Transcript Slide 1

HYPOTHERMIA
POST CARDIAC ARREST
2011
M. Nelson January 2011
OBJECTIVES
1. History
2. Pathophysiology
3. Changes & Side Effects During
Hypothermia
4. Indications/Exclusions
5. Overview of the UOHI Protocol
HISTORY
The concept of induced hypothermia in medicine
has ebbed and flowed through the years. Benson
et al (1959) studied hypothermia post cardiac
arrest in humans and showed decreased
mortality. Lack of sufficient evidence kept
hypothermia from general acceptance.
Using mild hypothermia post cardiac arrest to
preserve neurological function came to the
forefront with the publishing of two landmark
trials in the NEJM in 2002.
HISTORY
Both studies cooled out of hospital survivors of
ventricular fibrillation and ventricular tachycardia
arrests to 32°C-34°C for 12-24 hours. They
showed decreased mortality and improved
neurological function.
After these studies were published, ILCOR and
AHA recommended the use of therapeutic
hypothermia post cardiac arrest. The beneficial
results of these studies have subsequently been
supported by other studies.
HISTORY
Despite this evidence, the use of hypothermia is
limited at best even though survival of out of
hospital cardiac arrest is very poor. Less than ½
of the victims who develop ROSC and survive to
hospital leave the hospital alive and, in most
cases, the cause of death is anoxic brain injury.
CARDIAC ARREST – WHAT
HAPPENS?
CARDIAC ARREST
Depletes ATP in
4 min. failure
of Na/K and Ca
pumpscellular
depolarization &
injury
Lipolysis free fatty
acidsfree oxygen
radicalsApoptosis
ROSC
ISCHEMIA
Activates
inflammatory
cascade –
inflammatory
cytokines likely
contribute to
cerebral edema
CEREBRAL BLOOD FLOW
ALTERATION
1. first 5-30 minHyperemia
2. then cerebral
hypoperfusion (about 50%
of normal) for up to 12 hrs
Cerebral microvascular occlusions
from thrombi formed during arrest
Impaired cerebral reflow

CARDIAC ARREST – WHAT
HAPPENS?
Brain injury occurs at 2 time points:
1. Ischemia which activates multiple
inflammatory and proapoptotic pathways
&
2. Reperfusion which increases neuronal injury
by alterations in blood flow autoregulation,
production of reactive oxygen species and
more excitotoxic injury
CARDIAC ARREST – WHAT
HAPPENS?
Reperfusion Injury
MANIFESTATIONS OF
BRAIN INJURY
•Coma
•Seizures
•Myoclonus
•Cognitive dysfunction
•Persistent vegetative state
•Secondary Parkinsonism
•Cortical or spinal stroke
•Brain death
HYPOTHERMIA –
HOW DOES IT WORK?
The many processes that cause brain injury are
temperature dependant – fever stimulates the
destructive pathways and mild to moderate
hypothermia can block or mitigate these
processes.
PROTECTIVE EFFECTS OF MILD TO
MODERATE HYPOTHERMIA.
HYPOTHERMIA –
THE PROCEDURE
The process of hypothermia involves cooling a
patient to a prescribed temperature (32-34°C), for
a period of time (12-24 hours) and then allowing
the patient to rewarm or decool gradually.
The goal temperature, how quickly to cool, how
to cool, how long to stay at target temperature,
how slow to rewarm, these remain moving targets
as further research becomes available.
HYPOTHERMIA –
THE PROCEDURE
The 2005 American Heart Association guidelines
regarding the use of hypothermia post cardiac
arrest are summarized as follows:
•Unconscious patients with ROSC after out-ofhospital cardiac arrest should be cooled to 3234°C from 12-24 hrs when the initial rhythm was
VF (class lla)
•May be beneficial for patients with non VF arrest
or in-hospital arrest (class llb)
•Hemodynamically stable patients post ROSC with
spontaneous mild hypothermia should not be
actively rewarmed
HYPOTHERMIA –
THE PROCEDURE
•Cardiac arrests from VF or VT have the most
favorable results with hypothermia. Asystole
and PEA are much less positive.
•Most of the literature suggests cooling to a
temperature of 33°C and to remain at that
temperature for 24 hours.
•Many animal studies have shown that starting
cooling as soon as possible and attempting to
reach target temperature quickly is the most
effective procedure.
