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! Instructor presentation of 2011 BLS
Nurses Educational Opportunities
www.nursesed.net
Toll Free 866.266.2229
Copyright 2011
5*(-4.#6!
8:00 Welcome/Introduction
8: 15 AHA ACLS Overview Video
8:30 Instructor presentation of lethal rhythms & pretest
8:45 AHA Video ACLS Primary/Secondary Survey
9:00 AHA ACLS Video Airway Management
9:30 AHA BLS Video
9:45 Practice BLS with manikins/BMV/Barrier/AED
10:00 Instructor presentation of ACLS
11:00 AHA video of Heart Attack and Stroke
12:00 AHA video of Mega Code
12:15 Instructor presentation of Mega Code
Skills stations
Written exam
!"#$%&'()*'+#*,-(-.&,-)$'
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8:00 Welcome, Introduction, Pretest!
8:30 Lethal Rhythm Review & Practice!
9:30 Primary and Secondary Survey Video/Practice
10:00 Airway Management
11:00 BLS Practice
12:00 Lunch
1:00 VF/PEA/Asystole
2:00 Bradycardias
Tachycardias
Acute Coronary Syndrome/Stroke
Practice Skills
Airway Management
Defibrillation
Cardioversion
3:00 Scenario Discussions if time allows
4:00 Mega Code instructor presentation
"#$!()*!
8:00 Putting it all together
9:00 Mega Code Review
10:00 Mega Code and Written evaluation
11:00 Remediation if appropriate
2
 9:;('4+$(-!
Upon the completion this ACLS course the learner will be able to:
Simulate a team leader and a team member
Simulate airway management
Verbalize the steps to assist in intubation
Verbalize 5 steps in confirming ET tube placement
Verbalize the definition of ROCS
Verbalize the Hs and Ts with the signs and symptoms
and interventions
Verbalize the four interventions for Bradycardia
Verbalize the technique of managing the pacemaker
Discuss an unstable tachycardia and the steps in cardioversion
Discuss a stable tachycardia and appropriate drug interventions
Verbalize the time frame required to initiate stroke
interventions
Discuss the signs and symptoms of ACS and interventions
Discuss the signs and symptoms of acute stroke and interventions.
Discuss therapeutic hypothermia
Upon completion of the ACLS course the learner will be able to recognize and
select appropriate drugs for the following rhythms:
Ventricular Fibrillation
PEA
Asystole
Supraventricular Tachycardia
Rapid Atrial Fibrillation
Torsades de Pointes
Bradycardia
1st, 2nd, 3rd Degree Blocks
Paced rhythm
Upon completion of this ACLS course the learner will be able to
Demonstrate BLS with the AED
Demonstrate Respiratory Management with a pulse
Demonstrate Respiratory Management without a pulse
Demonstrate interventions of Bradycardia VF Asystole
Demonstrate intervention of Unstable Tachycardia VF PEA ROSC
Demonstrate intervention of Stable Tachycardia VF PEA ROSC
3 4
.<=(!>/('4*+'%/!?@3./-( !
!
When the electricity goes through the heart it travels from the
SA node to the AV node. As that occurs it causes the atrium to contract
and a P wave appears on the EKG paper. When the electricity travels on
through the Bundle Branches it causes the ventricles to contract and the
QRS complex appears. When the heart goes through its resting phase the
T wave appears. If you have a P wave, QRS complex, and a T wave
you have a Sinus Rhythm.
A Q wave is an abnormal wave and should no
appear. It is a downward deflection in the QRS complex.
It indicates an infarction has or is occurring.
To determine the age of the infarction we must examine the
isoelectric line. The isoelectric line should be level as it is seen in
the tracing on the following page. The dark heavy line that enters
the QRS complex is at the same level that comes out of the QRS
complex. This line may come out of the QRS complex elevated or
depressed. Note the elevation in the above complex. Examine the
12-lead EKG on page 6. Note the elevation in Lead I and Lead
AVL. Note the depression in V3 and V4.
Q waves with ST segment elevation may indicate an ST
segment elevated myocardial infarction (STEMI) and rapid and early
reperfusion is essential for optimal outcome
There are several ways to determine the rate of the rhythm. Your
NEO instructor will show you the following way in class. Memorize the
numbers in red on the next page. You may want to memorize them in
groups of three. (300-150-100) (75-60-50) Then find a complex that
lands on a bold line. Go to the next bold line and say 300, then 150,
then 100, then 75, then 60. The second complex landed between
60 and 75. In resuscitation. Approximate rates are all that you need to
know.
The following rhythm is a sinus rhythm with a rate 60-75 bpm.
There is no Q wave. The isoelectric line is level. The T wave is upright.
 A EFG0(%#!>LM

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:(7+&&+&7!,1!4=(!8 !
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! H(7+&&+&7!,1!4=(!I!
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B)0(.,C+A'D( Q = Infarction
! H(7+&&+&7!,1!4=(!I! ST (depression = ischemia)
!
4,!4=(!(&#!,1!4=(!2 (elevation = acuteness)
T inversion = Ischemia
Q waves with ST segment elevation may indicate an ST segment
elevated myocardial infarction (STEMI) and rapid and early reperfusion
is essential for optimal outcome.
5 6
 ?&4(*3*(4%4+,&! 5*%'4+'(!4=(!8=64=@
Rate: !
About 75/min
Rhythm:
Generally regular Sinus Rhythm with occasional PVCs. QRS is less
!
than 0.12 sec; therefore, there is no Bundle Branch Block.
Interpretation:
!
There are significant Q waves in I and AVL.
ST segments are elevated in I and AVL.
!Do you see Q waves? _______________
ST segments are depressed V1, V2, V3 and V4.
T waves are inverted in AVF and flat in II, III, and all chest
!IsIs the T wave upright? ______________
the isoelectric line level? __________

Comments:
leads. !What is the rate? ___________________
This is a normal sinus rhythm.
Patients with coronary atherosclerosis may develop a spectrum of
clinical syndromes representing varying degrees of coronary artery
!
occlusion. These syndromes include are as follows:
ST segment elevation MI (STEMI)
!
Characterized by ST-segment elevation in two or more contiguous
precordial leads or 2 or more adjacent limb leads or by a new left
!
bundle branch block. !
non-ST segment elevation MI (NSTEMI)
Characterized by ischemic ST segment depression or dynamic T-wave
inversion with pain or discomfort.
!Do you see Q waves? _______________
Is the T wave upright? ______________
Unstable angina (UA) !Is the isoelectric line level? __________
!A sinus tachycardia usually does not exceed a rate of 120-130 bpm.
Characterized by chest pain without exertion and normal or What is the rate? ___________________
nondiagnostic ECG.

!Atachycardia
STEMI: rate of greater than 180 bpm is referred to as a supraventricular
The ST segment elevated MI is the most time critical myocardial

!The
infarction. Early reperfusion with clot busters called fibrinolytics or
most important principle in managing a sinus tachycardia is
balloon dilatation or stent placement called PCI (Percutaneous
Coronary Intervention) will reduce mortality and minimize
identify the cause.
myocardial injury if achieved within 12 hours of onset. Fibrinolytics
are generally not recommended for patients that present greater that 12
!
hours of onset.
Bundle Branch Blocks:
!
BBB are easily diagnosed with an ECG by merely measuring the QRS
complex. If the QRS complex measures greater than 0.10 seconds a
!Do you see Q waves? _______________
BBB exist. It can slow on the right (Right Bundle Branch Block) or
slow on the left (Left Bundle Branch Block). A RBBB will have a
!IsIs the T wave upright? ______________
the isoelectric line level? __________
rabbit ear configuration
whereas a LBBB will look
!What is the rate? ___________________
A rate of less than 60 beats per minute is a Bradycardia
slurred. !A Bradycardia that is symptomatic requires intervention. The drug of
choice for a symptomatic Bradycardia is Atropine at 0.5 mg.*
7 8
!
!

