classification of cardiovascular

emergency
1. Cardiac arrest
2. Acute coronary syndrome
1. Unstable angina pectoris
2. NSTEMI (Non- ST elevation miocard
infark)
3. STEMI (ST elevation miocard infark)

Cardiac arrest
Definition
Condition that the circulation of blood
stop because heart cant contraction
effectively
Etio:

ventricular fibrillation
Pulseless ventriculat tachycardia
Pulseless electrical activity (PEA)
Asistol

Karakter Klinis Cardiac

Arrest
PRODROMAL
Angina
Dyspnea
Palpitasi
Mudah lelah
Gejala tidak spesifik
untuk cardiac arrest.

: perubahan status
ONSET
kardiovaskular akut
yang dapat
menimbulkan cardiac
arrest dalam waktu 1
jam.
EKG : perubahan
aktivitas elektrik (VF,
VT)
Kesuksesan resusitasi
bergantung pada
interval waktu antara
onset & tindakan
intervensi.

Tanda & Gejala

Tidak responsif
Tidak ada pulsasi
nadi
Pernapasan
dangkal &
terengah selama
beberapa menit
Biasanya disertai :
Sakit dada

Dyspnea
Palpitasi
Kejang
Segera setelah
henti jantung
terjadi :
Shock atau
hipotensi
Gangguan status
mental

Diagnosa Banding
Hilang kesadaran mendadak dengan
pulsasi teraba :
Syncope
Seizure
Acute stroke
Hypoglycemia
Acute airway obstruction
Head trauma
Toxins

Ventricular fibrilation
Definisi :bentuk gambaran gelombang
yg naik turun dlm berbagai bentuk
amplitudo ( Tidak ada kompleks QRS
atau segmen ST )
Fibrilasi halus di tandai dengan
amplitudo < 0,2mv

Risk Factor

Smoking
Elevated Cholesterol
serum
Elevated blood
presure
Diabetes

Obesity
Lack of physical
exercise
Family History
Age

Etiologi

Coroner heart disease

Accumulation ion Ca
Free radikal
Disorder of cell metabolic
Modulation otonom
Hipokalium
Toksisitas obat-obatan

Clinical appreance
Henti jantung
Henti nafas

Ventriculer fibrilation
Heart is composed of several normal myocardial
regions interspersed by regional ischemia
myocardial, injury or infarction were not
synchronized and chaotic.
Without regular ventricular depolarization
ventricles cant be contracted as a unit & dont
result in cardiac output (CO). Heart "shaking /
shivering" and does not pump blood

Criteria for determining based on

ECG
Value / QRS complex: cant be determined: no P
wave, QRS or T that can be known.
Rhythm: not determinable; deflection pattern up
(peak) & down (trough) sharp
Amplitude: measured from peak to trough; Fine
(2-4 mm), medium (5-9mm), coarse (10-14mm),
very coarse (> 15mm)

Clinical manifestation
Pulse disappeared with the onset of
VF. The pulse may disappear before
the onset of VF when a common sign
for VF (rapid VT) occurred before VF
Fainting, can not respond
Gasping, breathing very difficult
Begins an irreversible death /
irreversible

Etiology
Acute coronary syndrome that causes myocardial
ischemic areas
VT is stable to unstable, untreated
Premature ventricular complexes / premature
ventricular complexes (PVC) with R on T
phenomenon (R on T)
Some drugs, electrolyte or acid-base
abnormalities that prolong the refractory period is
relatively
QT prolongation primary or secondary
Death due to electricity, hypoxia and more

GAMBAR EKG

PEA (pulse less electric

activity)
A clinical situation there is no pulse,
while impulse conduction in the heart
is still there and should be able to
generate patterns that pulse
Because the electrical activity of the
heart does not result in myocardial
contraction / inadequate ventricular
filling at diastole

Determinants based on ECG criteria:

Rhythm showed irregular electrical
activity (not VF / VT without pulse)
Generally noT irreguler a normal
sinus rhythm
Can narrow (QRS <0.10), wide
(QRS> 0.12); fast (> 100 per
minute), slow (<60/menit)
Can narrow (non-cardiac etiology),
wide (often cardiac etiology), slow
(cardiac etiology), fast (non-cardiac

Clinical manifestations
Fainting can not respond
Gasping for breath, difficulty
breathing or apnea greatly
No pulse that can be detected by
palpation (a very low blood pressure
is still possible in the case of the socalled pseudo-PEA)

Etiology
6H & 5T (hypovolemia, hypotermia,
hypoglycaemia, H+ acidosis,
hypo/hyper kalemia, hypoksia,
Trauma, Toxin, Tamponade, Tension
pneumothorax, Trombosis)

PEA

Asistol
Determinants based on ECG criteria:
Published as a "flat line" heart stops
contracting

