PP EAKEAK EMERGENCY RESPONSE TRAINING
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CC A R D I A C AA R R E S T MM A N A G E M E N T :: AA EE DD PP R O T O C O L TT R A I N I N G MM A N U A L
S eventh Edition Revised December 20 1 6
Written and D eveloped by , Jeffrey Burko , Executive Medical Director
Special Contributions by , Alastair Thurley , Quality Assurance Direct or Emma Holden - Hindley , Operations Director Kayla Pocock , Corporation of Delta Heather McRae - Moloney , Corporation of Delta
Medical Direction Team and Standing Orders provided by
Dr. William Akeroyd, M.D., M.C.F.P. (EM) Dr. Gordon Bird, M.D., B.Sc., C.C.F .P. (EM) Dr. Steve Collyer, M.D., M.B.,Ch.B Dr. Angus Gilchrist, M.D., B.Sc., M.Sc., C.C.F.P. Dr. Bruce McKnight, M.D., B.Sc., C.C.F.P. (EM) Dr. Hazel Park, M.D., C.C.F.P. (EM), F.C.F.P. Dr. Stephan Samoyloff, M.D., C.C.F.P. (EM), F.C.F.P. Dr. Michael Slo an, M.D., M.B.,Ch.B Dr. Simon Ward, M.D., M.B.Ch.B, F.C.E.M., DipIM.C. (RCSEd)
1717 Beach Grove Road, South Delta ( Tsawwassen ) , British Columbia, Canada, V4L 1P4 Tel 778 899 7325 (PEAK), Fax 604 648 8120 Email [email protected] Web www.peakemergencytraining.com
C ARDIAC A RREST M ANAGEMENT : AED P ROTOCOL T RAINING M ANUAL
© All rights reserved. This document may not be reproduced, in any form without written permission from Peak Emergen cy Response Training, a division of Peak Project Management, Inc.
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T A B L E O F C O N T E N T S
Acknowledgements 1 - 2 Notice to Students 3 - 4 Overview & Liability 7 Medical Direction 7 Sudden Cardiac Arrest (SCA) 8 - 9 Respiratory / Cardiac Anatomy & Physiology 10 - 16 Coronary Artery Disease 17 Coronary Artery Disease – Angina Pectoris 18 Coronary Artery Disease – Myocardial Infarction 18 MI Induced SCA 19 Heart Rhythm s 19 - 21 Heart Rhythms Resulting in SCA 21 - 22 AED Use & Defibrillation 22 - 23 Purpose & Benefits 23 Indication for Use 24 Contraindications 24 Safety, Storage & De livery Precautions 24 Post Treatment – Termination of Use 25 Transfer of Care 25 Documentation 25 Algorithms 27 CPR / AED Algorithm – 1 Rescuer 29 CPR / AED Algorithm – 2+ Rescuer 31 CPR / AED (with BVM & OPA) Algorithm – OFA Le vel 2/3 Attendants 33 Child / Adult Conscious Choking 35 Child / Adult Unresponsive Choking – 1 Rescuer 37 Appendices 39 Appendix 1 – Use of a B ag - V alve - M ask Device 4 1 Appendix 2 – Use of a Suction Device 4 3 Post Course Quiz 4 5 - 48 Glossary 49 - 5 1 Notes 5 3 - 5 4
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A C K N O W L E D G E M E N T S
PEAK acknowledges the following individuals and organizations for their involvement, direct or indirect, with the development of this training manual:
National Ski Patrol – Outdoor Emergency Care Lifesaving Society of Canada Global Medical Services – CAM 1(Holmes) Royal Life Saving Society (UK) H eart and Stroke Foundations of Canada Surf Life Saving Australia American Heart Association
O PERATIONS , A DMINISTRATION AND I NSTRUCTIONAL T EAM :
