9. Normal Valve Function
Maintain forward flow and
prevent reversal of flow.
Valves open and close in
response to pressure
differences (gradients)
between cardiac chambers.
10. Abnormal Valve Function
Valve Stenosis
Obstruction to valve flow during that phase of the cardiac cycle when the
valve is normally open.
Hemodynamic hallmark -“pressure gradient” ~ flow// VA
Valve Regurgitation, Insufficiency, Incompetence
Inadequate valve closure--- back leakage
A single valve can be both stenotic and regurgitant.
Combinations of valve lesions can coexist
Single disease process
Different disease processes
One valve lesion may cause another
Certain combinations are particularly burdensome (AS & MR)
11. Mitral Valve Competence:
Integrated function of several
anatomic elements
1) Posterior LA wall
2) Anterior & Post.v. leaflets
3) Chordae tendineae
4) Papillary muscles
5) Left ventricular wall where
papillary muscles attach
12. Mitral Valve Competence:
Integrated function of several
anatomic elements
1) Posterior LA wall
2) Anterior & Post.v. leaflets
3) Chordae tendineae
4) Papillary muscles
5) Left ventricular wall where
papillary muscles attach
13. Valvular Heart Disease
Types of valvular heart disease depend on :
Valve or valves affected
Two types of functional alterations
Stenosis
Regurgitation
14. Pathophysiology
Stenosis- narrowed valve, increases afterload
Regurgitation or insufficiency- increases preload. The
heart has to pump same blood
Blood volume and pressures are reduced in front of the
affected valve and increased behind the affected valve.
This results in heart failure
All valvular diseases have a characteristic murmur
15. Valvular Stenosis
Pressure in upstream chamber IS HIGHER than
Pressure in downstream chamber during time of flow
(when valve is normally open).
Hemodynamic abnormality = "PRESSURE GRADIENT"
Upstream Down stream
High pressure low pressure
16. Valvular Regurgitation
Upstream Down stream
Volume overload
Retrograde flow of blood "upstream" during time when
valve is normally closed.
Hemodynamic abnormality = "VOLUME OVERLOAD"
24. Cardiac Physiology
Systole AV/PV – opens-------Aortic Stenosis
S1-S2 MV/TV – closes------Mitral Regurg
Diastole AV/PV – closes------Aortic Regurg
S2-S1 MV/TV – opens-------Mitral Stenosis
Regurg/ Insuff – leaking (backflow) of blood across a closed valve
Stenosis – Obstruction of (forward) flow across an opened valve
These concepts are set in stone, it can’t occur any other way,
It would be anatomically impossible
48. Mitral valve prolapse
General features
Occurs in 2-6% of the general population
Twice as common in women.
Due to myxomatous proliferation of the mitral valve.
Usually occurs as a primary condition, but may be a secondary
finding in connective tissue diseases e.g. Marfan’s syndrome.
Vast majority of patients are asymptomatic.
Symptoms may include palpitations, dizziness, syncope,
or chest discomfort.
The principal physical finding is the mid-systolic click, followed by
a late systolic murmur in the presence of regurgitation.
