CHF ec. MR
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Present by
FARINA DWINANDA F
(C111 09 887)
Supervisor :
dr. Khalid Saleh, Sp.PD-KKV, FINASIM
Chf nyha iII ec. MITRAL REGURGITATION
CASE PRESENTATION
Department of Cardiology and Vascular Medicine Medical Faculty of Hasanuddin University
Makassar 2014
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PATIENT IDENTITY
• Name : TN.M• Age : 50 years old• Gender : male• MR : 669126• Day of Admission : 25 Juni 2014
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Chief Complaint : Shortness of breath
It was felt since ± 2 month ago and got worsen 3 days before
admitted to the hospital. It was experienced while doing physical
activity. There is no complaint while doing the same activity. Since 2
days ago, patients do nothing but still feel the SOB during rest.
Patient can not sleep since the Sob getting worse with lying flat.
Sometimes awaked during at night time that caused by sudden
shortness of breath. History of chest pain (-). Cough(-), Wheezing (-)
Fever (-), history of fever 1 day before admitted to the hospital.
Nausea (-), Vomite (-), palpitation (-), Cold sweats (-). Oedema
extremities (+) in pretibial. Defecation and urination: Normal.
HISTORY TAKING
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Family History
Past Medical History
• History of DM (-)• History of
hypertension (+)• History of smoking
(+)
Family History
• History of cardiovascular disease in family (-)
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RISK FACTORS
ModifiedNon- Modified
• Gender : Male
• Age 50 years old
• Hypertension
• Smoking
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General Status
*Moderate illness/ Well nourished/ Conscious
*Nutritional Status: Normal
*Weight : 60 kg
*Height :165 cm
*BMI : 22,0 kg/m2
Vital Sign
*Blood Pressure : 160/100 mmHg
*Pulse Rate : 76 bpm
*Respiratory Rate : 28 bpm
*Temperature : 36.5 0C (axilla)
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PHYSICAL EXAMINATION
Head and Neck ExaminationsEye : Conjunctiva anemic (-/-), Sclera icteric (-/-) Lip : Cyanosis (-)
Neck : JVP R+3 cmH₂O potition 30º
Chest ExaminationInspection : Symmetric between left and right chest.Palpation : No mass, no tenderness.Percussion : Sonor between left and right chest, Auscultation: Respiratory sound: Vesicular Additional sound : Ronchi +/+ (mediobasal) ,Wheezing -/-
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• Inspection : Heart apex was not visible
• Palpation : Heart apex was not palpable • Percussion : Right heart border in ICS
II right parasternal. Left heart border in ICS 7 midclavicular.
• Auscultation : Heart Sounds : S I/II regular, murmur (+) sistolik at apex
Heart• Inspection : Flat, follows breathing
movement• Auscultation : Peristaltic sound (+),
normal• Palpation : No mass, no tenderness,
liver and spleen unpalpable
• Percussion : Tympani (+)Abdomen
• Pretibial edema +/+• Dorsal pedis edema +/+Extremitie
s
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Electrocardiogram (ECG)
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ECG interpretation
Rhythm: Sinus rhythmHeart rate : 70 bpmRegularity : regulerAxis : Right Axis DeviationP wave : 0,08 sPR interval : 0,16 sQRS complex : duration 0,12 s, configuration QS in II,III, aVFST Segment : 0,08 sT wave : 0,12 sConclution : Sinus rhythm, HR70 bpm, RAD, LVH , configuration QS in II,III,aVF
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Radiology findings
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THORAX FOTO INTERPRETATION
• Cardiomegaly with lung oedeme
• Bilateral efusion pleura
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LABORATORIUM
HEMATOL
OGY
RESULT NORMAL
VALUE
UNIT
WBC 13,9 4,00-10,0 (10³/UI)
RBC 5,46 3 4,00-6,00 (106/UI)
HGB 18,5 12,0-16,0 (gr/dL)
HCT 54 37,0-48,0 (%)
PLT 237 150-400 (103/uL)
GDS 110 140 Mg/dL
ureum 30 10-50 Mg/Dl
Creatinin 2,3 <1,3 Mg/dL
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Na 140 136-145 mmol/L
SGOT 3,6 <41 mmol/L
SGPT 99 <38 Mg/dL
PT 11.9 10-14 detik
APTT 31,6 22-30 detik
CK 97,7 L<190,P<18
7
u/L
CKMB 25,5 <25 u/L
TROPONIN T 0,26 <0.05
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ECHOCARDIOGRAPHY
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INTERPRETATIONConclusion
* Dysfunction sistolic and diastolic LV,
* EF 50%
* LVH (+)
* Dilation of LA and LV
* MR mild
* Decrease of systolic LV function, EF 50%
* Dimensional chambers of heart : LA and LV dilatation
* LVH (+)
* Global hipokinetic
* Insdequate RV systolic function, TAPSE 1,3 cm
* Heart valves :
- Mitral: MR mild
- Aorta : 3 cuspis, calsification (-)
- Tricuspid : TR trivial
- Pulmonal : normal function and movement
* E/A >2 (pseudonormal)
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Working DIAGNOSIS
CHF e.c HHDHT Grade IIMR Mild
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MANAGEMENT Bed rest
Oxygen 3-4 lpm via nasal canule
Cardiac diet
IVFD NaCl 0.9% 500 cc/24 hr
Angiotensin receptor Blocker
Valsartan 1x80 mg
Laxative
Laxadyne syr 0-0-II cth
Diuretic
Lasix 2am/8jam/iv
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DISCUSSION
HEART FAILURE
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The state in which abnormal circulatory congestion occurs as the result of heart failure.
