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Title: ROSC Now what


1
ROSC! Now what??!!
  • An EMS Guide to the Management of Post Cardiac
    Arrest Syndrome
  • Jay Lance Kovar, MD, FACEP
  • Montgomery County Hospital District
  • PHI Air Medical Texas

2
Objectives
  • Review
  • Background and Epidemiology of Cardiac Arrest
    Survival
  • Detail
  • Pathophysiology of Post Cardiac Arrest Syndrome
  • Discuss
  • Monitoring, Therapeutic Strategies, and Protocols
    they apply to the Pre-Hospital Environment
  • Propose
  • Integrated EMS Protocols for Improved Intact
    Neurologic Survivability

3
Background
  • 1966 Nat'l Academy Sciences Nat'l Research
    Council on CPR describes ABCDs
  • 1972 Dr Valdimir Negovsky The Second Step
  • Advances in CPR and cardiac care has not resulted
    in improved survivability in 50 years
  • Post Cardiac Arrest Syndrome
  • Brain Injury
  • Myocardial Dysfunction
  • Systemic Ischemia/Reperfusion Response
  • Unresolved Pathological Process

4
Background
  • Barriers to Optimal Outcomes
  • Multiple Teams/Hand-0ffs
  • Wide variation in Treatments (multicenter trials)
  • Early Prognostication Inaccuracies lt 72 hrs
  • Research focus on ROSC
  • Improved ROSC
  • w/o Improved Survival

5
Epidemiology
  • Early Mortality rates after ROSC varies greatly
    between studies, regions, and hospitals
    indicating variability in Post Cardiac Arrest
    Care
  • Advances in Critical Care over past 5 decades
    fails to produce improved outcomes
  • Data Definition Confusion
  • ROSC
  • Mortality Location
  • OOH/IH
  • Mortality Time

6
Epidemiology
  • Physiologic Phases of Post Cardiac Arrest Care
  • Immediate 0-20 minutes
  • CPR interventions
  • Early 20 minutes 6 to 12 hours
  • Early interventions most effective
  • Intermediate 6 to 12 hours 72 hours
  • Aggressive management of Injury pathways
  • Recovery beyond 3 days
  • Prognostication Reliable
  • Outcomes Predictable

7
Epidemiology
  • Mortality Rates Inadequate
  • Neurologic and Functional Outcomes
  • Cerebral Performance Category

8
Epidemiology
  • Quality of Life?
  • Limitation and Withdrawal of Therapy
  • 63 made DNR, 43 withdrew Therapy in Early and
    Intermediate time periods ltlt Prognostic period
  • Can better Care w/i 72 hours result in improved
    Survivability or increased Organ Donation and
    Quality?

9
Pathophysiology
  • Unique Process involving Multiple Organ Systems
  • Ischemic Injury
  • Additional Damage During and After Reperfusion
  • Additive to PreArrest Pathology
  • Post Cardiac Arrest brain Injury
  • Post Cardiac Arrest Myocardial Dysfunction
  • Systemic Ischemia/Reperfusion Response
  • Persistent Precipitating Pathology (P5)

10
Brain Injury
  • 68 OOH Mortality 23 IH Mortality
  • Limited Tolerance of Ischemia
  • Unique Reperfusion Response post ROSC lasting
    Hours to Days
  • Excitotoxicity
  • Disrupted Ca Homeostasis
  • Free Radical Formation
  • Pathologic Protease Cascades
  • Activation of Cell Death Pathways

11
Brain Injury
  • Protracted Injury Phase opens Broad Therapeutic
    Window
  • Cerebral Perfusion becomes dependent upon CePP
    not Autoregulation or Neuronal Activity
  • Migratory Intravascular Thrombosis with CPR gt 15
    minutes (No Reflow)
  • Hyperemic Flow increases Edema
  • Luxuriant Hyperperfusion
  • Excessive Oxygen Free radical Formation

