Valvular heart disease for finals

19th March 2013 Bori Dimitrova FY1 Surgery

Outline

Very broad subject Common conditions & presentations AS,AR,MS,MR,IE

Simple pathophysiology
Exam tips Questions

Valvular disease
Aortic & Mitral valves are mainly involved Tricuspid valves- secondary effects Pulmonary valves- mainly congenital disease

Why do valves go wrong?

Rheumatic fever valve disease later

Degenerative
Congenital bicuspid valve in AS Congenital plus degenarative Infection of the valve infective endocarditis (I.E.) Inflammatory disease

What problems do abnormal valves cause (pathophysiologically)?

Problems relate to effects on 1.Ventricle 2.Atrium

Intracardiac pressures - particularly raised pressures in the atria LA pressure pulmonary oedema RA pressure hepatic distension, ascites & oedema

What problems do abnormal valves cause (clinically)?

Nothing- maybe for years

exercise tolerance (all eventually) Heart failure (all eventually) Blood clots emboli (MS++ & MR) Angina (AS) Syncope & sudden death (AS)

Heart Sounds- Lub Dub

SYSTOLE (ventricular ejection)

Closure of mitral and tricuspid valves at the start of systole

DIASTOLE (ventricular filling)

Closure of the aortic and pulmonary valves, marking the end of systole

Normal valve function SYSTOLE

Aortic valve open
tricuspid

Ao Mitral valve closed

bicuspid

LA LV

Normal valve function

DIASTOLE
Aortic valve closed Ao

LA LV

Mitral valve open

AORTIC STENOSIS (AS)

Systole Aortic Stenosis

Thickening of the aortic valve causes obstruction to outflow

Ao

LA LV

Systole- AS Turbulent flow

Pressure gradient develops across the valve & turbulent flow causes a loud murmur in systole

Ao

LA LV

Systole -Aortic stenosis

LV is pressure loaded because of obstruction to flow & hypertrophies Ao

LA LV

AS Causes

Congenital- bicuspid aortic valve Rheumatic fever- also usually with AR Senile degeneration- age >60 , calcified immobile cusps

AS- S&S
Symptoms Effects of blocked outflow from the LV SAD (Syncope, Angina, Dyspnoea), dizziness, heart failure, sudden death, nil Signs Ejection systolic murmur radiates to carotids/ diamond shape (bur-dee) Slow-rising pulse Heaving, non-displaced apex LV heave

Investigations

ECG evidence of LVH or LV strain

ECG: LVH. S wave V2 + R wave of V5 > 35mm

CXR LVH, cardiac enlargement, calcification of the aortic valve; often normal except in advanced disease ECHO key diagnostic tool; assesses LV function (TTE or TOE) Cardiac catheterisation assess valve gradient, LV fx, coronary artery disease, BUT risks emboli

CXR: LVH in a pt with AS

Management
Medical therapy Risk factors modification- anti hypertensives, anti-arrhythmic drugs

BAV

Surgical therapy Aortic valve replacement (AVR) Balloon aortic valvuloplasty (BAV)

TAVI (Transcatheter aortic valve implanation)- method of AVR w/out risks of surgery
TAVI

AORTIC REGURGITATION (AR)

Diastole- Aortic regurgitation

Turbulent flow

Ao
LA

LV

Diastole- Aortic regurgitation

Ao
LA

LV

The backflow in diastole overloads the LV with volume & it dilates. This produces a murmur in early diastole.

AR Causes
Acute: Infective endocarditis

Aortic dissection Chest trauma

Chronic: Congenital Connective tissue & inflammatory conditions (eg.Marfans, RA, SLE)

Hypertension Aortic root pathology Aortic root distortion eg. chronic dissection, syphilis

AR S&S
Symptoms effects due to volume overload since the volume of blood leaking into the LV in diastole has to be pumped out again Nil of years- heart become very big Exertional dyspnoea Heart failure- orthopnea/PND Angina Syncope Signs Early diastolic murmur at LSE (lub-taaar) Collapsing pulse (water hammer/Corrigans pulse) Displaced, hyperdynamic apex beat

Eponyms-Corrigans sign (visible carotid pulsation), de Mussets sign (head nodding with each heartbeat), Quinckes sign (nailbed pulsation), Austin Flint murmur (severe AR)

Investigations

ECG- LVH

CXR- cardiomegaly, pulmonary oedema, dilated ascending aorta

ECHO- key examination in dx and quantification of AR severity Cardiac magnetic resonance (CMR)recommended for evaluation of the aorta in pts with Marfan's syndrome Cardiac angiography- assess coronary anatomy before surgery in patients with the appropriate age and risk factor profile

