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Advanced Cardiac

Life Support
dr. Atep Supriadi

The 3 Unequivocally Effective


Interventions
Basic cardiopulmonary resuscitation
Oxygenation and ventilation of the
lungs through a patent secure airway
Defibrillation for ventricular
fibrillation or pulseless ventricular
tachycardia

Airway Adjuncts
Oropharyngeal airways
Nasopharyngeal airways
Laryngeal mask airway
64-100% success

Combitube
69-100% success

Cuffed oropharyngeal
airways (COPA)
Suction devices

Combitube

Endotracheal Intubation
Optimal airway

Secure and clear airway


Protect airway
No gastric inflation
Drug
Bronchial toilet

Need 3 minutes of preoxygenation


Ventilation should not be interrupted for > 30
seconds
Cricoid pressure
Use of stylet or gum elastic bougie
Confirm and secure tube position

Breathing

FiO2 of 1.0
Manual resuscitators or ventilators
12-15 breaths/minute
Tidal Volume
10-12 ml/kg, if intubated
6-7 ml/kg, if not unintubated

Circulation
Closed chest compression at
100/minute
Open chest CPR should be restricted
to operating theatre and selected
instances of penetrating thoracic
injury

Routes of Drug
Administration

Peripheral veins
Central veins
Tracheal
Intraosseous
Intracardiac

Peripheral Venous Route


Peak effect 1.5-3 min. after injection
at antecubital fossa
IV push
20 ml NS flush after drug injection
circulation time by 40%
Comparable to drug delivery through a
central vein

Tracheal Route
Second line route due to impaired absorption and
unpredictable pharmacodynamics
Need 2-3 times the IV dose, diluted to at least 10
ml in 0.9% NS
Non-ionic drugs only:
adrenalin, atropine, lignocaine and naloxone

NEVER calcium or sodium bicarbonate

Cardiovascular Physiology
Review
Cardiac Output = Heart Rate x
Stroke Volume
Stroke Volume is affected by
Preload, Afterload, & Contractility
Preload then Stroke Volume
Afterload then Stroke Volume
Contractility then Stroke Volume

Blood Pressure = Cardiac Output


x Afterload

Acetylcholine Overview and


Effects
Heart Decrease in
Heart Rate by
Reducing the Firing
Rate of the SA
node and
Increasing
Conduction Time
through the AV
node.
Blood Vessels
Cause Mild
Dilatation of Blood

Cholinergic Antagonists Atropine


Atropine
Blocks Muscarinic Receptors Post-Ganglionic Receptors
in Parasympathetic Transmission
SA Node Effects - Increase Firing Rate
AV Node Effects Decrease Conduction Time
Overall Increased Heart Rate, Minimal BP Effect
No Effects on Transplanted Hearts
Indications for Atropine
Symptomatic Bradycardia (i.e. hypotension), asystole,
Pulseless Electrical Activity (PEA) if rate is slow.
Treatment of Choice for Hemodynamically Significant
Bradycardia
Pacing is Preferable for Severe Bardycardia

Reference: Grauer Page 78

Alpha Adrenoreceptor
Review
1 Receptors Stimulation leads to
Constriction of Vascular
Smooth Muscle,
primarily Skin and
Splanchnic vessels.
Increases Peripheral
Vascular Resistance
(PVR).

2 Receptors
Stimulation Inhibits NE
Release

Beta Adrenoreceptor Review


1 Receptors Stimulation Results
in Increased Heart
Rate, Conduction
Velocity and
Contractility
2 Receptors Relaxation of
Vascular Smooth
Muscle, Skeletal
Muscle and Bronchial
Smooth Muscle. ???
Effects on PVR

Epinephrine
Stimulates and Adrenergic Receptors
Low Doses - Effects Predominate
High doses, effects Predominate.
Increases Heart Rate, Increased Contractility.
Net Effect - Increase in Cardiac Output due to
effect of 1 Receptor
Constricts Arterioles of Skin, Mucous Membranes, and
Viscera.
Net Effect Increase in PVR due to effect of 1
Receptor
If Given at LOW Dose, may see a Slight Drop in
Diastolic Blood Pressure because of 2 Dilatory Effects
may Dominate Receptor Effects
Indication Ventricular Fibrillation, Pulseless
Ventricular Tachycardia, Asystole, PEA, Severe
Symptomatic Bradycardia

Reference: Grauer Page 75

Norepinephrine (ContD)

NE Indications
Sepsis to improve Renal Blood Flow and Urine Output
Severe Hypotension (Systolic <70) and Low PVR who
Fail to Respond to Less Potent Adrenergic Agents
such as Dopamine, Phenylephrine, or Methoxamine

Dopamine

Binds , , and Dopamine Receptors.


