INFECTIOUS DISEASE AND HEART VALVE DISEASE.

3rd modul

By 14B

ZulhermanIkrima Ainal QalbiWulan Purnama SariNurul Trisna MuchtarPuji Aulia ZaniRidhatul Afifah IkhwanVani MorinaFatmi 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.

Infeksieksudatblock the respiratory tractO2

2.fever infection ISPAthroat become sore not eatingtired

Lactat acid

uncomfortable in breathing.

3.has relation. susceptible4. 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 disease7.no.. Teridifteri miocarditis

others child rheumatic fever

scheme

difterino

immunization

-fever-breathless-stridor-cianosys-retraction

Teri 5th

infection

difteri faringitis

Heart valve

PJB

Joint pain

Rheumatic fever autoimun

Anak lain

Learning Objective

1. abnormalities in heart valves2. 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 ↑ in pulmonary venous pressure → ↑ in pulmonary arterial pressure*

Atrial fibrillation Transudation of fluid into pulmonary interstitial spaceThrombus formationSystemic thrombo-embolism ↓ed pulmonary compliance

↑Work of breathing

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 dilatationRV 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 low cardiac output’

• Cardiac auscultation– Opening snap– Rumbling diastolic murmur best heard at apex radiating to the

axilla– Loud S2: pulmonary hypertension

• 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 surgeryMild / 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. β-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/RVF1. Oxygen2. Diuretic

Loop diureticsHigh dose deleteriousCombine with vasodilator

3. Digitalis4. 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

PathophysiologyMitral regurgitation

Systolic (Retrograde) ejection into LA

Acute Chronic

Volume overload in LA & LV ↓ed LV afterload (into LA)

↑ed LA, LV Pressure ↑ed LA/LV size/ compliance

Pulmonary edema ↓ed Cardiac output LA dilatation ↓ed contractility

AF ↓ COPulmonary 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 & ↑ed Pulm vascul pressure systemic circulation

↓ cardiac output Pulmonary congestion/edema

Chronic compensated MR

Slow development of MRChronic 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 LAfrom 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 tightnessFainting, also called syncopePalpitations or a feeling of heavy, pounding,

or noticeable heartbeatsDecline 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:CongenitalEndocarditisRheumatoid

- Dilatation of the aortic root:Aotic aneurismAortic dissection

PATHOPHYSIOLOGYACUTE

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.

CHRONICAdaptive 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 exertionFatigueDecreased exercise toleranceUncomfortable sensations of a forceful heartbeat associated with the high pulse pressure

EXAMINATIONS

Austin flint murmurIt 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. Heart : The pulse was always regular, rarely are

patients with atrial fibrillation. Heart failure may also occur.

2. Chronic sepsis : Fever, anemia, leukocytosis moderate, elevated erythrocyte sedimentation rate, spleen enlargement, and clubbing.

3. Skin : Petekiae and nodulus osler.4. Kidney : Renal infarction causes a disorder called

focal nephritis.5. Embolism6. 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.