Transcript Post cardiac arrest syndrome and post ROSC care

Roshan Manasia
POST CARDIAC ARREST SYNDROME
AND
POST ROSC CARE
CLINICAL OUTCOMES POST CARDIAC ARREST
CLINICAL OUTCOMES POST ARREST
The first large multicentre report on patients treated for
cardiac arrest was published in 1953. The in-hospital
mortality rate for the 672 adults and children whose
‘‘heart beat was restarted’’ was 50%.
(Stephenson et al.,1953)
In Japan, one study reported that patients with ROSC
after witnessed out-of-hospital cardiac arrest of
presumed cardiac origin had an in-hospital mortality rate
of 90%
(Mashiko et
al, 2002)
CLINICAL OUTCOMES POST ARREST
In-hospital mortality rates for patients with out-ofhospital cardiac arrest who were taken to 4 different
hospitals in Norway averaged 63% (range 54–70%) for patients
with ROSC, 57% (range 56–70%) for patients arriving in the
emergency department (ED) with a pulse, and 50% (range 41–
62%) for patients admitted to the hospital.
(Langhelle et al., 2003) al., 2002).
In a comprehensive review of nontraumatic out-of-hospital
cardiac arrest in children, the overall rate of ROSC was 22.8%,
and the rate of survival to discharge was 6.7%, resulting in a
calculated post-ROSC mortality rate of 70%
(Donoghue et al., 2005).
CLINICAL OUTCOMES POST ARREST
In Sweden the 1-month mortality rate for 3853 patients
admitted with a pulse to 21 hospitals after out-ofhospital cardiac arrest ranged from 58% to 86%
(Herlitz et al., 2006).
The largest modern report of cardiac arrest
epidemiology was published by the National Registry of
CPR in 2006.
Among the 19,819 adults and 524 children who regained
any spontaneous circulation, in-hospital mortality rates
were 67% and 55%, respectively.
(Nadkarni et al., 2006).
CLINICAL OUTCOMES POST ROSC
The largest published in-hospital cardiac arrest database
(NRCPR) includes data from >36,000 cardiac arrests
Recalculation of the results of this report reveals that the
in-hospital mortality rate was 67% for the 19,819 adults
with any documented ROSC, 62% for the 17,183 adults
with ROSC > 20 min, 55% for the 524 children with any
documented ROSC, and 49% for the 460 children with
ROSC > 20 min
(Nadkarni et al., 2006).
24,132 patients in the United Kingdom who were
admitted to critical care units after cardiac arrest, the inhospital mortality rate was 71%
(Nolan et al., 2007).
CLINICAL OUTCOMES POST ROSC
Data from the Canadian Critical Care Research Network
indicates a 65% in-hospital mortality rate for 1483
patients admitted to the intensive care unit (ICU) after
out-of-hospital arrest.
(Keenan et al., 2007)
In the United Kingdom, 71.4% of 8987 patients admitted
to the ICU after out-of-hospital cardiac arrest died before
being discharged from the hospital.
(Nolan et al., 2007).
RETURN OF SPONTANEOUS CIRCULATION
(ROSC)
ROSC is defined as a brief (approximately >30 s)
return of pulse or spontaneous circulation
sustained for >20 min
PHASES OF ROSC
POST CARDIAC ARREST SYNDROME
Post-cardiac arrest syndrome is a unique and
complex combination of pathophysiological processes
including
 Post-cardiac arrest brain injury
 Post-cardiac arrest myocardial dysfunction
 Systemic ischaemia/reperfusion response.
 Persistent precipitating pathology
If ROSC is rapidly achieved after onset of cardiac arrest,
the post-cardiac arrest syndrome will not occur.
BRAIN AUTOREGULATION
POST CARDIAC ARREST BRAIN INJURY
POST CARDIAC ARREST BRAIN INJURY
 The unique vulnerability of the brain is attributed to its
limited tolerance of ischaemia as well as its unique
response to reperfusion.
