©2010 MFMER | slide-1

Jason Persoff, M.D., S.F.H.M.

Resuscitation: What Works, What Doesn’t, and What’s Coming Down the

Tube

©2010 MFMER | slide-2

Financial Disclosures

None to report

Motivational Disclosures

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.Herlitz et al. Resuscitation 2001.

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

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.

New BCLS Guidelines Emphasize What Works

Neurologically Intact Survival

(CPC 0-1)

Survival to Hospital Discharge

Return of Spontaneous Circulation

Death

CPC Status

•0 Normal•1 Good•2 Mod Disability•3 Major Disability•4 Persistent Vegetative State•Brain Death

Cerebral Performance Category

88% of all In-Hospital Cardiac Arrests Occur on Patients with DNR Status

Hodgetts et al. Resuscitation 54: 2002

Neurologically Intact Survival

(CPC 0-1)

Survival to Hospital Discharge

Return of Spontaneous Circulation

Death

CPC Status

•0 Normal•1 Good•2 Mod Disability•3 Major Disability•4 Persistent Vegetative State•Brain Death

Outcomes in VF / VT

54-76%

17-57%

58-75%

14-27% of Pediatric In-Hospital Arrests

24% of Adult In-Hospital ArrestsSamson et al. NEJM 354: 2006

Nadkarni, et al. JAMA 295: 2006

Total Surviving Neurologically

Intact ~12%

Neurologically Intact Survival

(CPC 0-1)

Survival to Hospital Discharge

Return of Spontaneous Circulation

Death

CPC Status

•0 Normal•1 Good•2 Mod Disability•3 Major Disability•4 Persistent Vegetative State•Brain Death

Outcomes in PEA / Asystole

53-52%

10-20%

61-62%

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

Total Surviving Neurologically

Intact ~6.8%

Untreated V-Fib/VT

Electrical Phase

0-4 minutes

High Countershock Receptivity

Circulatory Phase

4-10 minutes

CPR Needed Before Shock

Metabolic Phase

10+ minutes

Comprehensive Multisystem Approach

After Mader T,

Resuscitation 2007

Cardiac Arrest Physiology

Circulatory Collapse0-3 Mins

•Pulse Check?•Call Code?•CPR?

Code Team Arrival3-6 Mins

•How quickly does the team arrive and who leads?

CPR, Drugs, Intubation6-10 Mins

•Arrhythmia Recognition?

•Airway, Breathing•Shocks•Drugs

Code Team Begins to Integrate10+ Mins

•Kitchen Sink•Txfr or

Pronounced

Acute VF Arrest

Metabolic Phase

Electrical Phase

Circulatory Phase

Fibrillating myocardium

deplete of ATP

Losing Time, Losing Life

Weisfeldt ML and Becher LB. JAMA 2002;

288: 3035.

Decreased Survival Predictable

CPR Initiated >1-2 Minutes

After Collapse

Survival ↓↓↓↓34% to 14%

Herlitz et al.Resuscitation

49: 2001

Cooper et al.Resuscitation

68: 2006

Code Team Arrival > 3

Minutes After Collapse

Survival ↓↓↓↓Starts

@ 2MinsSurvival 0%

@ 6 Mins

Skrifvars et al. Resuscitation

70: 2006

ACLS Training Status of Nurses

SHD 31% vs. 20%

30 day26% vs. 5.9%

1 year21% vs. 0%

Moretti et al.Resuscitation

72: 2007

Quality of CPR Lots o’ Stuff

Chest Compressions

Start Now

Good Recoil

Push Hard

Pump Fast

Compressions Matter

CPR when done

perfectly provides only…

–1/3 normal cardiac output

–10-15% normal cerebral

blood flow

–1-5% normal cardiac

blood flowSanders et al. Resuscitation 1985.

Compressions Matter

• Compressions too shallow 62.6% of the time

• Compressions too slow 71.9% of the time

* p < 0 .0083

*75% 25%

ROSC No ROSC

Quartile 1

95.5 - 138.7 cpm

*24%76%Quartile 2

87.1 – 94.8 cpm

58% 42%Quartile 3

72.4 – 87.1 cpm

*42% 58%Quartile 4

40.3 – 72.0 cpm

Abella. Circulation 2005; 111:428-34

*

Compressions Matter

62%

0%

42%

0% 20% 40% 60% 80%

%Too Shallow

% Too Deep

%

IncompleteRelease

Wik et al. JAMA 2005: 293:299-304

The Hands Off Interval

Yu et al. Circulation 2002; 106:368-72

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.

