1. MANAGEMENT OF PATIENT FOLLOWING CARDIAC RESUSCITATION
Diagnosis and Implications of Brain Death
Dr. Manish chopra
University College of Medical Sciences & GTB Hospital, Delhi

2. Part 9: Post–Cardiac Arrest Care
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Mary Ann Peberdy, Clifton W. Callaway, Robert W. Neumar; Romergryko G. Geocadin; Janice L. Zimmerman; Michael Donnino; Andrea Gabrielli; Scott M. Silvers; Arno L. Zaritsky; Raina Merchant; Terry L. Vanden Hoek; Steven L. Kronick

3. Applying Classification of Recommendations and Level of Evidence
Class IIa
Class IIb
Class III
Benefit >>> Risk
Procedure/Treatment SHOULD be performed/ administered
Benefit >> Risk Additional studies with focused objectives needed
IT IS REASONABLE to perform procedure/ administer treatment
Benefit ≥ Risk Additional studies with broad objectives needed; Additional registry data would be helpful
IT IS NOT UNREASONABLE to perform procedure/ administer treatment
Risk ≥ Benefit No additional studies needed
Procedure/Treatment should NOT be performed/ administered SINCE IT IS NOT HELPFUL AND MAY BE HARMFUL
Level A
Multiple (3-5) population risk strata evaluated
Multiple RCT or metaanalysis
o Recommendation that procedure or treatment is useful/effective
o Sufficient evidence from multiple randomized trials or meta-analyses
o Recommendation in favor of treatment or procedure being useful/effective
o Some conflicting evidence from multiple randomized trials or meta-analyses
o Recommendation's usefulness/efficacy less well established
o Greater conflicting evidence from multiple randomized trials or meta-analyses
o Recommendation that procedure or treatment not useful/effective and may be harmful

4. Applying Classification of Recommendations and Level of Evidence
Class Iia
Class IIb
Class III
Level B
Limited (2-3) population risk strata evaluated
Single RCT or nonrandomized studies
o Recommendation that procedure or treatment is useful/effective
o Limited evidence from single randomized trial or non-randomized studies
o Recommendation in favor of treatment or procedure being useful/effective
o Some conflicting evidence from single randomized trial or non-randomized studies
o Recommendation's usefulness/efficacy less well established
o Greater conflicting evidence from single randomized trial or non-randomized studies
o Recommendation that procedure or treatment not useful/effective and may be harmful
Level C
Very limited (1-2) population risk strata evaluated
Only consensus opinion of experts case studies
o Only expert opinion, case studies, or standard-of-care
o Only diverging expert opinion, case studies, or standard-of-care

5. Introduction
Increasing recognition of return of spontaneous circulation (ROSC) - good quality of life post cardiac arrest
Randomized controlled clinical trials
Post–cardiac arrest syndrome*#
Post–cardiac arrest care has significant potential to reduce early mortality caused by hemodynamic instability and later morbidity and mortality from multiorgan failure and brain injury
*HACA. Hypothermia After Cardiac Arrest Study Group. Mild therapeutic
hypothermia to improve the neurologic outcome after cardiac
arrest. N Engl J Med. 2002;346:549 –556.
#Bernard SA, Gray TW, Buist MD, Jones BM, Silvester W, Gutteridge G,
Smith K. Treatment of comatose survivors of out-of-hospital cardiac
arrest with induced hypothermia. N Engl J Med. 2002;346:557–563.

6. (contd.)
Post–cardiac arrest care is a critical component of advanced life support
Most deaths occur during the first 24 hours after cardiac arrest
Multiple organ systems are affected after cardiac arrest

7. (contd.)
Significant cardiovascular dysfunction - requiring support of blood flow and ventilation- intravascular volume expansion, vasoactive and inotropic drugs, and invasive devices.
Therapeutic hypothermia, treatment of the underlying cause of cardiac arrest- improves survival and neurological outcomes
Protocolized hemodynamic optimization
Multidisciplinary early goal-directed therapy protocols - bundle of care
Proactive titration of post–cardiac arrest hemodynamics
Difficult to distinguish between any specific component of care that is most important.

8. What should be our approach
Comprehensive
Structured
Multidisciplinary system of care

10. Interventions Therapeutic hypothermia
Optimization of hemodynamics and gas exchange
Immediate coronary reperfusion- percutaneous coronary intervention (PCI)
Glycaemic control
Neurological diagnosis, management, and prognostication.