 The mechanisms of brain injury triggered by cardiac
arrest and resuscitation are complex and include
excitotoxicity, disrupted calcium homeostasis, free
radical formation, pathological protease cascades, and
activation of cell death signaling pathways.
 Both neuronal necrosis and apoptosis have been
reported after cardiac arrest. Prolonged cardiac arrest
can also be followed by fixed and/or dynamic failure of
cerebral microcirculatory reperfusion despite adequate
cerebral perfusion pressure (CPP).This impaired reflow
can cause persistent ischaemia and small infarctions in
some brain regions.
POST CARDIAC ARREST BRAIN INJURY
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Although resumption of oxygen and metabolic substrate
delivery at the microcirculatory level is essential, a growing body of
evidence suggests that too much oxygen during the initial stages of
reperfusion can exacerbate neuronal injury through production of
free radicals, nitric oxide, catecholamines, cytokines, and calcium
shifts, which all lead to mitochondrial damage and cell death. This
process may last as long as 24 to 48 hours.
Despite cerebral microcirculatory failure, macroscopic
reperfusion is often hyperaemic in the first few minutes after
cardiac arrest because of elevated CPP and impaired
cerebrovascular autoregulation These high initial perfusion
pressures can theoretically minimize impaired reflow. Yet
hyperaemic reperfusion can potentially exacerbate brain edema
and reperfusion injury.

The first 24—48 h after resuscitation from cardiac arrest, there is
increased cerebral vascular resistance, decreased CBF, decreased
cerebral metabolic rate of oxygen consumption (CMRO2), and
decreased glucose consumption
POST CARDIAC ARREST BRAIN INJURY
 Beyond the initial reperfusion phase, several
factors can potentially compromise cerebral oxygen
delivery and possibly secondary injury in the hours to
days after cardiac arrest. These include hypotension,
hypoxaemia, impaired cerebrovascular autoregulation, brain
oedema, pyrexia, hypergycemia, seizures
 There is limited evidence that brain oedema or elevated
intracranial pressure (ICP) directly exacerbates post-cardiac
arrest brain injury. Although transient brain oedema is observed
early after ROSC, most commonly after asphyxial cardiac
arrest, it is rarely associated with clinically relevant increases in
ICP. In contrast, delayed brain oedema, occurring days to weeks
after cardiac arrest, has been attributed to delayed hyperaemia;
this is more likely the consequence rather than the cause of
severe ischaemic neuro degeneration
POST CARDIAC ARREST BRAIN INJURY
 Hyperglycaemia is common in post-cardiac arrest patients
and is associated with poor neurological outcome. elevated
post ischaemic blood glucose concentrations exacerbate
ischaemic brain injury.
 Seizures in the post-cardiac arrest period are associated with
worse prognosis and are likely to be caused by, as well as
exacerbate, post-cardiac arrest brain injury.
 In a small case series, patients with temperatures >39 ◦C in the
first 72 h after out-of-hospital cardiac arrest had a significantly
increased risk of brain death.
 the risk of unfavorable outcome is increased for every degree
Celsius that the peak temperature exceeded 37 ◦C. Maximal
recorded temperature >37.8 ◦C was associated with increased
in-hospital mortality
POST CARDIAC ARREST BRAIN INJURY
POST-CARDIAC ARREST MYOCARDIAL
DYSFUNCTION
SYSTEMIC ISCHAEMIC-REPERFUSION
SYSTEMIC ISCHAEMIC-REPERFUSION
 Cardiac arrest represents the most severe shock state, during
which delivery of oxygen and metabolic substrates is abruptly
halted and metabolites are no longer removed.
 Inadequate tissue oxygen delivery can persist even after ROSC
because of myocardial dysfunction, pressor dependent
haemodynamic instability, and microcirculatory failure.
 oxygen debt leads to endothelial activation and systemic
inflammation106 and is predictive of subsequent multiple organ
failure and death.
 As early as 3 h after cardiac arrest, blood concentrations of
various cytokines, soluble receptors, and endotoxin increase, and
the magnitude of these changes are associated with out come.