Effects via Adrenergic Receptors are Dose
Dependent
Low Doses (1-2 g/kg/min) - Activation of D1
receptors which Results in Dilation of the Renal and
Mesenteric Blood Vessels
Little Hemodynamic Effect, Urine Output is not
Appreciably Increased
Moderate Dose (2-10 g/kg/min) - Predominant 1
Effect
Increased Contractility, Some Increase in HR,
Increased Cardiac Output
Modest Effect on PVR and BP
High Dose (above 10 g/kg/min) - Predominant
Effect
Increased BP
Reference: Grauer Page 77

Dopamine
(ContD)
Indications
Symptomatic Bradycardia
(i.e.hypotension) not
responding to Atropine
(pacing unavailable)
Cardiogenic Shock
If you have Severe
Bradycardia (ie slow
ventricular escape with a
barely palpable pulse)
physicians favor
Epinephrine Infusion

Adrenergic Antagonists
Blockers Not Part of ACLS Protocol
Blockers Can Block 1 and/or 2. Can be Combined with
Blockers.
Metoprolol, Atenolol, and Esmolol are 1 Selective
Propanolol is 1 and 2 Selective
Esmolol, Metoprolol, and Propanolol are IV Agents
Propanolol, Atenolol, and Metoprolol are Oral Agents
Indications for Blockers
Acute Myocardial Infarction (MI) Mortality Reduced
because of lower risk of Ventricular Fibrillation
Drug Choice for Benign Premature Ventricular
Contractions (PVCs), Selected Cases of Refractory
Ventricular Tachycardia(VT) and Ventricular Fibrillation (V
Fib) (Due to Excess Sympathetic Tone)
Supraventricular Tachycardias (SVTs)
Reference: Grauer Page 89

Beta Blockers
What Effects will They Have?
SA Node Effects - Decreased Firing
Rate
AV Node Effects Increased
Conduction Time
Overall Decreased Heart Rate,
Decreased Contractility, Decreased
BP

Nitrates
Nitrates are used for their ability to relax vascular
smooth muscle. Nitroglycerin is the initial treatment of
choice for suspected ischemic-type pain or discomfort.
Action of Nitroglycerin is Mediated through Local
Endothelial Production of Nitric Oxide, particularly in
the Venous Capacitance System.
Sub Lingual, Oral, Topical and IV.
Can Drop the BP so Check BP Before Administration
Can Produce Tachycardia, Paradoxical Bradycardia,
Hypoxemia caused by Increased Pulmonary VentilationPerfusion Mismatch, and Headache.
Avoid if Patient has used Viagra or Levitra within Past
24 Hours

Calcium Channel Blockers


Two Main Categories: Dihydropyridine (Amlodipine)
and Non-Dihydropyridine (Verapamil, Diltiazem)
Non-Dihydropiridines are used in ACLS. By Blocking
Certain Calcium Channels they:
Decrease the Force of Cardiac Contraction
Decrease the Rate of SA Node Firing
Increase Conduction Time Through the AV Node
Relax Vascular Smooth Muscle.
Can be Used to Treat HTN, Coronary Spasms, SVTs (A
Fib, A Flutter, PSVT, and MAT)
DO NOT GIVE an IV Blocker with IV
Verapamil/Diltiazem (Excessive Bradycardia or
Asystole)

Digoxin
Half-Life is 36 Hours in Young Adult, 5 Days in Old Adult
with Renal Failure
Inhibits the Na/K pump. This Leads to an Increase in
Intracellular Na, thereby Driving the Na/Ca Exchanger,
Resulting in Increased Intracellular Ca.
Increases contractility, decreases the speed of
conduction and firing of SA node
Increases Vagal (Parasympathetic) Tone
Indications Limited
Rapid A Fib / A Flutter Slows the Ventricular
Response
Does not convert A Fib any better than Placebo (50%
Spontaneous Conversion within 24 Hours)
Less Likely to Work if Sympathetic Tone is Increased

Antiarrhythmics

There are Many Antiarrhythmics and the Different


Mechanisms of Action are Way Beyond the Scope of
This Class
All Interact with Electrolyte Channels in Atrial Muscle
and/or Ventricular Muscle and/or SA Node and/or AV
Node and/or Purkinjie Fibers
Brief Strong Points
Magnesium Treatment of Choice for Torsades de
Pointes
Amiodarone Cardiac Arrest for Refractory V Fib and
Sustained V Tachycardia Antiarrhythmic of 1st
Choice
Also SVTs (Atrial Tachycardias, Wolf Parkinson
White (WPW) Rhythms, A Fib/ A Flutter

Antiarrhythmics
Class I Sodium Channel Blockers:
Procainamide, Lidocaine, Flecainide,
Propafenone
Class II Blockers
Class III K Channel Blockers: Amiodarone,
Sotalol, Ibutilide.
Class IV Calcium Channel Blockers: Non
Dihydropyridines.
Other Adenosine, Digoxin, Magnesium
Sulfate

