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 All rescuers should, at a minimum, provide

chest compressions.
 If bystander not trained (adult arrest): Hands-
Only CPR
 If bystander trained and able: perform
compressions and ventilations at rate of 30:2
 Healthcare provider: perform compressions
and ventilations at rate of 30:2
 Compression Depth
 AT LEAST 2 inches (2005 rec : 1 ½ to 2 inches)
 Without effective chest compressions
 Oxygen flow to brain stops
 Oxygen flow to heart stops
 Drugs go nowhere

 Compression rate  AT LEAST 100x/min


 Eliminations of Look Listen and Feel
 Why? Minimizes delay to action
 Cricoid pressure is NOT reccomended in
routine use
 Why? Interfere with ventilation and advanced
airway placement
 Team resuscitation
 Minimizes interuptions in compression
 Myocardial infarction
 Definition
 Stable angina
 chest or arm discomfort that may not be described as pain
but is reproducibly associated with physical exertion or
stress and is relieved within 5–10 min by rest and/or
sublingual nitroglycerin
 Unstable angina
 equivalent ischemic discomfort + 1 of 3 features:
 occurs at rest (or with minimal exertion), lasting >10 min
 severe and of new onset (within the prior 4–6 weeks)
 occurs with a crescendo pattern
 NSTEMI
 clinical features of UA develops evidence of myocardial
necrosis
 Pathophysiology
 oxygen supply < +/ myocardial oxygen demand > +
atherosclerotic coronary plaque
 plaque rupture or erosion with superimposed
nonocclusive thrombus
 dynamic obstruction (coronary spasm, as in
Prinzmetal's variant angina)
 progressive mechanical obstruction (rapidly advancing
coronary atherosclerosis)
 myocardial oxygen demand and/or decreased supply
(tachycardia, anemia)
 History & physical examination
 chest pain (substernal region or sometimes in the
epigastrium  radiates to the neck, left shoulder,
and left arm)
 Diaphoresis
 pale cool skin
 sinus tachycardia
 third and/or fourth heart sound
 basilar rales
 sometimes hypotension
 Electrocardiogram
 ST-segment depression, transient ST-segment
elevation, and/or T-wave inversion  30-50%

 Cardiac biomarkers
 CK-MB and troponin >
 minor troponin elevations have been reported and can
be caused by congestive heart failure, myocarditis, or
pulmonary embolism  false positive value
 Diagnostic pathways
 Short term management
 placed at bed rest with continuous ECG monitoring
for ST-segment deviation and cardiac rhythm
 Ambulation is permitted if
 patient shows no recurrence of ischemia (discomfort or
ECG changes)
 does not develop a biomarker of necrosis for 12–24 h

 Medical therapy
 Anti-ischemic & anti-thrombotic treatment
 Anti-ischemic therapy
 Include bed rest, nitrates, beta blockers

 Nitrates
 sublingually or by buccal spray (0.3–0.6 mg)
 Persist after three doses given 5 min apart  IV nitroglycerin
(5–10 ug/min using nonabsorbing tubing)  may be
increased by 10 ug/min every 3–5 min  pain relieved or
systolic arterial pressure <100 mmHg
 pain-free for 12–24 h  Topical or oral nitrates replace the IV
nitroglycerin
 Beta blockers
 IV followed by oral beta blockers  heart rate of 50–60
beats/min
 Antithrombotic therapy
 Invasive VS conservative strategy
 Invasive strategy (high risk patients / class I indication)
 anti-ischemic and antithrombotic agents
 coronary arteriography is carried out within ~48 h of
admission
 coronary revascularization (PCI or coronary artery bypass
grafting

