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Adult BLS & ACLS 2015

RECENT MOST GUIDELINES of BLS & ACLS as per AHA GUIDELINES , 2015

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Adult BLS & ACLS 2015

  1. 1. ADULT BLS & ACLS : 2015 Presenter- Dr. SUBHANKAR PAUL Emergency Medicine, GAUHATI MEDICAL COLLEGE & HOSPITAL
  2. 2. CONTENTS • BLS (BASIC LIFE SUPPORT )GUIDELINES • CPR TECHNIQUE • CHOKING • ACLS (ADVANCED CARDIAC LIFE SUPPORT) ALGORHYTHMS
  3. 3. BLS : Healthcare Provider Adult Cardiac Arrest Algorithm—2015 Update
  4. 4. HIGH QUALITY CPR • Position patient on hard surface in supine position • speed of compressions: 100-120/minute • Adequate depth of compressions: 2-2.4” (5-6cm) • Allow complete recoil of chest (avoid leaning • on the chest between compressions) • Ventilate adequately (2 breaths after 30 compressions, each breath delivered over 1 second, each causing chest rise) • Do not over ventilate • Minimal interruptions for ventilation (<10Sec)
  5. 5. AIRWAY HEAD TILT – CHIN LIFT JAW THRUST
  6. 6. Breathing MOUTH TO MOUTH
  7. 7. BREATHING : MOUTH TO MASK
  8. 8. Breathing : AMBU BAG
  9. 9. Automated External Defibrillator
  10. 10. Electrode Placement 4 pad positions • anterolateral, • anteroposterior, • anterior-left infrascapular, and • anterior-rightinfrascapular • For adults, an electrode size of 8 to 12 cm is reasonable • Any of the 4 pad positions is reasonable for defibrillation
  11. 11. SUMMARY
  12. 12. ADULT CHILDREN INFANTS
  13. 13. CHOKING
  14. 14. Advanced Cardiac Life Support • CARDIAC ARREST (PULSELESS ARREST ALGORHYTHM ) • ADULT BRADYCARDIA ALGORHYTHM • ADULT TACHYCARDIA ALGORHYTHM • AMI ALGORHYTHM
  15. 15. PULSELESS ARREST ALGORHYTHM
  16. 16. REVERSIBLE CAUSES of CARDIAC ARREST H’s • HYPOVOLEMIA • HYPOXIA • HYDROGEN IONS(ACIDOSIS) • HYPO/HYPERKALEMIA • HYPOTHERMIA T’s • TENSION PNEUMOTHIRAX • TAMPONADE • TOXINS • THROMBOSIS, PULMONARY • THROMBOSIS, CORONARY
  17. 17. Cardiac rhythms during Arrest Shockable • PULSELESS ELECTRICAL ACTIVITY (PEA) • ASYSTOLE Non-shockable • Ventricular Tachycardia (VT)  Monomorphic  Polymorphic • Ventricular Fibrillation (VF)  Coarse  Fine ( Close d/d for asystole )
  18. 18. MONOMORPHIC VT POLYMORPHIC VT COARSE VF FINE VF A R R E S T R H Y T H M S SHOCKABLE
  19. 19. PULSELESS ELECTRICAL ACTIVITY ASYSTOLE A R R E S T R H Y T H M S NON-SHOCKABLE
  20. 20. Management of Cardiac Arrest
  21. 21. CARDIAC ARREST
  22. 22. NON SHOCKABLE RHYTHM ( PEA/ ASYSTOLE ) SHOCK
  23. 23. CPR in PREGNANT FEMALES
  24. 24. Monitoring During CPR Physiologic parameters • Monitoring of PETCO2 (35 to 40 mmHg) • Coronary perfusion pressure (CPP) (15mmHg) • Central venous oxygen saturation (ScvO2) • Abrupt increase in any of these parameters is a sensitive indicator of ROSC that can be monitored without interrupting chest compressions
  25. 25. Quantitative waveform capnography • If Petco2 <10 mm Hg, attempt to improve CPR quality Intra-arterial pressure • If diastolic pressure <20 mm Hg, attempt to improve CPR quality • If ScvO2 is < 30%, consider trying to improve the quality of CPR
  26. 26. Interventions Not Recommended for Routine Use During Cardiac Arrest • Atropine : Available evidence suggests that routine use of atropine during PEA or asystole is unlikely to have a therapeutic benefit • Sodium Bicarbonate : routine use of sodium bicarbonate is not recommended for patients in cardiac arrest. In some special resuscitation situations, such as preexisting metabolic acidosis, hyperkalemia, or tricyclic antidepressant overdose, bicarbonate can be beneficial
  27. 27. • Calcium : Routine administration of calcium for treatment of in-hospital and out-of-hospital cardiac arrest is not recommended • Fibrinolysis : Fibrinolytic therapy should not be routinely used in cardiac arrest • Pacing : Electric pacing is not recommended for routine use in cardiac arrest • Precordial Thump : The precordial thump may be considered for termination of witnessed monitored unstable ventricular tachyarrhythmias when a defibrillator is not immediately ready for use(Class IIb, LOE B), but should not delay CPR and shock delivery
  28. 28. When Should Resuscitative Efforts Stop? • Withholding and Withdrawing CPR • (Termination of Resuscitative Efforts) • Related to In-Hospital Cardiac Arrest
  29. 29. (30ml/kg) or Paco 35– 45 To keep MAP>65mm Hg
