STEMI Inferior Onset >24 Jam Killip IICase Report

Cardiology Department Case ReportMedical Faculty April 2013Hasanuddin University

Austein Wedyanto C 111 08 346

Supervisor: dr. Muzakir Amir, Sp.Jp.FIHA FICA

 HASANUDDIN UNIVERSITY

MAKASSAR2013

Patient’s Identity

Name Mr. D

Gender Male

Age 69 years old

Address Riso Enrekang

Medical Record No. 599669

Date of Admission March 18th 2013

History Taking• Chief Complain : Chest Pain

• It was felt 28 Hours before admitted to the hospital, penetrated to

back and radiated to left arm. It was felt for more than 20 minutes

and didn’t relieve by taking a rest. During the attack, patient feel

sweating, nausea, vomit (-), palpitations (+), shortness of

breath (+).

Cough (-), history of cough(-)

Dizziness (-), Headache (-) , Fever (-)

• PND (-), DOE (+)

• Defecation and urination : normal

Previous Illness• History of coronary heart diseases (-)• History of Hypertension and uncontrolled (+)• History of diabetic (-)• Asthma (-), family history with asthma (-)• Family history with CVD (-)• Cigarette smoking (+), 1-2 pack each day• Alcoholism (-)

Physical Examination• General status:

• Moderate Ilness/ Overweight/Conscious (Alert and Oriented)• Body Weight : 60 kg• Body Height : 165 cm• Body Mass Index : 22,8 kg/m2

• Vital Status• Blood Pressure : 140/100 mmHg• Heart Rate : 72 x/mnr• Respiratory Rate : 26 x/mnt• Body Temperature : 36,5 °C

Physical Examination• Head : Normochepalic• Eye : Anemis (-), Icteric (-)• Pupil : Equal, round, diameter 2,5 mm, reactive to

light• Nares : Appearent is normal• Mouth : No cyanosis• Neck : JVP +3 CM H2O, no lymphadenopathy, no

thyroid enlargement

Physical Examination• Lung

• Inspection : Equal expension bilaterally• Palpation : No tenderness, no mass palpable• Percussion : Normal resonance bilaterally• Auscultation :

• Breath Sounds : Vesicular• Adventitious breath sound : Ronchi (-) , No wheezing

Physical Examination• Cardiac Examination

• Inspection : Ictus cordis was invisible• Palpation : Ictus cordis was palpable in ICS V about 1

finger from lateral of medioclavicularis sinistra line, Thrill (-)• Percussion : Right heart border in right parasternalis

line, left heart border in left midclavicle line ICS V.• Auscultation : Heart Sounds = S I/II regular.

Physical Examination• Abdominal

• Inspection : Flat, following breath movement• Auscultation: Peristaltic sound (+), normal• Palpation : Liver and spleen are unpalpable• Percussion : shifting dullness (-)

• Extremities • Oedema pretibial -/-• Oedema dorsum pedis -/- • Cyanosis (-), Clubbing finggers (-)

ECG Finding (18/03/2013)

•Rhythm : Junctional rhythm•P wave : Invisible P wave•Heart Rate : 72/minutes•Duration QRS : 0,06 s•Axis : 105 Degree•ST Segment : ST Elevation at Lead II,III, AVF. ST depresi at AFL, Lead I, V4, V5, V6•T wave : T Inverted Lead II, III, AVF

CONCLUSION : 1. Junctional Rhythm2. STEMI Inferior

Laboratory Findings1/03/13

WBC 13,09 x 103 Na 142

RBC 5,27 x 106 K 4,7

HGB 15,3 Cl 107

HCT 46,5% PT 11,3

PLT 204 APTT 26,5

Ur 67 GDS 111

Cr 1,3

SGOT 816 CKMB 675

SGPT 135 Trop T >2,0

Echocardiography findings• LV systolic function decrease,

EF 42%• Dilated LA and LV• Hypokinetic at Inferior,

inferoseptal and inferior• No LVH• RV Function decrease, TAPSE

0,9 cm• Mpa 30 mmHg• Heart valves :

• Mitral : MR Mild• Aorta : no calcification• Trikuspid : TR Mild• Pulmonal : function and

motility are good

Conclusion :