 Conservative strategy
 anti-ischemic and antithrombotic
 watchfull waiting
 coronary arteriography
 If rest pain or ST-segment changes
recur
 evidence of ischemia on a stress test
 Risk stratification & prognosis
 Pathophysiology
 coronary blood flow < + atherosclerotic thrombus 
 atherosclerotic plaque disruption (by cigarette, HT, lipid
>)
 various agonists (collagen, ADP, epinephrine, serotonin)
 platelet activation  thromboxane A2 > 
 local vasoconstrictor, further platelet activation
 conformational change in the glycoprotein IIb/IIIa receptor
 high affinity to fibrinogen  platelet cross-linking and
aggregation
 Factors VII and X are activated  prothrombin ~
thrombin  fibrinogen ~ fibrin  further coagulation
cascade
  occlusion of coronary artery by thrombus
 Clinical presentation
 precipitating factor
 vigorous physical exercise, emotional stress, or a medical or
surgical illness
 Deep & visceral pain (heavy, squeezing, and crushing;
stabbing, burning)
 occurs at rest, more severe, and lasts longer
 central portion of the chest and/or the epigastrium, occasion
it radiates to the arms, abdomen, back, lower jaw, and neck
 weakness, sweating, nausea, vomiting, anxiety, and a
sense of impending doom
 when it begins during a period of exertion  does not
usually subside with cessation
 Physical findings
 anxious and restless, attempting unsuccessfully to relieve
the pain (moving about in bed, altering their position, and
stretching)
 Pallor
 substernal chest pain > 30 min + diaphoresis
 precordium is usually quiet, apical impulse difficult to
palpate
 murmur due to dysfunction of the mitral valve
 Transmural STEMI
 pericardial friction rub is heard
 systolic pressure declines by approximately 10–15 mmHg
 laboratory findings
 Electrocardiogram
 total occlusion of an epicardial coronary artery  ST-
segment elevation + Q waves on the ECG
 Cardiac imaging
 early detection of the presence or absence of wall
motion abnormalities by echocardiography
 high-resolution cardiac magnetic resonance imaging
 radionuclide imaging techniques
 Serum cardiac biomarkers
 Cardiac-specific troponin T (cTnT) and cardiac-specific
troponin I (cTnI) >20 times higher than the upper
reference limit
 Creatine phosphokinase (CK) rises within 4–8 h and
generally returns to normal by 48–72 h (CK activity
>=2.5  suggest MI)
 Initial management
 Prehospital care
 Management in the emergency department
 Aspirin, buccal absorption of a chewed 160–325 mg
tablet
 Hypoxemia  O2 by nasal prongs or face mask (2–4
L/min) for the first 6–12 h  reassessed

 Control of discomfort
 Sublingual nitroglycerin (three doses of 0.4 mg at about 5-
min intervals)
 Morphine IV (2–4 mg every 5 min)
 IV beta blockers
 metoprolol, 5 mg every 2–5 min for a total of 3 doses 
15 min  oral regimen is initiated of 50 mg every 6 h for
48 h  100 mg every 12 h
 Management strategies  reperfusion therapy (PCI or
fibrinolytics)
 Cardiogenic shock & pulmonal edema
  life-threatening conditions that should be
treated as medical emergencies

 Etiology
 severe left ventricular (LV) dysfunction 
pulmonary congestion and/or systemic
hypoperfusion
 systemic hypoperfusion due to severe depression
of the cardiac index [<2.2 (L/min)/m2]
 sustained systolic arterial hypotension (<90
mmHg)
 elevated filling pressure [pulmonary capillary
wedge pressure (PCWP) > 18 mmHg]