Jeffrey Burko (Executive Director) , EMA - 2, PCP - A, ACLS - P, EMT - I, NUEC 3 - IT, NUOFA 3 - IT, AP - IT, AWFA - I T , BLS - IT, AVI - OPS - 1 Emma Holden - Hindley (Operations Director), BA , P ARAMEDIC (UK) , BLS - I Terry Makos ( Corporate Liaison ) , C.P ED .C AN ., CSGA L EV 2, ACMG ( HIKING ), NUEC 3 - I , NUOFA 3 - I , AP - I, AWFA , BLS - I, AVI - OPS - 2
John Baril, PCP - A, AP - I, BLS - I, B . S C . Trevor Beckley, PCP, NUEC 3 - I , NUOFA 3 - I, AP - I , BLS - I Mike Bowman , PCP, NUEC 3 - IT , NUOFA 3 - IT, AP - I T, BLS - I, AVI - OPS - 1 Alison Harper, PCP, EMT - A, NUEC 3 - I , NUOFA 3 - I , AP - I , BLS - I Mike Haug, PCP, NUEC 3 - I , NUOFA 3 - I, AP - I , BLS - I, AVI - OPS - 1 Brad Herman, NUEC 3 - I, NUOFA 3 - I, AP - I , BLS - I, AVI - OPS - 2 Shelly Hicks, PCP, NUEC 3 - I , NUOFA 3 - I, AP - I , BLS - I, AVI - OPS - 2 Melissa Huntley , NUEC 3 - I, NUOFA 3 - I, AP - I , BLS - I, AVI - OPS - 1 Chelsea Kerr, NUEC 3 - I, NUOFA 3 - I, AP - I , BLS - I , A ST - 2 Brent Lon skii , PCP , NUEC 3 - I T , NUOFA 3 - IT, AP - IT, BLS - I, AVI - OPS - 1 Bernie Palmer, PCP, EMR, WFA - I, NUEC 3 - I , NUOFA 3 - I, AP - I , BLS - I, A ST - 2 Graeme Parke, ACP, PCP , NUEC 3 - I, NUOFA 3 - I, AP - I, BLS - I, AVI - OPS - 1 Chris Rhind, B S C . , P ARAMEDIC (UK) , NUEC 3 - I , NUOFA 3 - I , AP - I , BLS - I Clayton Skwarok, EMT - P, ACP, NUEC 3 - I, NUOFA 3 - I, AP - I , BLS - I, A ST - 2 Shauna Speers, PCP, NUEC 3 - I , NUOFA 3 - I , AP - I , BLS - I, AVI - OPS - 1 Phil Vaughan - Jones, P ARAMEDIC (UK), NUEC 3 - I , NUOFA 3 - I , AP - I , BLS - I
Greg Golovach ( Technical Rescue Advisor ) , ACMG / IFMGA M TN . G UIDE , NUEC 3 , AP - P, BLS - P, AVI - OPS - 2 Derek Robinson ( Aviation Rescue Advisor), E CLIPSE H ELICOPTERS - OWNER
M EDICAL D IRECTION AND O VERSIGHT T EAM : Dr. William Akeroyd Dr. Gordon Bird Dr. Steve Collyer Dr. Angus Gilchrist Dr. Bruce McKnight Dr. Hazel Park Dr. Stephan Samoyloff Dr. Michael Sloan Dr. Simon Ward
The International Liaison Committee on Resuscitation (ILCOR) provides a forum between principal resuscitation organisations wor ldwide. The Canadian guidelines for the performance of emergency cardiac care (ECC) are based on the guidelines established by ILCOR. PEAK's Advanced Protocol Training Program adheres to the standards set by ILCOR.
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N O T I C E T O S T U D E N T
Welcome to the Cardiac Arrest Management: AED Protocol Training Program developed by PEAK Emergency Response Training ( PEAK ) , a division of Peak Project Management, Inc. , for use by the Corporation of Delta.
W e look forward to instruc ting you and we anticipate a rich, two - way exchange of knowledge and experience. To ensure that your educational experience is as beneficial as possible, we strongly urge you to commit the time to fully understand and assimilate the information contained in this Cardiac Arrest Management: AED Protocol Training Manual . It is as condensed as possible to ensure that you have to study only this essential information .