!
!
!
This is a First Degree Block because the PR interval is greater than 0.20
seconds.
Each little box measures 0.04 seconds. There are 8 little boxes from
the beginning of the P to the beginning of the Q.
The PR interval in this strip is 8 x .04 = .32 seconds.
This heart rate is about 40 bpm. If this patient is symptomatic and
probably is, Atropine is the drug of choice at 0.5 mg.
This is a Mobitz I, Second Degree Block.
It is also called the Wenckebach.
The PR interval progressively lengthens until a QRS complex is
dropped.
The patient has a heart rate of about 60 bpm and may be
asymptomatic and may require no intervention, but you wont
know until you check on this patient. If the patient is symptomatic
you may consider Atropine at 0.5 mg.
!
!
! This a Third Degree/Complete Heart Block.
! The atrium is working. The ventricles are working. But they are not
working together.
! The P waves are marching across. The QRS complexes are marching
! across. But they are not marching together.
! The P wave does not cause the QRS complex to occur. There is a
complete block. This is serious. Your patient will require a
! Transcutaneous Pacemaker. Atropine speeds up the SA node and since
! there are P waves that are blocked. You need a transcutaneous
pacemaker. You should consider Atropine while preparing for the
! pacemaker*. (AHA 2010 Update)
!
!
!
! This is another sample of a Third Degree/Complete Heart Block
! Notice the PR intervals are not consistent.
! Try Atropine but dont rely on atropine to do the job
! Try Epinephrine and/or Dopamine for its vasoconstrictive properties.
Try Transcutanious Pacing

This is a Mobitz II, Second Degree Block. Epinephrine dose is 2-10 mcg/min
The QRS complexes are dropped following some of the P waves. whereas
There is no progression of PR intervals as in the Mobitz I. Dopamine dose is 2-10 mcg/kg/min
Do you see the similarities
This is a serious situation!! Do you see the differences
This requires a Transcutaneous Pacemaker.
You may consider Atropine 0.5 mg while awaiting the pacemaker. Keep in mind check the pulse
Atropine speeds up the SA 9node and since there are P waves that are 10
If there is no pulse- administer Epinephrine 1 mg*
blocked it is not a good drug for these high degree blocks. (AHA 2010
Update)
++ Atropine is no longer recommended. (AHA 2010 Update)
Give priority to IV/IO access.
! Do not routinely insert an advanced airway unless bag/mask is
ineffective
! !
!
!
This is a fibrillating heart and often referred to as a
! Ventricular Fibrillation sometimes called a VF.
! To defibrillate a fibrillating heart shock it to stop it.
Like rebooting your computer!!!.
This is a Torsades de Pointes.
!
This is a rhythm that is wide and ugly.
This rhythm is appropriate to defibrillate
Wide and ugly is usually ventricular in origin.
There are two ways to defibrillate Monophasic or Biphasic
! Monophasic defibrillators direct the electrical energy into one
Look closely at this rhythm it appears in groups.
That indicates it is jumping its focus.
Biphasic defibrillators direct the! electrical energy into both pads
Pad and out the other - Use 360 joules
Magnesium is the drug of choice.
at the same time. Biphasic is better because you only
have to use half as many joutles 200 joules

!
! This is called a polymorphic tachycardia.
This is another tachycardia that is wide and ugly!!
! Wide and ugly is usually ventricular in origin.
The complexes are irregular.
! If a patient has polymorphic VT, the patient is likely to be unstable, and
This is an Asystole. It is also referred to as an agonal rhythm. rescuers should treat the rhythm as VF. They should deliver high-
You must not call this a Flat Line. energy defibrillations. (2005 Update)
A Flat Line occurs when the leads come off your patient.
An Asystole occurs when the heart dies.
To confirm the difference between asystole and flat line turn up the
gain or sensitivity on your monitor.
An Asystole is the final rhythm of a patient initially in VF or VT
Prolonged efforts are unnecessary and futile unless special situations
exsist such as hypothermia and drug overdose.
Keep up with your high-quality CPR
Try some Epinephrine 1 mg every 3-5 minutes.
Try some Vasopressin 40 units for EITHER the first dose of This is called a monomorphic tachycardia.
Epinephrine or the second dose. NOT in addition to Epi.. This is another tachycardia that is wide and ugly!!
11 This may or may not be ventricular 12in origin.
The complexes here are uniform.
There are two rules about wide complex tachycardias.
Rule #1 Always assume they are ventricular in origin
!
!
!
!
This is a Supraventricular Tachycardia. This rhythm is going very
! fast. It is going super fast. It is originating above the ventricles. This is a Tachycardia with the Vagal Maneuver.

! Therefore supra-ventricular tachycardia. Check your patient.

If this patient is stable try Adenosine. The initial dose is 6
! mg* If that doesnt work you may try 12 mg and if that doesnt
work try again 12 mg.
! Push it fast and flush it fast. Anticipate a 6 second asystole.
! You could try the Vagal Maneuver. The AHA considers the vagal
maneuver your first intervention.* Be careful, your hospital may not
want you to do this. You may vagal! your patient down to a complete
heart block.
!
This is a wide-complex tachycardia. Assume it is ventricular in
origin until you prove otherwise. Therefore, this is a ventricular
tachycardia..
!
This is another example of a Supraventricular Tachycardia. If the patient is stable you should consider Amiodarone for treatment.
(AHA 2010 Update)
Supraventricular Tachycardias: If the patient is unstable you should check his pulse.
Usually go faster than 180 If he is unstable with a pulse you would need to
cardiovert.
Have an abrupt start
If there is no pulse this is a pulseless ventricular tachycardia
Have narrow complexes and you need to defibrillate.

Note you may not see the abrupt start on the ECG strip (like on your
test)!!! The test question states that the patient suddenly felt dizzy,
indicating a SVT may have occurred. If this patient is stable:*
Try the vagal maneuver*
If that doesnt work, try adenosice 6-12-12
If that doesnt work, try cardioversion

