This document provides guidelines for adult BLS and ACLS. It discusses CPR techniques including compressions at a rate of 100-120 per minute with a depth of 2-4 inches. It also discusses airway management, use of an AED, and monitoring during CPR. The document then summarizes algorithms for pulseless arrest, bradycardia, tachycardia, and acute coronary syndrome. It provides details on the management of different cardiac rhythms and guidelines for prognostication, organ donation, and targeted temperature management after cardiac arrest.

1. ADULT BLS & ACLS : 2015
Presenter- Dr. SUBHANKAR PAUL
Emergency Medicine,
GAUHATI MEDICAL COLLEGE & HOSPITAL

3. CONTENTS
• BLS (BASIC LIFE SUPPORT )GUIDELINES
• CPR TECHNIQUE
• CHOKING
• ACLS (ADVANCED CARDIAC LIFE SUPPORT) ALGORHYTHMS

4. BLS : Healthcare Provider Adult Cardiac
Arrest Algorithm—2015 Update

7. 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)

9. AIRWAY
HEAD TILT – CHIN LIFT JAW THRUST

10. Breathing
MOUTH TO MOUTH

11. BREATHING : MOUTH TO MASK

12. Breathing : AMBU BAG

14. Automated External Defibrillator

15. 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

16. SUMMARY

17. ADULT CHILDREN INFANTS

19. CHOKING

22. Advanced Cardiac Life Support
• CARDIAC ARREST (PULSELESS ARREST ALGORHYTHM )
• ADULT BRADYCARDIA ALGORHYTHM
• ADULT TACHYCARDIA ALGORHYTHM
• AMI ALGORHYTHM

23. PULSELESS ARREST ALGORHYTHM

24. 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

25. 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 )

26. MONOMORPHIC
VT
POLYMORPHIC
VT
COARSE VF
FINE VF
A
R
R
E
S
T
R
H
Y
T
H
M
S
SHOCKABLE

27. PULSELESS
ELECTRICAL
ACTIVITY
ASYSTOLE
A
R
R
E
S
T
R
H
Y
T
H
M
S
NON-SHOCKABLE

28. Management of Cardiac
Arrest

29. CARDIAC ARREST

31. NON SHOCKABLE RHYTHM ( PEA/ ASYSTOLE )
SHOCK

34. CPR in PREGNANT FEMALES

36. 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

37. 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

38. 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

39. • 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

40. When Should Resuscitative Efforts Stop?
• Withholding and Withdrawing CPR
• (Termination of Resuscitative Efforts)
• Related to In-Hospital Cardiac Arrest

41. (30ml/kg)
or Paco 35– 45
To keep MAP>65mm Hg

42. 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

43. • 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

44. 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

45. 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

46. 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

47. ADULT BRADYCARDIA WITH A PULSE
ALGORHYTHM

48. 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

49. 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

50. 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)

53. ADULT TACHYCARDIA WITH A PULSE
ALGORHYTHM

54. 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

55. SINUS TACHYCARDIA
SUPRAVENTRICULAR
TACHYCARDIA
ATRIAL FLUTTER
VT MONOMORPHIC
VT POLYMORPHIC
N
A
R
R
O
W
W
I
D
E

58. ACUTE CORONARY SYNDROME ALGORHYTHM

59. 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.

60. CLINICAL FEATURES

61. 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

62. 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

63. 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)

65. 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

66. LOCATION WISE CLASSIFICATION

67. 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

68. 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

70. 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.

71. 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

73. DIAGNOSIS ??
ANS : INFERIOR WALL STEMI

74. DIAGNOSIS ??
ANS : ANTERIOR WALL STEMI

75. MANAGEMENT ALGORHYTHM

79. 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

82. DRUGS IN STEMI

84. DRUGS IN NSTEMI

86. REFERENCES
• AHA 2015 GUIDELINES : BLS & ACLS
• TINTINALLI’S 8TH EDITION
• HARRISON’S 19TH
• BRAUNWALD’S 10TH

87. Action in time can save a life!!!
THANK YOU