12
Brain Injury
  • Global CBF is reduced but adequate to meet
    Oxidative Metabolic Demands in first 48 hours
  • Transient Edema common post Arrest but rarely
    increases ICP
  • Delayed Edema attributable to Ischemic
    Neurodegradation
  • Pyrexia
  • Poor Outcome Increases with each degree gt 370C
  • Hyperglycemia
  • Common and Potentially Mitigated with Insulin
    Rx
  • Seizures
  • Associated with Worst Prognosis
  • -- Caused by and Exacerbates Injury

13
Myocardial Dysfunction
  • Responsive to Therapy and Reversible
  • Detectible within minutes of ROSC
  • Decreased EF (stunned)
  • Increased LVEDP (stiff)
  • Coronary Blood Flow Normal Myocardial Stunning
  • Nadir _at_ 8 Hrs, Improve _at_ 24 Hrs, Normal _at_ 72 Hrs
  • Dobutamine improves LVEF and Diastolic
    Dysfunction

14
Systemic Response
  • CPR generates poor Cardiac Output, O2 delivery
    ,and Metabolite Clearance
  • Oxygen Debt leads to Endothelial Activation and
    Systemic Inflammation
  • Predictive of MOSF and Death
  • Common Sepsis Features
  • Adrenal Insufficiency
  • Responsive to Therapy and Reversible
  • Early Goal Directed Therapy may Optimize Outcomes

15
Persistent Pathology
  • Precipitating or Contributory Pathology
  • ACS
  • AMI gt50 OOH Adult Arrests
  • 48 Acute Coronary Occlusion w/o apparent STEMI
  • Biomarker Specificity Reduced yet 96 Sensitive
    for AMI

16
Persistent Pathology
  • Precipitating or Contributory Pathology
  • Pulmonary Embolism
  • Up to 10 Incidence in Sudden Death
  • Unknown ROSC Rate
  • COPD, Asthma, or Pneumonia
  • Pulmonary Function often Worsens post ROSC
  • Brain Injury and Edema more common after Asphyxic
    Arrest
  • Sepsis
  • Infections more common cause of In Hospital
    Arrests
  • Toxins
  • Environmental

17
Insanity defined
  • Insanity doing the same thing over and over
    again and expecting different results.

18
Therapeutic Strategy
  • Critical Care Standards for EMS and ED
  • Time Sensitive
  • Account for In/Out of Hospital Settings
  • Sequential care by multiple Diverse Teams
  • Accommodate Spectrum of patients
  • Awake, Stable to Unstable Comatose

19
Out-of-Hospital Cardiac Arrest Survival after the
Sequential Implementation of 2005 AHA Guidelines
for Compressions, Ventilations, and Induced
Hypothermia J. Brent Myers, MD MPH Medical
Director Wake County EMS System
October 2007
11.6
8.2
Plt0.05
7.3
4.6
when compared with baseline
20
What about the ACLS Drugs?
  • Class IIb
  • more studies are needed.

21
I want a new drug
  • A study of ventricular fibrillation victims, 75
    of the surviving patients had a return of
    spontaneous circulation without injection of a
    vasopressor the remaining 25 of patients who
    required a vasopressor indicated that, if basic
    life support does not restore spontaneous
    circulation, the general outcome is most probably
    poor.
  • Bunch TJ, White RD, Gersh BJ, Meverden RA, Hodge
    DO, Ballman KV, Hammill SC, Shen WK, Packer DL
    Long-term outcomes of out-of-hospital cardiac
    arrest after successful early defibrillation.
  • N Engl J Med 2003, 3482626-2633.
  • Accordingly, once advanced cardiac life support
    drugs are necessary, rescuers need to understand
    that the chance the patient will be discharged
    from the hospital is lt10
  • Wenzel V, Krismer AC, Arntz HR, Sitter H,
    Stadlbauer KH, Lindner KH A comparison of
    vasopressin and epinephrine for out-of-hospital
    cardiopulmonary resuscitation.
  • N Engl J Med 2004, 350105-113.

