FRCA Notes

Aortic stenosis

Aortic stenosis is, perhaps, the 'classic' Final FRCA exam question and has appeared in CRQs in 2019 and 2022.

Both had pass rates of 67%, with examiners commending the degree of knowledge; marks were lost on LV pathophysiological changes and knowledge of TAVI.

Resources

  • Aortic stenosis is the commonest major valve lesion, with an incidence of 3% in those >75yrs and 4% in those >85yrs
  • Isolated AS of non-rheumatic origin is more common in males than females

Degenerative calcification of the valve

  • Most common form of AS (50% of cases)
  • Typically affects those >70yrs old
  • Associated with other risk factors for coronary artery disease such as smoking, hypertension>, diabetes and dyslipidaemia

  • Mechanical stress over time leads to progressive fibrosis and calcification of an otherwise normal valve
  • There is antecedent, irregular valve thickening known as aortic sclerosis, without any LVOT obstruction

Congenital bicuspid aortic valve

  • Is the commonest congenital cardiac malformation (2% of population)
  • Typically affects those aged 30 - 50yrs
  • Accounts for 50% of AS in under 70yr olds but only 25% of AS in over 70yr olds

  • There is turbulent flow through the abnormal two-leaflet valve, which causes fibrosis, calcification and orifice narrowing due to trauma

Others

  • Rheumatic heart disease
  • Supra- and sub-valvular stenosis
  • SLE
  • Fabry's disease
  • Paget's disease

  • AS can be classified according to degree of LV impairment (none, mild, moderate or severe), though is more commonly classified by aortic valve area and the mean pressure gradient across the valve:
Class Aortic valve area (cm2) Mean pressure gradient (mmHg)
Normal 2.5 - 3.6 <5
Mild 1.5 - 2.0 15 - 25
Moderate 1.0 - 1.5 25 - 40
Severe <1 40 - 50
Critical <0.8 >50

  • A narrowed aortic valve area with a surprisingly low mean pressure gradient is a worrying sign
  • It implies LV failure to the extent that it is unable to generate a decent pressure gradient

  • The LV undergoes concentric hypertrophy (described as LV diastolic thickness >1cm)
    • This allows it to maintain a pressure gradient across the narrowed valve without dilation or reduced CO
  • As the obstruction increases with progressive stenosis:
    • The hypertrophied ventricle becomes stiff and poorly compliant
    • This leads to diastolic dysfunction
    • There is normally a preserved LV systolic function
  • Eventually there is a fixed, low cardiac output state which renders the heart unable to compensate for systemic vasodilation

Reliance on preload and sinus rhythm

  • The poorly compliant ventricle requires higher filling pressures
  • As such, a normal LVEDP may actually represent hypovolaemia in these patients
  • This reliance makes the LV sensitive to changes in either preload or cardiac rhythm

  • Indeed, LV filling becomes more dependent on atrial systole
  • Atrial systole contributes 40% to LVEDV (vs. 20% in health) and there is associated atrial hypertrophy
  • Maintenance of sinus rhythm becomes vital for maintenance of CO

  • Haemodynamic compromise typically manifests once the aortic valve area is <1cm2
  • Eventually SV and CO fall, as does pressure gradient across the valve

Myocardial oxygen supply-demand imbalance

  • Left ventricular myocardial O2 demand increases (at rest 3ml/100g/min), because:
    • There is increased LV muscle mass i.e. hypertrophy
    • There is increased LVESP and therefore increased LV wall tension i.e. increased afterload

  • However, myocardial oxygen supply falls
    • There is reduced aortic (and thus coronary) blood flow
    • There is reduced diastolic time
    • Increased LV diastolic pressure compromises left coronary blood flow during diastole

  • The net effect is angina, even with normal coronary arteries (relative LV ischaemia)

Symptoms

  • Long asymptomatic phase
  • Described as a triad of:
    1. Angina
    2. (Pre-)syncope
    3. Dyspnoea inc. exertional dyspnoea, PND, orthopnoea, pulmonary oedema
  • Appearance of symptoms a poor prognostic factor, with median survival from onset of:
    • Angina - 5yrs
    • Syncope - 3yrs
    • Cardiac failure - 2yrs

Signs

  • Low volume, slow rising pulse
    • May be normal in mild disease, AR or in those with poorly compliant vascular beds e.g. elderly
  • There may be low SBP and narrowed PP
  • A pre-cordial thrill heard loudest when leaning forwards
  • Ejection systolic murmur heard loudest over the aortic valve, radiating to the carotids and apex
    • May be comes less audible in severe disease with LV failure due to reduced flow through the stenotic valve

Investigations

  • 12-lead ECG
    • Signs of LVH (85% of those with severe AS)
      • Sokolov-Lyon criteria: depth of S-wave in V1 + height of R wave height in V5 - 6 >35 mm
    • P-wave enlargement
    • Signs of worsening hypertrophy: T-wave inversion and ST-depression in lateral leads
    • Heart (AV nodal) block or interventricular block
      • The AVN is close to the aortic valve and calcification infiltrating the conduction system can result in heart block

