Pulseless Emergencies

Transcription

1 Pulseless Emergencies Nicole M. Acquisto, Pharm.D., BCPS Emergency Medicine Clinical Pharmacy Specialist University of Rochester Medical Center Nothing to disclose Disclosures Objectives Understand the medications used in the AHA ACLS algorithms Discuss the literature regarding some of these medications Explain the responsibilities that a pharmacist has as part of the code team Be able to discuss the patient outcomes available in the literature regarding pharmacists as members of the code team Describe the use of simulation as a training modality for pharmacists Determine ways to incorporate code response training into your institution

2 Code Response Do you currently have pharmacists responding to cardiopulmonary arrest codes at your institution? A. Yes 24/7 response B. Sometimes pharmacy not open 24/7 C. Sometimes pharmacy open 24/7, but a pharmacist does not respond all of the time D. No response currently Code Response Is there interest in expanding pharmacist services during code response at your institution? A. Yes B. No American Heart Association ACLS Algorithms for general action plans for cardiac arrest and other acute cardiovascular problems Modifications reflect new data in resuscitation and further the principles of evidence-based medicine Emphasis on rapid application of high quality basic life support (CPR) and quick defibrillation Additional focus is placed on the concepts of strong Team Dynamics

3 Adapted from: 2006 American Heart Association Patient Case Blue 100 response call to the medicine floor 72 y/o male admitted for CAP PMH: NIDDM, hypothyroidism, COPD, CHF There is no pulse and CPR is in progress The current rhythm check shows: Audience Response Question What therapy would you want to initiate? A. Defibrillation/shock B. Have the team obtain endotrachial tube access for medication administration C. Administration of epinephrine or vasopressin D. Administration of amiodarone

4 Asystole/ Pulseless Electrical Activity (PEA) Adapted from: 2006 American Heart Association Adapted from:cvpharmacology.com Why is Catecholamine/Vasopressor Support Needed? Enhances organ perfusion Increases arterial and aortic diastolic pressure Increases cerebral and coronary perfusion pressure Reduces blood flow to visceral and muscle tissue Increased coronary perfusion pressure + blood flow Increased success of defibrillation + ROSC Adrenergic Activity α 1 Vascular smooth muscle Coronary arteries β 1 Heart β 2 Vascular smooth muscle Skeletal muscle V 1a Vascular smooth muscle Vasoconstriction shunts blood away from non-vital areas HR, force of contractility Increase myocardial oxygen demand Vasodilation Vasoconstriction, smooth muscle contraction

5 Epinephrine Stimulates endogenous α and β receptors Alpha 1 agonist Vasoconstriction Shunts blood to vital organs Beta 1,2 agonist Increases inotropy Increases chronotropy Some bronchodilatory effect Dager WE, et al. Pharmacotherapy 2006;26: Epinephrine Concerns Increases myocardial oxygen demand Increases myocardial workload Increases risk of ventricular arrhythmias Post resuscitation myocardial dysfunction High dose epinephrine found to have no benefit for survival 0.01 mg/kg to 1 mg vs. 0.1 mg/kg to 5 mg Dager WE, et al. Pharmacotherapy 2006;26: Vasopressin Adapted from: cvpharmacology.com

6 Vasopressin Higher plasma vasopressin levels in patients post ventricular arrhythmias with ROSC vs. nonresuscitated patients Porcine model ( ) Higher level of vasopressin during CPR Improved coronary perfusion pressure, myocardial blood flow Coronary venous ph 1999 ROSC more likely with epinephrine vs. vasopressin Lindner KH, et al. Anesthesiology 1992;77:662-8 Lindner KH, et al. Heart 1996;75: Vasopressin 1 st human study (1996) n=8, in-hosp cardiac arrest (VF) Vasopressin 40 units after failure with a minimum of epinephrine 1mg and defibrillation 8/8 ROSC, 3/8 survival to hospital discharge Lindner KH, et al. Ann Intern Med 1996;124: Vasopressin Double-blind, RCT Out of hosp arrest VF/pVT Unresponsive to initial shock (n=40) Epinephrine 1 mg (n=20) Vasopressin 40 units (n=20) Repeated shocks q 60-90s and ACLS (including epi) Lindner KH, et al. Lancet 1997;349:

7 Vasopressin Epi (n=20) Vaso (n=20) p ROSC 11 (55%) 16 (80%) 0.18 Hosp admission 7 (35%) 14 (70%) 0.06 Survival 24 hrs 4 (20%) 12 (60%) 0.02 Hosp discharge 3 (15%) 8 (40%) 0.16 Mean GCS 10.7 (3.8) 11.7 (1.6) 0.78 Lindner KH, et al. Lancet1997;349: Vasopressin Multi-center, Double-blind, RCT Out of hosp arrest VF/pVT/Asystole/PEA Unresponsive to initial shock (n=1186) Epinephrine 1 mg IV q3min x 2 prn (n=597) Vasopressin 40 units IV q3min x 2 prn (n=589) + additional epinephrine at the physician s discretion Wenzel, et al. NEJM 2004;350: Vasopressin Combined VF/pVT, Asystole, PEA No diff in ROSC, survival to hosp admission or discharge Logistic regression Witnessed and BLS within 10 minutes associated with increased survival ROSC not restored with study drug (n=732) Additional treatment with epi improvement in survival in the vaso group (p=0.007) Wenzel, et al. NEJM 2004;350:105-13

8 Asystole subgroup Epi (n=597) Vaso (n=589) p Odds Ratio (95% CI) ROSC with study drug 44/266 (16.5%) 42/262 (16%) ( ) Hosp admission 54/266 (20.3%) 76/262 (29%) ( ) Hosp discharge 4/262 (1.5%) 12/257 (4.7%) (0.1-1) Wenzel, et al. NEJM 2004;350: Vasopressin + Epinephrine Multi-center, randomized, double-blind, placebo controlled, out of hosp Epinephrine 1mg + vasopressin 40 units or epi 1 mg + placebo for the 1 st dose, subsequent doses with epi alone c5 Gueugniaud, et al. NEJM 2008;359:21-30 AHA Vasopressin Recommendations No data to support one over the other Dose 40 units IV/IO x 1 Half-life: minutes Replace 1 st or 2 nd dose of epinephrine Do not need to wait 10 minutes until the next epinephrine

9 Slide 23 c5 I take it this is okay? Did we decide that or should you make your own? cevans, 3/19/2010

10 Patient Case Blue 100 response call to the CCU 58 y/o male admitted for STEMI, s/p LAD stent placement PMH: HTN, hyperlipidemia, CAD, previous MI 2005 There is no pulse and CPR is in progress The current rhythm check shows: Audience Response Question What therapy would you want to initiate? A. Defibrillation/shock B. Have the team obtain endotrachial tube access for medication administration C. Administration of atropine D. Administration of magnesium Ventricular Fibrillation/Tachycardia Adapted from: 2006 American Heart Association

11 Major Determinants of Successful Resuscitation Adequacy of ventilation/oxygenation Re-establishment of effective coronary flow Control of electrical instability Restoration of cerebral blood flow Larsen MP, et al. Ann Emerg Med 1993;22: Why Do We Use Antiarrhythmic Agents? Normalize abnormally depolarizing myocardial cells Normalize cardiac conduction Adapted from: heart.med.upatras.gr/prezentare_adi/apphases.jpg Amiodarone Inhibits Na, Ca, K channels Slows intraventricular conduction (Na) Slow heart rate and blocks AV node conduction (Ca) Prolongs A-V repolarization (K) Alpha- and beta- adrenergic suppression Less pro-arrhythmic tendencies than other anti-arrhythmic agents

