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.
post-cardiac arrest brain injury,
2.
3.
4.
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
In-hospital VF Arrests
Small subset within HACA: favorable survival
Out-of-hospital all-rhythms, or non-VF
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
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 nonspecific 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 nonspecific 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
Initial rhythm
arrests
VT/VF is the first monitored rhythm in only 15-23% of inhospital 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
Vascular Anesthesia (2009) 13(1):19-30
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)
33:237-245
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
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
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)
33:237-245