  30. 30. Targeted Temperature Management • comatose adult patients with ROSC after cardiac arrest & in- hospital cardiac arrest should have TTM for “nonshockable”) • Core Temperature Measurement If Comatose • Induce therapeutic Hypothermia ( if no contraindications) • Surface or endovascular cooling • Cold IV fluid Bolus 30 mL/kg • Selecting & maintaining a constant temperature of 32°C–34°C×24 hours • After 24 hours, Slow rewarming 0.25°C/hr • to actively prevent fever in comatose patients after TTM • routine prehospital cooling of patients after ROSC with rapid infusion of cold intravenous fluids is NOT recommended
  31. 31. • An EEG for the diagnosis of seizure should be promptly performed and interpreted, and then should be monitored frequently or continuously in comatose patients after ROSC. • The same anticonvulsant regimens for the treatment of status epilepticus caused by other etiologies may be considered after cardiac arrest
  32. 32. Prognostication After Cardiac Arrest • The earliest time to prognosticate a poor neurologic outcome using clinical examination in patients not treated with TTM is 72 hours after cardiac arrest, but this time can be even longer after cardiac arrest if the residual effect of sedation or paralysis is suspected to confound the clinical examination • In patients treated with TTM, where sedation or paralysis could confound clinical examination, it is reasonable to wait until 72 hours after return to normothermia before predicting outcome
  33. 33. POOR NEUROLOGICAL OUTCOME • Absence of pupillary reflex to light at 72 hours or more after cardiac arrest • Presence of status myoclonus (different from isolated myoclonic jerks) during the first 72 hours after cardiac arrest • Absence of the N20 somatosensory evoked potential cortical wave 24 to 72 hours after cardiac arrest or after rewarming • Presence of a marked reduction of the gray-white ratio on brain CT obtained within 2 hours after cardiac arrest • Extensive restriction of diffusion on brain MRI at 2 to 6 days after cardiac arrest • Persistent absence of EEG reactivity to external stimuli at 72 hours after cardiac arrest • Persistent burst suppression or intractable status epilepticus on EEG after rewarming
  34. 34. Organ Donation • All patients who are resuscitated from cardiac arrest but who subsequently progress to death or brain death should be evaluated as potential organ donors. • Patients who do not achieve ROSC and who would otherwise have resuscitation terminated may be considered as potential kidney or liver donors in settings where rapid organ recovery programs exist
  35. 35. ADULT BRADYCARDIA WITH A PULSE ALGORHYTHM
  36. 36. RECOGNITION of BRADYCARDIA SIGNS & SYMPTOMS  LIGHT-HEADEDNESS  PRESYNCOPE/SYNCOPE  PALPITATIONS  HYPOTENSION  DECREASED LEVEL OF CONSCIOUSNESS  SHOCK  POOR END ORGAN PERFUSION  RESPIRATORY DISTRESS /FAILURE  SUDDEN COLLAPSE ECG CHARACTERISTICS  SLOW HEART RATE for Age  P-Wave may/may NOT be Visible  QRS Complex may be Narrow / may be Wide  AV Dissociation may be present
  37. 37. NORMAL SINUS BRADYCARDIA 1ST DEGREE 2ND DEGREE MOBIZ TYPE-1 (WENCKEBACH PHENOMENON) 2ND DEGEREE MOBIZ TYPE-2 3RD DEGREE COMPLETE HEART BLOCK A V B L O C K
  38. 38. CAUSES • HYPOXIA • HYPOTENSION • ACIDOSIS • ELECTROLYTE IMBALANCE(HYPERKALEMIA) • DRUGS ( β-BLOCKER, CCB, DIGOXIN)/ TOXINS • INCREASED VAGAL TONE • INTRINSIC SA/AV NODAL DISEASE • CONGENITAL HEART/ CONDUCTION DEFECT • CARDIOMYOPATHY/MYOCARDITIS/MI • ACUTE RHEUMATIC FEVER (1st Degree AV Block)
  39. 39. ADULT TACHYCARDIA WITH A PULSE ALGORHYTHM
  40. 40. TACHYCARDIA : RECOGNITION SIGNS/SYMPTOMS • NONSPECIFIC & Differ acc to Age of the Child • Palpitation • Light-headed ness/ syncope • Respiratory distress • Shock • Altered mental status • Sudden collapse with rapid ,weak pulse ECG • HR > FASTER for Age A.NARROW COMPLEX(≤0.09sec) 1. ST (MC) HR 2. SVT( MC tacchyarrythmia cardio- vascular compromise in Infancy) 3. ATRIAL FLUTTER B. WIDE COMPLEX ( ≥0.09sec) 1. VT 2. SVT with Aberrant Conduction
  41. 41. SINUS TACHYCARDIA SUPRAVENTRICULAR TACHYCARDIA ATRIAL FLUTTER VT MONOMORPHIC VT POLYMORPHIC N A R R O W W I D E
  42. 42. ACUTE CORONARY SYNDROME ALGORHYTHM
  43. 43. Acute Coronary Syndrome a constellation of symptoms related to obstruction of coronary arteries with acute chest pain being the most common symptom in addition to nausea, vomiting, diaphoresis etc. Chest pain concerned for ACS is often radiating to the left arm or angle of the jaw, pressure-like in character, and associated with nausea and sweating. Chest pain is often categorized into typical and atypical angina.