11. What I Will Talk About ??

12. Hemodynamic
Neurological
Metabolic

13. Initial objectives of post–cardiac arrest care

14. Optimize cardiopulmonary function and vital organ perfusion
Out-of-hospital cardiac arrest - appropriate hospital - comprehensive post–cardiac arrest treatment system of care
In-hospital post–cardiac arrest - appropriate critical-care unit capable of providing comprehensive post–cardiac arrest care
Try to identify and treat the precipitating causes of the arrest and prevent recurrent arrest

15. Subsequent objectives of post–cardiac arrest care

16. Control body temperature to optimize survival and neurological recovery
Identify and treat acute coronary syndromes (ACS)
Optimize mechanical ventilation to minimize lung injury
Reduce the risk of multiorgan injury and support organ function if required
Objectively assess prognosis for recovery
Assist survivors with rehabilitation services when required

17. Overview of Post–Cardiac Arrest Care
Avoid using ties that pass circumferentially around the patient's neck
Elevate the head of the bed 30°
Avoid 100% oxygen - titrate inspired oxygen SpO2 of >94%, oxygen toxicity
Avoid Hyperventilation or "overbagging" the patient
Ventilation_ 10 to 12 breaths per minute
Titrated to achieve a PETCO2 of 35 to 40 mm Hg or a PaCO2 of 40 to 45 mm

18. (Contd.)
Assess vital signs and monitor for recurrent cardiac arrhythmias
Intravenous / intraosseous access
Systolic blood pressure < 90 mm Hg- fluid boluses can be considered
Titrated vasoactive drug infusions - minimum SBP (90 mm Hg) or a MAP (65 mm Hg)
Therapeutic hypothermia
Coronary reperfusion (PCI)

19. Remember
Most common cause of cardiac arrest- cardiovascular disease and coronary ischemia - 12-lead ECG to detect ST elevation or new left bundle-branch block
High suspicion of acute myocardial infarction (AMI) - treatment of AMI and coronary reperfusion should be activated
Absence of ST elevation - medical or interventional treatments may be considered for treatment of ACS

20. Identify and treat - cardiac, electrolyte, toxicological, pulmonary, and neurological precipitants of arrest
Review the H's and T's mnemonic to recall factors

21. Targeted Temperature Management
Induced Hypothermia
For protection of the brain and other organs - helpful therapeutic approach in comatose patients
Specific indications
Timing and duration of therapy
Methods for induction, maintenance, and subsequent reversal of hypothermia

22. (contd.)
Studies of animal models of cardiac arrest showed that short-duration hypothermia (1 hour) achieved < minutes after ROSC had a beneficial effect
Optimal duration of induced hypothermia is at least 12 hours and may be >24 hours
Hypothermia was maintained for 12 or 24 hours in the studies of out-of-hospital patients presenting in VF
Hypothermia for up to 72 hours was used safely in newborns

23. Methods for inducing hypothermia
Multiple, no single method has proved to be optimal.
Feedback-controlled endovascular catheters and surface cooling devices are available
Cooling blankets, application of ice bags - require more labor and closer monitoring.
Iced isotonic fluid can be infused to initiate core cooling but must be combined with a follow-up method for maintenance of hypothermia#
# Bernard S , Buist M, Monteiro O, et al. Induced hypothermia using large volume, ice cold intravenous fluid in comatose survivors of out of hospital cardiac arrest: a preliminary report. Resuscitation 2003;56:9-13

24. (contd.)
Patient's core temperature - Esophageal thermometer, bladder catheter, pulmonary artery catheter, Axillary and oral temperatures are inadequate for measurement of core temperature
Tympanic temperature - rarely available, unreliable
Bladder temperatures - anuric patients
Rectal temperatures - differ from brain or core temperature

25. Potential complications
Coagulopathy
Arrhythmias
Hyperglycemia
Pneumonia
Sepsis
Infections
Decrease immune function
Impairs coagulation
Ongoing bleeding

26. (contd.) Recommendation
Comatose adult patients with ROSC after out-of-hospital VF cardiac arrest should be cooled to 32°C to 34°C for 12 to 24 hours. (Class I, LOE B)
Induced hypothermia also may be considered for comatose adult patients with ROSC after in-hospital cardiac arrest of any initial rhythm or after out-of-hospital cardiac arrest with an initial rhythm of pulseless electric activity or asystole. (Class IIb, LOE B)
Active rewarming should be avoided in comatose patients who spontaneously develop a mild degree of hypothermia (>32°C) after resuscitation from cardiac arrest during the first 48 hours after ROSC.(Class III, LOE C)

27. Hyperthermia
After resuscitation, temperature elevation above normal can impair brain recovery
Etiology of fever after cardiac arrest - inflammatory cytokines.
There are no randomized controlled trials evaluating the effect of treating pyrexia with either frequent use of antipyretics or "controlled normothermia" using cooling techniques compared to no temperature intervention in post–cardiac arrest patients.
Patients can develop hyperthermia after rewarming posthypothermia treatment. This late hyperthermia should also be identified and treated. Providers should closely monitor patient core temperature after ROSC and actively intervene to avoid hyperthermia (Class I, LOE C).

