Post Resuscitation Care (PRC) refers to life support

given to Patients from Return of Spontaneous

Circulation(ROSC) after Cardiac Arrest (CA) until
they achieve a reasonable stable clinical state.

This is clearly the most difficult and prolonged part of

the resuscitation taken as a whole.
Statistics show :

 < 20% of pre hospital arrest pts are resuscitated

successfully
 Of those only < 10% resume pre arrest level of
activity.

Neurologic injury is the earliest to occur and most

difficult to treat -- Hence P R C centres around
cerebral resuscitation.
Physiology (to recollect)
 Normal CBF is about 50 mls/100gm/min

700mls/min in a 70kg individual

 At least 20% of CBF is required to maintain neuronal

viability.

 When there is no Flow for :

15 secs - Loss of consciousness
1 min - Cessation of brainstem functions
4-5 mins - glucose &ATP stores depleted
anaerobic metabolism starts
5-6 mins - irreversible damage
The key to Improve Neurological outcome in
patients who have suffered Cardiac arrest is
achieving early Return of Spontaneous
Circulation.
 Pre-arrest Conditions
 Pre-arrest Hyperglycemia has negative effects
on Neurologic outcome.

 Pre-arrest Hypoxia may result in a worse

outcome after ischemia.

 Pre-arrest Hypothermia is protective during

ischemia.
 Arrest Time
 CBF achieved with CPR is inversely
proportional to arrest time.

 When CPR started after

2 mins - CBF 50% of normal
5 mins - CBF 28% of normal
10 mins - CBF 0 %
 Hypoxic cerebral injury
 Myocardial injury
 Subsequent multi organ failure

are the predominant causes of

morbidity and mortality after cardiac arrest.
 Aims of Post resuscitation care
Should be to :
 Continue respiratory support

 Maintain adequate cerebral perfusion.

 Treat & prevent cardiac arrhythmias

 Determine & treat the cause of Cardiac Arrest.

ARC guidelines-July 2003

 IN ADDITION
Treatable causes need to be addressed

 Hypoxemia  Tamponade
(pericardial)
 Hypovolemia
 Tension pneumo thorax
 Hypo/Hyperthermia
 Toxins/poisons/drugs
 Hypo/Hyperkalemia
 Thrombosis (PE,MI)
 Metabolic derangements
Neurologic damage is caused by both Ischemic event
and Reperfusion that follows later on …
 Increased free radicals.

 Increased excitatory neuro transmitters.

( glutamate,aspartate)
 Loss of Potassium into Extra cellular space.

 Increased Intracellular calcium .

 Release of cytotoxins.
Problem we face after ROSC

POST – RESUCITATION
CEREBRAL SYNDROME
 Post-resuscitation cerebral syndrome

 Occurs after 10 – 20 mins of absence of

spontaneous cerebral blood flow in
normothermic conditions.

 Consists of 4 main components…

 Failure of cerebral perfusion – with less oxygen
supply to brain
 Cerebral reoxygenation – causing damage through

cascade of chemical events

 Extra cerebral abnormalities :
Hyperthermia / Renal &Hepatic failure
Hypoxemia / Acid base disturbances
Hypercapnia

 Blood abnormalities secondary to stasis:

- aggregates of WBC/macrophages release free radicals
- micro infarctions.
 Post Resuscitation Therapy

Obviously involves Multisystem interventions

 Cardiovascular
 Pulmonary
 Water & electrolytes
 Haematological
 Metabolic
 Therapeutic Hypothermia
 Cardiovascular measures
 Maintaining systemic perfusion pressure with vaso active
drugs + Fluid resuscitation

 Transient induced Hypertension (1-5 mins) with MAP

>130mm Hg after ROSC helps.(Hypertensive flush)

 Head end of bed elevated to 30 deg facilitates cerebral

venous drainage / decreases ICP

 Adequate Haemodynamic monitoring to guide

cardiovascular Mx.
 Pulmonary Measures
 Can range from Oxygen thru Face mask to Mechanical
Ventilation.

 2-12 hrs after ROSC is the highest Oxygen extraction period.

 In cases of coma following CA Mechanical ventilation is

recommended for atleast 12 hrs.

 Hyperventilation in Post resuscitation pts should be avoided

unless signs of cerebral herniation present.

