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INFECTIOUS DISEASE AND HEART VALVE

DISEASE.

By 14B
Zulherman
Ikrima Ainal Qalbi
Wulan Purnama Sari
Nurul Trisna Muchtar
Puji Aulia Zani
Ridhatul
Afifah Ikhwan
Vani Morina
Fatmi Eka Putri

from the throat to the heart

Teri boy five years old his mother brought to Pukesmas because of
shortness of breath, and breathing sounds from a few days ago. history
showed that his son had a fever since three days ago, looked very tired and
did not want to eat because of a sore throat. teri never immunized.
obtained from the examination of heart sounds weak and irregular. doctor
explained to her that the anchovies should immediately refer to the
hospital.
ECG results obtained, the PR interval lengthens. in the hospital, the mother
saw the child with anchovies cardiac abnormalities with different
symptoms, namely joint pain to move.
how you explain as a doctor?

terminology
Stridor :is an abnormal, high-pitched, musical

breathing sound. It is caused by a blockage in the

throat or voice box (larynx). It is most often heard
when taking in a breath.
Retraction:interested state backward.
PR interval : The PR Interval indicates AV
conduction time.

questions
why teri shortness of breath and wheezing since 3 days ago?
interpretation of history?
relationship situation with no immunization?
interpretation of physical examination and examination of

the heart?
Interpretation of EKG?
whether abnormalities of the heart together with the
children in addition?
why pain in the joints move?
working diagnosis for teri and next friend?

1. breathlessO2. blood supply

obtruction of respiratory
tract.
uncomfortable in
breathing.

Infeksieksudatblock the
respiratory tractO2
2.fever infection ISPAthroat become sore

not eatingtired

Lactat acid

3.has relation. susceptible

4. retraction because of respiratory muscles is

assisted by a respirator with a maximum.

5. heart valve disease.
long PR interval : mitral valve vegetation ->
inhibitory power the SA node to AV node.
6.because its autoimmune disease
7.no.. Teridifteri miocarditis
others child rheumatic fever

scheme
infectio
n
no
difteri
immunization

difteri

Teri 5th

faringitis

-fever
breathless
-stridor
-cianosys
retraction

Heart
valve
PJB

Rheumatic
fever

Joint
pain

Anak
lain
autoimun

Learning Objective
1. abnormalities in heart valves
2. infectious diseases of heart

MITRAL STENOSIS

Mitral Stenosis

Mitral valve is present between LA & LV

Normal mitral valve orifice area (MVA): 4-6cm2
MVA <2.5cm2 leads to symptoms
Decrease in Mitral valve orifice area leading to chronic & fixed mechanical
obstruction to LV filling is termed as MS.

Causes

Rheumatic Heart disease

SLE
Carcinoid syndrome
Active Infective Endocarditis
Left atrial myxoma
Congenital mitral stenosis
Massive Annular Calcification

Rheumatic mitral stenosis

More common in females (2/3rd of all pts)

Symptoms occur two decades after onset of Rheumatic fever
Age of presentation
Earlier in 20s-30s
Now in 40s-50s (slower progression)
Isolated MS in 40% cases of RHD
Remaining 60% cases associated with other valvular diseases- MR/AR

Patho-physiology

Immunological disorder initiated by Group A beta hemolytic streptococcus.

Antibodies produced against streptococcal cell wall proteins & sugars react
with connective tissues & heart; result in rheumatic fever and symptoms like
Carditis
Arthritis
Subcutaneous nodules
Chorea
Erythema marginatum

Chronic cardiac & valvular inflammation leads to cardiac & valvular

pathology

Rheumatic fever involving mitral valves

Valve leaflet thickening and fusion of commissures
Increased rigidity of valve leaflets
Thickening, fusion and contracture of chordae & papillary heads
Leaflet calcification (long standing MS)
Progressive reduction in mitral valve orifice area
Mitral Stenosis

Mechanical obstruction to left ventricular diastolic filling

Adaptative in LAP to maintain LV filling
------------------------------------------------------------------------LA enlargement

