Post cardiac arrest syndrome

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  • Cardiac arrest is the terminal event in any fatal disorder. Statistics would show, despite the use of CPR , mortality rates for cardiac arrest are 80 to 97% for infants and children. The mortality rate is almost 25% for respiratory arrest alone. Neurologic outcome is often severely compromised. But for those who survive… for the cardiac arrest survivor, the story does not end there. These group of patients go into experiencing various complex, multi-systemic pathologic processes, known as the POST-CARDIAC ARREST SYNDROME, which should be addressed appropriately, timely and aggressively, to ensure their continued survival.Good morning!
  • The objectives for today’s presentation are to: To define and describe post-cardiac arrest syndrome among cardiac arrest survivorsTo impart knowledge regarding the pathophysiology, treatment and prognosis of patients who regain spontaneous circulation after cardiac arrestTo provide basic guideline for optimization of post-cardiac arrest care.
  • To begin with, we have a case of C. J.. A 7 year old female from project 7 QC, admitted last March 18 for DOB.
  • The Birthmaternal, nutritional, immunization, and immunization are non-contributory to the
  • Asphyxia can be clinically defined as airway obstruction or inadequateventilation leading to hypoxemia and hypercarbia. Examples includedrowning, choking, and coma accompanied by loss of airway patency.The typical progression of untreated asphyxia is hypertension and increasedwork of breathing (where possible), followed by bradycardia, hypotension,pulseless electrical activity, and eventually, asystole.Before complete respiratory arrest, patients with intact neurologic function may be agitated, confused, and struggling to breathe. Tachycardia and diaphoresis are present; there may be intercostal or sternoclavicular retractions. Patients with CNS impairment or respiratory muscle weakness exhibit feeble, gasping, or irregular respirations and paradoxical breathing movements. Patients with a foreign body in the airway may choke and point to their necks. With respiratory arrest, the patient is unconscious, or about to become so, and cyanotic (unless markedly anemic). If uncorrected, cardiac arrest follows within minutes from onset of hypoxemia.
  • The most common cause of nontraumatic cardiopulmonary arrest in childrenis airway compromise . Although ventricular fibrillation (VF) orventricular tachycardia (VT) occurs less commonly in children than inadults, it is not rare: approximately 5% to 15% of children with prehospitalarrest have VF/VT
  • In contrast to adults, in whom most cardiac arrests are due to cardiac arrhythmia and intrinsic heart disease, most cardiac arrests in children, including in-hospital and out-of-hospital arrests, are due to asphyxia.
  • This is the result of a large meta-analysis done to determine the etiology of out-of-hospital cardiac arrest in children. It showed that respiratory diseases or asphyxia as a cause ranked top three among the top causes and clearly outnumbers cardiac causes. Among other causes of cardiac arrest would include...A large meta-analysis showed that ROSC from all causes of cardiac arrest was achieved in 13% of pediatric patients. Where the cardiac arrest occurs—in-hospital or out-of-hospital—has a large impact on ROSC, which is achieved in 24% of children with in-hospital and 9% of children with out-of-hospital cardiac arrest (157). Mortality after cardiac arrest in children is very high, estimated to be greater than 90% and, despite the potential for plasticity in the developing brain, children who survive have dismally poor neurologic outcomes, similar to adults. This finding may be related in part to the prearrest hypoxemia and brain hypoperfusion prior to no-flow ischemia seen during asphyxial cardiac arrest (Fig. 59.2). Morbidity is equally dismal. Of the survivors, over half will develop some degree of HIE.
  • Do the differences between asphyxial-mediated and cardiac-mediated injury have clinical relevance?
  • They do to the extent that asphyxialinjuries are more severe, because asphyxial cardiac arrest produces a physiologically different milieu compared with VT/VF arrest due to the fact that hypoxemia, acidosis, hypercarbia, and hypotension precede the cardiac arrest. Both injuries, however, demonstrate selective vulnerabilityand delayed neuronal death.. The most prominent of these ‘‘selectively vulnerable’’regions are the hippocampus and reticular thalamus. Thus, althoughan asphyxial injury may be more severe than a cardiac-mediated injury foran equivalent period of ischemia, asphyxial injuries should respond similarlyto neuroprotective therapies.
  • Asphyxial cardiac arrest produces a physiologically different milieu compared with VT/VF arrest due to the fact that hypoxemia, acidosis, hypercarbia, and hypotension precede the cardiac arrest.It has been reported that an asphyxial arrest of 7 mins produces severe impairment of neurologic function, comparable to a VT/VF arrest with a duration of 10 mins (34). Furthermore, compared head-to-head, asphyxial cardiac arrest in dogs resulted in more prevalent and prominent microinfarcts and petechialhemorrhage compared with VT/VF cardiac arrest of similar duration (149).
  • Before going further, we would define several terms that would help us understand more post-cardiac arrest syndrome.Resumption of spontaneous circulation (ROSC) after prolonged,complete, whole-body ischemia is an unnatural pathophysiologicalstate created by successful cardiopulmonary resuscitation (CPR).
  • In the early 1970s, Dr Vladimir Negovsky recognized that thepathology caused by complete whole-body ischemia and reperfusionwas unique in that it had a clearly definable cause, time course,and constellation of pathological processes. Negovskynamed this state "postresuscitation disease.
  • Although appropriateat the time, the term "resuscitation" is now used more broadlyto include treatment of various shock states in which circulationhas not ceased. Moreover, the term "postresuscitation" impliesthat the act of resuscitation has ended.
  • Negovsky himself statedthat a second, more complex phase of resuscitation begins whenpatients regain spontaneous circulation after cardiac arrest.1For these reasons, we propose a new term: "post–cardiacarrest syndrome."