13 14
 "!0+44/(!H+4!":,.4
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' <=(!B(O!FCEE!)58!
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Atrial flutter is a dysrhythmia that occurs in adults with severe
damage to the heart muscle. The A-V node does not allow conduction of
all the atrial impulses to the ventricles. The atrial response may be 240-
360 beats per minute while the ventricular response may be 75-150 beats
per minute. The ECG tracing has a saw tooth appearance.
The clinical significance of atrial flutter is the ventricular response
rate. If the ventricular response rate is 75 beats per minute, it should be
well tolerated. If, on the other hand, the ventricular response rate is 150
beats per minute, it could cause angina, congestive heart failure or other
signs of cardiac decompensation. The following strip shows flutter
waves. If the ventricular rate is greater than 150 bpm, cardioversion is
indicated.
! Bag/Mask Ventilation (demo in class)
"4*+%/!N+:*+//%4+,&!
Atrial fibrillation is asynchronous contraction of the atrial
muscles that causes the atria to contract irregularly and faster than the
ventricles. This atrial fibrillation results in complete incoordination of
atrial contractions so that atrial pumping ceases altogether. When the
muscle fibrillates, the muscle fibers of the atrium quiver individually
instead of contracting together. The quivering cancels out the pumping of
the atrium and blood may pool in the atrium of the heart. This pooling
can promote thrombus formation within the atria. If the patient is
unstable cardiovert. Do not cardiovert a stable patient without expert
consultation.
15
!
!
2011 CPR starts with scene safety and then:
Check your patient for unresponsiveness and if your patient is
unresponsive you must immediately call the hospitals emergency
response system Call the Code!!
Then return to the patient and take no more that 10 seconds to assess for
breathing and pulse. Patients that are gasping or agonal breathing do not
have adequate breathing. If there is no pulse or breathing begin chest
compressions immediately at a rate of 100 X min.* (AHA 2010 Update)
Push hard (demo in class)
Push fast (demo in class)
Allow the chest to recoil (demo in class)
Minimize interruptions. If interruptions are needed, take 10 sec or
less.*
High-quality CPR can easily be performed without advanced equipment
until the AED arrives.
There are 3 ways to provide rescue breaths
Mouth to mouth (demo in class)
Mouth to barrier device (demo in class)
The BLS survey includes the following:
Check for unresponsiveness
Activate the EMS and get the AED
Check for circulation
Early defibrillate if appropriate*
The best chance of survival:
2 minutes of CPR then 1 shock then 2 more minutes of CPR
Switch providers every 2 minutes.which is 5 cycles*
If the AED indicates no shock advised or does not promptly analyze the
rhythm, you must resume CPR beginning with chest compressions and
continue for 2 minutes which is 5 cycles*
16

)%//+&7!4=(!),#(!
5*+@%*6!2.*$(6!P!"H)Q-!%&#!K(1+:*+//%4+,&!
!
Assessment begins with checking for stability. You must
call the code if your patient:
Is unresponsive.
If your hospital has a Rapid Response Team you may want to call the RR
Team for identifying and treating early clinical deterioration.*
Severe respiratory distress.
Chest Pain or Facial Droop, Arm Drift, Slurred Speech
Symptomatic Bradycardia
After you call the code call return to your patient and take only 10
seconds to determine if your patient is breathing or has a pulse. If there is
no pulse begin CHEST COMPRESSIONS (C for compressions)
Effective Chest Compressions:
Changes in the ACLS treatment of cardiac arrest have
been designed to minimize interruptions in chest compressions
for rhythm check, pulse check, and ACLS therapies. There is
much more emphasis on CPR with minimal interruptions in
chest compression. Two of three studies showed that 1 - 3
minutes of EMS CPR before attempted defibrillation improved
survival for victims of VF/SCA.(2005 Update)
Push Hard, Push Fast, and Allow the Chest to
Recoil. are the three components of high-quality
CPR.*
Minimize interruptions. Prolonged interruptions of chest
compressions is the most common mistake of managing
cardiac arrest.* When chest compressions are
interrupted, blood flow stops and coronary artery
perfusion pressure quickly falls. The lower the coronary
artery perfusion pressure the lower the victims chance
of survival. (2005 Update)
Successful resuscitation of a patient in cardiac arrest depends
greatly on the performance of high-quality CPR.
Compression-to-Ventilation ratio should be 30:2 for all
ages with 5 cycles which is 2 minutes of CPR.
17
Rotation of 2-man CPR is every 2 minutes. The switch
should be completed in 5 sec. (2005 Update)
Rescue Breaths without compressions =
10-12 breaths/min = 1 breath every 5-6 sec
Rescue Breaths for a victim with a pulse is also
10-12 breaths/min = 1 breath every 5-6 sec*
Rescue Breaths with advanced airway =
8-10 breaths/min = 1 breath every 6-8 sec. Each
breath given over 1 second*
(2005 Update)
OPEN THE AIRWAY (A for Airway)
There are three ways to open the airway:
Head tiltchin lift
Jaw thrust for the trauma patient
Suctioning the oropharyngeal airway if secretions are present
Yanker or catheter suction. Limit suctioning to 10 seconds
.
A patient is RESPIRATORY FAILURE with a heart rate that is
dropping rapidly, consider this patients bradycardia is caused by a
breathing problem and not a heart problem. Therefore, airway
management with simple airway maneuvers and assisted
ventilations is your highest priority for a heart rate that is dropping
rapidly.*
CHECK FOR BREATHING (B for Breathing)
Ventilations may be provided by choosing one of three ways:
Mouth to mouth
All rescuers should take a normal breath not a deep breath
before mouth-mouth or mouth to barrier device. The rescuer
should be able to make the chest rise without taking a deep
breath. (2005 Update)
One way valve Barrier Device using a normal breath.
Bag Mask Ventilation
Breaths that are given too quickly, too forcefully, or too
large of volume may be harmful for several reasons:
The positive pressure in the chest that is created by
rescue breaths will decrease venous return to the heart.
This limits the refilling of the heart, so it will reduce
18
 cardiac output created by subsequent chest
compressions.
Large tidal volumes and forceful breaths in the
unprotected airway are also likely to cause gastric
inflation and its complications. (2005 Update)
The rescuer should compress a 1 L bag about half.
The rescuer should compress a 2 L bag about a third
Less ventilations than previously are now recommended:
During the first minutes of CPR for VF and Sudden
Cardiac Arrest (SCA), the oxygen content in the blood
initially remains adequate but the blood delivery is
inadequate.
Therefore, chest compressions are more important for
the delivery than the ventilations.
H(!%!0(%#(*!
As a first responder you may be the code team leader until the
hospital code team arrives. As a code team leader
You will delegate roles and responsibilities according to scope of
practice
You will organize interventions to minimize interruptions in chest
compressions.
You will ask for confirmation of task that have been completed
Ask for good ideas for differential diagnoses. Ask if anything has
been overlooked.
Review on going record of drugs and treatments administered
Speak in a friendly, controlled tone of voice. Avoid shouting!!
H(!%!<(%@!R(@:(*!
As a team member
You should have a clear understanding of your role assignment
and be prepared to carry out those responsibilities.
A team member may be required to intervene if the action that is
about to occur is inappropriate.
Repeat the drug and dose that is to be administered and follow-up
with closed loop communication (ie Epi in)
Ask for new task if your unable to perform the task assigned.
Clearly draw attention to significant changes in the patients
clinical condition.
19
In the Megacode you will be evaluated on using your leader skills
and member skills.
The first two responders to your code call may be the RTs!!! I
found these guys to be Johnny on the spot. You might delegate them
to take over the CPR for you that frees you up to Be A Leader! The
RTs may want to maintain the airway with the following devices.
Oropharyngeal airway for the unconscious patient (demo)
Nasopharyngeal airway for the semiconscious patient (demo in
class)
They will be responsible for airway management of oxygen
administration and suction.
The next responder may be bringing the crash cart. You might
delegate someone to be the med nurse and open the cart and do the
following:
Start 2 IV sites in the anticubital if not already done Do not
interrupt CPR for IV access
Hang NS to each IV site
Pull up two 20 cc syringes of NS to use for fluid boluses
Prepare 2 syringes of Epinephrine each 1 mg (can be given ET)
Prepare 1 dose of Vasopressin (40 unites) as a alternative to
Epinephrine (can be given ET).
Prepare some other alternatives such as antiarrhythmics
Amiodarone 300 mg first dose: 150 mg second dose
Lidocaine 1-1.5 mg/kg first dose: 0.5-0.75 second dose
(both of the above can be given ET)
Intravenous or intraosseous drug administration is preferred to
endotracheal administration. For this reason, the endotracheal doses of
resuscitation medications are not listed in the ACLS Pulseless Arrest
Algorithm.
The optimal endotracheal dose of most drugs in unknown but is
typically 2-2 times the recommended IV dose. Providers should dilute
the recommended dose in 5-10 ml of water or normal saline and inject it
into the endotracheal tube. Some studies indicate that dilution in water
rather than normal saline may achieve a better drug absorption.
20
 Administration of drugs into the trachea results in lower blood
concentration than the same dose given by IV route. Thus, although the
endotracheal administration of some resuscitation drugs is possible, IV or
IO drug administration provides more predictable drug delivery and
pharmacological effect. (2005 Update)
You may want to delegate the next responder to scribe the code.
That should be someone that is familiar with the drugs, is an ACLS
provider, and is good with charting details.
You may want to delegate someone to be in charge of the
defibrillator and attach the defibrillator to the patient. Most defibrillators
have jell pads and some have quick look paddles. Jell pads or self
adhesive pads referred to as hands free pads allow for more rapid
defibrillations* and will reduce the risk of electrical arcing. If you are
using quick look paddles dont forget to put conductive jell on the
paddles.
Once the defibrillator is attached to the patient by placing a pad or
paddle on the upper right chest and a second pad or paddle on the lateral
left chest you will be able to determine the rhythm that needs to be
treated. If the following rhythm appears on your monitor it is a
ventricular fibrillation and you must defibrillate the fibrillating heart.
Determine the type of monitor you have
Monophasic One way current
Use one single shock at 360 joules for an adult.
Biphasic Two way current
Use one single shock at 150-200 joules for adults.
Before the machine can discharge the shock it needs to be
charged. CPR should be continued during the charging of the
defibrillator to minimize interruptions* New defibrillators charge rapidly
(<10 sec). Before defibrillation always - keep yourself safe. and check
others to make sure everyone is clear. Keep in mind IV tubing can
21
conduct electricity. The IV nurse should not be administering drugs into
the IV ports.
Im clear
Youre clear
Oxygen clear*
Defibrillate one time and one time only and then direct the RTs
(if thats who you delegated to do CPR) to continue chest compression
along with bag/mask ventilation for two additional minutes without
interruptions. Do not pause for greater than 10 seconds to recheck the
rhythm. Providing quality compressions immediately before a
defibrillation increases the chance of successful conversion of VF.*
Delegate the med nurse to administer the drug of your choice.
For most team leaders that would be Epinephrine 1 mg IV followed with
a 20 cc NS fluid bolus.
When VF cardiac arrest is present for several minutes, the heart
has probably used up most of the available oxygen needed to contract
effectively. The VF is therefore, fine VF and defibrillation is not
typically successful. If it is successful, it is unlikely to pump blood
effectively for several seconds or even minutes after defibrillation. A
period of CPR BEFORE shock delivery will provide some blood flow to
the heart, delivering some oxygen and substrate to the heart muscle. This
will make a shock more likely to eliminate the VF and will make the
heart more likely to resume an effective rhythm and effective pumping
function after shock delivery. (2005 Update)
After one shock of either biphasic or monophasic current begin
uninterrupted chest compressions for 2 minutes/5 cycles at a ratio of 30:2
with a compression rate (speed) of 100 X minute. (2005 Update)
With most defibrillators now available, the first shock eliminates
VF more than 85% of the time. In cases where the first shock fails,
resumption of CPR is likely to confer a greater value than another shock.
Even when a shock eliminates VF, it takes several minutes for a
normal heart rhythm to return and more time for the heart to create blood
flow. A brief period of chest compressions can deliver oxygen and
sources of energy to the heart, increasing the likely that the heart will be
able to effectively pump blood after the shock. (2005 Update)
22

