Brain Injury due to Cardiac Arrest:
Neuropsychological Outcomes and a Model for
Early Rehabilitation Management
Kyle Harvison, PhD, LP, ABPP-CN
Cindy Kosek, OT
• Review of cardiac arrest and associated
mechanisms of brain injury
• Overview of therapeutic hypothermia as a
neuroprotective strategy post-cardiac arrest
• Overview of neuropsychological outcomes
and early non-cardiac rehabilitation needs
• Introduce a model of care focused on these
rehabilitation issues
Cardiac Arrest
• Sudden Cardiac Arrest
• Not always “heart attack”
• Cessation of productive cardiac mechanical activity
– Defined by absence of palpable pulse and
spontaneous respiration (Tiainen et al., 2007)
Cardiac Arrest: Causes
Problems with heart rhythm
Myocardial infarction
Coronary artery disease
Respiratory arrest
Enlarged heart
Valve disease
Congenital heart defect
Coronary artery dissection
Severe physical stress (e.g., blood loss)
Fluid buildup
Metabolic disruption
In Cohen and Gunstad (2010), pp. 127-28
Cardiac Arrest: Causes
Electrophysiologically, most common
underlying problems are:
– Ventricular fibrillation (VF)- Quivering of the
heart’s lower chambers
– Pulseless ventricular tachycardia- Extremely
rapid but ineffective beating of the heart’s
lower chambers
Out of Hospital Cardiac Arrest: Annual U.S.
(Schulman, Hartman, & Geocadin, 2006; Holzer, 2010)
Cardiac Arrest: Management and
• Interventions include cardiopulmonarycerebral resuscitation, defibrillation,
intubation, and heart stimulating drugs, as
well as management of underlying causes
• Crucial prognostic factors:
– Whether a heart rhythm is detected early
– Whether underlying causes of arrest been
identified and treated
Young (2009)
Post Cardiac-Arrest Syndrome
(Holzer, 2010)
• Includes:
– Brain Injury
– Myocardial Dysfunction
– Systemic ischemia
– Reperfusion responses
– Consequences of disorder that caused CA
How does cardiovascular disease affect
the brain?
• Cardioembolic stroke
• Global cerebral ischemia
• Cerebrovascular disease
associated with systemic
vascular changes
• Metabolic disruption from
injury to other organs
• Psychiatric comorbidities
• Medication effects
• Adverse postsurgical effects
Cohen (2010), pp. 21-22
Cardiac arrest and Brain Injury: Where?
More vulnerable
Less vulnerable
• Brainstem
• Thalamus/hypothalamus
Cerebral cortex
Basal ganglia
-Memory impairment in out-of-hospital cardiac arrest survivors has been
associated with global cerebral atrophy, rather than selective hippocampal
damage (Grubb et al., 2000)
Geocadin et al. (2008), p. 489
Cardiac Arrest and Brain Injury:
(Holzer, 2010)
• Immediate:
– Oxygen and energy stores deplete quickly
– Neuronal firing is disrupted
– Excessive stimulation kills nerve cells
• Reperfusion injury:
– Initial increase in blood flow followed by
delayed, prolonged hypoperfusion
– Toxic cell injury due to oxidative stress
– Inflammatory response can injure tissue and
disrupt O2 delivery
Cascade of events in Ischemia
Cardiac Arrest: Neurological Prognosis
• Brain damage occurs quickly (seconds to
minutes) and is permanent in half or more
with conventional treatment (Young, 2009)
• Estimated 12,000 survivors with persistent
neuro deficits/year with a prevalence of
~50,000 impaired survivors (Lim et al., 2004)
Cardiac Arrest: Neurological
• Early neurological prognosticating often occurs
during coma or early stages of confusional state
– Focused on likelihood that patient will achieve no
better than vegetative state or severe disability
(Young, 2009)
• Some patients may remain comatose for extended
periods but still have favorable neurological recovery
• Assessment complicated by interventions (Holzer,
• Difficult questions of when to withdraw care
Cardiac Arrest: Neuropsychological
• Roine, Kajaste, & Kaste (1993) published the
first prospective, consecutive, communitybased neuropsychological study of nontraumatic out-of-hospital VF cardiac arrest
– Part of a larger investigation of nimodipine
treatment to improve cognitive outcome
