Transcript No Slide Title

Valvular Disorders
&
Infecive Endocarditis
Normal Valve Function


Prevent backward flow of blood
Permit forward flow of blood
Abnormal valve function

Allows backward flow
Valve is “leaky;” “regurgitant;” “incompetent”
 Backwards jet causes turbulence that is audible as
murmur


Prevents forward flow
Valve does not open well
 Greek stenōsis, a narrowing
 Typically causes hypertrophy and dilatation of the
cardiac chamber

All valvular diseases have
characteristic murmurs


Damaged valve disrupts blood flow=turbulence &
sound!
Caused by
Rheumatic Heart Disease
 Acute conditions (infective endocarditis)
 Acute MI
 Congenital Heart Defects


Aging
Auscultation



Use the diaphragm for high pitched sounds and
murmurs
Use the bell for low pitched sounds and murmurs
Sequence of auscultation { Z Pattern }
Apex
 Lower left sternal border (LLSB)
 Upper left sternal border (ULSB)
 Upper right sternal border (URSB)

Common Murmurs and Timing
Systolic Murmurs
 Aortic stenosis
 Mitral insufficiency
 Mitral valve prolapse
 Tricuspid insufficiency
Diastolic Murmurs
 Aortic insufficiency
 Mitral stenosis
S1
S2
S1
Grading the Intensity of Murmurs

Grade 1


Grade 2


Murmur associated with a thrill
Grade 5


Murmur hears with stethoscope on chest wall, louder than grade 2 but
without a thrill
Grade 4


Faint murmur heard with stethoscope on chest wall
Grade 3


Murmur heard with stethoscope, but not at first
Murmur heard with just the rim held against the chest
Grade 6

Murmur heard with the stethoscope held away and in from the chest wall
Cardiac Murmurs

Most mid systolic murmurs of grade 2/6 intensity or
less are benign

Associated with physiologic increases in blood velocity:



Pregnancy
Elderly
In contrast, the following murmurs are usually
pathologic:



Systolic murmurs grade 3/6 or greater in intensity
Continuous murmurs
Any diastolic murmur
Innocent Murmurs
Common in asymptomatic adults

Characterized by

Grade I – II @ LSB
Systolic ejection pattern - no  with Valsalva
–
–
–
–
S1
S2
Normal precordium, apex, S1
Normal intensity & splitting of second sound (S2)
No other abnormal sounds or murmurs
No evidence of LVH

Characteristic Pathological Murmur




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Diastolic murmur
Loud murmur - grade IV or above
Regurgitant murmur
Murmurs associated with a click
Murmurs associated with other signs or
symptoms e.g. cyanosis
Abnormal 2nd heart sound – fixed split,
paradoxical split or single
Valvular Aortic Stenosis

Normal valve area 3-4 cm2

Failure of valve to open normally during systole, requiring LV to
develop excess pressure to overcome increased resistance

Mild AS >1.5 cm2
Moderate >1.0 cm2
Severe AS when area ¼ normal


<1 cm2 for large person
 <0.75 cm2 for normal person
Causes concentric hypertrophy
Symptoms of exertional chest pain, syncope, dyspnea
 Mandate valve replacement to prevent sudden death



A.S : Etiology
Clinical Presentation of Aortic Stenosis

Cardinal symptoms:
 Angina
 Syncope
 CHF
Physical Findings
S1
S2
Mild-Moderate
S1
S2
Severe
Management of Aortic Stenosis



Prognosis in asymptomatic disease excellent
Conservative approach with monitoring for
symptoms recommended
Once symptoms occur, AVR needed

Only should be considered:
If other cardiac surgery (such as CABG) planned
 Severe LVH or systolic dysfunction
 Women contemplating pregnancy

Aortic Regurgitation
Aortic Regurgitation: Etiology


Any conditions resulting
in incompetent aortic
leaflets
Congenital



Acquired




Bicuspid valve

Aortopathy


Cystic medial necrosis
Collagen disorders (e.g.
Marfan’s)
Rheumatic heart disease
Dilated aorta (e.g.
hypertension..)
Degenerative
Connective tissue disorders


E.g. ankylosing spondylitis,
rheumatoid arthritis, Reiter’s
syndrome, Giant-cell arteritis )
Syphilis (chronic aortitis)
Acute AI: aortic dissection,
infective endocarditis, trauma
Aortic Regurgitation: Symptoms


Dyspnea, Orthopnea, PND
Chest pain.

