UNSTABLE ANGINA

PECTORIS
BY : Radinal Irwinsyah

Supervisor : dr. Hakim Alkatiri, Sp.JP (K), FIHA

CASE REPORT
PATIENT IDENTITY
 MR number : 44-80-02
 Name : Mr. NS
 Age : 54 years old
 Date administered : November 5th 2014
History Taking
Chief complaint: Chest pain
It was felt since ± 2 days ago
Get worse 6 hours before admitted to the hospital
Chest pain occur with mild activity . Duration of chest pain is more
than 20 minutes
 Shortness of breath (-), sweating (-), and nausea (-), Cough (-),
PND (-), DOE (-) , Ortopneu (-)
Defecation and urination : normal
History of Past Illness
 History of angina pectoris in 2012 and admitted to
hospital for PCI
Risk Factor
Modifiable
Smoking (+) about 1 pack per day for 15 years

Hypertension (+)

Non Modifiable
Gender : Man

Age : 54 years old

Physical Examination
 General status
Moderate illness/over weight/conscious
 Vital sign
BP : 120 / 80 mmHg
HR : 98 x/min
RR : 18 x/min
T : 36.30 C
 Head Examination
o Eyes : anemia (-), icterus (-)
o Lip : cyanosis (-)
o Neck : lymphadenopathy (-), JVP R + 1 cmH2O

 Thoracal Examination
o Inspection : symmetric, normochest
o Palpation : mass (-), tenderness (-), VF R=L
o Percussion : sonor
o Auscultation : breath sound : bronchovesicular
additional sound : ronchi -/-,
wheezing -/-
 Heart Examination
o Inspection : IC wasn’t visible
o Palpation : IC wasn’t palpable
o Percussion : normal heart size
 Upper border : left 2nd ICS
 Lower border : left 5th ICS
 Right border : right parasternalis line
 Left border : left medioclavicular line
o Auscultation : Regular of I/II heart sound,
murmur (-)
 Abdominal Examination
o Inspection : flat and following breath movement
o Auscultation : peristaltic sound (+) , normal
o Palpation : liver and spleen unpalpable
o Percussion : tympani, ascites (-)

 Extremities
o Oedema : pretibial (-), dorsum pedis (-)
Electrocardiography
Interpretation
 Rhythm : Sinus
 Heart rate : 75 bpm
 Regularity : reguler
 PR interval : 0,16 s
 Axis : Normoaxis,
 P wave : 0,08 s
 Conclution : Sinus Rhythm, Normoaxis,
Complete blood
WBC : 11.3 x 103 /mm3 (↑) Blood chemistry
HGB : 14.6 g/dl Random blood sugar: 108 mg/dl
HCT : 42.1 %
RBC : 5.15 x 106 /mm3 SGOT : 19 u/l
PLT : 357x 103 /mm3 SGPT : 29 u/l
Ureum : 13
Cardiac enzyme
CK : 64
Creatinin : 0.90
CK MB : 9.9 Total Cholesterol : mg/dl
Troponin T :- HDL : 34 mg/dl
LDL : 130 mg/dl
Electrolyte
Triglyseride :
Sodium : 145 mmol/l
Uric acid : 6.1
Potassium : 4.1 mmol/l
Chloride : 108 mmol/l
WORKING DIAGNOSIS
 Unstable Angina Pectoris
Management
Bed Rest Anti cholesterol
Oxygen 2-4 lpm via nasal
canule •HMG-Co A reductase inhibitor

IVFD NaCl 0,9% 500cc/day (Simvastatin) 20 mg 0-0-1

Anti platelet Nitroglycerin
 ASA (Aspilet) 320mg (4 tab) loading dose
Clopidogrel ( Plavix ) 600 mg ( 8 tab) •Isosorbid Dinitrat (Fasorbid) 2
loading dose mg/hour/SP -> 10 cc/hour
Anti Hypertension
 Angioten 50 mg/24hrs/oral
Anxiolytic
•Benzodiazepin (Alprazolam) 0,5 mg
Trizedon MR 1tab/12hrs/oral ½-0-1
Carvedilol (V-Block) 3.12 mg/24hrs Laxative
•Laxadin syrup 1 x 2 cth
Pathophysiology of ACS
( Braunwald: Heart Disease: A Textbook of Cardiovascular
Medicine, 6th ed., Copyright © 2001 W. B. Saunders Company )

TEXTBOOK READING
Structure of the normal artery

A, Elastic artery. Note the concentric

laminae of elastic tissue that form
sandwiches with successive layers of
smooth muscle cells. Each level of the
elastic arterial tree has a characteristic
number of elastic laminae

B, Muscular artery. The smooth muscle cells are surrounded by a

collagenous matrix but lack the concentric rings of well-organized

elastic tissue character istic of the larger arteries .

Acute Coronary Syndrome
 The majority of patients with acute coronary
syndrome have significant obstructive coronary
atherosclerosis
 increase in myocardial oxygen demand (e.g.,
precipitated by tachycardia or hypertension) and/or
by a reduction in supply (e.g., due to reduction in
coronary lumen diameter by platelet-rich thrombi
or vasospasm)
INITIATION OF
ATHEROSCLEROSIS
 If a sufficient quantity of thrombogenic substances
is exposed when plaque rupture occurs, the
coronary artery lumen may become obstructed by a
combination of fibrin, platelet aggregates, and red
blood cells . An adequate collateral network that
prevents necrosis from occurring can result in
clinically silent episodes of coronary occlusion. The
rupture of plaques is now considered to be the
common pathophysiological substrate of the acute
coronary syndromes