Adrenaline
Adrenaline 1 mg (10 ml of 1:10,000
dilution) IV boluses every three minutes
until pulse returns
Short half life of 3-5 minutes
-effect (vasoconstriction)
aortic pressure to maintain myocardial
and cerebral blood flow

Vasopressin

40 U IV: powerful vasoconstriction


V1 receptors in smooth muscle

Longer half-life of 10-20 minutes


If there is no response 10-20 min. after 40 U of IV
vasopressin, resume epinephrine 1 mg IV push
every
3 to 5 minutes
Used in VF/VT
? role in asystole or PEA

Drugs for Persistent VF


Amiodarone
Class IIb
Rapid infusion of 300 mg in 20-30 ml NS IV push
(cardiac arrest dose)
If VF/pulseless VT recurs,
Supplementary doses of 150 mg IV by rapid infusion
Followed by 1 mg/min for 6 hours and then 0.5
mg/min
Maximum daily dose of 2 g

Atropine
Good for haemodynamically
significant bradycardia from high
vagal tone, hypoxia or nodal
ischaemia
? For asystole or PEA
1 mg up to 3 doses or single dose of
3 mg will produce a fully vagolytic
effect

The Universal Advanced Life


Support Algorithm
Two arrest rhythms
VF/Pulseless VT
Ventricular fibrillation
Pulseless ventricular tachycardia

Non-VF/VT
Pulseless electrical activity
Asystole

Defibrillation Energy
Adults
200J 200/300J 360J 360J thereafter
(monophasic)
Non-escalating 200J (biphasic)

Children
2J/kg 2-4J/kg 4J/kg 4J/kg thereafter

Possible Underlying Reversible


Causes

Hs
Hypovolemia
Hypoxia
Hydrogen ion
(acidosis)
Hyperkalemia/
hypokalemia/
metabolic disorders
Hypothermia/
hyperthermia

Ts
Toxins/tablets
(drug overdose)
Tamponade, cardiac
Tension pneumothorax
Thrombosis, coronary
Thrombosis,
pulmonary

New Recommendations
2 breaths chest compressions
All breaths (mouth-mouth, mouth-bag,
bag-mask) given over 1 sec see chest
rise
Longer uninterrupted chest compression
Compression:Breath (30:2)
Push hard and push fast (100/minute)
2 min of compression before rhythm/pulse
check in pulseless arrest
Pulseless VF/VT: 1 shock (instead of
stacked)

CPR
Compress at the center of the chest
at the nipple line
Compress the chest approximately
1.5-2 inches using heel of hands

Monophasic vs Biphasic
Defibrillators
1st-shock efficacy of monophasic < 1stshock efficacy of biphasic
Goal: delivery of current through chest to
the heart to depolarize myocardial cells
and eliminate VF/VT
Monophasic:
delivers current of one polarity
1-shock 360J

Biphasic :

<200J as safe and w/ higher efficacy than


higher voltage in monophasic
120J, 150J, 200J

Synchronized Cardioversion
Shock delivery timed with QRS complex
Indicated for Rx of unstable
tachyarrhythmias associated with organized
QRS complex and a perfusing rhythm
Rx unstable SVT
Atrial Fibrillation mono=100-200J,
bi=100-120J
Atrial flutter mono=50-100J, bi=100120J
Unstable monomorphic VT 100J,
bi=100-120J

PULSELESS ARREST
VF/VT

1ST-shock (M=360J, B=120-200J)


CPR X 2 minutes
1-shock
Epi 1mg Q 3-5min OR Vasopressin 40U
1-shock
Amiodarone 300mg (then 150) OR
lidocaine 1-1.5mg/kg x 1 (then 0.5 - 0.75 mg/kg x
2)

Magnesium 2 gms IV for Torsades


***CPRRHYTHM CHECKSHOCK

PULSELESS ARREST
ASYSTOLE/PEA
CPR x 2 min
Epi 1mg Q 3-5 min OR VP 40U
CPR x 2 minutes
Atropine 1 mg Q 3-5 minutes (max 3 doses)
for asystole or slow PEA
***CPR: PUSH HARD , PUSH FAST
(100 COMPRESSIONS PER MINUTE )

***1 DOSE VP SUBSTITUTES 2 DOSES OF EPI

PULSELESS ARREST
PULSELESS ELECTRICAL ACTIVITY (PEA)

6 Hs
Hypovolemia
Hypoxia
Hydrogen ion
(acidosis)
Hypo-/Hyperkalemia
Hypoglycemia
Hypothermia

5 Ts
Toxins
Tamponade
Thrombosis
(coronary or
pulmonary)
Tension PTx
Trauma

Tachyarrythmia
Narrow Complex
QRS<0.12

Sinus Tachycardia
AF/AFl
AV-nodal reentry
Atrial Tachycardia
(ectopic,reentrant)
MAT
Junctional
tachycardia

Wide Complex
QRS>0.12

VT
SVT with aberrancy

Thank You