group 16 problem 1b
TRANSCRIPT
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Group 16 Problem 1B
Emergency Medicine Plenary
October 4th2013
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No Nim Nama
1. 405090026 Erwin Sanders Anggota
2. 405090102 Yessica Theresia Ibrahim Anggota
3. 405090143 Nyimas Destriani Varissa Ketua
4. 405090170 Kresensianes Yolia Haur Anggota
5. 405090220 Meidy Regianto Anggota
6. 405100048 Priskila Wulan Sucipto Penulis
7. 405100162 Yunica Anggota
8. 405100177 Ines Syadza Anggota
9. 405100244 Septiany Indahsari Anggota
10. 405100253 Nyoman Rama Aditya K. Ketua
11. 405100257 Indah Novianty Sekretaris
12. 405100296 Holan Adi N.S. Anggota
dr. Hendra
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Problem 1B A 58 year-old-man came to the Emergency Department with severe chest pain
extending to his jaw and left arm. He suddenly felt the chest pain 3 hours agowhile he was watching television, accompanied by excessive cold sweat, nausea,and vomiting. He also felt shortness of breath since an hour ago.
He has a history of hypertension, diabetes melitus, hypercholesterolemia in thepast 3 years. He is not taking his medication regularly, has been smoking since thelast 10 years and never exercises. Previously, he had suffered an episode of mildchest pain but the symptom disappeared after resting. No history of stroke in the
past. Physical examination result: compos mentis (GCS 15), looks in pain, agitated,
overweight and having mild-dyspneu. Blood pressure 170/90 mmHg, heart rate120 beats per minute (regular with enough volume and firmness), respiratory rate30 breaths per minute ( slow and superficial), afebrile and slight increase in JVP.Insprection, palpation and percussion of the heart are in normal limits; S1 and S2in heart auscultation are normal, no murmur is found. Inspection, palpation and
percussion of the lungs are in normal limits but fine rales at the basis of the lungcan be heard in auscultation. Abdomen examination is normal. His extremities arewarm.
ECG examination results: tachycardia sinus rhythm, QRS rate 130x/ minut, QRS axisLAD normal P-wave, P-R interval 0.12 sec, QRS duration 0.08 sec, Q-pathologic (-),ST segment elevation in V1-V6 lead, inverted T-wave (-) and lVH (-) .
What can you learn from this problem?
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Learning Objectives
Acute Coronary Syndrome
Cardiac arrest
Basic Life Support Cardiopulmonar Resuscitation
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Definition ACS
Acute Coronary Syndrome refers to the
constellation of clinical diseases occurring as a
result of myocardial ischemic.
Spectrum : Asympthomatic CAD and stable
angina to UA,AMI, sudden cardiac death
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EPIDEMIOLOGY ACS
>50% of all detahs occur in women
The majority of fatalities from CAD occur
outside the hospital -- Aritmia Maligna (VT/VF)
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Classification
STABLE ANGINA
Myocardial Ischemic
Transient, episodic chest
discomfort Physical Exertion ,
emotional stress, anemia,
dysrhythmia, environment
exposure
Resolve with rest, NTG
UNSTABLE ANGINA
Minimal exertion / at rest
New onset angina
Worsening change previous
stable angina Rest anginaLasting >20
minute, Occurring within 1week of presentation
New onset anginaclass II
onset within the last 2 month Progressive angina : more
frequent, longer duration,class III
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UNSTABLE ANGINA
This is characterized by Pain that occurs with lessexcertion , cumulating pain at rest.
platelet-fibrin thrombus associated with a
ruptured atheromatous plaque
withoutcomplete occulation of the vessels.
The risk of infraction issubtanial, and the main aim
of therapy is to reduce this.
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Unstable angina
is that characterized by rapidlyworsening chest pain on minimal
exertion or at rest.
= ulcerated atheroma+ thrombusformation>>> reduction of coronary
blood flow caused by thrombus>>
angina at rest
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Unstable angina
Recent onset (less than 1 month).
Increase frequency and duration of episode.
Angina at rest not responding readily totherapy.
If the pain more than 20 min.