  • The immediate postarrestphase could be defined as the first 20 minutes after ROSC. Theearly postarrest phase could be defined as the period between20 minutes and 6 to 12 hours after ROSC, when early interventionsmight be most effective. An intermediate phase might be between6 to 12 hours and 72 hours, when injury pathways are still activeand aggressive treatment is typically instituted. Finally, aperiod beyond 3 days could be considered the recovery phase,when prognostication becomes more reliable and ultimate outcomesare more predictable.
  • Cj was spontaneously revived after 5 mins of CPR. However, this was followed by onset of seiures, characterized as generalized tonic-clonic , had hypotensive episodes which were addressed with intravenous fluids and inotropic support. Signs and symptoms of asthma persisted such as wheezing all over lung field areas.
  • The 4 key components of post–cardiac arrest syndromeare post–cardiac arrest brain injury, (2) post–cardiacarrest myocardial dysfunction, (3) systemic ischemia/reperfusionresponse, and (4) persistent precipitating pathology .
  • The severity of these disorders after ROSC is not uniform andwill vary in individual patients based on the severity of theischemic insult, the cause of cardiac arrest, and the patient’sprearrest state of health. If ROSC is achieved rapidly afteronset of cardiac arrest, the post–cardiac arrest syndromewill not occur.
  • Common cause of morbidity and mortality68% of out-of-hospital cardiac arrests23% of in-hospital cardiac arrests
  • Cardiac arrest produces global ischemia with consequences at the cellular level that adversely affect patients following resuscitation. The main consequences involve direct cellular damage and edema formation. Edema is particularly harmful in the brain, which has no room to expand, resulting in increased intracranial pressure and corresponding decrease in cerebral perfusion post-resuscitation. A number of successfully resuscitated patients have short- or long-term cerebral dysfunction.
  • Studies in adult animal models of cardiac arrest demonstrate that CBF in the postarrest period can be divided into four phases (Fig. 59.2): multifocal no reflow (Phase I), global hyperemia (Phase II), delayed hypoperfusion (Phase III), and restitution of normal blood flow (Phase IV) (8,46,68).
  • This phase is characterized by localized areas of the brain that fail to reperfuse after ROSC. At a microscopic level, areas of no reflow are interspersed with areas of restored blood flow and microinfarcts.Brain regions that are selectively vulnerable include the thalamus, amygdala, hippocampus, and striatum. It is hypothesized that vasospasm, perivascularedema, and increased blood viscosity play a role in the development of this “noreflow” phenomenon.
  • The second phase of CBF after cardiac arrest is characterized by increased global CBF immediately after ROSC and is often referred to as the hyperemic phase. This phase is present for 15-30 mins after ROSC. Global CBF during this phase is typically two to three times higher than baseline CBF. Some believe that this hyperemic phase is essential for neuronal functional recovery (100). This opinion is based on studies that show that hypertensive reperfusion improves neurologic outcome, whereas postarrest hypotension worsens neurologic outcome.
  • The third phase of CBF after cardiac arrest begins 15-30 minsafter ROSC, can persist for several hours, and is often referred to as the delayed hypoperfusion phase. During this phase, regional heterogeneity of the CBF is seen, with areas of high, normal, and low flow .(8,46). The severity, or duration and degree, of delayed hypoperfusion is associated with more severe impairment of functional recovery, especially if not matched by a lower metabolic rate (34). Therefore, interventions that increase CBF and minimize delayed hypoperfusion during phase III after ischemia may improve neurologic recovery.
  • Less information exists regarding CBF after cardiac arrest in infants and children.In neonatal asphyxia, CBF velocities have been estimated by Doppler ultrasonography and have suggested that the development of high CBF velocities after 24 hrs is predictive of poor prognosis (63). A study of CBF in 9 children in a persistent vegetative state several days after cardiac arrest (phase IV) of different etiologies (near-drowning, SIDS, postsurgery) showed CBF values that ranged from 12 to 56 mL/100 g brain tissue/min. In this series, CBF measurements in 2 children who were clinically brain dead at the time of the study were 0.2 and 2 mL/100 g brain tissue/min.A study of CBF in 9 children in a persistent vegetative state several days after cardiac arrest (phase IV) of different etiologies (near-drowning, SIDS, postsurgery) showed CBF values that ranged from 12 to 56 mL/100 g brain tissue/min. In this series, CBF measurements in 2 children who were clinically brain dead at the time of the study were 0.2 and 2 mL/100 g brain tissue/min. CBF values of <10 mL/100 g brain tissue/min are thought to be reflective of brain death, and CBF of >10–15 mL/100 g brain tissue/min is associated with potential for patient survival (9).Ashwal S, Schneider S, Thompson J. Xenon computed tomography measuring cerebral blood flow in the determination of brain death in children. Ann Neurol 1989;25:539–546.
  • This is an MRI image of the brain from a patient after asphyxial cardiac arrest
  • In a small case series,patients with temperatures >39°C in the first 72 hoursafter out-of-hospital cardiac arrest had a significantly increasedrisk of brain death.
  • When serial temperatures were monitoredin 151 patients for 48 hours after out-of-hospital cardiac arrest,the risk of unfavorable outcome increased (odds ratio 2.3, 95%confidence interval [CI] 1.2 to 4.1) for every degree Celsiusthat the peak temperature exceeded 37°C.
  • A subsequentmulticenter retrospective study of patients admitted after out-of-hospitalcardiac arrest reported that a maximal recorded temperature>37.8°C was associated with increased in-hospital mortality(odds ratio 2.7, 95% CI 1.2 to 6.3).
  • Hyperglycemia is common in post–cardiac arrest patientsand is associated with poor neurological outcome after out-of-hospitalcardiac arrest.Found in the first 24-48 hours after ROSC and is secondary to decreased glucose consumption.
