Transcript CBP: Cardiac Arrest - UBC Critical Care Medicine, Vancouver BC

CBP: Cardiac
Arrest
Case Presentation
A 55 year old business man collapses at work. This is
witnessed by his colleagues who find him pulseless.
They initiate CPR and call 911.
 EMS arrive 5 minutes later. They confirm the pulseless
state and place the patient on a monitor; he is in V.
Fib. Standard ACLS protocols are initiated; the
patient is intubated and transported to the closest ED.
 The patient arrives at the ED 7 minutes later. He has
received 2 doses of Epinephrine and one dose of
Atropine. He has received 2 shocks and is currently in
PEA arrest.
 In the ERP confirms ETT placement, the rhythm of
PEA, and performs a quick bedside ECHO, all the
while continuing with CPR. The ECHO shows
cardiac motion.
 The patient is given another dose of Epinephrine
and Atropine. By 6 minutes of his arrival, he is
noted to have Return of Spontaneous
Circulation and to have reverted to NSR.
 ICU is consulted
 Vital signs: HR – 112, RR – 6/poor effort, BP 65/40 (MAP
48), 36.5 Rectal Temp, Glucose 17.8, Sat’n 100%.
 Quick exam reveals: A: ETT in place. B: GBS x2. +ve
ETCO2 Capnography. C: As above. N HS. D: GCS of
3T, absent gag/corneal/papillary response. E:
Nothing obvious. And no calf edema.
 Past medical history reveals a 30 pack-year smoking
history. He is on no meds and has no known drug
allergies. He is known to travel abroad frequently with
his work.
Question 1
 Please define Post-Cardiac Arrest Syndrome and
its 4 pathophysiologic components. (Erik)
Definition
 Post-cardiac arrest syndrome is a unique and
complex combination of pathophysiological
processes, which include
1.
2.
3.
post-cardiac arrest brain injury,
post-cardiac arrest myocardial dysfunction, and
systemic ischemia/reperfusion response.
 This state is often complicated by a fourth
component:
4. the unresolved pathological process that caused
the cardiac arrest.
Phases – for Therapy & for Science
 The immediate post-arrest phase could be
defined as the first 20 minutes after ROSC.
 The early post-arrest phase could be
defined as the period between 20 minutes
and 6 to 12 hours after ROSC, when early
interventions might be most effective.
 An intermediate phase might be between 6
to 12 hours and 72 hours, when injury
pathways are still active and aggressive
treatment is typically instituted.
 Finally, a period beyond 3 days could be
considered the recovery phase, when
prognostication becomes more reliable and
ultimate outcomes are more predictable.
Pathophysiology
 The 4 key components of post-cardiac arrest
syndrome are:
1.
2.
3.
4.
post-cardiac arrest brain injury,
post-cardiac arrest myocardial dysfunction,
systemic ischemia/reperfusion response, and
persistent precipitating pathology.
Pathophysiology
 The unique features of post-cardiac arrest
pathophysiology are often superimposed on the
disease or injury that caused the cardiac arrest,
as well as underlying comorbidities.
 Therapies that focus on individual organs may
compromise other injured organ systems.
 The severity of these disorders after ROSC is not
uniform and will vary in individual patients based
on the severity of the ischemic insult, the cause
of cardiac arrest, and the patient’s pre-arrest
state of health.
Foundation on which to grow…
 In a study of dogs with induced cardiac arrest…
 In a single observational human study…
 Biochemical and neurohormonal models suggest…
 A growing body of evidence…
 These findings suggest, in theory, that…