 Speed: no visible activity ventricular

or 6 complexes per
minute;"asystole P waves" only
possible with atrial impulse (P waves)
Rhythm: no visible activity of
complex ventricular or 6 per
minute
PR: not specified, sometimes looks a
P wave, R wave but by definition
should not appear

clinical manifestations
gasping, breathing very hard (at the
beginning); unable to provide a
response
No pulse or blood pressure
cardiac arrest

etiology
End of life (death)
Ischemia / hypoxia from many causes
Acute respiratory failure (no oxygen,
apneu, asphyxiation)
Electroshock high level (eg, death due
to electrical, struck by lightning)
Can show "faint" of heart soon after
defiibrilasi, before the commencement
of the spontaneous rhythm

Differensial Diagnose of Cardiac

Arrest

Differensial Diagnose of Cardiac

Arrest
Sudden loss of consciousness with a
palpable pulse:
Syncope
Seizure
Acute stroke
Hypoglycemia
Acute airway obstruction
Head trauma, Toxins

Treatment (BCLS)
Melakukan survey primer ABCD &
lanjutkan RJP sambil menunggu alat
kejut listrik datang
Jika sudah datang pasang sadapan
pada pasien tnpa menghentikan RJP
Berhenti RJP (tidak boleh lebih dari
10 menit) Lihat ke monitor irama apa
yg terlihat

 Jika VT /VF ,kejut listrik unsynchronized

dengan energi 360 j (kejut listrik
monofasik)/200 J( kejut listrik bifasik)
RJP selama 5 siklus ( 2 menit) &lihat
monitor EKG
Jika msh VT,lakukan sama seperti di
atas & berikan EPINEPHRINE 1mg IV
/IO(ulang 3-5 menit) atau vasopresin
40 U IV/IO (hnya 1x smpai RJP selesai)

 Lakukan survey sekunder ,lakukan

intubasi

Acute coronary syndrome

UNSTABLE ANGINA
This is characterized by Pain that occurs with
less excertion , cumulating pain at rest.
platelet-fibrin thrombus associated with a
ruptured atheromatous plaque without
complete occulation of the vessels.
The risk of infraction is
subtanial, and the main aim
of therapy is to reduce this.

Unstable angina

is that characterized by
rapidly worsening chest pain
on minimal exertion or at
rest.
= ulcerated atheroma+
thrombus formation>>>
reduction of coronary blood
flow caused by thrombus>>
angina at rest

Unstable angina
Recent onset (less than 1 month).
Increase frequency and duration of
episode.
Angina at rest not responding readily
to therapy.
If the pain more than 30 min.????
MI

Causes:
Decrease in myocardial blood supply
due to increased coronary resistance
in large and small coronary arteries:
1. Significant coronary atherosclerotic
lesion
2. Coronary spasm (ie, Prinzmetal angina)

Causes:
3. Abnormal constriction or deficient
endothelial-dependent relaxation of
resistant vessels associated with diffuse
vascular disease
4. Syndrome X
5. Systemic inflammatory or collagen
vascular disease

Risk factors:
Major risk factors for atherosclerosis: like family
history of premature CAD, cigarette
smoking,DM,hypercholesterolemia(
Metabolic syndrome)
Other risk factors: These include LV
hypertrophy, obesity,

Precipitating factors:
These include factors such as severe
anemia, fever, tachyarrhythmias,
catecholamines, emotional stress, and
hyperthyroidism, which increase myocardial
oxygen demand.

Preventive factors:
Factors associated with reduced
risk of atherosclerosis are a high
serum HDL cholesterol level,
physical activity, estrogen, and
moderate alcohol intake (1-2
drinks/d).

Stable Angina
Exercise Testing
The goal of exercise testing is to
induce a controlled, temporary
ischemic state during clinical and
ECG observation

ECG
ST segment depression with or
without T wave inversion that
reverse after ischemia disappears.

N.A.N 2009

ECG
Elevation of ST segment in
prinzmentals angina.

N.A.N 2009

ECG
The resting ECG may be normal
between attacks however it may
show old MI, heart block or LVH

Exercise Testing
Contraindications
MIimpending or
acute
Unstable angina
Acute
myocarditis/pericarditi
s
Acute systemic illness

Severe aortic stenosis

Congestive heart
failure
Severe hypertension
Uncontrolled cardiac
arrhythmias

NON-ST ELEVATION
MYOCARDIAL
INFARCTION
a subtotally blockage in the coronary artery
in the first few hours and disappear over
time and there is evidence myocardial
infarction (elevated cardiac biomarker)

Pathophysiology
oxygen supply or myocardial
oxygen demand superimposed on a
lesion (coronary arterial obstruction
atherothrombotic coronary plaque)