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.

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

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

Oxygen is Rapidly

Consumed

•2-4 Minutes•Asymmetric distribution

Switch to Anaerobic Metabolism

•Hepatic perfusion necessary to clear•pKa, pH and other changes change medication effects

CO2 Rapidly Rises

•Adds to acid burden•Needs lung perfusion and ventilation to

clear

Low Flow

•Functional reductions in compression-

assisted forward flow•Arteriole failure with low effective blood

volumes

Hypoxia

Circulatory

Collapse

Lactic Acidosis

Hypercarbia

Whatever Happened to the ABC’s?

“The

Drain”

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: CCRNew Paradigm: CCR

Michard F. Anesthesiology 2005

New Paradigm: CCR

• Phenomenon of auto-PEEP usually referred to patients on a ventilator

• 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

New Paradigm: CCR

•Abella. Circulation 2005; 111:428-34.

• Aufderheide, et al. Resuscitation 2004.

Oral Airways

Oral Airways

• Contraindicated in conscious patients• Can premote retching and laryngospasm

• Trauma

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.

External Cooling

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

Cold is Cool

0%

10%

20%

30%

40%

50%

60%

70%

Good Neuro Bad Neuro Death

Hypothermia

Normothermia

After data from SA Bernard, et al. NEJM 2002; 346: 557-63.

Cold is Cool

0%

10%

20%

30%

40%

50%

60%

Good Neuro Death

Hypothermia

Normothermia

After data from THACASG. NEJM 2002; 346: 549-56.

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

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

Universal Algorithm

Shockable Rhythm?

Yep

V-Fib

Pulseless VT

Have no idea

Nope

PEA

Asystole

360JMono

150JBiphasic

150JBiphasic

or

5 Cycles

(150 Compressions)

Pressor (Epi vs. Vaso)

Shock

Drug

Shock

Antiarrhythmic

(Amiodarone)

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?

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

Universal Algorithm

Shockable Rhythm?

Yep

V-Fib

Pulseless VT

Have no idea

Nope

PEA

Asystole

360JMono

150JBiphasic

150JBiphasic

or

5 Cycles

(150 Compressions)

Pressor (Epi vs. Vaso)

Shock

Drug

Shock

Antiarrhythmic

(Amiodarone)

PEA: A Common Cause of Arrest

Desbiens NA, Crit Care Med 2008; 36:391.

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 ensuesincreasing 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

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

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.

Methyl-Prednisolone 40mg

IV after Epinephrine

Hydrocortisone 300mg qd x 7 days

Mentzelopoulos SD, et al. Arch Int Med2009; 169: 15.

Steroids

Low Relative Cortisol Levels

Sillberg VAH, et al. Resuscitation2008; 79: 380.

Wyer, et al. Ann Emergency Med 2006; 48: 86.

Koshman, et al. Ann of

Pharmacology2005; 39: 1687.

Vasopressin

Non-Adrenergic Vasoconstrictor

Sillberg VAH, et al. Resuscitation2008; 79: 380.

Yup in animals, not so in humans largely due to study design heterogeneity.

Epinephrine

plus Vasopressin

Smoke if You Got ‘Em

Sillberg VAH, et al. Resuscitation2008; 79: 380.

Epinephrine

αααα/ββββ Agonist

Resuscitation Medications

External Cooling

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

0%

10%

20%

30%

40%

50%

60%

70%

Good Neuro Bad Neuro Death

Hypothermia

Normothermia

After data from SA Bernard, et al. NEJM 2002; 346: 557-63.

Cold is Cool

0%

10%

20%

30%

40%

50%

60%

Good Neuro Death

Hypothermia

Normothermia

After data from THACASG. NEJM 2002; 346: 549-56.

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

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.

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 inmortality, but decrease in ICU admission rate

• No: MERIT Study. Crit Care Resusc 2007; 9: 206.

• MET not called for >15 mins prior to CA

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????