Nocturnal angina >> exertional angina
Peripheral Signs of Severe
Aortic Regurgitation

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Quincke’s sign: capillary
pulsation
Corrigan’s sign: water
hammer pulse
Bisferiens pulse (AS/AR >
AR)
De Musset’s sign: systolic
head bobbing
Mueller’s sign: systolic
pulsation of uvula



Durosier’s sign: femoral
retrograde bruits
Traube’s sign: pistol shot
femorals
Hill’s sign:BP Lower
extremity >BP Upper
extremity by



> 20 mm Hg - mild AR
> 40 mm Hg – mod AR
> 60 mm Hg – severe AR
Aortic Regurgitation:
Physical Exam

Widened pulse pressure



Systolic – diastolic = pulse pressure
High pitched, blowing, decrescendo
diastolic murmur at LSB
Best heard at end-expiration &
leaning forward
S1
S2
S1
Aortic Regurgitation:
Natural History
Asymptomatic
 Normal LV function (~good prognosis)
 Abnormal LV function


Progression to cardiac symptoms (25 % )
Symptomatic (Poor prognosis)

Mortality > 10 %
TX: Medical  Surgery BEFORE LV dysfunction
Mitral Stenosis


Almost always rheumatic in origin
>40% of cases of RHD result in mitral stenosis



Presentation 20-40 years after the initial episode of
rheumatic fever
Diastolic murmur



Women affected more than men (2:1)
classic presentation is during vaginal delivery. Tachycardia,
straining, volume increase cause pulmonary edema
Patients eventually have exertional dyspnea, atrial
fibrillation (often with thromboembolism), chest pain
Always look for MS in patient with new Atrial fibrillation
Mitral Stenosis Pathophysiology


Normal valve area: 4-6 cm2
Mild mitral stenosis:
MVA 1.5-2.5 cm2
 Minimal symptoms


Mod mitral stenosis


MVA 1.0-1.5 cm2 usually does not produce symptoms
at rest
Severe mitral stenosis

MVA < 1.0 cm2
Mitral Stenosis Symptoms


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Fatigue
Palpitations
Cough
SOB

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Orthopnea
PND
Palpitation

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A. Fibrillation
Systemic embolism
Pulmonary infection
Hemoptysis
Right sided failure


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Hepatic Congestion
Edema
Worsened by conditions that 
cardiac output.

Exertion,fever, anemia,
tachycardia, Afib, intercourse,
pregnancy, thyrotoxicosis
Mitral Stenosis Physical Exam
S1




S2 OS
S1
First heart sound (S1) is accentuated
Opening snap (OS)
Low pitch diastolic rumble at the apex
Pre-systolic accentuation (esp. if in sinus rhythm)
MS Mortality



Minimal symptoms >80% 10 year survival
Limiting symptoms <15% 10 year survival
Untreated patients
60-70% progressive pulmonary edema
 20-30% systemic embolism
 1-5% endocarditis/infection

Mitral Regurgitation


Incompetent mitral valve allows loss of stroke
volume back into Left Atrium
Mitral valve prolapse most common cause


Rheumatic disease and endocarditis
Physical Examination
Loud pan-SYSTOLIC murmur, loudest at apex and
radiating into axilla
 Typically soft S1
 Presence of S3 suggests severe MR

Mitral Regurgitation: Etiology

Valvular-leaflets



Rheumatic
Endocarditis
Chordae





Fused/inflammatory
Torn/trauma
Degenerative
Endocarditis
Annulus


Papillary Muscles


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Calcification, IE
(abcess)
CAD (Ischemia,
Infarction, Rupture)
LV dilatation &
functional regurgitation
Trauma
MR Symptoms





Dyspnea, Orthopnea, PND
Fatigue
Pulmonary HTN, Right sided failure
Hemoptysis
Systemic embolization in A Fib
Mitral Insufficiency:
Physical Exam
S1

Mitral regurgitation
S2
S1
MR Treatment


No medical therapy
Most difficult clinically


By the time symptoms occur, it may be too late
Drop in Ejection Fraction or development of
atrial fibrillation enough to justify surgery
Mitral Valve Prolapse : Epidemiology






Affects 5-10% of population
Most common cause of isolated severe MR
Females >> males; Ages of 14 - 30years
Strong hereditary component (? Autosomal Dominant)
2º to failure of apposition/coaptation of the anterior
and posterior mitral valve leaflets.
Cause is unknown in a majority of pts
Mitral Valve Prolapse: Symptoms



Majority are asymptomatic for entire life
Palpitations
Chest pain (atypical).