SYSTEMIC ISCHAEMIC-REPERFUSION
 Activation of blood coagulation without adequate activation
of endogenous fibrinolysis is an important pathophysiological
mechanism that may contribute to microcirculatory
reperfusion disorders.
 Anticoagulant factors such as antithrombin, protein S, and
protein C are decreased and are associated with a very
transient increase in endogenous activated protein C soon
after the cardiac arrest—resuscitation event
 The stress of total body ischaemia/reperfusion causes adrenal
insufficiency
PERSISTENT PRECIPITATING PATHOLOGY
 Diagnosis and management of persistent precipitating
pathologies such as acute coronary syndrome (ACS),
pulmonary diseases, haemorrhage, sepsis, and various
toxidromes can complicate and be complicated by the
simultaneous pathophysiology of the post-cardiac arrest
syndrome.
POST ROSC CARE
 Post ROSC protocol
 Post arrest therapeutic hypothermia
COOL BODY SAVES BRAIN
Beneficial Effects
of Hypothermia
 Decrease in cerebral metabolism
 Hypothermia reduces the cerebral metabolic rate for oxygen (CMRO2) by 6% -
7% for every 1°C reduction in brain temperature >28°C so as oxygen
consumption.
 Maintains integrity of membranes and ion homeostasis. Hypothermia helps to
stabilize the influx of calcium and glutamate by slowing the neuroexcitatory
processes, thereby reducing the disruptions in the blood–brain barrier and
preventing premature cell death.
 Hypothermia is also thought to decrease many of the chemical reactions that
occur during reperfusion, such as free radical production.
 Preserves Mild hypothermia is thought to suppress many of the chemical
reactions associated with reperfusion injury.
 Temperatures less than 35°C lead to decreased neutrophil and macrophage
functions. This reduces the inflammatory response that is initiated after
ischemia
Treatment of Comatose
Survivors of Out-of-Hospital
Cardiac Arrest with Induced
Hypothermia
 Bernard SA, et al.
 2002 –
 Melbourne, Australia
N Engl J Med 2002;346:557-63.
Aussie Arrest – Continued…
 Multicenter rCT 77 Pts who remained unconscious
s/p out of hospital cardiac arrest (V-fib @ scene).
 Randomized (by day) to hypothermia group (33 oC 2
hrs after return of spont circulation, maintained for
12 hours) or normothermia.
 Outcome: survival to hospital discharge with
sufficiently good neurologic function to be
discharged to home or to a rehabilitation facility.
Aussie Arrest – Continued…
 Survival to home/rehab was
Mortality did not
reach statistical sig
51% v. 68% (p=0.145)
49% in the hypothermia
group v. 26% in normothermia
group (p=0.046).
 Odds ratio (adjusted for age &
arrest time) was 5.25.
50%
45%
40%
35%
30%
25% 49%
20%
15%
10%
5%
0%
Hypo
70%
60%
50%
40%
30%
26%
20%
68%
51%
10%
Normo
0%
Hypo
Normo
Mild Therapeutic Hypothermia
to Improve the Neurologic
Outcome after Cardiac Arrest
 Michael Holzer, The Hypothermia after Cardiac
Arrest Study Group
 2002 –
 Vienna, Austria
N Engl J Med 2002;346:549-56.
Euro Arrest – Continued…
 Multictr RCT, Blinded assessment outcome.
 275 Pts s/p witnessed V-fib arrest randomized
to hypothermia (32-34 oC) x 24 hrs v.
normothermia (37-38 oC).
 Primary endpoint: favorable neuro outcome*
w/in 6 mo; secondary: 6 mo mortality & 7 day
complication rate.
* Pittsburgh cerebral-performance category, 1 [good recovery] or 2 [moderate disability]
Euro Arrest – Continued…
Favorable neuro outcome was
55% in the hypothermia
group v. 39% in the
normothermia group.
