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resusitasiPRADITA DIAH PERMATASARI

Definition

Sudden cardiac death natural death from cardiac causes, heralded by abrupt loss of consciousness within 1 hour of the onset of an acute change in cardiovascular status

Braunwald’s hearts disease 9th e, part 41 Cardiac arrest and sudden cardiac death

TERM DEFINITION QUALIFIERS MECHANISMSSudden cardiac death

Sudden, irreversible cessation of all biologic functions

None —

Cardiac arrest

Abrupt cessation of cardiac mechanical function, which may be reversible by a prompt intervention but will lead to death in its absence

Rare spontaneous reversions; likelihood of successful intervention relates to mechanism of arrest, clinical setting, and prompt return of circulation

Ventricular fibrillation, ventricular tachycardia, asystole, bradycardia, pulseless electrical activity, mechanical factors

Cardiovascular collapse

Sudden loss of effective blood flow due to cardiac and/or peripheral vascular factors that may reverse spontaneously (e.g., neurocardiogenic syncope; vasovagal syncope) or require interventions (e.g., cardiac arrest)

Nonspecific term; includes cardiac arrest and its consequences and transient non–life-threatening conditions that usually revert spontaneously

Same as cardiac arrest, plus vasodepressor syncope or other causes of transient loss of blood flow

Terms Related to Sudden Cardiac Death


Four temporal perspectives of sudden cardiac death


Epidemiology

Fewer than 250,000 SCDs annually when the etiologic definition is limited to coronary heart disease

More than 460,000 SCDs per year when all causes are included.


Braunwald’s hearts disease 9th e, part 41

Cardiac arrest and sudden cardiac death

Causes and contributing factors in sudden cardiac death Coronary artery abnormalities Hypertrophy of ventricular myocardium Myocardial diseases and heart failure Inflammatory, infiltrative, neoplastic, and degenerative processes Diseases of the cardiac valves Congenital heart disease Electrophysiologic abnormalities Electrical instability related to neurohumoral and central nervous system

influences Sudden infant death syndrome and sudden death in children Miscellaneous


Pathology dan Pathophysiology

Pathologic studies in SCD victims reflect the epidemiologic and clinical observations that coronary atherosclerosis is the major predisposing cause

CORONARY ARTERIES Extensive atherosclerosis has long been recognized as the

most common pathologic finding in the coronary arteries of victims of SCD


The role of active coronary artery lesions, characterized by plaque fissuring, plaque erosion or rupture, platelet aggregation, and thrombosis, as a major pathophysiologic mechanism of the onset of cardiac arrest has become clarified


Coronary artery spasm, an established cause of acute ischemia and SCD is commonly associated with nonobstructive plaques, and spasm itself has been recognized at postmortem examination in rare cases

MYOCARDIUM

Healed myocardial infarction is a common finding in SCD victims, with most investigators reporting frequencies ranging from 40% to more than 70%.


VENTRICULAR HYPERTROPHYheart weights are higher in SCD victims than in those whose death is not sudden, despite similar prevalences of history of hypertension before death

SPECIALIZED CONDUCTING SYSTEM IN SUDDEN CARDIAC DEATHFibrosis of the specialized conducting system may be observed in SCD victims


CARRDIAC NERVES AND SUDDEN CARDIAC DEATHDiseases of cardiac nerves have been postulated to have a role in SCD


Mechanism of Sudden Cardiac Death

Triggering factors ischemia, hemodynamic changes, fluctuations in the autonomic nervous system, electrolyte abnormalities, proarrythmic effect of drugs

TACHYARRYHTMIAS IN SCD VF first recorded rhythm in approximately 75% SCD VT degenerating into VF

Hurst’s The Heart 12th edition, Chapter 49 Sudden cardiac death

BRADYARRHYTHMIAS IN SCDBradyarrhytmias were documented infrequentlyThe basic electrophysiologic mechanism in this form of arrest is failure of normal subordinate automatic activity to assume the pacemaking function of the heart in the absence of normal function of the sinus node, AV junction, or both


Electrophysiologic Effects of Ischemia Acute myocardial ischemia intracellular and extracellular

acidosis and loss of myocellular membrane integrity with efflux of potassium and influx of calcium decrease in the amplitude and upstroke velocity of the cardiac action potential, inhomogeneous depolarization of the resting membrane potential, and shortening of action potential duration.


