PROBLEM 5 – EMERGENCY

MEDICINE
GROUP 11
Tutor : dr. Ria Buana
Leader : Lisa Alverina 405130096
Secretary : Jessica Nadia Dinda 405120140
Notulent : Dennis Aditya 405130220

Members :
• Maxend Arselino Silooy 405120110
• Rini Wulandari 405120224
• Vanessa Angela Mercy 405120225
• Kevin Rayadi 405130042
• Kevin Hardisto 405130070
• Cecillia Young 405130140
• Sheila Zivana Pakuan 405130162
• Mike Jamila Wanane 405130198
• Fransisca Nathalia C. K. 405130215
 Help me, I am Fainting!
Male, 32 years old, came to the emergency department because he felt
chest discomfort and shortness of breath since 4 hours ago. He also had
diaphoresis and felt nauseous. He was known to have hypertension since
5 years ago, but was left untreated. His daily blood pressure was around
160/100 mmHg.
On initial physical examination, he appeared to be severely ill, fully alert,
his blood pressure was 200/120 mmHg, heart rate of 100 beats per
minute and irregular, respiratory rate of 32 breaths per minute,
temperature of 360 C, his first and second heart sounds were irregular,
his extremities were clammy. This image below was his 12 lead ECG:
Ten minutes later, the patient suddenly became unconscious his
carotid pulse was not palpable and he was not breathng. His ECG
monitor showed us this result.

Identify the problem chronologically in this case, discuss it, and plan
the proper treatnent while considering all the possibilities!
 Unfamiliar Terms
• Diaforesis  keringat dingin karna rangsang saraf
simpatis yang berlebihan
 Rumusan Masalah
1. Apa penyebab rasa tak nyaman pada dada, nafas pendek,
diaforesis dan mual pada pasien?
2. Apa yang menyebabkan TD-nya bisa naik menjadi 200/120
mmHg?
3. Jelaskan apakah ada hubungan riwayat hipertensi sejak 5 tahun
yang lalu dengan keluhan pasien sekarang?
4. Apa yang menyebabkan ekstremitasnya basah?
5. Saat dilakukan pemeriksaan fisik didapatkan frekuensi jantung
yang ireguler, BJ pertama dan kedua ireguler, dan takipneu.
Apa yang menyebabkan hal tersebut?
6. Interpretasi EKG awal?
7. Mengapa 10 menit kemudian pasien tiba-tiba tidak sadarkan
diri, nadi di a.carotis tidak teraba, dan tidak bernapas?
Interpretasi EKG yang kedua?
8. Penanganan pertama untuk pasien ini setelah EKG yang kedua?
 Curah Pendapat
1-4.
• Hypertension since 5y ago: long term untreated  left
ventricular hypertrophy  compress the chamber’s blood
vessel (coronary arteries)  complication: myocardial
ischemic, arrhythmia, cardiac arrest !
• Dyslipidemia: if atherosclerosis occuring in the coronary
arteries  atheroma plaque occludes the lumen 
perfusion of myocardium  ischemic  angina pectoris
(stable/unstable), myocardial infarction
• Myocardial ischemic/infarction stroke volume & cardiac
output try to maintain CO  in sympathetic activity (
HR, diaphoresis and clammy skin) and parasymphatetic
activity (nauseous)
• Anaerobic metabolism in myocardial ischemic/infarction 
activate sensory pain fibres in the myocardium  chest pain
or chest discomfort
5. Symphatetic nervous activation  tachycardia (arrythmia -> irregular
heart sound)
CO  tissue hypoxia  stimulus to breathe  tachypnea
6. Lead I, aVL, V5, V6  lateral: STEMI @ V5 and V6
II, III, aVF  inferior: ST depression (ischemic)
V1 – V4  antero-septa: STEMI @ V2 – V6
V2 – V3  Q pathologic: previous myocardial infarction
7. 10 minutes later: the ECG result  Ventricular Fibrilation (VF)
8. Shockable rhythm  Shock with defibrilator manual  CRP 2
minutes and give IV line  assessing rhythm  shockable  shock +
CRP 2min and give Epinephrin 1mg/3-5min  assessing  shockable
 shock + CRP 2min and give Amiodaron 300mg/bolus
Review
CHEST
DISCOMFORT

ACUTE
STABLE CORONARY
ANGINA SYNDROME
(ACS)

UAP STEM NSTEMI

I
 Learning Objectives
• Menjelaskan tentang Cardiac Arrest (PVT, VF,
Asistol, PEA)
• Menjelaskan tentang Non-Cardiac Arrest (ACS,
AHF, Krisis Hipertensi)
LO 1

