Acquired heart diseases...............ppt
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Aug 21, 2024
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About This Presentation
Tttt
Slide Content
Tadesse Getahun, Pediatrician, Pediatric
Cardiologist
Lecture for C-1
ACQUIRED HEART DISEASES IN
CHILDREN
Cardiologist
Lecture for C-1
ACQUIRED HEART DISEASES IN
CHILDREN
RHEUMATIC FEVER
Introduction
Acute rheumatic fever (RF) occurs as a result of a complex
interaction between group A streptococcus (GAS), a
susceptible host, and the environment.
An abnormal immune response to GAS infection leads to an
acute inflammatory illness that most commonly affects the
joints, brain, heart, or skin.
The most common form of acquired heart disease in all age
groups
Accounts 50% of cardiac diseases & cardiac admissions.
Peak age, 5 – 15yrs (rare before 5yrs of age).
No sex predilection
Acute rheumatic fever (RF) occurs as a result of a complex
interaction between group A streptococcus (GAS), a
susceptible host, and the environment.
An abnormal immune response to GAS infection leads to an
acute inflammatory illness that most commonly affects the
joints, brain, heart, or skin.
The most common form of acquired heart disease in all age
groups
Accounts 50% of cardiac diseases & cardiac admissions.
Peak age, 5 – 15yrs (rare before 5yrs of age).
No sex predilection
Pathogenesis
Several theories proposed for pathogenesis of ARF,
Only 2 considered; cytotoxicity & immunologic theories
Cytotoxic theory:
GAS produces several enzymes that are cytotoxic for
mammalian cardiac cells, such as streptolysin O,
Which has a direct cytotoxic effect on mammalian cells in
tissue culture
The cytotoxicity hypothesis is its inability to explain the latent
period between GAS pharyngitis and the onset of acute
rheumatic fever.
Several theories proposed for pathogenesis of ARF,
Only 2 considered; cytotoxicity & immunologic theories
Cytotoxic theory:
GAS produces several enzymes that are cytotoxic for
mammalian cardiac cells, such as streptolysin O,
Which has a direct cytotoxic effect on mammalian cells in
tissue culture
The cytotoxicity hypothesis is its inability to explain the latent
period between GAS pharyngitis and the onset of acute
rheumatic fever.
Pathogenesis …
Immunologic theory:
Clinical similarity of acute rheumatic fever to other
illnesses produced by immunopathogenic processes and
the latent period between the GAS infection and acute
rheumatic fever.
Antigenic mimicry and cross reactivity.
Immunologic theory:
Clinical similarity of acute rheumatic fever to other
illnesses produced by immunopathogenic processes and
the latent period between the GAS infection and acute
rheumatic fever.
Antigenic mimicry and cross reactivity.
Pathogenesis …
Distinct structural characteristics of M proteins
(Epitopes shared with human heart tissue).
Heavily encapsulated forming mucoid colonies.
Resistance to phagocytosis.
Susceptible host (genetic predisposition).
Distinct structural characteristics of M proteins
(Epitopes shared with human heart tissue).
Heavily encapsulated forming mucoid colonies.
Resistance to phagocytosis.
Susceptible host (genetic predisposition).
Pathology…..
Exudative & proliferative inflammatory rxns involving
connective or collagen tissue → fibrinoid degeneration →
edematous and eosinophilic interstitial connective tissue →
mononuclear cell infilteration (including large modified
fibrohistiocytic cells (Aschoff cells) → Aschoff Giant cells
(Aschoff nodules).
Aschoff nodules are Pathognomonic of rheumatic carditis and
are found only in the heart.
Inflammation of valvular tissue is the most common
manifestation of rheumatic carditis.
Valvular insufficiency is the initial feature while stenosis is due
to fibrosis and calcification.
Exudative & proliferative inflammatory rxns involving
connective or collagen tissue → fibrinoid degeneration →
edematous and eosinophilic interstitial connective tissue →
mononuclear cell infilteration (including large modified
fibrohistiocytic cells (Aschoff cells) → Aschoff Giant cells
(Aschoff nodules).
Aschoff nodules are Pathognomonic of rheumatic carditis and
are found only in the heart.
Inflammation of valvular tissue is the most common
manifestation of rheumatic carditis.
Valvular insufficiency is the initial feature while stenosis is due
to fibrosis and calcification.
Clinical manifestation & diagnosis
No clinical or laboratory finding is pathognomonic for acute
rheumatic fever.
Revised Jones criteria is used to diagnose ARF
Five major & four minor criteria.
Microbiologic or serologic evidence of recent GAS infection
Diagnosis; two major or one major and two minor criteria with
supporting evidences of recent streptococcal infection.
Exceptions for this criteria:
Chorea
Indolent carditis
Recurrence
No clinical or laboratory finding is pathognomonic for acute
rheumatic fever.
Revised Jones criteria is used to diagnose ARF
Five major & four minor criteria.
Microbiologic or serologic evidence of recent GAS infection
Diagnosis; two major or one major and two minor criteria with
supporting evidences of recent streptococcal infection.
Exceptions for this criteria:
Chorea
Indolent carditis
Recurrence
CM & DX…
Major criteriaMinor criteria Supporting evidence
Carditis Clinical features:
Arthralgia & Fever
Positive throat culture or
PolyarthritisLaboratory features:
Elevated acute phase
reactants:
rapid streptococcal
antigen test
Erythema
marginatum
Erythrocyte sedimentation
rate
Elevated or increasing
streptococcal antibody
titer
Subcutaneous
nodules
C-reactive protein
Chorea Prolonged PR interval
Major criteriaMinor criteria Supporting evidence
Carditis Clinical features:
Arthralgia & Fever
Positive throat culture or
PolyarthritisLaboratory features:
Elevated acute phase
reactants:
rapid streptococcal
antigen test
Erythema
marginatum
Erythrocyte sedimentation
rate
Elevated or increasing
streptococcal antibody
titer
Subcutaneous
nodules
C-reactive protein
Chorea Prolonged PR interval
2020 Updated Australian criteria for ARF diagnosis
HIGH-RISK GROUPS LOW-RISK GROUPS
Definite initial episode of ARF2 major manifestations + evidence of preceding Strep A infection, or 1 major + 2 minor
manifestations + evidence of preceding Strep A infection
Definite recurrent§ episode of ARF in
a patient with a documented history of
ARF or RHD
2 major manifestations + evidence of preceding Strep A infection, or 1 major + 2 minor
manifestations + evidence of preceding Strep A infection‡ , or 3 minor manifestations + evidence
of a preceding Strep A infection‡
Probable or possible ARF (first
episode or recurrence§
A clinical presentation in which ARF is considered a likely diagnosis but falls short in meeting the
criteria by either:
• one major or one minor manifestation, or
• no evidence of preceding Strep A infection (streptococcal titres within normal limits or titres not
measured) Such cases should be further categorised according to the level of confidence with
which the diagnosis is made:
• Probable ARF (previously termed ‘probable: highly suspected’)
• Possible ARF (previously termed ‘probable: uncertain’)
Major manifestations Carditis (including subclinical evidence of
rheumatic valvulitis on echocardiogram)
Polyarthritis¶ or aseptic monoarthritis or
polyarthralgia Sydenham chorea†† Erythema
marginatum‡‡ Subcutaneous nodules