  • Animal studies suggest that elevatedpostischemic blood glucose concentrations exacerbate ischemicbrain injury, and this effect can be mitigated by intravenousinsulin therapy
  • Seizures in the post–cardiac arrestperiod are associated with worse prognosis and are likely tobe caused by, as well as exacerbate, post–cardiac arrestbrain injury
  • This global dysfunction is transient, and full recovery canoccur. In a swine model with no antecedent coronary or otherleft ventricular dysfunction features, the time to recoveryappears to be between 24 and 48 hours
  • Cardiac index values reached their nadir at8 hours after resuscitation, improved substantially by 24 hours,and almost uniformly returned to normal by 72 hours in patientswho survived out-of-hospital cardiac arrest.More sustaineddepression of ejection fraction among in- and out-of-hospitalpost–cardiac arrest patients has been reported with continuedrecovery over weeks to monthsThe responsiveness of post–cardiacarrest global myocardial dysfunction to inotropic drugs is welldocumented in animal studiesKern KB, Hilwig RW, Berg RA, Rhee KH, Sanders AB, Otto CW, Ewy GA. Postresuscitation left ventricular systolic and diastolic dysfunction: treatment with dobutamine. Circulation. 1997; 95: 2610–2613
  • For example, the severityand duration of post–cardiac arrest myocardial stunningin pediatric animal models are substantially less than in adult
  • Cardiac arrest represents the most severe shock state, duringwhich delivery of oxygen and metabolic substrates is abruptlyhalted and metabolites are no longer removed. CPR only partiallyreverses this process, achieving cardiac output and systemicoxygen delivery (DO2) that is much less than normal. DuringCPR, a compensatory increase in systemic oxygen extraction occurs,which leads to significantly decreased central (ScvO2) or mixedvenous oxygen saturation
  • Cardiac arrest represents the most severe shock state, duringwhich delivery of oxygen and metabolic substrates is abruptlyhalted and metabolites are no longer removed. CPR only partiallyreverses this process, achieving cardiac output and systemicoxygen delivery (DO2) that is much less than normal. DuringCPR, a compensatory increase in systemic oxygen extraction occurs,which leads to significantly decreased central (ScvO2) or mixedvenous oxygen saturation
  • Cardiac arrest represents the most severe shock state, duringwhich delivery of oxygen and metabolic substrates is abruptlyhalted and metabolites are no longer removed. CPR only partiallyreverses this process, achieving cardiac output and systemicoxygen delivery (DO2) that is much less than normal. DuringCPR, a compensatory increase in systemic oxygen extraction occurs,which leads to significantly decreased central (ScvO2) or mixedvenous oxygen saturation
  • Inadequate tissue oxygen deliverycan persist even after ROSC because of myocardial dysfunction,pressor-dependent hemodynamic instability, and microcirculatoryfailure. Oxygen debt (the difference between predicted oxygenconsumption [normally 120 to 140 mL · kg–1 ·min–1] and actual consumption multiplied by time duration)quantifies the magnitude of exposure to insufficient oxygendelivery. Accumulated oxygen debt leads to endothelial activationand systemic inflammation106 and is predictive of subsequentmultiple organ failure and death.107,108
  • Primary pulmonary disease such as chronic obstructive pulmonarydisease, asthma, or pneumonia can lead to respiratory failureand cardiac arrest
  • When cardiac arrest is caused by respiratoryfailure, pulmonary physiology may be worse after restorationof circulation. Redistribution of blood into pulmonary vasculaturecan lead to frank pulmonary edema or at least increased alveolar-arterialoxygen gradients after cardiac arrest.
  • Other precipitating causes of cardiac arrest may require specifictreatment during the post–cardiac arrest period. For example,drug overdose and intoxication may be treated with specificantidotes, and environmental causes such as hypothermia mayrequire active temperature control. Specific treatment of theseunderlying disturbances must then be coordinated with specificsupport for post–cardiac arrest neurological and cardiovasculardysfunction.
  • Care of the post–cardiac arrest patient is time-sensitive,occurs both in and out of the hospital, and is provided sequentiallyby multiple diverse teams of healthcare providers. Given thecomplex nature of post–cardiac arrest care, it is optimalto have a multidisciplinary team develop and execute a comprehensiveclinical pathway tailored to available resources.In all cases, treatment must focuson reversing the pathophysiological manifestations of the post–cardiacarrest syndrome with proper prioritization and timely execution
  • Additionalmonitoring should be added depending on the status of the patientand local resources and experience. The impact of specific monitoringtechniques on post–cardiac arrest outcome, however, hasnot been validated prospectively.
  • .This approach focuses on optimizationof preload, arterial oxygen content, afterload, contractility,and systemic oxygen utilization
  • The goals in these studies have included a central venous pressureof 8 to 12 mm Hg, MAP of 65 to 90 mm Hg, ScvO2 >70%, hematocrit>30% or hemoglobin >8 g/dL, lactate 2 mmol/L, urine output0.5 mL · kg–1 · h–1, and oxygen deliveryindex >600 mL · min–1 · m–2. Theprimary therapeutic tools are intravenous fluids, inotropes,vasopressors, and blood transfusion. The benefits of early goal-directedtherapy include modulation of inflammation, reduction of organdysfunction, and reduction of healthcare resource consumption
  • Theprimary therapeutic tools are intravenous fluids, inotropes,vasopressors, and blood transfusion. The benefits of early goal-directedtherapy include modulation of inflammation, reduction of organdysfunction, and reduction of healthcare resource consumption
  • Existing guidelines emphasize the use of a fraction of inspiredoxygen (FIO2) of 1.0 during CPR, and clinicians will frequentlymaintain ventilation with 100% oxygen for variable periods afterROSC. Although it is important to ensure that patients are nothypoxemic, a growing body of preclinical evidence suggests thathyperoxia during the early stages of reperfusion harms postischemicneurons by causing excessive oxidative stressMost relevant to post–cardiac arrest care, ventilationwith 100% oxygen for the first hour after ROSC resulted in worseneurological outcome than immediate adjustment of the FIO2 toproduce an arterial oxygen saturation of 94% to 96%This can be achieved by adjusting the FIO2 toproduce an arterial oxygen saturation of 94% to 96%.
