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Advanced Responder

ACLS Prestudy With the 2011 AHA Updates Recertification & Certification
8:00 8: 15 8:30 8:45 9:00 9:30 9:45 10:00 11:00 12:00 12:15

Advanced Cardiovascular Life Support Prestudy


Agenda for Recertification
Welcome/Introduction AHA ACLS Overview Video Instructor presentation of lethal rhythms & pretest AHA Video ACLS Primary/Secondary Survey Instructor presentation of 2011 BLS AHA ACLS Video Airway Management AHA BLS Video Practice BLS with manikins/BMV/Barrier/AED Instructor presentation of ACLS AHA video of Heart Attack and Stroke AHA video of Mega Code Instructor presentation of Mega Code Skills stations Written exam

Agenda for Certification


Day One 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 Day Two 8:00 Putting it all together 9:00 Mega Code Review 10:00 Mega Code and Written evaluation 11:00 Remediation if appropriate

Nurses Educational Opportunities www.nursesed.net Toll Free 866.266.2229 Copyright 2011

Objectives
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

.The

Electrical Impulse

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.

12-Lead EKG

P Wave
Originates in the SA Node

P-R Interval
0.12 - 0.20 Beginning of the P to the beginning of the R

T Wave

QT interval
Beginning of the Q To the end of the T

ST segment
End of the S To the beginning of the T Note: Depression or Elevation

QRS Complex
Beginning of the Q to the end of the S

Q = Infarction ST (depression = ischemia) (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.

Interpretation
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. ST segments are depressed V1, V2, V3 and V4. T waves are inverted in AVF and flat in II, III, and all chest leads. Comments: 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. Unstable angina (UA) Characterized by chest pain without exertion and normal or nondiagnostic ECG. STEMI: The ST segment elevated MI is the most time critical myocardial infarction. Early reperfusion with clot busters called fibrinolytics or balloon dilatation or stent placement called PCI (Percutaneous Coronary Intervention) will reduce mortality and minimize 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 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 rabbit ear configuration whereas a LBBB will look slurred.

Practice the Rhythm

Do you see Q waves? _______________ Is the T wave upright? ______________ Is the isoelectric line level? __________ What is the rate? ___________________ This is a normal sinus rhythm.

Do you see Q waves? _______________ Is the T wave upright? ______________ Is the isoelectric line level? __________ What is the rate? ___________________ A sinus tachycardia usually does not exceed a rate of 120-130 bpm. A rate of greater than 180 bpm is referred to as a supraventricular tachycardia The most important principle in managing a sinus tachycardia is identify the cause.

Do you see Q waves? _______________ Is the T wave upright? ______________ Is the isoelectric line level? __________ What is the rate? ___________________ A rate of less than 60 beats per minute is a Bradycardia A Bradycardia that is symptomatic requires intervention. The drug of choice for a symptomatic Bradycardia is Atropine at 0.5 mg.*

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 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 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 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 Transcutanious Pacing Try Epinephrine and/or Dopamine for its vasoconstrictive properties. Epinephrine dose is 2-10 mcg/min whereas Dopamine dose is 2-10 mcg/kg/min Do you see the similarities Do you see the differences Keep in mind check the pulse 10 If there is no pulse- administer Epinephrine 1 mg*

This is a Mobitz II, Second Degree Block. The QRS complexes are dropped following some of the P waves. There is no progression of PR intervals as in the Mobitz I. This is a serious situation!! This requires a Transcutaneous Pacemaker. You may consider Atropine 0.5 mg while awaiting the pacemaker. Atropine speeds up the SA 9 node and since there are P waves that are blocked it is not a good drug for these high degree blocks. (AHA 2010
Update)

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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 rhythm is appropriate to defibrillate There are two ways to defibrillate Monophasic or Biphasic Monophasic defibrillators direct the electrical energy into one Pad and out the other - Use 360 joules Biphasic defibrillators direct the electrical energy into both pads at the same time. Biphasic is better because you only have to use half as many joutles 200 joules

This is a Torsades de Pointes. This is a rhythm that is wide and ugly. Wide and ugly is usually ventricular in origin. Look closely at this rhythm it appears in groups. That indicates it is jumping its focus. Magnesium is the drug of choice.

This is an Asystole. It is also referred to as an agonal rhythm. You must not call this a Flat Line. 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 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 rescuers should treat the rhythm as VF. They should deliver highenergy defibrillations. (2005 Update)

Epinephrine or the second dose. NOT in addition to Epi.. 11

This is called a monomorphic tachycardia. This is another tachycardia that is wide and ugly!! This may or may not be ventricular in origin. 12 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. 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 Tachycardia with the Vagal Maneuver.

This is another example of a Supraventricular Tachycardia. Supraventricular Tachycardias: Usually go faster than 180 Have an abrupt start Have narrow complexes 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

This is a wide-complex tachycardia. Assume it is ventricular in origin until you prove otherwise. Therefore, this is a ventricular tachycardia.. If the patient is stable you should consider Amiodarone for treatment.
(AHA 2010 Update)

If the patient is unstable you should check his pulse.


If he is unstable with a pulse you would need to cardiovert. If there is no pulse this is a pulseless ventricular tachycardia and you need to defibrillate.

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A Little Bit About Atrial Fibrillation and Atrial Flutter Atrial Flutter
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 240360 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.

