1. Resuscitation: What Works, What
Doesn’t, and What’s Coming Down the
Tube
Jason Persoff, M.D., S.F.H.M.
©2010 MFMER | slide-1
Financial Disclosures
None to report
Motivational Disclosures
©2010 MFMER | slide-2

2. Explain the Gorilla Again…
• How much time did that video take?
• Exactly 82 seconds
• In the hospital, how long does it take to recognize
cardiac arrest?
Herlitz et al. Resuscitation 2001.

3. Are We Sure He’s Dead, Jim?
• Eberle confirmed our skills at pulse check
• Sensitivity 90%
• Specificity 55%
• Accuracy 65%
• Median time needed to identify presence or absence of pulse:
• 24 seconds overall, 32 seconds for pulse absent patients
• In 2009, Tibbells confirmed we’d only gotten a little better
• Sensitivity 86%
• Specificity 64%
• Accuracy 78%
• Bottom line: in controlled circumstances, we don’t know if a
patient has a pulse or not Eberle et al. Resuscitation 1996 (33)
Tibballs J and Russell Philip. Resuscitation
2009; 80: 61
Clinically Futile Cycles
• Pulse Check
• Rhythm Analysis
• Failure to Simulate, Rehearse, React
• “…the typical cardiac arrest victim receives a faster
response as a casino patron than they do as a hospital
inpatient.”
• Adams BA, et al. Resuscitation 2009; 80: 65.

4. New BCLS Guidelines Emphasize What Works

5. Cerebral Performance Category
Neurologically Intact Survival
(CPC 0-1) CPC
Status
Survival to Hospital Discharge
•0 Normal
•1 Good
•2 Mod Disability
Return of Spontaneous Circulation •3 Major Disability
•4 Persistent
Vegetative State
•Brain Death
Death
88% of all In-Hospital Cardiac Arrests Occur on Patients with DNR Status
Hodgetts et al. Resuscitation 54: 2002

6. Outcomes in VF / VT
Total Surviving Neurologically
Intact ~12%
Neurologically Intact Survival
58-75% CPC
(CPC 0-1)
Status
Survival to Hospital Discharge 17-57%
•0 Normal
•1 Good
54-76% •2 Mod Disability
Return of Spontaneous Circulation •3 Major Disability
•4 Persistent
Vegetative State
•Brain Death
Death
14-27% of Pediatric In-Hospital Arrests
24% of Adult In-Hospital Arrests Samson et al. NEJM 354: 2006
Nadkarni, et al. JAMA 295: 2006
Outcomes in PEA / Asystole
Total Surviving Neurologically
Intact ~6.8%
Neurologically Intact Survival
61-62% CPC
(CPC 0-1)
Status
Survival to Hospital Discharge 10-20%
•0 Normal
•1 Good
53-52% •2 Mod Disability
Return of Spontaneous Circulation •3 Major Disability
•4 Persistent
Vegetative State
•Brain Death
Death
Usually preceded up to 8 hours prior to arrest by
marked changes in SBP, HR, or oxygen
saturation Skrifvars et al. Resuscitation 70: 2006
Nadkarni, et al. JAMA 295: 2006

7. Cardiac Arrest Physiology
Untreated
V-Fib/VT
After Mader T,
Resuscitation 2007
Electrical Phase Metabolic Phase
Circulatory Phase
0-4 minutes
4-10 minutes 10+ minutes
High Countershock
CPR Needed Before Comprehensive
Receptivity
Shock Multisystem Approach
Losing Time, Losing Life
Circulatory Metabolic
Acute VF Electrical
Arrest Phase Phase
Fibrillating myocardium
Phase
deplete of ATP
Weisfeldt ML and
Becher LB. JAMA 2002;
288: 3035.
Circulatory Code Team CPR, Drugs, Code Team
Collapse Arrival Intubation Begins to
0-3 Mins 3-6 Mins 6-10 Mins Integrate
10+ Mins
•Pulse Check? •How quickly does •Arrhythmia
•Call Code? the team arrive Recognition?
and who leads? •Airway, Breathing •Kitchen Sink
•CPR? •Txfr or
•Shocks
•Drugs Pronounced