28. Organ-Specific Evaluation and Support
Pulmonary System Pulmonary dysfunction after cardiac arrest is common.
Etiologies - hydrostatic pulmonary edema from left ventricular dysfunction
Noncardiogenic edema from inflammatory, infective, or physical injuries
Pulmonary atelectasis
Aspiration
Mismatch of ventilation and perfusion
ARDS/ ALI
Role of Positive end-expiratory pressure (PEEP), a lung-protective strategy for mechanical ventilation, and titrated FiO2

29. (contd.)
Diagnostic tests in intubated patients - chest radiograph, ABG. Verify correct position of the ET tube, distribution of pulmonary infiltrates, edema
Identify complications - rib fracture, pneumothorax, and pleural effusions, pneumonia
Adjust mechanical ventilatory support - oxyhemoglobin saturation, ABG, MV and patient-ventilator synchrony
Reduce the work of breathing
Titrate oxygen administration - maintain the SpO2 94%.

30. (contd.)
Significant metabolic acidosis after cardiac arrest- temptation to institute hyperventilation to normalize blood pH
1-mm Hg decrease in PaCO2 - decrease in cerebral blood flow of approximately 2.5% to 4%
Cerebral blood flow remains CO2-reactive after cardiac arrest - diminished for 1 to 3 hours after reperfusion
Initial hyperemic blood flow response that lasts 10 to 30 minutes, followed by a more prolonged period of low blood flow. During this latter period of late hypoperfusion, a mismatch between blood flow and oxygen requirement may occur. Hyperventilation at this stage may lower PaCO2, cause cerebral vasoconstriction, and exacerbate cerebral ischemic injury.

31. (contd.)
In one study, controlled ventilation with specific goals to keep PaCO to 45.1 mm Hg (5 to 6 kPa) and SaO2 95% to 98% as part of a bundle with multiple other goals (including hypothermia and blood pressure goals) increased survival from 26% to 56%.
Hyperventilation also may compromise systemic blood flow because of occult or auto-PEEP and is deleterious in all low-flow states, including cardiopulmonary resuscitation (CPR) and hypovolemia.

32. (contd.)
Recommendation - TV of 6 to 8 mL/kg and inspiratory plateau pressure 30 cm H2O to reduce ventilator-associated lung injury.
Furthermore, a recent historical comparison of ventilation practice after cardiac arrest reported no differences in pneumonia, oxygenation, lung compliance, and ventilator days when a low VT strategy versus a more liberal "old practice" VT was applied
Maintain PaCO2 (40 to 45 mm Hg) or PETCO2 (35 to 40 mm Hg) while avoiding hemodynamic compromise (Class IIb, LOE C)

33. Treatment of Pulmonary Embolism After CPR
Use of fibrinolytics to treat pulmonary embolism after CPR has been reported
Surgical embolectomy
Mechanical thrombectomy
In post–cardiac arrest patients with arrest due to presumed or known pulmonary embolism, fibrinolytics may be considered (Class IIb, LOE C).

34. Sedation After Cardiac Arrest
Post–cardiac arrest - cognitive dysfunction, agitation, frank delirium with purposeless movement, risk of self-injury
Opioids, anxiolytics, sedative-hypnotic agents, adrenergic agonists, butyrophenones
Neuromuscular blocking agents can be used for short intervals with adequate sedation
Daily interruptions and titrated to the desired effect.

35. Cardiovascular System
ACS is a common cause of cardiac arrest- 12-lead ECG and cardiac markers - aggressive treatment of STEMI - regardless of coma or induced hypothermia - emergent coronary angiography.
PCI alone or as part of a bundle of care - improved myocardial function and neurological outcomes.
Therapeutic hypothermia safely combined with primary PCI after cardiac arrest caused by AMI.
Antiarrhythmic drugs- lidocaine or amiodarone
There is no evidence to support or refute continued or prophylactic administration of these medications.