Carditis (including subclinical evidence of
rheumatic valvulitis on echocardiogram)
Polyarthritis¶ Sydenham chorea†† Erythema
marginatum‡‡ Subcutaneous nodules
Minor Manifestations Fever§§ ≥38°C Monoarthralgia¶¶ ESR ≥30 mm/h
or CRP ≥30 mg/L Prolonged P-R interval on ECG
Fever ≥38.5°C Polyarthralgia or aseptic
monoarthritis¶¶ ESR ≥60 mm/h or CRP ≥30
mg/L Prolonged P-R interval on ECG
HIGH-RISK GROUPS LOW-RISK GROUPS
Definite initial episode of ARF2 major manifestations + evidence of preceding Strep A infection, or 1 major + 2 minor
manifestations + evidence of preceding Strep A infection
Definite recurrent§ episode of ARF in
a patient with a documented history of
ARF or RHD
2 major manifestations + evidence of preceding Strep A infection, or 1 major + 2 minor
manifestations + evidence of preceding Strep A infection‡ , or 3 minor manifestations + evidence
of a preceding Strep A infection‡
Probable or possible ARF (first
episode or recurrence§
A clinical presentation in which ARF is considered a likely diagnosis but falls short in meeting the
criteria by either:
• one major or one minor manifestation, or
• no evidence of preceding Strep A infection (streptococcal titres within normal limits or titres not
measured) Such cases should be further categorised according to the level of confidence with
which the diagnosis is made:
• Probable ARF (previously termed ‘probable: highly suspected’)
• Possible ARF (previously termed ‘probable: uncertain’)
Major manifestations Carditis (including subclinical evidence of
rheumatic valvulitis on echocardiogram)
Polyarthritis¶ or aseptic monoarthritis or
polyarthralgia Sydenham chorea†† Erythema
marginatum‡‡ Subcutaneous nodules
Carditis (including subclinical evidence of
rheumatic valvulitis on echocardiogram)
Polyarthritis¶ Sydenham chorea†† Erythema
marginatum‡‡ Subcutaneous nodules
Minor Manifestations Fever§§ ≥38°C Monoarthralgia¶¶ ESR ≥30 mm/h
or CRP ≥30 mg/L Prolonged P-R interval on ECG
Fever ≥38.5°C Polyarthralgia or aseptic
monoarthritis¶¶ ESR ≥60 mm/h or CRP ≥30
mg/L Prolonged P-R interval on ECG
High-risk groups are those living in communities with high rates of ARF (incidence
>30/100,000 per year in 5–14-year-olds) or RHD (all-age prevalence >2/1000).
Recurrent definite, probable or possible ARF requires a time period of more than 90 days
after the onset of symptoms from the previous episode of definite, probable or possible
ARF.
A definite history of arthritis is sufficient to satisfy this manifestation. Note that if
polyarthritis is present as a major manifestation, polyarthralgia or aseptic monoarthritis
cannot be considered an additional minor manifestation in the same person.
Chorea does not require other manifestations or evidence of preceding Strep A infection,
provided other causes of chorea are excluded.
In high-risk groups, fever can be considered a minor manifestation based on a reliable
history (in the absence of documented temperature) if anti-inflammatory medication has
already been administered.
If polyarthritis is present as a major criterion, monoarthritis or arthralgia cannot be
considered an additional minor manifestation.
If carditis is present as a major manifestation, a prolonged P-R interval cannot be
considered an additional minor manifestation
>30/100,000 per year in 5–14-year-olds) or RHD (all-age prevalence >2/1000).
Recurrent definite, probable or possible ARF requires a time period of more than 90 days
after the onset of symptoms from the previous episode of definite, probable or possible
ARF.
A definite history of arthritis is sufficient to satisfy this manifestation. Note that if
polyarthritis is present as a major manifestation, polyarthralgia or aseptic monoarthritis
cannot be considered an additional minor manifestation in the same person.
Chorea does not require other manifestations or evidence of preceding Strep A infection,
provided other causes of chorea are excluded.
In high-risk groups, fever can be considered a minor manifestation based on a reliable
history (in the absence of documented temperature) if anti-inflammatory medication has
already been administered.
If polyarthritis is present as a major criterion, monoarthritis or arthralgia cannot be
considered an additional minor manifestation.
If carditis is present as a major manifestation, a prolonged P-R interval cannot be
considered an additional minor manifestation
Clinical & diagnosis…
1. Migratory polyarthritis
Occurs in about 75% of patients with ARF
Typically involves larger joints (knees, ankles, wrists, & elbows):
but involvement of the spine, small joints of the hands and feet,
or hips is uncommon.
Migratory, severely inflamed joints; arthritis typically not
deforming and has dramatic response to even small doses of
salicylates.
Synovial fluid in ARF usually has wbc=10,000-100,000 /mm3
with > neutrophils, a protein level of about 4
g/dL, a normal
glucose level.
Arthritis is the earliest manifestation & correlate with peak ASO
titers.
Inverse relationship between the severity of arthritis and the
severity of cardiac involvement.
1. Migratory polyarthritis
Occurs in about 75% of patients with ARF
Typically involves larger joints (knees, ankles, wrists, & elbows):
but involvement of the spine, small joints of the hands and feet,
or hips is uncommon.
Migratory, severely inflamed joints; arthritis typically not
deforming and has dramatic response to even small doses of
salicylates.
Synovial fluid in ARF usually has wbc=10,000-100,000 /mm3
with > neutrophils, a protein level of about 4
g/dL, a normal
glucose level.
Arthritis is the earliest manifestation & correlate with peak ASO
titers.
Inverse relationship between the severity of arthritis and the
severity of cardiac involvement.
Clinical & diagnosis…
2. Carditis
Carditis occurs in about 50-60% of all cases of ARF
Carditis is almost always associated with a murmur of
valvulitis
Most serious manifestation responsible for morbidity &
mortality
pancarditis
Tachycardia & cardiac murmurs
Cardiomegally and CHF
The major consequence of acute rheumatic carditis is chronic,
progressive valvular disease, particularly valvular stenosis,
which can require valve replacement.
2. Carditis
Carditis occurs in about 50-60% of all cases of ARF
Carditis is almost always associated with a murmur of
valvulitis
Most serious manifestation responsible for morbidity &
mortality
pancarditis
Tachycardia & cardiac murmurs
Cardiomegally and CHF
The major consequence of acute rheumatic carditis is chronic,
progressive valvular disease, particularly valvular stenosis,
which can require valve replacement.
Clinical & diagnosis…
3. Chorea
Occur in 10-15% of ARF
Presents as an isolated, frequently subtle, neurologic behavior disorder.
Emotional lability, incoordination, poor school performance,
uncontrollable movements, and facial grimacing, exacerbated by stress
and disappearing with sleep, are characteristic
Occasionally unilateral.
Clinical maneuvers;
a)milkmaid's grip (irregular contractions of the muscles of the hands while
squeezing the examiner's fingers),
b) spooning and pronation of the hands when the patient's arms are extended,
c) Wormian darting movements of the tongue upon protrusion, and
d) examination of handwriting to evaluate fine motor movements
3. Chorea
Occur in 10-15% of ARF
Presents as an isolated, frequently subtle, neurologic behavior disorder.