MI
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STEMINSTEMI
Occluding thrombus
sufficient to cause
tissue damage & mild
myocardial necrosis
ST depression +/-
T wave inversion on
ECG
Elevated cardiac
enzymes
Complete thrombus
occlusion
ST elevations on
ECG or new LBBB
Elevated cardiac
enzymes
More severe
symptoms
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4 pathophysiologic processes development of
NSTEMI
1. plaque rupture or erosion NSTEMI
(embolization of platelet aggregates or
atherosclerotic debris)
2. dynamic obstruction (coronary spasm)
3. progressive mechanical obstruction
4. increased myocardial oxygen demand and/or
decreased supply (e.g., tachycardia, anemia)
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Myocardial Infarction
RISK FACTOR:
1. Smoking2. Hypertension
3. hypercholesterolemia
thrombus coronary artery
Decrease coronary artery blood flow
Arterosklerosis plaque
Ruptur plaqueThrombosit activation
Agonis (kolagen, ADP, epinefrin dan serotonin)
Tromboxan A2
Aggregasi platelet
Myocardial Infarction
Coronary artery Occlusion
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CLINICAL MANIFESTATION
Classic angina pectorissqueezing , pressure,tightness, fullness , heaviness, burning sensation .
Substernal/ precordial , may radiate to neck, jaw,
shoulders, arm Anginal Equivalent symptoms :+/ dsypneu ,
nausea, vomitting, diaphoresis, weakness,dizziness, excessive fatigue.
Occasionally, an apical systolic murmur or mitralinsufficiency due to papillary muscle and leftventricular dysfunction is present.
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DIAGNOSIS
1. STRESS (EXERCISE) TEST.
2. ECG (ELECTROCARDIOGRAPHY)
3. CHEST X-RAY4. CARDIAC ANGIOGRAPHY/ CARDIAC
CATHETERIZATION
5. ERGONOVINE TEST6. BLOOD TEST (BIO-MARKERS)
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1. EXERCISE TEST/STRESS TEST
Used to measure hearts response to exercise
Patient asked to walk on a treadmill while thephysician takes the ECG
So any changes in heart function can be
determined Alternatively the patient recieves an injection
of a radioisotope (generally Thallium) whichmakes the heart visible to a special-linkedcamera
90% accurate
But doesnt identify the exactly where andhow the coronary arteries are blocked.
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2. ELECTROCARDIOGRAM (ECG)
Measures electrical activity of the heart Provides info about the changes or damages to
the heart muscle Doesnt detect the narrowing of the coronary
arteries During an Anginal attack the ECG may show1. S-T phase depression.2. T- phase inversion and/or
3. Ventricular arrythmia
ECG- more abnormal with Unstable Anginawhere the elevation in S-T segment is found.
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3. CHEST X-RAY
Performed to rule out any lung
disease or heart damage that may be
causing the pain.
Also may reveal enlargement of heart
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4. CARDIAC ANGIOGRAPHY/ CARDIAC
CATHETERIZATION
Shows the precise size and location ofblockages within the Coronary arteries
A cathereter is inserted through the
blood vessels from the forearm or groin It is snaked through arteries till it
reaches the heart
A fluid is pumped
So the arteries and the heart are clearlyvisible
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5. ERGONOVINE TEST
Generally done if the person is assumed
to suffer from Coronary Spasm
Done along with angiography
The artery-narrowing drugErgonovine
or Ach is given to cause Coronary Spasm
The persons response to ergonovanine
is measured
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6. BLOOD TEST/BIOMARKERS
Blood test for amount of Lipidswithin the
blood
Because lipids major cause of anginal attack
Lipid profile for :- 1. HDL 2. LDL 3.TRIGLYCERIDES
Recently the newer biomarkers like the C-
reactive protein andB-type natriuretic
protein have been found out and the testsfor each of them is done
These tests are predictive of the moratality of
heart disease
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Terapi fibrinolisis Terapi invasif (PCI)
Onset 3 jm
Tidak tersedia pilihan invasif terapi
-Kontak door-ballon >90 mnt
-Door ballon minus door-needle
lbh dr 1 jm
Tersedia ahli PCI
-Kontak door-ballon
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Terapi PCI :
PCI primer dilakukan pada :
Syok kardiogenik
STEMI >75 thn & syok kardiogenik
Pasien KI fibrinolisis
Terapi penunjang lain :
LMWH
Clopidogrel
Statin
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Prognosis
NSTEMI exhibit a wide spectrum of early (30
days) risk of death, ranging from 1 to 10%, and
of new or recurrent infarction of 35% or
recurrent ACS (5-15%).
