This document discusses regurgitant murmurs, focusing on aortic regurgitation (AR) and mitral regurgitation (MR). It covers the etiology, pathophysiology, epidemiology, presentation, workup, management, and natural history of both conditions. For chronic MR, the left ventricle undergoes eccentric hypertrophy to compensate for the increased preload. Severe MR is defined by a regurgitant volume over 60mL/beat or an effective regurgitant orifice area over 0.40cm2. Surgery is generally recommended for symptomatic patients or those with progressive left ventricular dysfunction.

1. Regurgitant murmurs
KIBROM.MULUGETA
updated OCT 2016
SPHMMC
Lecture-1

2. outline
Etiology
Pathophysiology
Epidemiology
Presentation
Work up
Management
AR & MR

3. Etiology
acute

4. pathophysiology
The total stroke volume ejected by the LV
is increased in patients with AR.
 the increase in LV end-diastolic volume
(i.e., increased preload) provides
hemodynamic compensation.
In compensated AR , LV systolic function
is maintained through the combination of
chamber dilation and hypertrophy
(eccentric hypertrophy).

5. CON…
As the LV decompensates, LVcompliance
declines, and LV end-diastolic pressure
and volume rise.
Ultimately, these adaptive measures fail.
As LV function deteriorates, the end-
diastolic volume rises further and the
forward stroke volume and EF decline.

6. Con…
 In patients with acute severe AR, the LV is
unprepared for the regurgitant volume
load.
 LV compliance is normal or reduced, and
LV diastolic pressures rise rapidly,
occasionally to levels >40 mmHg.
 The LV pressure may exceed the LA
pressure toward the end of diastole, and
this reversed pressure gradient closes the
mitral valve prematurely.

7. Con…
 Myocardial ischemia may occur in
patients with AR because myocardial
oxygen requirements are elevated by
 LV dilation
 hypertrophy
 elevated LV systolic tension

8. Con…

9. EPIDEMIOLOGY
 The prevalence of AR varied with age and
disease severity.
 For mild AR, the prevalence was
 3.7% in men at ages 50 to 59
 12.1 % …. …. 60 to 69
 12.2 % …….. ….70 to 83
 moderate to severe AR, the prevalence
was 0.5, 0.6, and 2.2 % in men at ages 50
to 59, 60 to 69, and 70 to 83, respectively

10. Con…
three-fourths of patients with pure or
predominant AR are men.
women predominate among patients
with primary valvular AR who have
associated rheumatic mitral valve
disease.

11. Presentation
 History
 Hx cardiac illness
 Duration (acute or chronic)
 Palpitations
 exertional dyspnea
 Anginal pain
 do not respond satisfactorily to sublingual
nitroglycerin
 ankle edema

12. Con…
Physical Findings
Arterial Pulse
water-hammer
Corrigan's pulse
Quincke's pulse
pistol-shot(Traube's sign)
to-and-fro murmur (Duroziez's sign)
The arterial pulse pressure (widended)

13. Con…
 Bobbing motion of the head with each
systole(De Musset’s sign)
 A rapidly rising "water-hammer" pulse,
which collapses suddenly as arterial
pressure falls rapidly during late systole
and diastole
 Prominent carotid artery
pulsations(Corrigan's pulse)
 Quincke's pulse (capillary pulsations)

14.  Traube's sign, A booming "pistol-shot"
sound can be heard over the femoral
arteries
 Duroziez's sign, A to-and-fro murmur is
audible if the femoral artery is lightly
compressed with a stethoscope.
 Wide pulse pressure, elevation of the
systolic pressure and a depression of the
diastolic pressure.

15. Con…
 Precordial exam
 the LV impulse is heaving and displaced laterally and
inferiorly.
 A diastolic thrill is often palpable along the left sternal
border
 A prominent systolic thrill may be palpable in the
suprasternal notch
 A2 is usually absent, S3 and systolic ejection sound
are frequently audible, S4.
 A high-pitched, blowing, decrescendo diastolic
murmur, heard best in the 3rd intercostal space along
the LSB.

16. Con…
 A mid-systolic ejection murmur is
frequently audible and best at the base
of the heart
 Austin Flint murmur, a soft, low-pitched,
rumbling mid-diastolic murmur.
 The auscultatory features of AR are
intensified by strenuous handgrip,
which augments systemic resistance

17. Progress…
 Asymptomatic patients with left ventricular
dysfunction, however, develop symptoms
(angina, heart failure) at a rate of greater
than 25 % per year.
 symptomatic patients with severe aortic
regurgitation have an expected mortality
that exceeds 10 %per year.

18. Stages /AHA valvular heart
disease 2014

19. Work up
ECG:
 chronic severe AR,Left LV hypertrophy.
◦ ST-segment depression and T-wave inversion
in leads I, aVL, V5, and V6 ("LV strain").
◦ Left axis deviation and/or QRS prolongation
CXR:
 Cardiomegaly, aortic calcification, aortic root
dilatation

20. Echocardiography
 is useful in determining the cause of AR
 thickening and failure of coaptation of the
leaflets may be noted
 Colour flow Doppler ECHO is very
sensitive in the detection of AR,

21. 2014 AHA/ECHO follow up

22. Medical treatment
- Diuretics, digoxin, salt restriction
- Vasodilators
- Endocarditis prophylaxis
◦ Without surgery, death usually
occurs within 4 years of developing
angina and within 2 years after
onset of heart failure.