S,.Q*(!-4+//!4=(!0(%#(*TT!
Most leaders choose Epinephrine as the first line drug in VF for the
following reasons:
Speeds up the heart
Increases the contractility
Improves coronary artery pressure
IV/IO 1 mg
The recommended route in cardiac arrest is the peripheral IV.*
Always bolus after administration
Push it in the IV port
Push it up with a fluid bolus
Push it around with some UNINTERRUPTED CHEST
COMPRESSIONS
Repeat defibrillation if your patient remains in VF or Pulseless VT
after 2 minutes/5 cycles of Compression/Ventilations
Epinephrine may be given every 3-5 minutes. The scriber must
keep track of the times the medications are given.
One dose of Vasopressin (40 units) may be given IV or IO instead
of EITHER the first or second dose of Epinephrine. Give
Vasopressin one time and one time only. (2005 Update)
Drug Administration:
When drug administration is indicated, the drugs should be
administered during CPR, as soon as possible after the rhythm is
checked. A drug may administered during the CPR that is performed
while the defibrillator is charging, or during the CPR performed
immediately after the shock is delivered. Drug delivery should not
interrupt CPR. Rescuers should prepare the next drug dose before it is
time for the next rhythm check so that the drug can be administered as
soon as possible after the rhythm check.
The timing of the drug is less important than minimizing
interruptions in chest compressions.
A drug may be administered:
During the CPR
While the defibrillator is charging
Immediately after the shock (2005 Update)
23
When VF or pulseless VT persist after 2-3 shocks plus CPR and
administration of a vasopressor, consider administering an
antiarrhythmic such as Amiodarone or Lidocaine for refractory
(unresponsive) VF or VT. . The arrest dose of Amiodarone is 300 mg*
and the follow up dose if needed is 150 mg and given only one time.
The arrest dose of Lidocaine is 1-1.5 mg/kg and additional doses of
0.5-0.75 mg/kg (2005 Update)
Amiodarone Lidocaine
(Cordarone) (if Amio not avail)
300 mg IVP (1st dose) 1-1.5mg/Kg. IVP
Every 3-5 minutes Every 3-5 minutes
Additional dose, 150 mg IVP Additional doses,
Max dose, 2.2 gm/24 hours 0.5-0.75 mg/Kg
Not OK for ET tube Max dose, 3mg/Kg
OK for ET tube
!
>-4%:/+-=!%&!"#$%&'(#!"+*O%6!
After 2 minutes of CPR following the defibrillation you may
want to establish an advanced airway.Because insertion of an advanced
airway may require interruption of chest compressions for many seconds,
the rescuer should weigh the need for compressions against the need for
insertion of an advanced airway. Rescuers may defer insertion of an
advanced airway until the patient fails to respond to initial CPR and
defibrillation. As a Code Team Leader you may want to direct the
intubator not to intubate until 2 minutes of effective chest
compressions have been completed.
Insertion of an advanced airway may not be a high priority.
Because insertion of an advanced airway may require interruption
of chest compressions for many seconds, the rescuer should weigh
the need for compressions against the need for insertion of an
advanced airway. Airway insertion may be deferred until several
minutes into the attempted resuscitation. (2005 Update)
Once the ET tube is in continuous chest compression must be
given with no pauses for ventilation.*
Do not use ties to secure the ET tube around the neck because
it can occlude venous return*
If the ET tube requires suctioning, suction during withdrawal
and take no more than 10 sec.*
24

