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CBP: Cardiac Arrest

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Title: CBP: Cardiac Arrest


1
CBP Cardiac Arrest
2
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.

3
  • 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

4
  • Vital signs HR 112, RR 6/poor effort, BP
    65/40 (MAP 48), 36.5 Rectal Temp, Glucose 17.8,
    Satn 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.

5
Question 1
  • Please define Post-Cardiac Arrest Syndrome and
    its 4 pathophysiologic components. (Erik)

6
Definition
  • Post-cardiac arrest syndrome is a unique and
    complex combination of pathophysiological
    processes, which include
  • 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.

7
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.

8
Pathophysiology
  • The 4 key components of post-cardiac arrest
    syndrome are
  • post-cardiac arrest brain injury,
  • post-cardiac arrest myocardial dysfunction,
  • systemic ischemia/reperfusion response, and
  • persistent precipitating pathology.

9
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 patients
    pre-arrest state of health.

10
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11
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

12
Forrest through the trees
13
Fundamentals
  • Who remembers 51, 152, 302, 101, 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)

14
Question 2
  • How do you treat Post-Cardiac Arrest Syndrome.
    (Federico)

15
  • 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

16
  • MAP Goals gt65, lt90
  • 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)

17
  • Avoid hyperoxia
  • Ptl for increased free radical production
  • PaO2 goals of 92 96
  • Aim for normocarbia
  • Volume resuscitate
  • Consider intropes/vasopressors

18
  • Treat for ACS
  • Noemie
  • Hypothermia
  • Ibrahim
  • Treat seizures
  • Increase cerebral metabolism
  • No Evidence for prophylaxis
  • Myoclonus
  • Clonazepam

19
  • Treat hyperglycemia
  • No evidence for Neuroprotective medications
  • Adrenal dysfunction
  • Renal failure
  • Infection
  • More prone to aspiration pneumonia

20
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)

21
Who should be cooled?
  • Out-of-hospital VF/PVT Arrest
  • RCTsHACA 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 (gt37C--gt poor neuro
    outcomes), all patients

22
Bernard, 2002, NEJM
23
HACA, 2002, NEJM
24
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

25
Complications of TH
  • Technical Shivering, use of ongoing sedation and
    NMB, to prevent shivering (with 30 dec clearance
    with T34C), fluctuations of temp
  • HD inc SVR, dec COP, arrhythmias (esp brady)
  • Diuresis, hypovolemia, dec K, Ca, Mg, PO4 --gt
    arrhythmia
  • MgSO4 NMDA blocker, so dec shivering,
    vasodilator, so facilitate cooling induction,
    antiarrhythmic, and ? additive Neuroprotective
    (animal data)

26
  • Impaired glucose tolerance (dec insulin level and
    sensitivity)
  • Coagulopathy
  • Lower immunity--gt infections
  • Higher pneumonias in TH group in HACA, but NS

27
Should we cool this patient?
  • Yes! Out-of-hospital VF arrest

28
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)

29
. What do you tell them and how do you
prognosticate patients post arrest?
  • Timing
  • What is a poor outcome?
  • Prognostication
  • Clinical
  • EEG
  • Biomarkers
  • Imaging

30
Timing
  • Very difficult to prognosticate in the first 24
    hours
  • Most evidence is derived on testing at 72 hours
  • Therapeutic hypothermia changes the timeline

31
What is a poor outcome?
32
What is a poor outcome?
  • Poor outcome is defined as death, unconsciousness
    after one month, or unconsciousness or severe
    disability after six months.

33
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

34
Clinical Signs
  • Which are not good prognositcators
  • Age
  • Sex
  • Cause of arrest
  • Type of arrhythmia
  • Total arrest time
  • Duration of CPR

35
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36
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

37
SSEPs
  • Tests integrity of the neuronal pathways from
    peripheral nerve, spinal cord, brainstem, and
    cerebral cortex

38
N20
  • Best studied waveform
  • Robust as it is not strongly influence by meds
    and metabolic derangements
  • LR 12 (CI 5.3-27.6)

39
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40
Biomarkers
  • Dead brain releases biomarkers
  • 3 have been well studied
  • Neuron specific enolase (NSE)
  • S-100
  • Creatinine kinase BB isoenzyme (CK-BB)

41
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42
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

43
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44
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45
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)

46
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?

47
Etiology of cardiac arrests
48
65-70
10
5-10
15 to 35
49
Etiology of Sudden Cardiac Death
  • Age lt 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 1991689(13)1388-1392
50
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?

51
NEJM 19973361629-1633
  • 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

52
  • poor predictive value of CP and ECG changes for
    coronary-artery occlusion.

53
Recommendations for cath post cardiac arrest
54
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 (gt30 s) monomorphic ventricular
    tachycardia or nonsustained (lt30 s) polymorphic
    ventricular tachycardia. (Level of Evidence B)

55
If he arrested again, would you thrombolyse him?
56
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57
  • 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

58
  • 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.

59
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?

60
  • ECMO in cardiac arrest Extracorporeal Life
    Support (ECLS)
  • Few small, observational and retrospective
    studies (5 studies 3 adult, 2 pediatric)
  • All in hospital arrests

61
  • 2005 ACLS guidelines, consider in
  • In hospital patient
  • Brief pulseless period (rapid ECLS response
    teams)
  • Reversible causes (ODs, revascularization/heart
    transplant)
  • Realistically, not feasible for every patient
  • Modality of choice for severe hypothermia in
    cardiopulmonary arrest

62
Question 7
  •  
  • Assuming he survives to discharge, should he get
    an ICD implanted? (Marios)

63
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-of-hospital cardiac arrest?
    What can be done to improve the outcome of in
    hospital cardiac arrest? (Marios)

64
Question 7 Indications for ICD implantation
post-arrest
65
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 117e350.
66
Question 8a Are there any differences between
in-hospital and out-of-hospital cardiac arrest?
VS
67
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)
33237-245 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
68
Question 8b What can be done to improve the
outcome of in hospital cardiac arrest?
69
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)
33237-245
70
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)
33237-245
71
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)
33237-245
72
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 lt 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)
33237-245
73
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
74
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) 10193201
75
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 28N207N209.
76
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 28N207N209.
77
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)
33237-245
78
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)
33237-245
79
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