Professional Documents
Culture Documents
Life Support
dr. Atep Supriadi
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
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
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
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
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
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
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
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
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
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
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
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
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 :
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
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 )
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