– Occurred in Helsinki between 1986-88
Roine, Kajaste, & Kaste (1993)
• Follow-up assessments at 3 and 12 months
• Of 155 who met entry criteria, 70 (45%) were
alive at 3 months and 59 (38%) at 12 months
• Descriptives:
– Average age = 65 (range 36-85)
– Approximately 70% were men
– Average WAIS VIQs ~100
Roine, Kajaste, & Kaste (1993): Summary
• Moderate to severe deficits (i.e. < 2nd percentile)
present in 60% at 3 months and 48% at 12
• Findings generally stable between 3 and 12
months, but 23% improved and 8% declined (of
those who survived)
• Most common cognitive impairment was delayed
memory, with visuoconstruction, psychomotor
function, PIQ, and arithmetic also being
commonly affected
• Depression evident in 35% at 3 months and 31%
at 12 months
Cardiac Arrest: Neuropsychological
• Subsequent studies (Grubb et al., 1996; Suave’ et
al., 1996 ; van Alem et al, 2004) have
demonstrated cognitive deficits in 28-50% of
survivors at intervals ranging 6 -12 months
• Most common pattern is combination of
memory, psychomotor, and executive deficits (Lim
et al., 2004)
• Mayo study (Mateen et al., 2011) of survivors at 8
years found primarily memory difficulties but the
group (n=47) retained strong verbal IQ, normal
MMSE and high rates of functional independence
2002, Volume 346 (8)
Mild Therapeutic Hypothermia to Improve the Neurologic Outcome after Cardiac Arrest
The Hypothermia after Cardiac Arrest Study Group
Treatment of Comatose Survivors of Out-of-Hospital Cardiac Arrest
with Induced Hypothermia
Stephen A. Bernard, M.B., B.S., Timothy W. Gray, M.B., B.S., Michael D. Buist, M.B., B.S.,
Bruce M. Jones, M.B., B.S., William Silvester, M.B., B.S., Geoff Gutteridge, M.B., B.S., and Karen Smith, B.Sc.
“Favorable” Neurological Outcome
and Cerebral Performance Category
• CPC1= Good outcome: conscious, alert, able to work, possible
mild neurologic or psychologic deficit
• CPC2= Moderate disability: conscious, sufficient cerebral
function for independent activities of daily life. Able to work in
sheltered environment.
• CPC3 = Severe cerebral disability, functionally dependent;
includes severe dementia states
• CPC4 = Coma or vegetative state
• CPC5 = Brain death
Safar P. Resuscitation after Brain Ischemia, in Grenvik A and Safar P
Eds: Brain Failure and Resuscitation, Churchill Livingstone, New York,
1981; 155-184.
Rates of favorable neurological recovery in
survivors after therapeutic hypothermia (TH)
Discharged to home 21/43 (49%)
or rehab facility
(Bernard et al., 2002)
9/34 (26%)
Category 1 or 2 @ 6
Months (HACA,
54/137 (39%)
75/136 (55%)
“…hypothermia provides protection against numerous
deleterious biochemical mechanisms” Safar & Kochanek (2002)
TH Protocol
• Cooling initiated ASAP, typically within at least 4 hours of return
of spontaneous circulation
• Target core body temperature is 33-36 degrees Celsius
• Hypothermia continued for 24 hours
• Followed by passive rewarming
• Broader care includes ventilation, hemodynamic support,
cardiovascular intervention, dialysis, infection management,
glucose management, etc…
Cooling Methods
• Include:
– Surface cooling
• Pre-cooled pads
• Water-circulating pads
– Core cooling
• Cold IV fluids
• Catheter based endovascular delivery of cool
TH Mechanisms of Action
(Hopkins, 2008, Holzer, 2010)
Reduced brain metabolism
Decreased levels of excitatory substances
Attenuated oxidative stress
Decreased inflammation
Better regulated cerebral microcirculation
Decreased cell death
• Could also have beneficial effects on non-CNS
aspects of post-CA syndrome
• Therapeutic hypothermia after cardiac arrest.
An advisory statement by the Advanced Life Support Task Force of the
International Liaison Committee on Resuscitation
Resuscitation 57 (2003) 231-235
• Unconscious adult patients with spontaneous circulation
after out-of-hospital cardiac arrest should be cooled to
32-34 dgs. C for 12-24 hrs. when the initial rhythm was
• Such cooling may also be beneficial for other rhythms or
in-hospital cardiac arrest.
