ACLS REVIEW

by casualH.R.R.

JVD 7/02
MOCK CODES:
PRIMARY SURVEY
Airway: open airway, head tilt, chin lift
Breathing: assess, bag mask ventilation
Circulation: check pulse, begin CPR
Defibrillate: pulseless VT or VF 200, 300, 360 Joules
SECONDARY SURVEY
Airway: secure with endotracheal intubation
Breathing: check breath sounds
Circulation: place IV, check EKG, starts appropriate medication
DDX: treat reversible causes
VF/PULSELESS VT
Shock, shock, shock: non-synchronized 200, 300 360 joules: survival is determined primarily by length of
time from onset of VF to electrical defibrillation, SHOCK FAST
Ø Valenzuela et al. reported in NEJM 10/2002, a prospective observational case series of 148 patients
with out of hospital cardiac arrests in casinos (105 had VF, 17 PEA and 26 asystole), where they
trained security officers to use defibrillation on arrival. Primary outcome was survival to discharge
from hospital. Subgroup analysis was preformed on 90 patients with witnessed VF. Results revealed a
significant improvement in survival of those defibrillated within 3 minutes of collapse (74%) vs. those
defibrillated more than three from collapse (49%). 1
Ø Valenzuela et al. reported in Circulation 1997, a logistic regression analysis of two retrospective study
groups (total of 1872 patients) with out of hospital witnessed cardiac arrests due to VF, with main
outcome of survival to hospital discharge. Results identified only two significant predictors for
improved survival, which were time from collapse to CPR and defibrillation. 2
Vasopressin 40 units IV (potent vasoconstrictor, elevated in patients with shock and post cardiac
resuscitation, animal studies revealed increased coronary blood flow and cerebral blood flow), clinical
studies reveal conflicting results; possible increase survival of initial resuscitation.
Ø Steil et al. reported in The Lancet 7/2001, a DBRCT of 200 patients with in-hospital arrests (95 PEA,
61 asystole, 42 VF) when according to ACLS protocol when epinephrine was indicated, patients were
randomized to 40 units vasopressin or 1 mg epinephrine. Primary endpoint was a measurable pulse
post one hour of arrest and secondary outcome was a combination of survival to hospital discharge and
MMSE. Results revealed no difference in either outcome.3
Ø Linder et al. Reported in Lancet 1997, small DBRCT of 40 patients with out of hospital cardiac arrest
due to VF refractory to shock, randomized to either 1 mg epinephrine or 40 units vasopressin. Primary
outcome was successful resuscitation (admission into ICU requiring no further resuscitation),
secondary outcome was a combination of survival at 24 hours, survival to hospital discharge and
neurologic outcome. Results revealed a significantly increased survival of initial resuscitation (35%
vs. 10%); all other endpoints were not significantly different. 4
Ø Presently, Voelker and Linder are conducting a large, multi-center trial to evaluate 40 units of
vasopressin vs epinephrine in out of hospital cardiac arrest patients due to VF, PEA and asystole,
primary endpoint is hospital admission.
1 Valenzuela et al. “Outcomes of Rapid Defibrillation by Security Offices after Cardiac Arrest in Casinos”
NEJM. Vol. 343, 2000.
2 Valenzuela et al. “Estimating effectiveness of Cardiac Arrest Interventions” Circulation. Vol. 96, 1997
3 Steill et al. “Vasopressin versus Epinephrine for in hospital Cardiac Arrest: a randomized control trial”
The Lancet. Vol. 358, 2001.
4 Linder et al. “Randomized Comparison of Epinephrine and Vasopressin in Patients with out of Hospital
Ventricular Fibrillation” The Lancet. Vol. 349, 1997.
Epinephrine 1mg IV q 3-5 minutes, no clinical trial evidence of efficacy over placebo.
Ø Steill et al. reported in NEJM 1992, a DBRCT of 600 patients with in and out of hospital arrests,
randomized to either 7 mg epinephrine or 1 mg epinephrine. Primary endpoint was successful
resuscitation. Results revealed no change in outcome. 5
.
Amiodarone 300 mg IV bolus, antiarrythmic, two trials that confirm that amiodarone increases survival
to ICU admission, better that placebo or lidocaine, not powered to see effect on hospital discharge or death
Ø Dorian et al. reported in the NEJM 3/2002, a DBRCT of 347 patients with out of hospital cardiac
arrests due to VF refractory to shock and 1 mg epinephrine, randomized to either lidocaine or
amiodarone (5 mg/kg). Primary endpoint was survival to ICU admission, secondary endpoint survival
to hospital discharge. Results revealed significantly increased survival to ICU admission in
amiodarone group (22 % vs. 12%, ARR 10%, RRR 80%, NNT 10), secondary endpoint was not
significantly different. 6
Ø Kudenchuck et al. reported in NEJM 9/99 a DBRCT of 504 patients with out of hospital VF/NSVT
cardiac arrests that were refractory to shock and 1 mg epinephrine, randomized to either 300 mg
amiodarone or placebo. Primary endpoint was survival to hospital admission. Results revealed a
significant increase in survival to admission in amiodarone group (44% vs. 34%, ARR 10, RRR 30%,
NNT 10).
Lidocaine 100mg IV, antiarrythmic, no clinical trial evidence of its efficacy..
Ø Herlitz et al. reported in Resuscitation 1997, a retrospective study of 1360 patients with out of hospital
VF arrests, which compared outcomes of those that received lidocaine and those that did not. Results
revealed an increase in survival to hospital admission (38% Vs 18%) but no change in discharge. 7