Emotional lability, incoordination, poor school performance,
uncontrollable movements, and facial grimacing, exacerbated by stress
and disappearing with sleep, are characteristic
Occasionally unilateral.
Clinical maneuvers;
a)milkmaid's grip (irregular contractions of the muscles of the hands while
squeezing the examiner's fingers),
b) spooning and pronation of the hands when the patient's arms are extended,
c) Wormian darting movements of the tongue upon protrusion, and
d) examination of handwriting to evaluate fine motor movements
Clinical & diagnosis…
4. Erythema Marginatum
It is a rare (<3% of patients with acute rheumatic fever) but characteristic
rash of acute rheumatic fever.
It consists of erythematous, serpiginous, macular lesions with pale
centers that are not pruritic. It occurs primarily on the trunk and
extremities, but not on the face, and it can be accentuated by warming
the skin. It is usually associated with carditis.
4. Erythema Marginatum
It is a rare (<3% of patients with acute rheumatic fever) but characteristic
rash of acute rheumatic fever.
It consists of erythematous, serpiginous, macular lesions with pale
centers that are not pruritic. It occurs primarily on the trunk and
extremities, but not on the face, and it can be accentuated by warming
the skin. It is usually associated with carditis.
Clinical & diagnosis…
5. Subcutaneous Nodules
It is rare (≤1% of patients with ARF)
Consist of firm nodules approximately 1
cm in
diameter along the extensor surfaces of tendons
near bony prominences.
Associated with significant RHD.
5. Subcutaneous Nodules
It is rare (≤1% of patients with ARF)
Consist of firm nodules approximately 1
cm in
diameter along the extensor surfaces of tendons
near bony prominences.
Associated with significant RHD.
Clinical & diagnosis…
Minor manifestations
Two clinical:
Arthralgia in the absence of polyarthrtis & fever
temperature > 102°F occurring early in the
course of the illness.
Two laboratory:
Elevated acute phase reactants and prolonged P-
R interval
Minor manifestations
Two clinical:
Arthralgia in the absence of polyarthrtis & fever
temperature > 102°F occurring early in the
course of the illness.
Two laboratory:
Elevated acute phase reactants and prolonged P-
R interval
Treatment
Anti-inflammatory agents (e.g., salicylates, corticosteroids) should
be withheld if arthralgia or atypical arthritis is the only clinical
manifestation of presumed acute rheumatic fever
Patients with typical migratory polyarthritis and those with carditis
without cardiomegaly or congestive heart failure should be treated
with oral salicylates.
The usual dose of aspirin is 100
mg/kg/day in 4 divided doses PO
for 3-5 days, followed by 75
mg/kg/day in 4 divided doses PO for
4
wk.
Patients with carditis and cardiomegaly or congestive heart failure
should receive corticosteroids.
The usual dose of prednisone is 2
mg/kg/day in 4 divided doses for
2-3
wk followed by a tapering of the dose that reduces the dose by
5
mg/24 hr every 2-3 days
Anti-inflammatory agents (e.g., salicylates, corticosteroids) should
be withheld if arthralgia or atypical arthritis is the only clinical
manifestation of presumed acute rheumatic fever
Patients with typical migratory polyarthritis and those with carditis
without cardiomegaly or congestive heart failure should be treated
with oral salicylates.
The usual dose of aspirin is 100
mg/kg/day in 4 divided doses PO
for 3-5 days, followed by 75
mg/kg/day in 4 divided doses PO for
4
wk.
Patients with carditis and cardiomegaly or congestive heart failure
should receive corticosteroids.
The usual dose of prednisone is 2
mg/kg/day in 4 divided doses for
2-3
wk followed by a tapering of the dose that reduces the dose by
5
mg/24 hr every 2-3 days
Treatment
At the beginning of the tapering of the prednisone dose, aspirin
should be started at 75
mg/kg/day in 4 divided doses for 6 wk.
Supportive therapies for patients with moderate to severe carditis
include digoxin, fluid and salt restriction, diuretics, and oxygen.
The cardiac toxicity of digoxin is enhanced with myocarditis.
Anti-inflammatory agents are usually not indicated in chorea.
Sedatives may be helpful early in the course of chorea;
For mild cases no need to treat
Supportive measures plus anticonvulsant therapy with
carbamazepine or sodium valproate for moderate and sever cases.
Some clinicians add risperidone or haloperidol when the response
to anticonvulsant therapy is poor, but the evidence base is limited
At the beginning of the tapering of the prednisone dose, aspirin
should be started at 75
mg/kg/day in 4 divided doses for 6 wk.
Supportive therapies for patients with moderate to severe carditis
include digoxin, fluid and salt restriction, diuretics, and oxygen.
The cardiac toxicity of digoxin is enhanced with myocarditis.
Anti-inflammatory agents are usually not indicated in chorea.
Sedatives may be helpful early in the course of chorea;
For mild cases no need to treat
Supportive measures plus anticonvulsant therapy with
carbamazepine or sodium valproate for moderate and sever cases.
Some clinicians add risperidone or haloperidol when the response
to anticonvulsant therapy is poor, but the evidence base is limited
Complication
The arthritis and chorea of acute rheumatic fever resolve
completely without sequelae. Therefore, the long-term
sequelae of rheumatic fever are usually limited to the heart.
Approximately 70% of patients with carditis during the
initial episode of acute rheumatic fever recover with no
residual heart disease; the more severe the initial cardiac
involvement, the greater the risk is for residual heart
disease.
The arthritis and chorea of acute rheumatic fever resolve
completely without sequelae. Therefore, the long-term
sequelae of rheumatic fever are usually limited to the heart.
Approximately 70% of patients with carditis during the
initial episode of acute rheumatic fever recover with no
residual heart disease; the more severe the initial cardiac
involvement, the greater the risk is for residual heart
disease.
Prevention
Primary prophylaxis: Appropriate antibiotic therapy before the
9th day of symptoms of acute GAS pharyngitis is highly effective in
preventing 1st attacks of ARF
About 30% of patients with acute rheumatic fever do not recall a
preceding episode of pharyngitis.
Secondary prophylaxis: continuous antibiotic prophylaxis, which
should begin as soon as the diagnosis of acute rheumatic fever has
been made and immediately after a full course of antibiotic therapy
has been completed.
Benzanthine pencillin G 600,000IU IM for < 27kg
1.2million IU for >27kg
Cotrimoxazole or Erythromycine/azithromax for pencillin allergy
Primary prophylaxis: Appropriate antibiotic therapy before the
9th day of symptoms of acute GAS pharyngitis is highly effective in
preventing 1st attacks of ARF
About 30% of patients with acute rheumatic fever do not recall a
preceding episode of pharyngitis.
Secondary prophylaxis: continuous antibiotic prophylaxis, which
should begin as soon as the diagnosis of acute rheumatic fever has
been made and immediately after a full course of antibiotic therapy
has been completed.
