Emergency Medical Training Services

is an approved training center to provide

American Heart Association
emergency cardiac care courses.
T raining Division of EMTS
Main Training Center
100 N. Central Suite L-15
Richardson, TX 75080
EMTS
(972) 527-3687 www.emts911.com
CPR Training and More...
(214) 324-1119 www.cprtrainingandmore.com
ACLS
Advanced Cardiac Life Support
2010 Guidelines
Bring this study packet to class.
May not copy this packet without permission.
Packet is for classroom application only.
To help participants better prepare for the program the
AHA offers an online pre-exam/self assessment. The
self assessment covers basic ACLS knowledge to be
obtained upon successful completion of the program.
The web page and login code can be
found on the inside cover of the AHA
course textbook and/or the confirmation
e-mail participants receive once
successfully registered.
Contact our office if you have any questions.
Table of Content

GENERAL TOPICS
2 Advanced Airway Management
2 Airway Care Prior to Advanced Airway
Placement
2 Airway Placement Confirmation
3 Automated External Defibrillator
1 Basic Airway Management
3 Cardioversion
9 Conveying News of Death to Family
3 Defibrillation
8 Electrical Shock & Lightning Strikes
3 Emergency Pharmacology
2 Endotracheal Tube Intubation
2 Esophageal-Tracheal Combitube
1 Evaluating Airway Delivery & Tools
7 Hypoperfusion/Shock
7 Hypothermia
2 Laryngeal Mask Airway
3 Monophasic vs. Biphasic
1 Mouth-to-Mask & Bag-Valve-Mask
9 Miscellaneous ACLS Information
1 Nasopharyngeal Airway
7 Near-Drowning
1 Opening the Airway
1 Oropharyngeal Airway
3 Pacing (TCP)
2 Pharyngotracheal Lumen Airway
3 Precordial Thump
8 Pregnancy & Cardiac Arrest
2 Sellicks (Criocoid Pressure) Maneuver
7 Special Resuscitation Situations
8 Stroke
2 Suction
1 Tidal Volume & Inspiratory Times
8 Traumatic Cardiac Arrest
3 Vascular Access
10 12-Lead EKG (Basics Only)

PHARMACOLOGY
4 ADENOSINE
5 AMIODARONE
4 ATROPINE SULFATE
5 BETA-BLOCKERS
5 CALCIUM CHANNEL BLOCKER
5 CALCIUM CHLORIDE
5 CARDIZEM (Calcium Channel Blocker)
5 DILTIAZEM (Calcium Channel Blocker)
5 DISOPYRAMIDE
6 DOBUTAMINE
6 DOPAMINE
4 EPINEPHRINE
5 ESMOLOL (Beta-Blocker)
6 FUROSEMIDE
5 LIDOCAINE
6 MAGNESIUM SULFATE
5 METOPROLOL (Beta-Blocker)
6 MORPHINE SULFATE
6 NITROGLYCERIN
6 NOREPINEPHRINE
4 OXYGEN
5 PROCAINAMIDE
5 PROPRANOLOL (Beta-Blocker)
6 SODIUM BICARBONATE
6 THROMBOLYTIC AGENTS
4 VASOPRESSIN
5 VERAPAMIL (Calcium Channel Blocker)

ALGORITHMS
11 V-Fib & Pulseless V-Tach
12 Asystole
13 Pulseless Electrical Activity
14 Bradycardia
15 Narrow Complex Tachycardia
16 V-Tach: Monomorphic & Polymorphic
17 Pulmonary Edema, Hypotension, & Shock
It is recommended that participants
purchase the Handbook of Emergency
Cardiovascular Care for Healthcare
Providers. This pocket reference has
more specific information than what is
provided in this study packet. It also lists
all the algorithms in greater detail. The
book can be ordered by calling EMTS or
CPR Training and More...
The information, instructions and algorithms within
this packet are educational tools only to build a
learning foundation to aid in successful completion of
the course and should not be considered to be the
standard of care for patient use. Algorithms in this
packet are to assist learners to complete this course
only. Healthcare professionals must follow their
facilities/employers specific policies/procedures and
algorithms. Patients may need care not included within
this packet and when clinically appropriate, alterations
in care giving is acceptable. This packet is intended as
a study packet and/or review learning tool only. This
packet does not replace the need for the American
Heart Association's "Textbook of Advanced Cardiac
Life Support". By contacting our office we can make
the book available to participants for a fee. Any fees
charged do not represent income to the American
Heart Association. References: EMTS staff (general
knowledge), Mosby-Nursing Assessment, Para Emer
Care Pharmacology)-Brady.
ACLS Survey - Airway Management
Opening the Airway
Basic airway management begins with opening and
maintaining the airway. The main goal is to prevent
the tongue from blocking the airway. For a non-
trauma patient a head-tilt chin-lift method is
preferred. For a trauma patient the jaw-thrust with
spinal neutralization method is used.
Head-tilt, Chin-Lift Jaw Thrust
Evaluating the Airway
Evaluating the airway is always a top priority. Normal
respirations should be quiet, effortless, and with equal
chest rise. Ventilatory assistance is required if the
patient is breathing less than 8 times per minute. A
non-breathing patient should receive two slow and
smooth breaths lasting 1 second in length to evaluate
the airway passage for a blockage.
Basic Airway Delivery Tools and Care
Oropharyngeal Airway (OPA)
An oropharyngeal (OPA) airway is used to help
establish a patients airway when a gag reflex is not
present. OPAs come in many sizes. To ensure proper
size the rescuer should measure by placing one end of
the device on the corner of the mouth and the other
end to the earlobe. To insert the OPA, hold the device
at its flange end and insert it into the mouth with the
tip pointing toward the roof of the patients mouth.
Once the distal end of the OPA
reaches the posterior wall of the
pharynx, rotate the OPA 180
degrees so that it is positioned
over the tongue. The flange
should rest on the lips when
properly inserted. Use of the OPA
does not eliminate the need for
maintaining proper head position.
Nasopharyngeal Airway (NPA)
The NPA is used when the oral pharynx is not
accessible or the patient has a gag reflex. The device is
contraindicated in patients with facial fractures and
used with caution if skull fractures are present. To
ensure proper size the rescuer should measure from
the corner of the nose to the earlobe. Lubricate the
device prior to placement with a water based
substance. When inserting the NPA in an emergency
one should pick the largest and straightest nostril.
Place the bevel of the NPA to the
nasal septum. Hold the device like
you would a pencil and slowly insert
the NPA into the patients nostril
until the flange is flush with the
nostril. Do not force the device. Use
of the NPA does not eliminate the
need for maintaining proper head position.
Mouth-to-Mask and Bag-Valve-Mask
Mouth-to-mask breathing is the preferred method of
ventilating a nonbreathing patient. It is a simple one
person device, and because of the
two-handed mask seal it provides
excellent ventilatory volumes. The
device when not connected to
supplemental oxygen will deliver
16% oxygen to the patient. When
attached to >10 LPM of
supplemental oxygen the device
delivers approximately 50%
oxygen.