Management
Symptomatic Tx- chronic severe AR Prevent development of heart failure

Aortic valve replacement (AVR). Indications for surgery: -symptomatic, acute severe AR -enlarged heart on CXR/echo -ECG deterioration (TWI in lateral leads) -IE refractory to medical therapy Monitor Echo 6-12 monthly

MITRAL STENOSIS (MS)

Diastole Mitral stenosis

Mitral valve is thickened. This is usually due to rheumatic fever in past

Ao

LA LV

Diastole Mitral stenosis

Blood flow is turbulent in diastole and produces a murmur in diastole

Ao

LA LV

Turbulent obstructed flow out of the LA

Diastole Mitral stenosis

Back pressure into the LA enlarges it, pressure back through the lungs to pulmonary artery & right heart

Ao

LA LV Clots can form in the big LA

MS Causes

Rheumatic fever Congenital

Malignant carcinoid disease SLE RA

Rare

MS S&S
Symptoms Blood unable to reach LVPressure LA LA failure PA pressure strain on RV ( stretch TR) Nil, SOB (back pressure to lungs), fatigue, palpitations, chest pain, haemoptysis, AF (atria stretched by back pressure), emboli (large LA with pressure), heart failure & congestion Signs Mid-diastolic murmur best heard with pt on left lateral position with bell (LUB de-durr) Loud S1 with an opening snap in early diastole Malar flush on the cheeks Low-volume pulse/ AF Tapping, non-displaced apex beat RV heave

Investigations

ECG- AF, LA enlargement, RVH, p-mitrale (bifid p wave) LA hypertrophy, RVH/RAD

CXR-left atrial enlargement, pulmonary oedema ECHO- diagnostic, assesses valve orifice, main method to assess severity & consequences of MS

Management
Medical therapy If in AF- rate control, anticoagulate Diuretics- preload & pulmonary venous congestion Surgical therapy Balloon valvuloplasty Open mitral valvotomy Mitral valve repair (MVR)

MITRAL REGURGITATION (MR)

Systole- Mitral regurgitation

Ao LA

LV

Turbulence in the LA as blood regurgitates in systole This cause a loud Murmur in systole

Systole- Mitral regurgitation

Ao LA

LV

LV and LA are overloaded with volume and enlarge

MR Causes
Rheumatic fever Infective endocarditis Mitral valve prolapse Functional (LV dilataion) Annular calcification elderly Ruptured chordae tendinae- e.g. post MI Papillary muscle dysfunction/rupture

MR S&S
Symptoms Due to back pressure (as MS) into LA. LV enlarges due to volume Nil, exercise tolerance,dyspnoea,fatigue, palpitations, AF, emboli, heart failure Signs Pansystolic murmur at apex radiating to axilla (burrr) Loud P2 (pulmonary HTN) Displaced, hyperdynamix apex RV heave

MR Ix & Mx
Similar to MS ECG- AF CXR-large LA & LV Echo- LV function Manage AF Valve replacement

Infective Endocarditis quick overview

Causes Streptococci- Strep. Viridans Staphylococci- Staph. A Enterococci Psuedomonas

Culture negative (5-10%) Moderate risk Mitral valve prolapse Tricuspid valve disease Pulmonary stenosis HOCM IVDU Dental procedures

Risk factors High-risk Prosthethic heart valves Valvular lesions aortic>mitral Cyanotic congential heart disease

IE S&S
General manifestations of sepsis Fever (PUO) Rigors Night sweats N&V

Manifestations of immune complex deposition Petechiae Splinter haemorrhages Oslers nodes- small, tender nodules Janeway lesions- non-tender Cardiac manifestations erythematous/haemorrhagic Tachycardia, hypotension areas on palms/soles Valve Clubbing destructionnew/changing Roth spots- retinal murmur haemorrhages with pale Heart failure/pulmonary oedema centres
Complications Haemolytic anaemia, Meningitis, Renal failure

Oslers nodes

Janeway lesions

Splinter haemorrhage Roths spot

Clubbing

Dukes diagnostic criteria

Major criteria 1. +ve BCs 2. Evidence of Minor criteria Predisposing heart condition or ivdrug use

endocardial involvement +ve

T>38C Vascular phenomena Immunological phenomena/microbiological phenomena: +ve but does not meet a major criterion or serological evidence of active infection with organism consistent with IE

echo: oscillating intracardiac mass on valve/ supporting structures abscess new partial dehiscence of prosthetic valve new valvular regurgitation