DEFINITION
Heart failure is no longer able to pump an adequate supply of blood in relation to the venous return and in relation to the metabolic needs of the body tissues at the particular moment
Congestive
Heart
Failure
Heart
Failure
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ETIOLOGY OF HEARTFAILURE
Miocard Disease
CAD
Cardiomyopathy
Iatrogenic
Miocarditis
Miocard Mechanical Dysfunction
Pressure overloaded (Stenosis Aortae, Hypertension, Coartatio Aortae)
Volume Overloaded(Mitral/Aortae Regurgitation, Congenital Heart Disease, Hipertransfusion)
Miocard Filling Inhibitating(Cardiac Tamponade,
Pericarditis)
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The Framingham criteria for CHFCHF considered present if 2 major or 1 major & 2 minor
Major Criteria Minor Criteria
• Paroxysmal Nocturnal
Dyspnea
• Cardiomegaly
• Gallop S3
• Hepatojugular reflux
• Increased of JVP
• Rales or ronchi
• Acute pulmonary edema
• Prolonged circulation
time(> 25 sec)
• Weigh loss ≥ 4,5 kg in 5
days in
response to treatment of
CHF
• Extremity edema
• Nocturnal cough
• Decreased vital
pulmonary capacity
(1/3 of maximal)
• Hepatomegaly
• Pleural effusion
• Tachycardia (≥
120bpm)
• Dyspnea d’effort
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clASSIFICATION OF CHF
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PATHOPHYSIOLOGY OF CHF
Plaque in coronary artery
Blood flow to heart muscle is reduced. Heart muscle lacking of oxygen
Ischemia of heart muscle can lead to myocardial infarction
Symptomatic Congestive Heart Failure
Pulmonary edema Abnormal Heart rhythm
The heart muscle can’t pump adequately
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Sign & symptomp of chf
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Managing afterload
Managing preload
Neurohormonal modulation
Managing contractility
Inotropic agents : • Cardiac glycosides• B- adrenergic
• Diuretics• Venodilator
•ACE inhibitors•ARB•β blockers•CCB
•β blockers•ACE inhibitors•ARB
CHF MANAGEMENT
Farmakologi
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MITRAL REGURGITATION
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Normal mitral valve function depends on perfect function of the complex interaction between the mitral leaflets, the subvulvar apparatus (chordae tendinae and papillary muscles), the mitral annulus, and the left ventricle. An imperfection in any one of these
components can cause the valve to leak.
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Mitral regurgitation is retrograde flow of blood from LV to LA through incompetent mitral valve during systolic phase.
Causes by Primary (intrinsic valvular disease) and
Functional (regional or global LV remodelling )
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Primary (intrinsic valvular
disease)
*MR is almost always (90%) associated with MS in RHD
*Degenerative processes of leaflets and chordal structures
*Infective endocarditis
*Mitral annular calcification
Functional (regional or global LV
remodelling )
Structurally normal leaflets and chordae tendineae
*Ischemic heart disease (Ischemic MR)
*Idiopathic dilated cardiomyopathy
*Mitral annular dilatation
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Etiology
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• Dyspnea
• Fatigue
• Orthopnea
• Palpitation
• Pulmonary edema (often the initial manifestation)
Symptoms of MR
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Physical ExamPalpation may reveal the following:
*Brisk carotid upstroke and hyperdynamic cardiac impulse
*Prominent LV filling wave
Auscultation may reveal the following:
*Diminished S1 in acute MR and chronic severe MR with defective valve leaflets
*Wide splitting of S2 as a result of early closure of the aortic valve
*S3 as a result of LV dysfunction or increased blood flow across the MV
*Accentuated P2 if pulmonary hypertension is present
*Characteristic murmur
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Clinical Features
Acute
*Present with sudden onset of pulmonary edema, hypotensio, cardiogenic shock
*Murmur early systolic, soft inaudible
*Normal LA size and compliance
Chronic
*Usually asymptomatic, if there is present with low CO symptom
*Over time CHF features
*Increased LA size
*Lower CO
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• CXR: LA and LV enlargement
• ECG: LV hypertrophy, sometimes AF
• Echocardiografi:
– LAE
– LV enlargement
Diagnostic Tests
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Medical Therapy
*ACE-Inhibitor
*Diuretic
*Nitrat
*Digoxin
*Antibiotic
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• Symptomatic with severe MR
• Asymptomatic with severe MR and preserved LV function
• Asymptomatic with severe MR and LVESD > 45 mm and EF < 55%
Surgical intervention
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Thank You