23. surgical
 AVR(aortic valve replacement )
is indicated for the Tx of severe AR in
symptomatic pts irrespective of LV
function
It should be carried out in asymptomatic
pts with severe AR and progressive LV
dysfunction defined by
LVEF <50%,
an LV end-systolic dimension >55mm ,
or

24.  without indications for operation
should be followed by clinical and
ECHO examination every 3–12
months

26. 2014 AHA/ACC Valvular Heart
Disease Guideline

28. Etiology

29. Con…
 Valve leaflets
- myxomatous degeneration
- rheumatic heart disease
- infective endocarditis
 Chordae tendinae
- congenital, infective endocarditis,
trauma, rheumatic fever, myxomatous
 Papillary muscles
- myocardial ischaemia, congenital
abnormalities, infiltrative disease
 Mitral annulus
- dilatation eg. ischaemic or dilated
cardiomyopathy
- calcification due to degeneration,
hypertension, diabetes, CKD

30. Pathophysiology
 The resistance to LV emptying (LV afterload) is
reduced in pts with MR. As a consequence, the
LV is decompressed into the LA during ejection.
 The initial compensation to MR is more complete
LV emptying leading to a reduced end-systolic
LV volume.
 As regurgitation becomes chronic, the LV end-
diastolic volume increases and the end-systolic
volume returns to normal.
 The resultant increase in LV end-diastolic volume
and mitral annular diameter may create a vicious
circle in which “MR begets more MR.

31. Ctd.
 In patients with chronic MR , LV mass is also
increased (typical volume overload
(eccentric) hypertrophy)
 The reduced afterload in MR permits
maintenance of ejection fraction in the normal
to supranormal range ,thus even a modest
reduction in the EF (<60%) reflects significant
dysfunction.
 As the disease progress and LV contractile
function deteriorates LV volume increases
accompanied by a reduced forward CO.

32. Clinical features
 Symptoms usually occur with LV decompensation:
Fatigue, exertional dyspnea, and orthopnea are the
most prominent complaints in pts with chronic
severe MR
 Palpitations with AF
 Sx and SSx of right-sided HF in pt who have
associated pulmonary vascular disease and
marked pulmonary HTN
 Acute pulmonary edema is common in pts with
acute severe MR b/c of markedly increase LA and
pulmonary venous pressures.

33. Chronic versus Acute MR
Finding Chronic MR Acute MR
Symptoms subtle onset obvious
Appearance normal/mildly
severely ill
dyspnoeic
Tachycardia not striking always present
Apex beat displaced not displaced
Systolic thrill common absent
Murmur harsh pansystolic soft or absent
early systolic
component
ECG-LVH usually present
absent
CXR severe cardiomegaly normal heart size

34. Physical findings
- Pulse: sharp upstroke
- BP is usually normal
- Apex:
displaced, hyperdynamic
◦ A systolic thrill is often palpable at the
cardiac apex
◦ In acute severe MR, BP may be reduced
with a narrow pulse pressure, the apical
impulse is not displaced, and signs of
pulmonary congestion are prominent.
◦ S1 is absent or soft
◦ S3

35. CON…
◦ S 4 in acute severe MR
◦ holosystolic murmur most prominent
at the apex and radiates to the axilla,
intensified by isometric exercise
(handgrip)
◦ In pts with ruptured chordae
tendineae, the systolic murmur may
have a cooing or "sea gull" quality

36. Ctd.
 ECG
◦ evidence of LA enlargement
◦ AF
◦ signs of LV hypertrophy
 Chest X-Ray
◦ Pulmonary venous congestion,
interstitial edema, and Kerley B lines
◦ Calcification of the mitral annulus
may be visualized

37. Ctd.
Natural history
 The natural history of chronic MR depends on the
volume of regurgitation, the state of the
myocardium and the underlying cause.
 Preoperative LV end-systolic volume or diameter
is a useful predictor of function and postoperative
survival in chronic MR.
 The preoperative LV end-systolic diameter should
be < 45mm to ensure normal postoperative LV
function

38. CON...
Severe MR is defined by
a regurgitant volume 60 mL/beat,
regurgitant fraction (RF) 50%,
effective regurgitant orifice area 0.40
cm2

39. MR and Colour flow imaging of MR

40. Management strategy for pts with chronic severe
MR

41. Medical treatment
 Symptomatic patients may benefit from the
following drug therapy while awaiting surgery:
 ACE inhibitors
 Diuretics
 Digoxin / Beta-blockers in presence of atrial
fibrillation. Plus Warfarin with a target INR of 2–3.
 Endocarditis prophylaxis
 Pts with acute severe MR require urgent
stabilization and preparation for surgery.
[Diuretics, intravenous vasodilators (sodium
nitroprusside), and even IABC].

42. Surgical treatment
 Surgery is indicated
◦ If symptoms developed or LV end systolic diameter
≥45mm
◦ recent-onset AF and pulmonary hypertension, (a PA
pressure 50 mmHg at rest or 60 mmHg with exercise).
◦ For asymptomatic pts when LV dysfunction is progressive,
with LVEF declining below 60% and/or ESD on ECHO
rising above 40 mm.
 Mitral valve repair or replacement.
◦ Mitral repair and valvuloplasty maintain LV function to a
relatively greater degree and avoids the need for chronic
anticoagulation.
 In pts with significantly impaired LV function (EF
<30%), the risk of surgery rises, the recovery of LV
performance is incomplete, and the long-term
survival is reduced.

43. Ctd.
 Natural history
 Benign prognosis in most patients
 Complications may occur in patients
with a systolic murmur, thickened
leaflets, an increased LV or LA size,
especially in men > 45 years old
• Complications include progressive
MR, infective endocarditis, cerebral
emboli, arrhythmias and rarely sudden
death.

44. summary
 In patients with chronic MR , LV mass
is also increased (typical volume
overload (eccentric) hypertrophy
- Apex: displaced, hyperdynamic
◦ A systolic thrill is often palpable at the
cardiac apex.
◦ a regurgitant volume < 60
mL/beat….severMR