  44. 44. CLINICAL FEATURES
  45. 45. Acute coronary syndrome • Based on ECG and cardiac enzymes, ACS is classified into: – STEMI: ST elevation, elevated cardiac enzymes – NSTEMI: ST depression, T-wave inversion, elevated cardiac enzymes – Unstable Angina: Non specific ECG changes, normal cardiac enzymes
  46. 46. Universal Definition of Myocardial Infarction • The term acute myocardial infarction (MI) should be used when there is evidence of myocardial necrosis in a clinical setting consistent with acute myocardial ischemia. Under these conditions, any one of the following criteria meets the diagnosis for MI • Detection of a rise and/or fall of cardiac biomarker values (preferably cardiac troponin [cTn]) with at least one value above the 99th percentile upper reference limit (URL) and with at least one of the following: • • Symptoms of ischemia • • New or presumed new significant ST-segment T-wave (ST-T) changes or new left bundle branch block (LBBB) • • Development of pathologic Q waves in the electrocardiogram (ECG) • • Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality • • Identification of an intracoronary thrombus by angiography or autopsy
  47. 47. Classification of Myocardial Infarction • Type I: Spontaneous Myocardial Infarction • Type 2: Myocardial Infarction Secondary to an Ischemic Imbalance • Type 3: Myocardial Infarction Resulting in Death When Biomarker Values Are Unavailable • Type 4a: Myocardial Infarction Related to Percutaneous Coronary Intervention (PCI) • Type 4b: Myocardial Infarction Related to Stent Thrombosis • Type 5: Myocardial Infarction Related to Coronary Artery Bypass Grafting (CABG)
  48. 48. ECG  STEMI: Q waves , ST elevations, hyper acute T waves; followed by T wave inversions. Clinically significant ST segment elevations: > than 1 mm (0.1 mV) in at least two anatomical contiguous leads  or 2 mm (0.2 mV) in two contiguous precordial leads (V2 and V3) Note: LBBB and pacemakers can interfere with diagnosis of MI on EKG
  49. 49. LOCATION WISE CLASSIFICATION
  50. 50. ECG • NSTEMI: – ST depressions (0.5 mm at least) or T wave inversions ( 1.0 mm at least) without Q waves in 2 contiguous leads with prominent R wave or R/S ratio >1. – Isolated T wave inversions: • can correlate with increased risk for MI • may represent Wellen’s syndrome: – critical LAD stenosis – >2mm inversions in anterior precordial leads • Unstable Angina: – May present with nonspecific or transient ST segment depressions or elevations
  51. 51. Unstable Angina • Occurs at rest and prolonged, usually lasting >20 minutes • New onset angina that limits activity • Increasing angina: Pain that occurs more frequently, lasts longer periods or is increasingly limiting the patients activity
  52. 52. Cardiac Enzymes • Troponin is primarily used for diagnosing MI because it has good sensitivity and specificity. – CK-MB is more useful in certain situations such as post reperfusion MI or if troponin test is not available • Other conditions can cause elevation in troponin such as renal failure or heart failure • The increasing troponin trend is the important thing to look for in diagnosing MI. Order Troponin together with ECG when doing serial testing to rule out ACS.
  53. 53. Levels of cTnI and cTnT may remain elevated for 7–10 days after STEMI. CK rises within 4–8 h and generally returns to normal by 48–72 h
  54. 54. DIAGNOSIS ?? ANS : INFERIOR WALL STEMI
  55. 55. DIAGNOSIS ?? ANS : ANTERIOR WALL STEMI
  56. 56. MANAGEMENT ALGORHYTHM
  57. 57. Thrombolysis in Myocardial Infarction Thrombosis in Myocardial Infarction (TIMI) score is a seven item tool that helps stratify patients with potential ACSs in the ED. Patients with a score of 0 to 2 have a 2% to 9% 30-day risk of death, myocardial infarction, or revascularization. Patients with higher scoreshave higher risks
  58. 58. DRUGS IN STEMI
  59. 59. DRUGS IN NSTEMI
  60. 60. REFERENCES • AHA 2015 GUIDELINES : BLS & ACLS • TINTINALLI’S 8TH EDITION • HARRISON’S 19TH • BRAUNWALD’S 10TH
  61. 61. Action in time can save a life!!! THANK YOU

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