HACA Trial Neuropsychological
Outcome (Tiainen et al., 2007)
• 27 TH and 18 Normothermia (NT) at 3 months
• Most CPC 1 or 2
• Most living at home but only 25-33% back to
• Psychometric testing focused on memory,
executive, and psychomotor speed
• No significant group differences
HACA Trial Neuropsychological
Outcome (Tiainen et al., 2007)
TH (n = 27)
NT (n = 18)
n (%)
Intact or subtle deficits
(0-2/8 tests impaired*)
18 (67)
8 (44)
Moderate impairment (34/8 tests impaired*)
5 (19)
5 (28)
Severe impairment (5-8/8 4 (15)
tests impaired*)
5 (28)
-”The use of therapeutic hypothermia was not associated with
cognitive decline…”
*<1.5 SDs
Post TH outcomes: Study 2
(Cronberg et al., 2009)
• Prospective study of all patients with CA treated with
hypothermia at intensive care units at two university
hospitals and one regional hospital in Sweden
• 43/48 survivors agreed to follow-up at ~7 months
• Cognitive, mood, and quality of life measurement
• Encouraging findings but let’s consider from a rehab
Post TH outcomes: Study 2
(Cronberg et al., 2009)
“mild cognitive impairment is
Cognitive Outcomes (Cronberg et al.,
n (%)
n (%)
n (%)
n (%)
19 (44.2)
20 (46.5)
3 (7)
1 (2.3)
Frontal Lobe
25 (62.5)
Battery (n = 40)
5 (12.5)
10 (25)
BMT (n = 39)
8 (20.5)
18 (46.2)
11 (28.2)
2 (5.1)
Memory (n =
15? (35.7)
17? (40.5)
4 (9.5)
6 (14.3)
Self Reported
(n = 43)
Post TH outcomes: Study 2
(Cronberg et al., 2009)
“mild cognitive impairment is
But moderate memory and executive
impairment not uncommon
Post TH outcomes: Study 2
(Cronberg et al., 2009)
“mild cognitive impairment is
“high level of functioning as
reflected in the CPC categories”
Indeed, but meaning what? Also,
moderate memory and executive
impairment not uncommon
CPC insensitivity
Post TH outcomes: Study 2
(Cronberg et al., 2009)
“mild cognitive impairment is
But moderate memory and executive
impairment not uncommon
“high level of functioning as reflected
in the CPC categories”
“quality of life is good”
CPC insensitivity.
QofL <90% with 1/4 below 70%; plus
14% depressed and 22% can’t sleep
Post TH outcomes: Study 2
(Cronberg et al., 2009)
“mild cognitive impairment is
But moderate memory and executive
impairment not uncommon
“high level of functioning as reflected
in the CPC categories”
“quality of life is good”
CPC insensitivity.
“Overt neurological findings are
QofL <90% with 1/4 below 70%; plus
14% depressed and 22% can’t sleep
But ~25% showed motor difficulties
causing difficulties in handling daily
Post TH outcomes: Study 2
(Cronberg et al., 2009)
“mild cognitive impairment is
“high level of functioning as reflected
in the CPC categories”
“quality of life is good”
“Overt neurological findings are
“Clearly the outcome following THtreated CA is dichotomized into
survival with good neurological
outcome or death”
Indeed, but meaning what? Also,
moderate memory and executive
impairment not uncommon
So what? We knew that.
But most reported QofL <90% with
1/4 below 70%; plus 14% depressed
and 22% can’t sleep
But ~25% showed motor difficulties
causing difficulties in handling daily
Clearly it’s not that simple!
Post TH outcomes: Study 3
( Torgersen et al., 2010)
• 24 CA survivors post TH with CPC 1 or 2; seen at 13–
28 month follow up in university hospitals in Sweden
• 52% showed deficits in memory and executive
functioning on the CANTAB
• Group level QoL consistent with population norms;
QoL not correlated with cognitive outcomes
• Mild cognitive deficits are common in OHCA survivors
with a high functional status treated with TH but do
not affect HRQOL. (p. 7).
• Problems include small sample and poorly validated
test which samples limited domains
Post TH outcomes: Study 4
( Fugate et al., 2013)
• Prospective study from Mayo of OOH CA survivors
post TH (n=56); short post-CA coma
• Followed at 20 months using a telephone-based
interview of cognitive status
– 91% living independently
– 40% cognitively impaired, primarily weak delayed recall
– 79% of those employed at time of CA had returned to
– Long time to ROSC did not preclude good outcome (avg
20 mins in both groups)
Post TH outcomes: Study 5
( Larsson et al., 2014)
• Quality of life and mood outcomes in 26 survivors
post CA at discharge, one month and six months
• Changes in reporting of low QofL from 73% at
discharge to 50% at one month and 41% by six
• Physical problems most common complaint
affecting QofL
• Correlation with depressive symptoms; rates of
clinically significant depressive symptoms 11% or
Conclusions from literature
• Cardiac arrest causes heterogeneous brain damage via
global ischemia; injury continues through reperfusion
• Usually fatal, but survival improving with community
resources and improved treatments
• TH associated with “favorable neurological outcome,”
relatively speaking
• Memory, psychomotor, and executive problems common
but functional status often essentially normal
• Quality of life improves over about first six months; longerterm outcome less clear
• Need better operationalized definition of “impairment”
Next Steps
• From ICU to Discharge…..