55. Mitral Stenosis
Etiologies
• Rheumatic – almost all cases in adults
• Mitral Annular Ca+ - massive (rare)
• Congenital – rare
60% of pts don’t have a history of ARC
50% of pts who have ARC don’t develop VHD
60. Mitral Stenosis
Physical Exam
– Loud S1
– Opening Snap
– Diastolic Apical Rumble (murmur)
– May be associated with:
• MR or AS
• Right Sided Murmurs
o PI – Graham Steel Murmur
o TR
61. Mitral Stenosis
Diagnosis
– ECG
(– A Fib, LAE, RAE, RVH )
– Echo 2D/color doppler –test of choice
– Cardiac Cath – helpful, confirmatory, needed if
the pt is older – look at the coronaries
62. Mitral Stenosis
Treatment of Symptomatic Mitral Stenosis
Medical Therapy – treats the symptoms not the cause
• Diuretics – for congestion
• Digoxin, Beta and Ca Channel Blockers for Afib
rate control
• Anticoagulation – for AFib and LA clots
• SBE Prophylaxix – prevent endocarditis
63. Mitral Stenosis
Treatment of Symptomatic Mitral Stenosis
Surgical Therapy – treats the cause
• Percutaneous Ballon Valvulaoplasty – Non-
calcified, pliable valve
65. Mitral Stenosis
Treatment of Symptomatic Mitral Stenosis
Surgical Therapy – treats the cause
• Open Commisurotomy – valve repair
• Mitral Valve Replacement
66. Mitral Valve Disease :
(Summary Treatment )
Mitral Stenosis
Medical Rx for Class I & II
HR control – Dig & BB
Anticoagulation
Afib, >40yrs, LAE, MR,
prior embolic event
Surgical Rx -Class III &IV
Balloon Mitral Valvuloplasty
Commissural fusion
pliable, noncalcified leaflets
No MR of LA thrombus
Mitral Valve Surgery
Open commissurotomy
MV replacement
Chronic Mitral Regurgitation
Medical Rx for mild to mod MR
with vasodilators, diuretics,
anticoagulation
Surgical Rx –ideally before LV
systolic function declines.
MV replacement
MV ring & CABG
MR repair :
(associated with improved long-
term LV function )
MVP, ruptured chords,
infective endocadritis, pap ms
rupture.
79. Aortic Stenosis
Diagnosis
– ECG – LAE, LVH
– Echo 2D/color doppler –test of choice
– Cardiac Cath – helpful, confirmatory, needed if
the pt is older – look at the coronaries
80. Aortic Stenosis
Treatment of Symptomatic Aortic Stenosis or
Decreased LV Function
Medical Therapy – treats the symptoms not the cause
Aortic Valve Replacement
Bioprosthetic vs Mechanical AVR
89. Aortic Regurg – Austin Flint Murmur
Due to the vibration of the anterior leaflet of the mitral valve
as it is buffetted simultaneously by the blood jets from the left
atrium and the aorta.
90. Aortic Regurgitation
Diagnosis
– ECG – LAE, LVH
– Echo 2D/color doppler –test of choice
– Cardiac Cath –
(Helpful, confirmatory, needed if
the pt is older – look at the coronaries
91. Aortic Regurgitation
Treatment of Asymptomatic Aortic Regurg
Medical Therapy – treats the symptoms not the cause
• Serial Check ups with Echos (eval EF, Severity AR)
• SBE Prophylaxis
• Vasodialators (Nifedipine, ACE-I)
• Diuretics
Treatment of Symptomatic Aortic Regurg
Aortic Valve Replacement
Bioprosthetic vs Mechanical AVR
92. Balloon Aortic Valvuloplasty
Indications for BAV in critical Aortic Stenosis
Younger patients with congenital AS and predominant
commissural fusion
Bridge to eventual AVR
Moderate to severe heart failure/cardiogenic shock
Extremely high risk for AVR
Urgent/emergent need for noncardiac surgery
Patient with limited lifespan – cardiac or noncardiac
Patient refuses surgery
93. Aortic Valve Surgery: Ross procedure
Autotransplant of pulmonic
valve to the aortic position
Reimplantation of the
coronary arteries
Homograft valve in the
pulmonic position
Indications
Younger patients
No anticoagulation
Requires similar sized
aortic and pulmonic roots
97. Etiology of Primary Tricuspid Valve
Disease
• *Congenital
—Cleft valve generally in association with atrioventricular canal defect
—Ebstein’s anomaly
—Congenital tricuspid stenosis
—Tricuspid atresia
* Acquired
• Rheumatic disease, generally in ass.with rheumatic mitral valve disease
• Infective endocarditis
• Carcinoid heart disease
• Toxic (eg, Phen-Fen valvulopathy or methysergide valvulopathy)
• Tumors (eg, myxoma)
• Iatrogenic—pacemaker lead trauma
• Trauma—blunt or penetrating injuries
• Degenerative—tricuspid valve prolapse
98. Clinical Presentations
• Pure or predominant tricuspid stenosis
• Pure or predominant tricuspid regurgitation
• Mixed
99. Tricuspid valve disease—
Symptoms
• Fatigue
• Liver/gut congestion
• Right upper quadrant discomfort
• Dyspepsia
• Indigestion
• Fluid retention with leg edema
• Ascites
100. Tricuspid stenosis
• Always Rheumatic .