To assist you further in this regard , ‘ essential information ’ has been identified in this manual by ‘KEY Icon ’ (immediately below). As such , sections containing this icon are considered to contain ‘essential information ’ and required to be successful in this course.
The serious nature of th is protocol demands that the examination proces s accurately evaluates your integration of this material, to ensure that the AED P rotocol is initiated safely.
N OTICE OF L IABILITY
W E MAKE YOU AWARE OF THE FOLLOWING : This Cardiac Arrest Management: AED Protocol Training Manual is not exhaustive. It is designed to be used in conjunction with an extensive practical and theoretical training program. Candidates must demonstrate competency in a practical skills development session and achieve no less than 80% on a written evaluation to attain PEAK ’ s c ertification. Annual re - certification is required for maintenance of PEAK ’ s AED certification; as well , as 90 - day ‘skills refreshers’ in the first year following initial certification and bi - annual refreshers every year after .
This Protocol has been spec ifically designed for the exclusive use by certified staff of the Corporation of Delta . Potential students must hold a current ( less than 1 year ) appropriate level CPR certification .
No trained responder will be permitted to initiate the ‘AED Protocol’ without the written authorization of PEAK (certification). Th is ‘Protocol’ is as printed and carr ies no guarantee whatsoever. PEAK assumes no responsibility to any party for loss or damage caused by the information contained or by any omission in this Card iac Arrest Management: AED Protocol Training Manual .
Furthermore, PEAK prohibits anyone or corporation from copying, altering, loaning or using the ‘Protocol’ or this Cardiac Arrest Management: AED Protocol Training Manual in full or in part without pri or expressed written permission and involvement of PEAK .
Should you have any questions or comments , please do not hesitate to contact us.
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PP EAKEAK EMERGENCYEMERGENCY RESPONSERESPONSE TRAININGTRAINING
CC A R D I A C AA R R E S T MM A N A G E M E N T :: AA EE DD PP R O T O C O L
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O VERVIEW & L IABILITY
This Cardiac Arrest Management: AED Protocol Training Manual is not exhaustive. It is designed to be used in conjunction with an extensive practical and theoretica l training program. Candidates must demonstrate competency in a practical skills development session and achieve no less than 80% on a written evaluation to attain PEAK ’ s certification. Annual re - certification is required for maintenance of PEAK ’ s AED ce rtification; as well , 90 - day ‘skills refreshers’ in the first year following initial certification and bi - annual refreshers every year after .
This Cardiac Arrest Management: AED Protocol Training Manual has been specifically designed for the exclusive use by certified staff of the Corporation of Delta and is intended to be utilized by staff. No responder will be permitted to initiate this AED Protocol under PEAK ’ s Medical Direction and Oversight without the written authorization of PEAK ( PEAK certificatio n) and that of the Corporation of Delta’s AED Program Coordinator.
This Cardiac Arrest Management: AED Protocol Training Manual is as printed and carries no guarantee whatsoever. PEAK assumes no responsibility to any party for loss or damage alleged to b e caused by the information contained or by any alleged omission in this Cardiac Arrest Management: AED Protocol Training Manual.
Furthermore, PEAK prohibits any individual, corporation, or entity from copying, altering, loaning or using this ‘Cardiac A rrest Management: AED Protocol’ or this ‘Cardiac Arrest Management: AED Protocol Training Manual’ in full or in part without prior expressed written permission of PEAK .
M EDICAL D IRECTION
The ‘Aquatic Certified AED Responder’, once cert ified, is delegated to use an AED under the license of the AED Program Medical Director(s). PEAK’ S medical direction team is comprised of nine BC licensed physicians: Dr. Bill Akeroyd, Dr. Steve Collyer, Dr. Stephan Samoyloff, Dr. Angus Gilchrist, Dr. Haz el Park, Dr. Bruce McKnight, Dr. Michael Sloan, Dr. Gordon Bird and Dr. Simon Ward; together they provide the medical oversight for the Corporation of Delta’s AED Program.