Fast sodium and slow calcium channels in partially depolarized fibers may remain inactiveprolonging refractoriness electrical inhomogeneities within and around the ischemic zoneconduction delays, unidirectional block, and reentrant arrhythmias


Mechanoelectrical Feedback

acute changes in the mechanical state of the heart related to altered preload and contractility can have direct electrophysiologic effects that may precipitate arrhythmias; this relationship is referred to as mechanoelectrical feedback.


Cardiac disease associated with sudden death1. ISCHEMIC HEART DISEASE Coronary atherosclerosis

2. NONISCHEMIC HEART DISEASECardiomyopathies Idiopathic Dilated Cardiomyopathy Hypertropic Cardiomyopathy Hypertensive Cardiomyopathy Arrhythmogenic Right Ventricular DysplasiaValvular Heart Disease Mitral Valve ProlapsInfammatory and Infiltrative Myocardial DiseaseCongenital Heart DiseaseElectrolyte abnormalities


Primary Electrical Abnormality WPW Syndrome Idiopathic Ventricular Tachycardia Idiopathic Ventricular Fibrillation Brugada Syndrome

Drug and Other Toxic Agents Pro-arrhythmia Coccain


Clinical Features

Prodromal Symptoms patients at risk for SCD can have prodromes such as chest pain, dyspnea, weakness or fatigue, palpitations, syncope, and a number of nonspecific complaints.


Onset of the Terminal Event the period of 1 hour or less between acute changes in cardiovascular status and the cardiac arrest itself is defined as the “onset of the terminal event”.

Cardiac arrest characterized by abrupt loss of consciousness caused by lack of adequate cerebral blood flow due to failure of cardiac pump function.


Progression to Biologic Death The time course for progression from cardiac arrest to biologic death is related to the mechanism of the cardiac arrest, the nature of the underlying disease process, and the delay between onset and resuscitative efforts


Survivors of Cardiac Arrest

Cardiac arrests during the acute phase of myocardial infarction are classified as : - primary (electrical event not associated with hemodynamic dysfunction). Patients who are resuscitated immediately from primary VF associated with acute coronary syndromes usually stabilize promptly- secondary (electrical event linked to hemodynamic dysfunction).


Risk Stratification for SCD

Clinical history Left ventricular function Electrocardiographic abnormalities Autonomic markers Signal-averaged electrocardiography T-wave alternans Electrophysiologic studies


Treatment options for patients at risk of SCD

Β-blockers ACE-I HMG Co-A reductase inhibitor Dofetilide Amiodarone Device therapy ICD


ROLE OF SURGERYRevascularizationAntiarrythmia surgeryCatheter ablation therapy


Management of cardiac arrest

Basic life support- Chest tump- Airway This process includes tilting the head backward and lifting the chin, in addition to exploring the airway for foreign bodies, including dentures, and removing them- Breathing With the head properly placed and the oropharynx clear, mouth-to-mouth resuscitation can be initiated if no specific rescue equipment is available


- Circulation The palm of one hand is placed over the lower sternum and the heel of the other rests on the dorsum of the lower hand. The sternum is then depressed, with the resuscitator's arms straight at the elbows to provide a less tiring and more forceful fulcrum at the junction of the shoulders and back. By use of this technique, sufficient force is applied to depress the sternum about 4 to 5 cm, with abrupt relaxation, and the cycle is carried out at a rate of about 100 compressions/min.


ACLS AHA 2010

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