 Most common etiologies


 acute myocardial infarction
 cardiomyopathy or myocarditis
 cardiac tamponade
 Other etiologies
 Post cardiac arrest  RV failure
 Refractory sustained  Refractory sustained
tacchyarrhythmias bradyarrhythmias
 Pulmonary embolus  Toxic metabolic
 Severe valvular heart  Beta blocker/CCB
disease overdose
 Severe acidosis &
 Critical aortic / mitral
hypoxemia
stenosis
 Acute severe aortic /
mitral regurgitation
 Incidence
 leading cause of death of patients hospitalized with
MI
 LV failure accounts for ~80% of the cases of CS
complicating acute MI
 fell from 20% in the 1960s but has plateaued at ~8%
for >20 years
 typically associated with ST elevation MI (STEMI)
 Pathophysiology
 Large infarctions and
shock  SIRS
 Inflammatory cytokines,
inducible nitric oxide
synthase  shock
 Pump failure 
 Poor tissue perfusion 
lactic acidosis
 Pulmonary edema 
hypoxemia
 vicious cycle of
worsening MI &
hypotension
 Risk factors  Timing
 acute MI  1/4 of MI patients
 older age develop CS rapidly
 female sex (within 6 hour of MI
onset)
 prior MI
 3/4  later on the 1st
 diabetes day
 anterior MI location  Subsequent onset of CS
 reinfarction soon after 
MI  reinfarction,
 marked infarct
expansion,
 a mechanical
complication
 Clinical findings
 Continuing chest pain &  Tachypnea, Cheyne-
dyspnea Stokes respirations
 Pale, apprehensive,  jugular venous distention
diaphoretic  S1 is usually soft, and an
 Altered consciousness S3 gallop may be audible
 weak and rapid pulse  Acute, severe MR and
 90–110 beats/min VSR  systolic murmurs
 Systolic BP <90 mmHg +  LV failure causing CS 
narrow pulse pressure rales
(<30 mmHg)  Oliguria
 quiet precordium + weak  urine output < 30 mL/h
apical pulse
 Laboratory findings  ECG
 WBC count > with left  acute MI with LV
shift failure
 BUN & creatinin >>  Q waves and/or >2-mm
ST elevation in multiple
 Hepatic transaminase leads
>>  LBBB
 Lactic acid >  1,5 of infarct  anterior
 Arterial blood gases  severe left main
 hypoxemia and stenosis  global
metabolic acidosis
ischemia
 creatine  severe (e.g., >3 mm) ST
phosphokinase, depressions in multiple
troponin I & T > leads
 Chest X ray  Echocardiogram
 pulmonary vascular  left-to-right shunt in
congestion patients with VSR
 pulmonary edema  Pulmonary embolism
 CS results from a first  Proximal aortic
MI  heart’s size is dissection with aortic
normal regurgitation or
tamponade
 Pulmonary artery catheterization
 Prognosis
 wide range of expected death rates
 age, severity of hemodynamic abnormalities, severity of
the clinical manifestations of hypoperfusion, and the
performance of early revascularization
 Independent risk factors
 advanced age; depressed cardiac index, ejection
fraction, and BP; more extensive coronary artery
disease; and renal insufficiency
 Etiology
 Cardiogenic & non
cardiogenic
 Pathophysiology (cardiogenic)
 Cardiac abnormality  pulmonary venous & hydrostatic
pressure >  fluids exit the capillary  interstitial &
alveolar edema  pleural effusion  breathing
discomfort