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S UDDEN C ARDIAC A RREST (SCA)
Sudden Cardiac Arrest (SCA) is the leading cause of death among adults striking nearly 45,000 Canadians annually. The Canadian Heart and Stroke Foundation supports implementing the "Chain of Survival" to rescue people who suffer a cardiac arrest in the community. The adult chain consists of:
► Early Rec ognition & Activation ► Early CPR ► Rapid Defibrillation ► Effective Advanced Life Support Care ► Integrated Post - Cardiac Arrest Care
It is estimated that for every minute a person remains in cardiac arrest, survivability is reduced by 7 - 10%. The defin itive treatment for Ventricular Fibrillation (the most common ‘treatable’ type of cardiac arrest) or Ventricular Tachycardia is defibrillation. Early defibrillation, in conjunction with cardiopulmonary resuscitation (CPR), increases survival rates by near ly 50%.
What is Sudden Cardiac Arrest (SCA)? SCA is death resulting from an abrupt loss of heart function (cardiac arrest). Most victims of SCA are middle - aged or elderly: the average victim is about 65 years old; however, some victims are in their 40 ’s and even younger. Very often, there is no previous history of heart problems; in many cases SCA is the first symptom. All known heart diseases can lead to SCA and death.
Most deaths resulting from SCA occur when the electrical impulses in the disea sed heart become too rapid ( Ventricular Tachycardia ) or chaotic ( Ventricular Fibrillation ) – originating from incorrect parts of the heart. These irregular heart rhythms ( arrhythmias ) produce ineffective or absent contractions resulting in the cessation o f blood flow and – ultimately – death.
CPR / AED – Survival Rates
Early CPR CPR Delayed Defibrillation Defibrillation 2 - 8% s urvive
Early CPR Defibril l ation 2 0 % survive Early CPR Defibrillation
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SCA ( CONT ’ D )
What Causes Sudden Cardiac Arrest?
When SCA occurs in young adults (up to approximately 35 years of age), pre - existing heart abnormalities and/or respiratory compromise is likely the cause. Adrenalin released during intense physical or athletic activity often acts as a trigger for sudden death when these abnormalities are present.
Also, under certain conditions , some heart medications and other drugs (as wel l as recreational drugs) can lead to abnormal heart rhythms that can cause SCA.
In 90% of the adult victims of SCA, two or more major coronary arteries are found to be narrowed by fatty build - ups. In addition, heart muscle scarring from a prior heart att ack (often presented as a ‘silent’ attack), is observed in two - thirds of the victims.
In order to understand how these narrowings and blockages of coronary arteries can lead to SCA, it’s essential to review our knowledge of the anatomy & physiology (‘mea t and motion’) of the respiratory & cardiac systems.
Following this review, we must understand the electrical anatomy & physiology of the heart in order that we can understand how it is that arterial blockages lead to death of heart muscle tissue and int errupt electrical cardiac signals. Subsequently this may lead to malfunctioning of the cardiac muscle, decreased blood flow and ultimately SCA.
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R ESPIRATORY / C ARDIAC A NATOMY & P HYSIOLOGY
► T HE R ESPIRATORY S YSTEM
We a lready know that our Primary Survey includes making sure our patient has a clear airway and adequate breathing, or by providing the necessary critical interventions. To ensure that we have a firm foundation upon which to add the AED protocol – should it b e required – it is important to go through a quick review of the anatomy & physiology (A&P) of the respiratory system.
The airway is separated into two sections: the upper airway and the lower airway . The upper airway is composed of the mouth , nose , phar ynx and epiglottis . The tongue is located in the upper airway and is the most common source of airway obstruction in an unresponsive patient. The lower airway is made up of the larynx , trachea , bronchi , bronchioles and alveoli .
Air Flow Through The R espiratory System
Air enters through the nose or mouth , where it is warmed and filtered before passing through to the pharynx . The pharynx is divided into two sections: the nasopharynx (located behind the nose), and the oropharynx (located behind the mou th).