  • Studies in brain-injured patients have shown that the cerebralvasoconstriction caused by hyperventilation may produce potentiallyharmful cerebral ischemia.148–150 Hyperventilation alsoincreases intrathoracic pressure, which will decrease cardiacoutput both during and after CPR.151,152 Hypoventilation mayalso be harmful, because hypoxia and hypercarbia could increaseICP or compound metabolic acidosis, which is common shortlyafter ROSC.Ventilationshould be adjusted to achieve normocarbia and should be monitoredby regular measurement of arterial blood gas values.
  • Other causes of out-of-hospital cardiac arrest include pulmonaryembolism, sepsis, hypoxemia, hypovolemia, hypokalemia, hyperkalemia,metabolic disorders, accidental hypothermia, tension pneumothorax,cardiac tamponade, toxins, intoxication, and cerebrovascularcatastrophes. The incidence of these causes is potentially higherfor in-hospital cardiac arrest.5 These potential causes of cardiacarrest that persist after ROSC should be diagnosed promptlyand treated.
  • Hypothermia, now a class IIb recommendation from the American Heart Association (AHA) for postresuscitation treatment of cardiac arrest, typically decreases CBF, but this occurs via a coupled reduction in cerebral metabolism (recent guidelines for resuscitation and use of hypothermia are shown in Tables 59.3 and 59.4). Hypothermia also has suppressive effects on excitatory neurotransmission and oxygen radicals. In animal studies, hypothermia and induced hypertension were associated with improved survival (54,124). Two randomized, multicentered, clinical trials in adult patients after primarily VT/VF cardiac arrest certainly support the use of hypothermia after cardiac arrest (3,22) and suggest that therapies that include metabolic suppression may have clinical utilityMild, induced hypothermia has come to the forefront as a promising strategy for improving survival and neurologic outcome after cardiac arrest in adult patients, but the benefits in pediatric patients remain to be determined.
  • Some Evidence to support…Level 1: Randomized clinical trials or meta-analysis of multiple clinical trials with substantial treatment effectsLevel 2: Randomized clinical trials with smaller or less significant treatment effectsLevel 3: Prospective, controlled, nonrandomized cohort studiesLevel 4: Historic, nonrandomized cohort or case-controlled studiesLevel 5: Case series: patients compiled in serial fashion, control group lackingLevel 6: Animal or mechanical model studiesLevel 7: Extrapolations from existing data collected for other purposes, theoretical analysesLevel 8: Rational conjecture (common sense); common practices accepted before evidence-based guidelinesAdapted from The International Liaison Committee on Resuscitation (ILCOR) Consensus on Science with Treatment Recommendations for Pediatric and Neonatal Patients: Pediatric basic and advanced life support. Pediatrics 2006;117:e955–77
  • Adequate sedation will reduce oxygen consumption,which is further reduced with therapeutic hypothermiaIn summary, critically ill post–cardiac arrest patientswill require sedation for mechanical ventilation and therapeutichypothermia. Use of sedation scales for monitoring may be helpful.Adequate sedation is particularly important for prevention ofshivering during induction of therapeutic hypothermia, maintenance,and rewarming. Neuromuscular blockade may facilitate inductionof therapeutic hypothermia, but if continuous infusions of neuromuscular-blockingdrugs become necessary, continuous EEG monitoring should beconsidered.In summary, prolonged seizures may cause cerebral injury andshould be treated promptly and effectively with benzodiazepines,phenytoin, sodium valproate, propofol, or a barbiturateTight control of blood glucose (4.4 to 6.1 mmol/L or 80 to 110mg/dL) with insulin reduced hospital mortality rates in criticallyill adults in a surgical ICU220
  • Findingsof prognostic value include the absence of pupillary light reflex,corneal reflex, facial movements, eye movements, gag, cough,and motor response to painful stimuli.
  • Of these, the absenceof pupillary light response, corneal reflex, or motor responseto painful stimuli at day 3provides the most reliable predictorof poor outcome (vegetative state or death).211Poor neurological outcome is expected with these findings becauseof the extensive brain injury involving the upper brain stem(midbrain), which is the location of the ascending reticularformation (responsible for arousal) and where the pupillarylight response and motor response to pain are facilitated.
  • In all cases, treatment must focuson reversing the pathophysiological manifestations of the post–cardiacarrest syndrome with proper prioritization and timely execution.The clinical goals for pediatric cardiac arrest are effective cardiopulmonary resuscitation (CPR), rapid ROSC, and prevention of secondary injury. Time to initiation and quality of CPR can strongly impact survival and neurologic outcome.