 Clinical findings
 rapid onset of dyspnea at rest, tachypnea, tachycardia,
and severe hypoxemia
 Rales and wheezing
 due to airway compression from peribronchial cuffing
 Hypertension
 due to release of endogenous catecholamines
 Other examinations
 Echocardiography
 systolic and diastolic ventricular dysfunction and valvular
lesions
 Electrocardiography
 ST elevation and evolving Q waves is usually diagnostic of acute
MI
 Brain natriuretic peptide levels >  heart failure as the etiology
 X ray
 peribronchial thickening, prominent vascular markings in the
upper lung zones, and Kerley B lines
 patchy alveolar filling (in perihilar distribution)  diffuse
alveolar infiltrates
 Swan-Ganz catheter
 high pressure PCWP
 Treatment
 Oksigen therapy
 Positive pressure ventilation
 Diuretics
 Furosemide <=0.5 mg/kg
 Nitrates
 Sublingual nitroglycerin (0.4 mg x 3 every 5 min)  IV
nitroglycerin, commencing at 5–10 ug/min
 Morphine
 2- to 4-mg IV boluses
 ACE-I
 A low dose of a short-acting agent may be initiated and
followed by increasing oral doses
 Other Preload-Reducing Agents
 IV recombinant brain natriuretic peptide (nesiritide) 
potent vasodilator + diuretic (refractory patients & not
recommended in ischemia or MI)
 Physical Methods
 Patients without hypotension should be maintained in the
sitting position with the legs dangling along the side of the
bed
 Inotropic and Inodilator Drugs
 dopamine and dobutamine
 bipyridine phosphodiesterase-3 inhibitors (inodilators)
 milrinone (50 g/kg followed by 0.25–0.75 ug/kg per min) 
stimulate myocardial contractility + peripheral and
pulmonary vasodilation
 Digitalis Glycosides
 rarely used at present
 Intraaortic Counterpulsation
 IABP
 Treatment of Tachyarrhythmias and Atrial-Ventricular
Resynchronization
 a primary tachyarrhythmia may require cardioversion
 patients with reduced LV function and without atrial
contraction / with lack of synchronized atrioventricular
contraction  atrioventricular sequential pacemaker
 Stimulation of Alveolar Fluid Clearance
 IV Beta-adrenergic agonist treatment decreases extravascular
lung water
 4 irama penyebab cardiac arrest
 Ventricular Fibrilation(VF)
 Pulseless Ventricular Tachycardia(VT)
 PEA(Pulseless Elecetrical Activity)
 Asystole
 Occurs when the heart starts beating
chaotically and is unable to pump blood to the
body (no pulse or breathing)

 Etiology: electrical malfunction


Step 1: Pacemaker Impulse
Generation
Step 2: AV Node Impulse
Conduction
Step 3: AV Bundle Impulse
Conduction
Step 4: Purkinje Fibers Impulse
Conduction
The heart muscle contracts

pulse, blood pressure, breathing &other signs of circulation


Signs of cardiac arrest
 Sudden loss of responsiveness

 No normal breathing
kegawatdaruratan

Henti Takiaritmi
Bradikardi
jantung a
Sinus
VF/VT PEA Asistole AV blok
bradikardi

Derajat I
Artial Ventrikel Derajat
II.1
Takiaritmia Takiaritmia Derajat II
SVT ventrikuler Derajat
Sinus Ventrikel II.2
takikar takikardi Derajat III
di monomorfik
Atrial Ventrikel
fibrilasi takikardi
polimorfik
Atrial
flutter Biasa
SVT
takikard Torsades de
i pointes
Ventrikel takikardi
 Frekuensi = 100-250 x/mnt
 Irama = tidak teratur
 Gel.P = tdk ada hub gel P dgn QRS (AV disosiasi)
 PR interval = tidak kelihatan
 Lebar QRS = > 0,25 dtk,morfologi berbeda dgn
biasa,bila da multifokal = QRS kompleks akan
terlihat berbeda-beda
 Gambaran gelombang naik turun dalam
berbagai bentuk dan amplitudo yang berbeda-
beda  spt cacing bergerak naik turun, tidak
beraturan
 Tidak tampak kompleks QRS, segmen ST, gel.
T
 Amplitudo <0,2mv  VF halus, sering pada
VF lama, mirip asistol
 VT  VF
 Etiologi:
 SKA,
 VT stabil/ tidak stabil yg tidak diobati
 Premature ventricular complexes dgn fenomena R
pada T
 Obat, ketidakseimbangan elektrolit/ asam basa
 Perpanjangan QT primer/ sekunder
 Kematian karena listrik, hipoksia, dll
 Patofisiologi
 Iskemik/ cedera/ infark pada miokard ventrikel 
depolarisasi dan repolarisasi ventrikel yang tidak
sinkron/ kacau
 Manifestasi klinis
 Megap-megap  sangat sulit bernafas  henti nafas
 Henti jantung, nadi menghilang
 Pingsan  tidak berespon
 Jantung hanya bergetar tanpa memompa
 Kriteria EKG :
 QRS tidak dapat ditentukan dan tidak ada
gelombang yang dikenali
 Gel. Pada garis dasar 150-500x/ menit
 Irama tidak dapat ditentukan
 Pola puncak (naik) dan palung (turun) tajam
 Amplitudo
 Halus  puncak ke palung 2 - <5mm
 Medium  5 - <10mm
 Kasar  10 - <15mm
 Sangat kasar  > 15mm
 1. CAB + RJP sambil menunggu defibrilator + EKG
datang
 2. pasang EKG segera tanpa menghentikan RJP 
perhatikan monitor (<10s)  VT/VS  defibrilator
 Kejut listrik 360J pada defibrilator bifasik dan 200J pada
defibrilator monofasik
 3. RJP 5 siklus (2 menit)  EKG  VT/VS  defibrilator
 RJP 5 siklus + epinefrin / vasopresin* / amiodarone
(jika IV line terpasang),. dst.
 * epinefrin 1mg IV/IO
 *vasopresin 40 U IV/IO  hanya 1x
 *amiodarone 300mg IV/IO  dapat diganti lidokaine
 VT/VF yang disaksikan trakeostomi ditunda
jika oksigenasi baik; tidak disaksikan  intubasi
trakea segera
 Adanya gambaran elektrik pada EKG tapi
tidak ditemukan denyut nadi pada perabaan
arteri karotis
 Ventrikel masih kontraksi tapi tidak cukup
kuat menimbulkan pulsasi sampai p.d.