Benzanthine pencillin G 600,000IU IM for < 27kg
1.2million IU for >27kg
Cotrimoxazole or Erythromycine/azithromax for pencillin allergy
Prevention…
Duration of secondary prophylaxis
CATEGORY DURATION
Rheumatic fever without carditis
5
yr or until 21 yr of age, whichever is
longer
Rheumatic fever with carditis but
without residual heart disease (no
valvular disease*)
10
yr or until 21 yr of age, whichever
is longer
Rheumatic fever with carditis and
residual heart disease (persistent
valvular disease*)
10
yr or until 40 yr of age, whichever
is longer, sometimes lifelong
prophylaxis
Duration of secondary prophylaxis
CATEGORY DURATION
Rheumatic fever without carditis
5
yr or until 21 yr of age, whichever is
longer
Rheumatic fever with carditis but
without residual heart disease (no
valvular disease*)
10
yr or until 21 yr of age, whichever
is longer
Rheumatic fever with carditis and
residual heart disease (persistent
valvular disease*)
10
yr or until 40 yr of age, whichever
is longer, sometimes lifelong
prophylaxis
RHEUMATIC HEART DISEASES
Rheumatic heart diseases
It is the result of rheumatic fever.
The mitral valve is affected most often, followed in frequency by
the aortic valve;
Right-sided heart manifestations are rare.
As the inflammation subsides, the verrucae tend to disappear and
leave scar tissue.
With repeated attacks of rheumatic fever, new verrucae form near
the previous ones, and the mural endocardium and chordae
tendineae become involved.
It is the result of rheumatic fever.
The mitral valve is affected most often, followed in frequency by
the aortic valve;
Right-sided heart manifestations are rare.
As the inflammation subsides, the verrucae tend to disappear and
leave scar tissue.
With repeated attacks of rheumatic fever, new verrucae form near
the previous ones, and the mural endocardium and chordae
tendineae become involved.
RHD, Mitral insufficiency
Pathophysiology:
MR is the result of structural changes some loss of valvular substance
and shortening and thickening of the chordae tendineae.
Back flow blood from LV to LA during systole
The left atrium dilates as blood regurgitates into this chamber.
Pulmonary congestion and symptoms of left-sided heart failure.
Spontaneous improvement usually occurs with time.
The lesion is most often mild or moderate.
Patients can be asymptomatic.
In patients with severe chronic mitral insufficiency, pulmonary arterial
pressure becomes elevated, the right ventricle and atrium become
enlarged, and right-sided heart failure subsequently develops.
Pathophysiology:
MR is the result of structural changes some loss of valvular substance
and shortening and thickening of the chordae tendineae.
Back flow blood from LV to LA during systole
The left atrium dilates as blood regurgitates into this chamber.
Pulmonary congestion and symptoms of left-sided heart failure.
Spontaneous improvement usually occurs with time.
The lesion is most often mild or moderate.
Patients can be asymptomatic.
In patients with severe chronic mitral insufficiency, pulmonary arterial
pressure becomes elevated, the right ventricle and atrium become
enlarged, and right-sided heart failure subsequently develops.
RHD, Mitral insufficiency..
Clinical manifestation:
Depends on its severity
High holo systolic murmur at apex which radiates to axilla
CHF in sever cases
Accentuated second heart sound when pulmonary HTN.
CXR = prominent Lt atrium
ECG= Lt ventricular hypertrophy, prominent bifid p waves.
Echocardiography
Enlargement of the left atrium and ventricle, an abnormally
thickened mitral valve,
and Doppler studies demonstrate the severity of the mitral
regurgitation.
Clinical manifestation:
Depends on its severity
High holo systolic murmur at apex which radiates to axilla
CHF in sever cases
Accentuated second heart sound when pulmonary HTN.
CXR = prominent Lt atrium
ECG= Lt ventricular hypertrophy, prominent bifid p waves.
Echocardiography
Enlargement of the left atrium and ventricle, an abnormally
thickened mitral valve,
and Doppler studies demonstrate the severity of the mitral
regurgitation.
RHD, Mitral insufficiency
Treatment:
Mild mitral insufficiency, prophylaxis against recurrences of rheumatic
fever.
Prophylaxis against bacterial endocarditis is warranted for dental
procedures
Treatment of complicating heart failure, arrhythmias and infective
endocarditis.
Afterload-reducing agents (ACE inhibitors or angiotensin receptor
blockers) may reduce the regurgitant volume and preserve left ventricular
function.
Surgical treatment is indicated for patients who despite adequate medical
therapy have persistent heart failure, often with pulmonary hypertension
Treatment:
Mild mitral insufficiency, prophylaxis against recurrences of rheumatic
fever.
Prophylaxis against bacterial endocarditis is warranted for dental
procedures
Treatment of complicating heart failure, arrhythmias and infective
endocarditis.
Afterload-reducing agents (ACE inhibitors or angiotensin receptor
blockers) may reduce the regurgitant volume and preserve left ventricular
function.
Surgical treatment is indicated for patients who despite adequate medical
therapy have persistent heart failure, often with pulmonary hypertension
RHD, Mitral stenosis
Pathophysiology:
Mitral stenosis is a result of
Fibrosis of the mitral ring,
Commissural adhesions,
And contracture of the valve leaflets, chordae, and papillary muscles
over time.
It usually takes ≥10
yr for the lesion to become fully established.
Rarely occur before adolescent and it usually seen in adults.
Significant mitral stenosis results in:
Increased pressure and enlargement & hypertrophy of the LA
Pulmonary venous hypertension, pulmonary hypertension.
tricuspid regurgitation, and clinical signs of right-sided heart failure.
Pathophysiology:
Mitral stenosis is a result of
Fibrosis of the mitral ring,
Commissural adhesions,
And contracture of the valve leaflets, chordae, and papillary muscles
over time.
It usually takes ≥10
yr for the lesion to become fully established.
Rarely occur before adolescent and it usually seen in adults.
Significant mitral stenosis results in:
Increased pressure and enlargement & hypertrophy of the LA
Pulmonary venous hypertension, pulmonary hypertension.
tricuspid regurgitation, and clinical signs of right-sided heart failure.
RHD, Mitral stenosis
Clinical manifestations:
Mild lesions are asymptomatic
Sever degree of obstruction & exercise intolerance and dyspnea.
Critical lesions can result in orthopnea PND, and overt pulmonary
edema, as well as atrial arrhythmias.
Pulmonary HTN
Functional tricuspid insufficiency.
Hemoptysis : rupture of bronchial or pleurohilar veins and/ or by
pulmonary infarction
Atrial fibrilation, heart failure and cardiomegaly.
Opening snap, low pitched, rumbling diastolic murmur.
Holosystolic murmur due to TR.
Clinical manifestations:
Mild lesions are asymptomatic
Sever degree of obstruction & exercise intolerance and dyspnea.
Critical lesions can result in orthopnea PND, and overt pulmonary
edema, as well as atrial arrhythmias.
Pulmonary HTN
Functional tricuspid insufficiency.
Hemoptysis : rupture of bronchial or pleurohilar veins and/ or by
pulmonary infarction
Atrial fibrilation, heart failure and cardiomegaly.
Opening snap, low pitched, rumbling diastolic murmur.
Holosystolic murmur due to TR.