The bag-valve-mask (BVM) consists of a one-way
valve, self-inflating bag, oxygen reservoir, and a
transparent mask. The device delivers 21% oxygen
concentration with room air and once connected to
high flow supplemental oxygen it can deliver up to 80
to 100% oxygen concentration. The BVM technique
commonly creates a poor seal around the patients
mouth and is designed for two trained rescuers to use.
The BVM typically delivers less volume than mouth-to-
mask technique. When using a
BVM during a cardiac arrest
the rescuer needs to be aware
of the pop-off valve status
because greater ventilatory
pressure is usually required.
This device is most effective
when the patient is intubated
and the BVM is attached to an
endotracheal tube (ETT) because the trachea is then
isolated.
Tidal Volumes and Inspiratory Times
If supplemental oxygen is not available, tidal volumes
and inspiratory times should be approximately 8-
10mL/kg (800mL) and delivered over 1 second which
is sufficient to make the chest rise. At room air deliver
1 breath every 5 to 6 seconds. With supplemental O2
and advanced airway in place deliver 1 breath every 6
to 8 seconds.

ETCO2 (Capnography) goals in an arrest patient is >
10 torr. In a perfusing patient in respiratory arrest
titrate to 35 to 40 torr. SpO2 goal is >94%.
Emergency Medical Training Services Page 1
Sellicks Maneuver (Cricoid Pressure)
Sellicks maneuver reduces gastric inflation during
ventilatory efforts. By placing downward pressure
on the cricoid cartilage the diameter of the
e s o p h a g u s i s
decreased therefore
restricting the flow of
air into the stomach.
The routine use of
cricoid pressure in
cardiac arrest is not
recommended.
Suction
If a patients airway is compromised by fluids, turn
the victims head to one side and remove large
particles. Once suction is available the remaining
fluids and fine particles should be removed. For
oral suctioning the pressure should be set at
approximately 300mmHg and suction limited to 15
seconds. For tracheal suctioning the pressure
should be around 80 to 120mmHg and suction time
limited to 5 seconds. Only suction on the way out
and always measure for proper advancement depth
of the suction catheters.

Advanced Airway Management
Esophageal-Tracheal Combitube (ETC)
The ETC allows ventilation of the lungs and reduces
the risk of aspiration of gastric contents. The device
is blindly inserted to ventilate the trachea,
regardless of esophageal or tracheal placement. If
the tube is placed in the trachea the distal cuff is
inflated with up to 15mL of air. If the ETC was
placed in the esophagus inflate the proximal cuff
with up to 100mL of air to
seal the pharynx and inflate
the distal cuff with up to
15mL of air to seal the
esophagus. Air will then be
directed to the trachea.
Contraindications: gag reflex
present, suspected esophageal
disease, ingestion of caustic
substance and patients less than 4 feet tall.
Pharyngotracheal Lumen Airway (PTL)
A duel-lumen tube that allows either tracheal or
esophageal placement. The PTL is blindly inserted
just like the ETC. Consists of two parallel tubes of
equal length and two balloon cuffs that inflate
simultaneously when air is
blown into the inflation port
with a bag-valve device. When
inflated one cuff closes the
oropharynx and the other cuff
secures the esophagus or
trachea depending on distal
placement. Contraindications: gag reflex present, patients
less than 5 feet tall, patients less than 14 years old,
suspected esophageal disease, and ingestion of caustic
substance.
Laryngeal Mask Airway (LMA)
The LMA may be used as an alternative to either the
endotracheal tube (ETT) or the face mask with either
spontaneous or positive-pressure ventilation. The LMA
may be used as the primary airway, as a channel for an
ETT, or as an option in the management of a difficult
airway when intubation is unsuccessful. The device
consists of a tube that is fused to a elliptical, spoon-shaped
mask at a 30-degree angle. When inserted, the tube
protrudes from the patients mouth and is connected to a
ventilation device. The mask is
advanced until resistance is felt.
Then the mask is inflated, it
provides a low-pressure seal
around the laryngeal inlet.
When the LMA is properly
placed, the black line on the
tube should rest in the midline
against the patients upper lip.
The LMA is contraindicated if a
risk of aspiration exists.
Endotracheal Tube (ETT) Intubation
ETT intubation is the airway of choice for all critical
patients who cannot protect their own airway. Tube
advancement is directly into the trachea and a cuff is
inflated with up to 10mL of air to secure the trachea.
Advantages to ETT intubation are isolation of the trachea,
reduction in the risk of aspiration, eliminates the need to
maintain a mask seal, direct route for tracheal suction and
certain medications can be administered via the ETT.
Disadvantages are that it takes more skill than other
airway devices, ETT can be dislodged easily, and takes
more equipment than other methods to secure an airway.
It is also recommended to use a commercial grade tube tie
device to secure the ETT. Most reliable assessment tool for
monitoring correct placement is capnography.
Prior to Advanced Airway Placement
Non-cardiac arrest patients should be hyperventilated and
well oxygenated for 1 to 2 minutes before placement of an
advanced airway device. The attempt to establish the
airway device should take no longer than 30 seconds to
complete. If the device cannot be established within 30
seconds the patient should be hyperventilated again for 1
to 2 minutes before the next attempt.
Airway Placement Confirmation
Whenever airway assistance is being provided the rescuer
should ensure proper ventilation of the patient two ways:
with primary confirmation techniques and secondary
confirmation techniques.
Emergency Medical Training Services Page 2
Primary confirmation techniques include 5-point
auscultation, bilateral chest expansion, and mask or
tube condensation. In secondary confirmation
techniques, esophageal detector devices are
preferred for intubation confirmation in adult
cardiac arrests; end-tidal CO2 detectors
(capnography, capnometry, capnometer) are
preferred in non-cardiac arrest victims.

Defibrillation, Cardioversion, and AED
Defibrillation and Precordial Thump
The most common lethal arrhythmia in an adult
cardiac arrest is ventricular fibrillation (V-fib). V-
fib and pulseless ventricular tachycardia (V-tach)
should be defibrillated immediately at 360J (or
equivalent Biphasic defibrillation ((approx 120-
200J)) followed by 2 minutes of immediate CPR.

Transthoracic resistance to electrical current
therapy is reduced with the use of a conductive
medium, increased paddle pressure (or use of
hands-free defibrillation pads), and successive
shocks.

Precordial thumps are seldom effective and are
usually reserved for witnessed cardiac arrests if a
defibrillator is not readily available.