The air then continues to travel down the pharynx and past the epiglottis ( the flap that covers the larynx preventing food and liquid from entering the lower airway when eating). The air then enters the lower airway.
The air enters the larynx ( voice box) after passing the epiglottis. The larynx lies between the areas that you palpate (feel) when checking the carotid pulse.
The cricoid cartilage makes up the bottom portion of the larynx, and the trachea lies just below the larynx.
Air pass es through the trachea and follows the bronchus which branches off into the left and right bronchi - leading to the left and right lungs.
The air follows the bronchi which further divide into many bronchioles , which eventually end in alveolar sacs locate d in the lung tissue.
Once the air reaches the capillaries within the alveoli, gas exchange occurs (CO 2 [carbon dioxide] is off - loaded from the blood cells, and O 2 [oxygen] is loaded onto the blood cells – ‘oxygenating’ the blood for its return back to the heart). The lungs are referred to as the ‘ pulmonary ’ component of the respiratory system.
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R ESPIRATORY / C ARDIAC A NATOMY & P HYSIOLOGY ( CONT ’ D )
► T HE C ARDIO - P ULMONARY S YSTEM – M ECHANICAL A & P
P ULMONARY (R) S IDE S YSTEMIC (L) S IDE The heart is an involuntary muscle that is about the size of two clenched adult fists. It is composed of cardiac muscle, called myocardium , and it is responsible for pumping oxygen - rich blood to the body (including its own heart t issue) and oxygen - depleted blood back to the lungs.
The heart is divided into four chambers, with the septum separating the left & right sides. Each side is further divided in half with the atria being the upper chambers and the ventricles being the lo wer.
Blood Flow Through The Cardio - Pulmonary System
The superior vena cava receives oxygen - depleted blood from the head and the upper body, and the inferior vena cava receives blood from the lower body.
This blood is delivered into the ‘relaxed’ righ t atrium , which, when the atria contract, expels the blood through a one - way valve (the tricuspid valve) into the right ventricle. This creates the ‘lub’ of the familiar ‘lub - dub’ sound associated with a heart - beat.
While the atria are contracting, th e ventricles are ‘relaxing’ or re - expanding – allowing them to refill with the next influx of blood.
Immediately after the atria contract, contraction of the ventricles occurs (‘dub’) and the blood is delivered into the pulmonary arteries via the pulmonar y valve . ( S ee lub - dub in the glossary for an in - depth explanation . )
While the ventricles are contracting, the atria are ‘relaxing’ or re - expanding – allowing them to refill with the next influx of blood.
The blood pumped from the right ventricle travels to the lungs where gas exchange occurs.
This oxygenated blood then travels via the pulmonary veins to the left atrium.
When again the atria contract, the blood in the left atrium then passes through the bicuspid valve ( also known as the mitral valv e ) to the most muscular chamber, the left ventricle.
Contraction of the ventricles occurs again, and the oxygenated blood is then pushed through the aortic valve to the aorta and then on to the entire body – including the coronary arteries . It is impor tant to note that the coronary arteries are located at the start of the aorta and they provide the heart muscle with its own supply of oxygenated blood.
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R ESPIRATORY / C ARDIAC A NATOMY & P HYSIOLOGY ( CONT ’ D )
► C ARDIAC S YSTEM – E LECTRICAL A & P (Electr ophysiology)
Now that we’ve reviewed the A&P , we can start to build on that foundation by exploring the electrical aspect of the heart – that aspect which the AED addresses so effectively.
The heart has its own electrical system which controls the seque ncing , rate and rhythm of the contractions of the heart.
Heart Contraction Sequencing
The heart’s electrical system controls the timing or sequencing of the separate contractions of the upper & lower pairs of chambers. Think of it this way: if the whol e heart muscle contracted at the same time, there would be no effective pumping, because the chambers wouldn’t be able to effectively pump and refill at the same time. Therefore, the timing of the contractions of the two pairs of chambers are slightly off set (‘lub - dub’ = atria, then ventricles) to allow the chambers time to effectively refill before their next pumping cycle.
