group 16 problem 1b

8/10/2019 Group 16 Problem 1B

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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

39


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Tanda2 henti jantung & henti napas

40


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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

group 16 problem 1b

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