RHD, Mitral stenosis
Clinical manifestations:
pulmonary hypertension, the pulmonic component of the 2nd heart sound is
accentuated.
An early diastolic murmur of rheumatic aortic insufficiency or pulmonary
valvular insufficiency secondary to pulmonary hypertension.
EKG may be normal in mild cases, Prominent & notched P wave, RV
hypertrophy, lately atrial fibrilation.
CXR- signs of atrial enlargement, calcifications may be seen.
Echo - shows thickening of the mitral valve, distinct narrowing of the mitral
orifice during diastole and left atrial enlargement.
Treatment :
Manage CHF if there is sever obstruction
Surgical valvotomy or
Balloon catheter mitral valvuloplasty
Clinical manifestations:
pulmonary hypertension, the pulmonic component of the 2nd heart sound is
accentuated.
An early diastolic murmur of rheumatic aortic insufficiency or pulmonary
valvular insufficiency secondary to pulmonary hypertension.
EKG may be normal in mild cases, Prominent & notched P wave, RV
hypertrophy, lately atrial fibrilation.
CXR- signs of atrial enlargement, calcifications may be seen.
Echo - shows thickening of the mitral valve, distinct narrowing of the mitral
orifice during diastole and left atrial enlargement.
Treatment :
Manage CHF if there is sever obstruction
Surgical valvotomy or
Balloon catheter mitral valvuloplasty
RHD, Aortic insufficiency
Sclerosis of the aortic valve results in distortion & retraction of
the cusps.
Regurgitation of blood – Volume over load to LV results in
dilatation & Hypertrophy.
Combined MR & AR is common than AR alone.
Clinical manifestation:
Asymptomatic
palpitation due to large SV & forceful contraction.
Sweating & heat intolerance due to excessive vasodilation.
Dyspnea, orthopnea, pulmonary edema.
Angina precipitated by heavy exercise.
Nocturnal attacks with sweating, tachycardia, chest pain, and
hypertension may occur
Sclerosis of the aortic valve results in distortion & retraction of
the cusps.
Regurgitation of blood – Volume over load to LV results in
dilatation & Hypertrophy.
Combined MR & AR is common than AR alone.
Clinical manifestation:
Asymptomatic
palpitation due to large SV & forceful contraction.
Sweating & heat intolerance due to excessive vasodilation.
Dyspnea, orthopnea, pulmonary edema.
Angina precipitated by heavy exercise.
Nocturnal attacks with sweating, tachycardia, chest pain, and
hypertension may occur
RHD, Aortic insufficiency
Clinical manifestation…
Wide pulse pressure with bounding peripheral pulse
Sever AR enlarged heart with LV apical heave.
Diastolic thrill
Austin Flint murmur- Heard as result of the large regurgitant
aortic flow in diastole preventing the mitral valve from
opening fully.
CXR- enlarged LV and aorta
ECG- LV hypertrophy with prominent P waves
Echo- shows a large LV and diastolic mitral valve flutter or
oscillation caused by regurgitant flow hitting the valve leaflets
Clinical manifestation…
Wide pulse pressure with bounding peripheral pulse
Sever AR enlarged heart with LV apical heave.
Diastolic thrill
Austin Flint murmur- Heard as result of the large regurgitant
aortic flow in diastole preventing the mitral valve from
opening fully.
CXR- enlarged LV and aorta
ECG- LV hypertrophy with prominent P waves
Echo- shows a large LV and diastolic mitral valve flutter or
oscillation caused by regurgitant flow hitting the valve leaflets
RHD, Aortic insufficiency
Prognosis:
Mild & moderate lesions are well tolerated.
AR does not regress unlike MR
Pts with combined lesions during acute attack of ARF may
have aortic involvement only 1-2yrs later.
Treatment:
After load reducers (ACE inhibitors)
Prophylaxis against recurrence of ARF
Surgery – valve replacement- advanced heart failure,
pulmonary edema, angina, when myocardial performance
decreased.
Prognosis:
Mild & moderate lesions are well tolerated.
AR does not regress unlike MR
Pts with combined lesions during acute attack of ARF may
have aortic involvement only 1-2yrs later.
Treatment:
After load reducers (ACE inhibitors)
Prophylaxis against recurrence of ARF
Surgery – valve replacement- advanced heart failure,
pulmonary edema, angina, when myocardial performance
decreased.
INFECTIVE ENDOCARDITIS
Definition
Infective endocarditis - is an infection of the endocardial
surface of the heart.
Although heart valves are most often involved, the wall of
the heart may be involved
Patients with prosthetic valves and other foreign materials
are particularly susceptible.
Infective endarteritis - the infectious process involving
arteriovenous shunts, arterioarterial shunts (PDA), or COA.
Classification as acute or subacute not advised (obsolete).
Better classification based on etiologic agent.
Infective endocarditis - is an infection of the endocardial
surface of the heart.
Although heart valves are most often involved, the wall of
the heart may be involved
Patients with prosthetic valves and other foreign materials
are particularly susceptible.
Infective endarteritis - the infectious process involving
arteriovenous shunts, arterioarterial shunts (PDA), or COA.
Classification as acute or subacute not advised (obsolete).
Better classification based on etiologic agent.
Infective….
Etiology
Commonest etiology in children includes..
- Viridians type strepts/ alpha hemolytic usu. occur after
dental procedure.
- Staph. aureus – with no underlying cardiac lesion.
- HACEK,(haemophilus sp. Actinobacilus,
cardiobactrium,Ekinell, kinegella)
- Group D enterococci.
- Pseudomonas A.& serratia m. - iv. drug users
- Fungi , caugulase negative staph.
Etiology
Commonest etiology in children includes..
- Viridians type strepts/ alpha hemolytic usu. occur after
dental procedure.
- Staph. aureus – with no underlying cardiac lesion.
- HACEK,(haemophilus sp. Actinobacilus,
cardiobactrium,Ekinell, kinegella)
- Group D enterococci.
- Pseudomonas A.& serratia m. - iv. drug users
- Fungi , caugulase negative staph.
Infective…..
Epidemiology
Endocarditis takes place on normal and abnormal heart
valves, and on congenitally abnormal hearts.
Only highly virulent bacteria, e.g. S. aureus, infect normal
valves.
Low virulence, oral and skin microorganisms are more
likely to cause infection on abnormal valves (e.g. Viridans
streptococci and coagulase negative staphylococci).
Prosthetic valves are most susceptible and may be infected by all of the
above organisms in addition to bacteria attaching to the valve at the
time of its insertion.
Epidemiology
Endocarditis takes place on normal and abnormal heart
valves, and on congenitally abnormal hearts.
Only highly virulent bacteria, e.g. S. aureus, infect normal
valves.
Low virulence, oral and skin microorganisms are more
likely to cause infection on abnormal valves (e.g. Viridans
streptococci and coagulase negative staphylococci).
Prosthetic valves are most susceptible and may be infected by all of the
above organisms in addition to bacteria attaching to the valve at the
time of its insertion.
High risk
- prosthetic heart valves.
