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PATIENTS IDENTITY
Name
: Mr. a Gender : Male Umur : 59 y.o Reg. Number : 640971 Admitted Date : 9th, December 2013
HISTORY TAKING
Chief
Nausea (-), epigastric pain (-) Palpitation (-) Cold sweats (+)
of hypertension (+) since 5 years ago ( uncontrolled ) History of Diabetes (-) History of Dyslipidemia (-) Family History of having CVD (-) History of Smoking (+) since 15 yo, 1 pack/day and stop since 20 years ago
PHYSICAL EXAMINATION
General
cyanosis(-)
Thoracic Examination : Inspection : Symmetric left and right Palpation : No mass, no tenderness Percussion : Sonor Auscultation : Breath Sound : vesicular, Rh -/-, wh -/Cardiac Examination : Inspection : Ictus Cordis not visible Palpation : Ictus Cordis not palpable Percussion : left border 1 finger from ICS VI midclavicularis line sinistra right border ICS IV parasternalis line dekstra Auscultation : Regular of I/II Heart Sound, murmur (-) gallop (-)
movement Palpation : Liver and spleen unpalpable Percussion : Tympani Auscultation: Peristaltic sound (+), normal
breath
ECG
ECG (25/4/2013)
ECG INTERPRETATION
Rhythm HR PR interval Axis P Wave QRS complex : Configuration Duration ST segment T wave Conclusion
-
: Sinus Rhyth : 60 bpm : 0.12 sec : -30 LAD : 0,08 sec : Q patologis in lead III, AVF, V1-V2 : 0,08 sec : ST depretion in lead V3-V4 : inverted in lead V3-V4 : Sinus rhythm, HR 60 bpm, LAD, OMI inferoseptal, Anterior iskemik
LABORATORY FINDINGS
Complete Blood Count WBC : 8,9x103 uL HB: 13,1 g/dl HCT : 40,5% PLT : 362x103 uL
Blood chemistry SGOT : 23 SGPT : 22 Ureum : 19 Creatinin : 1,0 Uric acid : 6,2 Glucose : 99 mg/dl
ECHOCARDIOGRAM
WORKING DIAGNOSIS
UNSTABLE ANGINA PECTORIS
MANAGEMENT
O2 2-4 LPM via Nasal Canule IVFD NaCl 0,9% 12 dpm Nitrate : ISDN Fasorbid (10mg/cc) 2 mg/hour/SP Anti-platelet aggregation : Aspilet 80 mg 0-1-0 Clopidogrel (Plavix) 75 mg 1-0-0 ACE Inhibitor: captopril 3 x 6.25 mg Anti-coagulant : Arixtra 2,5mg/24/SC Statin : Simvastatin 20mg (0-0-1) Anti-anxiety : Alprazolam 0.5 mg (0-0-1) p.r.n Laxative: Laxadyne syr 0-0-2 C
PLANNING
ECG
/ day
DISCUSSION
ACS
CAD Stable Angina Pectoris
NSTEMI
STEMI
DIAGNOSIS
CLASSIFICATION
DIAGNOSIS
ECG
Yes
No
Lab
Yes
No
DEFINITION
Angina pectoris is a syndrome characterized by chest pain resulting from an imbalance between O2 supply & demand, and is most commonly caused by the inability of atherosclerotic coronary arteries to perfuse the heart under conditions of increased myocardial O2 consumption.
PATHOGENESIS
Plaque
rupture Thrombus formation Incomplete/ intermittent occlusion of the infactrelated vessel to the presence of collateral channels/ to small size of affected vessel
Cardiology, Desmond G. Julian, J.Campbell Cowan, James M. McLenachan, 8th edition, Elsevier, 2005
UAP - CASE REPORT CARDIOLOGY DEPARTMENT Figure 1. Pathophysiologic Events Culminating in the Clinical Syndrome of Unstable Angina. Numerous physiologic triggers probably initiate the rupture of a vulnerable plaque. Rupture leads to the activation, adhesion, and aggregation of platelets and the activation of the clotting cascade, resulting in the formation of an occlusive thrombus. If this process leads to complete occlusion of the artery, then acute myocardial infarction with ST-segment elevation occurs. Alternatively, if the process leads to severe stenosis but the artery nonetheless remains patent, then unstable angina occurs.
CAUSES
Reduction in oxygen supply to myocardium
Coronary artery narrowing from non-occlusive thrombus on a disrupted atherosclerotic plaque Dynamic obstruction by coronary vasospasm or vasoconstriction Severe narrowing without thrombus or spasm progressive atherosclerosis Restenosis after Percutaneous coronary intervention Arterial inflammation and /infection
Increased myocardial oxygen demand in the presence of fixed restricted oxygen supply
Fever, tachycardia, thyrotoxicosis, anemia
Ischemic symptoms
crushing, squeezing
Usually retrosternal location, radiating to left chest, left arm, can be epigastric
Dyspnea
Diaphoresis Palpitations
Nausea/vomiting
Mild headache
UAP
If the plaque become unstable caused by bleeding, rupture, or fissure and result in thrombus formation which blocked the vascularisation, angina may occur. Angina become progressive crescendo and have no relation to activity. Moreover, angina can occur anytime, even resting time. This kind of angina called by the Unstable Angina Pectoris
DIAGNOSIS
Clinical -
history: Increase frequency and severity of the pain Pre-existing angina Last longer than 10 minutes to several hours Not related to activities Pain may be intermitten Not relieve by nitrate
Cardiology, Desmond G. Julian, J.Campbell Cowan, James M. McLenachan, 8th edition, Elsevier, 2005
BRAUNWALD CLASSIFICATION
Characteristic
Severity I II
Class/Category
Details
Symptoms with exertion Subacute symptoms at rest (2-30 d prior)
III
A B C
1 2 3
Tan, A Walter. Unsta ble Angina Pectoris Clinical Presentation (updated 7th Dec 2011) http://emedicine.medscape.com/article/159383-overview#showall
PROGNOSIS
The presence of any of the following variables constitutes 1 point, with the sum constituting the patient risk score on a scale of 0-7: - Aged 65 years or older - Use of aspirin in the last 7 days - Known coronary stenosis of 50% or greater - Elevated serum cardiac markers - At least 3 risk factors for coronary artery disease (including diabetes mellitus, active smoker, family history of coronary artery disease, hypertension, hypercholesterolemia) - Severe anginal symptoms (2 or more anginal events in the last 24 h) - ST deviation on ECG The inflection point for myocardial infarction or death starts at a TIMI Risk Score of 3. Therefore, patients with a score of 3-7 should be considered for use of intravenous glycoprotein IIb/IIIa agents, heparin (low molecular weight or unfractionated), and early cardiac catheterization
RISK FACTORS
Modifiable:
Hypertension Diabetes
Non-modifiable:
Gender: male Age >45 years old Personal history of Coronary Artery Disease Family history of Coronary Artery Disease
MANAGEMENT
http://www.cardiosmart.org/HeartDisease