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CARDIAC ARREST
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Sudden cardiac death
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Tanda2 henti jantung & henti napas
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Cardiac arrest from a primary
cardiac origin typically presents as:
VFold MI, acute MI
VT miocardial hypertrophy, cardiomiopathy, specific
structural abnormalities
PEA
Asystole
Metabolic hyperalemia result in progressive
widening of the QRS complex
can deteriorate to VT,VF, asystole or PEA.
Electrocution
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Ventricular Fibrillation
Occur in 30% of in-hospital cardiac arrest
More common in ischemic and infarction heart disease
More likely to respond to treatment
ECG : bizarre irregular waveform, random in both frequency
and amplitude Shows disorganized electrical activity in myocardium
The only effective treatment is early defibrillation
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Clinical Manifestations: Pulse disappears with onset of VF
Collapse, unconsciousness
Agonal breathsapnea in
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Treatment:
Early defibrillation is essential
Agents given to prolong period of reversible death
(oxygen, CPR, intubation, epinephrine,vasopressin)
Agents given to prevent refibrillation after a shock
causes defibrillation (lidocaine, amiodarone,
procainamide,
-blockers) Agents given to adjust metabolic milieu (sodium
bicarbonate, magnesium)
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Clinical Manifestations:
Collapse; unconscious
Agonal respirations or apnea
No pulse detectable by arterial palpation Etiologies
Hypovolemia
Tablets(drug OD, ingestions) Tamponade, cardiac
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Treatment:
Per PEA algorithm
Primary ABCD (basic CPR)
Secondary
AB (advanced airway and ventilation);
C (IV, epinephrine, atropine if electrical activity
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ALGORYTHMFOR
BRADYCARDIA
OR ASYSTOLE
Harrisons Principle of Internal Medicine 18th Ed52
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Copyright 2005 American Heart Association Circulation 2005;112:IV-58-IV-66
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BASIC & ADVANCE CPR
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Teknik Basic Life Support
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Teknik Basic Life SupportPeriksa Tindakan
Circulation
Periksa denyut a. carotis
Fungsi : memastikan tidak terabanya nadi saat dilakukan pertolongan
Pegang leher pasien dan cari trakea dengan 2-3 jari
Raba kearah lateral dan temukan batas trakea dengan otot samping leher
(tempat a. carotis)
Maksimal pemeriksaan : 10 detik
Kompresi dada
Fungsi : menciptakan aliran darah melalui tekanan intratorakal dan
penekanan langsung pada dinding jantung
Pasien dibaringkan di tempat yang datar dan keras
Lokasi : di bagiah bawah sternum, 2 jari diatas prosesus xiphoideus
Cara : telapak tangan saling berkaitan, dalam keadaan bertelutFrekuensi : minimal 100x/menit tanpa interupsi dilanjutkan kompresi
dengan ventilasi (30 : 2)
Kedalaman : 5cm (dewasa) atau 4cm (bayi)
Evaluasi : periksa denyut a. carotis setelah 5x siklus kompresi
Teknik Basic Life Support
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Teknik Basic Life SupportPeriksa Tindakan
*Airway and Breathing (ventilasi)*
Airway
Buka jalan nafas dengan metode :
Head tilt chin liftuntuk pasien non trauma cervical dan leherJaw thrustuntuk pasien dengan trauma cervical dan leher
Breathing Memberikan nafas bantuan (2x dalam 1 detik setiap tiupan) setelah 1x siklus
kompresi (30x kompresi)
Berikan sesuai kapasitas volume tidallihat pengangkatan dinding dada
Metode :
-Mulut ke mulut
-Mulut ke hidung
-Mulut ke sungkup
-Dengan kantung pernafasan
Evaluasi : raba a. carotisbila teraba : jaga airway tetap terbuka dan posisikan
dalam recovery positionDefibrillation Bisa menggunakan defibrillator manual atau AED
Untuk dewasa dengan VF/TV : th/ kejut listrik (monofasik : 360J atau bifasik :
200J)
Untuk anakth/ kejut listrik : dosis 2-4 J/kg, dosis ulangan 4-10 J/kg
Untuk neonatus : manual defibrillator
Tidak diindikasikan pada pasien asistole atau PEA
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Komplikasi Basic Life Support
Aspirasi regurgitasi
Fraktur costae-sternum
Pneumothorax, hematothorax, contusio paru
