Mitral Regurgitation

Mitral regurgitation is classified in two ways:

• Aetiology
  • Primary
    Due to valvular pathology.
  • Secondary/Functional
    Due to LV dysfunction interfering with normal valvular function.
• Temporality
  • Acute
    Pathology evolving faster than LA compensation, resulting in elevated LAPs, PAPs, and pulmonary oedema (classically severe and of rapid onset).
  • Chronic
    MR with LA compensation. Symptoms may only develop after many years when the LV fails.

MR classification is complex, and is based on echocardiographic findings:

Grading of Mitral Regurgitation

Measurement	Mild	Moderate	Severe
Regurgitant fraction	<30%	30-49%	>50%
Regurgitant volume	<30ml/beat	30-60mL/beat	>60mL/beat
Effective Regurgitant Orifice Area	⩽0.2cm2	0.2-0.39cm2	>0.4cm2

Epidemiology and Risk Factors

Pathophysiology

Acute MR:

• Sudden regurgitation leads to acute LV volume overload
  Results in:
  • ↑ LVEDP
  • Rapid LA dilation and ↑ in LAP
  • Pulmonary hypertension
  • Acute pulmonary oedema
  • RV failure
  • Sympathetic stimulation
    • Tachycardia
    • ↑ LV contractility

Progressive regurgitation leads to:

• Volume overload
• Progressive chamber dilatation
  Initially well-compensated with preserved systolic function.
  • ↑ LVEDV with normal LVEDP
• Eccentric hypertrophy
• Eventual decompensation when dilation and hypertrophy can no longer maintain forward SV
  • ↑ PAP
  • Pulmonary congestion
  • RV failure

Aetiology

Causes include:

• Acute
  • Chordae rupture
    • Myxomatous disease
    • Chest trauma
    • Acute rheumatic fever
  • Ischaemia
    • Papillary muscle rupture
  • Infective endocarditis
• Chronic
  • MV leaflet abnormalities
  • Annular dilatation
    LV dilation.
  • Rheumatic heart disease

Clinical Manifestations

History

Examination

Diagnostic Approach and DDx

Investigations

Echocardiography:

• Allows grading of severity
• LV assessment is confounded
  EF appears higher than it is due to the regurgitation fraction.
  • LVEF of ~70% is equivalent to ~55% in absence of MR.

Management

Medical management of acute MR involves:

• Reducing filling pressures
  • Diuretics
  • Nitrates
• Reducing afterload
  • Vasodilators
  • IABP
• Preservation of forward flow
  Maintain normal or high-normal heart rate, sinus rhythm.

Medical management of chronic MR involves treating cardiac failure, and cardioversion if required.

Surgical management of MR involves either repair (most common) or replacement (rare). Indications for surgery:

• Primary, severe, acute MR
  E.g. ruptured papillary muscle.
• Symptomatic chronic MR
• Asymptomatic MR with CVS sequelae:
  • LVEF <60%
  • AF
  • Pulmonary HTN

Anaesthetic Considerations

• C
  • Maintain preload
    Promotes forward flow.
  • Aim high-normal heart rate (80-100)
    Reduces diastolic regurgitant fine.
  • Afterload reduction
    Reduces regurgitant fraction. Particularly important around intubation.
  • Inotropes

In mixed valvular disease, management should prioritise the most haemodynamically significant lesion. That said, in general:

• In mixed AS and MR, the AS should generally be given precedence
  MR tends to be improved by anaesthesia, AS tends to be worsened and is more likely to cause intraoperative crises.

• In mixed AR and MR
  Similar haemodynamic goals, best defended by maintaining forward flow through ↓ SVR and defending BP through ↑ CO.

• In mixed MS and MR
  Competing haemodynamic disease that is a common conundrum in rheumatic disease. In general:

  • In asymmetric disease, prioritise the most significant lesion
  • Otherwise aim maintenance of stable pre-induction haemodynamic parameters, i.e.:
    • Maintain normal afterload
    • Maintain normal HR
    • Maintain normal contractility
    • Avoid ↑ PVR
    • Provide adequate preload

Marginal and Ineffective Therapies

Complications

Prognosis

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References

1. Holmes K, Gibbison B, Vohra HA. Mitral valve and mitral valve disease. BJA Educ. 2017;17(1):1-9. doi:10.1093/bjaed/mkw032