 PEEP should be avoided as it decreases Venous return to

heart.
 Water and Electrolytes
 Blood volume , Diuresis, Electrolytes should be evaluated
frequently to keep
- serum osmolality around 280 – 330m.osm/L
- normal electrolyte levels

 Fluids & Blood to be replaced where appropriate

 Dextrose infusions are best avoided

- increased lactic acid production
- worsens cerebral edema & damage
 Haematological

 Aim is to keep hematocrit between 30 – 35%

 But there is evidence to prove Normovolemic

hemodilution (20-25% hematocrit) improves
cerebral perfusion.

 Low dose thrombolytics to prevent

microvascular fibrinolytic clotting.
 Metabolic measures
 Hypo/Hyperglycemia should be corrected.

 Avoid Hyperthermia (which is common after

ROSC).

 Convulsions should be controlled & prevented

with anticonvulsants.
 Pharmacologic Measures
 Calcium channel blockers(nimodipine,lidoflazine)
Barbiturates
Corticosteroids
Free radical scavengers……
are all being studied.

 Results so far has shown no concrete benefits

that justify their use
 Therapeutic Hypothermia
 Induced Hypothermia has been used
successfully in cardiac surgeries to protect
against Global cerebral ischemia.

 Recent several animal & human studies have

demonstrated the potential for therapeutic
Hypothermia to improve survival & outcome
in victims of Cardiac arrest.
 Two multicentre randomised controlled trials
comparing Mild hypothermia &Normothermia in
Comatose survivors of Out of hospital survivors
(published-2002)

 1st study - 9 centres in 5 European countries.

(136 + 137 pts)

 2nd study - 4 centres in Melbourne,Australia.

(43 + 34 pts)

ref: circulation;July 2003

Criteria for pt selection in both studies were:

 Cardiac arrest due to presumed Cardiac origin

 Initial rhythm was VF

 Had ROSC but remained comatose

 Required intubation & ventilation

Results: European study

Hypothermic gp Normothermic gp
136 cases 137 cases

 Favourable
neurologic 55% 39%
Outcome

 Mortality
at 6 months 41% 55%
Results: Australian study

Hypothermic gp Normothermic gp
43 cases 34 cases

 Favourable
neurologic 49% 26%
Outcome

 Mortality
at 6 months 51% 68%
 International Liaison Committee On
Resucitation (ILCOR)
Recommendation – October 2002
 Unconscious adult patients with spontaneous

circulation after out of hospital cardiac arrest

should be cooled to 32 -34 deg celsius for 12 –
24 hrs when initial rhythm was VF.

 Such cooling may also be beneficial for other

rhythms or In hospital Cardiac arrest.
 Mechanism of action ( hypothermia):

 Reduces CMR02 by 6% for every

1 deg celsius reduction in brain
temperature.

 Thought to suppress chemical cascades

associated with reperfusion injury.
 But… Hypothermia may cause….
 Arrythmias

 Infection (pneumonia)

 Coagulopathy

when core temperature is < 32 deg celsius.

 Timing of cooling
 Initiated ASAP after ROSC but appears to be
successful even if delayed by 4 – 6 hrs.

 Further research is needed to determine :

* opitmal duration of hypothermia
* optimum target temperature
* rates of cooling and warming
 Cooling techniques
 External : Cooling blankets
Icepacks to groin/axillae/neck
Wet towels & fanning
Cooling helmet ( frigicap)

 Internal : Cold Crystalloid infusion

Peritoneal/bladder/pleural lavage
 Extra-corporeal cooling -- too invasive.

 Intra vascular heat exchange device has

become available recently.
 Not scientifically proven…but…
 Mannitol : increases CBF, free radical
scavenger… But optimal dose have not been
determined.
 Etomidate : depresses cerebral metabolism
without cardiotoxicity…but no human studies
exist confirming its usefullness.
 Corticosteroids : stabilize vascular memb,
prevent neuronal swelling, improve
intracranial compliance.
 Potential future therapies….
Suggested by current literature….
 Combinations of antioxidants,Calcium channel

blockers,sedatives.
 N-Methyl-D-aspartate scavengers.

 Lazaroids – 21-aminosteroid superoxide & lipid

hydroperoxide scavengers.
 ? ATP substitutes

 ?Immunotherapy

 ?Leukopheresis detoxification