1 / 54

CARDIAC ARREST

CARDIAC ARREST. DR. PRAKASH MOHANASUNDARAM Emergency & Critical care Physician Vinayaka Mission University SALEM. What is cardiac arrest?. Abrupt cessation of cardiac pump function which may be reversible by a prompt

nevaeh
Download Presentation

CARDIAC ARREST

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. CARDIAC ARREST DR. PRAKASH MOHANASUNDARAM Emergency & Critical care Physician Vinayaka Mission University SALEM

  2. What is cardiac arrest? Abrupt cessation of cardiac pump function which may be reversible by a prompt intervention but will lead to death in its absence

  3. NO Central Pulse

  4. Scenario 1 He was about to be shifted to the cathlab when he suddenly became drowsy and then unconscious

  5. CALL FOR HELP CHECK FOR RESPONSE OPEN THE AIRWAY CHECK FOR BREATHING

  6. NO BREATHING CHECK FOR CENTRAL PULSE GIVE 2 RESCUE BREATHS NO CENTRAL PULSE KEEP DEFIB PADDLES CHECK RHYTHM

  7. Identify the rhythm

  8. What is VF? Coarse fibrillatory waves Chaotic electrical activity If flatline increase gain - fine VF

  9. Identify the rhythm

  10. Ventricular tachycardia(VT) QRS has a wide morphology Rate is typically from 100-200 bpm P waves are hidden if present Can deteriorate rapidly to VF

  11. Polymorphic VT The QRS morphology keeps varying If preceded by a prolonged QT interval when in sinus rhythm – Torsades de pointes

  12. Primary ABCD Survey Basic Life Support: Airway Breathing Circulation Attach monitor/defibrillator

  13. Check rhythm Shockable Not Shockable VF/VT Aystole/PEA

  14. VF/Pulseless VT Give 1 shock Biphasic: 120 to 200 J Monophasic: 360 J Give the highest energy in that equipment Resume CPR immediately

  15. PADDLE PLACEMENT

  16. Persistent VF/Pulseless VT Give 1 shock Resume CPR Give vasopressor Epinephrine 1 mg IV repeat every 3 to 5 minutes OR Vasopressin 40 U IV

  17. If rhythm persists Consider antiarrhythmics

  18. Amiodarone – Class II b Na ,K and Ca channel blocker Also alpha and beta adrenergic effects 300 mg IV bolus followed by 1 dose of 150 mg IV If perfusing rhythm achieved: 1 mg/min for next 6 hrs 0.5 mg for next 18 hrs Preferred through central line

  19. Lidocaine – Class Indeterminate The initial dose 1 to 1.5 mg/kg IV push If VF / pulseless VT persists additional doses 0.5 to 0.75 mg/kg IV push 5 to 10min interval Maximum dose of 3 mg/kg

  20. Magnesium – Class IIa Polymorphic VT associated with prolonged QT interval (torsades de pointes) 1-2gm IV/IO in 10 ml of 5D over 5-20 mins If with pulse same 1-2gm in 100ml of 5D over 20-60 mins

  21. Reduce interruptions as much as possible !!!!!!!

  22. Key points of CPR Provide CPR while the defib is charging Push hard and push fast Allow chest recoil Minimize interruption during chest compressions Check rhythm only after delivery of 5 cycles / 2mins of CPR after shock delivery

  23. Vasopressor to be delivered only after 1 or 2 shocks Palpate for pulse if organized rhythm appears. If patient in hypothermic(< 30 deg C) with hold vasopressors until rewarmed.

  24. With advanced airway, compressions at 100/min ventilations at 8-10 breaths /min Avoid fatigue by rotation Drugs in peripheral lines- 20 ml chase fluids and elevate limb. Rule out the 6Hs and 5Ts.