12 ARREST Double-blind, RCT Out of hosp arrest VF/pVT Unresponsive to 3 shocks + Epinephrine 1 mg IV Amiodarone 300 mg IV (n=246) Placebo (n=258) + no changes in further treatment or use of additional antiarrhythmics Kudenchuk PJ, et al. NEJM 1999;341:871-8 ARREST Clinical Characteristics Amio (n=246) Placebo (n=258) Witnessed arrest 155 (70%) 185 (77%) Bystander CPR 155 (68%) 138 (59%) Initial rhythm VF/pVT 205 (83%) 216 (84%) Time to 1 st shock 8.9 ± 5.4 (7.6) 9.5 ± 7.5 (7.4) Time to admin of study drug 21.4 ± 8.3 (19.2) 20.5 ± 7 (19.3) + antiarrhythmic drug for 163 (66%) 187 (73%) VF/pVT Kudenchuk PJ, et al. NEJM 1999;341:871-8 ARREST % Hospital Survival Amiodarone Placebo p = All Patients VF Initial Asystole/PEA 64 ROSC No ROSC Kudenchuk, et al. NEJM 1999;341:871-8

13 ARREST No difference in survival to hosp discharge (n=67) 13.4% Amiodarone vs. 13.2% Placebo Not powered Adverse effects requiring treatment Hypotension 91/153 (59%) vs. 69/145 (48%), p=0.04 Bradycardia 63/153 (41%) vs. 36/145 (25%), p=0.004 Kudenchuk, et al. NEJM 1999;341:871-8 AHA Amiodarone Recommendations Amiodarone replaced Lidocaine as 1 st line therapy in 2000 update (ARREST) No in-hospital arrest data Dose 300 mg diluted in > 20 ml NS or D5W IV/IO bolus May repeat 150 mg Max 2.2 gm in 24hrs Infusion: 1 mg/min over 6 hrs, then 0.5 mg/min Lidocaine Class Ib antiarrhythmic agent Na channel blockade Reduces phase 4 depolarization Decreases automaticity Interferes with reentrant pathways

14 Lidocaine Retrospective analysis All out-of-hosp VF arrests from Sustained VF arrest after 4 shocks and epinephrine 1mg Lidocaine (n=185), No Lidocaine (n=105) Results ROSC 45% vs. 24%, p<0.01 Survival to hospital admission 38% vs. 18%, p<0.001 Survival to hospital discharge 14% vs. 8%, NS Herlitz J, et al. Resuscitation 1997;33: ALIVE Double-blind, controlled Out of hosp VF arrest Unresponsive to 4 shocks + Epinephrine 1 mg IV Amiodarone 5 mg/kg IV + Placebo (n=180) Lidocaine 1.5 mg/kg IV + Placebo (n=167) + second dose of study drug after additional shock if needed Dorian, et al. NEJM 2002;346: ALIVE Clinical Characteristics Amio (n=180) Lido (n=167) Witnessed arrest 136 (76%) 130 (78%) Bystander CPR 47 (26%) 47 (28%) Initial rhythm VF 140 (78%) 132 (79%) Time to 1 st shock 8 ± 3 (8) 9 ± 4 (9) Time to admin of study drug 25 ± 8 (24) 24 ± 7 (24) 2 nd study drug dose 87 (48%) 86 (52%) Dorian, et al. NEJM 2002;346:884-90

15 ALIVE % Hospital Survival p = 0.007, OR 2.49 ( ) 42 Amiodarone Lidocaine All Patients VF Initial Asystole/PEA ROSC No ROSC Dorian, et al. NEJM 2002;346: ALIVE Time From Dispatch to Study Drug % Survival to Hosp Admit Early Late 5 Amiodarone Lidocaine Median 24 minutes Dorian, et al. NEJM 2002;346: ALIVE No difference in survival to hosp discharge (n=41) 6.4% Amiodarone vs. 3.8% Lidocaine, p=0.32 Not powered Adverse effects requiring treatment Hypotension 13/180 (7%) vs. 6/167 (4%) Bradycardia 43/180 (24%) vs. 38/167 (23%) Dorian, et al. NEJM 2002;346:884-90