The New 2011 CPR


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) Bag/Mask Ventilation (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*

Atrial Fibrillation
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.

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Calling the Code Primary Survey ABCs and Defibrillation


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.

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

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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.

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.

Be a Leader
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!!

Be a Team Member
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.

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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.

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)

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

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Youre still the Leader!!


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)

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 (Cordarone) 300 mg IVP (1st dose) Every 3-5 minutes Additional dose, 150 mg IVP Max dose, 2.2 gm/24 hours Not OK for ET tube Lidocaine (if Amio not avail) 1-1.5mg/Kg. IVP Every 3-5 minutes Additional doses, 0.5-0.75 mg/Kg Max dose, 3mg/Kg OK for ET tube

Establish an Advanced Airway


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.

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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

If you get a rhythm check the pulse Any organized rhythm without a pulse is a PEA *

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*

Youre still the leader!! Continue CPR*


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

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Hypothermia
Clues: Intervention: Caution: Hyperkalemia Clues: Intervention: Hypokalemia Clues: Intervention: Cold skin Low core temperature Use warmed NS not dead till warm and dead. Peaked T waves History of renal failure Infuse Na Bicarb Flat T waves Infuse K+ (not be confused with K+ bolus!) metabolic acidosis Small amplitude QRS History of renal failure Altered LOC D5w check breath sounds Deviated trachea Neck vein distention Needle decompress the chest Bulging neck veins Rapid heart rate Pericardiocentsis coronary and/or lung Coronary = ST segment elevation = STEMI Lung = Distended neck vein Call the surgeon. Bradycardia Try some Narcan

Asystole

Hydrogen ion excess


Clues:

Hypoglycemia
Clues: Intervention: Tension Pneumothorax Clues: Intervention: Tamponade Clues: Intervention: Thrombosis Clues: Clues:

Prognosis is poor Continue CPR IV access is a priority over advanced airway management unless bag/mask ventilation is ineffective. Do not routinely insert an advanced airway unless ventilations with a bag-mask are ineffective. Start 2 IV sites in the anticubital if not already done Do not interrupt CPR for IV access Try more Epi 1 mg or Vasopressin as an alternative for EITHER the first or second dose of epinephrine The standard epinephrine dose is 1 mg IV/IO every 3-5 minutes of 1:10,000 solution*. High-dose epinephrine is not routinely recommended. The AHA no longer recommends Atropine for the asystole (2010
Update)

Remember this is a nonshockable rhythm Be aware of some reasons to terminate resuscitative efforts, such
as rigor mortis, indications of DNR and threat to safety.

Toxins - (drug overdose)


Clues: Intervention: 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.

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The Bradycardia
Heart Rates less than 60 BPM

Pacemaker
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!!!

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

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

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The Tachycardias
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.

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?

Unstable Tachycardia Cardiovert


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.

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.

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100j-200j for monophasic and 100j-120j for biphasic waveforms.


(Depending on the acuity of your patient). Atrial flutter and SVTs generally require less joules at 50j 100j. (2005 Update)

Narrow
Regular
SVT Adenosine

Wide
Regular
Monomorphic Amiodarone or Adenosine

Go
Charge the defibrillator and announce what you are doing.
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. You might want to bolus with an antiarrhythmic drug followed with an infusion.

Irregular
A-Fib Calcium Channel Blockers

Irregular
Torsades Magnesium

Stable Tachycardia - Medicate


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 narrowcomplex 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*

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Acute Coronary Syndromes


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 STsegment elevation.

Treatment of ACS involves the initial use of drug to relieve discomfort, dissolve clots, and inhibit thrombin and platelets. These drugs are: 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.

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Stroke
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.

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

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Trauma Abnormal coagulation studies


The indications for tPA are as follows: If the age is greater than 18 years If the clinical diagnosis of stroke is measurable with neurologic deficit If the onset of signs and symptoms is within 3 hours before treatment can begin. A patient that presents is less than 3 hours without contraindications is a candidate for IV fibrinolytic therapy. General Stroke Care includes the following: Support ABC Monitor blood glucose Monitor for complications of fibrinolytic therapy Monitor for hypertension. The risk of fibrinolytic therapy: Cerebral hemorrhage

Return to Spontaneous Circulation


ROSC is deemed to have occurred when chest compressions are not required for 20 consecutive minutes and signs of circulation persist. If ROSC occurs for the hypotensive patient after cardiac arrest,
bolus the patient with 1-2 L or NS or RL*

Maintain a systolic BP at 90 mm/Hg* which may be accomplished


with Dopamine. Continue to optimize ventilation and oxygenation*

Mega Code
Your ACLS mega code will follow the guidelines on page 151-155 which includes the following Respiratory Management with a pulse Respiratory Management without a pulse and use of the AED Bradycardia VF Asystole Unstable Tachycardia VF PEA ROSC Stable Tachycardia VF PEA ROSC

Therapeutic Hypothermia
Mild hypothermia (cooling of the brain to about 89-93 F or 32-34 C has 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.

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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

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 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

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. CAUTION: Hyperventilation in trauma victims decreases intracranial pressure (IPP) by decreasing the intracranial blood flow. The result is cerebral ischemia.

Pretest Questions 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 epigastric pain. Her vitals are stable along with the O2 sat. What is you first interevention?_______________________________ (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)

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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).

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)

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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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