  • Post cardiac arrest syndrome

    1. 1. POST-CARDIAC ARREST SYNDROME<br />Darla Kay A. de Guzman, M.D.<br />Fellow-in-Training<br />Pediatric Critical Care Center<br />
    2. 2. INTRODUCTION<br />
    3. 3. OBJECTIVES<br />To define and describe post-cardiac arrest syndrome among cardiac arrest survivors<br />2. To impart knowledge regarding the pathophysiology, treatment and prognosis of patients who regain spontaneous circulation after cardiac arrest<br />3. To provide basic guideline for optimization of post-cardiac arrest care.<br />
    4. 4. GENERAL DATA<br />C. J.<br />7 yr old , female<br />From Project 7, Q.C.<br />Admitted last March 18, 2009<br />
    5. 5. Chief Complaint<br /> difficulty of breathing<br />
    6. 6. INTERVAL HISTORY<br />Patient is a diagnosed case of bronchial asthma since 4 years old<br />On Salbutamol nebulization PRN basis<br />Usual triggers : URTI, climate changes, dust<br />Last attack was January 2009<br />
    7. 7. HISTORY OF PRESENT ILLNESS<br />2 days PTA- cough, colds, no fever<br /> given Ambroxol. No consult done<br /> 1 day PTA- symptoms persisted<br />difficulty of breathing <br /> Salbutamol nebulization (total of 9 doses)<br /> DOA - DOB persisted<br /> consult at St. Agnes Hosp <br /> 2 doses of Salbutamol + Ipratropium Br nebulization<br /> Advised admission , opted THOC.<br /> PCMC<br />
    8. 8. FAMILY HISTORY<br />30<br />30<br /> Construction worker<br /> Housewife<br />(+) asthma<br />(+) asthma<br />3/12<br />
    9. 9. BIRTH AND MATERNAL HISTORY<br />Born to a 23 y/o primigravid, NABD, RPNCU <br /> c/o LHC, (+)MVS, Feso4<br />No illnesses during pregnancy<br />No exposure to teratogen, viral exanthem <br /> nor radiation<br />Del FT via NSD at EAMC, BW- 2.7kg, good cry and activity at birth<br />No fetomaternal complications noted<br />Discharged after 1 day <br />
    10. 10. NUTRITIONAL HISTORY<br />Breastfed x few weeks of life<br />Shifted to MF (Alacta – alactamil-<br /> alactagen)<br />Complementary feeding: started at <br /> 3-4 mos old<br />
    11. 11. IMMUNIZATION HISTORY<br />BCG<br />DPT/OPV x 3 doses with booster<br />Hepa B x 3 doses<br />Hib x 1<br />Measles<br />
    12. 12. GROWTH AND DEVELOPMENT<br />At par with age<br />Grade 2 average student at San Antonio Elementary School<br />
    13. 13. PAST MEDICAL HISTORY<br />No history of previous hospitalization<br />No known food or drug allergy<br />
    14. 14. PHYSICAL EXAMINATION<br /><ul><li>Awake, irritable, in respiratory distress</li></ul>CR- 130/min RR- 68/min T- 36.7 <br /><ul><li>SKIN: warm, no rashes
    15. 15. HEENT: pink palpebral conjunctiva, white sclera, </li></ul> (-)alar flaring<br /><ul><li>NECK: supple, (-) CLAD
    16. 16. CHEST/ LUNGS: symmetrical chest expansion, (+)subcostal, intercostal retractions, tight air entry
    17. 17. HEART: adynamicprecordium, tachycardic, regular rhythm, no murmur</li></li></ul><li>PHYSICAL EXAMINATION<br />ABDOMEN: Flat, normoactive bowel sounds, soft, no organomegally<br />EXTREMITIES: poor distal pulses, <br /> cyanotic nailbeds<br /> CRT 2-3 secs <br />
    18. 18. SEQUENCE OF Events...<br /> RESPIRATORY FAILURE <br /> HYPOXEMIA<br /> HYPERCARBIA & ACIDOSIS<br /> HYPOTENSION<br /> PEA<br />ASYSTOLE<br />irritable<br />tachycardia<br />tachypnea<br />subcostal, intercostal retractions, tight air entry<br />cyanotic nailbeds<br />poor distal pulses<br />
    19. 19. Cause of Cardiac Arrest: VF or Asphyxia? <br />Asphyxia- most common cause <br /> in children: 80-90%<br />VF- 5-15% of children<br />R.W.Hickey,M.D., M.J.Painter M.D., Brain Injury from Cardiac Arrest in Children; Neurol Clin 24 (2006) 147-158<br />
    20. 20. Adult and Pediatric Differences...<br />Adults: Common <br /> Causes<br /><ul><li>cardiac diseases
    21. 21. non-cardiac </li></ul> diseases<br />Pediatrics: Common Causes<br /><ul><li>respiratory disorders (eg, airway obstruction, smoke inhalation, drowning, infection, sudden infant death syndrome).