In order to accomplish this, the body has developed a sophisticated system of cardiac pacemakers, signal retarders and electrical p athways to ensure the coordinated pumping of blood through the heart and on to the lungs and the body.
The heart muscle needs electricity running through it in order to contract. The heart has built - in pacemaker tissue (instead of a battery) located in the area of the heart which contracts first – the atria.
This pacemaker tissue is called the sinoatrial node (the word ‘sino’ - refers to opening or hole – think of your sinuses), and in this case refers to the opening in the right atrium through which th e inferior and superior vena cava deliver the blood from the body.
The sinoatrial node (or SA node), acting as a pacemaker, sends out an electrical impulse across the tissues closest to it (both atria). This jolt or impulse causes the atria to contract w hich pumps the blood down into the ventricles.
What prevents the ventricles contracting at the same time as the atria? That’s where the signal retarding tissue comes in.
As that electrical signal from the SA node follows the electrical pathways around a nd through the contracting atria, the pathways gather together again just above the right ventricle at the retarding atrioventricular node (or AV node obviously named for its location between the atria and the ventricles). The signal takes about 0.08 seco nds to reach the AV node.
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R ESPIRATORY / C ARDIAC A NATOMY & P HYSIOLOGY ( CONT ’ D )
Although the AV node can serve as a secondary, slower pacemaker if the SA node fails, its primary function is to slow the SA node’s signal momentarily before it electrifi es the ventricles.
The AV node tissue has a slightly higher electrical resistance than the atrial tissue above it. So, as the signal is gathered in the AV node, this resistant tissue holds the impulse back very briefly (about 0.12 seconds) before allowin g it to race on at its previous speed down through and around the ventricular tissues. An analogy we can use to describe this process is that of a dog racing along the length of a beach. When the dog runs into a crashing wave, it is slowed down only temp orarily before continuing on as before. As this electrical signal races on from the AV node , it follows the long ventricular pathways – the right & left bundle branches and the purkinje fibres , and causes the respective ventricles to contract simultaneous ly.
To summarize, the SA node or pacemaker sends an electrical signal through the atria – causing them to contract – pumping the blood to the ventricles. The SA node’s signal is gathered and slowed in the AV node – allowing the ventricles time to relax af ter their last contraction and refill with blood from the atria. The signal then races on through the ventricles – causing them to contract – pumping the blood to the lungs and the body. Simultaneously, while the ventricles are contracting, the atria are relaxing and refilling, and the SA node is recharging to start the next signal and the next cycle.
Heart Rate
The SA node is the primary rate - setter or ‘pacemaker’ in a healthy heart. It generates electrical impulses (and therefore contractions) 60 - 10 0 times / minute, thereby establishing a healthy, perfusing heart rate. It is important to note, however, that any of the electrical conductive tissue of the heart has the ability to act as the heart’s pacemaker. The SA node generates an electrical impul se faster than any other tissue, which is why it is typically in control. However, if the SA node should fail (e.g. in the event of inadequate perfusion of that tissue due to arterial blockage), other tissues – like the AV node – may take over.
SA node: 60 - 100 times / minute Pacemaker Rates of Fire AV node: 40 - 50 times / minute Purkinje fibr e s : 30 - 40 times / minute
As the pacemaker rate table above shows, the lower (more inferior) place or tissue in the heart that the secondary pacemaker is established, the slower, and therefore less effective, the heart rate will be.
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R ESPIRATORY / C ARDIAC A NATOMY & P HYSIOLOGY ( CONT ’ D )
A healthy heartbeat for an adult is 60 - 100 beats / minute. It is normal and healthy for your heartbeat to speed up or slow down during the day as your activity level changes. However, it is not healthy for your heart to beat out of rhythm. Th is arrhythmia will compromise the blood flow to the rest of your body.