  • CXR
    • May be normal
    • May demonstrate cardiomegaly
    • Calcified aortic valve on lateral
    • Post-stenotic dilatation of the aortic root

  • Echocardiography is used to:
    1. Assess valvular anatomy
    2. Check valve area & pressure gradient
    3. Assess degree of LV (dys)function

Valve anatomy

  • 2-D examination is used to check valve leaflet number, thickening, mobility and degree of calcification

Valve pressure gradient

  • Continuous Doppler wave recordings of the LVOT are made
    • Maximum velocity in the LVOT corresponds to flow through the valve at peak systole
    • Modified Bernoulli equation can be used to calculate pressure across the valve (maximum pressure gradient across the valve (mmHg) = 4 x velocity2)
  • Mean pressure gradient is also measured

Valve area

  • AVA is calculated using the continuity equation
  • AVA = cross sectional area of the LVOT x (velocity time integral of the LVOT / velocity time integral of the aortic valve)

Medical management

  • Aims at addressing coalescing cardiovascular comorbidities
  • 1yr mortality of severe symptomatic AS without interventional procedure is 40-50%

Surgical AV replacement [Gold standard]

  • Relatively high risk procedure, with 30-day mortality ~3% but may be much higher in patients with greater perioperative risk
  • Indications:
    • Severe, symptomatic AS
    • Severe, asymptomatic AS with EF <50%
    • Severe, asymptomatic AS with risk of rapid progression, planned major surgery or abnormal response to exercise
    • Moderate AS undergoing simultaneous cardiac procedure
  • Replacement valves are either metallic (mechanical) or bioprosthetic; the former require lifelong anticoagulation

Transcatheter Aortic Valve Implantation (TAVI)

  • See separate page on TAVI

  • Less invasive than surgical valve replacement
  • Generally considered in those at higher risk from surgical replacement
  • Still carries significant risk of complications including heart failure, stroke and death

Balloon Valvuloplasty

  • Stenosis is relieved by inflation of a balloon at the aortic valve, which fractures calcium deposits and stretches the aortic valve annulus
  • Does not demonstrate a long-term outcome benefit due to high re-stenosis rates
  • May, however, be used for palliation or as a bridge to definitive treatment

Perioperative management of the patient with aortic stenosis


  • A full history and examination, elicity features of the disease as above

Investigations

  • ECG
  • TTE is a must
    • If not present must be treated as if they have moderate AS
    • Re-examination warranted if >2yrs since last TTE due to progression of disease (0.1cm2 valve area lost/year)

  • A chinwag with the Cardiologists/Cardiothoracic surgeons if the patient is:
    • An asymptomatic patient having major, elective surgery (abdominal, vascular, orthopaedic) if their valve gradient is >50mmHg i.e. critical stenosis
    • Symptomatic and having elective, non-cardiac surgery

  • Consider pre-medication to reduce stress response i.e. reduce tachycardia

Monitoring

  • Careful haemodynamic monitoring:
    • AAGBI as standard
    • Arterial line pre-induction
    • ± CVC
    • ± Oesophageal Doppler
    • ± PA catheter

Haemodynamic goals

Cardiovascular feature Goal of management Rationale
Heart rate Avoid tachycardia (HR <90bpm)
Avoid bradycardia (HR >60bpm)		 Tachycardia reduces diastolic time and therefore myocardial perfusion
CO is heart-rate dependent due to fixed stroke volume
Heart rhythm Maintain sinus rhythm with rapid treatment of arrhythmia Increased dependence on atrial systole for LV filling (40% vs. the normal 20%)
Afterload Prevent decreases in SVR
Prevent large increases in SVR		 Fixed CO state and cannot compensate for reductions in SVR
Increased SVR will increased myocardial workload and oxygen requirements
Contractility Avoid negative inotropy and provide inotropic support Relatively fixed stroke volume
Diastolic BP Maintain DBP As CPP = AoDBP - LVDEP, maintain DBP to ensure adequate coronary perfusion

  • Maintain adequate preload and high-normal SVR
    • Hypotension will cause a downwards spiral of poor myocardial perfusion, myocardial ischaemia, poor contractility, low MAP, low coronary perfusion
    • Neuraxial anaesthetic techniques are relatively contraindicated
    • Use vasoconstrictors inc. metaraminol, phenylephrine, noradrenaline
    • Treat underlying cause (e.g. haemorrhage) aggressively

  • Remain at increased risk in the post-operative period
  • NCEPOD recommendation that if AVA <1cm2, especially if reduced LVSF, then should be managed in an HDU setting
  • Avoid NSAIDs if possible as at high risk of renal dysfunction