Neurocritical care
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post cardiac arrest neurocritical care in comatose patients
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Neurocritical care
- 1. POST ARREST CARE IN NEURO ICU DR TUSHAR KUMAR PDCC NEUROANAESTHESIA
- 2. BURDEN OF DISEASE • Neurologic injury is a leading cause of death after ROSC. • In- hospital mortality after successful resuscitation is about 70%. • 2/3rd of Remaining 30% live with moderate to severe cognitive defects. • Survival rates for out-of hospital cardiac arrest (OHCA) is 9.5%. • In in-hospital cardiac arrest (IHCA) only 22.3% patients goes home. • 10 to 30 % cardiac arrest survivors progress to vegetative state. • Cost of care is 1 billion dollar per year.
- 3. CANDIDATES FOR NEUROPROTECTION: • WHO??? patients who don’t regain consciousness after ROSC following cardiac arrest. • It could be VF/VT or PEA / asystole followed by coma. • Transient ischemic insult then followed by reperfusion injury. • Series of biochemical events that start, ultimately causing unfavorable outcome.
- 4. WHAT HAPPENS TO BRAIN AFTER CA? • Permanent neuronal damage occurs after 5-10 min of cardiac arrest. • Hypoxic brain has impaired ATP production i. Anaerobic glycolysis ii. Disruption of ion homeostasis iii. Disruption of structural integrity of cells
- 5. WHAT HAPPENS TO BRAIN AFTER CA?
- 6. NEUROPROTECTION AFTER CARDIAC ARREST: • American heart association now recommends Therapeutic hypothermia for comatose patients with ROSC. • OHCA due to VF/VT • IHCA/OHCA due to non- shockable rhythm. • Therapeutic hypothermia (TH) is decreasing the temperature of the target tissue in normothermic patients (mild hypothermia of 33–35°C) or induced normothermia (cooling patients to 37°C) in hyperthermic patients. • It is now referred as TTM ( targeted temperature management) Magnus D.B. et al. A systematic review of neuroprotective strategies after cardiac arrest: from bench to bedside (Part I – Protection via specific pathways).Med Gas Res 2014; 4: 9.
- 8. MECHANISM OF TTM: Global hypoxic insult Decreased ATP production Increased release of glutamate Cell swelling Enzyme induction Membrane degradation Inflammatory mediators DNA damage Mitochondrial damage Microglial activation Leucocyte infiltration Apoptosi s Free radical generation
- 9. PHASES OF TARGETED TEMPERATURE MANAGEMENT: 1. Identification of patient: • Comatose cardiac arrest survivors • GCS < 8 • Patients excluded are: • Reanimated longer than 60 min • ROSC > 6 Hrs • In coma previous to CA • Pregnancy • Active bleed / coagulopathy • Uncontrolled hemodynamically unstable arrhythmias • Major surgery < 14 days • Cardiogenic shock / septic shock. • Terminally ill patients. • Drug over dose. • Pre existing hypothermia (T<34ºC) Rech T H; Vieira S R R. Mild therapeutic hypothermia after cardiac arrest: mechanisms of action and protocol development. Rev. bras. ter. intensiva.2010;22(2):196-205.
- 10. PHASES OF TTM 2. Hypothermia induction: • Target temperature: 32 -34 º C • Best is to keep at 33 º C Monitoring: • ECG • Fluid balance • IBP • Central temperature monitoring Lab test: • CBC • Coagulation profile • S. electrolytes • Arterial blood gas analysis Baseline and every 6-12 hrs M. Tiainen, H.J. Parikka, M.A. Makijarvi, et al., Arrhythmias and heart rate variability during and after therapeutic hypothermiaafter cardiac arrest, Critical Care Medicine 39 (2011) 57 -64. Rech T H; Vieira S R R. Mild therapeutic hypothermia after cardiac arrest: mechanisms of action and protocol development. Rev. bras. ter. intensiva.2010;22(2):196-
- 11. PHASES OF TTM • Not major but mild coagulation changes. • Pulse oxymetry is not accurate. • Monitor oxygenation from ABG • Electrolyte imbalance : causes arrhythmia. k K+ Ca2+ Mg2+ PO4³¯ Replace electrolytes.