8. Decreased Survival Predictable
Survival ↓
34% to 14%
Herlitz et al. CPR Initiated Quality of
Resuscitation Lots o’ Stuff
49: 2001
>1-2 Minutes CPR
After Collapse
Cooper et al.
Resuscitation
68: 2006
SHD
Survival ↓ 31% vs. 20%
Starts
@ 2Mins 30 day
Survival 0% Code Team ACLS 26% vs. 5.9%
@ 6 Mins Arrival > 3 Training
1 year
Skrifvars et al.
Minutes After Status of 21% vs. 0%
Resuscitation Collapse Nurses
70: 2006 Moretti et al.
Resuscitation
72: 2007
Compressions Matter
Pump
Fast
Push Good
Hard Recoil
Chest Compressions CPR when done
perfectly provides
only…
Start –1/3 normal cardiac
Now output
–10-15% normal cerebral
blood flow
–1-5% normal cardiac
blood flow
Sanders et al.
Resuscitation 1985.

9. Compressions Matter
• Compressions too shallow 62.6% of the time
• Compressions too slow 71.9% of the time
ROSC No ROSC
Quartile 1
95.5 - 138.7 cpm 75% 25% *
Quartile 2
76% 24% *
87.1 – 94.8 cpm
Quartile 3 58% 42% *
* p < 0 .0083
72.4 – 87.1 cpm
Quartile 4 42% 58% *
40.3 – 72.0 cpm
Abella. Circulation 2005; 111:428-34
Compressions Matter
%
42%
Incomplete
Release
% 0%
Too Deep
% 62%
Too Shallow
0% 20% 40% 60% 80%
Wik et al. JAMA 2005: 293:299-304

10. The Hands Off Interval
Yu et al. Circulation 2002; 106:368-72

11. Physiologic Consequences
Physiologic Consequences
• Compression depth inversely correlates with
likelihood of successful defibrillation
• Mechanisms of why this may happen
• Rapid drops in aortic diastolic pressure
• Expansion of the right heart (compromising left
ventricular size and flow)
• Delays in resuming chest compressions following
defibrillation decrease ROSC and neurological
intact survival
Edelson DP, et al. Resuscitation 2006; 71: 137.
Yu et al. Circulation 2002; 106: 368.
Chamberlain D, et al. Resuscitation 2008; 77: 10.
Berg RA, et al. Resuscitation 2008; 78: 71.

12. Shock ‘Em
• AEDs
• Widely available but with long hands-off times
• Shock ‘Em NOW!
Chan PS, et al. NEJM 2008; 358: 9.
Lloyd MS, et al. Circulation 2008; 117: 2510.
Op Ed: Perkins GD. Resuscitation 2008; 79: 1.
Shock ‘em Yesterday
• Risk of shock: negligible
• Brave volunteers didn’t die
• Few case reports
Op Ed: Perkins GD. Resuscitation 2008; 79: 1.

13. Er…I Can’t Check The Rhythm Due to
Compressions…So…Hands Off, Right?
• Wrong…Zoll (among other manufacturers have
accelerometer pads that “zero out” compressions

14. Shocking
• Delayed defibrillation
• Black race associated with delays in defibrillation
(p<0.001)
• Small hospital size (<250 beds)
• “After hours” (nights/weekends)
• Non-monitored bed
Chan PS, et al. NEJM 2008; 358: 9.
Herlitz et al. Resuscitation 2001.
So If We Can’t Check A Pulse…?
• Continuous capnography
• Increasingly appears to be predictive of excellent
perfusion
• Markers of perfusion include a sudden increase in PCO2
• Ventilations can be titrated to accommodate for EtCO2 of
35-40mmHg