Often substernal, prolonged, poorly related to exertion,
and rarely resembles typical angina
Syncope
Mitral Valve Prolapse:
Physical Exam
S1


C
S2
Most important finding: mid  late systolic click.
Variable murmurs:
 high pitched late systolic crescendo-decrescendo
murmur,
Mitral Valve Prolapse: Complications




Arrhythmias (Usually PVC, PSVT>>VT)
Transient cerebral ischemic (embolic – rare)
Infective endocarditis (if associated with MR)
Sudden death (rare)
Tricuspid Valve Disease

Tricuspid stenosis is rare



Associated with rheumatic heart disease
More common than regurgitation
Result in R. atrial enlargement > inc. systemic venous pressure > atrial fibrillation,
peripheral edema, ascites

TR usually occurs secondary to:

Pulmonary hypertension
 RV chamber enlargement with annular dilatation
 Endocarditis (associated with IV drug use)
Other secondary causes: carcinoid, radiation therapy


Symptoms are manifestations of systemic venous congestion
Ascites & Pedal edema
Echo is diagnostic in most cases



Severe tricuspid regurgitation is difficult to treat and carries a poor
overall clinical outcome
Other Valve disorders:

Pulmonic stenosis





Thrombus on valves – Hypercoag., DIC, Malignancy, etc.
May cause strokes, sec. bacterial infection.
Libman-Sacks:


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Uncommon valve disorders
NBTE: Non bacterial thrombotic…


Result in R. ventricular hypertension and hypertrophy
Fatigue , loud midsystolic murmur
Sterile Immune complex vegetations
SLE.
Carcinoid Heart Disease:


Carcinoid tumour, 5HT, seratonins etc..
Endocardial fibrosis
Valvular Disease

Rheumatic fever



Endocarditis causes regurgitation


Regurgitation frequently present acutely
Long term predominant effect is stenosis
Patients with valve disease should take antibiotics prior to dental
work to prevent endocarditis
All patients with symptomatic valvular disease (i.e.
dyspnea, chest pain, syncope) need to be evaluated for
surgical correction

Some asymptomatic subjects also need correction “before it’s
too late”
Valvular Disease
General Principles




Left sided valvular disease more prone to cause serious
hemodynamic problems
Regurgitation causes volume overload- eccentric
hypertrophy (dilatation)
Stenotic lesions cause pressure overload on proximal
chamber- concentric hypertrophy (thickened walls)
Stenotic lesions cause symptoms sooner than
regurgitant lesions but respond to therapy better
Common Murmurs and Timing
Systolic Murmurs
 Aortic stenosis
 Mitral insufficiency
 Mitral valve prolapse
 Tricuspid insufficiency
Diastolic Murmurs
 Aortic insufficiency
 Mitral stenosis
S1
S2
S1
General Appearance

Marfan Syndrome





Large stature, coarse facial
features, “spade” hands
Associated with: Cardiac
hypertrophy
Turner Syndrome



Tall, long extremities
Associated with: aortic root
dilitation, MV prolapse
Acromegaly

Web neck, hypertelorism, short
stature
Associated with: Aortic coarctation,
pulmonary stenosis
Pickwickian Syndrome



Severe obesity, somnolence
Associated with: Pulmonary
hypertension
Fredreich ataxia



Duchenne muscular dystrophy



Pseudohypertrophy of the calves
Cardiomyopathy
Ankylosing spondylitis



Lurching gait, hammertoe, pes
cavus
Associated with: hypertrophic
cardiomyopathy
Straight back syndrome, stiff
(“poker”) spine
Associated with: AI, CHB (rare)
Lentigines (LEOPARD
syndrome)


Brown skin macules that do not
increase with sunlight
Associated with: HOCM, PS
General Appearance- 2