Defibrillation and cardioversion on children is at a
much lower energy level and is determined by
weight.
Cardioversion
Cardioversion, also known as synchronized
shocking, is indicated for lethal rhythms with a
pulse, such as, V-tach with a pulse and
supraventricular tachycardia (SVT). By using
synchronized cardioversion on a patient, one is
avoiding the R on T phenomenon that may result in
V-fib.
*A-fib first shock at 120 to 200J biphasic.
*SVT first shock at 50 to 100J biphasic.
*Monomorphic V-Tach at 100J biphasic.
All monophasic energy starts at 200J. If additional
shocks are needed increase the dose in a stepwise
fashion. The rescuer should also evaluate for a pulse
after each shock.
AED
Automated External Defibrillators (AED) are very
popular in both the healthcare and public settings.
This device requires minimal training, is easy to use,
and is very safe to the rescuer. The device is placed
on a patient who is over 8 years of age once they are
determined to be in cardiac arrest. The
defibrillation pads are placed on the chest which
results in the AED analyzing the patients cardiac
rhythm. If V-fib or V-tach is present the machine
will defibrillate at 360J (or equivalent Biphasic
defibrillation) one time followed by 2 minutes of
immediate CPR. If the cardiac rhythm is not a shockable
rhythm the machine will instruct the rescuer to perform 2
minutes of CPR if no pulse is present. After 2 minute the
machine will then re-analyze to see if shocks are now
indicated and so on.
4 Alternative electrode placement positions:
*Apex / sternum (most common)
*Anterioposterior (sandwich the heart)
*Left anterior / left infrascapular
*Left anterior / right infrascapular
Monphasic vs. Biphasic Energy
Many studies are now suggesting that Biphasic delivery of
energy requires a lower energy setting and fewer shocks to
convert. Energy is delivered in waveforms that flow
between two electrodes or paddles. Monophasic means the
energy flows one direction. Biphasic energy is delivered in
two phases by passing through the heart and then back
again. At this time the American Heart Association (AHA)
still acknowledges Monophasic energy in the algorithms.
Until more data is collected the AHA does support
Biphasic use at this time, if available, at energy levels set
by the manufactures.

Pacing (TCP)
Transcutaneous cardiac pacing (TCP) is the preferred
initial ACLS pacing method of choice as it can be
established rapidly and is the least invasive techniques.
Pacing is indicated for unstable patients with bradycardias
especially for high degree heart blocks (Mobitz 2 and 3
rd
degree AV blocks). Override pacing to slow a cardiac
rhythm is usually not recommended as an initial treatment
for a tachyarrhythmia. The energy used to pace a patient
is different than shocking a patient, therefore it is safe to
touch a patient while pacing them.

Vascular Access
The largest and most accessible vein that does not interfere
with resuscitation efforts is the best choice. The
antecubital vein is the preferred IV site in most cardiac
arrests for initial IV placement. Complications include
extravasation, thrombosis and tissue trauma. An added
concern with IV establishment is catheter shear. Under the
current guidelines intraosseous (IO) is now acceptable on
any aged patient, if needed as a last resort.

Emergency Pharmacology
Many ACLS drugs are delivered as
recommended standard doses, but most should
be administered based on body weight when
possible.

Related to the goals of this course participants should focus
on First Line Cardiac Drugs.
Emergency Medical Training Services Page 3
The acronym LEAN is used to identify medications
that can be delivered via the ETT or other devices
that allow isolation and direct access to the lungs.
L - Lidocaine -last option not well absorbed via lungs
A - Atropine
E - Epinephrine -last option not well absorbed via lungs
N - Narcan