  25. Causes of pulseless arrest-6Hs Hypovolemia Hypoglycemia Hypoxia H+ ion - acidosis Hypothermia Hypo / hyperkalemia

  26. 5Ts Tension Pneumothorax Toxins Trauma Tamponade - cardiac Thrombosis

  27. Scenario 2 A 65 year old male was admitted in the ICU with a diagnosis of hemorrhagic stroke, on ventilator support Suddenly nurse noticed a fall in the GCS and alerted you You find that there is no central pulse and the monitor shows this rhythm

  28. Pulseless Electrical Activity (PEA) Pulseless patients with minimal electrical activity Force of contractions not enough to produce a perfusing rhythm Often caused by reversible conditions Treat the cause(6Hs and 5Ts)

  29. What to do if you see this?

  30. Asystole Check the pulse Check the leads first! Change the leads Increase the gain. Why? PLEASE DON’T DELIVER SHOCK

  31. Evidence for no shock In 1989 Losek- 49 children in asystole delivered shock with no positive results 1993 Nine city high dose epinephrine study group- “no benefit from shock for asystole” CIRCULATION 2005

  32. PEA and Asystole May give 1 dose of vasopressin 40IU to replace 1st or 2nd dose of adrenaline A,B,C, start CPR IV/IO give inj.adrenaline 1mg(repeat every 3-5 mins) Atropine 1mg IV when slow PEA / Asystole Max 3 doses PEA / Asystole VF / VT Go to shockable rhythm management Check rhythm after 5 cycles of CPR If NSR go to post resuscitation care

  33. Management of PEA / Asystole Focus on high quality CPR Airway ASAP Minimize interruptions in chest compressions Deliver IV/IO medications once CPR is started Epinephrine every 3-5 mins Atropine is 1mg , max of 3 doses Vasopressin can replace adrenaline during the first or second dose

  34. Causes of Pulseless arrest Hypovolemia Hypoxia Hydrogen ion Hypo/ hyperkalemia Hypoglycemia Hypothermia Toxins Tamponade ,cardiac Tension pneumothorax Thrombosis (coronary/pulmonary) Trauma

  35. The drugs in cardiac arrest Epinephrine Vasopressin Atropine Amiodarone Magnesium Lidocaine

  36. Class I Class II -a Class II - b Class - Indeterminate Class III Definitely useful Probably useful Possibly useful No supporting evidence Harmful Classification of ACLS drugs

  37. Epinephrine – Class II b Alpha adrenergic effects- beneficial But Beta adrenergic effects increase myocardial oxygen demand and also reduces subendocardial perfusion 1mg IV/IO every 3-5 mins If IO/IV unable to get, ET tube dose of 2-2.5mg

  38. Vasopressin – Class Indeterminate Noradrenergic peripheral vasoconstrictor that also causes coronary and renal vasoconstriction Benefit no better than epinephrine in survival Significantly less neurological deficit 40 IU IV / IO

  39. Atropine – Class Indeterminate Atropine reverses cholinergic mediated, decrease in heart rate Asystole could be precipitated by excessive vagal tone 1 mg every 3-5 mins upto max of 3 mg

  40. Buffers Adequate Oxygenation & Ventilation is the best buffer Soda bicarb- only buffer authorised for use (Class II b) Acidosis – accumulation of CO2 and lactate No adequate tissue perfusion during prolonged CPR or late start

  41. How does it work Corrects acidosis, improves vascular response Decreases defibrillation threshold Post resuscitation- increases myocardial contractility

  42. Cont… Currently no evidence for empirical use! Supported only in hyperkalemia(CRF), TCA overdose or preexisting metabolic acidosis 0.5-1 meq/kg over 10 mins or ABG guided.

  43. Pediatric arrest 2 rescuers 15 : 2 CPR technique Drugs: No atropine in PEA/ Asystole 2 Joules / kg then 4 joules/ kg

  44. DRUGS Adrenaline 0.01mg/kg IV/IO 0.1 mg/kg ET Amiodarone 5mg/kg upto 15/mg/kg max of 300 mg.

  45. Neonate arrest Start CPR when HR Less than 60 bpm Ratio is 3 : 1 Turn the mask Adrenaline 0.01mg/kg IV 0.1 mg/kg in ET

  46. Definite NO NOs Precordial thump Procainamide in VF Nor adrenaline - worse neurologic outcomes Volume expansion with IV fluids Pacing in asystole

  47. Be prepared Emergency drugs kit Airway kit Regular drills Team work Debriefing

  48. Summary Anticipate Remember to change leads and increase gain in Asystole Basics of CPR Please don’t shock Asystole / PEA Constant update

More Related