CARDIAC ARREST
 Cardiac arrest from a primary
cardiac origin typically presents as:
• VF  old MI, acute MI
• VT  miocardial hypertrophy,
cardiomiopathy, specific structural
abnormalities Cardiopulmonary arrest
• PEA is defined by the triad of
• Asystole unconsciousness,
apnea, and
• Metabolic  hyperkalemia 
pulselessness.
result in progressive widening of
the QRS complex  can
deteriorate to VT, VF, asystole or
PEA.
• Electrocution
 Physical Examination
Physical examination of a cardiac arrest patient
is necessarily focused on a few key goals:
• (1) ensure adequacy of airway maintenance
and ventilation,
• (2) confirm the diagnosis of cardiac arrest,
• (3) find evidence of cause, and
• (4) monitor for complications of therapeutic
interventions.
 Monitoring
• Arterial Blood Pressure and Coronary
Perfusion Pressure
• End-tidal Carbon Dioxide
• Central Venous Oxygen Saturation
• Echocardiography
• Laboratory Testing
PEA- H’s and T’s of ACLS
(major contributing factors)
PEA-H’s and T’s of ACLS
(major contributing factors)
LO 2

NON-CARDIAC ARREST
(AHF, ACS, HYPERTENSIVE CRISIS)
ACUTE HEART FAILURE
ETIOLOGY
PATOPHYSIOLOGY
PATOPHYSIOLOGY
SIGN & Symptoms:
SYMPTOMS fatigue, shortness of breath/dyspnea, orthopnea, cheyne-stokes respiration,
feeling uncomfortable when lying flat more than a few minutes, anorexia, nausea,
abdominal pain & fullness, weight loss

Sign: (found in physical examination)

•SBP: early HFnormal/high, advanced HF low (due to ↓ stroke volume
• cool peripheral extremities
•Cyanosis (lips and nail bed)
•Pitting edema
•JVP (early stagemay be normal, then may become elevated (positive
abdominojugular reflux)
•Pulmonary: crackles (rales or crepitations)
•Cardiac examination:
-cardiomegaly: PMI below the 5th ICS& lateral to the midclavicular line
-S3 (protodiastolic gallop)
-murmur
•cachexia
ADDITIONAL ECG, chest X-ray, echocardiography,
CHECKS Lab: CBC, electrolytes, BUN, serum creatinine, hepatic enzymes,urinalysis, blood
glucose, lipid profile
Biomarker:
-natriuretic peptide: BNP (B-type natriuretic peptide) & N-terminal pro-BNP
-Troponin T and I
 EVALUATION OF THE PATIENT WITH
AHF
1. Establishing definitive diagnosis of AHF as
rapidly & efficiently as possible
2. Emergent treatment for potentially life
threatening condition
3. Identifying & adressing any relevant clinical
triggers
4. Risk stratification for triage of the patient to an
appropriate level of care
5. Defining clinical profile of the patientthe most
appropriate therapy
TREATMENT (DIURETIC)
Furosemide 20–40 mg qd or bid 400 mg/da

Torsemide 10–20 mg qd bid 200 mg/da

Bumetanide 0.5–1 mg qd or bid 10 mg/da

Hydrochlorthiazide 25 mg qd 100 mg/da

Metolazone 2.5–5 mg qd or bid 20 mg/da

 From: 2013 ACCF/AHA Guideline for the Management of Heart Failure: A Report of the American College of
Cardiology Foundation/American Heart Association Task Force on Practice Guidelines
J Am Coll Cardiol. 2013;62(16):e147-e239. doi:10.1016/j.jacc.2013.05.019

Figure Legend:
Date of download: 10/19/2016 Copyright © The American College of Cardiology. All rights reserved.
Classification
TABLE 26-3 -- New York Heart Association Functional Classification of Heart
Failure
CLASS SYMPTOMS
Class I (mild)
No limitation of physical activity

Ordinary physical activity does not cause undue fatigue, palpitation, or dyspnea (shortness of
breath)

Class II (mild)
Slight limitation of physical activity

Comfortable at rest, but ordinary physical activity results in fatigue, palpitation, or dyspnea

Class III (moderate)

Marked limitation of physical activity

Comfortable at rest, but less than ordinary activity causes fatigue, palpitation, or dyspnea

Class IV (severe)
Unable to carry out any physical activity without discomfort

Symptoms of cardiac insufficiency at rest

If any physical activity is undertaken, discomfort is increased

ACUTE CORONARY SYNDROME
(UAP/NSTEMI, STEMI)
 UA & NSTEMI
• UA (unstable angina):
– Angina pectoris or equivalent ischaemic discomfort
with at least 1 of 3 features:
• Occurs at rest/minimal exertion, usually lasting > 10 min
• Severe, new onset (within the prior 4-6 wks)
• Crescendo pattern (more severe, prolonged or frequent)