HYPOTHERMIA –
THE PROCEDURE
However, many centres have had positive results
even when the initiation of cooling and
attainment of target temperature have been
delayed. This suggests that hypothermia should
be inclusive rather than exclusive and that other
factors, such as age, likely play a role.
THE OTTAWA EXPERIENCE
In 2008, the stats for Ottawa (pop.~ 900,000):
•400 VSA patients in field due to cardiac arrest
•61% had “cease resuscitation” order
•39% were transported to the ED
•18% continued resuscitation efforts in ED
•14% were admitted to hospital
•8% survived to discharge
Justin Maloney
HYPOTHERMIA –
CHANGES & SIDE EFFECTS
•Hypovolemia: from cold diuresis which can
result in hypotension
•Cardiovascular changes: BP, CVP, mixed
venous saturation;  HR, CO
•ECG changes: Bradycardia, PR & QT intervals,
wide QRS complex; arrhythmias when temp
30°C (a.fib at 30°C, VT/VF at 28°C)
•Electrolyte disorders: K, Mg, P, Ca (risk of
hyperkalemia in warming)
HYPOTHERMIA –
CHANGES & SIDE EFFECTS
•Hypocoagulation/risk of bleeding:
thrombocytopenia
•Shivering: warming, O2 consumption, metabolic
demands and intracranial pressure
•Risk of Infections: inflammatory response is
suppressed by cooling
•Hyperglycemia: Hypothermia suppresses insulin
release and causes insulin resistance
•Skin Problems: from vasoconstriction,
immobilization and immune suppression
HYPOTHERMIA –
CHANGES & SIDE EFFECTS
•Lab Changes: amylase, liver enzymes, lactate,
ketonic acid, and glycerol; WBC & platelets;
mild hematocrit; mild acidosis
•Prolonged Drug Clearance: Delays metabolism &
clearance of sedatives, NMBAs, anticonvulsants,
& analgesics
INDICATIONS
•Cardiac Arrest Patients with
less than 30 minutes down
time
Down time is defined as time of
cardiac arrest to initiation of ACLS
•Cardiac arrest patients who
are not responding
appropriately to verbal
commands
•Hemodynamically stable
•VT, VF; consider PEA &
Asystole
EXCLUSIONS
•Unwitnessed cardiac arrest with no CPR 15
minutes
•More than 30 minutes from arrest to ACLS
•Refractory shock despite treatment with IV fluids
and vasopressors
•Persistent or repeated episodes of cardiac
arrhythmias
•Refractory hypoxia (O2 sat less than 85% for
more than 15 min despite adequate ventilation)
•Severe coagulopathy with evidence of bleeding
METHODS OF COOLING
Ice Packs
Cooled IV fluids (4°C)
Trans Nasal Evaporative Cooling
Commercial Surface Cooling
Cooling
Intravascular
Cooling
UOHI PROTOCOL
1.
2.
3.
4.
Patient Selection
STEMI versus non STEMI
Blood Work
Baseline assessment including VS, Neuro,
Skin, RASS, TOF
5. Insert nasopharyngeal temperature probe,
oral gastric tube & foley catheter
6. Central Venous Access & arterial line
7. Ensure second temperature source: foley, PA
line, tympanic
UOHI PROTOCOL
8. Set target temperature to 33°C
9. IV Sufentanil & IV Propofol
10. Neuromuscular blockade with IV Cisatacurium
to maintain TOF at 2:4 and to suppress
shivering
Maintain target temperature at 33°C for 24 hours
1. Temperature, VS, NVS (pupils), TOF q1h –
maintain MAP of ≥ 65
2. Bedside Shivering Assessment Scale
UOHI PROTOCOL
3.
4.
5.
6.