- previous endocarditis
- complex cyanotic CHD TGA,TOF, single ventricle
- systemic to pulmonary artery shunts
Moderate risk pts
-Most other congenital heart diseases (not included in high &
negligible risk)
-Acquired valve dysfunction( RHD)
-HCM
Negligible risk pts
-Isolated ASD,
-Surgical repair of ASD,VSD, PDA
- prosthetic heart valves.
- previous endocarditis
- complex cyanotic CHD TGA,TOF, single ventricle
- systemic to pulmonary artery shunts
Moderate risk pts
-Most other congenital heart diseases (not included in high &
negligible risk)
-Acquired valve dysfunction( RHD)
-HCM
Negligible risk pts
-Isolated ASD,
-Surgical repair of ASD,VSD, PDA
Infective…..
Pathogenesis:
Formation of vegetations reflects two pathogenic
mechanisms
-hypercoagulability
-endothelial damage
Bacterial adherence to the platelet-fibrin thrombus is a
critical factor for infective endocarditis.
In high pressure areas of blood flow
Adhere b/s of their specific products.
Emboli to the brain, kidney, spleen, skin etc…
Pathogenesis:
Formation of vegetations reflects two pathogenic
mechanisms
-hypercoagulability
-endothelial damage
Bacterial adherence to the platelet-fibrin thrombus is a
critical factor for infective endocarditis.
In high pressure areas of blood flow
Adhere b/s of their specific products.
Emboli to the brain, kidney, spleen, skin etc…
Infective ….
Clinical manifestation:
Symptoms include- fever, chills, chest & abdominal pain,
dyspnea, malaise, night sweats, weight loss, CNS
manifestations.
Signs include- raised tem, tachycardia, embolic
phenomenon, new or changing murmur, splenomegaly,
arthritis , heart failure , arrhythmias, metastatic infections,
clubbing
Clinical manifestation:
Symptoms include- fever, chills, chest & abdominal pain,
dyspnea, malaise, night sweats, weight loss, CNS
manifestations.
Signs include- raised tem, tachycardia, embolic
phenomenon, new or changing murmur, splenomegaly,
arthritis , heart failure , arrhythmias, metastatic infections,
clubbing
Infective…..
Investigations and Diagnosis:
- ESR, CRP, Hct, WBC, U/A,
- CXR, RFT,
- Echocardiography- location, size ,cardiac function,
intracardiac complications.
- Complement levels
Diagnosis of infective endocarditis is based on certain
criteria.
The parameters in the criteria include :
Investigations and Diagnosis:
- ESR, CRP, Hct, WBC, U/A,
- CXR, RFT,
- Echocardiography- location, size ,cardiac function,
intracardiac complications.
- Complement levels
Diagnosis of infective endocarditis is based on certain
criteria.
The parameters in the criteria include :
Infective….
Definite IE
Pathological criteria
Microorganisms: demonstrated by culture or histology in a
vegetation,
Pathological lesions: vegetation or intracardiac abscess present,
confirmed by histology showing active endocarditis.
Possible IE
Clinical criteria, using.
2 major criteria, or 1 major and 3 minor criteria, or
5 minor criteria
Findings consistent with IE that fall short of “Definite” but not
“Rejected
Definite IE
Pathological criteria
Microorganisms: demonstrated by culture or histology in a
vegetation,
Pathological lesions: vegetation or intracardiac abscess present,
confirmed by histology showing active endocarditis.
Possible IE
Clinical criteria, using.
2 major criteria, or 1 major and 3 minor criteria, or
5 minor criteria
Findings consistent with IE that fall short of “Definite” but not
“Rejected
Infective….
Rejected
Firm alternate diagnosis for manifestations of endocarditis, or
Resolution of manifestations of endocarditis with antibiotic
therapy for ≤4 days, or
No pathological evidence of IE at surgery or autopsy, after
antibiotic therapy for ≤ 4 days
Major criteria
1. Positive blood culture for IE
A. Typical microorganism consistent with IE from 2 separate
blood cultures as noted below:
Rejected
Firm alternate diagnosis for manifestations of endocarditis, or
Resolution of manifestations of endocarditis with antibiotic
therapy for ≤4 days, or
No pathological evidence of IE at surgery or autopsy, after
antibiotic therapy for ≤ 4 days
Major criteria
1. Positive blood culture for IE
A. Typical microorganism consistent with IE from 2 separate
blood cultures as noted below:
Infective ….
B. Microorganisms consistent with IE from persistently positive
blood cultures defined as
- (i) ≥ 2 positive cultures of blood samples drawn>12 hours apart
or
-(ii) all of 3 or a majority of ≥ 4 separate cultures of blood (with
first and last sample drawn ≥ 1 hour apart)
2. Evidence of endocardial involvement
A. Positive echocardiogram for IE
B. New valvular regurgitation (worsening or changing of
preexisting murmur not sufficient)
B. Microorganisms consistent with IE from persistently positive
blood cultures defined as
- (i) ≥ 2 positive cultures of blood samples drawn>12 hours apart
or
-(ii) all of 3 or a majority of ≥ 4 separate cultures of blood (with
first and last sample drawn ≥ 1 hour apart)
2. Evidence of endocardial involvement
A. Positive echocardiogram for IE
B. New valvular regurgitation (worsening or changing of
preexisting murmur not sufficient)
Infective ….
Minor criteria
1. Predisposition: Intravenous drug use, HD
2. Fever: temperature >38.0°
3. Vascular phenomena: major arterial emboli, septic emboli,
hemorrhage. Janeway lesions.
4. Immunologic phenomena: glomerulonephritis, Osler’s nodes,
Roth spots, and rheumatoid factor
5.Microbiological evidence: positive blood culture but does not meet
a major criterion
6. Echocardiographic findings: consistent with IE but do not meet a
major criterion
Minor criteria
1. Predisposition: Intravenous drug use, HD
2. Fever: temperature >38.0°
3. Vascular phenomena: major arterial emboli, septic emboli,
hemorrhage. Janeway lesions.
4. Immunologic phenomena: glomerulonephritis, Osler’s nodes,
Roth spots, and rheumatoid factor
5.Microbiological evidence: positive blood culture but does not meet
a major criterion
6. Echocardiographic findings: consistent with IE but do not meet a
major criterion
Infective…
Complications:
CHF
Embolization
Rupture of chordae tendinae or papillary muscle
Myocarditis
Valve ring abscess
Prognosis
Depends on early diagnosis & management
Despite use of antibiotic agents mortality remains 20-25% .
50-60% - serious morbidity.
Complications:
CHF
Embolization
Rupture of chordae tendinae or papillary muscle
Myocarditis
Valve ring abscess
Prognosis
Depends on early diagnosis & management
Despite use of antibiotic agents mortality remains 20-25% .
50-60% - serious morbidity.
Infective…
Treatment:
Within vegetations, organisms are embedded in very high
concentrations.
Relatively low rates of bacterial metabolism and cell division
decreased susceptibility to beta – lactam and other cell wall
active antibiotics.
Bactericidal rather than bacteriostatic antibiotics preferred
Complete eradication of the organisms requires 4 to 6 weeks of
antibiotic treatment.
Parenteral administration recommended.
Combination of antibiotics against the commonest offending
agents.
Treatment:
Within vegetations, organisms are embedded in very high
concentrations.
