Download Rheumatic heart disease

Rheumatic heart disease
Mitral stenosis
Valvular heart disease
• Rheumatic
• Age related
• congenital
Mitral valve
• Stenosis
• Regurgitation
• Prolapse
Mitral stenosis
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2/3 females
Usually rheumatic
Rarely congenital
40% of all RHD
Structural defects
• Diffusely thickened –fibrous tissue /calcified
deposits
• Mitral commisures fuse
• Corde tendinae fuse /shorten
• Narrowing of the apex of funnel shaped valves
• Calcification of slender valves immobilises the
leaflet and narrows the orifice –thrombus
formation –arterial thrombus from calcified
Valves
Pathophysiology
• Normal mv –dia -4-6 cm2
• <2 cm 2-atrial to ventricular flow is
maintained by increased av pressure gradient
–the hallmark of ms
• <1 cm2 –LAP should be atleast 25mm hg is
required to maintain normal output .
• Increased Lap --------increased pulm pressure -----increased capillary pressure -----decreased
pulm compliance -------exertional dyspnoea.
• Increased heart rate –decreased transvalvular
gradient ----increased LAP
• Lv diastolic pressure in normal in ms
• Co is normal at rest ---at exercise –decreased
co.
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Clinical /hemodynamic Features –influenced by
Passive backward transmission of LAP
Pulmonary arteriolar constriction
Intertitial edema
Organic obliterative changes in the pul vascular
bed
• Phtn----Tr------rt sided failures---bornheimeffect
symptoms
• Carditis---ms-----2 decades,
• Dyspnoea on exertion ----4 th decade—
progressive worsening to death---2-5 yrs
• Doe ,orthopnoea ,pnd,arrthmia-premature
atraial complex,paroxysysmal
tachycardia,flutter,fibrilation
• Haemoptysis –increased pulm venous
pressure
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Recurrant pulm embolism
Pulm infection
Endocarditis
Chest pain -10%
Thrombus formation in the left atrium-af—
appendages of LA
• Pedunculated thrombus –ball valve thrombi
• -syncope-angina –changing ascultatory signs
On examination
• Malar flush-pinched blue facies
• JVP-a wave prominence –af –a wave absent
• Palpation-tapping apical impulse ,s1
loud,palpable ,s2 p2 loud
• Diastolic thrill
• Auscultation-s1 accentuated /snapping –
delayed –mv doesn’t close till LVP>LAP
• Qs prolongation ,p2 loud
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A2-p2-os -0.05-0.12
P2-os –severity of ms
Intensity of s1/os –pliability of leAFLET
MDM after os
Duration correlates with ms severity
S1-closure of mitral /tricuspid valve
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Intensity of s1
Pos of mv at onset of vent systole
Rate of increase in LAP
Degree of structural damage of the valve
Amt of tissue bet heart and sthetoscope
• S1 loud –diastole is shortened by tachycardia
• S1 split -10-30 msec
• S1 –m1t1-----prolonged in rbbb
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t1m1 –severe ms ,left atrial myoma lbbb
Mitrl regurgitation
etiology
• Chronic rhd –severe mr- 1/3
• Seen in males mostly
• Rheumatic processrigidity,deformity,retraction of the valve cuspscommisural fusion
• Congenital-endocardial cushion defects
• Fibrosis of papillary muscles in MI
• Ischeamia –paplillary dysfn
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Lv dilated in DCM
HOCM-ant displace ment of the ant leaflet
Mitral prolapse –MR
Acute MR-inf endocarditis
pathophysiology
• Clinical pic depends on p-v relation ship of LA
AND PUL -VENOUS BED
• Increased LAP-Increased pulm edema
• Effective forward pressure of lv decreases
• Inc-LA volume –due to atrial compliance
• Low cardiac out put
• Atrial fibrillation
SYMPTOMS
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FATIGUE
Doe
Orthopnea
Pnd
Haemoptysis
Sys embolism
Rh f-jvp inc,tr,phtn,hep congestion
Physical examination
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Sys thrill-left apex
Hyperdynmic apical impulse
Laterally displaced
Palpable p2
Parasternal heave
auscultation
• S1-absent/softor buried in systolic murmur
• Decreased co-aorta closes early-a2 early-wide
spliting of s2
• Os –indicates ms
• Gallop rhythm
• Pansystolic murmur
lab
• Ecg –sinus rhythm ,prominent p waves ,af lvh
• Echo
• Cxr-kerley b lines
management
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Medical
Dec exertion
Dec NA intake
Diuretics
Digitalis/vasodilators-inc co
Ace inhibitors /hydralazine
Surgical-valve replacement