Case Presentation Kardio Raissa

8/10/2019 Case Presentation Kardio Raissa

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MITRAL REGURGITATIONPresent by

Raissa Safitry

(C111 09 346)

Supervisor :

dr. Pendrik Tandean, Sp.PD-KKV.FINASIM

CAS E P RE S E NTATI O N

Department of Cardiology and Vascular Medicine

Medical Faculty of Hasanuddin University

Makassar 2014



PATIENT IDENTITY

• Name : Mr. E

• Age : 21 years old

• Gender : Male

• MR : 660467

• Address : Mamuju

• Date of Admission : April 23th 2014



HISTORY TAKING

A 21 years old man was admitted to Emergency Room Chief complaint : Dyspneu

It was felt since a week ago, worsen in 1 days before

hospital admission, DOE (+) PND (-) Orthopneu (-).

Fever (+) since a week ago, intermitten. Cough (-)

Chest pain (-), history of chest pain (-)

Nausea (-), vomiting (-), epigastric pain (-).

Palpitation (+), Cold sweats (+).

General weakness (+)

Micturition and defecation remains normal as usually.



History of DM (-)

History of hypertension (-)

History of smoking (+) 1 pack/day, stopped in

2009

Past Medical History

Family History

History of cardiovascular disease in family (-)



General Status

Moderate illness/ Well nourished/ Conscious

Nutritional Status: Normal◦ Weight : 50 kg

◦ Height : 155 cm

◦ BMI : 20.8 kg/m2

Vital Sign

Blood Pressure : 120/80 mmHg

Pulse Rate : 120 bpm Respiratory Rate : 30 tpm

Temperature : 38 0C (axilla)



PHYSICAL EXAMINATION

Head and Neck Examinations Eye : Conjunctiva anemic (-/-), Sclera icteric (-/-)Lip : Cyanosis (-)

Neck : JVP R +3 cmH O position 30º

Chest Examination Inspection : Symmetric between left and right chest.

Palpation : No mass, no tenderness.Percussion : Sonor between left and right chest,lung-liver border in ICS IV right anterior. Auscultation: Respiratory sound: Vesicular Additional sound :Ronchi -/- Wheezing /-



• Inspection : Heart apex was not visible

• Palpation : Heart apex was not palpable

•

Percussion : Right heart border in right parasternalline, Left heart border in left midclavicular lineICS V.

• Auscultation : Heart Sounds : S I/II regular, murmur (+)sistolic grade 3/6 in apexHeart

•

Inspection : Flat, follows breathing movement • Auscultation : Peristaltic sound (+), normal

• Palpation : No mass, no tenderness, liver andspleen unpalpable

• Percussion : Tympani (+)Abdomen

• Pretibial edema -/-

• Dorsal pedis edema -/-

Extremities



Electrocardiogram (ECG) 23/04/2014



ECG interpretation

Rhythm : Sinus rhythm

Heart rate : 115 bpmRegularity : regular Axis : +115P wave : P mitral 0,12 s on II,avL leadPR interval : 0,16 sQ pathologies : -

QRS complex : duration 0,08 s, ICRBBBST Segment : 0,08 s isoelectricT wave : 0,12 sConclusion :Sinus tachycardi rhythm, Normoaxis, ICRBBB



Chest X Ray

• Increased bronchovascular

marking,

• Suprahilar vascular dilatation,• No specific process in both of

lung

• CTI: 0,8, double contour

(LAE), cardiac waist

disappear, apex upward(RVE), small aorta knob.

• Normal sinus and

diaphragma.