Once the tube is inserted the placement needs to be confirmed:
Mist in the tube may be first seen.
Check for gastric sounds next.
Check for lung sounds left first then right.
CO2 detector turning gold.
Continuous capnography waveform is the most reliable method of
confirming and monitoring placement of the ET tube*
Capnography is now recommended by the AHA to confirm and
monitor the endotracheal tube as well as the adequacy for CPR*
based on end-tidal CO2. Update 2010
Recall lab values of CO2 level of a blood Gas should be
35-40. Therefore, the closer your capongrahy reading is to
normal values, the more effective the resuscitation
technique.
Such as after ROSC the PETCO2 should be 35-40 mg/h
A PETCO2 level of >10 would be a sign of effective CPR.*
whereas, a PETCO2 level of 8 would indicate ineffective CPR*
?1!6,.!7(4!%!*=64=@!P!'=('U!4=(!3./-(!
"&6!,*7%&+V(#!*=64=@!O+4=,.4!%!3./-(!+-!%!5>"!W!
S,.Q*(!-4+//!4=(!/(%#(*TT!!
Continue CPRW!
Delegate your team to look for the Possible Causes
P = Possible cause (?)
E = Epinephrine 1 mg *. which is a vasopressor
No vasopressor has been shown to increase survival
from PEA. Because vasopressors (epinephrine and
vasopressin) can improve aortic diastolic blood pressure
and coronary artery perfusion pressure, vasopressors
such as epinephrine continue to be recommended*.
A = No longer is Atropine recommended for PEA.. The AHA
recommends Vasopressin (2010 Update)

The ability to achieve a good resuscitation outcome, with return of a

perfusion rhythm and spontaneous respirations of a PEA depends on
rapid assessment and identification of an immediately correctable cause.
The two most common causes of PEA are hypovolemia and Hypoxia
The American Heart refers to the causes as the Hs and Ts They are as
follows:
Hypovolemia
Clues: Poor skin color (pallor).
Rapid heart rate with narrow complex
Flat neck vein
Intervention: Open up the bag of NS
Hypoxia
Clues: Cyanosis
Slow heart rate
Intervention: Check the FIO2
Check airway placement
!

25 26
 Hypothermia "-6-4,/(!
Clues: Cold skin
Low core temperature
Intervention: Use warmed NS
Caution: not dead till warm and dead.
Hyperkalemia
Clues: Peaked T waves
History of renal failure
Intervention: Infuse Na Bicarb Prognosis is poor
Hypokalemia Continue CPR
Clues: Flat T waves IV access is a priority over advanced airway management unless
Intervention: Infuse K+ (not be confused with K+ bag/mask ventilation is ineffective.
bolus!) Do not routinely insert an advanced airway unless ventilations with
Hydrogen ion excess metabolic acidosis a bag-mask are ineffective.
Clues: Small amplitude QRS Start 2 IV sites in the anticubital if not already done Do not
History of renal failure interrupt CPR for IV access
Hypoglycemia Try more Epi 1 mg or Vasopressin as an alternative for EITHER
Clues: Altered LOC the first or second dose of epinephrine
Intervention: D5w The standard epinephrine dose is 1 mg IV/IO every 3-5 minutes
Tension Pneumothorax check breath sounds of 1:10,000 solution*. High-dose epinephrine is not routinely
Clues: Deviated trachea recommended.
Neck vein distention The AHA no longer recommends Atropine for the asystole (2010
Intervention: Needle decompress the chest Update)
Tamponade Remember this is a nonshockable rhythm
Clues: Bulging neck veins Be aware of some reasons to terminate resuscitative efforts, such
Rapid heart rate as rigor mortis, indications of DNR and threat to safety.
Intervention: Pericardiocentsis
Thrombosis coronary and/or lung
Clues: Coronary = ST segment elevation =
STEMI
Clues: Lung = Distended neck vein Call the
surgeon.
Toxins - (drug overdose)
Clues: Bradycardia
Intervention: Try some Narcan This delegating is kinda nifty!! You may like being the code team
leader!!
Trauma

If the following rhythm appears on the monitor you must call this an
asystole. Do not call this rhythm a flat line.
27 28
 <=(!H*%#6'%*#+%
X(%*4!8%4(-!/(--!4=%&!YC!H5R!
Immediate supplemental oxygen as needed to keep sats >94%
Quickly obtain an IV access.
Call for a 12-lead ECG
The bradycardias may include the following:
Sinus Bradycardia
First Degree Block
Second Degree Block (Mobitz I and Mobitz II)
Third Degree Block
To determine if the patient is symptomatic you may want to use the
pneumonic CHAPS.!
C for color = patients that are pale and pasty
H for hypotensive = blood pressures less that 90/60
A for altered level of consciousness
P for signs of poor perfusion
S for SOB = dont forget the oxygen
Treatment is determined by the severity: To determine the intervention
you may want to use the pneumonic Bradycardias are to darn easy.
A for Atropine = O.5 mg IV every 3-5 minutes to a maximum dose
of 3 mg is the first intervention*.
Use cautiously in presence of MI. Atropine may worsen
ischemia and increase infarct size.
Do no rely on Atropine in high degree blocks. but for the test,
always give Atropine first while waiting for TCP
T for Transcutaneous Pacing if there is no response to
atropine and if the patient has a high degree block
D for Dopamine if the blood pressure needs to be supported
2-10 mcg/kg/min and titrate to patient response*
E for Epinephrine = while waiting for TC pacing.
2-10 mcg/min and titrate to patient response
29
5%'(@%U(*!
For a complete heart block you will need to consider a transcutaneous
pacemaker. Heres the skinny on the dials!!
There will be a pacemaker mode on your
defibrillator. There will be 2 dials.
Rate Dial
You may want a rate to be 60.
mA Dial
The energy is measured in milliamps.
Select the amps (usually 2 mA above the
dose at which consistent capture is observed)
Place the TC electrodes on the patient:
Anterior electrode to the left of the sternum
Posterior electrode on the back
Begin pacing
Check for spike with capture
Capture is usually characterized by a widening of the QRS
complex (looks like a PVC)
Dont forget to give your patient analgesia!!!
Precautions
TCP is contraindicated in severe hypothermia and/or asytole
Conscious patients require analgesia but do not delay if the
sedation will cause/contribute to deterioration.
Do not assess the carotid pulse to confirm mechanical capture ;
electrical stimulation causes muscular jerking that may mimic the
carotid pulse.
Assess Response
Asses response to patients clinical response.
Patients with ACS should be paced at the lowest heart rate that
allows clinical stability.
Start pacing at a rate of 60 and adjust to clinical response
30

