Acute mitral regurgitation (MR) is a critical medical and surgical emergency characterized by decompensated heart failure and potential misdiagnosis as pulmonary disease. Management varies based on the underlying cause, with surgical interventions for ruptured chordae and medical treatments focusing on stabilization. Imaging, particularly echocardiography, plays a crucial role in diagnosis and monitoring, while newer transcatheter techniques offer less invasive options for high-risk patients.

1. ACUTE MITRAL REGURGITATION
Suvendu Choudhury , 2nd
year
Percepter - Asst Prof Dr Ashok Kumar Behera

2. OVERVIEW
Importance –
 acute MR is a medical & surgical
emergency as the patients present with
acute decompensated HF with a reduced
cardiac output.
 often misdiagnosed as acute pulmonary
disease (dyspnea , abnormal chest
radiograph , no audible murmur )
Management depends on specific
etiology

3. Mitral regurgitation is an abnormal reversal
of blood flow from LV to LA
STAGES
•Acute
•Chronic compensated
• Chronic decompested

4. ANATOMY : MITRAL VALVE
Mitral valve Apparatus consists of
• LA wall
• MV annulus - fibrous ring , connects with
leaflets , acts as a spinchter during systole
dilatation causes MR
•MV leaflets - are like continuous veils ,
free edges have 2 major indenentations
which divide the leaflets into Anterior
leaflet and Posterior leaflet
Inflammatory , degenerative,
infectious diseases can result in
poor coaptation  MR

5. • Chordae tendinae
Fibrous string like , originate from PM or Ventricular
wall
Inserted to MV leaflets
Chordal rupture  poor coaptation  MR
•Papillary muscle & Vent. Wall
Comprise the muscular component of MVA
PM arise from apex and middle 1/3rd
of V.wall
Ant lateral PM is larger than Post. Medial PM
and is supplied by LAD, LCX while the later is supplied
by
RCA
Rupture, infarction  MR

6. CAUSES OF ACUTE MR
Primary causes or Causes due to organic diseases of MV
• Infective Endocarditis
•Myxomatous degeneration of MV
•Spontaneous Rupture of Chordae and Valve leaflets

7. Secondary causes
• Ischaemic (as in AMI)
Without PM rupture
•Leaflets become tethered due to
•RWMA / GWMA
Due to PM rupture poor coaptation
Of leaflets
• PM rupture occurs more in case of
IWMI> AWMI

8. OTHER SECONDARY CAUSES
•Penetrating trauma
•Systemic inflammatory diseseases eg SLE
•TAKOTSUBO cardiomyopathy
•Iatrogenic

10. HEMODYNAMICS
Two most important determinants are
LA Compliance
LV Compliance

11. HEMODYNAMICS (Contd)
In chronic MR , LA and LV gradually compensate by increase in volume
Enlarged , compliant LA maintains
low systolic pressure despite
the regurgitant flow
Enlarged LV is able to maintain forward
Stroke volume

12. In Acute MR
LA doesnt have time to
adapt to volume overload
LA pessure
LV initially try to compensate
With hyperdynamicity to maintain
C.O. But since LV is of normal size
It cant provide enough forward SV
Low C.O

14. CLINICAL FEATURES
Sudden volume overload on LA
LA pressure
Pulmonary edema
Dyspnea
LV unable to maintain forward
Stroke volume
Hypotension
Cardiogenic Shock

15. Physical examintion
Auscultation is elusive
There may be a soft systolic murmur which disappears in late
Systole as the LA& Lvpressure gradient reduces to zero ,
due to markedly increased LA pressure.
In 30% cases of Acute MR no murmur is audible
Even if the murmur is audible the soft systolic murmur may be
missed in emergency as the pt presents with severe resp. distress.
Basal crepitations are heard in resp system examination

16. IMAGING
ECG is non specific
CXR findings are consistent with acute pulmonary edema
Echocardiography is the investigation of choice
TTE is the 1st
line in assesment of acute pulmonary edema
,if available bedside / ER.
Color Doppler ECHO
• reliably identifies MR
•Provides clue to etiology

17. Continuous wave Doppler regurgitant flow velocity curve
often shows the characteristic triangular (instead of rounded)
shape due to a rapid decline in late systolic velocity reflecting
the abrupt increase LA pressure.

18. Ruptured PM – Observed as a triangular mass swinging
back & forth between LA & LV

19. Impending PM rupture - evidenced by newly
developed leaflet
prolapse
Leaflet tethering - evident as RWMA in the region of
culprit coronary A  leaflet tenting  poor
coaptation MR
Serial followup ECHO needed in such cases as MR
dramatically
Improves after PCI

21. Careful monitoring of TOE or TTE is also needed during
placement of transcatheter devices e.g Transcatheter Aortic
Valve replacment (TAVR) or insertion of axial flow left ventricular
assist device

22. In TAKOTSUBO cardiomyopathy with SAM the
ECHO findings are
-LV apical ballooning
- abnormal MV motion i.e SAM

23. MANAGEMENT
Management of acute MR depends on
Etiology
Degree of Cardiac dysfunction
Comorbidity

24. Surgical correction is indicated in
Ruptured chordae – MV repair
PM rupture
Infective Endocarditis
MV replacement
Post operative mortality is
highest in case of acute ischaemi MR
Lowest in chronic degenerative MR

25. In patients with secondary MR or when the pt is too sick
for surgical intervention 
Pharmacological afterload reduction
Mechanical circulatory support like IABP,
Veno Arterial extracorporeal membraneoxygenetion ,
Ventricular assist device
are condsidered

26. In certain condition without organic involvement of
Valve like Takotsubo cardiomyopathy medical treatment
is first choice to stabilise & expecting spontaneous recovery

27. REVSCULARISATION THERAPY FOR acute ischaemic MR
Acute ischaemic MR has worse short term&
long term prognosis even its mild to moderate.
Emergency coronary revascularisation can reduce
the degree of MR both in early stage & later stage
However in certain cases MR can persist despite successful
Primary coronary intervention

28. Percutaneous Transcatheter Intervention for acute MR
Transcatheter MV edge to edge repair / replacement
are newly developed & less invasive approaches
Though surgical intervention are 1st
line t/t for acute
Severe MR , Transcatheter repair is considered as a
rescue therapy for patients who are deemed to high risk
For surgical interventions.