Atrial fibrillation

in pulmonary venous pressure in pulmonary arterial pressure*

Transudation of fluid into pulmonary interstitial space

Thrombus formation
Systemic thrombo-embolism
Work of breathing

ed pulmonary compliance

Progressive dyspnoea on exertion/rest

Acute conditions like AF, Pregnancy, Pain, sepsis
( HR/CO)
Acute in LAP

Pulmonary edema

in pulmonary arterial pressure*-------- Pulmonary arterial hypertrophy ( Pulmonary HTN)

RV hypertrophy and dilatation

RV failure

Effect of heart rate

Tachycardia shortens diastole more proportionately than systole

Decreases the overall time for transmitral flow,
In order to maintain CO, the flow rate per unit time must increase
Pressure gradient increase proportionate to square of flow rate
LAP Pulmonary venous congestion and symptoms.
So, patients with MS do not tolerate tachycardia.

Effect of Atrial fibrillation in

MS

Increased chances of thrombus formation & systemic thrombo-embolism

Normally effective atrial contraction is important in LV diastolic filling
In presence of AF
Loss of effective atrial contraction
ed ventricular rate (ed diastolic filling time)

Impaired LV filling (ed LV preload)

decreased cardiac output

Diagnosis
Clinical presentation
Dyspnea, fatigue, orthopnea, PND, cough, hemoptysis,.
10% patients have anginal type chest pain not attributable to CAD
Systemic thromboembolism (first symptom in 20% cases).

Physical examination
Low volume pulse
Sign & Symptoms of right sided heart failure - engorged neck veins,
enlarged tender liver

 Mitral facies
Pink purple patches on the cheeks, cyanotic skin changes from
cardiac output

Cardiac auscultation
Opening snap
Rumbling diastolic murmur best heard at apex radiating to the axilla
Loud S2: pulmonary hypertension

low

 ECG
Broad notched P
wave (left atrial
enlargement)

Atrial fibrillation

 Chest X-ray
Normal to ed cardiac
shadow
Straightening of the left heart
of border and elevation of left
main bronchus (left atrial
enlargement)
mitral calcification
Evidence of pulmonary
edema/ HTN

LAA: Left atrial appendages, MPA: Main pulmonary artery, LPA: left
pulmonary artery, RPA: Right pulmonary artery, Ao- Aortic
knuckle (Ao)

 Echocardiography
Anatomy/size of mitral valve & its appendages
severity of MS (area of orifice)
Size & function of ventricles
Estimation of pulmonary artery pressure

Cardiac catheterization and invasive

measurement
Are almost never necessary
Reserved for situations ECHO sub-optimal/conflict with clinical
presentation

Guidelines
Symptomatic MS (progressive dyspnoea on exertion, exertional pre-syncope,
heart failure) is an active cardiac condition & pt should undergo evaluation
& treatment before non cardiac surgery

Emergency surgery
Mild / Moderate MS

High risk
Continue medication
Proceed with surgery
Severe MS

Very high risk consent

Post- op ventilatory consent

Pre-operative Optimization of patient

Atrial fibrillation
Sinus rhythm/control of ventricular rate

1. Digoxin (emergent IV digitalization:- loading dose

0.25mg iv over 15 minutes followed by 0.1mg every
hour till response occur or total dose of 0.5-1.0mg.
Monitor ECG, BP, CVP; HR <60bpm- Stop)
2. CCB (verapamil/diltiazem: 0.075-0.15mg/kg IV)
3. -blocker (esmolol: 1mg IV)
4. Amiodarone (loading: 100mg IV, infusion: 1mg/min
IV for 6 hrs.
0.5mg/min for next 18 hrs)
5. Cardioversion in hemodynamic unstable patients

 Pulmonary HTN/Edema/RVF

1. Oxygen
2. Diuretic
Loop diuretics
High dose deleterious
Combine with vasodilator

3. Digitalis
4. Morphine (0.1mg/kg)

MITRAL REGURGITATION

Definition:
Retrograde flow of blood from LV to LA through incompetent
mitral valve during systolic phase
Causes:

90% associated with MS in RHD

Degenerative processes of leaflets and chordal structures
Infective endocarditis
Mitral annular calcification

Pathophysiology
Mitral regurgitation
Systolic (Retrograde) ejection into LA
Acute
Volume overload in LA & LV
ed LA, LV Pressure

Chronic
ed LV afterload (into LA)
ed LA/LV size/ compliance

Pulmonary edema ed Cardiac output

LA dilatation ed contractility
AF
CO
Pulmonary congestion

Acute MR
Sudden onset MR
Sudden increase in LV preload
Enhanced LV contractility
ed LAP (acute)
(LV size: N)
(LA size: N)
Ejection into LA &
systemic circulation

ed Pulm vascul pressure

cardiac output

Pulmonary congestion/edema

Chronic compensated MR
Slow development of MR

Chronic LV overloading
Eccentric LV hypertrophy

LA dilatation

LV radius, ed wall tension Maintenance of LAP

Maintenance of LV systolic function
Change in LV compliance
(LVEDP maintained)
After load/CO: maintained
Gradual decline in LV systolic function
Decompensated phase

Decompensated phase
Progressive LV dilatation
Mitral annular dilatation

ed wall stress/afterload

Increased regurgitation
deteoration in LV syslolic
& diastolic function
ed LAP
Atrial enlargement

Pulmonary congestion/edema/HTN

Atrial Fibrillation

RV dysfunction/failure

Pathophysiology of MS with MR
MS

MR

Obstruction of blood flow

systolic (retrograde) ejection into LA
from LA to LV during diastole
Volume overload in LA
Volume overload in LV
ed LV filling
LAP
LV dysfunction
ed CO
ed CO
LA dilatation
PVP/PAP
(LV size/function: N)
RV dysfunction

Diagnosis
Clinical presentation

Fatigue, dyspnoea, orthopnoea/Systemic thrombo-embolism

Physical examination
Arterial pressure: N/
Pulse (Water Hammer pulse- DBP, SBP)
Signs of RVF like JVP
Systolic thrill at apex (hyperdynamic circulation)
Cardiac auscultation
Holosystolic murmur
S1 is absent, soft or buried in the systolic murmur

 ECG

Non-specific findings
Atrial fibrillation
LA enlargement/LV hypertrophy

Chest X-ray

Left heart chamber enlargement

Pulmonary congestion

Echocardiography

Diagnosis/mechanism/severity of MR/MS
Impact on cardiac chamber size, pressure & function
Pulmonary artery pressure
Presence of thrombus

Cardiac catheterization with left ventriculography

invasive
Reserved for pts in whom ECHO is sub-optimal

AORTIC
STENOSIS

Aortic stenosis
- Aortic stenosis is a
narrowing of the aortic
valve opening.
- Aortic stenosis
restricts the blood flow
from the left ventricle
to the aorta and may
also affect the pressure
in the left atrium.

Etiology
Calcium buildup on the aortic valve. As you age,

calcium can build up on the valve, making it hard

and thick. This buildup happens over time, so
symptoms usually don't appear until after age 65.
A heart defect you were born with (congenital).
Rheumatic fever or endocarditis. These infections
can damage the valve.

Symptoms of aortic stenosis may include:

Breathlessness (Feeling tired and being short of

breath).
Chest pain, pressure or tightness
Fainting, also called syncope
Palpitations or a feeling of heavy, pounding, or
noticeable heartbeats
Decline in activity level or reduced ability to do
normal activities requiring mild exertion

Pathophysiology

In addition to the symptoms of aortic stenosis, which

may cause a patient to feel faint, weak, or lethargic, the
wall of the left ventricle may also show muscular
thickening because the ventricle must work harder to
pump blood through the narrow valve opening into the
aorta.
The thickened wall takes up more space inside the lower
heart chamber which allows less room for an adequate
amount of blood to be supplied to the body, which in
turn may cause heart failure. Early treatment can help to
reverse or slow down the progress of this disease.