    22. 22. trauma
    23. 23. poisoning
    24. 24. cardiac diseases </li></li></ul><li>Etiology of out-of-hospital cardiac arrest in children<br />Cause of arrest n (%) Survival to hosp d/c<br />Sudden infant death syndrome 136 (23) 0<br />Trauma 118 (20) 5<br />Respiratory 96 (16) 21<br />Submersion 73 (12) 17<br />Cardiac 48 (8) 8 <br />Central nervous system 35 (6) 3<br />Burn 6 (1) 0<br />Poisoning 6 (1) 17<br />Other 63 (10) 10<br />Unknown 0 (3) 6<br /> Data from Young KD, Gausche-Hill M, McClung CD, et al. A prospective, population based<br /> study of the epidemiology and outcome of out-of-hospital pediatric cardiopulmonary<br /> arrest. Pediatrics 2004;114(1):157–64<br />
    25. 25. Do the differences between asphyxial-mediated and cardiac-mediated injury have clinical relevance?<br />
    26. 26. Clinical implication...<br />Asphyxial injuries- more severe<br />Both: selective vulnerability and delayed neuronal death<br />Asphyxial injuries respond similarly to neuroprotective strategies<br />R.W.Hickey,M.D., M.J.Painter M.D., Brain Injury from Cardiac Arrest in Children; Neurol Clin 24 (2006) 147-158<br />
    27. 27. Comparison of injury from ventricular fibrillation versus asphyxial cardiac arrest<br />R.W.Hickey,M.D., M.J.Painter M.D., Brain Injury from Cardiac Arrest in Children; Neurol Clin 24 (2006) 147-158<br />
    28. 28. Return of Spontaneous Circulation (ROSC)<br />an unnatural pathophysiological state<br /> created by successful CPR<br />
    29. 29. Postresuscitation Disease<br /> 1970’s Dr. Vladimir Negovsky- <br /> recognized pathology caused by whole body ischemia and reperfusion that had a clearly definable cause, time course and constellation of pathological processes.<br />
    30. 30. Postresuscitation Disease<br />“resuscitation”- treatment of shock states in w/c circulation has not ceased<br />“postresuscitation”- the resuscitation has ended<br />
    31. 31. Post-Cardiac Arrest Syndrome<br /> Dr. Negovsky- a second, more complex <br /> phase of resuscitation begins when px regain spontaneous circulation after cardiac arrest.<br />
    32. 32. Phases of Post-Cardiac Arrest syndrome<br />Immediate Postarrest<br />Early Postarrest<br />Intermediate Phase<br />Recovery Phase<br />-Early interventions are most effective<br />-limit ongoing injury<br />-organ support<br />-prevent recurrence<br />-Injury pathways are still active<br /><ul><li>Aggressive treatment instituted
    33. 33. same goals</li></ul>-Prognostication reliable<br />- Outcomes more Predictable<br />
    34. 34. Going back to pxC.J. ...<br />Spontaneously revived after 5 mins<br /> of CPR<br />onset of seizures, anisocoric<br />hypotensive<br />Wheezes, BLF<br />
    35. 35. PATHOPHYSIOLOGY<br />4 Key Components:<br />Post-cardiac arrest brain injury<br />Post-cardiac arrest myocardial dysfunction<br />Systemic ischemia/perfusion response<br />Persistent precipitating pathology<br />-seizures, anisocoria,<br />posturing<br />-peristent hypotension<br />-wheezes BLF<br />R.W. Neumar, M.d., PhD, et.al., ILCOR Consensus Statement Post-Cardiac Arrest syndrome; Circulation Oct. 2008; 118:2452-2483<br />
    36. 36. 4 Key Components:<br />Severity of these disorders is based upon:<br /> - severity of theischemic insult<br /> - the cause of cardiac arrest<br /> - patient’sprearrest state of health<br />Post-cardiac arrest brain injury<br />Post-cardiac arrest myocardial dysfunction<br />Systemic ischemia/perfusion response<br />Persistent precipitating pathology<br />R.W. Neumar, M.d., PhD, et.al., ILCOR Consensus Statement Post-Cardiac Arrest syndrome; Circulation Oct. 2008; 118:2452-2483<br />
    37. 37. POST-CARDIAC ARREST BRAIN INJURY<br />
    38. 38. Post-cardiac arrest brain injury...<br />Common cause of morbidity and mortality<br />68% of out-of-hospital cardiac arrests<br />23% of in-hospital cardiac arrests <br />
    39. 39. From the ER to the PICU...<br />Phenobarbital<br />Phenytoin<br />Midazolam drip<br />Head cooling measures<br />Head elevation- 30 degrees<br />Mannitol <br />Insulin drip<br /><ul><li>had episodes of hypotension, but was eventually stabilized
    40. 40. continued to have seizures </li></ul> Status epilepticus<br /><ul><li>Febrile during the initial hours of stabilization
    41. 41. hyperglycemic</li></ul>-GCS 6 (E1V1M4)<br /><ul><li>Pupils mid-dilated, NRTL
    42. 42. (+) papilledema</li></li></ul><li>PATHOPHYSIOLOGY: BRAIN INJURY<br />CARDIAC ARREST<br />Cardiac arrest<br />Global Ischemia<br />GLOBAL ISCHEMIA<br />DIRECT CELLULAR DAMAGE<br />EDEMA FORMATION<br />ICP<br />CBF<br />
    43. 43. Cellular Mechanisms <br />Excitotoxicity<br />Disturbances in calcium hemostasis<br />Oxidative stress<br />Energy failure<br />Release of subs. triggering cell- death pathways <br />
    44. 44. CEREBRAL PERFUSION<br />Phase IV: Normal Blood Flow<br />
    45. 45. CEREBRAL PERFUSION<br />
    46. 46. CEREBRAL PERFUSION<br />
    47. 47. CEREBRAL PERFUSION<br />
    48. 48. CEREBRAL PERFUSION<br />9 pxs post-arrest...CBF values ranged from 12 to 56 mL/100 g brain tissue/min. <br />2 Children ...clinically brain dead at the time of the study were 0.2 and 2 mL/100 g brain tissue/min.<br />Ashwal S, et al, Xenon Computed tomography measuring cerebral blood flow in the determination of brain death in chlidren. Ann Neurol 1989; 25:539-546<br />CBF values of <10 ml/100 g brain tissue: brain death<br />CBF: >10-15 ml/100 g- potential for survival<br />poor prognosis<br />
    49. 49. Roger’s Textbook of Intensive Care 4th edition<br />
    50. 50.
