Postresuscitation care

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Postresuscitation care

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• 40 of victims are initially resuscitated, but
  fewer than an average of 5 leave the hospital
  alive and neurologically intact.
• cardiopulmonary resuscitation (CPR) is only
  successful if it is instituted within 5 min after
  the heart stops beating.

Max Harry Weil and Shijie Sun Critical Care
2005, 9287-290doi 27 September 2004
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How long to resuscitate ?

• CPR can be continued for 30 minutes if the time
  to onset of CPR is less than 6 minutes, but if
  there is a delay to onset of CPR longer than 6
  minutes, CPR should be terminated after 15
  minutes.

Crit care med 1985 13930-931
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Stages of Postresuscitation syndrome

• Stage I 010 hr
• -- rapid change of cerebral and systemic
  hemodynamic
• -- metabolic derangement leading to
  catabolism(37day)
• Stage II 1024 hr
• -- Normalization of CV function, persistent brain
  dysfunction, impaired microcirculation
• Cause of death recurrent cardiac arrest,
  increased bleeding, brain and lung edema.

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Stages of Postresuscitation syndrome

• Stage III 13 days
• -- normalization of systemic indices (brain too)
• -- increased intestinal permeability leading to
  bacteremia and pulmonary, hepatic, pancreatic and
  renal insufficiency (MODS)
• Stage IV gt 3 days
• -- localized or generalized infection
• -- prolonged metabolic derangement in severe
  cases

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Objectives of postresuscitation care

• Optimize cardiopulmonary function and systemic
  perfusion, especially perfusion to the brain
• Transport the victim of out-of-hospital cardiac
  arrest to the hospital emergency department (ED)
  and continue care in an appropriately equipped
  critical care unit
• Try to identify the precipitating causes of the
  arrest
• Institute measures to prevent recurrence
• Institute measures that may improve long-term,
  neurologically intact survival

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Precipitating causes of the arrest ? 6H6T

• After resuscitation , evaluate ECG, CXR ,serum
  electrolytes and cardiac biomarkers.
• Echocardiographic evaluation within the first 24
  hours if needed.

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Resuscitation related injury

• Clinicians should identify complications, such as
  rib fracture, hemopneumothorax, pericardial
  tamponade, intra-abdominal trauma, and misplaced
  tracheal tube.

Circulation. 2000 102(suppl I)I-166I-171.
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Respiratory system

• ETT ventilator (Mode CMV AC)
• Sustained hypocapnea (low PCO2) may reduce
  cerebral blood flow
• Hyperventilation ? auto PEEP ? increase in
  cerebral venous and intracranial pressures.
  (CPPMAP-ICP)
• there is inadequate data to recommend for or
  against the use of a defined period of sedation
  or neuromuscular blockade after cardiac arrest
  (Class Indeterminate).

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Cardiovascular system

• Both the ischemia/reperfusion of cardiac arrest
  and electrical defibrillation can cause transient
  myocardial stunning and dysfunction that can last
  many hours but may improve with vasopressors.

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Cardiovascular system

• The severity of postresuscitation myocardial
  dysfunction is minimized by
• 1. early resuscitation
• 2. reducing the numbers and the energy
• levels of shocks delivered by
  defibrillator
• 3. use of biphasic rather than monophasic
• waveform shocks

Max Harry Weil and Shijie Sun Critical Care
2005, 9287-290doi 27 September 2004
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Cardiovascular system

• Titrate volume administration and vasoactive
  (eg, norepinephrine), inotropic(eg, dobutamine),
  and inodilator (eg, milrinone) drugs as needed to
  support blood pressure, cardiac index, and
  systemic perfusion.
• The ideal target blood pressure or hemodynamic
  parameters associated with optimal survival have
  not been established.
• prophylactic administration of antiarrhythmic
  drugs (Class Indeterminate).
• given the cardioprotective effects of B-blockers
  in the context of ischemic heart disease, if no
  contraindications.