Drugs delivered via the ETT should be 2-2.5 times
the IV amount and in a total solution of 8-10mL.
When a drug is given down the ETT the maximum
dose is also increased 2-2.5 times the IV maximum
dose.
Oxygen - First Line Cardiac Drug
The highest oxygen concentration should be
administered as soon as possible to all patients in
respiratory or cardiac arrest and patients suspected
of hypoxemia regardless of cause including COPD.
The administration of enriched oxygen increases the
oxygen concentration in the alveoli, which
subsequently increases the oxygen saturation of
available hemoglobin. Indications: Hypoxia. Dose:
Oxygen administration should be monitored by use
of pulse oximetry. 100% oxygen for cardiac arrest
and other critical patients and titrate to effect on
others, but when in doubt give high flow oxygen.
Titrate SpO2 >94% and PETCO2 approx 40 torr.
Epinephrine 1:10,000 - First Line Cardiac Drug
Epinephrine is a naturally occurring catecholamine.
It is a potent alpha and beta adrenergic stimulant,
however its effect on beta receptors is more
profound. Epinephrine can stimulate spontaneous
firing of myocardial conduction cells. In the
emergency setting, it is used to convert fine
ventricular fibrillation to coarse ventricular
fibrillation. In asystole, it is used to initiate
electrical activity in the myocardium. The effects of
epinephrine usually appear within 90 seconds of
administration and they are usually of short
durations. Therefore, it must be administered every
3-5 minutes to maintain therapeutic levels. The
effects of epinephrine include increased heart rate,
increased cardiac contractile force, increased
electrical activity in myocardium, increased blood
pressure, and increased automaticity. Indications:
Cardiac arrest (asystole, ventricular fibrillation,
pulseless ventricular tachycardia, pulseless
electrical activity). Dose: Epinephrine can be
administered IV, IO, and ETT. The American Heart
Association recommends l mg doses every 3-5
minutes.
Vasopressin - First Line Cardiac Drug
Vasopressin is equivalent to epinephrine for
pulseless arrest. The initial agent for refractory V-
Fib or pulseless V-Tach can be either epinephrine or
vasopressin. As a vasoconstrictor, vasopressin appears as
effective as epinephrine, with fewer negative effects on the
heart. Despite decades of use, the effectiveness of
epinephrine in human cardiac arrest has not been shown
in prospective, randomized human clinical trials.
Vasopressin lasts much longer (10 to 20 minutes);
therefore, only 1 dose is recommended. 40 Units IV bolus
given only once. By consensus, vasopressin can be
substituted for the first or second dose of epinephrine.
Atropine Sulfate - First Line Cardiac Drug
Atropine is a parasympatholytic that is derived from parts
of the Atropa Belladonna plant. Atropine is a potent
parasympatholytic and is used to increase the heart rate in
hemodynami cal l y si gni f i cant bradycardi as .
Hemodynamically significant bradycardias are those slow
heart rates accompanied by hypotension, shortness of
breath, chest pain, altered mental status, congestive heart
failure, and shock. Atropine acts by blocking acetylcholine
receptors thus inhibiting parasympathetic stimulation.
Indications: Hemodynamically significant bradycardias.
Dose: Atropine can be administered IV, IO and ETT. The
American Heart Association recommends 0.5 mg doses
every 3-5 minutes with a maximum dose of 3mg or
0.04mg/kg. Precautions: Atropine may actually worsen the
bradycardias associated with second-degree type II and
third degree AV blocks. In these cases, go straight to
transcutaneous pacing when available instead of trying
atropine.
Adenosine (Adenocard) - First Line Cardiac Drug
Adenosine is a naturally occurring nucleoside that slows
AV conduction through the AV node. It has an
exceptionally short half-life and a relatively good safety
profile. Adenosine decreases conduction of the electrical
impulses thought the AV node and interrupts AV re-entry
pathways in supraventricular arrhythmias such as PSVT.
The half-life of adenosine is approximately 5 seconds. Due
to its short half-life the administration of adenosine is
sometimes referred to as "chemical cardioversion."
Adenosine does not appear to cause hypotension to the
same degree as does verapamil (described below).
Indications: SVT (including that associated with Wolff
Parkinson-White syndrome) refractory to common vagal
maneuvers. Dose: The initial dose of adenosine is 6mg
given as a rapid IV bolus over a 1-2 second period with a
flush. To be certain that the drug rapidly reaches the
central circulation, it should be given directly into a vein or
into a proximal medication port of a functioning IV line. If
the initial dose does not result in conversion of the SVT
within 1 to 2 minutes, a 12mg dose may be given.
Emergency Medical Training Services Page 4
Calcium Channel Blockers
Calcium channel blockers cause a relaxation of
vascular smooth muscle and slows conduction
through the AV node. The advantages are twofold.
First, it will inhibit arrhythmias caused by a
re-entry mechanism such as with PSVT. Second, it
will decrease the rapid ventricular response seen
with atrial tachyarrhythmias such as atrial flutter
and fibrillation. This class of drug also reduces
myocardial oxygen demand because of its negative
inotropic effects and causes coronary and
peripheral vasodilation. Indications: PSVT
refractory to adenosine. Precautions: Can cause
systemic hypotension. Calcium chloride can be used
to prevent the hypotensive effects of calcium
channel blockers and in the management of calcium
channel blocker overdose. Calcium channel blockers
should not be administered to patients receiving IV
beta blockers because of an increase risk of CHF,
bradycardia, and asystole. Dose: Verapamil is
administered IV and the initial dose is 2.5-5mg
during a 2-3 minute interval. A repeat dose of
5-10mg can be given in 15-30 minutes if PSVT
persists. The total dose of verapamil should not
exceed 30mg in 30 minutes. Diltiazem/cardizem .25
mg/kg over 2 minutes.
Disopyramide (Norpace)
Inhibits sodium influx through fast sodium channels
in the cell membrane of the myocardium, decreases
myocardial conduction velocity, excitability, and
contractibility. Indications: Patients with atrial
fibrillation/atrial flutter and normal left ventricular
function, and stable V-tach. Dose: 2mg/kg over 15
minutes, then 1 to 2mg/kg by infusion over 45
minutes.
Beta-Blockers
Esmolol 0.5mg/kg over 1 minute, metoprolol 5mg IV
push over 5 minutes, and propranolol may
significantly reduce the occurrence of ventricular
fibrillation in post MI patients. Precautions:
Bradycardias, AV delays and hypotension.
Calcium Chloride
Calcium chloride replaces calcium in cases of
hypocalcemia. Calcium chloride causes a significant
increase in the myocardium contractile force and
appears to increase ventricular automaticity.
Indications: Hyperkalemia, hypocalcemia, calcium
channel blocker toxicity. Dose: Standard dose is
2-4mg/kg IV. Repeated every l0 minutes as
required.
Amiodarone (Cordarone) - First Line Cardiac Drug
Blocks sodium channels, inhibits sympathetic
stimulation, and blocks potassium channels as well
as calcium channels. Slows conduction through the
His-Purkinje system and in patients with Wolff-
Parkinson-White syndrome. Inhibits both alpha
and beta receptors and possesses both vagolytic and
calcium channel blocking properties. Indications: Shock-
refractory pulseless V-tach/V-fib, Polymorphic V-tach,
wide complex tachycardia of uncertain origin, stable V-
tach when cardioversion unsuccessful, and conversion of
atrial fibrillation. Dose: Pulseless V-tach/V-fib - 300mg IV
bolus diluted in 20 to 30mL of NS or D5W. Repeat dose of
150mg every 3 to 5 minutes. If defibrillation successful,
follow with 1mg/min IV infusion for 6 hours. Maximum
