Cardiac Arrest

classification of cardiovascular emergency

1. Cardiac arrest2. Acute coronary syndrome

1. Unstable angina pectoris2. NSTEMI (Non- ST elevation miocard infark)3. STEMI (ST elevation miocard infark)

Cardiac arrest

• Definition– Condition that the circulation of blood stop

because heart can’t contraction effectively– Etio: • ventricular fibrillation• Pulseless ventriculat tachycardia• Pulseless electrical activity (PEA)• Asistol

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 can’t be contracted as a unit & don’t result in cardiac output (CO). Heart "shaking / shivering" and does not pump blood

Criteria for determining based on ECG

• Value / QRS complex: can’t 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 etiology)

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 so-called pseudo-PEA)

Etiology

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

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

• QRS complex: no visible deflection consistent

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

The Canadian Cardiovascular Society grading scale

• is used for classification of angina severity, as follows:

• Class I : Angina only during strenuous or prolonged physical activity

• Class II : Slight limitation, with angina only during vigorous physical activity

• Class III : Symptoms with everyday living activities, ie, moderate limitation

• Class IV : Inability to perform any activity without angina or angina at rest, ie, severe limitation

N.A.N 2009

The New York Heart Association classification

• is also used to quantify the functional limitation imposed by patients' symptoms, as follows:

• Class I : No limitation of physical activity (Ordinary physical

activity does not cause symptoms.) • Class II : Slight limitation of physical activity (Ordinary physical

activity does cause symptoms.) • Class III : Moderate limitation of activity (Patient is comfortable

at rest, but less than ordinary activities cause symptoms.) • Class IV : Unable to perform any physical activity without

discomfort, therefore severe limitation (Patient may be symptomatic even at rest.)

N.A.N 2009

Causes:

• Decrease in myocardial blood supply due to increased coronary resistance in large and small coronary arteries:

1. Significant coronary atherosclerotic lesion2. Coronary spasm (ie, Prinzmetal angina)

N.A.N 2009

Causes:

3. Abnormal constriction or deficient endothelial-dependent relaxation of resistant vessels associated with diffuse vascular disease (ie, microvascular angina)

4. Syndrome X 5. Systemic inflammatory or collagen vascular

disease, (scleroderma, systemic lupus erythematous, Kawasaki disease, polyarteritis nodosa, and Takayasu arteritis)

N.A.N 2009

Risk factors:

• Major risk factors for atherosclerosis: like family history of premature CAD, cigarette smoking,DM,hypercholesterolemia(Metabolic syndrome), or systemic HTN

• Other risk factors: These include LV hypertrophy, obesity,

N.A.N 2009

http://emedicine.medscape.com/article/150916-overview

http://emedicine.medscape.com/article/165124-overview

Precipitating factors:

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

N.A.N 2009

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).

• ???!! Plz Don’t drink and smoke 4u life.

N.A.N 2009

Stable AnginaExercise Testing

• The goal of exercise testing is to induce a controlled, temporary ischemic state during clinical and ECG observation

N.A.N 2009

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 prinzmental’s angina.

N.A.N 2009

ECG

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

N.A.N 2009

Exercise TestingContraindications

• MI—impending or acute• Unstable angina• Acute myocarditis/pericarditis• Acute systemic illness• Severe aortic stenosis• Congestive heart failure• Severe hypertension• Uncontrolled cardiac arrhythmias

N.A.N 2009

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.Smoking2.Hypertension3.hypercholesterolemia

thrombus coronary artery

Decrease coronary artery blood flow Arterosklerosis plaque

Ruptur plaqueThrombosit activationAgonis (kolagen, ADP, epinefrin dan serotonin)

Tromboxan A2

Aggregasi platelet

Myocardial Infarction

Coronary artery Occlusion

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


• 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


• 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 ST-segment 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 3–5% or recurrent ACS (5-15%).

AMERICAN HEART ASSOCIATION

CHANGES IN THE 2010 CHANGES IN THE 2010 GUIDELINES AFFECTING GUIDELINES AFFECTING

ALL RESCUERSALL RESCUERS

AMERICAN HEART ASSOCIATION:AMERICAN HEART ASSOCIATION:2010 GUIDELINES2010 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 1.5" infant 2" child

Avoid excessive ventilations

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


• 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


AHA ECC Adult Chain of Survival - New

Simplified Universal BLS algorithm


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 2

3 4

CPR - Children

• Use heel of one hand

• Keep airway open with other hand

• 30 compressions:2 ventilations if alone (2 rescuers use 15:2)

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• Water• Transdermal

medication patches

• Implanted defibrillators or pacemakers

• Metal surfaces• Jewelry and glasses

Assess • Check your patient

Universal Steps

Power↓

Patient↓

Analyze↓

Shock

Power

• Turn the power on

Patient

• Apply pads to patient

Analyze

• Stay clear while patient’s 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

Cardiac Arrest

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