 These findings do not rule out the potential effect of…
 Limited evidence is available to guide…
Forrest through the trees
Fundamentals
 Who remembers 5:1, 15:2, 30:2, 10:1, vs continuous?
(AHA, ACC, ILCOR)
 ETT vs supraglottic device? (AHA, ACC, ILCOR)
 BLS plus AED vs ACLS (OPALS, PAD)
 Push hard, push fast, push often! (ROC-BC)
Question 2
 How do you treat Post-Cardiac Arrest Syndrome.
(Federico)
 Early HD optimization
 No evidence based guidelines
 Suggestion is to have a similar approach as EGDT
for Sepsis
 MAP goals undefined
 Loss of Cerebral Autoregulation
 CPP dependent on MAP
 ICP generally not elevated
 MAP Goals >65, <90
 Mixed venous gases
 Venous Hyperoxia
 Falsely elevated levels due to poor tissue
extraction related to epi use and mitochondrial
failure
 Follow urine output (careful in hypothermia)
 Follow lactates (need to follow trends)
 Avoid hyperoxia
 Ptl for increased free radical production
 PaO2 goals of 92 – 96%
 Aim for normocarbia
 Volume resuscitate
 Consider intropes/vasopressors
 Treat for ACS
 Noemie
 Hypothermia
 Ibrahim
 Treat seizures
 Increase cerebral metabolism
 No Evidence for prophylaxis
 Myoclonus
 Clonazepam
 Treat hyperglycemia
 No evidence for Neuroprotective medications
 Adrenal dysfunction
 Renal failure
 Infection
 More prone to aspiration pneumonia
Question 3
 Should we cool this patient? Who do we cool,
what parameters do we use, what are the
complications of hypothermia therapy? What if
the original documented rhythm was PEA?
(Ibrahim)
Who should be cooled?
 Out-of-hospital VF/PVT Arrest
 RCTs:HACA and Bernard et al (NEJM, 2002):
significant survival to d/c and neuro recovery (NNT 6
in a meta-analysis)
 In-hospital VF Arrests
 Small subset within HACA: favorable survival
 Out-of-hospital all-rhythms, or non-VF
 4 retrospective studies for all (Oddo 2006, Scott 2006,
Arrich 2007, Hay 2008), one retrospective and 2
observational for non-VF: possible benefit
 Pyrexia within 72 Hr (>37C--> poor neuro
outcomes), all patients
Bernard, 2002, NEJM
HACA, 2002, NEJM
What are the parameters of
cooling protocol?
 Target core temp: 33C, or 32-34C
 Onset: variable, ASAP (2-8 Hr, up to 24Hr)
 Duration: 12-24 Hr
 Further data required
 NRCPR, HACA-R
Complications of TH
 Technical: Shivering, use of ongoing
sedation and NMB, to prevent shivering
(with 30% dec clearance with T=34C),
fluctuations of temp
 HD: inc SVR, dec COP, arrhythmias (esp
brady)
 Diuresis, hypovolemia, dec K, Ca, Mg,
PO4 --> arrhythmia
 MgSO4: NMDA blocker, so dec shivering,
vasodilator, so facilitate cooling induction,
antiarrhythmic, and ? additive
Neuroprotective (animal data)
 Impaired glucose tolerance (dec insulin level
and sensitivity)
 Coagulopathy
 Lower immunity--> infections
 Higher pneumonias in TH group in HACA, but NS
Should we cool this patient?
 Yes! Out-of-hospital VF arrest
Question 4
 His wife has just arrived with his 3 kids (16, 15, and
9 years old). They want to know what his
prognosis is. What do you tell them and how do
you prognosticate patients post arrest? Please
discuss clinical and lab findings and imaging
modalities. Would things be looked at
differently if he was cooled? (Neil)
. What do you tell them and how
do you prognosticate patients
post
arrest?
 Timing
 What is a “poor outcome”?
 Prognostication
 Clinical
 EEG
 Biomarkers
 Imaging
Timing
 Very difficult to prognosticate in the first 24 hours
 Most evidence is derived on testing at 72 hours
 Therapeutic hypothermia changes the timeline
What is a poor outcome?
What is a poor outcome?