Treatment
- Surgery
digitalis, diuretics, and angiotensin-converting
enzyme (ACE) inhibitors might attempted, whereas
beta-blockers might be used if the predominant
symptom is angina
Antibiotic prophylaxis

AORTIC
REGURGITATION

ETIOLOGY
Also termed aortic insufficiency, may

result of:

Diseases of the aortic leaflets:

Congenital
Endocarditis
Rheumatoid

Dilatation of the aortic root:

Aotic

aneurism
Aortic dissection

PATHOPHYSIOLOGY
ACUTE
LV

is of normal size and relatively

noncompliant. Thus, the volume load of
regurgitation causes the LV diastolic
pressure to rise substantially. The sudden
high diastolic pressure is transmitted to the
LA and pulmonary circulation, often
producting dyspnea and pulmonary edema.
Acute AR is usually a surgical emergency,
requiring immediate valve replacement.

CHRONIC

Adaptive

LV and LA enlargement
have occurred, such that a
greater volume of regurgitation
can be accommodated with less
of an increase in diastolic LV
pressure, so that pulmonary
congestion is less likely

CLINICAL MAIFESTATIONS

Dyspnea on exertion
Fatigue
Decreased exercise tolerance
Uncomfortable sensations of a

forceful heartbeat associated

with the high pulse pressure

EXAMINATIONS
Austin flint murmur
It

is thought to reflect turbulence of blood

flow through the mitral valve during of
diastole owing to downward displacement
of the mitral anterior leaflet by regurgitant
stream of AR.
It can be distinguished from the murmur
of mitral stenosis by the absence of an OS
or presystolic accentuation of the murmur.

Chest radiograph shows an enlarged left

ventricular silhouette.
Doppler echocardiography can identify and

quantify the degree of AR and often can identify its

cause.
Cardiac catheterization with contrast angiography

is useful for evaluation of LV function,

quantification of the degree, and assessement of
coexisting coronary artery disease.

TREADMENT

Calcium channel Beta blocker

Angiotensin-converting

enzyme inhibitor (when

hypertension is present)
Surgical correction

INFECTIOUS
DISEASES OF
HEART

INFECTIVE
ENDOCARDITIS

Etiology : Streptococcus virudans (75%),

Staphylococcus species (20%), E.coli,

Pneumococcus, Streptococcus beta haemolyticus,
Pseudomonas, Haemophylus influenza, fungi,
ricketsia, and virus.
Pathogenesis : The microorganisms enter the
blood vessels and affects endocardial which has
been damaged by disease or trauma, these
microorganisms can grow. Abnormalities of these
microorganisms is easily covered with a defective
valve and the lesion a loud gushing stream.

In these places, there is a growth called vegetation. The amount

of vegetation varies, sometimes as small as verruca small and
sometimes large and irregularly shaped. Verruca was originally
found on the edges of the valve cover, then the rest of the valve,
eventually also in the atrial and ventricular endocardial and
khordae tendineae. These warts are easily damaged, and off
come the bloodstream as emboli and thrombi can be a seed in
other places.If cured, healing is accompanied by the growth of
connective tissue and scar formation that forms the valve to be
changed. This thrombus composed of fibrin, platelets,
erythrocytes, and leukocytes and consequently many
microorganisms in it. Of thrombus is always issued to the
microorganisms in the blood to chronic sepsis.

Clinical symptoms :
1.

2.

3.
4.

5.
6.

Heart : The pulse was always regular, rarely are patients

with atrial fibrillation. Heart failure may also occur.
Chronic sepsis : Fever, anemia, leukocytosis moderate,
elevated erythrocyte sedimentation rate, spleen
enlargement, and clubbing.
Skin : Petekiae and nodulus osler.
Kidney : Renal infarction causes a disorder called focal
nephritis.
Embolism
Central nervous system : Headache, dizziness, and
vomiting.

Therapy : Penicillinase-resistant penicillin such

oxacillin or methicillin, gentamicin, ampicillin,

vancomycin and surgical intervention.
Prognosis : Without antibiotics, the cure rate is
only 0.5%. With sulfonamide cure rate of
approximately 5%. With antibiotics, the cure rate
can reach 70% -80%. Successful treatment
depends heavily on rapid initiation of therapy.