Management of Cardiac Arrest Based on : 2010 American Heart Association Guidelines

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Transcription:

Management of Cardiac Arrest Based on : 2010 American Heart Association Guidelines www.circ.ahajournals.org Elham Pishbin. M.D Assistant Professor of Emergency Medicine MUMS

C H E S Advanced Life Support A B C T C O M p

C H Defibrillator attached E S T C O M p

Check Rhythm VT, VF PEA, Asystole

Asystole / PEA PEA : a heterogeneous group of organized electric rhythms, with either absence of mechanical ventricular activity or mechanical ventricular activity that is insufficient to generate a clinically detectable pulse. Asystole : absence of detectable ventricular electric activity with or without atrial electric activity.

DON T INTERRUPT CHEST COMPRESSION Periodic pauses in CPR should be as brief as possible and only as necessary to assess rhythm, shock VF/VT, perform a pulse check when an organized rhythm is detected, or place an advanced airway.

High quality CPR Monitoring and optimizing quality of CPR on the basis of 1- Mechanical parameters: Coronary Perfusion Pressure = (rate & depth of compressions, (Aortic Relaxation P.) (R.A Relaxation P) relaxation, and minimization of pauses) It correlate with both Myocardial blood flow & ROSC. 2- Physiologic parameters : (PETCO2, arterial pressure during the relaxation phase of chest compressions, or ScvO2 )

Asystole / PEA (cont ) The ability to achieve a good resuscitation outcome depends on: 1-Provide effective CPR 2-Identify and correct a cause of PEA / Asystole All resuscitation team members must simultaneously Conduct a search for a underlying and treatable cause of the PEA in addition to performing their assigned role.

Asystole / PEA (cont )

Asystole : It is should be confirm that: -Not another rhythm masquerading as a flat line -Not the result of an operator error that is creating a flat line Causes of an Isoelectric ECG: -Loose leads or leads not connected to the patient or defibrillator/monitor -No power -Signal gain too low

Drug Therapy in Asys / PEA A vasopressor can be given as soon as feasible with the primary goal of increasing myocardial and cerebral blood flow during CPR and achieving ROSC. Available evidence suggests that the routine use of atropine during PEA or asystole is unlikely to have a therapeutic benefit, SO Atropine has been removed from the cardiac arrest algorithm.

Rhythm Shockable Nonshockable VF Pulseless VT Asystole PEA

V.F / Pulse-less V.T The foundation of successful ACLS is : high quality CPR, and, for VF/pulseless VT, attempted defibrillation within minutes of collapse. For victims of witnessed VF arrest, early CPR and rapid defibrillation can significantly increase the chance for survival to hospital discharge. In comparison, other ACLS therapies such as medications & advanced airways, although associated with an increased rate of ROSC, have not been shown to increase the rate of survival to hospital discharge and should be performed without compromising quality of CPR or timely defibrillation.

V.F / Pulse-less V.T In other words : vascular access, drug delivery, and advanced airway should not cause significant interruptions in chest compression or delay defibrillation. There is insufficient evidence to recommend a specific timing or sequence (order) of drug administration and advanced airway placement during cardiac arrest.

Chest comp

V.F / Pulse-less V.T When VF is present for more than a few minutes, myocardium is depleted of oxygen and metabolic substrates. A brief period of chest compressions can deliver oxygen and energy and unload the volume- overloaded R.V, increasing the likelihood of returning a perfusing rhythm after shock. Performing CPR while a defibrillator is readied for use is strongly recommended for all patients in cardiac arrest

V.F / Pulse-less V.T The shorter the time interval between the last chest compression and shock delivery, the more likely the shock will be successful. A reduction of even a few seconds in the interval from pausing compressions to shock delivery can increase the probability of shock success

V.F / Pulse-less V.T The value of intentionally delaying defibrillation to perform CPR is less clear. At this time the benefit of delaying defibrillation to perform CPR before defibrillation is unclear

C Shock? H E S T C O M p Monophasic Biphasic Children 360 J / at beginning 120 J / then 200 J first 2 J/kg then 4 J/kg

Drug Therapy in V.F / Pulse-less V.T When VF/pulseless VT persists after at least 1 shock and a 2-minute CPR period, a vasopressor can be given with the primary goal of increasing myocardial blood flow during CPR and achieving ROSC. If a shock fails to generate a perfusing rhythm, then giving a vasopressor soon after the shock will optimize the potential impact of increased myocardial blood flow before the next shock.

Drug Therapy in V.F / Pulse-less V.T Amiodarone is the first-line antiarrhythmic agent given during cardiac arrest because it has been clinically demonstrated to improve the rate of ROSC and hospital admission in adults with refractory VF/pulseless VT. Amiodarone considered when VF/VT is unresponsive to CPR, defibrillation, and vasopressor therapy. If amiodarone is unavailable, lidocaine may be considered. Magnesium sulfate should be considered only for torsades de point.

As A Rule : All drugs in CPR are given I.V Push. and then 20 cc N.S.

During cardiac arrest, provision of high-quality CPR and rapid defibrillation are of primary importance and drug administration is of secondary importance. After beginning CPR and attempting defibrillation for identified VF or pulseless VT, providers can establish IV or IO access. This should be performed without interrupting chest compressions.

If IV or IO access cannot be established, epinephrine, vasopressin, and lidocaine may be administered by the endotracheal route during cardiac arrest. The optimal endotracheal dose of most drugs is unknown, but typically the dose is 2 to 21 2 times of the recommended IV dose.

C H E S T C Do not check pulse until The rhythm changed O M p

Drugs Antiarrhythmic: Amiodarone : 300 mg first dose if needed after 15-20 min, 150 mg max, 450 mg Lidocaine : 1.5 mg/kg first dose if needed Q 10 min--- 0.75 mg/kg for 2 doses max. 3 mg/kg

Vasopressors Epinephrine hydrochloride: S & NS rhythms 1 mg- IV, IO, ET Q 3-5 min/ cont to END Atropine: Forget about it!

C Drug rout H E S T C O M As a law: Drugs injections in CPR must be: PUSH ETT administration: 2-2.5 times as IV doses plus 5-10 ml distilled water p

C H E S T C O M p Prolonged CPR Hypothermia Toxicity Drowning C H E S T C O M p

Post Cardiac Arrest Care

Post cardiac arrest care has significant potential to reduce early mortality caused by hemodynamic instability and later morbidity and mortality from multiorgan failure and brain injury.

Subsequent objectives of post cardiac arrest care are : Control body temperature to optimize survival and neurological recovery Identify and treat acute coronary syndromes (ACS) Optimize mechanical ventilation to minimize lung injury Reduce the risk of multi-organ injury and support organ function if required Objectively assess prognosis for recovery Assist survivors with rehabilitation services when required

Multi System Approach to Post Cardiac Arrest Care 1- Ventilation 2- Hemodynamics 3- Cardiovascular 4- Neurological 5- Metabolic