1 / 53

Overview of ACLS

andrew
Télécharger la présentation

Overview of ACLS

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. Overview of ACLS May 2006

    2. Slide 16. Acute Myocardial Infarction Acute myocardial infarction (MI) represents a major health issue in the United States today. About 900,000 people in the U.S. experience an MI each year. Of these, approximately 225,000 die. More than half of them, about 125,000, die “in the field,” before reaching the hospital. Most MI deaths are arrhythmic in etiology.1 Reference 1. Ryan TJ, Anderson JL, Antman EM, et al. ACC/AHA guidelines for the management of patients with acute myocardial infarction. J Am Coll Cardiol. 1996;28:1333.Slide 16. Acute Myocardial Infarction Acute myocardial infarction (MI) represents a major health issue in the United States today. About 900,000 people in the U.S. experience an MI each year. Of these, approximately 225,000 die. More than half of them, about 125,000, die “in the field,” before reaching the hospital. Most MI deaths are arrhythmic in etiology.1 Reference 1. Ryan TJ, Anderson JL, Antman EM, et al. ACC/AHA guidelines for the management of patients with acute myocardial infarction. J Am Coll Cardiol. 1996;28:1333.

    3. Mechanisms of CA 80-90% of non-traumatic cardiac arrests in adults are due to VF or PVT The key action is early defibrillation Most arrests in children are respiratory The key action is ventilation

    4. Success of Defibrillation is Time-Dependent

    5. AED The AED assesses the rhythm and advises shocks for VT/VF After shocks resume CPR and reassess rhythm after 5 cycles (two) minutes If pulse returns, assess and assist breathing

    6. Pulseless VT/VF Witnessed: Consider precordial thump (optional, may be harmful) Unwitnessed: CPR for 2 minutes prior to shock Shock 1 time. Level of energy with monophasic shock: 360 J. Biphasic: 120-200J. Resume CPR immediately after shock. Check rhythm after 2 minutes

    7. Pulseless VT/VF Persists After Shock Start Drugs The key drug in CA mgmt is epinephrine For every type of CA, epinephrine is given every 3-5 minutes until a pulse is restored Vasopressin ( 40 u) may be given instead of the first or second dose of epinephrine Simultaneously, intubate, oxygenate ventilate

    8. CPR Pointers The compresssion rate is 100 per minute. Be sure compressions are full (1 ½-2”) and fast , but be sure that chest recoil is complete between compressions. Hand position is mid-sternal at nipple line

    9. CPR Pointers Minimize all CPR interruptions Once the patient is intubated do not interrupt chest compressions for ventilation Following intubation: Ventilation rate is 8-10 per minute. Do not hyperventilate

    10. Pulseless VT/VF Proceed with a drug/shock sequence. Do CPR for 5 cycles (2 minutes) after a drug is administered, then shock Still in VF: amiodirone 300 mg IV. May give an additional 150 mg if VF persists Minimize interruptions in CPR for pulse checks

    11. Anti-Arrhythmics for PVT/VF After amiodirone: Lidocaine 1-1.5 mg/kg IV, may repeat in 3-5 min (max 3 mg/kg) Magnesium sulfate: 1-2 gm IV for suspected hypomagnesemia or torsades Procaineamide: 30 mg/min or 100 mg q5 min (max 17mg/kg) Consider bicarbonate: 1mg/kg for pre-existing acidosis, drug OD, prolonged code

    12. Endotracheal Drug Adm VALEN: Vasopressin, atropine, lidocaine, epinephrine, naloxone IV administration is preferable: indicated only when iv access cannot be obtained Dose is 2-5X the iv dose. Dilute in sterile water

    13. Central vs Peripheral Line Peripheral iv is preferred because of less interruption of CPR Peripherally administered drugs should be followed by fluid bolus and arm elevation to facilitate delivery to central circulation

    14. 80 yo comes into ER with weakness. On exam he is pale and diaphoretic, but alert and oriented and complaining of weakness. PMH: CABG, diabetes Initial EKG:

    16. Acute anterior MI Initial evaluation

    17. Evaluate ABC If adequate start O2, monitor (EKG and pulse ox), IV (OMI) iv site-antecubital Asa, heparin, pain control cardiology consult

    18. His rhythm changes

    20. What do you want to know?

    21. Stable or unstable-presence of serious signs and symptoms? In this case starts out with BP114/70, ie stable

    22. Treat with amiodarone 150mg iv over 10 minutes and then infusion of 1mg/min Patient remains in VT-develops MS changes and pulse weakens Stable or unstable? Treatment

    23. VT with pulse, unstable-cardiovert This means a synchronized shock-you press the synch button on the defib Consider sedation Start with 100j Patient changes as machine is charging-now pulseless and apneic

    25. Shock 360j (or 200 biphasic) if the sync button is still pressed it won’t work-turn off Do CPR for 2 minutes before checking rhythm Ventilate with BVM and 100% O2, intubate Start iv, give epi or vasopressin

    26. Intubation Secures the airway Allows administration of 100% oxygen and correction of respiratory acidosis Allows administration of some medications (VALEN-3X iv dose) What if you can’t intubate??

