pleno minggu 3 blok 3.2
DESCRIPTION
3.2TRANSCRIPT
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.