CARDIAC ARREST

ETIOLOGI

• most often caused by heart disease– Heart attack– Congestive heart failure, aortic stenosis–Cardiomyopati (95%) : heart muscle does not

contract properly -> iskemi– Myocarditis

• Pulmonary emboli• Young: hypertropic cardiomyopati (ventrikel

>) and anomalous coronary arteries

ETIOLOGY FREQUENCY

Coronary Artery Disease Acute Coronary Syndrome Chronic Myocardial Scar

Approximately 80%

CardiomyopathieDilated Cardiomyopathies Hypertrophic Cardiomyopathies

Approximately 10% to 15%

Uncommon Causes Valvular/Congenital Heart Disease Myocarditis, Genetic Ion-Channel Abnormalities, etc.

< 5%

Contributing Causes Of Cardiac Arrest

6H 5T

HypovolemiaHypoxiaHydrogen ion (acidosis)Hypokalemia/Hyperkalemia HypothermiaHypoglycemia

ToxinsTamponade, cardiacTension, pneumothoraxThrombosis (coronary or pulmonary)Trauma

symptomp• the heart stops beating and blood is not supplied

to the body • The presentation is not subtle• immediate loss of consciousness occurs → not

aroused →fall over• No pulse will be able to be palpated and no signs

of breathing• pulses paradoxus, elevated jugular venous

pulsation, distant heart sounds, and electrical alternans on ECG

Heart attack warning sign

• Chest discomfort (center of the chest that lasts more than a few minutes, or that goes away and comes back. It can feel like uncomfortable pressure, squeezing, fullness or pain)

• Discomfort in other areas of the upper body (one or both arms, the back, neck, jaw or stomach)

• Shortness of breath• Other signs: cold sweat, nausea or

lightheadedness

PATOFISIOLOGI

diagnosis

• Sudden cardiac arrest is an unexpected death in a person who had no known previous diagnosis of a fatal disease or condition. The person may or may not have heart disease.

DIFFERENTIAL DIAGNOSIS

• Acute insults (hypoxia, ischemia, acidosis, electrolyte imbalances, and toxic effects of certain drugs)

• DRUGS:– tricyclic antidepressants– neuroleptics– macrolide and quinolone antibiotics– antifungal agents– procainamide, quinidine, disopyramide (class IA

antiarrhythmics)– sotalol, dofetilide, and ibutilide (class III antiarrhythmics)

treatment• Do CPR !!!• Farmako: Epinephrine and atropine – IV or endotrakeal tube– Perifer >

• Advanced life support: treats cardiac arrest definitively with drugs, fluids, DC countershock or artificial pacemaker when appropriate

• Continous of effective Basic Life Support remains important to maintain vital organ perfusion assure circulation of lifesaving drugs

• ELECTRICAL PHASE: defibrillation is the most effective

• CIRCULATORY PHASE: good quality CPR gains increasing importance along with defibrillation

• METABOLIC PHASE(global ischemic injury): focus on metabolic derangements are critical. Therapeutic hypothermia for comatose survivors of SCD may assist in neurologic recovery at this stage.

• Sodium bicarbonate (NaHCO3) and calcium chloride (CaCl2) should never be given through the endotracheal tube

• Children as in adults defibrilation of adult/ child receiving digoxin can result in irreversible cardiac arrest

• In such patients, defibrillation should begin with the lowest energy setting that the defibrillator will deliver, then cautiously increased

• Epinephrine – n a- and b-receptor agonist– increased peripheral vascular resistance via the

stimulation of a-receptors of the blood vessels. – redistribution of blood flow from visceral organs to

the heart and brain.• Atropine– asystole and slow PEA along with epinephrine and

vasopressin• Vasopresin, amiodarone, lidocaine

PROGNOSIS

• related to the frequency of coronary artery disease.

• In the adolescent population, increased awareness of hypertrophic cardiomyopathy and appropriate screening may decrease the frequency of sudden death.

• Public education and widespread availability of AEDs will increase survival.

• BAD !!• Brain death and permanent death start to

occur in just 4 to 6 minutes after someone experiences cardiac arrest

• more than 95 percent of cardiac arrest victims die before reaching the hospital

Factors Associated With Improved Outcomes in Cardiac Arrest

Presenting rhythm of VT/VF Presenting rhythm of VT/VFEarly/bystander CPR Early/bystander CPREarly defibrillation Early defibrillationCPR prior to defibrillation in the circulatory phase of cardiac arrest Minimal interruptions to chest compressions In-hospital and out-of-hospital use of AEDs Amiodarone use in shock-resistant VT/VF Therapeutic hypothermia in comatose cardiac arrest victims