    27. Laryngeal Mask Airway

    28. LMA The LMA is inserted by slipping the mask along the palate into the hypopharynx with subsequent inflation of the mask rim

    29. Epi-1 mg q3-5 min or vasopressin 40 units Shock-still VF Amiodarone 300mg-shock, then 150 mg then infusion (max 2.2 grams per 24 hours) Lidocaine 1-1.5 mg/kg. Repeat x1 max 3mg/kg.

    30. How do you check that the ETT is properly placed? How do you know CPR is adequate

    31. ETT placement Listen over both lateral lung fields and the stomach Use end tidal CO2 (but no CO2 if CPR is not adequate)

    32. Adequate CPR Palpable carotid or femoral pulse Pulse oximeter or A-line CO2 production

    33. Vasopressin in CA Half life is 10-20 minutes, so consider waiting at least 10 minutes to give epinephrine Comparing survival in out of hospital arrest, no advantage of vasopressin over epinephrine (in one study, it looked better for asystole)

    34. What if they come back with a pulse but inadequate BP?

    35. Low BP Fluid bolus Dopamine-5 micrograms/kg/min titrate (put 200 mcg in 250cc and start at 30 drops/min)

    36. When to Stop ? CV unresponsiveness You get more info about situation and code status

    37. Asystole/PEA Confirm asystole in more than one lead (use lead select to move between limb leads) Transcutaneous pacing is ineffective for asystole and is no longer recommended Epinephrine: 1mg IV q3-5 min (or vasopressin*) Atropine: 1mg IV q 3-5 min (up to 3 doses)

    38. Consider Causes: 6H’s Hypovolemia Hypoxia Hyper, hypokalemia Hydrogen ions (acidosis) Hypothermia Hypoglycemia

    39. 5T’s Toxins Tamponade, cardiac Tension pneumothorax Thrombosis (pulmonary, coronary) Trauma

    40. PEA Thinking of and correcting one of the reversible causes of PEA early (eg chest tube placement for pneumothorax) can be lifesaving

    41. Improving Survival After Cardiac Arrest After restoration of spontaneous circulation, poor neurologic outcome is one of major causes of death 2 studies have now demonstrated improved neurologic outcome post arrest with the use of mild hypothermia

    42. Mild Hypothermia after VF Arrest 136 patients comatose after VF arrest (the arrest was witnessed) were randomized to mild hypothermia, target 32-34 C measured with a bladder probe. Patients were sedated with fentanyl and midazolam and paralyzed with pancuronium and temperature was maintained for 32 hours

    45. ACLS: Management of Tachycardias and Bradycardias

    46. Bradycardia and Tachycardia Algorithms The main important point is the distinction between stable vs unstable with serious signs and sx including: Hypotension Shock Pulmonary edema Loss of consciousness, confusion agitation MI , angina

    47. Tachycardia with a Pulse Main distinction is wide vs narrow complex tachycardia. Also consider LV function. Assume wide complex tachycardia is VT and treat with amiodarone, lidocaine or procaineamide if stable or synchronized cardioversion if unstable Synchronized cardioversion: sedate first, start with 100j

    48. Wide Complex Tachycardia Always assume it is VT The drugs of choice for stable VT or wide complex tachycardia of unknown origin are amiodarone and procaineamide Adenosine and verapamil are contraindicated for the treatment of wide complex tachycardia

    49. Narrow Complex Tachycardia Identify the rhythm (carotid massage, adenosine), consider cause, duration, LV function Tachycardia may be secondary to fever, dehydration, hypoxemia-treat the underlying cause rather than the rhythm No cardioversion for: sinus tachycardia, MAT, junctional tachycardia Avoid using > one drug

    50. Atrial Flutter-Fibrillation >48h Agents that control rate rather than convert the rhythm are preferred, unless the patient is adequately anticoagulated Normal LV function: diltiazem or beta blockers (I) Abnormal LV function(EF<40%): digoxin, diltiazem or amiodarone (use 1) (IIb)

    51. Atrial Fibrillation <48h Consider cardioversion Normal LV function: IIa: ibutilide, amiodarone, flecainide, procaineamide, propafenone Abnormal LV function: IIb: amiodarone

    52. Bradycardia If hypotensive, prepare for pacing Transcutaneous pacing as a bridge Use drugs to support blood pressure: dopamine or epinephrine drip Never give iv bolus epinephrine for bradycardia with pulse unless you give tiny doses (0.1mg)

    53. Avoid Panic on the First Day of Internship Learn the basics of ACLS including drug doses

More Related