daily dose 2.0g IV/24 hours. Other protocol doses if patient
has a pulse are 150mg IV bolus over 10 minutes. May
repeat every 10 minutes as needed. After conversion infuse
360mg over next 6 hours.
Lidocaine (Xylocaine) - First Line Cardiac Drug
Lidocaine is indicated in this course only if Amiodarone is
not available. Lidocaine is an amide-type local anesthetic.
It is frequently used to treat life-threatening ventricular
dysrhythmias. Lidocaine is
probabl y t he mos t
f r e q u e n t l y u s e d
antiarrhythmic agent in
the treatment if life
t hreat eni ng cardi ac
emergencies. Moreover, it
has been shown to be
effective in suppressing
premature ventricular contractions, treating ventricular
tachycardia and some cases of ventricular fibrillation, and
increasing the fibrillation threshold in acute myocardial
infarction. Lidocaine depresses depolarization and
automaticity in the ventricles. It has very little effect on
atrial tissues. Lidocaine is most apt to suppress ventricular
arrhythmias only when the level of the drug in the blood is
between 1.5 and 6.0mcg/ml of blood. A 75-100mg bolus of
lidocaine will maintain adequate blood levels for only 20
minutes. Therefore, once a ventricular arrhythmia is
suppressed, a lidocaine bolus should be followed by a 1-
4mg/min infusion to maintain therapeutic blood levels.
Indications: Ventricular tachycardia, ventricular
fibrillation and premature ventricular contraction
(malignant; more than six unifocal PVC's per minute,
multifocal PVC's, couplets, runs of PVC's, and R on T
phenomena). Dose: Lidocaine can be given IV, IO and
ETT. Ventricular fibrillation and pulseless ventricular
tachycardia is 1-1.5mg/kg every 3-5 minutes. Ventricular
tachycardia with a pulse and malignant PVC's is
1-1.5mg/kg initial dose every 5-10 minutes and repeat doses
are half the initial dose. The maximum dose of this drug is
3mg/kg.
Procainamide (Pronestyl)
Procainamide is an ester-type local anesthetic. It is
frequently uses to treat life-threatening ventricular
dysrhythmias Procainamide is effective in suppressing
ventricular ectopy.
Emergency Medical Training Services Page 5
It may be effective in cases where lidocaine and/or
amiodarone has not suppressed the ventricular
arrhythmia. Procainamide reduces the automaticity
of the various pacemaker sites in the heart.
Procainamide slows intraventricular conduction to
a much greater degree than lidocaine. Indications:
Persistent cardiac arrest due to ventricular
fibrillation, premature ventricular contractions, and
ventricular tachycardias. Dose: In treating PVC's or
ventricular tachycardia, 100mg should be
administered every 5 minutes at a rate of
20-50mg/min. This should be discontinued if any of
the following occur; arrhythmia is suppressed,
hypotension ensues, QRS has widened by 50% of its
original width and a total of 17mg/kg maximum
dose is reached. A maintenance infusion of
procainamide is 1-4mg/min. Precaution: If the
rhythm is suspected to be Torsades de Pointes
magnesium is the preferred drug of choice. Avoid
administering procainamide if the rhythm is a
known Torsades de Pointes rhythm.
Magnesium Sulfate - First Line Cardiac Drug
Magnesium is the treatment of choice for Torsades
de Pointes and it may be used in refractory
ventricular tachycardia and ventricular fibrillation.
Indication: Ventricular fibrillation, ventricular
tachycardia and Torsades de Pointes. Dose: 1-2g in
10mL given IV push. Several studies support use in
AMI patients as an infusion.
Sodium Bicarbonate
Ventilation is the initial treatment priority to
acid-base balance during early cardiac arrests.
Hyperventilation influences respiratory acidosis by
removing CO2. Sodium bicarbonate is indicated for
metabolic acidosis (DKA), hyperkalemia, and
overdoses (tricyclic, phenobarbital). Sodium
bicarbonate may be beneficial after prolonged
hypoperfusion or cardiac arrest situations. It is
generally not used within the first 10-15 minutes of
arrest unless diagnostic tools and/or history
supports metabolic acidosis is present. Indications:
Tricyclic overdose, phenobarbital overdose, and
severe acidosis refractory to hyperventilation. Dose:
Usual dose of sodium bicarbonate is 1mEq/kg can
be repeated every 10 minutes at half the original
dose. Precaution: Most catecholamines and
vasopressors (i.e. dopamine, epinephrine) can be
deactivated by alkalotic solutions. Make sure that
IV lines are flushed before and after administering
sodium bicarbonate.
Dopamine (Intropin) - First Line Cardiac Drug
Dopamine is a naturally occurring catecholamine. It
is a chemical precursor of norepinephrine. It acts on
alpha, beta and dopaminergic adrenergic receptors.
Its affects on alpha receptors is dose-dependent.
Indications: Hemodynamically significant
hypotension (70-100mmHg) not resulting from
hypovolemia and is also indicated for cardiogenic shock.
Dose: Intial dose: Low dose (2-10mcg/kg/min) stimulates
dopaminergic receptors causing dilation of mesentery,
coronary and cerebral areas. Medium dose
(10-15mcg/kg/min) stimulates beta effects for rate and
force. High dose (15-20mcg/kg/min) introduces alpha
effects and vasoconstriction.
Norepinephrine (Levophed) - First Line Cardiac Drug
A natural occurring alpha and beta agonist. It is indicated
in patients with severe hypotension (less than 70mmHg)
otherwise dopamine should be used. Norepinephrine
should be used cautiously due to its potent alpha
stimulation. Dose: IV infusion 0.5-30mcg/min.
Dobutamine (Dobutrex)
A synthetic catecholamine and a potent inotropic agent
used in treating heart failure patients. Dobutamine
increases the force of the systolic contraction (positive
inotropic effect) with little chronotropic activity. Dose:
2-20mcg/kg/min
Furosemide (Lasix)
A potent diuretic that inhibits sodium and chloride
reabsorption in the kidneys. This drug is used to treat
pulmonary edema and lower blood pressure. The effects
may occur within 5-20 minutes. Dose: 0.5-1 mg/kg slow IV.
Blood pressure must be able to support the fluid shift.
Nitroglycerin (Nitrostat) - First Line Cardiac Drug
Nitroglycerin is a potent smooth muscle relaxant used in
the treatment of angina pectoris. Nitroglycerin reduces
cardiac work load, and to a lesser degree, dilates the
coronary arteries. This results in increased coronary blood
flow and improved perfusion of the ischemic myocardium.
Indications: Chest pain with angina, chest pain with AMI,
and acute pulmonary edema (unless hypotensive). Dose:
0.4mg sublingual for routine angina pectoris. Repeated 3-5
minutes as required. IV infusion nitroglycerin is
10-20mcg/min.
Morphine Sulfate - First Line Cardiac Drug
Morphine is a central nervous system depressant that acts
on opiate receptors in the brain, providing both analgesia
and sedation. It increases peripheral venous capacitance
and decreases venous return. This effect is sometimes
called a "chemical phlebotomy." Morphine also decreases
myocardial oxygen demand. Indications: Severe pain
associated with MI. Pulmonary edema either with or
without associated pain (monitor for hypotension). Dose:
There are many different approaches to the administration
of morphine. An initial dose of 2-10mg IV is standard. This
can be augmented with additional doses of 2mg every few
minutes until pain is relieved, respiratory depression
occurs, or hypotension is noted.
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Clot Buster - Fibrinolytic Agents
Streptokinase, urokinase and tissue plasminogen
activator (tPA) are common agents. Therapy should
be initiated within 8 hours of onset of pain when all
of the following symptoms are presenting; ST
elevation 2mm in 2 contiguous leads, symptoms and
ST el evati on post SL NTG therapy.
Contraindications may include hemorrhage, aortic
dissections, prolonged CPR, HTN, CVA, recent
trauma, liver dysfunction and many more.