Procainimide 20-30 mg/min IV drip, no clinical trial evidence of its efficacy.
Ø No clinical trial evidence, there is one retrospective analysis that preformed a multivariate analysis of
post arrest patients and found procainimide was independently associated with hospital admission.
Magnesium 2 gram IV if hypomagnesemic state suspected, otherwise no clinical trial evidence of its
efficacy.
Ø Thel et al. reported in Lancet 1997, a small DBRCT, of 150 patients with in hospital arrests (all types,
except torsades) who received either 2 grams magnesium or placebo. NO statistical difference in
primary endpoint of restoration of spontaneous circulation at one hour. 8
Remember: perform CPR post medication infusion for at least 30 seconds to allow medication to
distribute, check rhythm, if still in VF/NSVT you must shock again, before starting new medication.
PEA ARREST
Ø Diagnose reversible causes: think out loud about your differential diagnosis 5H/5T’s , get labs
Hypovolemia, hypothermia, hyperkalemia, hypoxia, +H (acidosis)
Tamponade, tension pneumothorax, thrombosis (myocardial infarction, pulmonary embolism),
tablets (overdoses).
Ø Initiate empiric treatment, according to patient’s history and exam
Intubate and hyper ventilate, wide open fluids, bicarbonate bolus, calcium gluconate, D50 with
insulin, pericardiocentesis or needle decompression
Ø Epinephrine 1 mg IV q 3-5 minutes
Ø Atropine 1mg IV q3-5 mminutes if rate is slow
Ø Thrombolysis: tissue plasminogen activator, one clinical trial reported NO improvement survival.
Ø Abu-Laban et al. reported in NEJM 5/2002, a DBRCT of 233 patients with out of hospital cardiac
arrest due to PEA refractory to fluid bolus, 1 mg epinephrine, intubation and ventilation,
5 Steil et al. High Dose Epinephrine in Adult Cardiac Arrests” NEJM. Vol. 327, 1992.
6 Dorian et al. “ Amiodarone as compared with Lidocaine for Shock Resistant Ventricular Fibrillation”
NEJM. Vol. 346, 2002.
7 Herlitz et al. “Lidocaine in out of hospital Ventricular Fibrillation. Does it improve survival?”
Resuscitation. Vol. 33, 1997.
8
randomized to either 50 mg tPA or placebo. Primary outcome was survival to hospital discharge.
Results revealed no significant differences in any outcome 9
ASYSTOLE
Confirm true asystole in two leads, do not miss coarse VF, and search for reversible causes
Immediate transcutaneous pacing
Epinephrine 1 mg IV q3-5 minutes
Atropine 1 mg IV q 3-5 minutes
POST ARREST CARE
Hypothermia two clinical trials reported improved neurologic outcome at discharge and 6 months.
Ø Holzer et al. reported in NEJM 2/2002, an outcome BRCT of 275 patients’ s/p VF/pulseless VT arrest
that had been successfully hemodynamically resuscitated. Exclusion criteria included temp 30 minutes) and persistent hypoxemia (>15 minutes). Patients were randomized to
either hypothermia, goal bladder temp of 32-34 degrees, achieved with cooling blankets and ice packs
if needed, for 24 hours vs. normothermia treatment. All patients were sedated and paralyzed. Primary
outcome was favorable neurologic outcome in 6 months. Secondary outcomes were morality at 6
months and complication within 7 days. Results revealed a significant increase in favorable
neurological outcome in patients with hypothermia (55% vs. 39%, RRR 40 %, ARR 16%, NNT 6),
secondary endpoint of mortality was also improved (44 % vs. 55%) and no difference in complication
rates. 10
Ø Bernard et al. reported in NEJM 2/2002 an outcome BRCT of 77 patients’ s/p VF cardiac arrests that
had been successfully resuscitated . Exclusion criteria were patients with cardiogenic shock, or had
other possible etiologies of coma other than arrest. Patients were either randomized to hypothermia,
goal bladder temp of 33 degrees by active cooling with ice packs for 12 hours or normothermia.
Primary outcome was survival to hospital discharge with sufficiently good neurologic function to go
home or to rehab. Results revealed a significant increase in discharge form hospital with good
neurologic function in-patients with hypothermia (49% vs. 26%, 23 % ARR, 88% RRR, NNT 4). No
difference in complication rates. 11
COMMON ERRORS
Ø Leadership: failure to take control of session
Ø Procedural : unfamiliarity with defibrillator use12
STOPPING THE CODE
Ø Always a difficult decision.
Ø Prolonged CPR beyond 30 minutes without return of spontaneous circulation is usually futile. 13
Ø Walraven et al. reported in the Archives of Internal Medicine 1/99, a clinical predictive model, derived
from 1077 patients with in hospital codes (enrolled in RCT’s) and with logistic regression analysis
found the following three factors predict NO chance of discharge from the hospital: no pulse 10
minutes after the start of CPR, initial cardiac rhythm was not VF/pulseless VT, unwitnessed arrest.
They tested this model in their same cohort and found 100 sensitivity.
9 Laban et al. “ Tissue Plasminogen Activator in Cardiac Arrest with Pulseless Electrical Activity” NEJM.
Vol. 346, 2002.
10 Holzer et al. “Mild Therapeutic Hypothermia to Improve Neurologic Outcome after cardiac Arrest”
NEJM. Vol. 346, 2002
11 Bernard et al. “Treatment of Comatose Survivors of Out-of Hospital Cardiac Arrest with Induced
Hypothermia” NEJM, Vol. 346, 2002.
12 Eisenberg et al. “Cardiac resuscitation” NEJM. Vol. 344, 2001.
13 Walraven et al. Derivation of a Clinical decision Rule for the Discontinuation of In Hospital Cardiac
Arrest Resuscitation” Arch of Int Med. Vol. 159, 1999.

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