Monitor for frostbite q2h & prn
Counterwarming as needed
Routine blood work: ABGs, K, Mg, glucose
IV/SC Heparin, IV Insulin, Artificial tears eye
ointment
After 24 hours at target temperature, begin
rewarming or “decooling”
1. Use Arctic Sun to warm 0.25°C per hour
2. Discontinue NMBA at start of warming
UOHI PROTOCOL
3. Maintain temperature  37°C for 48 hours after
rewarming has begun
4. Continue sedation & analgesia till temperature
is 36°C and TOF is 4:4
5. When TOF is 4:4, wean analgesia
6. Wean sedation last
CHANGES & SIDE EFFECTS
SHIVERING
•Happens on induction at T of 35.5 and generally
stops when temperature is  than 33.5
•Older people tend to shiver less
Counterwarming: can help to lower the
shivering threshold by countering the feedback
loop from the skin temperature to the
hypothalmic thermoregulation centre;
focal or body
CHANGES & SIDE EFFECTS
SHIVERING
To Block Or Not To Block: We have routinely used
NMBA; problem has been that the TOF becomes
unreliable so more difficult to titrate; Sedation
and analgesia are needed even without NMBA
Pros
- very effective, does not cause hypotension
Cons
- Brain continues to try to make body shiver, may
mask seizures, prolonged paralysis  risk of
polyneuropathy
CHANGES & SIDE EFFECTS
SHIVERING
Bedside Shivering Assessment Scale
0: None – no shivering
1: Mild – localized to neck/thorax, may only
be seen on ECG
2: Moderate – intermittent involvement of
upper extremities +/- thorax
3: Severe – generalized shivering or sustained
upper extremity shivering
Maintain Normal Magnesium Level
CHANGES & SIDE EFFECTS
CARDIOVASCULAR
Hypotension
We have not seen cold diuresis, hypotension has
generally been due to cardiogenic shock prior to
induction and vasodilation on rewarming
Ensure adequate fluid volume prior to rewarming
Arrhythmias
Bradycardia, bradycardia and more bradycardia
Usually we have not needed to treat; if have BP
or MAP, or urine output, will treat with IV
Dopamine
If want PA line & hemodynamics need to use iced
injectate.
CHANGES & SIDE EFFECTS
ELECTROLYTE DISORDERS & HYPERGLYCEMIA
• Potassium & phosphate shift intracellularly
during cooling and extracellularly during
warming
• Magnesium for shivering
• IV Insulin continuous infusion is used frequently
for glucose
HYPOCOAGULATION/BLEEDING
• This has not been an issue for us even with the
STEMI patients on Plavix and possibly IV
Heparin
CHANGES & SIDE EFFECTS
INFECTION
•About 50% of our patients have developed
pneumonia due to ?aspiration, VAP
•Use rotation mode of the Total Care Bed, HOB at
least 30 degrees, chlorhexidine mouthwash
•We do not use prophylactic antibiotics
SKIN PROBLEMS
•Pads are easy to get on & off to check
•Positioning/rotation
CHANGES & SIDE EFFECTS
PROLONGED DRUG CLEARANCE
May also have renal or hepatic dysfunction from
prolonged cardiac arrest affecting metabolism &
elimination for ? Amount of time
•Use minimal doses for desired effect
•Choice of drugs – which is best?
SEIZURES
Some form of continuous
EEG monitoring is
suggested especially if
NMBA are used.
The other option is
Bispectral Index
Monitoring.
QUESTIONS?
Bernard, S. (2009). Hypothermia after cardiac arrest. Critical Care
Medecine 37(7Suppl.), S227-S233.
FAVORITE
ARTICLES
Chamorro, C.,et al. (2010). Anesthesia and analgesia protocol during
therapeutic hypothermia after cardiac arrest: A systemic Review.
Anesthesia and Analgesia 110(5), 1328-1335.
Geocadin, R.G., et al. (2008). Management of brain injury after
resuscitation from cardiac arrest. Neurologic Clinics 26, 487-506.
Hirsch, K.G., et al. (2009). Management of brain injury after cardiac
arrest. Continuum Lifelong Learning Neurology 15(3), 100-120.
ILCOR Consensus Statement (2008). Post-cardiac arrest syndrome.
Circulation 118, 2452-2483.
Polderman, K.H., et al. (2009). Therapeutic Hypothermia and controlled
normothermia in the intensive care unit: Practical considerations,
side effects, and cooling methods. Critical Care Medicine 37(3),
1101-1120
Polderman, K.H. (2009). Mechanism of action, physiological effects, and
complications of hypothermia. Critical Care Medicine 37(7 Suppl.),
S186-S202
Seder, D.B. (2009). Methods of cooling: Practical aspects of therapeutic
temperature management. Critical Care Medicine 37(7 Suppl.), S211S222