<=(!<%'=6'%*#+%-!
The tachycardias can be overwhelming to understand fully.
Lets make this as simple and basic as possible. If your patient has a fast
heart rate of greater than 100 bpm that would be a tachycardia. If your
patient has a heart rate greater than 150 bpm that would be a significant
tachycardia. The higher the heart rate the more likely symptoms are due
to the tachycardia. The most important intervention is to check your
patient. Determine first if he is seriously stable or unstable.
Z&-4%:/(!<%'=6'%*#+%!P!)%*#+,$(*4!
!
If your patient is unstable with serious signs and symptoms you will
cardiovert your patient.
Serious symptoms of instability
SOB
Chest pain
Weakness, fatigue, near-fainting (presyncope), and/or syncope
Altered LOC
Serious signs of instability
Pulmonary edema
Hypotension
Poor peripheral perfusion (cool extremities, decreased urine output)
Ischemic EKG change
The 2 keys to management of patients with unstable tachycardia are:
Rapid recognition that the patient is significantly symptomatic or
unstable
Rapid recognition that the signs and symptoms are caused by the
tachycardia
If your patient is unconscious with a tachycardia for the ACLS
test you will need to review the patients home medications!!* I
dont get this statement. If you do - let me know.
If your patient is seriously unstable Cardiovert:
Do not delay cardioversion if you think the tachycardia is causing the
unstable signs and symptoms or if the patient is clinically deteriorating.
31
In addition, you may consider a dose of Adenosine while preparing to
cardiovert. But do not delay to cardiovert to administer the drug or to
establish an IV access. (2005 Update)
If you have decided to cardiovert lets get ready.
Airway airway airway!! Always secure the airway.
Oropharyngeal for the unconscious
Nasophayrngeal for the semiconscious
BMV ready with oxygen source.
Make sure your suction is ready for use
Better have an IV
Automatic blood pressure cuff would be cool
Surely your patient is being monitored
Better have the crash cart available
Do you have time for a 12-lead and a chest film?
Lets get set
Premedicate with a sedative plus analgesic. Versed is cool.
You dont want your patient to wake up and remember you!!
Turn on the defibrillator
Attach monitor leads on the patient white on right
smoke (black) over fire (red)
Put the defibrillator in the sync mode
Look for markers on the R wave indicating sync mode
Adjust monitor gain if necessary until sync markers occur with
each R wave
Are the conductor pads in place? Usually cardioversion is not done
with hand held paddles.
Make sure the lead select switch is in the lead I, II, III
position and not the paddle position.
Select the energy dose for the specific type of rhythm.
For cardioversion of UNSTABLE atrial fibrillation, the
recommended initial monophasic energy dose is 100j to 200j with a
monophasic waveform. A dose of 100j to 120j is reasonable with a
biphasic waveform. Escalate the second and subsequent shock
dose as needed.
Cardioversion of atrial flutter and SVT generally requires less
energy. An initial energy dose of 50j to 100j monophasic.
32
 100j-200j for monophasic and 100j-120j for biphasic waveforms.
(Depending on the acuity of your patient). Atrial flutter and SVTs !!!!!!!!!!!((G$--,H( !!!!!!!!!!!!!!!!!56"'(
generally require less joules at 50j 100j. (2005 Update) Regular Regular
Go 2[<! R,&,@,*3=+'
Charge the defibrillator and announce what you are doing. Adenosine Amiodarone or Adenosine!
Im clear Youre clear - Oxygen clear
Depress the discharge button..
Check the monitor. - Check the patient.
You may have to up the joules and reattempt.
Irregular Irregular
You might want to bolus with an antiarrhythmic drug followed
with an infusion. "GN+: <,*-%#(-
Calcium Channel Blockers Magnesium
24%:/(!<%'=6'%*#+%!G!R(#+'%4(! !

The patients with stable tachycardia are the those with no signs of
serious signs and symptoms as discussed in the patients with unstable
tachycardia. There is 2 rules in treated the stable tachycardia.
Treat the underlying cause
Treat with medication and not cardioversion like you did in
unstable tachycardia. To determine which drug to treat these stable
tachycardias, the AHA suggests that you begin with classifying the
tachycardia into two categories:
Narrow Complex then further classify the rhythm into regular
and irregular
Supraventricular Tachycardia is a regular rhythm
Atrial fibs and flutters are irregular rhythms (2005 Update)
Wide Complex then further classify the rhythm into regular
and irregular(
Monomorphic VT is a regular rhythm
Torsades de Point and Polymorphic VT are irregular
Refer to the Tachycardia algorithm to determine which drug to use. The
following is an example of drug determination:
The basic ACLS provider is expected to recognize a stable narrow-
complex or wide-complex tachycardia and classify the rhythm as
regular or irregular. Regular narrow-complex tachycardias may be
treated initially with vagal maneuvers and adenosine.
SVT that is stable vagal and medicate with Adenosine
SVT tha is unstable cardiovert
For your test!! A scenario is presented with a patient with a normal
BP, RR, and Sats but has a heart rate of 200/min. You can not
respond appropriately until you know what kind of tachycardia is
present.. So you must get a 12-lead ECG. If it were me, I would
want a rhythm strip.
For your test!! A scenario is presented with abnormal BP, RR, Sats,
and patient is cool to touch and complaints of chest pain. The rhythm
is a wide complex tachycardia. This tachycardia is unstable so the
patient must be cardioverted. This patient is seriously unstable and
you should not take the time to medicate*