Relatively low rates of bacterial metabolism and cell division
decreased susceptibility to beta – lactam and other cell wall
active antibiotics.
Bactericidal rather than bacteriostatic antibiotics preferred
Complete eradication of the organisms requires 4 to 6 weeks of
antibiotic treatment.
Parenteral administration recommended.
Combination of antibiotics against the commonest offending
agents.
Infective…
Surgery with medical management: Indications
- Sever aortic or mitral valve involvement with refractory CHF.
- Uncontrolled infection despite optimal mgt.
- More than one serious embolic episode.
- Fungal endocarditis
- Local suppurative complications.
- Large vegetations (> 10mm) & increasing size of vegetation while on
treatment
Surgery with medical management: Indications
- Sever aortic or mitral valve involvement with refractory CHF.
- Uncontrolled infection despite optimal mgt.
- More than one serious embolic episode.
- Fungal endocarditis
- Local suppurative complications.
- Large vegetations (> 10mm) & increasing size of vegetation while on
treatment
Infective…
Prevention
Antimicrobial prophylaxis before various procedures.
Dental procedures
Dental and oral care
Amoxicillin 50mg/kg p.o. 30 to 60 min before procedure
(standard).
Ampicillin or cefazoline or ceftriaxone, IM or IV, if unable to take
oral medications.
Clindamycin or cephalexin or azithromycin or clarithromycin for
penicillin allergic patients.
Prevention
Antimicrobial prophylaxis before various procedures.
Dental procedures
Dental and oral care
Amoxicillin 50mg/kg p.o. 30 to 60 min before procedure
(standard).
Ampicillin or cefazoline or ceftriaxone, IM or IV, if unable to take
oral medications.
Clindamycin or cephalexin or azithromycin or clarithromycin for
penicillin allergic patients.
Diseases of myocardium & pericardium
Myocarditis
Acute or chronic inflammation of the myocardium is
characterized by inflammatory cell infiltrates, myocyte
necrosis, or myocyte degeneration
Caused by infectious, connective tissue, granulomatous,
toxic, or idiopathic processes
Etiologies
Viral- Coxsackievirus, enteroviruses, adenovirus,
parvovirus, Epstein-Barr virus, and cytomegalovirus are
the most common causative agents in children.
Bacterial- Less common, Diphtheria (common)
Acute or chronic inflammation of the myocardium is
characterized by inflammatory cell infiltrates, myocyte
necrosis, or myocyte degeneration
Caused by infectious, connective tissue, granulomatous,
toxic, or idiopathic processes
Etiologies
Viral- Coxsackievirus, enteroviruses, adenovirus,
parvovirus, Epstein-Barr virus, and cytomegalovirus are
the most common causative agents in children.
Bacterial- Less common, Diphtheria (common)
Myocarditis….
Pathophysiology:
Myocarditis is characterized by myocardial
inflammation, injury or necrosis, and ultimately fibrosis.
Cardiac enlargement and diminished systolic function
occur as a direct result of the myocardial damage.
Typical signs of congestive heart failure occur and may
progress rapidly to shock, atrial or ventricular
arrhythmias, and sudden death.
Viral myocarditis may also become a chronic process
with persistence of viral nucleic acid in the myocardium.
Pathophysiology:
Myocarditis is characterized by myocardial
inflammation, injury or necrosis, and ultimately fibrosis.
Cardiac enlargement and diminished systolic function
occur as a direct result of the myocardial damage.
Typical signs of congestive heart failure occur and may
progress rapidly to shock, atrial or ventricular
arrhythmias, and sudden death.
Viral myocarditis may also become a chronic process
with persistence of viral nucleic acid in the myocardium.
Myocarditis….
Clinical manifestation:
Infants and young children more often have a fulminant
presentation:
with fever, respiratory distress, tachycardia, hypotension,
gallop rhythm, and cardiac murmur.
Associated findings may include a rash or evidence of
end organ involvement such as hepatitis or aseptic
meningitis.
•Hepatic enlargement, peripheral edema, and pulmonary
findings such as wheezes or rales may be present in
patients with decompensated congestive heart failure.
Clinical manifestation:
Infants and young children more often have a fulminant
presentation:
with fever, respiratory distress, tachycardia, hypotension,
gallop rhythm, and cardiac murmur.
Associated findings may include a rash or evidence of
end organ involvement such as hepatitis or aseptic
meningitis.
•Hepatic enlargement, peripheral edema, and pulmonary
findings such as wheezes or rales may be present in
patients with decompensated congestive heart failure.
Myocarditis….
Diagnosis:
. CXR- cardiomegaly, pulmonary vascular prominence,
overt pulmonary edema, or pleural effusions
ECG
Echo- Cardiac chamber enlargement, mitral
insufficiency, and occasionally, evidence of pericardial
infusion.
Treatment: Diuretics, ACE inhibitors, and angiotensin
receptor blockers are of use in patients with
compensated congestive heart failure.
Diagnosis:
. CXR- cardiomegaly, pulmonary vascular prominence,
overt pulmonary edema, or pleural effusions
ECG
Echo- Cardiac chamber enlargement, mitral
insufficiency, and occasionally, evidence of pericardial
infusion.
Treatment: Diuretics, ACE inhibitors, and angiotensin
receptor blockers are of use in patients with
compensated congestive heart failure.
CARDIOMYOPATHY
•Disease of myocardium associated with cardiac
dysfunction.
•Myocardial dysfunction is not common early in the course
of majority of congenital heart diseases.
Etiologic
-primary or idiopathic
-secondary
Structural and functional abnormality
-Dilated cardiomyopathy
-Hypertrophic cardiomyopathy
-Restrictive cardiomyopathy
•Disease of myocardium associated with cardiac
dysfunction.
•Myocardial dysfunction is not common early in the course
of majority of congenital heart diseases.
Etiologic
-primary or idiopathic
-secondary
Structural and functional abnormality
-Dilated cardiomyopathy
-Hypertrophic cardiomyopathy
-Restrictive cardiomyopathy
CARDIOMYOPATHY….
•Dilated cardiomyopathy
•Commonest of all cardiomyopathies.
•Characterized by extensive dilatation and impaired
contraction of one or both ventricles.
•Varying degree of ventricular hypertrophy also present.
•Hemodynamics:
- increase systolic and diastolic volumes.
- decreased stroke volume.
- impaired systolic function.
- decreased ejection fraction
•Dilated cardiomyopathy
•Commonest of all cardiomyopathies.
•Characterized by extensive dilatation and impaired
contraction of one or both ventricles.
•Varying degree of ventricular hypertrophy also present.
•Hemodynamics:
- increase systolic and diastolic volumes.
- decreased stroke volume.
- impaired systolic function.
- decreased ejection fraction
CARDIOMYOPATHY…..
Etiology:
•Vast majority idiopathic:
• - 20% familial with AD, AR, X-linked, and
mitochondrial inheritance pattern.
• - 2-15% active myocarditis
•Infections- viral, bacterial, fungi, parasitic, ricketssial.
•Endocrine
•Metabolic
•Nutritional deficiencies
•Congenital and acquired abnormalities of coronary
artery.
Etiology:
•Vast majority idiopathic:
• - 20% familial with AD, AR, X-linked, and
mitochondrial inheritance pattern.