Myocardial Infarction
RISK FACTOR:
1. Smoking
2. Hypertension
3. hypercholesterolemia
Myocardial Infarction

thrombus coronary artery

Coronary artery Occlusio

Aggregasi platelet

Decrease coronary artery blood flow

Arterosklerosis plaque

Ruptur plaque

Tromboxan A2

Thrombosit activation
Agonis (kolagen, ADP, epinefrin dan serotonin)

Risk Factors
age > 65 years
three or more risk factors for CAD (carotid artery
disease),
documented CAD at catheterization,
development of UA/NSTEMI while on aspirin,
more than two episodes of angina within the
preceding 24 h
ST deviation 0.5 mm, and an elevated cardiac
marker

Clinical manifestation
chest pain
located in the substernal region or
sometimes in the epigastrium, that
radiates to the neck, left shoulder,
and/or the left arm
dyspnea and epigastric discomfort

Clinical manifestation

Diaphoresis
cool skin
sinus tachycardia
a third and/or fourth heart sound
basilar rales (crackles) inflamation, fluid or
infection.
Hypotension resembling the findings of large
STEMI.

Diagnosis
clinical history
ECG
Cardiac markers (recognize or
exclude MI )
Stress testing (coronary imaging is
an emerging option).

Electrocardiogram
ST-segment depression, transient STsegment elevation, and/or T-wave
inversion occur in 30 to 50% of
patients

Cardiac Biomarkers
elevated biomarkers of necrosis,
such as CK-MB > 3 ng/ml and
troponin >0.4 ng/ml
High risk mortality if troponin
incrase.

Therapy

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%).

AMERICAN HEART
ASSOCIATION

CHANGES IN THE 2010

GUIDELINES AFFECTING
ALL RESCUERS

AMERICAN HEART ASSOCIATION:

2010 GUIDELINES
Health Care Provider*
PUSH HARD AND PUSH FAST
At least 100 COMPRESSIONS / MINUTE*
Allow the chest to recoil -- equal compression and relaxation times
<10 seconds for pulse checks or rescue breaths
Compression Depth*
Adults 2
Child/Infant 1/3 depth of chest

Avoid excessive ventilations

1.5" infant

2" child

AMERICAN HEART ASSOCIATION:

2010 GUIDELINES
A-B-C changed to C-A-B*
Critical element is chest compressions
Delay in A-B
Avoidance of A & B

Early defib
If alone--call and retrieve AED
Exception asphyxial arrest

AMERICAN HEART ASSOCIATION:

2010 GUIDELINES
Cricoid pressure not recommended
Advanced airway = 1 every 6-8
seconds

Adult: 1 every 5-6 Peds: 1 every 3

With advanced airway- no pause

Dispatcher Identification
SCA = seizure & agonal gasps
Trained to ID ask if breathing is
normal
Only gasping???
Provide CPR instructions

AMERICAN HEART ASSOCIATION:

2010 GUIDELINES
AHA ECC Adult Chain of Survival - New

AMERICAN HEART ASSOCIATION:

2010 GUIDELINES
Simplified Universal
BLS algorithm

PRIMARY SURVEY
CARDIOGENIC SHOCK

PRIMARY SURVEY

SECONDARY SURVEY
CARDIOGENIC SHOCK

Survey sekunder
Anamnesis
Pasien dg infark miokard akut : nyeri dada akut, riwayat
penyakit jantung koroner sebelumnya
Komplikasi mekanik infark miokard : nyeri dada, gejala
tiba-tiba yg menunjukkan edema paru akut, atau bahkan
henti jantung.
Pasien aritmia : palpitasi, presikop, sinkop, merasakan
irama jantung berhenti sejenak, letargi akibat
berkurangnya perfusi ke SSP.

Pemeriksaan fisik

Sistolik < 90 mmHg

Takikardi
Takipneu
Ronki
Irama gallop
Regurgitasi mitral atau defek septal ventrikel
Bising murmur
Pasien dg gagal jantung kanan :
pulsasi di liver akibat regurgitasi trikuspid, terjadinya asites
Pulsasi arteri di ekstremitas perifeer menurun, edema
perifer
Sianosis dan ekstremitas teraba dingin

VARIABEL YANG SERINGKALI DIMONITOR PADA SYOK

PENGUKURAN
Tekanan darah pd
pemb.nadi
Denyut nadi
Tek.vena sentral
Hematokrit
Darah arteri
pH
pCO2
HCO3
Asam laktat
Air kemih
Volume
Berat molekul

NILAI
NORMAL

NILAI KHAS pd
SHOCK

120/80

<90 mmHg sistolik

80/menit
4-8cm saline
35-45%

>100/menit
<3cm
<35 %

7,4
95 mmHg
40 mmHg
23-25 mEq/liter
12 mg/liter

7,3
85 mmHg
<30 mmHg
<23 mEq/liter
>20 mg/100ml

50 ml/jam
1,015-1,025

<20 ml/jam
>1,025

Penemuan Laboratorium

Troponin I dan T meningkat

ABG biasanya menunjukkan hipoksemia dan asidosis metabolik
dimana dapat dikompensasi dengan alkalosis respiratorik
Cardiac markers, creatinin phosphokinase dan MB fractionnya
jelas meningkat
Perubahan pada ekg meliputi kompleks QRS gelombang T dan
segmen ST.