Hereditary hemorrhagic
telangiectasia (Osler-WeberRendu)




Butterfly rash on face, Raynaud
phenomenon- hands, Livedo
reticularis
Associated with: Verrucous
endocarditis, Myocarditis,
Pericarditis
Sarcoidosis



Lupus


Small capillary hemangiomas on
the face or mouth
Associated with: Pulmonary
arteriovenous fistula

Tuberous Sclerosis




Pale diaphoretic skin,
neurofibromatosis- café-au-lait
spots
Associated with: Catecholamineinduced secondary dilated CM
Angiofibromas (face; adenoma
sebaceum)
Associated with: Rhabdomyoma
Myxedema

Pheochromocytoma

Cutaneous nodules, erythema
nodosum
Associated with: Secondary
cardiomyopathy, heart block

Coarse, dry skin, thinning of
lateral eyebrows, hoarseness of
voice
Associated with: Pericardial
effusion, LV dysfunction
Prosthetic Valve Complications

Common complications include:




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Endocarditis prophylaxis required for patients with all types of prosthetic
valves
Suspect valve dysfunction in:






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Structural valve deterioration
Valve thrombosis
Embolism
Bleeding
Endocarditis
Acute CHF in the immediate postoperative period
New cardiac symptoms
Embolic phenomena
Hemolytic anemia
New murmurs
TEE is the diagnostic procedure of choice
Postoperative TTE should be done 2-3 months after surgery
2007: Who gets Prophylaxis?
Only patients with the highest risk of adverse
outcomes (heart failure, surgery, death) from
endocarditis:
1. Prosthetic cardiac valve
2. Previous Infective Endocarditis
3. Cardiac transplant recipients who develop
cardiac valvulopathy
4. Congenital Heart Disease
Which categories of Congenital Heart Disease?

Unrepaired cyanotic CHD



Tetralogy of Fallot, Transposition of Great Arteries, including
palliative shunts and conduits
Completely repaired congenital heart defect with prosthetic
material or device during 1st 6 months after surgery
Repaired CHD with residual defects at or near a prosthetic
patch/device (which inhibit endothelialization)
Dental Procedures

“If it bleeds, give prophylaxis”

High-risk pts undergoing all dental procedures that involve
manipulation of gingival tissues OR periapical region of
teeth OR perforation of oral mucosa


i.e. biopsies, suture removal, placing orthodontic bands
NO PROPHYLAXIS:



X ray, anesthetic injections, fluoride treatments
Shedding of deciduous teeth
Placement/adjustment of removable prosthodontic or
orthodontic appliances
Prophylaxis for Dental Procedures


Goal: cover Strep Viridans
Single dose, 30-60 min prior to procedure
PO
Amoxicillin 2g
PO,
PCNallergic
Cephalexin 2g
IV:
Ampicillin 2gm IV/IM
OR Clindamycine 600mg OR Azithromycine 500mg
**Don’t use Cephalexin if anaphylaxis, angioedema, or urticaria
w/PCNs or ampicillin
OR Cefazolin 1g IV/IM OR Ceftriaxone 1g IV/IM
IV, PCNallergic
Cefazolin 1g IV/IM
OR Ceftriaxone 1g IV/IM OR Clindamycine 600mg IV/IM
Summary: IE prophylaxis



Need high-risk pt PLUS high-risk procedure
High-risk pts:
1. Prosthetic cardiac valve
2. Previous IE
3. Cardiac transplants w/ valvulopathy
4. Congenital Heart Disease
High-risk procedures:
1.
2.
Dental: “If it bleeds, give prophylaxis”
Respiratory: Consider if pt will be cut or biopsied
No Prophylaxis


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Endotracheal intubation
Cardiac cath/stent
Pacer/ICD implantation
EGD, Colonoscopy
Barium Enema
TEE
Incision/Bx of surgically scrubbed skin
Circumcision
Vaginal delivery
Hysterectomy
Endocarditis


Etiology

Damaged valve (RHD) exposed to bacteria in blood stream

S. viridans, S. aureus
Clinical




acute, subacute, chronic
fever, new murmur, ESR
(+) blood cultures
Treatment


Antibiotic according to organism
Future prophylaxis for procedures
Endocarditis Classification

Acute




Subacute (SBE)