- 12. PHASES OF TTM • Sedation and analgesia: • Prevent shivering. • Heat generation counteract with hypothermia. • Increases Oxygen demand and raises ICP. • Use of neuromuscular blockers. • Methods of induction: • Could be invasive or non invasive • Should induce rapid hypothermia • No risk of overcooling / wide temp fluctuations • Non invasive: ice packs, thermal blankets, surface cooling devices, infusion of cold solution. • Unpredictable cooling • Difficult rewarming • Mean time of cooling: 1.4 ºC/ hr.
- 13. PHASES OF TTM • Invasive cooling methods: • Endovascular catheter • Better temperature control for induction, maintenance and rewarming • Rate of cooling: 2 -2.5 ºC/ hr. • But may increase the risk of infection • Risk of deep vein thrombosis • High cost. • Specially trained personnels • At present it is the most efficient method for TH.
- 14. PHASES OF TTM 3. Hypothermia maintenance phase: • Once target temperature achieved : keep for 24 hrs. • Things to remember during maintenance phase: 1. keep MAP >80 mmHg in CA survivors. 2. Correct insulin resistance. 3. No entral feeding: Delayed gastric emptying. Increased risk of VAP / Aspiration pneumonitis. 4. Sedation control : monitor with sedation scores, BIS (Bispectral Index). 5. Seizure activity: May be masked by sedation and NM Blockers. Monitor with EEG ,if available.
- 15. PHASES OF TTM: • When to interrupt: • Signs of awaking • Severe arrhythmias and bleeding • Bradycardia / Osborne waves do not indicate TH discontinuation. • Discontinuation of neuromuscular blockers: • Evaluate after 12 hrs of TH. • If no shivering stop NM blockers.
- 16. PHASES OF TTM 4. Rewarming: • Starts after 24 hours of cooling. • Rate of rewarming: 0.2ºC to 0.4 ºC/hour, for 12 hours, until a temperature between 35ºC and 37ºC is reached. • Methods: active or passive. • Takes 8 hrs to reach 35 ºC. • External cooling devices or endovascular catheters : rewarming speed is setted. • post-reperfusion syndrome: • Hemodynamic instability • Vasodilatation • Hyperkalemia • Hypoglycemia • Stop sedation when temp reaches 35 ºC.
- 18. COOLING METHODS:
- 19. NEUROPROTECTIVE STRATEGIES: • Other srtategies are employed with TH to enhance neurologic outcomes. • Mechanism: 1. Modulating neuronal cell death pathways. 2. Influencing oxygen free radicals. 3. Improving cerebral fluid dynamics. • Xenon and argon : successfully modulate neuronal cell death pathways. dose, initiation time and duration still require further study. • Ischemic post conditioning: reduces reperfusion injury. • CPR assisted with ACD or ITPR: improves cerebral perfusion. • 100% hyperoxia post resuscitation is harmful.
- 20. NEUROPROTECTIVE STRATEGIES: • Pharmacological approaches: • Adenosine: acts as a neurotransmitter • Growth factors/ hormones: • Brain-derived neurotrophic factor (BDNF) • Insulin-like growth factor-1 (IGF-1) and glycine- proline-glutamate (GPE) • Granulocyte colony stimulating factor (G-CSF) • Estrogen • Gas mediator approaches: • Hydrogen sulfide (H2S), hyperbaric oxygen (HBO) and hydrogen gas (H2) exert anti-oxidant, anti-inflammation and anti-apoptosis effects through regulation of variable signaling pathways. • A systematic review of neuroprotective strategies after cardiac arrest: from bench to bedside (Part I – Protection via specific pathways).Med Gas Res. 2014; 4: 9. • Huang l et al. A systematic review of neuroprotective strategies after cardiac arrest: from bench to bedside (part II-comprehensive protection) Med Gas Res. 2014; 4: 10
- 21. WHAT NEEDS TO BE DONE: • Only 30% of patients are treated with TH. • European resuscitation council and ILCOR strongly recommends TH in comatose cardiac arrest survivors from VF or VT. ( level I evidence) • With level IV evidence they also recommends TH for cardiac arrest survivors from non shockable rhythms. • TTM is not a contraindication for PCI. • Newer approaches are still at the level of animal models. • Effects of Cardiac arrest and CPR are not isolated but rather have diffuse systemic ramifications. Knot J et at. Therapeutic hypothermia after cardiac arrest—Part 1: Mechanism of action, techniques of cooling, and adverse events. cor et vasa 54 (2012) :243–247.