Special Resuscitation Situations
Several special situations are associated with
cardiopulmonary arrest that require the rescuer to
change their approach to resuscitation. Emergency
personnel should note carefully the differences in
triage, emphasis, and techniques.
Hypoperfusion/Shock
Shock is defined as inadequate tissue perfusion. It is
important to identify and treat the causes while
keeping the body hemodynamically stable.

Rate problems associated with tachycardias and
bradycardias can attributed to backing up of fluids.
Pump Problems could include MI, chordae
tendineae damage, valvular damage, myocarditis,
aortic aneurysm, pulmonary edema, cardiac
tamponade, and others. Volume complications from
hemorrhage or other fluid losses along with relative
vasodilation, redistribution, and drug induced
influences.

In treating a hypotensive patient the
"Cardiovascular
Triad" is applied. Rate, rhythm and lastly blood
pressure.

Signs and symptoms of hypotension may include but
are not limited to altered mental status, diaphoresis,
cool, pale skin, decreased distal pulses, dyspnea,
tachycardias, and decreased blood pressure.

Care includes ABC, EKG, pulse oximetry, IV,
history, physical exam, 12 lead and chest x-ray.
Treat rate, rhythm, and finally blood pressure in
most cases. For further information refer to
hypotension algorithm.
Hypothermia - Non-medically induced
Hypothermia is defined as a body temperature less
than 95 degrees Fahrenheit. Severe hypothermia is
a body temperature below 85 degrees and is
associated with depression of cerebral blood flow
and oxygen requirements, reduced cardiac output
and decreased arterial pressure. The patients
peripheral pulses and breathing efforts may be
difficult to identify and assess. Try to remove the
person from the environment or situation causing
the decrease in body temperature (weather, wet
clothes). One of the most important goalsin saving a
hypothermic patient is to prevent further heat loss.

Rescue breathing should be initiated if not breathing. Pulse
checks should last 30-45 seconds to compensate for the
decreased cardiac function. For body temperatures
between 85 to 93 degrees, apply external warming devices
to the trunk areas only. Airway management and
transportation should be handled as gently as possible to
decrease the possibility of ventricular fibrillation. Move
patient in a horizontal position to avoid aggravating
hypotension. If the body temperature is below 85 degrees
and the patient is in ventricular fibrillation or pulseless
ventricular tachycardia, only one round of shocks are
advised until the body temperature is above 85 degrees and
rewarming is established. Also avoid certain medications
until body temperature is increased.

Rewarming can be done by warmed humidified oxygen,
warm packs to the torso region, warmed IV fluids,
peritoneal lavage, extracorporeal blood warming and
esophageal rewarming tubes. As a rule, victims should not
be considered dead until they have a near normal core
temperature.

Since severe hypothermia is frequently preceded by other
disorders (drug overdoses, alcohol use, trauma, and others)
the healthcare provider must look for and treat underlying
conditions while simultaneously treating the hypothermia.
All cachectic, malnourished, or alcoholic patients should
receive thiamine (100mg) early during rewarming
procedures.
Near-Drowning
The most significant concern
regarding a drowning victim is
hypoxemia. Therefore, rescuers
should restore ventilation and
perfusion as quickly as possible.

The initial treatment for a
non-breathing drowning victim
is delivering rescue breaths.
Also suspect hypothermia and
head, neck, and back injuries
with diving accidents. THERE IS NO NEED TO CLEAR
THE AIRWAY OF ASPIRATED WATER. At most only
a modest amount of water is aspirated by a majority of
both freshwater and seawater drowning victims. Some
patients do not aspirate at all due to laryngospasms.
Maintain the victim horizontal and protect for possible
head, neck or back injuries when removing victim from
water.

If the victim is not breathing and pulses are absent begin
CPR. Intubation should be initiated as soon as possible.
End-tidal CO2 determinations may be helpful in making
the decision to continue resuscitation efforts. Aggressive
attempts to resuscitate should be made for a drowning
victim in icy water.
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Pregnancy and Cardiac Arrest
Cardi ac arrest of
pregnant patients is not
c ommon. Car di ac
output increases up to
30-50%. Heart rate,
ventilatory rate, and
o x y g e n d e ma n d s
increase. Respiratory function decreases due to
dramatic anatomical changes. Systemic and
pulmonary vascular resistance decrease as well.
Pregnant patients are more prone to major
cardiovascular and respiratory injuries than a
non-pregnant patient. The uterus may compress the
vena cava, aorta and others vessels resulting in
supine hypotension syndrome which may result in
a 20-25% decrease in cardiac output.

Standard life saving measures are recommended for
all severely unstable patients. Position the uterus to
the left side of the abdomen. Vasopressor drugs
should not be withheld as well as other
pharmacological agents. At less than 23 weeks
gestation, focus efforts on saving the mothers's life.

If after ACLS intervention there is no patient
response and there is possible viability of the fetus,
a cesarean section may be considered. Delivery
attempts should take place within 5 minutes of the
arrest when possible. Cesarean section may increase
the chances of survival for both patients.
Electrical Shock and Lightning Strikes
Electrical shock is associated with a fatality rate of
0.5 per 100,000 population per year in the United
States. It accounts for 1,000 deaths annually and
causes an additional 5,000 patients to require
emergency care. Electrical shock victims may
experience transient unpleasant sensation from
brief exposure to low-intensity current to cardiac
arrest.

Electrical injuries result from current passing
through the body and converting into heat energy.
Factors to consider include magnitude of energy
delivered, resistance to current flow, type of
current, duration of contact and current pathway.
High-tension current causes the most serious
injuries. Alternating current at 60 cycles per second
may cause tetanic skeletal contraction and delivery
of current to the myocardium resulting in an
increased chance of ventricular fibrillation.
Hand-to-hand pathways are more fatal than
hand-to-foot and foot-to-foot pathways.
Cardiopulmonary arrest is the primary cause of
immediate death due to electrical injury.
Ventricular fibrillation or ventricular asystole may
occur as a result of electric shock. Respiratory
arrest may occur secondary to electrical current
passing through the brain and causing inhibition of
the medullary respiratory center function, tetanic
contraction of the diaphragm and chest wall musculature
loss.

It is important that the rescuers be certain that rescue
efforts will not put him or her in danger. As soon as
possible secure an airway and oxygenate. CPR and
precautions for head, neck and back injuries as needed.
Transfer to a burn center may be indicated.
Traumatic Cardiac Arrest
Patients who develop cardiac
arrest in association with
trauma are treated differently
than non-trauma patients.
Cardiac arrest resulting from
trauma has many causes to
consider ranging from but not
limited to; severe central neurological injury, hypoxia
resulting from pneumothorax, obstructions and crushing
wounds to the airway, hypovolemia, and pericardial
tamponade.

The following suggest an approach of care for an injured
patient in cardiac arrest; treat ventricular fibrillation,
identify and treat potential reversible injuries, rapid
transport, and rewarming therapy.

Treatment includes identifying lethal dysrhythmias,
maintaining spinal alignment, intubation, CPR, surgical
airway, pericardiocentisis, seal open chest wounds, and IV
therapy. Many BLS and ACLS interventions are of no
benefit if surgical interventions are not provided quickly.
Stroke
A sudden onset caused by blockage
or aneurism of a cerebral blood
vessel. Ischemic strokes are caused
by thrombotic or embolic
occlusion. Hemorrhagic strokes are
caused by a rupture of a vessel
resulting in blood and brain cells
coming into direct contact leading
to a more violent insult to the
brain.

Common signs and symptoms include; AMS, headaches,
aphasia, facial weakness, asymmetry, ataxia, vertigo,
unilateral hearing loss, monocular blindness, N/V and
others.