Circulation 2005 112IV-84-IV-88
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Cardiovascular system

• Despite having no long-term survival benefit,
  intravenous amiodarone is now recommended for
  cases of V-fib and pulseless V-tach that are
  refractory to defibrillation and vasopressor
  drugs.
• Lidocaine is now recommended only as an
  alternative to amiodarone

ICU book (3rd edition) Paul L.Marino
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Central nervous system

• Autoregulation of cerebral blood flow is lost
  after extended hypoxemia or hypercarbia, or both,
  and cerebral blood flow becomes dependent on
  cerebral perfusion pressure. (CPPMAP-ICP) ?
  maintaining a normal or slightly elevated MAP and
  reducing ICP.
• Witnessed seizures should be promptly controlled
  and maintenance anticonvulsant therapy initiated
  (Class IIa).
• routine seizure prophylaxis (Class Indeterminate)

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Temperature regulation

• Hyperthermia and hyperglycemia compromise
  postresuscitation neurologic outcome, whereas
  mild to moderate induced hypothermia appears to
  improve neurologic outcome and decrease mortality

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Temperature regulation

• unconscious adult patients with ROSC after out-of
  hospital cardiac arrest should be cooled to 32C
  to 34C (89.6F to 93.2F) for 12 to 24 hours
  when the initial rhythm
• was VF (Class IIa).
• Similar therapy may be beneficial for patients
  with non-VF arrest out of hospital or for
  in-hospital arrest (Class IIb)

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Candidate of hypothermia therapy

• Patients with out-of-hospital cardiac arrest due
  to VF or pulseless VT who remain comatose after
  successful resuscitation.
• Inclusion criteria
• 1. cardiac arrest is cardiac origin
• 2. body temperature is not reduced.
• 3. patient is hemodynamically stable
• 4. patient is intubated and on a ventilator

ICU book (3rd edition) Paul L.Marino
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Cooling method

• 1. Cooling should begin within 12hr after CPR
• 2. Use cooling blanket to achieve a body
  temperature of 32C34C (More recent studies
  suggest that internal cooling(eg, cold saline,
  endovascular cooling catheter)
• 3. Use sedation and neuromuscular blockade
  (atracurium) to avoid shivering (can provoke
  vasospasm in diseased coronary arteries)
• 4. watch for hyperkalemia and hyperglycemia
  during hypothermia
• 5. maintain hypothermia for 24hr, and then allow
  passive rewarming

ICU book (3rd edition) Paul L.Marino
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• Temperature monitoring
• continuous core temperature monitor by
  Swan-Ganz catheter, foley temp. probe, rectal
  temp.probe
• General condition maintenance
• Mean arterial pressure between 80100mmHg

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Complications of cooling

• coagulopathy
• arrhythmias
• pneumonia and sepsis
• hyperglycemia
• Hyperkalemia
• frostbite

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Glucose control

• high blood glucose after resuscitation from
  cardiac arrest ?poor neurologic outcomes
• Control blood glucose ? decreased mortality from
  infectious

Circulation 2005 112IV-84-IV-88
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Renal system

• On Foley, assess I/O
• Differentiate prerenal from renal failure. (FENa,
  PAOP, cardiac output)
• Furosemide-maintain urine output despite renal
  failure
• Low dose dopamine (13 µg/kg per min) does not
  improve splanchnic blood flow or renal protection
  --gt no longer indicated in ARF.
• Avoid nephrotoxic drugs. Dose should be adjusted.
• Progressive renal failure --gt mortality are high
  --gt often require dialysis.

Circulation. 2000 102(suppl I)I-166I-171.
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GI system

• NG tube should be inserted.
• Start enteric feeding as soon as possible. If not
  tolerated, administer H2 blockers or sucralfate
  to reduce the risk of stress ulcer and GI
  bleeding.

Circulation. 2000 102(suppl I)I-166I-171.
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SIRS
Circulation. 2000 102(suppl I)I-166I-171.

• SIRS may occur after prolonged CPR.
• When infection is the cause --gtsepsis
• Initial management consists of volume
  replacement. Inotrope or vasopressin is usually
  required.--gt improved outcome has not been shown.
  (Dobutamine and norepinephrine)
• When sepsis is suspected, empirical antibiotic
  therapy is indicated.
• Glucocorticoid therapy-controversial , no
  evidence suggest that corticosteroid improve
  survival rates. Supraphysiological doses of
  corticosteroids may be beneficial for p'ts with
  persistent vasopressor-resistant shock maximally
  treated with broad-spectrum or organism-specific
  antibiotics. (class IIb)

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Prognostic factor

• Absent corneal reflex at 24 hours
• Absent pupillary response at 24 hours
• Absent withdrawal response to pain at 24 hours
• No motor response at 24 hours
• No motor response at 72 hours
• Bilateral absence of cortical response to median
  nerve SSEP measured 72 hours (in normothermic
  patient) after hypoxic ischemic (asphyxial) insult

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Thanks for your attention !