Emergency Medicine

Help Me, I’m Fainting!

Problem 5

Group 16
October 21 th, 2016
 Group 16
• Tutor : dr. Norbert
• Leader : Silvia Dwi Mustika
• Secretary : Suni Christina W
• Scribe : Florencia Santoso
• Members :
 Julia Jennifer M.
 Yofishia
 Albert
 Gishelly Marcella
 Andi Eka Putra
 Mutiara Lirendra
 Jesica
 Skolastika Indah A.
 Help Me, I’m 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 diaphoresis and felt nauseous. He was
known to have hypertension since 5 years ago, but was felt
untreated. His daily blood pressure was around 160/100
mmhg.
On his physical examination, he appeared to be severly ill,
fully alert, his BP was 200/120 mmhg, HR 100 beats per
minute and irregular, RR 32 breats per minute, T 36 degree C,
his first and second heart sounds were irreguler, his
extremities were clammy. This below his 12 lead EKG.
Ten minute later, the patient suddenly became unconscious,
his carotid pulse was not palpable, and he was not breathing.
His ECG monitor showed us this result.
Identify the problem chronologically in this case, discuss it,
and plan the proper treatment while considering all this
possibilities!
Unfamiliar Terms Perumusan Masalah
• None P.F:
Perumusan Masalah •Tampak sakit berat
Perempuan 32 thn : •Compos mentis
K.U (4 jam lalu) •BP: 200/120 mmHg
•Rasa tidak nyaman didada •HR: 100x/menit
•Nafas pendek •RR: 32x/menit
•Keringatan •T: 36 ◦C
•Mual •BJ I dan II: irreguler
Riwayat: HT selama 5 tahun yang
tidak diobati (BP: 160/100
mmHg)
Perumusan Masalah Perumusan Masalah
P.P (EKG):
•Irama: sinus dan irreguler P.P (EKG):10 menit kemudian
•HR: sekitar 100x/menit •Fibrilasasi ventrikel halus
•Axis: - Kondisi: tidak sadar, nadi tidak
•P wave: N teraba, napas tidak ada
•PR interval: -
•QRS complex: •Pertanyaan :
Q pato: - 1. Apa saja yang kemungkinan
R wave: N yang terjadi pada pasien
Rv5: N tersebut?
Rv5+Sv2: N
2. Tatalaksana awal dan terapi
•QRS interval : N
apakah yang dapat
•ST segmen: elevasi V2-V6
(anterolateral) diberikan?
•T wave: inversi V1, LIII, Avf (inferior)
•U wave: -
Curah Pendapat Curah Pendapat
1. Mungkin terjadi: 2. Sebelum 10 menit: ABC
- Anamnesa
• A: jaga pantensi jalan napas
• D.K: angina pektoris
• B: oksigenasi (nasal kanul: 4-
• DD: GERD, gagal jantung
(III-IV) 5L/menit
- PF • C: ISDN 5 mg SL (diulang tiap
• D.K: syok kardiogenik e.c 5 menit)
angina pektoris e.c suspek • 10 menit kemudian:
ACS defibrilasi dan IV line (NS/D5)
- EKG
• D.K: syok kardiogenik e.c
STEMI
- 10 menit kemudian:
• D.K: syok kardiogenik e.c
STEMI dan VF
 Mind mapping
Bapak 32 Anamnesis:
tahun Rasa tidak nyaman didada
Nafas pendek
Keringatan
Mual

ABC dan EKG

Anamnesa
D.K: angina pektoris
DD: GERD, gagal jantung (III-IV)
- PF
D.K: syok kardiogenik e.c angina
pektoris e.c suspek ACS
- EKG
D.K: syok kardiogenik e.c STEMI

- 10 menit kemudian: Defibrilasi

D.K: syok kardiogenik e.c STEMI dan VF
 Learning Objective
1. MM Angina
2. MM ACS
3. MM STEMI dan NSTEMI
4. MM Gangguan irama jantung (gawat
darurat)
5. MM Henti Jantung
6. MM Gagal Jantung (gawat darurat)
 LO1

MM Angina
 ISCHEMIC HEART DISEASE

Coronary Artery
Disease
Ischemic Heart
UA & NSTEMI
Disease
Acute Coronary
Syndromes
STEMI

Harrison’s Principle of Internal Medicine 18th Ed

 ISCHEMIC HEART DISEASE
• Main symptom : Angina Pectoris
– Stable : chest/arm discomfort reprudicibly associated with
physical exertion or stress and is relieved within 5-10mins
by rest or sublingual nutroglycerin
– Unstable : at least have one of three features
• Occurs at rest, lasting >10mins
• Severe and new onset
• Crescendo pattern
– Prizmetal: a syndrome of ischemic pain that occurs at rest
but not usually with exertion and associated with transient
ST elevation
• Caused by focal spasm of coronal artery  severe
myocardial infacrtion
• Managed by Nitrates and CCB.
Harrison’s Principle of Internal Medicine 18th Ed
 History
1. Characteristic of pain
2. Activity at the onset of pain
3. Severity of pain (onset, peak, present, & after intervention)
4. Location of pain
5. Radiation of pain
6. Duration of pain
7. Aggravating or Alleviating factors
8. Other associated symptoms (diaphoresis, hemoptysis, Near-syncope and
syncope, Dyspnea, N/V)
9. History of prior pain & diagnostic
10. Risk factors
 LO2

