ADULT BLS & ACLS : 2015

Presenter- Dr. SUBHANKAR PAUL

Emergency Medicine,
GAUHATI MEDICAL COLLEGE & HOSPITAL
 CONTENTS
• BLS (BASIC LIFE SUPPORT )GUIDELINES
• CPR TECHNIQUE
• CHOKING
• ACLS (ADVANCED CARDIAC LIFE SUPPORT) ALGORHYTHMS
BLS : Healthcare Provider Adult Cardiac
Arrest Algorithm—2015 Update
 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)
 AIRWAY

HEAD TILT – CHIN LIFT JAW THRUST

Breathing

MOUTH TO MOUTH
BREATHING : MOUTH TO MASK
Breathing : AMBU BAG
Automated External Defibrillator
 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
SUMMARY
ADULT CHILDREN INFANTS
CHOKING
 Advanced Cardiac Life Support
• CARDIAC ARREST (PULSELESS ARREST ALGORHYTHM )
• ADULT BRADYCARDIA ALGORHYTHM
• ADULT TACHYCARDIA ALGORHYTHM
• AMI ALGORHYTHM
PULSELESS ARREST ALGORHYTHM
 REVERSIBLE CAUSES of CARDIAC ARREST
H’s T’s
• HYPOVOLEMIA • TENSION PNEUMOTHIRAX
• HYPOXIA • TAMPONADE
• HYDROGEN IONS(ACIDOSIS) • TOXINS
• HYPO/HYPERKALEMIA • THROMBOSIS, PULMONARY
• HYPOTHERMIA • THROMBOSIS, CORONARY
 Cardiac rhythms during Arrest
Shockable Non-shockable
• Ventricular Tachycardia (VT) • PULSELESS ELECTRICAL ACTIVITY
Monomorphic (PEA)
Polymorphic • ASYSTOLE
• Ventricular Fibrillation (VF)
Coarse
Fine ( Close d/d for asystole )
 MONOMORPHIC A
VT R
R
E
POLYMORPHIC S
VT
T

R
COARSE VF H
Y
T
FINE VF H
M
S
SHOCKABLE
A
R
R
E PULSELESS
S ELECTRICAL
ACTIVITY
T

R
H
ASYSTOLE
Y
T
H
M
S
NON-SHOCKABLE
Management of Cardiac
Arrest
CARDIAC ARREST
NON SHOCKABLE RHYTHM ( PEA/ ASYSTOLE )

SHOCK
CPR in PREGNANT FEMALES
 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
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
 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
• 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
 When Should Resuscitative Efforts Stop?
• Withholding and Withdrawing CPR
• (Termination of Resuscitative Efforts)
• Related to In-Hospital Cardiac Arrest
 or Paco 35– 45

(30ml/kg)
To keep MAP>65mm Hg
 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
• 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
 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
 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
 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
ADULT BRADYCARDIA WITH A PULSE
ALGORHYTHM
 RECOGNITION of BRADYCARDIA
SIGNS & SYMPTOMS ECG CHARACTERISTICS
LIGHT-HEADEDNESS SLOW HEART RATE for Age
PRESYNCOPE/SYNCOPE P-Wave may/may NOT be Visible
PALPITATIONS QRS Complex may be Narrow / may
HYPOTENSION be Wide
DECREASED LEVEL OF CONSCIOUSNESS AV Dissociation may be present
SHOCK
POOR END ORGAN PERFUSION
RESPIRATORY DISTRESS /FAILURE
SUDDEN COLLAPSE
NORMAL

SINUS BRADYCARDIA

1ST DEGREE

2ND DEGREE A
MOBIZ TYPE-1 V
(WENCKEBACH
PHENOMENON) B
L
2ND DEGEREE O
MOBIZ TYPE-2 C
K
3RD DEGREE
COMPLETE HEART
BLOCK
 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)
ADULT TACHYCARDIA WITH A PULSE
ALGORHYTHM
 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
SINUS TACHYCARDIA
N
A
SUPRAVENTRICULAR R
TACHYCARDIA R
O
W

ATRIAL FLUTTER

VT MONOMORPHIC
W
I
D
E

VT POLYMORPHIC
ACUTE CORONARY SYNDROME ALGORHYTHM
 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.
CLINICAL FEATURES
 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
 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
 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)
 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

LOCATION WISE CLASSIFICATION
 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
 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
 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.
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
DIAGNOSIS ??

ANS : INFERIOR WALL STEMI

DIAGNOSIS ??

ANS : ANTERIOR WALL STEMI

MANAGEMENT ALGORHYTHM
 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
DRUGS IN STEMI
DRUGS IN NSTEMI
 REFERENCES
• AHA 2015 GUIDELINES : BLS & ACLS
• TINTINALLI’S 8TH EDITION
• HARRISON’S 19TH
• BRAUNWALD’S 10TH
Action in time can save a life!!!

THANK YOU