22
Epinephrine
  • employed in CPR for 100 years
  • dosage "lumps together" of all etiologies
    despite differences in myocardial energetics,
    postresuscitation function, neurological lesions,
    and mortality between ventricular fibrillation
    and other etiologies of arrest
  • ACLS dose of 1 mg bolus results in dose
    variability corresponding to 10 µg/kg in a 100-kg
    person but 25 µg/kg in a 40-kg person.
  • increases myocardial oxygen consumption during
    cardiopulmonary resuscitation
  • increases the likelihood of cardiac failure after
    restoration of spontaneous circulation via
    diastolic dysfunction
  • "But if you don't have a smashing alternative to
    the drug, you often just keep using it."

23
Vasopressin
  • successfully resuscitated cardiac-arrest patients
    found to have higher endogenous vasopressin
    levels than those patients who die
  • vasopressin increases blood pressure differently
    in the body, constricting the vessels in nonvital
    organs and dilating the blood vessels in the
    brain and in the heart
  • vasopressin appears to work best when ischemia is
    substantial
  • typically used only as alternative and late
  • Vasopressin is an orphan drug
  • Is marketing of vasopressin essential to the drug
    being used by emergency physicians treating
    cardiac-arrest patients?

24
Vasopressin versus continuous adrenaline during
experimental cardiopulmonary resuscitationResusci
tation, Volume 62, Issue 1, Pages 61-69
2004J.Johansson, R.Gedeborg, S.Rubertsson
  • Objective
  • To evaluate the effects of a bolus dose of
    vasopressin compared to continuous adrenaline
    (epinephrine) infusion on vital organ blood flow
    during cardiopulmonary resuscitation (CPR).
  • Results
  • Vasopressin generated higher cortical cerebral
    blood flow (Plt0.001) and lower cerebral oxygen
    extraction (Plt0.001) during CPR compared to
    continuous adrenaline.
  • Coronary perfusion pressure during CPR was higher
    in vasopressin-treated pigs (Plt0.001) and
    successful resuscitation was achieved in 12/12 in
    the vasopressin group versus 5/12 in the
    adrenaline group (P0.005).
  • Conclusions
  • In this experimental model, vasopressin caused a
    greater increase in cortical cerebral blood flow
    and lower cerebral oxygen extraction during CPR
    compared to continuous adrenaline. Furthermore,
    vasopressin generated higher coronary perfusion
    pressure and increased the likelihood of
    restoring spontaneous circulation.

25
Effects of epinephrine and vasopressin on
end-tidal carbon dioxide tension and mean
arterial blood pressure in out-of-hospital
cardiopulmonary resuscitation an observational
studyStefan Mally , Alina Jelatancev and Stefek
Grmec Centre for Emergency Medicine Maribor,
Ljubljanska 5, 2000 Maribor, SloveniaCritical
Care 2007, 11R39doi10.1186/cc5726
  • 1 mg of epinephrine intravenously every three
    minutes only vs vasopressin/epinephrine group 40
    units of vasopressin intravenously only or
    followed by 1 mg of epinephrine every three
    minutes during CPR. Values of end-tidal carbon
    dioxide and MAP were recorded, and data were
    collected according to the Utstein style.
  • Results
  • Final end-tidal carbon dioxide values and average
    values of MAP in patients with restoration of
    pulse were significantly higher in the
    vasopressin/epinephrine group (p lt 0.01).
    End-tidal carbon dioxide values as well as MAP at
    admission to the hospital were associated with
    survival at 24 hours and improved hospital
    discharge.
  • In the vasopressin group, significantly more
    pulse restorations and a better rate of survival
    at 24 hours were observed (p lt 0.05). Subgroup
    analysis of patients with initial asystole
    revealed a higher hospital discharge rate when
    vasopressin was used (p 0.04).
  • Neurological outcome in discharged patients was
    better in the vasopressin group (p 0.04).
  • Conclusion
  • End-tidal carbon dioxide and MAP are strong
    prognostic factors for the outcome of
    out-of-hospital cardiac arrest. This combination
    vasopressor therapy improves restoration of
    spontaneous circulation, short-term survival, and
    neurological outcome. In the subgroup of patients
    with initial asystole, it improves the hospital
    discharge rate.