MM ACS
 Coronary Heart Disease
• Asymptomatic CAD
• Stable Angina
• Unstable Angina*
• Acute Myocardial Infarct*
• Sudden Cardiac Death*
*belongs to acute coronary syndrome
 Coronary Heart Disease
Stable Angina
• Transient
• Episodic chest discomfort
• Discomfort usually is predictable and
reproducible
• Resolve spontaneously by rest or nitroglycerin
 Coronary Heart Disease
• Canadian Cardiovascular Society
classified:
 Coronary Heart Disease
Unstable Angina
• Also referred to as:
- pre-infarction angina
- crescendo angina
- intermediate coronary syndrome
- pre-occlusive syndrome
 Coronary Heart Disease
Unstable Angina
• Angina occurring with minimal exertion or at
rest, new onset angina, or worsening of
changes in preciously stable angina syndrome
• Rest angina
• New onset angina
• Printzmetal’s angina
 Coronary Heart Disease
Acute Myocardial Infarct
• Defined as myocardial cell death and necrosis
of myocardium
• According to ECG interpretation, AMI can
classified into two : STEMI and NSTEMI
 LO3

MM STEMI dan NSTEMI

 LO4

MM Gangguan irama jantung (gawat

darurat)
 Tachyarrhythmias
• Supraventricular tachycardia
• Atrial fibrillation
• Atrial flutter
• Ventricular tachycardia
» Monomorphic
» Polymorphic (Torsades de pointe)
• Ventricular fibrillation
 SVT
• Reentrant arrhythmia at AV node that is
spontaneous in onset
• May have neck fullness, hypotension and/or
polyuria due to ANP
• Narrow QRS with tachycardia
• First line is vagal maneuvers
• Second line is adenosine or verapamil
• For chronic SVT, class 1A or 1C or amiodarone or
sotalol work well
• Ablation will cure it too, but we usually do this
only in young patients
 A-Fib
• Can be due to HTN, cardiomyopathy, valvular
heart desease, sick sinus, WPW, thyrotoxicosis
or ETOH
• Therapy is either rate control via slowing AV
node conduction with stroke prophylaxis or
rhythm control
Atrial Fibrillation
 Ventricular Tachycardia

• Impulse is initiated from the ventricle itself

• Wide QRS, Rate is 140-250
• If unstable DC cardiovert
• If not, IV Amiodarone and/or DCCV
• Consider procainamide
• Nonsustained ventricular tachycardia needs no treatment
Ventricular Tachycardia
 Torsades de Pointes

• “Twisting of the points” is usually caused by medication

(quinidine, disopyramide, sotalol, TCA), hypokalemia or
bradycardia especially after MI
• Has prolonged QT interval
• Acute: Remove offending medication. Shorten the QT
interval with magnesium, lidocaine, isoproterenol, or
temporary overdrive pacing
• Chronic: may need pacemaker/ICD, amiodarone, beta-
blockers
 Ventricular Fibrillation

• Most common in acute MI, also drug overdose,

anesthesia, hypothermia & electric shock can
precipitate
• Absence of ventricular complexes
• Usually terminal event
• Use Amiodarone if refractory to DCCV.
 Classification of Anti-arrhythmics
Cla ss Actio n Exa mp le s Sid e Ef fe cts
1A Fa st so d ium chan ne l bloc ke r va ries Q uinid ine , Cla ss: na use a , vo miting
d e p o la riz a tio n a nd a ctio n p o te ntial p ro ca ina mide, Q uinid ine : h e mo lytic
d ura tio n d isop yra mid e a ne mia, thro mbo cyto pe nia ,
tinnitus
Proc ai na mid e : lup us
1B Lido ca ine, Lido ca ine: d iz z ines s,
Mex ile tine co nfusio n, seiz ure s, co ma
Mex ile tine : tre mo r, a ta xia,
ras h

1C Fle ca inid e, Fle ca inid e: p ro-a rrhythmia ,

Prop afen o ne na usea , diz zy ne ss
2 b eta-b lo cke rs SA nod e & AV no d e Prop ra no lo l, Cla ss: CHF, b ro ncho spa sm,
co nd uctio n me top ro lo l b ra dy ca rd ia , hypo tensio n
3 Pro lo ng a ctio n p oten tia l b y b lo cking Amio d a ro ne, Amio d a ro ne: he pa titis,
K+ c ha nne ls sota lo l p ulmo na ry fi b ro sis, thyroid
d iso rde rs, p e rip he ra l
neu ro pa thy
So ta lol: b ro ncho spa sm
4 cal cium cha nne l bloc ke rs AV no d e Ve ra p a mil, Cla ss: A V b lo ck,
co nd uctio n d ilit ia z e m hyp o te nsio n, b ra d ycar d ia,
co nstip a tio n
 LO5

