Post Cardiac Arrest Care American Heart Association Guidelines 2015 Dr. Ankit Jain
Primary Assessment – The ABCs Airway secured during CPR? Advanced Airway for Comatose patients Ensure patency and adequacy of airway. Avoid neck ties 30° Head High if acceptable Aspiration Risk Cerebral Oedema VAP
Primary Assessment – The ABCs Most patients mechanically ventilated Strategy for ventilator management Assess PCO2 using ABG ETCO2 using Quantitative waveform capnography Maintain Normocapnia PCO2 30-40 mm Hg ETCO2 35-45 mm Hg.
Primary Assessment – The ABCs Avoid hyperventilation. Hyperventilation→↓PCO2→Cerebral Vasoconstriction→ Cerebral Oedema→Poor Neurological Outcome Hyperventilation→↑PEEP→Hyperinflation→ ↑Intrathoracic Pressure→↓Preload→Hypotension Unless…… ↑PCO2 eg ALI, High airway pressure ↓PCO2 (Mild) eg. Raised ICP
Primary Assessment – The ABCs Oxygenation The issue of hyperoxia. (PaO2 >300 mmHg) Absorptive atelectasis, accentuation of preexisting hypercapnia, airway injury, parenchymal lung injury, and extrapulmonary toxicity. Hyperoxia may cause coronary vasoconstiction. Mediated by reactive oxygen species, which can promote inflammation and induce cell death.
Primary Assessment – The ABCs A Reasonable guideline… Preventing hypoxic (PaO2 <60 mm Hg) episodes with their ESTABLISHED side effects is more important than avoiding any POSSIBLE risks of hyperoxia. Use highest possible FiO2 until PaO2/SpO2 available; then titrate asap to an SpO2 of 94% or PaO2 60 mmHg. (Peripheral vasoconstriction post cardiac arrest may make SpO2 measurements unreliable. )
Primary Assessment – The ABCs Secure IV access if not secured during CPR Patients often hemodynamically unstable. How? Fluids vs Vasopressors?? No consensus. Use your clinical acumen.
Primary Assessment – The ABCs BP Goals Maintain End Organ perfusion MAP>65 mm Hg to reverse shock. MAP 80-100 mm Hg for cerebral perfusion. ↑MAP ↓MAP Reverse Acute Shock State Optimize Cerebral Perfusion Maintain CVP Adequate Urine Output Overstressing a Decompensated Heart
Primary Assessment – The ABCs Fluids Isotonic Saline or RL RL avoids Hyperchloremic Acidosis. Avoid Hypotonic fluids → Exacerbate Cerebral oedema. Target central venous pressure (CVP) of 8 to 12 mmHg. Adjuvant for TTM.
Primary Assessment – The ABCs Vasopressors Once an adequate CVP has been established patients whose MAP remains below 80 mmHg generally need treatment with an inotropic agent or vasopressor. Prior to CVP monitoring, it is reasonable to start vasoactive drugs in patients with hypotension that does not resolve after a rapid infusion of 2 liters of isotonic crystalloid. Choice of Vasopressor agent?? No superiority of any one agent in post arrest patients. IABP Role of Advanced cardiac monitoring. Targets for other hemodynamic or perfusion measures (such as cardiac output, mixed/central venous oxygen saturation) remain undefined in post–cardiac arrest patients.
CORONARY REVASCULARISATION POST CARDIAC ARREST
CORONARY REVASCULARISATION ACS common cause of out of hospital cardiac arrest. Obtain 12 lead ECG as soon as possible after ROSC after cardiac arrest. Emergent (same day) coronary catheterization if ST segment elevation myocardial infarction (STEMI) or new left bundle branch block (LBBB).
CORONARY REVASCULARISATION Non ST elevation on initial ECG High Incidence of CAD in OHCA due to VF or PVT. (435 patients; 70% CAD) Raising Troponin levels, RWMA on 2DEcho, hemodynamic instability due to cardiogenic shock.
CORONARY REVASCULARISATION CAG and COMA TTM not a contraindication to CAG. CAG NEURO PROGNOSTICATION Of ROSC <24 HOURS Benefit >72 HOURS
Targeted temperature management NEUROLOGIC CARE
TARGETED TEMPERATURE MANAGEMENT Why? Only intervention that has proven to improve neurological recovery after ROSC. High neurologic morbidity and mortality without any specific interventions. Temperature is an important variable for neurologic recovery. Who? Comatosed patients (No meaningful response to VC) with ROSC post cardiac arrest.