Perubahan klasik pada EKG

A: skema EKG normal, terdiri dari gelombg P < kompleks QRS,

gelombang T .
B: perubahan gelombang T , tinggi dan simetris. (hiperakut infark)
C: elevasi segmen ST (injury pd jam2 pertama )
D: inversi gelombang T : iskemik
E: gelombang Q abnormal lebar >1mm tinggi >25% tinggi gelombang R.

Iskemik : (<20 menit) : gel T tinggi, inversi gelombang T,

depresi segmen T
Injuri : (20-40 menit) : elevasi segmen T
Infark : (setelah 2 jam ) : gel Q abnormal

IMA

PEMERIKSAAN PENUNJANG
EKG
Membantu menentukan etiologi
IMA: bila lokasi infark di ventrikel kanan, maka
akan terlihat elevasi ST di sandapan V4R
Rontgen dada
Gagal ventrikel kiri berat kardiomegali, edema
paru
VSD / regurgitasi mitral akibat IMA kongesti
paru tanpa kardiomegali
102

 Ekokardiografi
Menilai fungsi ventrikel kanan
Menilai fungsi katup jantung (stenosis atau
regurgitasi)
Menilai tekanan ventrikel kanan
Mendeteksi adanya shunt (cth: VSD)
Mendeteksi adanya efusi perikardial / tamponade

103

 Pemantauan hemodinamik
Penggunaan kateter Swan-Ganz mengukur
tekanan arteri pulmonal dan tekanan baji pembuluh
kapiler, indikator evaluasi terapi
Saturasi O2
Dapat dilakukan saat pemasangan kateter SwanGanz
Dapat mendeteksi adanya VSD

104

Monitoring hemodinamik
Pengukuran tek pengisian ventrikel & curah jntg
gmbrn brtnya masalah, prognosis & hipovolemi
Pompa balon intra aorta
I : perburukan hemodinamik e.c ggl pompa jntg atau
g3 mekanik, yaitu bl :
Hipotensi (sistolik <90mmHG, tek arteri rata2
60mmHG atau <30mmHG dbwh tek basal sblmnya)
Tek baji arteri (>16-18mmHG)
Indeks jntg (<2L/mnt/m2)

CPR

CPR
Combines external chest
compressions with artificial
ventilation
Provides 30% (or less) of normal
circulation
Only effective for short period of time

CPR 1 Rescuer
Assess
responsiveness
Summon EMS
Position the
patient

CPR 1 Rescuer
Open the airway

CPR 1 Rescuer
Look, listen, and
feel for
breathing

CPR 1 Rescuer
If there is no
breathing, give
two breaths,
each lasting 1
second

CPR 1 Rescuer
Check for a
pulse ( 10
seconds)

CPR 1 Rescuer
If there is no
pulse, find your
landmarks,
lower half of the
sternum,
between the
nipples

CPR 1 Rescuer
Begin chest
compressions

CPR 1 Rescuer
Perform 30
chest
compressions
Push hard
Push fast
Allow the chest
to recoil after
each
compression

CPR 1 Rescuer
Administer two
ventilations
then return to
compressions

CPR 2 Rescuer
1

CPR - Children

Use heel of one

hand
Keep airway
open with other
hand
30
compressions:2
ventilations if
alone (2

CPR - Infant

Give chest thrusts

and puffs of air
30 compressions:2
ventilations if
alone
15 compressions: 2
ventilations with 2
rescuers

AEDs

Safe, accurate &

lightweight
Easy to operate
What is public
access defibrillation?

PAD
AEDs in public
places
Training the public
in CPR/AED

Special Considerations

Children
Clothing
Body hair
Implanted
Water
defibrillators or
pacemakers
Transdermal
medication patches Metal surfaces
Jewelry and glasses

AED

Assess

Check your
patient

Universal Steps

Power

Patient

Analyze

Shock

Power
Turn the power
on

Patient

Apply pads to
patient

Analyze

Stay clear
while patients
heart rhythm
analyzed

Clear

Head to toe
and toe to
head:
everyone is
clear!

Shock
Defibrillate

Patient

Standard is set of
1 shock
Immediately
restart CPR for 2
minutes then
check pulse