Investigations

Blood cultures- 3 sets from different sites at least 1 hour apart before Abx therapy FBC- normocytic anaemia U&Es, LFTS CRP- key marker for progress Urinalysis- microscopic haematuria ECG- confuction defects CXR- pulmonary oedema, infected/infarcted areas from septic emboli ECHO- confirm presence of valve lesions/ demonstrate vegetation OPG (panoramic dental XR) Swabs- any potential sites of infection

Management
Admit Await confirmation of diagnosis

Local micro + Abx guidelines -usually benzylpenicillin 1.2g QDS /gentamicin

4-6 weeks Rx PICC line IE Team- cardiologist & microbiologist

Description of Murmurs
Right-sided murmurs are heard best on Inspiration. Leftsided murmurs are heard best on Expiration Timing (diastolic or systolic) Intensity (soft or loud) Pitch or sensation of frequencies (high or low pitched) position (where the murmur is loudest) Radiation Tonal quality (blowing, rumbling, etc)

Grade (1-6)
I barely audible with stethoscope II soft but audible III medium intensity without a thrill, easily audible, and relatively loud IV medium intensity with a palpable thrill, is relatively loud V loudest murmur heard with stethoscope on chest +palpable thrill VI heard with stethoscope off the chest

If you havent got a clue

Likely AS/MR

Systolic murmur Best heard at.. Grade 3/6 No radiation My differentials are What I would like to do next is..

EMQs & Cases

A 72 year-old man becomes hypotensive 2 hours after apparently successful treatment for an inferior myocardial infarction. A right precordial lead ECG shows normal ST segments in V4R to V6R. On examination there is a new systolic murmur and the LV apex is thrusting. There is florid pulmonary oedema. pulmonary embolism inferior myocardial infarction cardiac tamponade left ventricular failure aortic dissection severe mitral regurgitation severe aortic stenosis right ventricular infarction hypertrophic cardiomyopathy coarctation of the aorta

a) b) c) d) e) f)

g)
h) i) j)

a) b) c) d) e)

f)
g) h) i)

j)

An 86 year-old man presents with a 2 week history of worsening dyspnoea and syncope. He has a weak pulse and his BP is 110/85. On auscultation there is a soft cresendo-decresendo systolic murmur. The first heart sound is present but S2 is absent. There are crackles throughout both lungs and CXR confirms pulmonary oedema. pulmonary embolism inferior myocardial infarction cardiac tamponade left ventricular failure aortic dissection severe mitral regurgitation severe aortic stenosis right ventricular infarction hypertrophic cardiomyopathy coarctation of the aorta

A 30 year old man attends for a routine pre-employment medical. On examination of the cardiovascular system, the doctor finds a soft (grade 2/6) ejection systolic murmur at the apex. He has no previous cardiac or respiratory problems, & has normal pulse & BP.
A B C D E F G Aortic stenosis Aortic regurgitation Mitral stenosis rheumatic Mitral regurgitation rheumatic Mitral regurgitation non-rheumatic Infective endocarditis Innocent murmur

H
I J K L M

Mixed aortic valve disease

Mixed mitral valve disease Mixed mitral & aortic valve disease Prolapsing mitral valve Congenital aortic stenosis Hypertrophic obstructive cardiomyopathy

EMQ
1. Pt with Hx of Mi 1 yr prior CO SOB & fatigue. The

A) AR

pts pansystolic murmur radiates into the axilla. 2.IVDU presents with fever & swollen ankles. OE pt has pulsatile hepatomegaly & pansystolic murmur, best heard at lower sternal edge upon inspiration. 3.OE pt has Corrigans sign, De Mussets sign, Quinckes sign & Ducosier sign - & for those that need it, pt also has collapsing pulse. 4.Pt presents with collapse on exertion. Pt known to have common problem with valve since birth. Slow rising pulse noticed on exam. 5. Pt admitted with SOB & chest pain. Echo reveals normal LV function. Pt admits to Hx of rheumatic fever. Malar flush is evident on pts face 6. 35 yr old pt, newly diagnosed with Fallots tetralogy, presents with epistaxis.
BGACDH

B) MR
C) AS D) MS E) M prolapse F) PR G) TR H) PS I) TS

J) Prosthetic R
K) Prosthetic S

Summary

Common valvular problems

pathophysiology presentation investigations treatment

Cases

Thank you