Care includes ABC's, V/S trending, general
medical/trauma assessment, physical and neurological
exams. Continued care
will consist of EKG monitoring, pulse oximetry, IV access,
lateral C-spine x-rays, arterial blood gases, 12 lead EKG,
chest x-ray, CBC, coagulant studies and electrolyte
monitoring. Further evaluation and continuation of
treatment includes neurological consult, IV therapy (NS or
LR at <30mL/hr, avoid D5W), and monitoring
intake/output.
Emergency Medical Training Service Page 8
Antihypertensive drugs (criteria and medication
choices will vary upon situation). Anticonvulsant
drugs prn (phenytoin, diazepam, phenobarbital).
Intracranial pressure can be addressed by
hyperventilation (PETCO2, 30mmHg) and
anti-inflammatory medications (mannitol 1-2g/kg
over 5-10 minutes).

Conveying News of a Sudden Death to Family
Call the family if they have not been notified.
Explain that their loved one has been admitted to
the ED or critical care unit and that the situation is
serious. If possible, survivors should be told of the
death in person, not over the telephone.

Obtain as much information as possible about the
patient and the circumstances surrounding the
death. Carefully go over the events as they
happened in the ED. Ask someone to take family
members to a private area. Walk in, introduce
yourself, and sit down. Address the closest relative.

Briefly describe the circumstances leading to the
death. Go over the sequence of events in the ED.
Avoid euphemisms such as "he's passed on," "she's
no longer with us," or "he's left us." Instead use the
words "death," "dying," or "dead." Allow time for
the shock to be absorbed. Make eye contact, touch,
and share. Convey your feelings with a phrase such
as "You have my (our) sincere sympathy.

Immediate Post-Cardiac Arrest Care
Return of Spontaneous Circulation (ROSC):
*Maintain a PETCO2 or PaCO2 of approx
35-40 torr. SPO2 >94%.
*Maintain BP >90mmHg.
-IV Bolus
-Dopamine drip
-Norepinephrine drip
-Epinephrine drip
*If comatose after ROSC induce hypothermia.
-1 to 2 L (30mL/kg) isotonic solution at
4 degrees Celsius. Maintain temperature of 32
to 34 degrees Celsius for 12 to 24 hrs.
*If MI cause consider PCI/Cathlab ASAP.
Miscellaneous ACLS Information
MONA greets all heart attach victims at the door.
Morphine, Oxygen, Nitro, and Aspirin.

Whenever a patient is moved the airway should be
re-evaluated.

CPR is 30 compressions to 2 ventilations unless the
patient is intubated. If advanced airway is placed
ventilator provides 8 to 10 ventilations per minute
and compressor provides compressions at a rate of at least
100 per minute without interruption.

Rescue breathing is at a rate of 12 to 15 per minute (8 to 10
if advanced airway is in use) and hyperventilation is 24 per
minute.
BLS versus ACLS Survey
*BLS Survey is step 1-2-3-4. It is used for CPR.
-1 Check for response
-2 Start compressions
-3 Open Airway and give breathes
-4 AED
*ACLS Survey is a more indepth assessment when not in
arrest. The traditional ABCD
-A Airway
-B Breathing
-C Circulation
-D Diagnostic deferential
Notes:
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12-LEAD EKG (Basics Only)
The precipitating event in acute
myocardial infarction is occlusion of
a coronary artery and interruption of
blood flow to a portion of the
myocardium it supplies. It is at this
moment that the clock starts
running. TIME IS MYOCARDIUM!

Initially, following coronary
occlusion, the affected tissue will
become deprived of oxygen and other
nutrients and will become ischemic.
Myocardial ischemia can often be
demonstrated on the EKG as ST
segment depression and T wave
inversion. The larger the quantity of
ischemic tissue, the more significant,
as a rule, will be the EKG findings. If
allowed to progress untreated, tissue
at the center of the myocardial injury
will transition from ischemic to
injury. The ST segment will become
elevated in the affected leads. In
addition, T waves in the affected
leads will become more peaked.

After approximately 6 hours and
provided blood supply has not been
restored, the injured tissue will begin
to die. As the infarction becomes
complete over the next 48-72 hours,
most ischemic and injured tissue will
have been replaced by infarcted
tissue causing decreased ST segment
elevation. A significant Q wave
usually persists and is an indication
of an old infarction.

Each EKG lead is designed to
visualize a part of the heart. The
following is a generalized description
of the various EKG lead groupings.

Anterior: leads VI, V2, V3, V4
Lateral: leads I, aVL, V5, V6
Inferior: leads II, III, aVF
(A finding in two or more leads per
grouping could be viewed as a
positive finding.)

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Primary Assessment
Airway (basic) - Breathing - Circulation (CPR)
Defibrillate at 360J (or equivalent Biphasic energy ((120-
200J)) followed by 2 minutes of immediate CPR
Secondary Assessment
Airway (advanced)
Breathing (confirm by at least 2 methods)
Circulation (IV/IO access)
Differential (search for and treat causes)
Antiarrhythmics
Amiodarone - 300mg IV bolus diluted in 20-30mL of NS. Consider repeat dose of 150mg in 3-5 minutes.
If defibrillation successful start 1mg/min infusion for 6 hours.
or
Lidocaine (only if Amiodarone is not available) - 1.5mg/kg bolus. Repeat at 1.5mg/kg 3-5 minutes after first dose.
If defibrillation successful start 1-4mg/min infusion.
Epinephrine 1mg every 3-5 minutes.
or
Vasopressin 40 U IV bolus given once. May substitute 1
st
or 2
nd
dose of EPI.
May resume epinephrine after 3-5 minutes.
Ventricular Fibrillation & Pulseless Ventricular Tachycardia
Note: ETT drugs - double dose in 10mL.
Note: Vasopressors are given on its own time schedule.
Note: Every 2 minutes reassess if additional defibrillation is needed.
V-Fib V-Tach
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Primary Assessment
Airway (basic) - Breathing - Circulation (CPR)
Epinephrine 1mg every 3-5 minutes
or
Vasopressin 40 U IV bolus given once. May substitute 1
st
or 2
nd
dose of EPI.
May resume epinephrine after 5-10 minutes.
Secondary Assessment
Airway (advanced)
Breathing (confirm by at least 2 methods)
Circulation (IV access)
Differential (search for and treat causes) PATCH-5-MD
Consider termination of efforts
Asystole
MOST COMMON CAUSES OF RAPID DETERIORATION OF PATIENT CONDITION
P pulmonary embolism Consult needed
A acidosis 1mEq/kg Sodium Bicarb
T tension pneumo Needle chest decompression
C cardiac tamponade Pericardiosentesis
H hypovolemia Fluid bolus 250-500mL may repeat
H hypoxia Oxygen delivery
H heat/cold Monitor and maintain based on condition
H hyper/hypokalemia Consult needed
H hypoglycemia Glucose administration
M MI STEMI protocol
D drug overdose Narcan 2mg may repeat
Asystole
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Primary Assessment
Airway (basic) - Breathing - Circulation (CPR)
Secondary Assessment
Airway (advanced)
Breathing (confirm by at least 2 methods)
Circulation (IV access)
Differential (search for and treat causes) PATCH-5-MD
Epinephrine 1mg every 3-5 minutes
or
Vasopressin 40 U IV bolus given once. May substitute 1
st
or 2
nd
dose of EPI.
May resume epinephrine after 5-10 minutes.
Consider termination of efforts
Pulseless Electrical Activity
Note: ETT drugs - double dose in 10mL.
Note: Epinephrine is given on its own time schedule.
Note: After rate adjustment fails consider dopamine.
Note: PEA is any pulseless rhythm other than asystole, V-tach, or V-Fib
P pulmonary embolism
A acidosis
T tension pneumo
C cardiac tamponade
H hypovolemia
H hypoxia
H heat/cold
H hyper/hypokalemia
H hypoglycemia
M MI
D drug overdose
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Primary Assessment
Airway (basic) - Breathing - Circulation
Secondary Assessment
Airway (advanced)
Breathing (confirm by at least 2 methods)
Circulation (IV access)
Differential (search for and treat causes)
Determine if STABLE or UNSTABLE
If stable continue work-up.
If unstable continue with algorithm.
Atropine 0.5mg IV every 3-5 minutes to max
dose of 0.04mg/kg
Narrow QRS Bradycardia
Sinus Brady
Junctional Rhythm
2 Degree AV Block, type 1
Complete AV Block
Wide QRS Bradycardia
2 Degree AV Block, type 2
Complete AV Block
Idioventricular Rhythm
TCP as soon as possible
TCP
(Rate) Dopamine 2-10mcg/kg/min
(BP) Dopamine 10-20mcg/kg/min
and/or
Epinephrine Drip - 2-10mcg/min
hen
Isoproterenol Drip - 2-10mcg/min
(Rate) Dopamine 2-10mcg/kg/min
(BP) Dopamine 10-20mcg/kg/min
and/or
Epinephrine Drip - 2-10mcg/min
then
Isoproterenol Drip - 2-10mcg/min
Bradycardia