36. Vasoactive Drugs for Use in Post–Cardiac Arrest Patients

37. (contd.)

38. (contd.) Hemodynamic instability is common after cardiac arrest.
Persistently low cardiac index during the first 24 hours - multiorgan failure
Metabolic acidosis - Vasodilation
Ischemia/reperfusion of cardiac arrest and electric defibrillation - myocardial stunning and dysfunction
Echocardiographic evaluation within the first 24 hours
Mean arterial pressure 65 mm Hg and an ScvO2 70% are generally considered reasonable goals.

39. Glucose Control
The post–cardiac arrest patient is likely to develop metabolic abnormalities such as hyperglycemia
Increased mortality or worse neurological outcomes
Optimum blood glucose concentration and interventional strategy to manage blood glucose in the post–cardiac arrest period is unknown
Hypoglycemia may be associated with worse outcomes in critically ill patients
Strategies to target moderate glycemic control (144 to 180 mg/dL) may be considered in adult patients with ROSC after cardiac arrest (Class IIb, LOE B)
Attempts to control glucose concentration within a lower range (80 to 110 mg/dL should not be implemented after cardiac arrest due to the increased risk of hypoglycemia (Class III, LOE B)

40. Steroids
Corticosteroids have an essential role in the physiological response to severe stress, including maintenance of vascular tone and capillary permeability
In the post–cardiac arrest phase - adrenal insufficiency
At present there are no human randomized trials investigating corticosteroid use after ROSC

41. Hemofiltration
Hemofiltration has been proposed as a method to modify the humoral response to the ischemic-reperfusion injury that occurs after cardiac arrest
Future investigations are required to determine whether hemofiltration will improve outcome in post–cardiac arrest patients.

42. Central Nervous System
Brain injury
Common cause of morbidity and mortality in post–cardiac arrest patients.
Cause of death in 68% patients (out-of-hospital), 23% a (in-hospital) cardiac arrest.
Clinical manifestations - coma, seizures, myoclonus, neurocognitive dysfunction (ranging from memory deficits to persistent vegetative state), and brain death.
Seizure Management Whether there is any disease-specific management of seizures after cardiac arrest remains unknown
Untreated seizures - detrimental to the brain
EEG - as soon as possible and should be monitored frequently or continuously in comatose patients after ROSC. (Class I, LOE C)
Neuroprotective agents with anticonvulsant properties- thiopental, diazepam or magnesium - not improved neurological outcome in survivors.
The same anticonvulsant regimens for the treatment of seizures used for status epilepticus caused by other etiologies may be considered after cardiac arrest. (Class IIb, LOE C)

43. Neuroprotective Drugs
Number of clinical trials performed to date is limited and has failed to demonstrate improved neurological outcome with potential neuroprotective drugs given after cardiac arrest.

44. Prognostication of Neurological Outcome in Comatose Cardiac Arrest Survivors
Early prognostication of neurological outcome - essential component of post–cardiac arrest care
Accurate and reliable tools to prognosticate poor outcome
Poor outcome is defined as death, persistent unresponsiveness, or the inability to undertake independent activities after 6 months
No pre-arrest or intra-arrest parameters alone or in combination accurately predict outcome in individual patients who achieve ROSC

45. (contd.)
No post-arrest physical examination finding or diagnostic study has as yet predicted poor outcome of comatose cardiac arrest survivors during the first 24 hours after ROSC.
After 24 hours - SSEPs - absence of confounders (such as hypotension, seizures, sedatives, or neuromuscular blockers) - most reliable early predictors of poor outcome
However, the decision to limit care should never be made on the basis of a single prognostic parameter, and expert consultation may be needed.

46. Neurological Assessment
Most widely studied parameter to predict outcome in comatose post–cardiac arrest patients – check confounding factors (hypotension, seizures, sedatives, or neuromuscular blockers)
No clinical neurological signs reliably predict poor outcome < 24 hours after cardiac arrest. Absence of both pupillary light and corneal reflexes at 72 hours after cardiac arrest predicted poor outcome with high reliability
The absence of vestibulo-ocular reflexes at 24 hours or Glasgow Coma Scale (GCS) score < 5 at 72 hours are less reliable for predicting poor outcome

47. (contd.)
EEG No electrophysiological study reliably predicts outcome in comatose patients during the first 24 hours after ROSC.
EEG pattern showing generalized suppression to <20 µV, burst-suppression pattern associated with generalized epileptic activity, or diffuse periodic complexes on a flat background is associated with a poor outcome – check confounders
In the absence of confounding factors such as sedatives, hypotension, hypothermia, neuromuscular blockade, seizures, or hypoxemia, it may be helpful to use an unprocessed EEG interpretation observed 24 hours after ROSC to assist with the prediction of a poor outcome in comatose survivors of cardiac arrest not treated with hypothermia (Class IIb, LOE B).
Evoked Potentials Abnormalities in evoked potentials are associated with poor outcomes.