26
A Comparison of Vasopressin and Epinephrine for
Out-of-Hospital Cardiopulmonary
ResuscitationVolker Wenzel, M.D., Anette C.
Krismer, M.D., H. Richard Arntz, M.D., Helmut
Sitter, Ph.D., Karl H. Stadlbauer, M.D., Karl H.
Lindner, M.D., for the European Resuscitation
Council Vasopressor during Cardiopulmonary
Resuscitation Study Group
  • Methods
  • 40 IU of vasopressin vs 1 mg of epinephrine,
    followed by additional treatment with epinephrine
    if needed.
  • Results
  • A total of 1186 patients.
  • Among patients with asystole, however,
    vasopressin use was associated with significantly
    higher rates of hospital admission (29.0 percent,
    vs. 20.3 P0.02) and hospital discharge (4.7
    percent vs. 1.5 percent, P0.04).
  • Among patients in whom spontaneous circulation
    was not restored with the two injections of the
    study drug, additional treatment with epinephrine
    resulted in significant improvement in the rates
    of survival to hospital admission and hospital
    discharge in the vasopressin group, but not in
    the epinephrine group (hospital admission rate,
    25.7 percent vs. 16.4 percent P0.002
  • hospital discharge rate, 6.2 percent vs. 1.7
    percent P0.002).
  • Cerebral performance was similar in the two
    groups.
  • Conclusions The effects of vasopressin were
    similar to those of epinephrine in the management
    of ventricular fibrillation and pulseless
    electrical activity, but vasopressin was superior
    to epinephrine in patients with asystole.
    Vasopressin followed by epinephrine may be more
    effective than epinephrine alone in the treatment
    of refractory cardiac arrest.

27
Combination vasopressin/epinephrine does not
improve cardiac-arrest outcomes
  • "The lack of superiority of combination therapy
    over epinephrine alone, regardless of the patient
    subgroup, suggests it may be futile to add
    vasopressin to epinephrine during cardiopulmonary
    resuscitation with advanced cardiac life
    support,"
  • Dr Pierre-Yves Gueugniaud et al,July 3, 2008 New
    England Journal of Medicine.
  • Investigators assigned 1442 adults to 1 mg of
    epinephrine and 40 IU of vasopressin and 1452
    adults to 1 mg of epinephrine alone, with the
    combination of drugs repeated if spontaneous
    circulation was not restored within three minutes
    after the first administration. Patients were
    subsequently given additional epinephrine alone
    if needed.
  • The combination therapy with vasopressin and
    epinephrine did not result in any significant
    improvement over epinephrine alone. The rates of
    survival to hospital admission, return of
    spontaneous circulation, survival to hospital
    discharge, survival at one year, and neurologic
    recovery at discharge were similar in both
    treatment arms.
  • Gueugniaud and colleagues point out that very few
    patients in their study had ventricular
    fibrillationless than 10 in both treatment
    armsand this "precludes a definitive conclusion
    against the use of vasopressin."
  • Survivorship to hospital discharge average 2 for
    both groups

28
Repeat?
  • Repeated Administration of Vasopressin but Not
    Epinephrine Maintains Coronary Perfusion Pressure
    After Early and Late Administration During
    Prolonged Cardiopulmonary Resuscitation in Pigs
  • Volker Wenzel, MD Karl H. Lindner, MD Anette C.
    Krismer, MD Egfried A. Miller, BS Wolfgang G.
    Voelckel, MD Werner Lingnau, MD

