THERAPEUTIC HYPOTHERMIA GAIL DELFIN MSN RN CCRN CCNS May 2011

THERAPEUTIC HYPOTHERMIA
GAIL DELFIN MSN RN CCRN CCNS
HOSPITAL OF THE UNIVERSITY OF PENNSYLVANIA
May 2011
Presenter Disclosure
Information
Gail Delfin MSN RN
Therapeutic Hypothermia
FINANCIAL DISCLOSURES:
No relevant financial relationships exist
UNLABELED/UNAPPROVED USES:
None
Prevalence
There are 200,000 – 300,000 deaths per year
due to cardiac arrest
(Nichol et al, 2008)
What Happens After Successful CPR?
How do we
improve
survival and
optimize
neurological
outcomes?
Mitochondria – Where the Action is!
“Oxygen deprivation is merely the start
of the cascade. Dying turns out to be
almost as complicated as living.”
– Lance Becker MD, Center for Resuscitation Science at Penn
Mitochondria Function
•
Energy
•
“Death control”
During ischemia followed by reperfusion, brain
cells partially / fully recover or enter a pathway
of programmed cellular death (apoptosis)
The key is…
Prevention of Mitochondrial Dysfunction!
The Apoptotic Pathway
•
ATP and other high-energy metabolites
breakdown, leading to increased
intracellular levels of lactate, H+ ions and
phosphates, resulting in intracellular acidosis
•
Ca+ influx induces mitochondrial dysfunction
•
Prolonged glutamate exposure causes
neuron hyperexcitability
(Polderman, 2009)
Other Effects of Reperfusion Injury
•
Increase in pro-inflammatory mediators
(tumor necrosis factor, interleukin-1,
cytokines) leads to accumulation of
inflammatory cells
•
Free radical production (i.e., superoxide,
hydrogen peroxide) damages cellular
components
•
Disruption of the blood-brain barrier leads to
cerebral edema
(Polderman, 2009)
An Historical View of TH
Hippocrates
450 BC
Baron Larrey
1814
Peter Safar
1960s
Packed Injured
Patients in Snow
Napoleonic
Wars
Father
of CPR
Landmark Studies
300
275
250
200
150
100
77
50
30
0
IDRISSI
BERNARD
HACA
Belgium
2001
Australia
2002
Austria
2002
Outcomes of mild induced therapeutic
hypothermia
HYPOTHERMIA
NORMOTHERMIA
Alive @ hospital discharge - favorable neurological recovery
HACA Study Group
Bernard
Hachimi-Idrissi
72/136 (53%)
21/43 (49%)
4/16 (25%)
50/137 (36%)
9/34 (26%)
1/17 (6%)
Alive at 6 months - favorable neurological recovery
HACA Study Group
72/136 (52%)
50/137 (36%)
Recommendations from the AHA
2010
Comatose out-of-hospital VF – Class I
Comatose in-hospital, other rhythms - Class IIb
Decision-making after ROSC

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Comatose with Glasgow Motor < 6
No alternative reason for coma
No uncontrolled bleeding
Hemodynamically stable; no uncontrollable
dysrhythmias
Absence of severe MODS or sepsis
Full code status prior to event
Pre-arrest cognition not meaningfully impaired
? Prolonged arrest time (> 60 minutes)
?Pregnancy – consult maternal-fetal medicine
Framework for TH Induction

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Apply all appropriate
ICU monitoring
equipment – intubate
(if not already done)
Immediate EKG;
ECHO if indicated
Blood work
Guarantee that
cooling equipment is
ready
Begin infusion of 2
liters of cold (4
degree C) NSS

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Arterial line (always
prior to cooling)
Central line
Temperaturefeedback device
If paralysis is part of
protocol, guarantee
sedation, baseline
TOF
Apply continuous EEG
if available
Goal: To Reach Target Temp of
32–34 Degrees C Within 4 Hours


But if the EKG looks unusual?
How do we incorporate catheterization?
Neumar et al (2008) recommend that
because CAD is present in the majority of
out-of-hospital arrest victims, patients with ST
segment elevation should undergo
immediate cardiac intervention
– If there is no clear cut EKG evidence but
suspicion for ACS is high, these patients
should also be considered for immediate
coronary angiography
– Studies have demonstrated that
intervention during TH is safe and may
improve outcomes
(Hovdenes et al, 2007)
Cardiac ECHO
May reveal global hypokinesis –
myocardial stunning
 May reveal segmental hypo- or
akinesis indicative of MI
 May be helpful in directing use of
vasoactive support related to the
ejection fraction

What Can Bloodwork Tell Us?