48. Neuroimaging MRI CT Single-photon emission computed tomography
Cerebral angiography
Transcranial Doppler

49. Blood and Cerebrospinal Fluid Biomarkers
NSE - most promising and extensively studied biomarker is serum for predicting poor outcome when measured between 24 and 72 hours after cardiac arrest
Routine use of any serum or CSF biomarker as a sole predictor of poor outcome in comatose patients after cardiac arrest is not recommended (Class III, LOE B).

50. Ethics
Advance directive – communicates thoughts, wishes, preferences for healthcare decisions in periods of inadequacy.
Living will – written direction to healthcare providers about the care that the individual approves should he or she becomes terminally ill and unable to make decisions.
Durable power of attorney for health care – legal document, appoints an authorized person to make healthcare decisions.
DNAR order – Licensed physician as per local regulation
Must be signed, valid date, preceded by discussion with family
AND (allow natural death) – allow natural consequences of a disease or injury, emphasize ongoing end of life care.

51. A decision to limit care or withdraw life support is justifiable
If the patient is determined to be brain dead
If the physician and patient/surrogate agree that treatment goals cannot be met, or if the burden to the patient of continued treatment believed to exceed any benefits.

52. Organ Donation After Cardiac Arrest
Despite maximal support and adequate observation, some patients will be brain-dead after cardiac arrest.
No difference in functional outcomes of organs transplanted from patients who are brain-dead as a consequence of cardiac arrest when compared with donors who are brain-dead due to other causes.
Adult patients who progress to brain death after resuscitation from cardiac arrest should be considered for organ donation (Class I, LOE B).

53. Brain Death
Refinements in critical care medicine- appropriate diagnosis of brain death.
No global consensus on brain death diagnosis.
Legal requirement for organ donation.

54. History First description of cessation of brain function – 1959
Criteria for brain death – first published in 1968
Brainstem definition for brain death Conference of Medical Royal Colleges and their Faculties in the United Kingdom.
The document in Criteria for the Diagnosis of Brain Stem Death encouraged the use of more correct term Brainstem Death.

55. The concept of Brain Death
Brain death – death of the organism and not merely death or necrosis of brain in a living body.
Physiologic significance of brain death and cardiac death are essentially equal- both represent irreversible loss of communication between the control centers and the peripheral cells.
Current concept - CNS, including the brain stem, is the control center, cessation of CNS functions represents cessation of harmony of life, without CNS control living organism is nothing more than an aggregation of living cells.

56. Diagnostic criteria for the clinical diagnosis of brain death
A Prerequisites
Brain death is the absence of clinical brain function when the proximate cause is known and demonstrably irreversible.
Clinical or neuroimaging evidence of an acute CNS catastrophe that is compatible with the clinical diagnosis of brain death.
Exclusion of complicating medical conditions that may confound clinical assessment
No drug intoxication or poisoning
Core temperature ≥ 32oC.

57. (contd.)
B Cardinal findings
1 Coma or unresponsiveness- no cerebral motor response to pain in all extremities.
2 Absence of brainstem reflexes
Pupils
no response to bright light
size: midposition to dilated

58. (contd.) Absent pupillary light reflex
Although drugs can influence pupillary size, the light reflex remains intact only in the absence of brain death
IV atropine does not markedly affect response
Paralytics do not affect pupillary size
Topical administration of drugs and eye trauma may influence pupillary size and reactivity
Pre-existing ocular anatomic abnormalities may also confound pupillary assessment in brain death

59. (contd.)