Six month mortality was 41%
in the hypo group v. 55% in
the normo group
60%
60%
50%
50%
40%
40%
30% 55%
30%
20%
39%
20% 41%
10%
10%
0%
0%
Hypo
Normo
55%
Hypo
Normo
Inclusion Criteria
 Adult patients (over age of 18years) whose initial cardiac
arrest rhythm was Ventricular Fibrillation (VF) or Pulseless
Ventricular Tachycardia (VT). Patients who had Pulseless
Electrical Activity (PEA) and Asystolic arrest may also benefit
from the therapeutic hypothermia and should be considered
for the therapy.
 ROSC following CPR within 60 minutes of collapse.
 Persistent coma following ROSC. It is defined as inability to
follow commands which is not attributed to pre-cardiac
arrest medical condition or GCS of < 8.
Exclusion Criteria
 Refractory shock that is mean arterial pressure (MAP) less than 60 mm
Hg for greater than 30 minutes requiring more than one vasopressor.
 Patients with terminal illness or multi-organ dysfunction.
 Persistent life threatening arrhythmias post ROSC
 Pregnancy
 Patients with no flow time more than 60 minutes
 Time laps of more than 12 hours from ROSC to hypothermia
 Primary coagulopathy or uncontrolled bleeding.
 Patients with DNR.
 Patient with traumatic brain injury
Note: Patients who have received thrombolytic agents or who are on
antiplatelet/anticoagulant therapy necessary to treat a primary cardiac
condition, is not a contraindication to cooling
General guidelines
 The patient must be on mechanical ventilation and on
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continuous cardiac monitoring.
Cooling should be initiated as soon as possible, preferably within
6 hours of ROSC.
Patient should be cooled as soon as possible to achieve the
target temperature of 32C – 34C ( 33C) within 4 hours of
initiation of initiating cooling measures.
Target temperature should be maintained for 24 hours, with time
beginning once patient reaches the goal temperature.
To optimize the positive outcomes of the hypothermia take
measures to maintain MAP 65-100mmHg; urine output > 0.5
ml/kg/hr; CVP 8-12 mmHg; O2 saturation 94%-96%; control
hyperglycemia following target blood sugar less than
150mmHg.
Pre induction phase
 Consent
 Continuous temperature monitoring (rectal, bladder, esophageal
or pulmonary artery catheter (PAC). .
 Obtain base line lab for blood sugar, serum electrolyte, arterial
blood gas, coagulation profile (PT,APTT.INR), CBC with
differentials, serum lactate and Beta-HCG
 12 Lead ECG,QT interval and assess for arrhythmias
 Assess baseline neurological status, vital signs and CVP reading.
 CVP and arterial line insertion. .
Note: Arterial line access may be more difficult to obtain due to
vasoconstriction, once the target temperature is reached.
 ETCO2 monitoring may be used to monitor variation in PCO2
during the treatment.
Induction phase
 Administer 500 mL of chilled (cooled at approximately 4C)
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Normal Saline or Ringers Lactate through peripheral intravenous
line every 10 minutes until rectal temperature reaches 34C or till
a total of 30 mL/kg of cold fluid is given.
Avoid using internal jugular or subclavian CVP lines to infuse cold
infusion to prevent cardioplegia.
Apply ice packs to the neck, torso, armpits, flanks and groin.
Initiate surface cooling device (K-thermia) with the goal
temperature set on the machine to prevent over cooling.
Monitor patient’s temperature, blood pressure, heart rate and O2
saturations and document every 15 minutes.
Monitor for adverse effects of hypothermia
 Assess patient for shivering every hour using following Bed Side
Shivering Assessment Scale (BSAS). Notify physician if score is more
than 0.
 Patient should be administered opioids analgesia (fentanyl, morphine
sulphate, pethedine) and hypnotics (propofol) or benzodiazepine
(midazolam) to prevent shivering.
 If shivering occurs despite optimal sedation, neuromuscular blocking
agent (atracurium, pancuronium, vecuronium) as a bolus or infusion
should be considered
SCORE
0
None
DEFINITION
No shivering noted on palpation of the masseter, neck or chest
wall.