16 AHA Lidocaine Recommendations Dose mg/kg IV/IO May repeat 0.5 to 0.75 mg/kg Max of 3 mg/kg Infusion: 1-4 mg/min infusion Can administer ETT NEJM 1972;287:151 Pharmacist Responsibilities Drug preparation Expedite drug delivery Dose and infusion rate calculations Drug use documentation Drug information Setting up/operating infusion devices AHA ACLS algorithm recommendations Shimp LA, et al. AJHP 1995;52:980-4 Draper HM, et al. Ann Pharm 2008;42:

17 How Common is Participation? Surveys sent to pharmacy directors of 181 general acute care hospitals in Michigan Results 46/160 (33%) pharmacists routine members of the CPR team 27/46 (59%) did not require BLS Participation varied Education Teaching affiliated hospitals Centralized vs. decentralized services Geographic location of the hospital Mean clinical pharmacist time 35 minutes Shimp LA, et al. AJHP 1995;52:980-4 What is the Benefit? 1992 NCPS and Medicare database 282/1029 (27%) hospitals surveyed had pharmacist participation in the CPR team Multivariate regression analysis Severity of illness Associated with a decrease in patient death by 17.9 deaths/year/hospital Bond CA, et al. Pharmacotherapy 1999;19: Is There a Benefit? 1998 NCPS and Medicare database 584 hospitals Specific information on 14 clinical services ADE reporting systems Multiple regression analysis Clinical pharmacy services, pharmacy staffing, ADRs Participation on the CPR team was associated with a 22% reduction in ADRs Slope , 95%CI to , p=0.008 Bond CA, et al. Pharmacotherapy 2006;26:735-47

18 ACLS Compliance Retrospective Consecutive in-hosp arrests 350 bed community teaching hospital Pharmacist present (n=27) Pharmacist not present (n=47) Draper HM, et al. Ann Pharmacother 2008;48: ACLS Compliance Pharmacist (n=27) No Pharmacist (n=47) Compliance with ACLS 581/650 (89.4%) 69/650 (10.6%) Compliance with drug therapy Incorrect dose Omission Delay > 5 minutes Deviation in sequence of treatment 15/46 (32.6%) 31/46 (67.4%) Draper HM, et al. Ann Pharmacother 2008;48: Barriers to Implementation Lack of advanced training for pharmacists Inadequate pharmacy department staff Lack of perception of the pharmacist s role Draper HM, et al. Ann Pharmacother 2008;42:469-74

19 Training - BLS 187 pharmacy graduates 72% - BLS should be mandatory 70% - Training is of value in their current practice 93% - Training would be of value in the future Bond CA, et al. Am J Hosp Pharm 1989;446: Training - ACLS Encourage/fund ACLS training and renewal Even if the pharmacist role is limited Understand the rationale of drug therapy Monitor for efficacy and adverse effects DiPiro, JT. Encyclopedia of Clinical Pharmacy 2003; 116 Mock Code/Simulation Pharmacy-only sessions ACLS review Medication tray review Medication/infusion pump manipulation

20 Mock Code/Simulation Multidisciplinary simulation Nursing Respiratory therapy Pharmacy Pharmacist educator Pharmacist Integration Pharmacist advocate Participation in hospital resuscitation committee Seize opportunities ACLS instructor Assign Responsibility Code pager Assignment determined by training Complete pharmacy session Complete simulation session Complete competency or ACLS certification Buddy system Education at the bedside

21 Monitor Progress Log all codes into a database Follow-up with code pharmacist Discuss clinical issues Other discipline issues Discuss ways to overcome barriers at the code Start small and build on responsibilities Conclusions Data are limited to show superiority of vasopressin vs. epinephrine and lidocaine vs. amiodarone Data are limited in showing the benefit of pharmacists on the resuscitation team Show what you can do to build acceptance There are several responsibilities for a pharmacy on the resuscitation team Start small and build Thank You! c7

22 Slide 60 c7 I think you chose an appropriate and amusing pic. cevans, 3/19/2010