29
Question
  • Should vasopressin be injected during CPR based
    on results from a subgroup analysis and
    retrospective studies?
  • The pragmatic answer is yes.
  • Basic life support saves the 'best' cardiac
    arrest patients any subsequent advanced cardiac
    life support intervention has a decreasing
    likelihood to restore spontaneous circulation
    over time. Vasopressin should therefore be
    employed rapidly if initial epinephrine does not
    restore spontaneous circulation. Our strategy is
    to alternate between an initial injection of 1 mg
    epinephrine i.v. and a subsequent injection of 40
    IU vasopressin i.v. every 35 minutes during CPR

Vasopressin combined with epinephrine during
cardiac resuscitation a solution for the
future? Volker Wenzel Karl H Lindner Department
of Anesthesiology and Critical Care Medicine,
Innsbruck Medical University, Austria Critical
Care 2006, 10125doi10.1186/cc4846
30
Steroids
  • Here we go again
  • Methylprednisolone
  • Enhances contractile function of heart during and
    after myocardial ischemia
  • Enhances contractile function of peripheral
    arteries during endotoxemia
  • Within 30 to 60 minutes
  • Myocardial dysfunction and vasoplegia are key
    components of post-resuscitation shock

31
Vasopressin, Epinephrine, and Corticosteroids for
In-Hospital Cardiac ArrestMentzelopoulos, et al.
Arch Internal Med vol 1 Jan 12, 2009
  • Single center, prospective trial 100 consecutive
    patients.
  • 20 IU Vaso 1mg Epi 40mg Methylprednisolone
    and Hydrocortisone taper vs. STD 1 mg Epi for up
    to 5 CPR cycles
  • ROSC 81 vs. 52 p.003
  • Survival to D/C 30 vs. 0
  • Hymodynamics and Svo2 improved
  • Less MOSF
  • Independent of Induced Therapeutic Hypothermia

32
Monitoring
  • General EMS capabilities
  • Pulse Oximetry
  • Capnography
  • EKG, Continuous Monitoring
  • Core Temperature
  • Mean Arterial Pressure Targets
  • Advanced
  • Biomarkers

33
Oxygenation
  • 100 Oxygen
  • Good for CPR/ROSC
  • Bad post ROSC
  • Hyperoxia in early reperfusion harms
    Post-Ischemic Neurons
  • 100 FIO2 in 1st Hour post ROSC Worsened Outcome
    over Immediate Adjustment to 94-96

34
Ventilation
  • Autoregulation is dysfunctional yet
    Cerebrovascular Changes to PaCO2 Preserved
  • Hyperventilation may cause Vasoconstriction and
    Further Ischemia
  • Hypoventilation/Hypoxia/Hypercarbia elevates ICP
    and Metabolic Acidosis
  • Adjust Rate and Tidal Volume to keep PaCO2 near
    Normal

35
Optimal Hemodynamics
  • Balance Oxygen Delivery and Demands
  • Should be Achieved in the Early Post Arrest Phase
  • Optimize (Not Maximize)
  • Preload
  • PaO2
  • Afterload
  • Contractility
  • Systemic Oxygen Utilization

36
Optimal Hemodynamics
  • Post Cardiac Arrest Syndrome shares
    Characteristics with Sepsis
  • EGDT in Post Cardiac Arrest Syndrome
  • Optimal MAP?
  • gt 100 mmHg w/i 5 minutes of ROSC Bad
  • Cerebral perfusion dependant on MAP in Early
    Phase
  • No Reflow Phenomenon may require 90-100 mmHg
    Range
  • AMI or Myocardial Stunning maybe better at 65-75
    mmHg Range

37
Optimal Hemodynamics
  • Post Cardiac Arrest Syndrome shares
    Characteristics with Sepsis
  • EGDT in Post Cardiac Arrest Syndrome
  • Optimal CVP 8 12 mmHg
  • Relative Intravascular Volume Depletion Exists
    post ROSC
  • Account for Pathologies causing Elevated CVPs
  • Cardiac Tamponade
  • RV Infarct
  • PE
  • Tension PTX
  • Poor Myocardial Compliance

38
Circulation Support
  • Hemodynamic instability manifests as
    Dysrhythmias, Hypotension, and poor Stroke
    Volume/Output
  • Early Reperfusion is Best AntiArhythmic Therapy
  • Optimize RV Filling Pressures 8 -12 mmHG
  • 3.5 6.5 Lt First 24 hours
  • Inotropes/Vasopressors After Volume Correction
  • Pressor Dependence up to 72 hours
  • Select Inotropes by BP, HR, CO, and SvO2
  • Dopamine??