1
Shivering localized to neck and/or thorax only. May only be
Mild
noticed on palpation.
2
Shivering involves gross muscle movement of upper
Moderate extremities in addition to neck and thorax .
3
Shivering involves gross movement of the trunk and upper and
Severe
lower extremities
Maintenance phase
 Once the target temperature 32C – 34C (33 C) is achieved,
continue with surface cooling measure (K-thermia) to maintain
target temperature for 24 hours.
 If the temperature rises above 34C during this phase, ice packs

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
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


may be reapplied to bring temperature to the required range.
K-thermia must be stopped if the temperature falls below
recommended range.
Continuously monitor patient’s temperature, blood pressure,
heart rate, and O2 sats and document at least every 30 minutes.
Monitor CVP and urine output every hour as per ICU protocol.
Shivering monitoring every hourly and PRN
Skin integrity every 2 hourly.
Probe placement every 2 hourly.
Monitor for adverse effects of hypothermia.
Reflo
Monitor blood glucose at least every 2 hourly as per
patient’s baseline or ICU protocol. If hyperglycemia
develops, monitor blood glucose every hou
PT/APTT/INR/Platelet
Every 12 hourly
CBC
Every day
Amylase and Lipase
Once per day
Electrolytes
Check electrolyte every 6 hour
QTc interval
Every 4 hourly
Rewarming phase
 Begins upon completion of 24 hours of maintenance phase.
 Allow patient to rewarm passively to a temperature of 36C, it

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should not be faster than 0.25 - 0.5 C per hour.
Monitor patient’s temperature, blood pressure, heart rate, and O2
sats and document every 30 minutes.
Use of K-thermia or bair hugger should only be reserved if
temperature does not rise in initial 6 hours of rewarming phase. Kthermia/Bair Hugger and all other measures must be stopped once
patient’s temperature reaches 36C.
Monitor for adverse effects that is hypotension, cerebral edema,
ICP, arrhythmias, and shift of electrolytes back into the
plasma
Efforts must be made to prevent pyrexia (38C) during initial 72
hours from the time of cardiac arrest.
Discontinuation of
hypothermia
 Hemodynamically unstable arrhythmia that is
refractory to the treatment.
 Severe bradycardia with hemodynamic
compromise (less than 40 beats per minute).
 Severe bleeding
 If hypothermia is aborted rewarming should not
be faster than 0.25 - 0.5 C per hour.

ADVERSE EFFECTS OF THERAPEUTIC
HYPOTHERMIA
Shivering
 It increases metabolic rate and oxygen consumption and makes
it difficult to achieve target temperature . Shivering is less likely
to occur during the maintenance and warming phases.
 Signs and symptoms of shivering include a drop in mixed venous
oxygen saturation, increase in RR, facial tensing, artifacts on ECG
and palpation of muscle fasciculations on the face or chest.
 Bedside shivering assessment scale (Target is 0)
Management of Shivering
 Analgesia and sedation.
 Sedation and analgesic drugs, such as midazolam, fentanyl, and

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propofol, have a 30% to 50% decrease in systemic clearance
during hypothermia. Vecuronium and atracurium, clearance is
decreased 10% for every 1C below 37C. Thus, their duration of
action is also increased. During hypothermia, the amount of drug
required may be less than what is typically used. Patient may
take longer to wake up after drugs are hold. (Doses)
train of 4 should be done in case of continuous paralytics and
goal is 1 out 4 . (Add in the policy, order and monitoring sheet)
The paralytic and sedation medications should be stopped as
soon as possible after the completion of induced hypothermia
treatment unless indicated otherwise.
The paralytic may be stopped during the warming phase.
Magnesium sulphate
Bradycardia and vasoconstriction
 patient’s normal response to hypothermia is to increase the heart
rate and vasoconstriction to conserve heat. Use of sedation and
paralytic agents prevents this normal response to hypothermia.
 Bradycardia and increased systemic vascular resistance will be
seen in the absence of shivering with a continued decrease in
temperature.