HCG on all women of child-bearing
age
ABG with ionized calcium
– pH of >7.25 to normal acceptable
– Keep CO2 normal (avoid hyper–
/hypoventilation)
– Maintain normal calcium levels
CBC, platelets, coags, fibrinogen
– Baseline Hgb
– Platelets may decrease with
cooling
– Rule out disseminated intravascular
clotting
Bloodwork (cont’d)

Electrolytes, magnesium, phos, glucose
– Expect decrease in potassium and
magnesium as cooling diuresis begins and
intracellular shifts occur
– Maintain phos at normal levels to support
ventilator weaning
– Glucose will rise during cooling and
fall during warming

Amylase, lipase, liver function
values may be elevated – expect to
return to normal
Bloodwork (cont’d)

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Lactate
– Abnormal lactate is to be anticipated should fall to normal; if elevates again,
investigate
Troponins, CK-MB
Cortisol level
Pan-culture
Toxicology panel if appropriate
Hgb/O2 sat (co-oximetry panel)
Temperature Measurement

Temperature accuracy for feedback
to cooling device
– Gold standard - jugular venous bulb or
pulmonary artery catheter; accurate, no
lag time
– Peripheral sites are never used
– Others (bladder, esophageal) have
some lag time and may be more
complicated to place
Sedation and Paralysis


Sedatives include propofol, lorazepam,
midazolam and fentanyl – most protocols
recommend both a benzodiazepine and
opiate (Chamorro et al, 2009)
Paralysis – Initiate prior to cooling;
initiating after cooling is begun could
drop temperature precipitously – prevent
shivering!
– Increases MVO2 40 – 100%
– May use other methods other than
paralysis
Sedation/Paralysis

BIS Monitor to
maintain sedation –
small study (62
patients)
demonstrated that
any patient that had a
BIS of 0 at any time
point did not survive
(Leary et al, 2010)

Train-of-four to monitor
paralysis
Post-resuscitation Care – A Critical Component of
Advanced Life Support (Circulation, 2005)

Providers should:
– Optimize hemodynamic, respiratory
and neurologic support
– Identify and treat reversible causes of
cardiac arrest
– Monitor and consider treatment for
disturbances of temperature regulation
and metabolism
Similarity of Post–arrest Syndrome to
Sepsis Syndrome
(Adrie et al, 2002)
Goal-Directed Therapy for
Hemodynamic Optimization*
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Maintain MAP 80 – 100 (may
consider lower if ACS)
Maintain CVP 8 – 15
Maintain ScvO2 equal to or
greater than 65
Monitor lactate to
determine cellular perfusion
*(Gaieski et al, 2009)
Determining Which
Vasoactive Drugs to Use

Unknown ejection fraction or < 40% – dobutamine

Add dopamine or epinephrine

Ejection fraction is normal – norepinephrine

Severe hypotension – consider IABP

Hypertension – nitroglycerin
(Gaieski et al, 2009)
Normal Side Effects of TH
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Tachycardia then bradycardia when temp < 35 C
Vasoconstriction – increased B/P
Increased CVP reading (venoconstriction) but
decreased CVP due to cooling diuresis
Cooling diuresis
Mottling of skin
Left shift of oxyhemoglobin curve
Decreased metabolic rate (8% for every degree C
drop)
Hyperglycemia (decreased insulin sensitivity)
Arrhythmias rare if temp >30
Change in drug metabolism
Re-Warming Considerations
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Should occur slowly - < 0.5 C/hr
Discontinue all K+ containing fluids to prevent
hyperkalemia
Hydrate patient to maintain CVP prior to/during
re-warming; consider fluid boluses for
hypotension
Frequent glucose monitoring to avoid
hypoglycemia
Observe for arrhythmias, shivering, seizures
Prevention of fever for at least 48 hours
Discontinue paralytics at 36 C; titrate sedation
Consider treatment plan – ? cath, ? ICD, followup
Adverse Effects