39
Therapeutic Hypothermia
  • The Only Post Cardiac Arrest Therapy Show to
    Increase Survival
  • Ongoing Evaluation of benefit in Patient
    Populations, Induction Techniques, Target
    Temperature, Duration of Therapy, and Rewarming
    Techniques.
  • Benefit Related to Time of Initiation of Therapy
  • Induction
  • IV Fluids and Cooling Pads
  • Maintenance
  • Cooling Pads and Catheters
  • ReWarming
  • 0.250C 0.50C/hr Current Consensus

40
Therapeutic Hypothermia
41
Sedation and Paralysis
  • Indicated for Failure to return to Awake Status
    w/i 5-10 minutes Post ROSC
  • Sedation reduces oxygen Consumption
  • Opoids and Hypnotics Required
  • EEG Monitoring for Sustained Neuromuscular
    Blockade

42
Seizures
  • Increases Cerebral Metabolism 3 Fold
  • Exclude ICH Electrolyte Imbalance
  • Myoclonus
  • Difficult to Control
  • Phenytoin Ineffective
  • Clonazepam most Effective
  • Improved Outcomes with Hypothermia despite Severe
    post Arrest Status Epilepticus

43
Prognostication
  • Pre-Cardiac Arrest Factors
  • Many Factors Associated with Poor Outcome
  • Advanced Age
  • Race
  • Poor Pre-Arrest health
  • Diabetes
  • Sepsis
  • Metastatic cancer
  • Renal failure
  • Homebound Status
  • Stroke
  • APACHE II III Scores
  • None are Reliable Predictors

44
Prognostication
  • Intra-Cardiac Arrest Factors
  • Factors Associated with Poor ROSC
  • Time To CPR
  • Duration of CPR
  • Quality of CPR
  • Maximum ETCO2 lt 10 mmHg
  • Asystole
  • Non cardiac Causes
  • None are Reliable Predictors Post ROSC

45
Prognostication
  • PostCardiac Arrest Factors
  • Retention of Neurologic Function Immediately
    after ROSC Best Predictor
  • Absence of Neurologic Function Immediately after
    ROSC is Not a Reliable predictor of Poor Outcome
  • Reliable Predictors occur at 72 Hours

46
PrognosticationIn the Age of Hypothermia
  • Therapeutic Hypothermia Improves Survival and
    Functional Outcome for 1 in every 6 Cardiac
    Arrest Survivors treated (NNT6)
  • Alters Progression of Neurological Injury
  • Changes the Evolution of Recovery
  • Changes in Timing and Interpretations are Needed
  • Do Not Withdraw Support Prematurely

47
Implementation
  • Clinical Guidelines Dont Change Practice
  • Barriers
  • Structural
  • Human and Financial Resources
  • Organizational
  • Leadership
  • Scientific
  • Personal
  • Intellectual
  • Attitudinal
  • Motivation
  • Environmental
  • Political
  • Economic
  • Cultural
  • Social

48
Implementation
  • Protocol changes
  • drop/downplay Epi
  • Vasopressin early and repeat
  • accept Pox 96-98
  • Follow eTCO2
  • Aim for MAP 65-95mmHg
  • Volume resuscitate
  • Dobutamine over Dopamine
  • Induce Hypothermia
  • Educate colleagues
  • Demand Outcomes
  • Transport to Resuscitation centers

49
Questions
  • What Will You Do Different Monday?
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