• Intact bone

Conclusion:

• Cardiomegaly with sign of

pulmonary oedema (MHD)



LABORATORIUM

HEMATOL

OGY

RESULT NORMAL

VALUE

UNIT

WBC 6,1 4,00-10,0 (10³/UI)

RBC 4,94 4,00-6,00 (106

/UI)

HGB 13,0 12,0-16,0 (gr/dL)

HCT 52,1 37,0-48,0 (%)

PLT 235 150-400 (103/uL)

GDS 117 140 Mg/dL

Ureum 18 10-50 Mg/Dl

Creatinin 0,7 <1,3 Mg/dL

6/1/2014



Na 138 136-145 mmol/L

SGOT 42 <41 mmol/L

SGPT 16 <38 Mg/dL

PT 11.1

10-14 detik

APTT 25,0 22-30 detik



ECHOCARDIOGRAPHY





Working DIAGNOSIS

CHF NYHA IIMITRAL REGURGITATION



MANAGEMENT

Bed rest

Oxygen 3-4 lpm via nasal canula

IVFD NaCl 0.9% 500 cc/24 hr

Furosemide 20 mg/24 hours/IV

Digoxin 0,25 mg 1x1

Captopril 12,5 3x1 2 mg 1x1

PCT 500 3x1



DISCUSSION

MITRAL REGURGITATION



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.



Mitral regurgitation is retrograde

flow of blood from LV to LA throughincompetent mitral valve during

systolic phase.

Causes by Primary (intrinsicvalvular disease) and

Functional (regional or global LVremodelling )



Primary

(intrinsic valvulardisease)

◦ MR is almost always

(90%) associated withMS in RHD

◦ Degenerative processesof leaflets and chordalstructures

◦

Infective endocarditis◦ Mitral annular

calcification

Functional

(regional or global LV

remodelling)

Structurally normal leaflets

and chordae tendinae

◦ Ischemic heart disease(Ischemic MR)

◦ Idiopathic dilated

cardiomyopathy

◦

Mitral annular dilatation



Etiology





Pathophysiology



Symptoms of MR

• Dyspnea

• Fatigue

• Orthopnea

• Palpitation

• Pulmonary edema (often the initial

manifestation)



Physical Exam Palpation may reveal the following:

Brisk carotid upstroke and hyperdynamic cardiacimpulse

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 flowacross the MV

Accentuated P2 if pulmonary hypertension is present

Characteristic murmur



Auscultation



Clinical Features

Acute

Present withsudden onset ofpulmonary edema,

hypotensio,cardiogenic shock

Murmur earlysystolic, softinaudible

Normal LA sizeand compliance

Chronic

Usuallyasymptomatic, ifthere is present

with low COsymptom

Over time CHFfeatures

Increased LA size

Lower CO



Diagnostic Tests • CXR: LA and LV enlargement

• ECG: LV hypertrophy,sometimes AF

• Echo:

– LAE – LV enlargement







Surgical intervention

• Symptomatic with severe MR

• Asymptomatic with severe MR and

preserved LV function

• Asymptomatic with severe MR and LVESD >45 mm and EF < 55%



DISCUSSION

HEART FAILURE

DEFINITION



The state in which abnormal

circulatory congestion occurs as

the result of heart failure.

DEFINITION

Heart is no longer able to pump anadequate supply of blood in relation to the

venous return and in relation to the

metabolic needs of the body tissues at the

particular moment

ETIOLOGY OF HEARTFAILURE



ETIOLOGY OF HEARTFAILURE

MiocardDisease

CAD

Cardiomyopathy

Iatrogenic

Miocarditis

Miocard MechanicalDysfunction

Pressure overloaded

(Stenosis Aortae, Hypertension,Coartatio Aortae)

Volume Overloaded

(Mitral/Aortae Regurgitation,Congenital Heart Disease,

Hipertransfusion)

Miocard Filling Inhibitating

(Cardiac Tamponade, Pericarditis)



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



clASSIFICATION OF CHF





PATHOPHYSIOLOGY OF CHF

Plaque incoronary artery

Blood flow toheart muscle isreduced. Heartmuscle lacking

of oxygen

Ischemia ofheart musclecan lead tomyocardial

infarction

Symptomatic

CongestiveHeart Failure

Pulmonaryedema

Abnormal Heartrhythm

The heartmuscle cant

pumpadequately



Sign & symptom of chf



CHF MANAGEMENT

Non-Farmakologi



Farmakologi



Thank You

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Case Presentation Kardio Raissa