    51. 51. Other Issues:<br />Pyrexia<br />Hyperglycemia<br />Seizures<br />
    52. 52. Other Issues:<br />In a small case series..patients with temperatures >39°C in the first 72 hoursafter out-of-hospital cardiac arrest had a significantly increasedrisk of brain death..<br />Takasu A, Saitoh D, et al, Hyperthermia: is it an ominous sign after cardiac arrest? Resuscitation. 2001; 49: 273–277.<br />Pyrexia<br />Hyperglycemia<br />Seizures<br />
    53. 53. When serial temperatures were monitored in 151 patients for 48 hours after out-of-hospital cardiac arrest…the risk of unfavorable outcome increasedfor every degree Celsiusthat the peak temperature exceeded 37°C…<br />Zeiner A. et al, . Hyperthermia after cardiac arrest is associated with unfavorable neurologic outcome. Arch intern. Med. 200; 161: 2007-2012<br />Other Issues:<br />Pyrexia<br />Hyperglycemia<br />Seizures<br />
    54. 54. Other Issues:<br />A multicenter retrospective study of patients admittted for out-of-hospitalcardiac arrest reported that a maximal recorded temperature>37.8°C was associated with increased in-hospital mortality...<br />Langhelle A, et al. In-hospital factors associated with improved outcome after out-of-hospital cardiac arrest: a comparison between four regions in Norway. Resuscitation. 2003; 56: 247–263<br />Pyrexia<br />Hyperglycemia<br />Seizures<br />
    55. 55. Other Issues:<br />Hyperglycemiais common in post-cardiac arrest patient and is associated with a poor neurological outcome after out-of-hospital cardiac arrest.<br />. <br />Langhelle A, et al. In-hospital factors associated with improved outcome after out-of-hospital cardiac arrest: a comparison between four regions in Norway. Resuscitation. 2003; 56: 247–263<br />Pyrexia<br />Hyperglycemia<br />Seizures<br />
    56. 56. Other Issues:<br />Animal studies suggest that elevatedpostischemic blood glucose concentrations exacerbate ischemicbrain injury and this effect can be mitigated by intravenous insulin therapy..<br />KatzLM, Wang Y, Ebmeyer U, Radovsky A, Safar P. Glucose plus insulin infusion improves cerebral outcome after asphyxial cardiac arrest. Neuroreport. 1998; 9: 3363–3367.<br />Pyrexia<br />Hyperglycemia<br />Seizures<br />
    57. 57. Other Issues:<br />...Seizures in the post–cardiac arrestperiod are associated with worse prognosis and are likely tobe caused by, as well as exacerbate, post–cardiac arrestbrain injury…<br />Krumholz A, Stern BJ, Weiss HD. Outcome from coma after cardiopulmonary resuscitation: relation to seizures and myoclonus. Neurology. 1988; 38: 401–405.[<br />Pyrexia<br />Hyperglycemia<br />Seizures<br />
    58. 58. Post-cardiac arrest myocardial dysfunction<br />
    59. 59. Post-Cardiac Arrest Myocardial Dysfunction<br />Contributes also to low survival rate<br />Transient global dysfunction<br />Time to recovery: 24-48 hours<br />Kern KB, Hilwig RW, Rhee KH, Berg RA. Myocardial dysfunction after resuscitation from cardiac arrest: an example of global myocardial stunning. J Am Coll Cardiol. 1996; 28: 232–240<br />
    60. 60. …The responsiveness of post–cardiacarrest global myocardial dysfunction to inotropic drugs is welldocumented in animal studies<br />Ruiz-BailénM, et Reversible myocardial dysfunction after cardiopulmonary resuscitation. Resuscitation. 2005; 66: 175–181<br />..Cardiac index values reachnadir at 8 hours, improved by 24 hours, return to normal by 72 hours among patients who survived out-of-hospital cardiac arrest..<br />Laurent I, et. Reversible myocardial dysfunction in survivors of out-of-hospital cardiac arrest. J Am CollCardiol. 2002; 40: 2110–2116<br />
    61. 61. Post-Cardiac Arrest Myocardial Dysfunction<br />the severityand duration of post–cardiac arrest myocardial stunningin pediatric animal models are substantially less than in adult<br />
    62. 62. SYSTEMIC ISCHEMIA/ PERFUSION ESPONSE<br />
    63. 63. SYSTEMIC ISCHEMIA/ PERFUSION RESPONSE<br />CARDIAC ARREST<br />OXYGEN<br />METABOLIC SUBSTRATES<br />METABOLITES<br />
    64. 64. SYSTEMIC ISCHEMIA/ PERFUSION RESPONSE<br />CARDIAC ARREST<br />OXYGEN<br />METABOLIC SUBSTRATES<br />METABOLITES<br />
    65. 65. SYSTEMIC ISCHEMIA/ PERFUSION RESPONSE<br />LESS CARDIAC OUTPUT<br />LESS THAN NORMAL DO2<br />INC. SYSTEMIC O2 EXTRACTION<br />CARDIAC ARREST<br />OXYGEN<br />METABOLIC SUBSTRATES<br />CPR<br />METABOLITES<br />
    66. 66. SYSTEMIC ISCHEMIA/ PERFUSION RESPONSE<br />Myocardial dysfunction, pressor-dependent hemodynamic instability<br />Microcirculatory failure<br />INADEQUATE O2 DELIVERY<br />MULTIPLE ORGAN FAILURE<br />INFECTION<br />DEATH<br />ENDOTHELIAL ACTIVATION<br />SYSTEMIC INFLAMMATION<br />OXYGEN DEBT<br />
    67. 67. PERSISTENT PRECIPITATING PATHOLOGY<br />
    68. 68. PERSISTENT PRECIPITATING PATHOLOGY<br />Chronic obstructive pulmonary disease<br />Asthma <br />pneumonia<br />
    69. 69. PERSISTENT PRECIPITATING PATHOLOGY<br />Cardiac arrest secondary to pulmonary physiology<br />worse pulmonary physiology<br />PULMONARY EDEMA<br />INCREASED ALVEOLAR-ARTERIAL OXYGEN GRADIENTS<br />