• - 2-15% active myocarditis
•Infections- viral, bacterial, fungi, parasitic, ricketssial.
•Endocrine
•Metabolic
•Nutritional deficiencies
•Congenital and acquired abnormalities of coronary
artery.
CARDIOMYOPATHY…..
•Clinical Manifestations:
•All age groups affected
•Onset- insidious and non specific like irritability,
anorexia, abdominal pain, cough
• - Infants and young children: respiratory
symptoms and failure to thrive.
• - Older children: nausea, anorexia
•P/E: -rales, wheezing,
•-cool and pale skin, feeble pulse, narrow pulse
pressure, tachycardia, raised JVP, hepatomegally,
edema, quite precordium, gallop and murmur of
MR or TR
•Clinical Manifestations:
•All age groups affected
•Onset- insidious and non specific like irritability,
anorexia, abdominal pain, cough
• - Infants and young children: respiratory
symptoms and failure to thrive.
• - Older children: nausea, anorexia
•P/E: -rales, wheezing,
•-cool and pale skin, feeble pulse, narrow pulse
pressure, tachycardia, raised JVP, hepatomegally,
edema, quite precordium, gallop and murmur of
MR or TR
CARDIOMYOPATHY…..
•Diagnosis:
•CXR- cardiomegally, pulmonary congestion
•ECG- combination of atrial enlargement, Left and right
ventricular hypertrophy.
•Echocardiography
- left atrium and ventricle dilatation,
- decreased ejection fraction
- Doppler studies- mitral regurgitation and decreased
flow velocity through aortic valve
- Pulmonary hypertension
•Myocardial biopsy
•PCR
•DNA study
•Diagnosis:
•CXR- cardiomegally, pulmonary congestion
•ECG- combination of atrial enlargement, Left and right
ventricular hypertrophy.
•Echocardiography
- left atrium and ventricle dilatation,
- decreased ejection fraction
- Doppler studies- mitral regurgitation and decreased
flow velocity through aortic valve
- Pulmonary hypertension
•Myocardial biopsy
•PCR
•DNA study
CARDIOMYOPATHY…..
Prognosis:
•Most have downhill course
•Complications include
- Ventricular arrhythmia: syncope and sudden death
- Pulmonary and systemic emboli
•Treatment
•Supportive (Vigorous treatment of heart failure gives
temporary remission, but relapse is common and in time
patients become resistant for therapy.)
- digoxine
- diuretics
- ACE inhibitors
- B-blockers - anticoagulants
-antiarrhythmic drugs - cardiac transplantation
Prognosis:
•Most have downhill course
•Complications include
- Ventricular arrhythmia: syncope and sudden death
- Pulmonary and systemic emboli
•Treatment
•Supportive (Vigorous treatment of heart failure gives
temporary remission, but relapse is common and in time
patients become resistant for therapy.)
- digoxine
- diuretics
- ACE inhibitors
- B-blockers - anticoagulants
-antiarrhythmic drugs - cardiac transplantation
CARDIOMYOPATHY…..
Hypertrophic cardiomyopathy
Restrictive cardiomyopathy
Hypertrophic cardiomyopathy
Restrictive cardiomyopathy
Diseases of the Pericardium….
•Acute Pericarditis:
•Inflammation of the pericardium may have only minor
pathophysiologic consequences in the absence of significant
fluid accumulation in the pericardial space.
•Clinical Manifestations:
•Sharp/stabbing chest pain most common, typically described as,
positional, radiating, worse with inspiration, and relieved by
sitting upright or prone.
•Cough, fever, dyspnea, abdominal pain, and vomiting are
nonspecific
•Signs and symptoms of organ system involvement.
•Muffled or distant heart sounds, tachycardia, narrow pulse
pressure, jugular venous distension, and a pericardial friction
rub provide clues to the diagnosis of acute pericarditis.
•Cardiac tamponade- Pulsus paradoxsus
•Acute Pericarditis:
•Inflammation of the pericardium may have only minor
pathophysiologic consequences in the absence of significant
fluid accumulation in the pericardial space.
•Clinical Manifestations:
•Sharp/stabbing chest pain most common, typically described as,
positional, radiating, worse with inspiration, and relieved by
sitting upright or prone.
•Cough, fever, dyspnea, abdominal pain, and vomiting are
nonspecific
•Signs and symptoms of organ system involvement.
•Muffled or distant heart sounds, tachycardia, narrow pulse
pressure, jugular venous distension, and a pericardial friction
rub provide clues to the diagnosis of acute pericarditis.
•Cardiac tamponade- Pulsus paradoxsus
Diseases of the Pericardium…
•Diagnosis:
ECG- abnormal though it is non specific
CXR- Significant effusion cardiac enlargement
Echo- is the most sensitive technique for identifying the size and
location of a pericardial effusion.
It differentiates pericarditis from myocarditis.
Purulent pericarditis.
Treatment-:
Supportive
Depends on the cause and system involved
Pericardiosynthesis for pericardial effusion.
•Diagnosis:
ECG- abnormal though it is non specific
CXR- Significant effusion cardiac enlargement
Echo- is the most sensitive technique for identifying the size and
location of a pericardial effusion.
It differentiates pericarditis from myocarditis.
Purulent pericarditis.
Treatment-:
Supportive
Depends on the cause and system involved
Pericardiosynthesis for pericardial effusion.
Diseases of the Pericardium….
Constrictive pericarditis:
Chronic pericardial inflammation can result in fibrosis,
calcification, and thickening of the pericardium.
Pericardial scarring may lead to impaired cardiac distensibility
and filling and is termed constrictive pericarditis.
Constrictive pericarditis can occur following ;
recurrent or chronic pericarditis,
cardiac surgery, or
radiation to the mediastinum as a treatment for malignancies
systemic venous hypertension predominate.
A pericardial knock, rub, and distant heart sounds might be
heard
Constrictive pericarditis:
Chronic pericardial inflammation can result in fibrosis,
calcification, and thickening of the pericardium.
Pericardial scarring may lead to impaired cardiac distensibility
and filling and is termed constrictive pericarditis.
Constrictive pericarditis can occur following ;
recurrent or chronic pericarditis,
cardiac surgery, or
radiation to the mediastinum as a treatment for malignancies
systemic venous hypertension predominate.
A pericardial knock, rub, and distant heart sounds might be
heard
Diseases of the Pericardium
Constrictive pericarditis may be difficult to distinguish
clinically from restrictive cardiomyopathy as both
conditions result in impaired myocardial filling.
Echo is important to differentiate, CT and MRI are very
much sensitive in the diagnosis of pericardial dieases.
typical chronic constrictive pericarditis will respond only to
surgical pericardiectomy with extensive resection of the
pericardium though acute constriction responds to
antiinflammatory agents
Constrictive pericarditis may be difficult to distinguish
clinically from restrictive cardiomyopathy as both
conditions result in impaired myocardial filling.
Echo is important to differentiate, CT and MRI are very
much sensitive in the diagnosis of pericardial dieases.
typical chronic constrictive pericarditis will respond only to
surgical pericardiectomy with extensive resection of the
pericardium though acute constriction responds to
antiinflammatory agents
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