 Manifestasi klinis
 Pingsan  tidak memberi respon
 Megap-megap  sulit nafas  henti nafas
 Tidak ada denyut yang dapat dideteksi dengan
palpasi
H T
 Hipovolemi  Toksin , ex obat
 Hipoksia  Tamponade jantung
 Hydrogen ion (asidosis)  Tension pneumothorax
 Hipo/ hiperkalemia  Trombosis koroner
 hipotermia  Trombosis paru
 Kriteria EKG
 Irama menunjukkan aktv. Listrik/ depol ventrikel
(bukan VT/VF tanpa denyut)
 Umumnya tidak seteratur irama sinus normal
 QRS interval
 Sempit  <0,10s
 Lebar >0,12s
 Cepat (>100x/ menit) atau lambat (<60x/menit)
 EKG QRS lebar dengan frek rendah (20-
40x/menit) atau <20x/menit

 Gambarannya  irama idioventrikular


 cardiac stand still with no cardiac output and
no ventricular depolarization
 Asystole is sometimes referred to as a “flat
line.”
 Jantung berhenti berkontraksi

 Keadaan puncak dari perjalanan henti jantung

 Etiologi
 Akhir dari kehidupan / kematian
 Iskemi/ hipoksia
 Gagal nafas akut (tidak ada O2, apnea, asfiksia)
 Kejut listrik tingkat tinggi, ex : tersambar petir
 Dapat menunjukkan “pingsan jantung”  setelah
defibrilasi sebelum dimulai irama sontan
 Kriteria penentu EKG
 Klasik  garis datar
 Irama  tidak dapat ditetapkan
 Kompleks QRS  tidak terlihat defleksi konsisten

 Manifestasi klinis
 Megap-megap  sulit nafas  berhenti nafas
 Tidak berespon
 Tidak ada denyut nadi

 Tatalaksana = PEA
 Tatalaksana = PEA/ VF
Jika sudah ada nafas spontan  posisi
pemulihan korban
near a true lateral position
head dependent

stable
no pressure on the chest to
impair breathing.
 Kompleks QRS melebar dengan frekuensi
rendah  20-40x/menit atau < 20x/menit
 Irama idioventrikuler
 Asistol  garis lurus tanpa aktivitas ventrikel
(tidak tampak kompleks QRS)