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CBP: Cardiac Arrest

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Page 1: Cardiac Arrest CBP (

CBP: Cardiac Arrest

Page 2: Cardiac Arrest CBP (

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.

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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

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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.

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Question 1

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

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Definition

Post-cardiac arrest syndrome is a unique and complex combination of pathophysiological processes, which include1. post-cardiac arrest brain injury,

2. post-cardiac arrest myocardial dysfunction, and

3. systemic ischemia/reperfusion response.

This state is often complicated by a fourth component: 4. the unresolved pathological process that

caused the cardiac arrest.

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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.

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Pathophysiology

The 4 key components of post-cardiac arrest syndrome are:1. post-cardiac arrest brain injury,

2. post-cardiac arrest myocardial dysfunction,

3. systemic ischemia/reperfusion response, and

4. persistent precipitating pathology.

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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.

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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…

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Forrest through the trees

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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)

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Question 2

How do you treat Post-Cardiac Arrest Syndrome. (Federico)

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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

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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)

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Avoid hyperoxia Ptl for increased free radical production PaO2 goals of 92 – 96%

Aim for normocarbia

Volume resuscitate

Consider intropes/vasopressors

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Treat for ACS Noemie

Hypothermia Ibrahim

Treat seizures Increase cerebral metabolism No Evidence for prophylaxis

Myoclonus Clonazepam

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Treat hyperglycemia

No evidence for Neuroprotective medications

Adrenal dysfunction

Renal failure

Infection More prone to aspiration pneumonia

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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)

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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

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Bernard, 2002, NEJM

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HACA, 2002, NEJM

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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

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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)

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Impaired glucose tolerance (dec insulin level and sensitivity)

Coagulopathy

Lower immunity--> infections Higher pneumonias in TH group in HACA, but NS

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Should we cool this patient?

Yes! Out-of-hospital VF arrest

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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)

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. What do you tell them and how do you prognosticate patients

post arrest? Timing

What is a “poor outcome”?

Prognostication Clinical EEG Biomarkers Imaging

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Timing

Very difficult to prognosticate in the first 24 hours

Most evidence is derived on testing at 72 hours

Therapeutic hypothermia changes the timeline

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What is a poor outcome?

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What is a poor outcome?

Poor outcome is defined as death, unconsciousness after one month, or unconsciousness or severe disability after six months.

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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

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Clinical Signs

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

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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

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SSEP’s

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

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N20

Best studied waveform

Robust as it is not strongly influence by meds and metabolic derangements

LR+ 12 (CI 5.3-27.6)

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Biomarkers

Dead brain releases biomarkers

3 have been “well” studied Neuron specific enolase (NSE) S-100 Creatinine kinase BB isoenzyme (CK-BB)

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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

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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)

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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?

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Etiology of cardiac arrests

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65-70 %

10%

5-10%

15 to 35%

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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

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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?

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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

NEJM 1997;336:1629-1633

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

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Recommendations for cath post cardiac arrest

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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)

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If he arrested again, would you thrombolyse him?

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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

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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.”

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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?

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ECMO in cardiac arrest = Extracorporeal Life Support (ECLS)

Few small, observational and retrospective studies (5 studies: 3 adult, 2 pediatric)

All in hospital arrests

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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

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Question 7

 

Assuming he survives to discharge, should he get an ICD implanted? (Marios)

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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)

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Question 7: Indications for ICD implantation post-arrest

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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.

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Question 8a: Are there any differences between in-hospital and out-of-hospital

cardiac arrest?

VS

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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) 33:237-245Dichtwald 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

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Question 8b: What can be done to improve the outcome of in hospital

cardiac arrest?

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“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) 33:237-245

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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) 33:237-245

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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) 33:237-245

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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

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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

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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

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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.

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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.

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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

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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) 33:237-245

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The End