Poor outcome is defined as death, unconsciousness after one month, or unconsciousness or severe disability after six months.
Clinical signs
 Absence of pupillary light reflexes
 100% specificity in meta analysis
 LR+ 10.5 (CI 2.1-52.4)
 Absence of motor response to pain
 100% specificity in meta analysis
 LR+ 16.8 (CI 3.4 – 84.1)
 Myoclonic status epilepticus
 Can be predictive early
 Much worse than SE
Clinical Signs
 Which are not good prognositcators
 Age
 Sex
 Cause of arrest
 Type of arrhythmia
 Total arrest time
 Duration of CPR
EEG
 Overall prognostication ability is not strong
 Variety of studies have looked into it
 Lack of a standardized classification system
 Concerning features
 Burst suppression
 Nonreactive alpha and theta patterns
 Generalized periodic complexes
SSEP’s
 Tests integrity of the neuronal pathways from
peripheral nerve, spinal cord, brainstem, and
cerebral cortex
N20
 Best studied waveform
 Robust as it is not strongly influence by meds
and metabolic derangements
 LR+ 12 (CI 5.3-27.6)
Biomarkers
 Dead brain releases biomarkers
 3 have been “well” studied
 Neuron specific enolase (NSE)
 S-100
 Creatinine kinase BB isoenzyme (CK-BB)
Imaging
 Although not strong enough to prognosticate
reliably, a bad scan is a bad scan
 Problem lies in that a good scan may not be a
good scan
Question 5
 His EKG shows normal sinus rhythm with non-
specific changes. Should he go to the cath lab?
If so, what are the recommendations for cath
post cardiac arrest? If he arrested again, would
you thrombolyse him? What is the etiology of
the vast majority of cardiac arrests? (Noamie)
Questions
 His EKG shows normal sinus rhythm with non-
specific changes. Should he go to the cath lab?
 If so, what are the recommendations for cath
post cardiac arrest?
 If he arrested again, would you thrombolyse
him?
 What is the etiology of the vast majority of
cardiac arrests?
Etiology of cardiac arrests
65-70 %
10%
5-10%
15 to 35%
Etiology of Sudden Cardiac
Death
 Age < 20:
 Myocarditis (22%), HCM (22%) and conduction
system abnormalities (13%)
 Age 20-29:
 CAD (24%), myocarditis (22%) and
HCM (13%).
 Age 29-39:
 CAD (58%), myocarditis (11%).
Am J Cardiol 1991;689(13):1388-1392
Should he go to the cath lab?
 Yes
 Even if no evidence of an ACS, need to exclude
stable/chronic CAD
 Sudden cardiac arrest may be first indication of
CAD
 But, does he need it right now?
NEJM 1997;336:1629-1633
 1994-1998
 Pt post cardiac arrest btw 30-75
 Immediate cath if no obvious non-cardiac
cause
 1st rhythm recorded: 93% VF/VT
 84% had 0 or 1 cardiac RF
 71% had clinically significant CAD
 poor predictive value of CP
and ECG changes for
coronary-artery occlusion.
Recommendations for cath post
cardiac arrest
Recommendations
 Recommendations for Coronary
Angiography in Patients With Known
or Suspected CAD Who Are Currently
Asymptomatic or Have Stable Angina.
 Class I: Patients who have been
successfully resuscitated from sudden
cardiac death or have sustained (>30 s)
monomorphic ventricular tachycardia or
nonsustained (<30 s) polymorphic
ventricular tachycardia. (Level of
Evidence: B)
If he arrested again, would you
thrombolyse him?
 TROICA (NEJM 2008)
 Tenecteplase vs placebo
 Stopped early for futility
 Lancet 2001
 rt-PA vs placebo
 Improved ROSC but no difference in 24HR survival or
survival to discharge
 AJC 2006
 No statistically significant benefit
 Treatment recommendation:
 “Fibrinolysis should be considered in adult patients with
cardiac arrest with proven or suspected pulmonary
embolism. There are insufficient data to support or refute the
routine use of fibrinolysis in cardiac arrest from other
causes.”
Question 6
 Patient arrests again and family wants
EVERYTHING done. His wife is a cardiac nurse
and asks if ECMO is an option. What do you tell
her?
 ECMO in cardiac arrest = Extracorporeal Life
Support (ECLS)
 Few small, observational and retrospective
studies (5 studies: 3 adult, 2 pediatric)
 All in hospital arrests
 2005 ACLS guidelines, consider in:
 In hospital patient
 Brief pulseless period (rapid ECLS response teams)
 Reversible causes (OD’s, revascularization/heart
transplant)
 Realistically, not feasible for every patient
 Modality of choice for severe hypothermia in
cardiopulmonary arrest
Question 7
 Assuming he survives to discharge, should he get
an ICD implanted? (Marios)
Question 8
 Patient does well and eventually gets
discharged to a ward bed. However, he has
another cardiac arrest. Are there any
differences between in-hospital and out-ofhospital cardiac arrest? What can be done to
improve the outcome of in hospital cardiac
arrest? (Marios)
Question 7: Indications for ICD
implantation post-arrest
Indications for ICD

