (mitral ‘plop’ and late diastolic murmur)
Differential diagnosis of Mitral stenosis
- Left atrial myxoma
2. Austin–Flint murmur
Investigation of Mitral stenosis
- ECG: p‐mitrale (broad, bifid) and atrial fibrillation
- CXR: enlarged left atrium (splayed of carina), calcified valve, pulmonary oedema
- TTE/TOE: valve area (<1.0 cm2 is severe), cusp mobility, calcification and left atrialthrombus, right ventricular failure
Management of Mitral stenosis
- Medical: + AF: rate control and oral anticoagulants, diuretics
- Mitral valvuloplasty: if pliable, non‐calcified with minimal regurgitation and no left atrial thrombus
- Surgery:
- —–> closed mitral valvotomy (without opening the heart) or
- —–> open valvotomy (requiring cardiopulmonary bypass) or
- —–> valve replacement
Prognosis of Mitral stenosis
Latent asymptomatic phase 15–20 years;
NYHA > II – 50% mortality at 5 years.
Pathophysiology of Rheumatic fever
• Immunological cross‐reactivity between Group A β‐haemolytic streptococcal infection,
e.g. Streptococcus pyogenes and valve tissue
Duckett–Jones diagnostic criteria of Rheumatic fever
Proven β‐haemolytic streptococcal infection diagnosed by throat swab, rapid antigen detection test (RADT), anti streptolysin O titre (ASOT) or clinical scarlet fever plus 2 major or 1 major and 2 minor:
** Major: ======================** Minor:
——> Chorea, ================——> Raised ESR,
——> Erythema marginatum, ====——> Raised WCC,
——> Subcutaneous nodules, ===——> Previous RhF,
——> Polyarthritis, =============——> Arthralgia,
——> Carditis =================——> Pyrexia,
=============================——> Prolonged PR interval
Treatment of Rheumatic fever
Rest, high‐dose aspirin and penicillin
Prophylaxis of Rheumatic fever
⚬⚬ Primary prevention: penicillin V (or clindamycin) for 10 days
⚬⚬ Secondary prevention: penicillin V for about 5–10 years
Clinical signs of Mitral incompetence
- Scars: lateral thoracotomy (valvotomy)
- Pulse: AF, small volume
- Apex: displaced and volume loaded
- Palpation: thrill at apex
- Auscultation:
- Pan-systolic murmur (PSM) loudest at the apex radiating to the axilla. Loudest in expiration.
- Wide splitting of A2 P2 due to the earlier closure of A2 because the LV empties sooner.
- S3 indicates rapid ventricular filling from LA, and excludes significant mitral stenosis. - Pulmonary oedema
- Evidence of the Cause: signs of endocarditis
- Severity: left ventricular failure and atrial fibrillation (late). Not murmur intensity
- Other murmurs, e.g. ASD
Congenital Causes of Mitral incompetence
There is an association between cleft mitral valve and primum ASD
Acquired Causes of Mitral incompetence
- Valve leaflets
- Acute
- > Bacterial endocarditis
- Chronic
- > Myomatous degeneration (prolapse)
- > Rheumatic
- > Connective tissue diseases
- > Fibrosis (fenfluramine/pergolide)
- Valve annulus
- Chronic
- > Dilated left ventricle (functional MR)
- > Calcification
- Chordae/papillae
- Acute
- > Rupture
- Chronic:
- > Infiltration, e.g. amyloid
- > Fibrosis (post‐MI/trauma)
Investigation of Mitral incompetence
- ECG: p‐mitrale, atrial fibrillation and previous infarction (Q waves)
- CXR: cardiomegaly, enlargement of the left atrium and pulmonary oedema
- TTE/TOE:
- Severity: size/density of MR jet, LV dilatation and reduced EF
- Cause: prolapse, vegetations, ruptured papillae, fibrotic restriction and infarction
Management of Mitral incompetence
1- Medical
⚬⚬ Anticoagulation for atrial fibrillation or embolic complications
⚬⚬ Diuretic, β‐blocker and ACE inhibitors
2- Percutaneous: mitral clip device for palliation in inoperative cases of mitral valve prolapse
3- Surgical
⚬⚬ Valve repair (preferable) with annuloplasty ring or replacement
⚬⚬ Aim to operate when symptomatic, prior to severe LV dilatation and dysfunction
Prognosis of Mitral incompetence
- Often asymptomatic for >10 years
* Symptomatic – 25% mortality at 5 years
Mitral valve prolapse
• Common (5%), especially young tall women
• Associated with connective tissue disease, e.g. Marfan’s syndrome and HOCM
• Often asymptomatic, but may present with chest pain, syncope and palpitations
• Small risk of emboli and endocarditis
• Auscultation
-> Mid-systolic ejection click (EC).
-> Pan-systolic murmur that gets louder up to A2.
-> Murmur is accentuated by standing from a squatting position or during the straining phase of the Valsalva manoeuvre, which reduces the flow of blood through the heart.
Clinical signs of Tricuspid incompetence
- Raised JVP with giant CV waves
- Thrill left sternal edge
- Auscultation:
- > Pan-systolic murmur (PSM) loudest at the tricuspid area (lower left sternal edge) in inspiration.
- > Reverse split second heart sound due to rapid RV emptying.
- > Right ventricular rapid filling gives an S3 - Pulsatile liver, ascites and peripheral oedema
- Endocarditis from IV drug abuse: needle marks
- Pulmonary hypertension: RV heave and loud P2
- Other valve lesions: rheumatic mitral stenosis
Causes of Tricuspid incompetence
• Congenital: Ebstein’s anomaly (atrialization of the right ventricle and TR)
• Acquired:
-> Acute: infective endocarditis (IV drug user)
-> Chronic: functional (commonest), rheumatic and carcinoid syndrome