MM Henti Jantung
 CARDIAC ARREST
Cardiac Arrest = Loss of cardiac function
resultant of:
1) Acute myocardial infarction, OR
2) Ischemia without infarction, OR
3) Structural alterations such as scar formation or
ventricular dilation secondary to prior infarction
or chronic ischemia
 Risk Factors of Cardiac Arrest
• Coronary Heart Disease
– Fibrous scar tissue formation on cardiac muscle
• Direct effect on pump mechanism and electrical
conduction pathways
– Ischemia; chronic or acute
• Coronary artery blockages
– Left ventricular dilation, myocardial stretch
• Muscle walls are fatigued
• Precursor to congestive heart failure
 Risk Factors of Cardiac Arrest
• Congestive Heart Failure
– Altered calcium regulation
• Decreased calcium = less contractile force
– Fibrous/Scar formation
• Contractile force is inhibited by lack of elasticity of the
cardiac muscle
– Left ventricular dilation, myocardial stretch
• Muscle walls are fatigued
– Hypertrophy (left ventricular)
• Increase in muscle mass, but the muscle does not increase
its pumping ability
• In pathological hypertrophy, the heart can increase its mass
by up to 150%.
 Risk Factors of Cardiac Arrest
• Shared Risk Factors
– Age
• From age 50 to 75 there is an 8x greater risk
– Hypertension
– Diabetes
– Smoking
– Obesity
– Renal disease
– Inflammation
– GENETICS!!!!
 Genetics and cardiac arrest
• Cholesterol
– Represents the strongest link genetically
– Elevated LDL (the bad one)
– Decreased HDL (the good one)
– Increases the risk of cardiac arrest at younger ages!
• Typically the sub-50 age group; as early as the mid-20’s!
– Taken in through food (controllable)
– Produced by the body (uncontrollable)
• Up to 1000mg/day
 Pathology of Cardiac Arrest
• Heart generally progresses through several
cardiac rhythm disburbancE
• With pulse
V-Tach
• Without pulse

• Course = early
in onset
V-Fib
• High survival
potential!

• Poor prognosis
Asystole for survival
• Same as PEA
http://cpr.heart.org/idc/groups/heart-
public/@wcm/@ecc/documents/image/ucm_478551.jpg
https://eccguidelines.heart.org/wp-
content/uploads/2015/09/BLS-Adult-Cardiac-Arrest-
Algorithm---2015-Update.png
https://eccguidelines.heart.org/index.php/circulation/cpr-
ecc-guidelines-2/part-7-adult-advanced-cardiovascular-life-
support/
http://circ.ahajournals.org/content/132/18_suppl
_2/S444
https://eccguidelines.he
art.org/index.php/circul
ation/cpr-ecc-
guidelines-2/part-8-
post-cardiac-arrest-care/
https://eccguidelines.heart.org/index.php/circulation/cpr-
ecc-guidelines-2/part-7-adult-advanced-cardiovascular-life-
support/
https://eccguidelines.heart.org/index.php/circu
lation/cpr-ecc-guidelines-2/part-9-acute-
coronary-syndromes/
 LO6

MM Gagal Jantung (gawat darurat)

Causes & precipitating factors of AHF

The European Society of Cardiology: Guidelines for the diagnosis and treatment of acute and chronic heart failure, 2008
Clinical presentation

The European Society of Cardiology: Guidelines for the diagnosis and treatment of acute and chronic heart failure, 2008
 Diagnosis

The European Society of Cardiology: Guidelines for the diagnosis and treatment of acute and chronic heart failure, 2008
 Assessment of Hemodynamic Profile

• The Forrester classification is based on clinical signs &

haemodynamic characteristics.
Patient Treatment Selection

Fonarow GC. Rev Cardiovasc Med. 2001;2(suppl 2):S7–S12.

AHF treatment strategy according to systolic BP

The European Society of Cardiology, Guidelines on the diagnosis and treatment of acute heart failure, 2005
 Conclussion
- Anamnesa Tatalaksan:
• D.K: angina pektoris Sebelum 10 menit: ABC
• DD: GERD, gagal jantung (III- • A: jaga pantensi jalan napas
IV) • B: oksigenasi (nasal kanul: 4-
- PF 5L/menit
• D.K: syok kardiogenik e.c • C: ISDN 5 mg SL (diulang tiap
angina pektoris e.c suspek 5 menit)
ACS 10 menit kemudian:
- EKG defibrilasi dan IV line (NS/D5)
• D.K: syok kardiogenik e.c
STEMI
- 10 menit kemudian:
• D.K: syok kardiogenik e.c
STEMI dan VF