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Stress ulcers – prophylaxis
Bleeding (very low incidence)
Risk of pneumonia, wound infections due
to impaired immune response
Atrial fibrillation progressing to VF if temp
drops < 30 degrees
Incidence of significant adverse effects is
low
Nursing Care
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Skin care – observe skin, turn Q 2 hours,
adjust skin wraps
Assessment for shivering, seizures
Eye care (paralysis)
Careful documentation of IV sites;
prevention of VAP, skin breakdown
Consider 2:1 nursing care of the patient
for first 6 hours, then 1:1 for remainder of
TH course
Family support
Family Needs
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Very difficult time – “marathon, not a sprint”
Encourage support by chaplain, social services
Provide information, websites, articles for
laypersons
Encourage family to take care by sleeping,
eating, reaching out to other family members
and friends, especially during 24 hours that
patient remains cooled
All health care providers should be on same
page when communicating with the family
Neuroprognostication
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Published prognostic
criteria are
not valid for these patients
(Rittenberger, 2009)
CT of brain commonly
shows swelling – without
prognosticating value
MRI of brain – poorly
studied in early phase of
post-arrest resuscitation
EEG alone is insufficient to
prognosticate futility
(Abella, 2009)
Neuroprognostication
(cont’d)

Some indications of poor outcome:
– No motor response to pain after three days
– Bilaterally absent somatosensory evoked potentials
after three days
– Status epilepticus during the post-cardiac arrest period
up to three days

Neuroprognostication should absolutely not
occur before 72 hours after ROSC! (and maybe
as long as 5 – 6 days)
(Abella, 2009)

Hypothermia Network Registry
Oct 2004-Oct 2008
986 OHCA pts > 18 yrs; 34 centers, 7
countries
OHCA to ROSC:

OHCA to initiation of hypothermia:

OHCA to goal temperature (≤34 C):
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– 20 (14–30) minutes
– 90 (60–165) minutes
– 260 (178–400) minutes
(Nielsen, 2009)
Results
•
VT/VF
>
412 survivors (61%)
380 good outcome (56%)
>
54 survivors (25%)
46 good outcome (21%)
>
18 survivors (27%)
(n = 686)
•
Asystole
(n = 217)
•
PEA
(n = 66)
15 good outcome (23%)
Penn Data
Total cooled since 2005 – 154 patients
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Initial rhythm:
Survival to discharge:
VT/VF – 45 (29%)
27 (60%)
PEA – 62 (37%)
20 (32%)
Asystole – 28 (18%)
5 (18%)
Other/unknown – 19 (13%)
6 (32%)
Total survived: 57 (37%)
Neurologically intact: 41 (72%)
A Successful TH Course…
TH improved survival and functional
outcome for every one in six comatose
survivors of cardiac arrest
In experienced hands, TH is safe and
highly effective
References
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2005 American Heart Association Guidelines for
Cardiopulmonary Resuscitation and Emergency
Cardiovascular Care. Circulation 2005; 12: Dec 13
Supplement.
Abella BS. Prognostication and setting family expectations.
Presentation, October 30 2009.
Adrie C, Adib-Conquy M, Laurent I et al. Successful
cardiopulmonary resuscitation after cardiac arrest as a
“sepsis-like” syndrome. Circulation 2002; 106: 562-68.
Chamorro C, Borrallo J, Romera M et al. Anesthesia and
analgesia protocol during therapeutic hypothermia after
cardiac arrest: A systematic review. Presentation, January
22 2010.
Gaieski DF, Band RA, Abella BS et al. Early goal-directed
hemodynamic optimization with therapeutic hypothermia
in comatose survivors of out-of-hospital cardiac arrest.
Resuscitation 2009; 80 (4): 418-24.
References (cont’d)
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Hovdenes J, Laake JH, Aaberge L et al. Therapeutic
hypothermia after out-of-hospital arrest: experiences with
patients treated with percutaneous coronary intervention and
cardiogenic shock. Acta Anaesthesiol Scand 2007; 51 (2): 137-42.
Leary M, Fried D, Gaieski D et al. Neurologic prognostication and
bispectral index monitoring after resuscitation from cardiac
arrest. Resuscitation 2010; doi: 1016/j.resuscitation.2010.04.021.
Nielsen N, Hovdenes J, Nilsson F et al. Outcome, timing and
adverse effects in therapeutic hypothermia after out-of-hospital
cardiac arrest. Acta Anaesthesiol Scand 2009; 53 : 926-34.
Neumar RW, Nolan JP, Adrie C et al. Post cardiac arrest
syndrome: Epidemiology, pathophysiology, treatment, and
prognostication – A consensus statement from the International
Liaison Committee on Resuscitation. Circulation 2008; 118: 245283.
Polderman KH. Mechanisms of action, physiological effects, and
complications of hypothermia. Crit Care Med 2009; 37
(7)(Suppl): S186-202.
Rittenberger JC. Post-arrest care: Coronary catheterization,
neuro monitoring. Presentation, October 30 2009.
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