• NSTEMI: clinical features of UA + evidence of

myocardial necrosis (elevated cardiac biomarkers)
ETIOLOGY & Oxygen supply↓ , +increase myocardial oxygen demand
PATOPHYSIOLOGY (atherothrombotic coronary plaque)
CLINICAL • Chest pain (substernal region or sometimes epigastriumradiates to
PRESENTATION the neck, left shoulder, and/or left arm
• Dyspnea
• Diaphoresis, pale & cool skin, sinus tachycardia, S3 or S4, basilar rales,
sometimes hypotension  large NSTEMI

ADDITIONAL • ECG (ST : depression or transient elevation, T –waves inversion)

EXAMINATION • Cardiac biomarkers: CK-MB, troponin (if elevated  NSTEMI, if not
elevated  UA)
• Coronary imaging  emerging option
Four major diagnostic tools: clinical history, ECG, cardiac markers, stress testing (coronary imaging)

TREATMENT
Anti-ischaemic treatment : nitrates, beta adrenergic blockers and other agents
Antithrombotic therapy
Invasive therapy : PCI (especially for high-risk patient)
Long term management
Clinical presentation
 Management
• The following medications are used in the management of unstable angina:
– Antiplatelet agents (eg, aspirin and clopidogrel)
– Lipid-lowering statin agents (eg, simvastatin, atorvastatin, pitavastatin, and
pravastatin)
– Cardiovascular antiplatelet agents (eg, tirofiban, eptifibatide, and abciximab)
– Beta blockers (eg, atenolol, metoprolol, esmolol, nadolol, and propranolol)
– Anticoagulants (eg, heparin)
– Low-molecular-weight heparins (eg, enoxaparin, dalteparin, and tinzaparin)
– Thrombin inhibitors (eg, bivalirudin, lepirudin, desirudin, and argatroban)
– Angina nitrates (eg, nitroglycerin IV)
– Angiotensin-converting enzyme inhibitors (eg, captopril, lisinopril, enalapril,
and ramipril)
• Surgical intervention in unstable angina may include the following:
– Cardiac catheterization
– Revascularization
http://emedicine.medscape.com/article/15938
3-overview
HYPERTENSIVE CRISIS
 Hypertensive Crisis
• A severe and quickly increase in blood pressure that
can lead to a stroke.
• Extremely high blood pressure, systolic pressure of
180mmHg/higher or diastolic pressure of
120mmHg/higher.
• Divided into two categories: urgent and emergency.
– Urgent : extremely high blood pressure without any damage
to your organs.
– Emergency : extremely high blood pressure and has caused
damage to your organs.
• SS/:
– Severe chest pain
– Severe headache,
accompanied by
confusion and blurred
vision
– Nausea and vomiting
– Severe anxiety
– Shortness of breath
– Seizures
– unresponsiveness
 Treatment
• Hypertensive emergency
– immediate BP reduction to limit continuing end-organ damage.
• not to normalize the BP (< 140/90 mmHg)
• reduce the mean arterial pressure (MAP = 1/3 systolic BP + 2/3 diastolic
BP) by -20% in the first half-hour.
• Aortic dissection  rapid reduction in systolic BP to < 100 mmHg & heart
rate to <60 bpm.
• intracranial hemorrhage  controversial  cautious reduction of systolic
BP <200 mmHg or diastolic BP < 110 mmHg is recommended + immediate
consultation with a neurosurgeon.
• hypertensive urgency  Immediate aggressive BP reduction
is contraindicated
– overzealous treatment  secondary cerebral hypoperfusion and CNS
ischemia.
– Gradually reduce the BP to normotensive limits over a period of 24-48
hours with the use of oral antihypertensive medicines.
 Hypertensive emergencies
Evaluation:
• Electrolyte, BUN creatinine levels, dipstick urinalysis
• CBC and peripheral blood smear
• Imaging (according to clinical presentation).
– Pulmonary edema or chest pain  chest radiography, ECG
– Neurological signs  head CT scan

Medscape: Hypertensive emergencies

 Case in fifth problem
• Untreated hypertension can be the risk factor
of acute coronary syndrome in this patient
• Non –cardiac arrest  cardiac arrest
• Last ECG: VF treatment plan : shock + CPR
(+pharmacological agents needed)
 Conclusion
• We have learned about:
– Non-cardiac arrest (AHF, ACS, hypertensive crisis)
– Cardiac arrest
 REFERENCES
• Longo D, Fauci AS, Kasper D, Hauser S, Jameson
JL, Loscalzo J, editors. Harrison’s Principles of
Internal Medicine. 18th ed. New York: McGraw-
Hill, 2001
• Braunwald’s heart disease : a textbook of
cardiovascular medicine 10th edition
• http://www.calgaryguide.ucalgary.ca/category/ca
rdiology
• AHA Guidelines update for CPR and ECC 2015
• https://acls-algorithms.com/