- 22. Thank you
Editor's Notes
- Emotional trauma for relatives Financial burden.
- Until recently, the postresuscitation acute management of survivors of cardiac arrest was directed mainly toward the systemic injury, and acute neurologic care focused mainly on prognostication, with some supportive care of neurologic complications.
- The problem with our brain is: Brain has high substrate requirement to generate ATP. Has no storage capacity. Brain constantly requires glucose and oxygen for oxidative phosphorylation. Blockade of substrate supply reduces ATP production by 95%. Anaerobic glycolysis: results in acidosis & free radical production. Disruption of ion homeostasis. Abnormal movement of Na+, K+, Ca2+ Disruption of structural integrity of cells: mitochondrial membrane damage, inhibition of protein synthesis.
- Lactate levels > 20 μmol / L to cause irreversible injury . So, more is the hyperglycaemia more production of lactate. So a diabetic patient being resuscitated after Cardiac arrest is more prone to neuronal injury.
- Mild hypothermia is able to modulate cell processes involving oxidative stress, excitatory amines release and cell necrosis and apoptosis induction, besides to reduce neuronal oxygen consumption. Neuroprotection takes place by several mechanisms.
- Cardiac arrhythmias frequent < 31. and < 28 risk of VT is high. 32 – 34 C easily achieved. Central temperature management: esophageal thermometer, vesical catheter, PA catheter Hypovolumia is very common: as TH causes profuse diuresis.
- Shivering is a normal physiological response, attempting to maintain the body temperature. It is counter-productive, as it generates heat and delays the cooling process, in addition to increase oxygen demand and intracranial pressure. Midazolam and phentanyl are routine drugs. Neuromuscular blockers are frequently required. combination of meperidine (± buspirone), skin warming and magnesium infusion can be used to reduce shivering and avoid thermal discomfort. Infusion of cold fluids at a 30 to 40 mL/kg dose, either peripheral or centrally, is able to induce a temperature drop by 2ºC to 4ºC.
- system uses a special coated metal central venous catheter where water circulates from an external cooler system. The catheter may be installed either via femoral, subclavian or jugular accesses.
- Hypothermia cause insulin resistance. Monitor blood glucose from central blood sample. Feeding is not indicated during TH, as stomach emptying is delayed in these patients. Additionally, there is an increased mechanic ventilation associated pneumonia (VAP) risk for possible aspiration during CA. Strict VAP prevention measures are thus recommended
- Just finish it off…
- Passive rewarming up to a 35ºC central temperature usually takes about 8 hours. If a thermal blanket is used, it should be removed when the temperature reaches 35ºC. If commercial external cooling devices or endovascular catheters are used, the rewarming speed is setted. This is one of the main advantages of these devices, a better control of the rate of temperature changes hemodynamic instability: Vasodilatation: vasopressors. Hyperkalemia stop all potassium and magnesium containing soln Hypoglycemia: stop insulin. When 35ºC is reached, sedation is discontinued. After the TH protocol ends, aggressive fever (if occurring) therapy is recommended, as it is associated with unfavorable outcomes after cardiac arrest 35 ºC.
- Anti excitatory amino acid Active compression decompression Intrathoracic pressure regulator IPC: 4 cycles of 20 seconds of chest compressions followed by a 20 second pause. Dustin B M, Huang L, Applegate P M et al, A systematic review of neuroprotective strategies after cardiac arrest: from bench to bedside (Part I – Protection via specific pathways) Medical Gas Research 2014, 4:9
- through activation of four specific G-protein-coupled adenosine (A) receptors: A1, A2A, A2B and A3 receptors IGF-1 exerts pleiotropic neuroprotection including potent antiapoptotic properties, modulation of BBB permeability and neuronal excitability Activation of hypoxia-inducible factor (HIF)-1α H2 is cost-effective and has low toxicity with little drug-drug interaction. These features could make H2 administration an ideal neuroprotection approach that could be implemented during CPR and/or after ROSC.
- International liaison committee on resuscitation.