1. Diastolic and systolic of both ventricle disfunction

2. Hypokinetic at Inferior, Inferoseptal and posterior

3. MR, TR, PH Mild

Working Diagnosis• STEMI Inferior onset > 24Hours Killip II• HT Grade I

Therapy• Bed Rest• O2 3 – 4 liter/min via nasal canule• Heart Diet• IVFD NaCl 0,9% 1000cc/24 hours• (Salysilic Acid) Aspilet 80 mg 1-0-0• (Clopidogrel) Plavix 75 mg 0-1-0• (ACE Inhibitor) Captopril 25 mg 1-0-1• (Statin) Simvastatin 20 mg 0-0-1• (Fondaparinux sodium) Arixtra 2,5 mg/24 hours/SC• (Isosorbide dinitrate) Cedocard 5mcg/minutes via syringe

pump• Alprazolam Tab 0,5 mg 0-0-1• (Bisacodyl)Laxadyn syrup 0-0-2

Management• Planning

• ECG Control• Coronary angiography

Discussion

ST ELEVATION MYOCARDIAL INFARCTION

DEFINITION

Myocardial infarction (MI) rapid development of myocardial necrosis caused by a critical imbalance between the oxygen supply and demand of the myocardium.

This usually results from plaque rupture with thrombus formation in a coronary vessels, resulting in an acute reduction of blood supply to a portion of the myocardium.

• Occurs when coronary blood flow decreases abruptly after a thrombotic occlusion of a coronary artery previously affected by atherosclerosis.

• In most cases, infarction occurs when an atherosclerotic plaque fissures, ruptures, or ulcerates.

PATHOPHYSIOLOGY

ACS describe a group of conditions resulting from acute myocardial

ischemia (insufficient blood flow to heart muscle) ranging from

unstable angina to myocardial infarction.

CLASSIFICATION

Gender and Age

Men, increased risk after age 45

Women, increased risk after age 55

Family History

Heart disease diagnosed before age

55 in father or brother

Heart disease diagnosed before age

65 in mother or sister

RISK FACTORS

Non- Modifiable

Smoking

Hypertension

Diabetis Mellitus

Dyslipidemia

Obesity

Lack of physical activity

Modifiable

1. Clinical history of ischaemic type chest pain lasting >20 minutes

2. Changes in serial ECG tracings3. Rise and fall of serum cardiac biomarkers

such as creatinine kinase-MB fraction and troponin

WHO Diagnostic Criteria

CLINICAL FEATURES

1. Chest pain, >30 minutes2. Usually tight, crushing, and band like3. Location in retrosternal4. May radiate to left arm, throat, and

jaw5. Associated features including

palpitation, sweating, breathlessness, and nausea.

ECG CHANGES IN AMI

• ST segment elevation over area of damage

• ST depression in leads opposite infarction

• Pathological Q waves• Reduced R waves• Inverted T waves

Diagnosis

No

Yes

Yes

No

Acute Myocardial Infarction (STEMI)

NSTEMI( Non ST-Elevation 

Myocardial Infarction )

Unstable   Angina

Signs of myocardial ischemia

 ↑ Biochemical cardiac markers ?

ECG

Lab

  ST segmen elevation  ?

Complication

• Congestive heart failure

• Myocardial rupture

• Arrhythmia

• Cardiogenic shock

• Pericarditis

Therapy

Managing chest pain and anxietyo Bed resto Diet o O2 2-4 lpmo Nitrate sublingual/oral/IVo Antiplatelet: aspirin and clopidogrelo Morphine/ pethidine

Stabilizing hemodynamic (blood pressure and peripheral pulse control)

o β-blockero Calcium channel blocker (CCB)o ACE-Inhibitor

Reperfusion of the myocardiumo Thrombolytic

TIMI PROGNOSIS IN STEMI

Risk Factor  ScoreAge > 65 years old 2Age > 75 years old 3

History of angina/hypertension/DM 1/1/1

Systolic BP <100 3Heart rate > 100 2

Killip II-IV 2Weight > 67kg 1

Anterior MI or LBBB 1Delay treatment >4hours 1

 Total Score  Risk of Death in 30 days0 0.8%1 1.6%2 2.2%3 4.4%4 7.3%5 12.4%6 16.1%7 23.4%8 26.8%

9-16 35.9%

PROGNOSIS KILLIP CLASSIFICATION

ClassClass DescriptionDescription Mortality Rate (%)Mortality Rate (%)

II no clinical signs of heart failureno clinical signs of heart failure 66

IIII rales or crackles in the lungs, an rales or crackles in the lungs, an SS33, and elevated jugular venous , and elevated jugular venous pressurepressure

1717

IIIIII acute pulmonary edemaacute pulmonary edema 30 - 4030 - 40

IVIV cardiogenic shock or cardiogenic shock or hypotension (systolic BP < 90 hypotension (systolic BP < 90 mmHg), and evidence of mmHg), and evidence of peripheral vasoconstrictionperipheral vasoconstriction

60 – 8060 – 80

Thank You