    70. 70. PERSISTENT PRECIPITATING PATHOLOGY<br />Other precipitating causes requiring specific treatment:<br /> - drug overdose, intoxication<br /> - hypothermia<br />
    71. 71. Therapeutic stRAtegies<br />
    72. 72. THERAPEUTIC STRATEGIES<br />Time-sensitive<br />Occurs in and out the hospital<br />Multiple diverse teams of healthcare providers<br />In all cases, treatment must focuson reversing the pathophysiological manifestations of the post–cardiacarrest syndrome with proper prioritization and timely execution.<br />
    73. 73. THERAPEUTIC STRATEGIES<br />Monitoring<br />Early Hemodynamic Optimization<br />Oxygenation <br />Ventilation<br />Precipitating Pathologies<br />Other Treatment Strategies<br />Long Term Management<br />
    74. 74. Post–Cardiac Arrest Syndrome: Monitoring Options<br />1. General intensive care monitoring<br />    Arterial catheter<br />    Oxygen saturation by pulse oximetry<br />    Continuous ECG<br />    CVP<br />    ScvO2<br />    Temperature (bladder, esophagus)<br />    Urine output<br />    Arterial blood gases<br />    Serum lactate<br />    Blood glucose, electrolytes, CBC, and general blood sampling<br />    Chest radiograph<br />2. More advanced hemodynamic monitoring<br />    Echocardiography<br />    Cardiac output monitoring (either noninvasive or PA catheter)<br />3. Cerebral monitoring<br />    EEG (on indication / ) : early seizure detection and treatment<br />    CT/MRI<br />
    75. 75. II. Early Hemodynamic Optimization<br /><ul><li>Preload
    76. 76. Arterial Oxygen Content
    77. 77. Afterload
    78. 78. Contractility
    79. 79. Systemic O2 Utilization</li></li></ul><li>II. Early Hemodynamic Optimization<br />Goals:<br />CVP: 8-12 mm Hg<br />MAP: 65-100 mm Hg<br />ScvO2 >70%<br />Hct >30% or Hgb >8g/dL???<br />U/O > 1 ml/kg/hr<br />O2 Delivery Index >600mL/min/m2<br />
    80. 80. II. Early Hemodynamic Optimization<br />Primary Therapeutic Tools:<br />Intravenous fluids<br />Inotropes<br />Vasopressors<br />Blood Transfusion<br />
    81. 81. II. Oxygenation<br /><ul><li>Use of FiO2 of 1.0
    82. 82. Hyperoxia harms postischemic neurons, by oxidative stress</li></ul>Most relevant to post–cardiac arrest care, ventilationwith 100% oxygenfor the first hour after ROSC resulted in worseneurological outcomethan immediate adjustment of the FIO2 toproduce an arterial oxygen saturation of 94% to 96%<br />BalanIS,et al, Oximetry-guided reoxygenation improves neurological outcome after experimental cardiac arrest. Stroke. 2006; 37: 3008–3013<br />
    83. 83. IV. Ventilation<br />Hyperventilation<br /> - cerebral ischemia<br /> - inc. intrathoracic pressure<br />Hypoventilation<br /> - hypoxia & hypercarbia ICP<br /> - metabolic acidosis <br />Ventilationshould be adjusted to achieve normocarbia and should be monitoredby regular measurement of arterial blood gas values.<br />
    84. 84. V. Other Persistent Precipitating Pathologies<br />Pulmonary embolism<br />Sepsis<br />Hypoxemia<br />Hypovolemia<br />Hyperkalemia<br />Metabolic disorders<br />Accidental hypothermia<br />Tension pneumothorax<br />Cardiac tamponade<br />Toxins<br />Intoxication<br />Cerebrovascular catastrophes<br />
    85. 85. VI. Other Treatment Modalities<br />Therapeutic Hypothermia<br /><ul><li>Promising strategy in adult patients
    86. 86. Class IIb recommendation from the AHA
    87. 87. Benefits in pediatrics: remains to be determined</li></ul>Benefits:<br />-decreases CBF<br />-suppresseive effects on excitatory neurotransmission and O2 radicals<br />
    88. 88. Evidence in support of the use of therapeutic hypothermia (32-34°C for 12-24 hrs) immediately after resuscitation from cardiac arrest<br />Rogers Textbook of Pediatric Intensive Care 4th Edition<br />
    89. 89. VI. Other Treatment Modalities<br />2. Sedation and Neuromuscular blockade<br /> - reduces oxygen consumption<br />3. Seizure Control and Prevention<br /> - prevent cerebral injury<br />4. Glucose Control<br /> -tight control:4.4-6.1 mmol/L or 80-110mg/dL.<br />
    90. 90. VI. Other Treatment Modalities<br />5. Adrenal Dysfunction<br /> - use of steroids? : no evidence yet<br />6. Renal Failure<br /> - indications for use of RRT’s: same with that of critically ill patients in general<br />7. Infection<br /> - pneumonia by aspiration or mech. Vent.<br />
    91. 91. VII. Long Term Management<br />cardiac and neurologicalrehabilitation and psychiatric disorders<br />nutrition<br />family counseling<br />
    92. 92. Algorithm for the management and treatment of post-circulatory arrest syndrome in infants and children<br />..<br />Roger’s Textbook of Pediatric Intensive care 4th ed<br />
    93. 93. Findings of Prognostic Value<br />Absence of pupillary light reflex<br />Corneal reflex<br />Facial Movements<br />Eye movements<br />Gag<br />Cough<br />Motor Response to painful stimuli<br />
    94. 94. Findings of Prognostic Value<br />Absence of pupillary light reflex<br />Corneal reflex<br />Facial Movements<br />Eye movements<br />Gag<br />Cough<br />Motor Response to painful stimuli<br />
    95. 95. SUMMARY<br />
    96. 96. THANK YOU!<br />

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