TARGETED TEMPERATURE MANAGEMENT Contraindications?? Essentially no patients in whom temperature control between 32 C and 36 C is contraindicated. Change from earlier guidelines Target temperature 32 to 34 Lead to various Contraindications Eg. Pregnancy, hemodynamic instability, active bleeding
TARGETED TEMPERATURE MANAGEMENT What temperature exactly? 32 C-36 C Higher temperatures in patients for whom lower temperatures pose some risk and vice versa. Temperature at onset.
TARGETED TEMPERATURE MANAGEMENT How long? No direct comparisons of different durations of TTM in post–cardiac arrest patients. The largest trials and studies of TTM maintained temperatures for 24 hours or 28 hours followed by a gradual (approximately 0.25ºC/hour) return to normothermia
TARGETED TEMPERATURE MANAGEMENT Methodology Measure Core body temperature Oesophageal Bladder PA No surface temperature. Cooling Techniques Intravascular Cooling Cold Saline @4 C Endovascular Catheters Surface Cooling Ice packs, cooling blankets, cooling vests, and cold water immersion.
TARGETED TEMPERATURE MANAGEMENT PRECAUTIONS: Shivering Natural response to hypothermia. Sedation and Analgesia via IV Boluses and Infusions to prevent pain and discomfort. Choose agent with short half life as elimination delayed in hypothermia Increases metabolism and delays achievement of target temperature. Usually between 35 and 37 C. Reduces once target temperature reached. Increase dose of sedatives/anesthetic agents. Neuromuscular Blocking agents Infusion or boluses. NMB may mask seizure activity, common cause of coma. Use EEG.
TARGETED TEMPERATURE MANAGEMENT PRECAUTIONS: Hemodynamics Initial Tachycardia and Hypertension during initiation of hypothermia due to shivering and cutaneous vasoconstriction. Then Bradycardia (prolonged PR, QTc, Sinus, junctional or ventricular rhythm). Treat bradycardia only if with hypotension. Target MAP>90 mm Hg. Target CVP 10-12 Rewarming may cause hypotension. Treat arrythmias as per medical protocol. Increase target temperature if arrhythmia or hypotension persists.
TARGETED TEMPERATURE MANAGEMENT PRECAUTIONS: Oxygenation and Ventilation. Mechanical Ventilation mandatory. PaO2 94-96 Avoid prolonged FiO2of 100 as it may ppt reactive oxygen radicals and neuronal damage. Ventilation to target normocarbia. Glucose Hyperglycemia secondary to reduced insulin secretion and resistance in hypothermia. Hypoglycemia during rewarming. Monitor sugars hourly. Stop Insulin if glucose <200 mg/dL. Potassium Hypothermia causes intracellular shift of potassium and hypokalemia. Monitor 4 hourly. Potassium replacement to target S.K of 3.5 mEq/L. Stop replacement 4 hours prior to initiating rewarming. Hyperkalemia during rewarming as efflux of potassium from cells.
TARGETED TEMPERATURE MANAGEMENT Rewarming After Therapeutic Hypothermia Begin 24 hours after initiation of cooling/ achieving target temperature. Rewarming at a rate of 0.25C per hour until normothermia 37 C. Watch for Hypotension, Hypoglycemia, Hyperkalemia. Avoid Hyperthermia which can be detrimental. Neurological evaluation 72 hours after normothermia as delayed neurological recovery after TH.
GLYCEMIC CONTROL No data suggest that the approach to glucose management chosen for other critically ill patients should be modified for cardiac arrest patients.
Other Investigations Chest Xray Respiratory dysfunction common after Cardiac arrest Pulmonary oedema secondary to LV failure. Aspiration during arrest or resuscitation. Complications of Chest Compressions Rib fractures. Pnueumothorax Lines and Tubes.
Identify and Treat Cause of Cardiac Arrest Remember 5 H and 5 T Fibrinolysis during or after CPR does not pose an unacceptable risk! 5 H 5 T Hypoxia Toxins Hypovolemia Tamponade H+ Ions Tension pneumothorax Hyper/Hypo Kalemia Thrombosis (Pulmonary) Hypothermia Thrombosis(Coronary)
Thank You. ANY QUESTIONS??