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Primary Assessment
Airway (basic) - Breathing - Circulation
Secondary Assessment
Airway (advanced)
Breathing (confirm by at least 2 methods)
Circulation (IV access)
Differential (search for and treat causes)
If Stable continue with algorithm.
If Unstable go to bottom box.
Attempt therapeutic diagnostic maneuver
A Vagal stimulation
A Adenosine 6mg rapid push IV, may repeat in 1-2 minutes at 12mg.
Normal Cardiac Function
A B-Blocker
A Ca2+ channel blocker
Normal Cardiac Function
A B-Blocker
A Ca2+ channel blocker
Normal Cardiac Function
Priority order:
A Ca2+ channel blocker
A B-Blocker
A Digoxin
A DC cardioversion
Stable Ectopic or
Multifocal Atrial Tachycardla
Stable Paroxysmal SVT
Stable Junctional tachycardia
If hemodynamically unstable, synchronize cardioversion:
*SVT 50-100J biphasic
*A-Fib 120-200J biphasic
*If using monophasic energy start at 200J
AFTER FIRST SHOCK ESCALATE AS NEEDED.
Remember to check for a pulse after each shock.
Narrow Complex Tachycardia
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Primary Assessment
Airway (basic) - Breathing - Circulation
Secondary Assessment
Airway (advanced)
Breathing (confirm by at least 2 methods)
Circulation (IV access)
Differential (search for and treat causes)
If Stable continue with algorithm.
If Unstable go to bottom box.
Normal baseline QT interval &
Normal Cardiac Function
A Treat ischemia
A Correct electrolytes
Medications: any one
A B-Blockers or
A Lidocaine or
A Amiodarone or
A Procainamide or
A Sotalol
Normal baseline QT interval &
Impaired Cardiac Function
Amiodarone
A 150 mg IV bolus over 10 minutes
or
Lidocaine (if Amiodarone is not
available)
A 0.5 to 1mg/kg IV push
then use
A Defibrillation not synchronized
cardioversion.
Prolonged baseline QT interval
(suggests torsades)
A Correct abnormal electrolytes
Medications: any one
A Magnesium
A Overdrive pacing
A Phenytoin
Note!!!!!
May go directly to
cardioversion
Stable Monomorphic V-tach
A Is cardiac function impaired?
Stable Polymorphic V-tach
AIs QT baseline interval prolonged?
Normal Cardiac Function
Amiodarone
A 150 mg IV bolus over 10 minutes
or
Lidocaine (if Amiodarone is not
available)
A 0.5 to 1mg/kg IV push
then use
A Synchronized cardioversion at
100J biphasic or 200J
monophasic. Then escalate as
needed.
If hemodynamically unstable, deliver electrical therapy as described above.
Remember to check for a pulse after each shock.
Ventricular Tachycardia: Monomorphic and Polymorphic
Note: To determine the QT Interval measure two consecutive R-R
waves. Then measure the QT Interval from the Q wave to the start
of the T wave. If the QT Interval is less than half the R-R
measurement the QT Interval is considered normal. If the QT
Interval measurement of more than half of the R-R measurement it
is considered long.
Note: Once a patient has received electrical therapy all ventricular
drugs should then be followed by another shock
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Clinical signs:
Shock, Hypoperfusion, CHF, Acute Pulmonary Edema
Most likely the problem?
Rate Problem Pump Problem
Pulmonary Edema
Go to
Bradycardia
or
Tachycardia
algorithms
Systolic BP 70 to 100 mmHg s/s of shock
Dopamine 2 to 20 mcg/kg/min IV
Blood
Pressure?
Volume Problem
Administer
A Fluids
A Blood transfusions
A Cause-specific
interventions
Consider vasopressors
1st - Acute pulmonary edema
A Furosemide IV 0.5 to 1.0mg/kg
A Morphine IV 2 to 4mg
A Nitroglycerin SL
A O2/CPAP/intubation as needed
Systolic BP
BP defines 2nd
line of action
Systolic BP <70 mmHg s/s of shock
Norepinephrine 0.5 to 30 mcg/min IV
2nd - Acute pulmonary edema
A Nitroglycerin/nitroprusside if
BP >100 mmHg
A Dopemine if BP = 70 to 100
mmHg, signs/symptoms of
shock
A Dobutamine if BP >100 mmHg,
no signs/symptoms of shock
Systolic BP 70 to 100 mmHg No s/s of shock
Dobutamine 2 to 20 mg/kg/min IV
Systolic BP >100 mmHg
Nitroglycerin 10 to 20 mcg/min IV
consider
Nitroprusside 0.1 to 5.0 mcg/kg/min IV
Acute Pulmonary Edema, Hypotension, Shock



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