• The anatomical changes and physiological principles are
similar to those of mitral stenosis.
• The low cardiac output state causes fatigue; abdominal
discomfort may occur due to hepatomegaly and ascites.
• The diastolic murmur of tricuspid stenosis is augmented by
inspiration.
• Medical management includes salt restriction and diuretics.
• Surgical treatment should be carried out in patients with a
valve area <2.0cm2 and a mean pressure gradient >5mmHg.
101. Tricuspid reurgitation
• Most common cause is annular dilatation due to RV failure of
any cause; may also be caused by intrinsic valve involvement
• Well tolerated in the absence of pulmonary hypertension; in
the presence of pulmonary hypertension, cardiac output
declines and RV failure may worsen.
• Symptoms and signs result from a reduced cardiac output,
ascites, painful congestive hepatomegaly and oedema.
• The pansystolic murmur of TR is usually loudest at the left
sternal edge and augmented by deep inspiration.
• Severe functional TR may be treated by annuloplasty or valve
replacement. Severe TR due to intrinsic tricuspid valve disease
requires valve replacement.
106. Pulmonary stenosis
• Most commonly due to congenital malformation and
usually an isolated anomaly.
• Survival into adulthood is the rule, infective
endocarditis is a risk and right ventricular failure is
the most common cause of death.
• Rheumatic involvement of the pulmonary valve is
very uncommon and rarely leads to serious deformity.
• Carcinoid plaques may lead to constriction of the
pulmonary valve ring.
107. Clinical Features & Diagnosis
1. Symptoms
Symptomatic, but less severe than neonates
30-40% are asymptomatic.
Effort dyspnea & cyanosis may appear.
2. Signs
Systolic murmur with a thrill
Pulmonary component of second sound is decreased.
3. Electrocardiography
RAE, RAD, RVH
T- waves in right precordial lead
4. Echocardiography, catheterization & cineangiography
PS in Infants, Children, Adults
108. Techniques of Operation
1. Comment
Percutaneous balloon valvotomy is treatment of
choice for valvar pulmonary stenosis, if not possible,
open surgical valvotomy is indicated.
2. Open operation during CPB
Pulmonary valvotomy
Infundibular resection
Transanular patch
PS in Infants, Children, Adults
111. Pulmonary regurgitation
• Most common cause is ring dilatation due to pulmonary
hypertension, or dilatation of the pulmonary artery secondary
to a connective tissue disorder.
• May be tolerated for many years unless complicated by
pulmonary hypertension.
• The clinical manifestations of the primary disease tend to
overshadow the pulmonary regurgitation.
• Physical examination reveals a right ventricular heave and a
high-pitched, blowing, early diastolic decrescendo murmur
over the left sternal edge, augmented by deep inspiration.
• Rx.
Pulmonary regurgitation is seldom severe enough to require
specific treatment. Surgery may be required because of
intractable RV failure.
116. Diagnosis
• History and physical findings
• EKG
• Chest x-ray
• Cardiac cath
• Echocardiogram
117. Medial Treatment
• Nonsurgical management focuses on drug
therapy and rest
• Diuretic, beta blockers, digoxin, O2,
vasodilators, prophylactic antibiotic therapy
• Manage A-fib, if develops, with conversion if
possible, and use of anticoagulation
118. Interventions
• Assess vitals, heart sounds, adventitious breath sounds
• ^ SOB
• O2 as prescribed
• Emotional support
• Give medications
• I/O
• Weight
• Check for edema
• Explain disease process, provide for home care with O2,
medications
120. What is new?
Percutaneous Transcatheter Heart Valve Implantation-
Metallic clip -for the treatment of mitral regurgitation
Longer-lasting replacement valves
Stem cell research and the use of endothelial cells
122. Prosthetic Valves
• MECHANICAL
– Durable
– Large orifice
– High thromboembolic
potential
– Best in Left Side
– Chronic warfarin therapy
– May cause hemolysis
• BIO-PROSTHETIC
– Not durable
– Smaller orifice/functional
stenosis
– Low thromboembolic
potential
– Consider in elderly
– Best in tricuspid position
– Anticoagulant for 3 mon.