Laserasi hati atau limpa
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BASIC LIFE
SUPPORT
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Simplified Universal
BLS algorithm
AMERICAN HEART ASSOCIATION:
2010 GUIDELINES
Rantai kelangsungan hidup
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Rantai kelangsungan hidup
berdasarkan rekomendasiAmerican Heart Association
Komponen Rantai Kelangsungan Hidup
Early Access Pengenalan kejadian henti hantung dan aktivasi sistem gawat
darurat segera
Early CPR Resusitasi jantung paru segera
Early Defibrillation Defibrilasi segera
Effective ACLS Perawatan kardiovaskuler lanjutan yang efektif
Integrated post
cardiac arrest care
Penanganan pasca henti jantung yang terintegrasi
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THEORY OF CHEST COMPRESSION
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THEORY OF CHEST COMPRESSION
HEART PUMP THEORY:squeezing the heartbetween the bony sternum & vertebral column
results in forward flow of blood.
THORACIC PUMP THEORY:proposes that chest
compression increases intrathoracic pressure thatpropels blood out of arteries into veins.
CPR 1 Rescuer
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CPR1 Rescuer
Assess
responsiveness
Summon EMS
Position the patient
CPR 1 Rescuer
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CPR1 Rescuer
Open the airway
CPR 1 Rescuer
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CPR1 Rescuer
Look, listen, and feel
for breathing
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CPR 1 Rescuer
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CPR1 Rescuer
If there is no pulse,
find your landmarks,
lower half of the
sternum, betweenthe nipples
CPR 1 Rescuer
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CPR1 Rescuer
Begin chest
compressions
CPR 1 Rescuer
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CPR1 Rescuer
Perform 30 chest
compressions
Push hard
Push fast
Allow the chest to
recoil after each
compression
CPR 1 Rescuer
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CPR1 Rescuer
Administer two
ventilations then
return to
compressions
CPR 2 Rescuer
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CPR2 Rescuer
1 2
3 4
If he is breathing normally
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If he is breathing normally
turn him into the recovery positionsend or go for help/call for an ambulance
check for continued breathing
Right angles
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Headtilt
Right angles
Right angles
If the victim has to be kept in the recovery positionfor more than 30 minturn him to the opposite side
to relieve the pressure on the lower arm.
CPR - Children
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CPR Children
Use heel of one
hand Keep airway open
with other hand
30 compressions:2
ventilations if alone
(2 rescuers use 15:2)
CPR - Infant
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CPR - Infant
Give chest thrusts and
puffs of air
30 compressions:2ventilations if alone
15 compressions: 2
ventilations with 2
rescuers
Special Considerations
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Special Considerations
Children
Clothing
Body hair
Water
Transdermal medication
patches
Implanted defibrillators
or pacemakers
Metal surfaces
Jewelry and glasses
AED
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AED
Assess Check your
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Assess ypatient
Universal Steps
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Universal Steps
Power
Patient
Analyze
Shock
Power
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Power
Turn the power
on
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Analyze
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Analyze
Stay clear while
patients heart
rhythm analyzed
Clear
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Clear
Head to toe and
toe to head:
everyone is clear!
Shock
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Shock
Defibrillate
Patient
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Patient
Standard is set of 1
shock
Immediately restart
CPR for 2 minutesthen check pulse
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REFERENCE
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REFERENCE
Subagjo,agus,dkk. BCLS (Basic cardiac lifesupport) ed.2011
ACLS (advance cardiac life support) ed.2011
Rossens
Harrison princple ed.18th