60. (contd.) Ocular movement no oculocephalic reflex
no deviation of eyes to irrigation (50ml, 1min, 5min)
Elevate the head by 30°
Irrigate one tympanic membrane with iced water
Observe patient for 1 minute after each ear irrigation, with a 5 minute wait between testing of each ear
Facial trauma involving the auditory canal and petrous bone can also inhibit these reflexes

61. Cold caloric test interpretation
Not comatose
Nystagmus; both eyes slow toward cold,
Coma with intact brainstem
Both eyes tonically deviate toward cold water
No eye movement
Brainstem injury / death
Movement only of eye on side of stimulus
Internuclear ophthalmoplegia
Suggests brainstem structural lesion

63. (contd.) Facial sensation and facial motor response no corneal reflex
no jaw reflex
no grimacing to deep pressure
Pharyngeal and tracheal reflexes
no response-posterior pharynx
no cough response- bronchial suctioning

64. (contd.) Apnea test Prerequisites Core temperature ≥ 36.5 OC
Systolic blood pressure ≥ 90 mmHg
Euvolemia: option- positive fluid balance in the previous 6 hours
Normal PaCO2: Option - PaCO2 ≥ 40 mmHg
Normal PaO2: Option - preoxygenation to obtain arterial PaO2 ≥ 200 mmHg

65. (contd) Connect a pulse oximeter – disconnect ventilator
Deliver 100 percent oxygen, 6L/min, into the trachea
Look closely for the respiratory movements
Measure arterial PaCO2, PaO2 and pH after approximately 8 min and reconnect the ventilator

66. Interpretation of Apnea test
Respiratory movements - absent
arterial PCO2 ≥ 60 mmHg (option: 20 mmHg increase over baseline) – apnea test positive
Respiratory movements observed - apnea test negative - test should be repeated
Connect the ventilator if - SBP ≤ 90 mmHg
Pulse oximeter indicates significant desaturation
Cardiac arrhythmias

67. (contd.) Immediately draw an arterial sample- ABG
PaCO2 ≥ 60 mmHg or PaCo2 increase ≥ 20 mmHg - Apnea test positive
If PaCO2 ≤ 60 mmHg or PaCo2 increase < 20 mmHg- result is indeterminate - additional confirmatory test can be considered.

68. Brain death guidelines in children
A History
Determination of the proximate cause of coma to ensure absence of remediable or reversible conditions
B Physical examination
Coma and apnea
Absence of brainstem functions
Midposition of fully dilated pupils
Absence of spontaneous eye movements
Absence of movements of bulbar musculature and corneal, gag, cough, sucking and rooting reflexes
Absence of respiratory movements with apnea testing
Patient must not be hypothermic or hypotensive for age
Flaccid tone and absence of spontaneous or induced movements
The examination results should remain consistent with brain death throughout the observation and testing period.

69. (contd.) C Observation period according to age
7 days - 2 months: 2 examinations and EEGs separated by hours
2 months - 1 yr: examinations and EEG seperated by at least 24 hours
> 1 year : observation period of atleast 12 hours/ more prolonged period of atleast 24 hours if it is difficult to assess the extent and reversibility of brain damage.

70. (contd.)
D Laboratory testing EEG – should be performed throughout a 30- min period using standardized techniques. Angiography – cerebral radionuclide angiogram – lack of visualization of cerebral circulation Techniques being investigated Xenon CT, DSA, Real time cranial USG, Doppler, Evoked potential

71. Confirmatory Testing for Determination of Brain Death
Cerebral angiography
Electroencephalograpgy
Transcranial Doppler USG
Cerebral Scintigraphy 99mTc- hexametazime
The diagnosis of brain death. N Engl J Med 344:1215,2001

72. Role of Anaesthesiologist in brain death/ Anaesthesiologists in Organ Donation

73. With the development of organ transplantation, the concept of brain death has been developed.
Permits multiple vital organ procurement for transplantation.
Dead – donor rule : requires that patients must be declared dead before the removal of any life sustaining organs- ethical and legal implications

74. Required request/ presumed consent- to improve the rate of organ donation.
“Non-heart beating organ donor” protocols: life sustaining therapy is withheld on an imminently dying patient with the removal of transplantable organs after the patients cardiac arrest.

75. Anaesthesiologists- ample knowledge about brain death and organ donation.
Involved not only in brain death diagnosis but also in anaesthetic management of brain dead patients for organ procurement.
Special care is required for anaesthetic management as the spinal cord is intact and somatic and visceral reflexes are present.

76. Vasodilators- suppress hypertension and tachycardia by noxious stimuli.
Muscle relaxants – suppress the motor activity mediated by spinal reflexes.
Sedation and analgesia – an opinion – theoretically unnecessary.

77. References
Circulation . The journal of American heart association 2010
Miller’s anaesthesia 7th edition
Morgan’s clinical anaesthesiology 4th edition
Cardio pulmonary resuscitation improve the quality of care. Indian journal of anaesthesia. 2010;54; (2) :91- 94

78. THANK YOU