Professional Documents
Culture Documents
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
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
MM Angina
ISCHEMIC HEART DISEASE
Coronary Artery
Disease
Ischemic Heart
UA & NSTEMI
Disease
Acute Coronary
Syndromes
STEMI
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 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
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 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