124. Prosthetic Valves
• MECHANICAL
– Durable
– Large orifice
– High thromboembolic
potential
– Best in Left Side
– Chronic warfarin therapy
– May cause hemolysis
• BIO-PROSTHETIC
– Not durable
– Smaller orifice/functional
stenosis
– Low thromboembolic
potential
– Consider in elderly
– Best in tricuspid position
– Anticoagulant for 3 mon.
132. INTRODUCTION
*RF. is major public health problem in Yemen.
*Clinicians & health workers should not forget
about acute rheumatic fever & fight against it.
*The relation between sore throat & rheumatic
fever is clear fact now.
135. Lancefeld Group A B.Hemolytic
Streptococcus(GAS).
In 0.3-2% of populations.
RF. 2-4 weaks later (10-20%)
50% RHD.
*BACTERIA OF IMPORTANT*
WHO referrence
136. Group A Streptococcus bacterium.
( 1998 J.L. Carson.)
(Reproduced by permission of Custom Medical Stock Photo.)
141. Sir Alexander Fleming, 1952
In 1929 he Isolated "penicillin" from a mold, Penicillium notatum.
142.
143. *Orally Penicillin for 5-10 days.
*IM Penicillin (LAP). Especially in
• 1-Unlikely to complete the 10 days course of oral
treatment.
• 2-Possitive family history of RF. Or RHD.
• 3-Group at high risk (as parents of young ,child
adolescence,crowded,teachers,physcions,nurse,
military persons, or low socioeconomic status )
Acute Sore Throat
+
144. Awareness ♦ Surveillance ♦ Advocacy ♦ Prevention
Secondary prevention: Duration
CATEGORY DURATION OF PROPHYLAXIS
All persons with ARF
with no or mild carditis
MINIMUM 10 years after most recent episode
or age 21
All persons with ARF
and moderate carditis
MINIMUM 10 years after most recent episode
or age 35
All persons with ARF
and severe carditis
MINIMUM 10 years after most recent episode
or age 35 and then specialist review for need
to continue.
Post surgical cases definitely lifelong.
145. Secondary Prevention
Stops sore throat, prevents recurrences of ARF and aids in
regression of RHD
Antibiotic Administration Dose
Benzathine benzyl
penicillin
Single IM injection
2-4 /Wks.
1.2 MU > 30kg
600 000 U < 30 kg
Phenoxymethyl
penicillin
(Pen VK)
BD PO daily 250-500mg bd
Erythromycin
ethylsuccinate
BD po daily Use same dose as above.
Oral penicillin has been shown to be less effective than Penicillin IMI
Anaphylaxis is extremely unusual
147. • Infection of heart valves
• Commonly bacterial
• Results in damage to valve structure
giving rise to senosis or regurgitation
Infective
endocarditis.
152. vegetation
• Def :- any plant like (fungoid neoplasm or
growth )
• Or called vegs
153.
154. Vegetations in the Heart
• Inflammatory cardiac valve lesions, composed
of bacteria, WBCs, macrophages, fibrin,
rouleaux, platelets , and edema
• Attached to the “flow side” of valves
• Amorphous and irregular in shape
158. Petechiae
Photo credit, Josh Fierer, M.D.