– The need for a program at ANW was identified by a
previous patient
• Therapeutic Hypothermia work group was established
(Goal: no patient will slip through the cracks)
Rehabilitation Approach
• Our challenges:
– Don’t let relief of survival overshadow need to focus on
rehab-relevant adverse outcomes
– Select array of tests with validity and reliability in
this population, acceptably easy to administer,
broad yet focused
• Screening model: find survivors with any cognitive
dysfunction after Cool-it knowing:
– would over-identify dysfunction
– not all dysfunction identified would necessarily be due to
effects of CA-related global cerebral ischemia
Work Group Outcomes
for Rehabilitation
• Routine orders sets now include:
– Therapies
– PM&R consult
– Neuropsych consult
• Discharge conference
– Team and patient
• Routine order for Outpt follow up
– Neuropsych and OT
Typical Patient Profile
• Multiple lines
• Impulsive
Therapy Roles:
• PT:
– Early mobilization
• Amnesia around the
– Family Education
– Early ADL’s
– Min-stim protocol
• Decreased Fine Motor
- Swallow screen
• Emerging Alertness
• Family Relief of survival
Social Work:
- Family connection
Telemetry Unit
Typical Patient Profile
• Most lines removed
• Impaired Balance persists
• Impulsivity
• Decreased Attention
• Impaired short term
Decreased Insight
Therapy Roles
• Progress Mobility
– Functional Cognition
– Assess high risk ADL’s
SLP /Neuropsych
– Formal Cognitive Testing
PM&R Consult
Cardiac Rehab
– Trains in CPR
– Outpatient referral
Patient Education:
Other Defaulted Consults
• Social work
– Will follow patients from admission to discharge
– Will coordinate Discharge Planning meeting
• Case management
– Will actively follow patients at time of transfer
– Will coordinate required After Discharge appointments
• Spiritual care
• Smoking cessation (if appropriate)
• Hospitalist/Cardiologist
– Manages non-cardiac or cardiac issues
Day of Discharge
Patient Profile
• Up and moving
• Varying levels of
• Anxious and focused
on discharge home
Day of Discharge Cont.
Discharge Conference
– Patient & Family
– Case Manager
– Social Worker
– Therapies
– MD Providers
– Physiatrist
– Neuropsych
• Discharge
– ADLs/mobility
– Supervision
– Driving
– Working
– Out patient therapies
– Cardiac Rehab
Outpatient Follow-up
• Brain Injury Case Manager Phone Follow Up
• 4-6 weeks s/p discharge
• Clinic Follow up:
• Neuropsychological Re-assessment
• Occupational Therapy
Case Manager
Phone Follow Up
– Confirm dates/ times of follow up appointment
– Notify Cardiology
– Checks on patient’s current status:
Assistance with personal cares
Living situation
Return to work?
Return to driving?
Any other concerns/ questions
Day of Follow Up
Neuropsychology Re-assessment
Neuropsychologist reviews the findings
Neuropsychologist updates OT on outcome
OT meets with patient
3 primary Roles of OT
1. Strategy identification in any areas of
inefficiency identified by
2. Education on core concepts
3. Provide assessment information to care
team to assist with interdisciplinary
recommendations in the area of higher
level IADL’s
Core Educational Concepts
• Multi-factor Model
• 6 Things that need to be Managed for Best
Cognitive Health
Multi-factor Model
Brain impairment combines in some fashion with personal and
situational factors to influence performance, social interactions
and coping with failures and other stresses.
• When individuals have had a cardiac event, their disability is
determined by:
– Brain impairment
– The effects of problematic factors, both personal and situational
Montgomery, 1995
Multi Factor Model
Personal Factors:
– Fatigue
– Arousal/Tension
– Physical symptoms (i.e. headaches, nausea)
– Negative thoughts
Situational Factors
– External environmental distracters
– Multi-task demands
– Information processing demands
Montgomery 1995
6 Key Areas That Need To Be
Managed For Cognitive Health
1. Good Nutrition
Stay hydrated
Eat consistently
Let Dr. know if nausea or
appetite are a problem
Use supplements
Get easy to prepare foods
Use external prompts
6 Key Areas That Need To Be
Managed For Cognitive Health
2. Good Sleep
Get up and go to bed at a set time
No caffeine after 2:00 pm
No TV in the bedroom
Relaxation prior to sleep
Medications may be helpful
Be mindful of napping
6 Key Areas That Need To Be
Managed For Cognitive Health:
3. Physical Exercise
 Resume some level of
 Take breaks
 Begin slowly and build
4. Stress Reduction
 Develop relaxation skills.
 Schedule relaxation time
into your day
6 Key Areas That Need To Be
Managed For Cognitive Health
5. Brain Engagement
It matters
It needs to challenge you
It needs to be fun
The list is endless…..just do
something each day!
6. Social Engagement
Need connections and interaction
Support groups
Consistent contact with family and
Case study
• As CA survival rates are improving,
neuropsychological outcomes are of
increasing importance
• Patients likely leave hospital below baseline,
but improvements may be made over several
months or more
• Roles for both cardiac and neuro-rehab

similar documents