ACLS DECEMBER 2005

ACLS DECEMBER 2005 - CARDIOPULMONARY RESUSCITATION...

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Unformatted text preview: CARDIOPULMONARY RESUSCITATION & EMERGENCY CARDIOVASCULAR CARE DECEMBER 2005 GUIDELINES Classification of Recommendations Classification of Recommendations and Level of Evidence ► CLASS I: Benefit>>>Risk ► Procedure/Rx/Diagnostic Test should be done ► CLASS IIa: Benefit>>Risk ► Procedure/Rx/Diagnostic Test reasonable to perform ► CLASS IIb: Benefit=Risk ► Procedure/Rx/Diagnostic may be considered ► Optional vs expert recommendation ► CLASS III: Risk>Benefit ► Procedure/Rx/Diagnostic should not be performed/harmful New Recommendations New Recommendations ► 2 breaths chest compressions ► All breaths (mouth­mouth, mouth­bag, bag­mask) given over 1 sec see chest rise ► Longer uninterrupted chest compression Compression:Breath (30:2) ► Push hard and push fast (100/minute) ► 2 min of compression before rhythm/pulse check in pulseless arrest ► Pulseless VF/VT: 1 shock (instead of stacked) CPR ► Compress at the center of the chest at the nipple line ► Compress the chest approximately 1.5­2 inches using heel of hands Electrical Therapies Electrical Therapies Automated Electrical Defibrillators(AED), Defibrillation, Cardioversion, Pacing ► Immediate CPR until defibrillator available ► 1­Shock vs 3­shock sequence ►No studies humans/animals comparing the two ►Animal studies: long interruptions in CPR assoc w/ post­resuscitation myocardial dysfunction and decr. survival ►RCT: interruptions in CPR assoc w/ decr. probability of conversion of VF to another rhythm ►3­Shock: 37 sec delay before 1st compression ►1­Shock: efficacy of conversion >90% (biphasic defibrillators) Monophasic vs Biphasic Monophasic vs Biphasic Defibrillators ► 1st­shock efficacy of monophasic < 1st­shock efficacy of biphasic ► Goal: delivery of current through chest to the heart to depolarize myocardial cells and eliminate VF/VT ► Monophasic: delivers current of one polarity 1­shock 360J ► Biphasic : <200J as safe and w/ higher efficacy than higher voltage in monophasic 120J, 150J, 200J AED AED ► Only useful for shockable rhythms ► If implantable medical device (pacemaker, AICD) place 1 inch away ► Do Not place on transdermal medication devicesburns, decrease energy to heart ► Individual wet/diaphoreticdry ► Decreasing impedance ► Shave chest hair ► Conductive gel ► Arched placement of AED in O2­rich environment can spark fires Synchronized Cardioversion Synchronized Cardioversion ► Shock delivery timed with QRS complex ► Indicated for Rx of unstable tachyarrhythmias associated with organized QRS complex and a perfusing rhythm ► Rx unstable SVT ► Reentry ► Atrial Fibrillation mono=100­200J, bi=100­120J ► Atrial flutter mono=50­100J, bi=100­120J ► Unstable monomorphic VT 100J, bi=100­120J ► NOT effective ► Junctional tachycardia ► Ectopic/multifocal­atrial tachycardia (automatic focus) ► Shocks to automatic focus can further increase HR Pacing Pacing ► Symptomatic bradycardia ► RCT: Asytolic patients and pacing ►No improvent in survivalClass III Medication for Arrest Rhythms Medication for Arrest Rhythms VASOPRESSORS No controlled trials demonstrating increased rate of neurologically intact survival to hospital discharge Evidence that Vasopressor agents favors initial ROSC EPINEPHRINE EPINEPHRINE ► Alpha­adrenergic vasoconstrictor properties increases coronary and CPP during CPR ► Beta­adrenergic properties controversial as they may increase myocardial work and reduce subendocardial perfusion ► 1mg dose vs High dose NSS in 8­RCT ► 1mg dose Q 3­5 min CLASS IIB VASOPRESSIN VASOPRESSIN ► Non­adrenergic peripheral vasoconstrictor ► Coronary and renal vasoconstrictor ► Meta­analysis of 5­RCT NSS between EPI and VP for ROSC, 1­hour survival, 24­hr­ survival, or survival to hospital d/c ► Dose: 40 Units ATROPINE ATROPINE ► Reverses the cholinergic mediated decrease in HR, SVR, BP ► No prospective controlled studies supporting its use in Asystole/ PEA ► Retrospective review: intubated pts w/ refractory asystole (in the field) increased survival to hospital admission ► Caution in ACS/AMI as may Incr HR and worsen ischemia ► May not be effective in cardiac transplant patients as the transplanted heart lacks vagal innervation ► Dose: 1mg Q 3­5 min (max 3mg) Amiodarone Amiodarone ► Affects Na, K, Ca­channels, alpha and beta­ adrenergic blocking properties ► RCT (in the field): Amio vs Placebo vs Lido ► Increased survival to hospital admission (SS) ► Improved defibrillator response (SS) ► Initial: 300mg, then 150mg ***(SS) Statistically Significant Magnesium Magnesium ► Observational studies termination of Torsades ► 1­2g in 50­100cc D5W over 5­20min ETT Medications ETT Medications NAVEL NALOXONE ATROPINE VASOPRESSIN EPINEPHRINE LIDOCAINE ***Dose at 2­2.5 x normal VF/VT VF/VT ► Most critical intervention during 1st min ►Immediate bystander CPR w/ min interruptions in chest compressions and Defib ASAP Class 1 ► 1­shock instead of 3­shocks (stacked) PULSELESS ARREST PULSELESS ARREST VF/VT 1ST­shock (M=360J, B=120­200J) CPR X 2 minutes 1­shock Epi 1mg Q 3­5min OR Vasopressin 40U 1­shock Amiodarone 300mg (then 150) OR lidocaine 1­1.5mg/kg x 1 (then 0.5 ­ 0.75 mg/kg x 2) Magnesium 2 gms IV for Torsades ***CPR RHYTHM CHECK SHOCK PULSELESS ARREST PULSELESS ARREST ASYSTOLE/PEA CPR x 2 min Epi 1mg Q 3­5 min OR VP 40U CPR x 2 minutes Atropine 1 mg Q 3­5 minutes (max 3 doses) for asystole or slow PEA ***CPR: PUSH HARD , PUSH FAST (100 COMPRESSIONS PER MINUTE ) ***1 DOSE VP SUBSTITUTES 2 DOSES OF EPI PULSELESS ARREST PULSELESS ARREST PULSELESS ELECTRICAL ACTIVITY (PEA) 6 H’s Hypovolemia Hypoxia Hydrogen ion (acidosis) Hypo­/Hyperkalemia Hypoglycemia Hypothermia 5 T’s Toxins Tamponade Thrombosis (coronary or pulmonary) Tension PTx Trauma Symptomatic Bradycardia Symptomatic Bradycardia ► HR<60, and inadequate for clinical condition change in mental status, ongoing severe ischemic CP, CHF, hypotension, shock ► Airway, oxygen, EKG monitor, IV ► TCP (immediate in type II 2nd,3rd AVB) CLASS 1 ► Atropine 0.5mg (may repeat to max 3mg) ► Epi 2­10mcg/min OR dopa 2­10mcg/kg/min ► TVP ► Glucagon 3mg IV3mg/hr for BB/CCB overdose refractory to atropine Tachyarrythmia Tachyarrythmia Narrow Complex QRS<0.12 Sinus Tachycardia AF/AFl AV­nodal reentry Atrial Tachycardia (ectopic,reentrant) MAT Junctional tachycardia Wide Complex QRS>0.12 VT SVT with aberrancy Narrow Complex Narrow Complex Regular Vagal Maneuver Adenosine 6, 12, 12 **If converts:reentrant SVT If not converted: CCB, BB, Amio (EF<40%) **Afl, Ectopic A.tach, J,tach Irregular CCB, BB, Amio (EF<40%) **AF, Afl, MAT Wide Complex Wide Complex ► VT or Uncertain rhythm ►Amiodarone 150mg ►Synchronized cardioversion ► AF+WPW (pre­excited AF) ►Amiodarone 150mg ►AVOID: adenosine, Digoxin, Diltiazem, Verapamil Review Review ► Pulseless VF/VT ► CPR, 120J, CPREPI/VPCPR,AirwayAmio 300 ► CPR X 2 min then shock ► Asystole/PEA ► Epi, Atropine ► Symptomatic Bradycardia ► TCP, Atropine, Epi/Dopa, TCP ► Narrow Complex Tachycardia: ► Vagal, Adenosine, CCB/BB/Amio ► Wide Complex Tachycardia ► Amio 58yo female with DM, HTN, found unresponsive, No Pulse 65 yo male with CODE BLUE, unresponsive and no palpable pulse 76 yo female with acute SOB and complaints of mild CP 50 yo male with HTN, DM, heroine abuse, CRI on HD found down and without palpable pulses ...
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This note was uploaded on 12/24/2011 for the course STEP 1 taught by Professor Dr.aslam during the Fall '11 term at Montgomery College.

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