15. Whatever Happened to the ABC’s?
Oxygen is CO2 Rapidly
Rapidly Rises
Hypoxia Hypercarbia
Consumed
•Adds to acid burden
•Needs lung perfusion
•2-4 Minutes and ventilation to
•Asymmetric clear
distribution
“The
Drain”
Switch to
Anaerobic Low Flow
Metabolism
•Functional reductions
Lactic Circulatory in compression-
•Hepatic perfusion Acidosis Collapse assisted forward flow
necessary to clear •Arteriole failure with
•pKa, pH and other low effective blood
changes change volumes
medication effects

16. New Paradigm: CCR
• “Iatrogenic hypotension”
– Over-zealous BVM use due to
• Desire to correct hypoxia
• Belief that hyperventilation will correct acid-base derangements
• What is the appropriate tidal volume for a
patient in cardiopulmonary arrest?
• Roughly 750cc
• What is the volume of an adult bag-valve-
mask?
• 1.5 liters
• Designed for 1-handed operation
New Paradigm: CCR
Michard F. Anesthesiology 2005

17. New Paradigm: CCR
• Phenomenon of auto-PEEP usually referred to
patients on a ventilator
New Paradigm: CCR
• Rate exceeded at least 60.9% of the time in humans
• In swine models, hyperventilation results in…
• …increased intrathoracic pressure
• …decreased coronary perfusion pressures
• …lower survival
•Abella. Circulation 2005; 111:428-34.
• Aufderheide, et al. Resuscitation 2004.

18. Oral Airways
Oral Airways
• Contraindicated in conscious patients
• Can premote retching and laryngospasm
• Trauma

19. Why is Airway De-Emphasized?
• Patients gasp during cardiac arrest
• Gasping…
• …is a forceful agonal respiration
• …is a marker of improved prognosis
• …increases cerebral blood flow
• …decreases intracranial pressure
• …improves upper airway patency
• …generates cardiac output
•Yang, et al. Crit Care Med 1994; 22: 879.
•Ristagno G, et al. Resuscitation 2007; 75: 366.
•Xie J, et al. Crit Care Med 2004; 32:238.
•Srinivasan V, et al. Resuscitation 2006; 69: 329.
•Ewy GA and Kern KB. J Am Coll of Cardiol 2009; 53:147.
GASP!!!!
Rats!
A hemorrhagic
model of PEA in rats
Suzuki M, et al.
Resuscitation 2009; 80:109.

20. External Cooling

21. Cold Is Cool
• Why hypothermia?
• Superoxide generation post-resuscitation
• Calcium influx into cells
• Decreased available glucose
• Increased oxidative phosphorylation
• Cooling preserves mitochondria
• The only “brain preserving” therapy post-arrest
• Hazards
• Coagulopathy
• Impaired WBC function
• Decrease in cardiac index
• Hyperglycemia (Real)
• Requires
• Continuous bladder or central monitoring of temperature
• Target 32-34°C
Cold is Cool
A. Aguila et al. / Resuscitation
81 (2010) 1621–1626

22. Cold is Cool
70%
60%
50%
40%
Hypothermia
30% Normothermia
20%
10%
0%
Good Neuro Bad Neuro Death
After data from SA Bernard, et al. NEJM 2002; 346: 557-63.
Cold is Cool
60%
50%
40%
30% Hypothermia
Normothermia
20%
10%
0%
Good Neuro Death
After data from THACASG. NEJM 2002; 346: 549-56.

23. Cold is Cool
After THACASG. NEJM 2002; 346: 549-56.
Cold Is Cool
• Therapeutic Hypothermia
• Depression in cardiac index from TH means pressors are indicated
• Maintenance of MAP 90-100mmHg
• Oddo M, et al. Crit Care Med 2006
• Paralysis is recommended but must be combined with sedation
• Paralysis is stopped once core temp is >35°C
• TH causes selective increases in CK-MB
• Standard resuscitation peak ~100 at 6 hrs
• TH resuscitation peak ~300 at 12 hrs
• Nevertheless, STEMI or suspicion of MI should NOT preclude PCI