 The patient may be pale and peripheral pulses may
be difficult to obtain because of the
vasoconstriction
Hypotension
Cooling phase
 Bradycardia is usually not hemodynamically significant and
usually refractory to atropine. It is not always necessary to
terminate treatment for patients who are bradycardic.
 Blood pressure is usually maintained without the use of
vasopressors secondary to the increased systemic vascular
resistance. If needed vasopressors may be used to maintain
mean arterial pressure > 65 mmHg.
Rewarming phase
 The greatest risk for hypotension is during the warming phase
secondary to vasodilation.
 kept well hydrated during cooling to help prevent hypotension
during warming when vasodilation occurs
ECG changes
 Dysrhythmias are rare in mild hypothermia.
 Tachyarrhythmias beginning by atrial fibrillation.
 Prolong PR, QRS and QT interval in case of temperature < 33 C.
QTc evaluation…notify if more than 0.5 sec to prevent torsades
de pointes.
 The patient is more at risk when the temperature drops below
32C. Temperatures below 30C may cause VF and may be
refractory to defibrillation.
 Osborne’s J waves.
 Osborne’s waves are camel-hump waves, or hypothermic
waves, are best seen in the inferior and lateral precordial
leads. A small extra wave is seen immediately after the QRS
complex. hey become more prominent as the body
temperature decreases, and they resolve gradually with
rewarming
Osborne’s J waves
Management related to ECG changes
 Prevent overcooling and electrolytes imbalance
 If treatment is aborted, rewarm slowly
Fluid and Electrolyte Imbalance
Cooling phase
 Cold diuresis occurs during hypothermia because there is a decrease in
the reabsorption of solute in the ascending limb of the loop of Henle.
Suppression of the antidiuretic hormone also exists.
 Electrolyte shifts from cold diuresis and from cellular acidosis that may
occur during hypothermia causing hypokalemia, hypomagnesemia,
hypophosphatemia, and hypocalcemia
Management
 Monitor urine output and replace fluid if needed.
 Monitor electrolytes
 Potassium replacement should be given during cooling, to
prevent dysrhythmias
 Replacement should be conservative and possibly discontinued
several hours before warming begins
fluid and electrolyte imbalance
Warming Phase
 Hyperkalemia during warming exists because the potassium
shifts back, out of the cells
 The patient is at particular risk for hyperkalemia if the
hypokalemia was over treated during the cooling phase.
Management
 Monitor urine output and replace fluid if needed.
 Monitor electrolytes
 The patient may still require replacement during the warming
phase if the potassium level is significantly low
Coagulopathy
 Occurs during hypothermia. Studies have shown that there is not
a significant risk of bleeding during hypothermia
 Platelet counts decrease, and there is an inhibition of enzyme
reactions of both the intrinsic and extrinsic pathways of the
clotting cascade.
Management
 Monitor PT, APTT/INR and Platelets.
 Platelets or fresh frozen plasma should be given only if a clinical
concern is present and not based on the laboratory test values
alone.
Increase risk of infection
 Hypothermia decreases the number of circulating white
blood cells.
Management
 Implement VAP bundle and other measures to prevent
infections.
 Beware that elevated temperatures related to infection
will be masked by hypothermia
Hyperglycemia
 It is caused by decreased release of insulin from the pancreas
and causes insulin resistance at the cellular level during cooling
phase.
Management
 Hyperglycemia should be controlled using insulin treatment
with frequent monitoring
 Glucose should be controlled at levels less than 150 mg/dL. Tight
glycemic control less than 110 mg/dL is not recommended and
carries risk of hypoglycemia.
Reduced Metabolism
 Decreased metabolic demand
 Decreased CO2 production
 Decreased oxygen consumption.
Management
 Frequent blood gases and adjustment of minute
ventilation.
Skin breakdown
 Peripheral vasoconstriction places the patient
at a particularly high risk for skin breakdown.
 Extra attention to skin assessment, skin care,
and frequent turning is necessary.
CPC scoring
Arrhythmias interpretation
References attached into TH
policy