Virulent! Staph aureus, Gram Negative Rods
Normal valves
Acute course with rapid valve destruction, Heart Failure
Streptococci, Enterococcus, Staph epidermoides
Underlying cardiac disease
More indolent presentation: low-grade fever, murmur
Native valve, addict, prosthetic valve, culture-neg
Diagnosis of IE




Fever, new murmur or heart failure, bacteremia
Systemic findings of emboli
Neurologic impairment
ECG


New AV block or BBB suggests perivalvular invasion
CXR

Septic pulmonary emboli
Trans Thoracic Echocardiography:

98% Specificity for veg

Sensitivity <60%; less in obesity, COPD

Begin with TTE if pt is good candidate for imaging surface, has native valves, or has low
probability of IE
Trans Esophageal Echocardiography:

Invasive, costly

Sens 75-95%, Spec 85-98%. Neg TEE: NPV >92%

Consider for pts w/prosthetic valves, high probability of endocarditis, and to evaluate
myocardial abscess, perivalvular extension
Septic Emboli








Osler's Nodes: Painful,
erythematous nodules associated
with bacterial endocarditis.
4 P’s:
Pink
Painful
Pea-sized
Pulp of fingers/toes
Splinter Hemorrhages: in the nail
bed.
Roth Spots
Janeway Lesions
Nontender, erythematous, hemorrhagic or pustular lesions on palms, soles
Petechiae
• Not specific for IE but
common
• Splinter Hemorrhages
–Linear, under nailbeds
• Conjunctival Petechiae
–Hemorrhages on eversion of
eyelid
Prosthetic Valve Endocarditis

Risk of IE


EARLY: < 2 months post-op




1% at 12 mos, 2-3% at 60 mos post-op
#1 cause: Staph aureus (used to be staph epi)
Usually acquired in the hospital: direct intra-op contamination or
post-op hematogenous spread
Anchoring sutures and valve ring are not yet endothelialized, so
more vulnerable
LATE: > 2 months post-op

Endothelialization occurs over months, making it more difficult
for bugs to adhere. Community-acquired.
IVDU

Classic teaching: IVDU  Right-sided IE





But left-sided IE may actually be more common
50% Staph Aureus
15% Enterococcus
8% each: Strep, GNR (Pseudomonas or
Serratia), Candida
May be polymicrobial
Major Duke’s Criteria
Definite IE: 2 major, 1 major + 3 minor, or 5 minor




(+) Blood cultures with appropriate organism
Evidence of Coxiella burnetii infection
New Valvular regurgitation
+ Echo findings
Minor Duke’s Criteria



High-risk for IE, or h/o IVDU
Temperature > 38oC
Vascular Phenomena


Immunologic phenomena



Arterial embolism, septic pulm infarcts, mycotic aneurysm,
intracranial hemorrhage, Janeway lesions
Osler’s nodes, Roth spots, GN, Rheumatoid factor
Serologic studies
Blood cultures or echo results not meeting the major
criteria
Therapy: General comments


Prolonged IV administration of bactericidal
agents(s) x 4-6 wks
Culture-negative native-valve endocarditis
should be individualized and generally includes
penicillin, ampicillin, ceftriaxone, or vanc, +/aminoglycoside
Indications for Surgery







Refractory CHF, Severe valvular dysfunction
Uncontrolled infection
Valve perforation, dehiscence, fistula, abscess
1 embolic event with persistent large vegetation, or >1
episode of embolization
Prosthetic valve infection
Fungal IE
New heart block…
Conclusions



Valvular heart disease associated with spectrum
of presentations
Recognition prior to the onset of symptoms
may be life saving
Careful physical exam almost always diagnostic
“Pearls”


Diastolic murmurs usually represent pathological conditions
as do most continuous murmurs.
Most important issue in patient with a cardiac murmur is the
presence or absence of symptoms.



Many asymptomatic children and young adults with grade 2/6
midsystolic murmurs and no other cardiac physical findings need no
further cardiac evaluation
Many asymptomatic elderly patients have midsystolic murmurs
related to sclerotic aortic valve leaflets, flow into tortuous,
noncompliant great vessels
Such murmurs must be distinguished from murmurs caused by mild
to severe valvular aortic stenosis (AS) which is prevalent in this age
group.