24. Cold Is Cool
• Therapeutic Hypothermia
• Goal: RAPID decrease in core temp to 32-34 Deg C
• Average 6 hours to achieve targets
• Oddo M, et al. Crit Care Med 2006
• Cold LR 30mL/kg bolus plus external cooling in comatose patients post-
resuscitation
• Bottom Line: HIGHER CPC SCORES, SIMILAR SURVIVAL
• CPC 0-1 seen in 54% of those treated vs. 30% of controls
• Review: Bro-Jeppensen J, et al. Resuscitation 2009; 80: 171.
• Theoretical decrease in diminishment of ECG VF to asystole
• Cooling DURING arrest seems to improve ROSC, but not survival
• Pre-Arrest and Intra-Arrest Hypothermia and VF. Menegazzi JJ, et al.
Resuscitation 2009; 80: 126.
Fin

25. Universal Algorithm
Yep Nope
V-Fib Shockable Rhythm?
PEA
Pulseless VT
Asystole
Have no idea
360J Antiarrhythmic
Mono
(Amiodarone)
or
Shock
150J
Biphasic
Drug
Biphasic Shock
150J 5 Cycles
(150 Compressions)
Pressor (Epi vs. Vaso)
Assignment #1
• You come across an unconscious patient who
appears unarousable and not particularly lively. As a
group, determine:
• Who will lead the code
• Determine interventions prior to defibrillator arrival
• When the defibrillator arrives, how would you set it up?

26. Debriefing #1
• Group leader, discuss what chaos ensued
• How did you figure out to use the defibrillator?
• How did you decide on a collective course of action?
• What areas of uncertainty existed?
• Take 2: new group leader, same exercise
VF/Pulseless VT
• Peripheral vs. Central Lines
• Precordial Thumps
• Cough CPR
• Pulse Checks

27. Universal Algorithm
Yep Nope
V-Fib Shockable Rhythm?
PEA
Pulseless VT
Asystole
Have no idea
360J Antiarrhythmic
Mono
(Amiodarone)
or
Shock
150J
Biphasic
Drug
Biphasic Shock
150J 5 Cycles
(150 Compressions)
Pressor (Epi vs. Vaso)
PEA: A Common Cause of Arrest
Desbiens NA, Crit Care
Med 2008; 36:391.

28. PEA: A Common Cause of Arrest
• All patients in PEA should receive:
• IVF wide open to “fill the tank”
• Patients will go into vascular collapse commonly as shock ensues
increasing the relative vascular volume by many liters
• Oxygen
• Systemic hypoxia causes vasoconstriction of the pulmonary
arteries leading to RV dysfunction and thus decreases in LV
preload
• Epinephrine
• Peripheral alpha-agonist can clamp down the vessels effectively
but will also increase myocardial workload via beta-agonist
effects. This is a short-term fix
• Chest Compressions
• Already discussed
Assignment #2
• Your team arrives on a patient who is agonally
breathing but appears to have a very faint, rapid
pulse.
• At what point would you institute chest compressions?
• What interventions should you initiate immediately and
why?
• Name some immediate causes that could have led to this
collapse

29. Debrief #2
• What were the difficulties this go around in deciding
course of action?
• Ultimately, what did your group decide was the
etiology for the collapse and how did you approach
it?
• What algorithms do you think may have helped you
perform better?
Bradycardia

30. Tachycardia
What, No Love for CCR?
• Effect of CCR on Alveolar Collapse and Recruitment
• More Atelectasis
• More Hypoxemia
• Worse Hemodynamics
• Effects Persist Even After Resumption of IPPV
• But…the pigs used were anesthetized
• Markstaller K, et al. Resuscitation 2008; 79: 125.