33 34
 "'.4(!),*,&%*6!26&#*,@(-!
dissolve clots, and inhibit thrombin and platelets. These drugs are:
A video will be shown in your class. The following information is
dramatized in the video.
The ACLS Provider Course emphasizes the need to acquire a 12 lead
ECG immediately if the patient is stable*. Then recognize ST segment
elevation to initiate early reperfusion therapy. The ACLS Experienced
Provider Course includes assessment, triage and treatment for non-ST
elevation myocardial infarction (NSTEMI) and high-risk unstable angina
Sudden cardiac death due to VF and Bradycardic hypotensive rhythms
also occur with ACS. VF is most likely to develop during the first 4
hours after onset of symptoms. You must anticipate these occurrences
and be prepared for interventions as learned previously.
Signs and symptoms suggestive of ACS starts with Dispatch and may
include the following:
Retrosternal chest discomfort that is described as pressure, fullness,
squeezing that radiates to the shoulders, neck, arms, jaw, or back
Lightheadedness, fainting, sweating, or nausea
Unexplained shortness of breath.
Women have vague signs and symptoms of ACS. She often will
complain of epigastric pain and will take antacids for this pain.
Dont overlook the women for ACS. Get a 12-lead ECG to rule
out an MI*..
Diagnosis begins with a 12-lead ECG. Note the Q wave with ST-
segment elevation.
35
Treatment of ACS involves the initial use of drug to relieve discomfort,
Oxygen in the first 6 hours of therapy 4 L/NC to keep sats >90%
Aspirin 160-325 mg (or 2 baby aspirin) to chew or rectal
suppositories for patients with nausea
Nitroglycerin sublingually or spray every 3-5 minutes up to three
doses if the systolic BP is greater than 90 mm and the patient has
no recent use of phosphodiesterase (Viagra). Do not give Nitro to
patients with tachycardia or bradycardia. Nitro opens or dialates
the coronary vessels. IV nitroglycerin may also be used to titrate
effect.
Morphine 2-4 mg and repeat as much as it takes to relieve pain,
to relax the smooth muscles, and to reduce the oxygen demand on
the heart. Monitor for hypotension.
Fibrinolytic or thrombolytic therapy - referred to as clot busters
if there are no contraindications of fibrinolytic infusion. Examples
of fibrinolytics are as follows:
tPA
Reteplase
Streptokinase which is not used as much as in the past.
Fibrinolytics are not recommended for patients presenting more
than 12 hours after onset of symptoms. Do not give fibrinolytics
to patients who present more than 24 hours after the onset of
symptoms.
Heparin if not contraindicated. The inappropriate dosing can
cause excess intracerebral bleeding and major hemorrhage in
STEMI patients.
PCI (precutaneous coronary intervention) as an alternative to
fibrinolytics. PCIs are time sensitive. See your text for appropriate
times for use.
'
'
36
 24*,U(!
A video will be shown in your class. The following information is
dramatized in the video.
Stroke is a general term. It is the third leading cause of death. It refers
to acute neurologic impairment that follows interruption in blood supply
to the brain. There are two types of strokes:
Ischemic Strokes occur with the occlusion of an artery to a region
of the brain.
Hemorrhagic Strokes occurs with the irruption of an artery to a
region of the brain therefore, anticoagulants need to be avoided.
The goal of stoke care is to minimize brain injury and maximize the
patients recovery. This can be accomplished with the following
guidelines: Referred to as the 7 Ds
Rapid detection
Rapid EMS dispatch and delivery
Rapid diagnosis with a noncontrast CT scan
Rapid data collection for drug administration.
Rapid discussion with the family and patient regarding treatment.
The warning sings and symptoms of a stroke may be subtle. They
include the following which is referred to as the Cincinnati Prehospital
Stroke Scale (CPSS).*
Facial droop have the patient smile and show teeth
Arm drift have the patient close eyes and hold both arms out
Trouble speaking have the patient say You cant teach an old
dog new tricks.
The presence of 1 finding indicates a 72% probability of stroke. The
presence of 3 findings indicates 85% probability of stroke.
The Los Angeles Prehospital Stroke Screen (LAPSS) is a more detailed
screen which builds on the physical findings of the CPPS, adding criteria
for age, lack of history of seizures, symptoms duration, blood glucose
levels, and lack of preexisting ambulation problems. A person with
positive findings in all 6 criteria has a 97% probability of a stroke.
The patient with acute stroke is at risk for respiratory compromise from
aspiration, upper airway obstruction and hypoventilation.
37
The general assessment and stabilization of the stroke patient is time
sensitive. Therefore, hospitals have organized Stroke Teams to
facilitate the assessment and stabilization. The goal of the Stroke Team
is assessment within 10 minutes upon arrival to the ED using the
following criteria:
Assess ABCs and baseline vital signs
Provide oxygen
Determine onset time is of essence.
Establish IV and draw electrolytes, CBC, coagulation studies, and
blood glucose with bedside glucose.
Preform neurologic assessment
To be completed within 25 minutes of patients arrival
Order noncontrast CT scan of the head* and 12-lead ECG and read
by a qualified physician. If your hospital does not have a CT
scanner, the patient should be averted to a nearby hospital with CT
capabilities.*
To be completed within 25 minutes of arrival and read within 45
minutes from performance
The presence of hemorrhage versus no hemorrhage determines the next
steps in treatmemt:
If the CT is positive there is hemorrhage present and the patient is
not a candidate for fibrinolytic therapy. Consult a neurologist or
neurosurgeon. This indicates an Acute Cerebral Hemorrhage.
If the CT is negative (normal) there is no hemorrhage present and
the patient is a candidate for fibrinolytic therapy. The physician
then discusses the risks and benefits of treatment with the patient
and family and may proceed with tPA. A good-to-excellent
outcome is tPA (fibrinolytic therapy) for the patient with ischemic
stroke within 3 hours of onset.
The contraindications to tPA are as follows:
Positive CT scan
Presentation suggestive of subarachnoid hemorrhage even with a
normal CT scan
Abnormal blood vessels in the brain
History of intracranial hemorrhage
Uncontrolled hypertension. Blood pressures should be less that
185/110 before treatment begins Labetalol may be used to bring
the BP under control if given within the 3 hour window.
Witnessed seizure at stroke onset
38
 Trauma
Abnormal coagulation studies 8(4.*&!4,!23,&4%&(,.-!)+*'./%4+,&!
The indications for tPA are as follows:
If the age is greater than 18 years ROSC is deemed to have occurred when chest compressions are
If the clinical diagnosis of stroke is measurable with neurologic not required for 20 consecutive minutes and signs of circulation
deficit persist. !
If the onset of signs and symptoms is within 3 hours before If ROSC occurs for the hypotensive patient after cardiac arrest,
treatment can begin. A patient that presents is less than 3 hours bolus the patient with 1-2 L or NS or RL*
without contraindications is a Maintain a systolic BP at 90 mm/Hg* which may be accomplished
candidate for IV fibrinolytic therapy. with Dopamine.
General Stroke Care includes the following: Continue to optimize ventilation and oxygenation*
Support ABC !
Monitor blood glucose R(7%!),#(!
Monitor for complications of fibrinolytic therapy !
Monitor for hypertension. Your ACLS mega code will follow the guidelines on page 151-155
which includes the following
The risk of fibrinolytic therapy: Respiratory Management with a pulse
Cerebral hemorrhage Respiratory Management without a pulse and use of the AED
Bradycardia VF Asystole
<=(*%3(.4+'!X63,4=(*@+%! Unstable Tachycardia VF PEA ROSC
Mild hypothermia (cooling of the brain to about 89-93 F or 32-34 C has Stable Tachycardia VF PEA ROSC
shown to improve survival from cardiac arrest and comatose patients.
Patients that are responding to verbal stimuli after cardiac arrest are not
candidates for therapeutic hypothermia* If the patient has a response to
verbal stimuli, he, therefore, has an intact brain which includes the
hypothalamus (the thermostat of the brain). If you put a patient on
external cooling the hypothalamus competes with the external cooling
system. The more the cooling system tries to cool the body, the more
the hypothalamus tries to heat the body.
Cooling can be achieved using external cooling (ice packs, cooling
blankets) or internal cooling (peripheral administration of ice cold
IV fluids).
Begin cooling within 4 hours of ROSC
Maintain cooling temperature for 12-24 hours then rewarm slowly.
Avoid shivering which generates heat and increase oxygen
consumption.
Monitor temperature from sites such as the bladder rather then
rectal temperatures which lags behind core temperature.
39 40
 NEW AHA UPDATE: CAPNOGRAPHY
The most reliable way to confirm proper tube placement is
waveform capnography. Waveform capnography is the
measurement of carbon dioxide (CO2) in each exhaled breath.
PETCO2 measures the level of CO2.
Waveform capnography is
Simple
Insert the sampling tube at the end of the ET tube. Watch
the waveform and PETCO2 values
Direct
Capnography provides an immediate picture or patients
apnea. Pulse oximetry is delayed several minutes.
Non-invasive
Reduces the need for arterial blood sampling.
CAUTION: You still need to assess for bilateral breath
sounds. Capnography cannot detect right main-stem intubation.
You use a capnograph to sample the exhaled CO2. The capnograph
is a device which has a sampling tube, and CO2 sensor.
Normal PETCO2 levels are 35 - 45 mm Hg
Capnography is a great way to
Confirm proper ET tube placement
Monitor quality and effectiveness of CPR
Detect return or loss of ROSC
Capnography is an early warning system of impending
respiratory crisis.
When a person hyperventilates, their CO2 goes
down PETCO2 < 35 mmHG
When a person hypoventilates, their CO2 goes up
PETCO2 > 45 mmHg
41
Hyperventilation: caused by anxiety, bronchospasm, pulmonary
embolus, cardiac arrest, decreased cardiac output, hypotension,
cold, severe pulmonary edema.
Hypoventilation: caused by overdose, sedation, intoxication, head
trauma, stroke, increased cardiac output with increased breathing,
fever, sepsis, pain, severe difficulty breathing, chronic hypercapnia
Pay more attention to the PETCO2 trend, than the actual
number. Patients with a steadily rising PETCO2 can soon
require assisted ventilations or intubation.
Capnography is the most reliable way to confirm proper tube
placement.
If PETCO2 = 0, the tube is in the esophagus
*Another possible reason is that the blood is blocked
entirely from the lungs by a massive pulmonary embolism.
ET TUBE OUT ET TUBE IN
Capnography is an indirect measure of metabolism.
Increased metabolism will increase the
production of carbon dioxide, increasing the
PETCO2.
A decrease in cardiac output will lower the
delivery of carbon dioxide to the lungs decreasing
the PETCO2.
Capnography measures the effectiveness of
CPR
Monitoring PETC02 measures cardiac output, thus
monitoring PETCO2 is a good way to measure the
effectiveness of CPR.
PETCO2 > 10 mm Hg indicates effective CPR.
Note: Patients with extended down times may have
PETCO2 readings so low that quality of
compressions will show little difference in the
number.
42
Capnography detects the return of ROSC.
Post-cardiac arrest PETC02 with ROSC is 35 - 40 mm Hg
During cardiac arrest, if you see PETCO2 shoot up, stop
CPR and check for the pulse.
There is an average sudden PETCO2 increase by
13.5mmHg with sudden ROSC before settling into a
normal range.
Capnography detects the loss of ROSC.
If PETCO2 significantly drops, check for the pulse. If no
pulse, start CPR.
'
'
/*#,#0,'12#0,-)$0'
'
1. The initial intervention for all bradycardia is__________
(Atropine 0.5 mg)
2. A patient has sinus bradycardia with a rate of 36 per minute.
Atropine has been administered to a total dose of 3 mg. A
transcutaneous pacemaker has failed to capture. The patient is
dizzy with SOB. Which drug would administer with what dose?
_______________( Dopamine 2-10 mcg/kg/min)