2008 ACC/AHA/HRS guidelines state that most survivors of VT/VF arrest
that are not due to reversible causes should be offered an ICD.

Reversible causes:



Polymorphic VT/VF clearly due to ischemia that is amenable to
revascularization.
Polymorphic VT in the setting of reversible QT prolongation
Exceptions:




Wolff-Parkinson-White syndrome – tx is ablation
Fulminant myocarditis in which LVAD will be used as a bridge to recovery
Drug-induced arrhythmias
Electrolyte abnormalities (rarely an isolated cause however)
Epstein, AE, DiMarco, JP, Ellenbogen, KA, et al. ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: a
report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines Circulation 2008; 117:e350.
Question 8a: Are there any differences
between in-hospital and out-of-hospital
cardiac arrest?
VS
Differences between in-hospital
and out-of-hospital cardiac
arrests
 Initial rhythm
 VT/VF is the first monitored rhythm in only 15-23% of in-
hospital cardiac arrests (IHCAs)
 In out-of-hospital arrests (OHCAs) VF/VT occur in 45% of
cases
 IHCAs more likely to be due to hypoxemia and hypotension
 more likely to cause PEA or asystole
 OHCAs more often precipitated by ischemia which more
commonly leads to VT/VF
Sandroni C, et al. In-hospital cardiac arrest: incidence, prognosis and possible measures to improve survival. Intensive Care Medicine (2007)
33:237-245
Dichtwald S, et al. Improving the outcome of in-hospital cardiac arrest: the importance of being earnest. Seminars in Cardiothoracic and
Question 8b: What can be done to
improve the outcome of in hospital
cardiac arrest?
“Survival” post in-hospital
cardiac arrests

Between 25% and 67% of successfully resuscitated patients die within 24h of ROSC

Survival to discharge ranges from 0% to 28%%, with major studies reporting ~ 20% survival
to discharge rate.

14% to 47% of patients discharged die within one year

In other words, IHCA is a bad prognostic sign.
Sandroni C, et al. In-hospital cardiac arrest: incidence, prognosis and possible measures to improve survival. Intensive Care Medicine (2007)
Strategies to improve outcomes
 MET teams:
 Initially showed positive effects in reducing both
cardiac arrests and in-hospital mortality
 Many of these studies were of low quality
 A recent meta-analysis showed no effect on
mortality despite a reduction in cardiac arrests (?
ICU arrests vs more patients being made DNR by
MET team)
Sandroni C, et al. In-hospital cardiac arrest: incidence, prognosis and possible measures to improve survival. Intensive Care Medicine (2007)
Strategies to improve outcomes
 DNR status:
 By addressing level of care, CPR may be targeted
to those who are more likely to benefit from it.
 This would be expected to improve survival rates of
in hospital arrests.
 No studies have looked at this.
Sandroni C, et al. In-hospital cardiac arrest: incidence, prognosis and possible measures to improve survival. Intensive Care Medicine (2007)
Strategies to improve outcomes
 ACLS training
 Chest compression rate and depth inadequate in a
third of codes
 Lower immediate survival rate in patients receiving
compression rates < 80/min
 Immediate survival rate nearly 4 times higher when
resuscitated by ALS-trained vs non-ALS-trained nurse.
 Immediate survival better in hospitals after
completion of a resuscitation training program.
Sandroni C, et al. In-hospital cardiac arrest: incidence, prognosis and possible measures to improve survival. Intensive Care Medicine (2007)
33:237-245
Strategies to improve outcomes
 CPR Adjuncts:
 Active Compression Decompression CPR
 Impedance Threshold Valve
 Though promising animal and physiologic date,
conclusive outcome data is still pending.
Dichtwald S, et al. Improving the outcome of in-hospital cardiac arrest: the importance of being earnest. Seminars in Cardiothoracic and
Vascular Anesthesia (2009) 13(1):19-30
Active
Compression/Decompression
CPR
Frascone RJ, et al. Combination of active compression decompression cardiopulmonary resuscitation and the inspiratory impedance threshold
device: state of the art. Curr Opin Crit Care.(2004): 10:193–201
Impedance threshold valve
Lurie K, Zielinski T, McKnite S, et al. Improving the efficiency of cardiopul- monary resuscitation with an inspiratory impedance threshold valve. Crit
Care Med 2000; 28:N207–N209.
Hemodynamic effects of
devices
Lurie K, Zielinski T, McKnite S, et al. Improving the efficiency of cardiopul- monary resuscitation with an inspiratory impedance threshold valve. Crit
Care Med 2000; 28:N207–N209.
Strategies to improve outcomes
 Early defibrillation
 Response time of code teams may be
unacceptably long in remote areas of hospitals
(up to 6 minutes in larger hospitals)
 One before-after study showed an improved
survival from VT/VF arrest from 2.2% to 15.6% after
implementation of an AED program
 Randomized controlled trials are needed
Sandroni C, et al. In-hospital cardiac arrest: incidence, prognosis and possible measures to improve survival. Intensive Care Medicine (2007)
33:237-245
Strategies to improve outcomes
 Post-resuscitation care
 Therapeutic hypothermia
 As opposed to out-of-hospital arrests, in-hospital
cardiac arrests are more often non-VT/VF.
 Neurological injury less often a cause of death in
IHCA patients
 Impact of therapeutic hypothermia may therefore
be reduced for in-hospital cardiac arrests
Sandroni C, et al. In-hospital cardiac arrest: incidence, prognosis and possible measures to improve survival. Intensive Care Medicine (2007)
The End