31. Resuscitation Medications
Epinephrine Vasopressin Epinephrine Steroids
plus
Vasopressin
Sillberg VAH, et al. Methyl-
Resuscitation Sillberg VAH, et al. Prednisolone 40mg
2008; 79: 380. Resuscitation IV after
Sillberg VAH, et al. 2008; 79: 380.
Resuscitation Epinephrine
Wyer, et al. Ann
2008; 79: 380. Yup in animals, not
Emergency Med Hydrocortisone
2006; 48: 86. so in humans 300mg qd x 7 days
largely due to
Koshman, et al. study design
Mentzelopoulos SD,
Ann of heterogeneity.
et al. Arch Int Med
Pharmacology
2009; 169: 15.
2005; 39: 1687.
α/β Agonist
β Non-Adrenergic Smoke if You Got Low Relative
Vasoconstrictor ‘Em Cortisol Levels
External Cooling

32. Cold Is Cool
• Why hypothermia?
• Superoxide generation post-resuscitation
• Calcium influx into cells
• Decreased available glucose
• Increased oxidative phosphorylation
• Cooling preserves mitochondria
• The only “brain preserving” therapy post-arrest
• Hazards
• Coagulopathy
• Impaired WBC function
• Decrease in cardiac index
• Hyperglycemia (Real)
• Requires
• Continuous bladder or central monitoring of temperature
• Target 32-34°C
Cold is Cool
70%
60%
50%
40%
Hypothermia
30% Normothermia
20%
10%
0%
Good Neuro Bad Neuro Death
After data from SA Bernard, et al. NEJM 2002; 346: 557-63.

33. Cold is Cool
60%
50%
40%
30% Hypothermia
Normothermia
20%
10%
0%
Good Neuro Death
After data from THACASG. NEJM 2002; 346: 549-56.
Cold is Cool
After THACASG. NEJM 2002; 346: 549-56.

34. Cold Is Cool
• Therapeutic Hypothermia
• Depression in cardiac index from TH means pressors are indicated
• Maintenance of MAP 90-100mmHg
• Oddo M, et al. Crit Care Med 2006
• Paralysis is recommended but must be combined with sedation
• Paralysis is stopped once core temp is >35°C
• TH causes selective increases in CK-MB
• Standard resuscitation peak ~100 at 6 hrs
• TH resuscitation peak ~300 at 12 hrs
• Nevertheless, STEMI or suspicion of MI should NOT preclude PCI
Cold Is Cool
• Therapeutic Hypothermia
• Goal: RAPID decrease in core temp to 32-34 Deg C
• Average 6 hours to achieve targets
• Oddo M, et al. Crit Care Med 2006
• Cold LR 30mL/kg bolus plus external cooling in comatose patients post-
resuscitation
• Bottom Line: HIGHER CPC SCORES, SIMILAR SURVIVAL
• CPC 0-1 seen in 54% of those treated vs. 30% of controls
• Review: Bro-Jeppensen J, et al. Resuscitation 2009; 80: 171.
• Theoretical decrease in diminishment of ECG VF to asystole
• Cooling DURING arrest seems to improve ROSC, but not survival
• Pre-Arrest and Intra-Arrest Hypothermia and VF. Menegazzi JJ, et al.
Resuscitation 2009; 80: 126.

35. Post-Cardiac Arrest Syndrome
Respect for the RRT?
• Does an RRT decrease mortality and frequency of codes:
Maybe
• Yes: Downey AW, et al. Crit Care Med 2008; 36: 477.
• Measured alteration in mental status
• Delay in MET call resulted in death (37% vs. 22%)
• Yes: Dacey MJ, et al. Crit Care Med 2007; 35: 2076.
• Yes: Sebat F, et al. Crit Care Med 2007; 35: 2568.
• Yes: Sharek PJ, et al. JAMA 2007; 298: 2267.
• No: Chan PS, et al. JAMA 2008; 300: 2506.
• Single hospital before and after intervention, no differences in
mortality, but decrease in ICU admission rate
• No: MERIT Study. Crit Care Resusc 2007; 9: 206.
• MET not called for >15 mins prior to CA

36. Respect for the RRT
• “Why doesn’t anyone call for help?”
• Buist M. Crit Care Med 2008; 36: 634.
• Implementation of an RRT improves vital sign recording
• Chen J, et al. Resuscitation 2009; 80: 35.
Break
Isn’t Orientation over yet????