3. A 52 year old female presents to the ED with persistent

CAUTION: Hyperventilation in trauma victims decreases epigastric pain. Her vitals are stable along with the O2 sat. What
intracranial pressure (IPP) by decreasing the intracranial blood is you first interevention?_______________________________
flow. The result is cerebral ischemia. (Obtain a 12-lead ECG))
'
' 4. High quality CPR includes 4 components. They are__________
' (push hard),_____________(push fast)___________,(allow the
' chest to recoil) and _____________(minimize interruptions)
'
' 5. The best chance of successful defibrillation is_____________
' _________________________________________________
' (perform high quality chest compressions prior to defibrillation)
'
' 6. What action would help to minimize interruptions during a code
' call that requires defibrillation? ______________________
' (Continuing Chest Compressions while the defibrillator is
' charging).
'
7. A defibrillator may be equipped with hands free pads are
'
better than paddles. Why are hands free pads
'
better?________________________________________
'
They can provide a more rapid defibrillation)
'
' 8. Many hospitals have Rapid Response Teams. What is their main
' purpose?____________________________________( Prevents
' deterioration to overt a code call)
'
'
'
43 44
9. Your patient with a code call received 2 doses of Epinephrine at
1 mg each which did not convert the patients VF. What
antirhythmic might work for this refractory
VF?____________________________(Amioderone at 300 mg)
10. Any organized rhythms without a pulse is referred to as _____
and you must continue CPR. The drug of choice for an
organized rhythm without a pulse is ______________
_________________________PEA, Epinephrine at 1 mg)
11. The preferred method of administering Epinephrine in a cardiac
arrest is__________________________________(peripheral)
12. High quality CPR includes push hard, push fast, allow the chest
to recoil and _________________________(prolonged
interruptions) which is a common fatal mistake in cardiac arrest
management.
13. If you are unsure the patient has a pulse or has a faint pulse you
must initiate__________________________immediately.
( chest compressions)
14. The BLS Survey includes check for unresponsiveness, activate
the EMS and get the AED, check for circulation, and
_____________________________(early defibrillation)
15. If chest compressions need to be interrupted you should allow
only_____________________(ten seconds) for the interruptions.
16. When doing chest compression with ventilations during a cardiac
arrest you should switch providers ever____________________
______________________________(2 minutes which is every 5
cycles).
17. If the patient has a pulse and is not breathing, you should deliver
one breaths every____________________(5 to 6 seconds)
18. Once an advanced airway is in place chest compressions should
continue without _________________pauses (without).
45
19. After placing an advanced airway you should secure with a
commercial device and not ties around the neck because it
can_____________________________(obstruct venous return. )
20. If the patient has an advanced airway the rate of ventilations
should be every________________________(8-10 breaths/min)
which is one breath every 6-8 seconds.
21. If you need to suction the ET tube you should take no longer
than_________________________(ten seconds)
22. There are 4 ways to confirm ET tube placement. They are
mist in the tube upon insertion, no gurgling in the stomach with
bag/mask ventilation, bilateral breaths sounds with bag/mask
ventilation and _______________________________________
(continuous waveform capnography)
23. The best way to monitor CPR of an intubated patient is
__________________________(Waveform Capnography)
24. PETCO2 refers to the amount of CO2 exhaled. The optimal
limits are _________________________with ROSC. The
PETCO2 level of ineffective CPR on the waveform
is____________________. (35-40 mm Hg) (< 8 mm Hg). The
PETCO2 level that indicated effective CPR is ____________
(> 10 mm Hg).
25. A patient with a sudden onset of palpitation or dizziness may be
experiencing a SVT and the first intervention is to determine if
the patient is stable or unstable. If the patient is stable, you may
________________________(ask the patient to vagal down)
26. If the vagal maneuver fails to convert the SVT to a sinus rhythm
the first drug intervention would you would use is
________________________________(adenosine at 6 mg)
27. If the first dose of adenosine does not work the second dose
should be ________________________(adenosine at 12 mg)
46
28. An EMS crew can terminate resuscitation if _____________
(rigor mortis) sets in.

29. Three signs of an acute stroke are facial drop, arm drift, and
slurred speech. This is referred to as the________________
(Cincinnati Prehospital Stroke Scale assessment)

30. With a positive prehospital stroke scale you would obtain a set of
vitals including blood glucose and order a ________________
___________________(noncontrast CT scan of the head)

31. If a patient is hypotensive who has achieved ROSC you should

bolus with ___________________(1-2 L) NS or LR

32. The minimum systolic blood pressure you should accept for a
hypotensive post cardiac arrest that has achieved ROSC is
________________(90 mg Hg)

33. Your priority in the care a patient with ROSC is optimizing

_________________and_______________(oxygenation and
ventilations)

34. A patient suddenly collapsed and is poorly responsive. The

monitor reveals a third-degree block. There is an IV access and
supplemental oxygen is being administered with a nonrebreather.
What would you first do?_____________(Give atropine 0.5 mg
and begin pacing as soon as the pacemaker is ready).

35. A patient becomes unresponsive and you are uncertain if a faint

pulse is present. What would you
do?___________________(Begin CPR with high-quality chest
compressions)
36. A patient with a wide-complex tachycardia that is unstable you
must_________________(cardiovert) You may not have time to
medicate this patient if he is severely unstable.
The American Heart Association strongly promotes knowledge and proficiency
in BLS, ACLS, and PALS and has developed instructional materials for this
purpose. Use of these materials in an educational course does not represent
course sponsorship by the American Heart Association. Any fees charged for
such a course, except for a portion of fees needed for AHA course material, do
not represent income to the Association.-ll

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