medicine.ucsd.edu/clinicalimg/ Eye-Petechiae.html
Harden Library for the Health Sciences
www.lib.uiowa.edu/ hardin/
md/cdc/3184.html
1. Nonspecific
2. Often located on extremities
or mucous membranes
dermatology.about.com/.../
blpetechiaephoto.htm
159. Splinter Hemorrhages
1. Nonspecific
2. Nonblanching
3. Linear reddish-brown lesions found under the nail bed
4. Usually do NOT extend the entire length of the nail
160. Osler’s Nodes
1. More specific
2. Painful and erythematous nodules
3. Located on pulp of fingers and toes
4. More common in subacute IE
American College of Rheumatology
webrheum.bham.ac.uk/.../ default/pages/3b5.htm www.meddean.luc.edu/.../
Hand10/Hand10dx.html
161. Janeway Lesions
1. More specific
2. Erythematous, blanching macules
3. Nonpainful
4. Located on palms and soles
168. Lab findings
• Serology
– Rheumatoid factor (40-50%)
– Circulating immune complexes
– Antinuclear antibodies
– Complement
• Blood culture
– Most important lab test
– Positive cultures in 97% of cases
169. Imaging
• Chest x-ray
– Look for multiple focal infiltrates and calcification of heart
valves
• EKG
– Rarely diagnostic
– Look for evidence of tachycardia ,ischemia, conduction
delay, and arrhythmias
*Echocardiography
• MRI. Or CT.
• Cath
– hemodyanmic and anatomic info for surgical intervention
176. Diagnosis
• Diagnosis of IE requires hospitalization
– Cultures
– Echocardiogram
– Clinical observation
• Duke Criteria – 90% sensitive
– Major Criteria
– Minor Criteria
177. Making the Diagnosis
Pelletier and Petersdorf criteria (1977)
Classification scheme of definite, probable, and possible IE
Reasonably specific but lacked sensitivity
Von Reyn criteria (1981)
Added “rejected” as a category
Added more clinical criteria
Improved specificity and clinical utility
Duke criteria (1994)
Included the role of echocardiography in diagnosis
Added IVDA as a “predisposing heart condition”
178. Duke criteria
Major criteria
1. Blood culture positive for
typical IE-causing
microorganism
2. Evidence of endocardial
involvement
Minor criteria
1. Predisposition – heart
condition or i.v. drug abuse
2. Fever – temp. >38 °C
3. Vascular phenomena –
arterial emboli etc.
4. Immunologic phenomena –
glomerulonephritis, Osler’s
nodes, Roth’s spots
5. Microbiological evidence –
positive blood cultures but do
not meet major criteria
Diagnosis
• 2 major criteria
• 1 major and 3 minor
• 5 minor criteria
179. Therapy
• Complete eradication takes weeks, relapses may occur. This is
due to:
1. The infection exists in an area of impaired host defense and is tightly
encased in a fibrin meshwork
2. The bacteria reach very high population densities, such that the
organism may exist in a state of reduced metabolic activity and cell
division
• Aspirin may decrease the growth of vegetative lesions and
prevent cerebral emboli
180. Therapy: General principles
• Etiologic agent must be isolated in pure culture. MIC and MBC should
be determined
• Parenteral antibiotics are recommended over oral drugs
• Bacteriostatic antibiotics are generally ineffective
• Antibiotic combinations should produce a rapid effect
• Selection of antibiotics should be based on susceptibility tests, and
treatment should be monitored clinically and with antimicrobial blood
levels
• Blood cultures should be obtained during the early phase of therapy
to ensure eradication
• Use of anticoagulants during therapy for native valve IE is not
recommended. With mechanical valves, anticoagulation should be
maintained (if indicated) within therapeutic range
181.
182.
183.
184.
185.
186.
187.
188.
189.
190.
191.
192.
193.
194.
195.
196. Summary
1. IE is rare but serious disease, with high mortality rate
2. Every case of fever of unknown origin should be suspected
for IE
3. Blood cultures are essential for diagnosis
4. TTE/TEE is the best method to monitor and follow-up of IE
5. Antibiotics are main treatment
6. CHF is the most common complication
7. Pharmacological prophylaxis is reserved for a narrow
group of high risk patients
198. Valvular Heart Disease
Follow up
Antibiotic prophylaxis
New symptoms
Change in symptoms
Change in physical findings
Echocardiography/other imaging