The ECG
Before we discuss the rhythm of a heart beat, it is important to understand the graphical measurement or representation of the heart’s electrical activity – the electrocardi ograph (ECG), and how it represents the heart’s mechanical activity. (Please note – this section is only an introduction to the ECG and in no way should it be misunderstood as providing training in ECG interpretation . )
The following ECG strip example ref lects healthy electrical (and hopefully mechanical) activity in the heart. If we were trained to ‘read’ an ECG, we would know that the electrical activity in this heart should be generating a healthy rate, sequencing and rhythm. That is – it shows a rate between 60 - 100 times / minute (normal), an impulse starting in the SA node (sinus) and recurring regularly (rhythm). This would be referred to as a ‘Normal Sinus Rhythm’ or NSR.
Electrocardiograph (ECG) Example
Note: In the diagram above, th e vertical axis measures the electrical current while the horizontal axis measures time.
How would a trained person recognize this as a NSR? They would attempt to identify recurring patterns , and then evaluate those patterns for frequency , regularity, and structure .
Identifying Recurring Patterns It is likely you’re able to see the following pattern recurring in the above ECG strip.
Evaluating for Frequency
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R ESPIRATORY / C ARDIAC A NATOMY & P HYSIOLOGY ( CONT ’ D )
Evaluating for Regularity It is easy to recognize that these patterns repeat regularly - approximately once every 4 vertical lines.
E valuating for Structure ( Sequencing ) This requires a deeper knowledge of what the components of these patterns represent. Let’s look at the pattern again with some of its landmarks labeled: 2. QRS
1. P
3. T
1. P - This is referred to as the P - w ave. It repr esents the electrical signal racing from the SA node through the atria (or the atrial depolarization ). It also therefore represents the contraction of the atria .
2. QRS - This is referred to as the QRS complex. It repre sents the electrical signal racing from the AV node through the ventricles (or the ventricular depolarization ). It also therefore represents the contraction of the ventricles .
3. T - The T - wave occurs when both ventricles of the heart are relaxing . T he ventricles are recovering and refilling before they must contract again ( repolarization is occurring).
2. QRS complex
1. P - wave
3. T - wave = repolarization / relaxation
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R ESPIRATORY / C ARDIAC A NATOMY & P HYSIOLOGY ( CONT ’ D )
These recurring patterns (the P - QRS patterns) on this strip have a structure revealing that the sequencing of the electrical signal is healthy – the signal begins at the SA node, crosses the atria, slows at the AV node, and then quickly crosses the ventricles.
In a very simplistic way this ECG strip example reveals si milarly structured, healthy patterns, recurring regularly at rate of approximately 60 - 100 beats per minute.
In summary then , it is clear that in a healthy Cardio - Respiratory System
an electrical event……………….
stimulates a mechanical event ………………….
and results in a coordinated pumping action……
w hich in turn results in the:
► Delivery of blood to the lungs for cleaning and oxygenation; and ► Delivery of oxygenated blood back to the coronary arteries, tissues, and body.
PEAK E MERGENCY R ESPONSE T RAINING P ROVIDED FOR US E BY THE C ORPORATION OF D ELTA C ARDIAC A RREST M ANAGEMENT : AED P ROTOCOL T RAINING M ANUAL 17 Now we can start to put all this together to form a greater understanding of how coronary artery disease leads to the blockages and heart rhythms (arrhythmias) which result in SCA.
C ORONARY A RTERY D ISEASE
Coronary Artery Disease (CAD) occurs when the art eries that supply blood to the heart muscle (the coronary arteries) become hardened and narrowed – due to buildup of plaque on the inner walls or lining of the arteries ( atherosclerosis ). As this plaque narrows the coronary arteries, blood flow to the hea rt is reduced. This, in turn, decreases the oxygen supply to the heart muscle . CAD can result in angina and / or myocardial infarction and / or SCA.
The following are the major risk factors which contribute to the development of coronar y artery disease and atherosclerosis:
► Age ► Male ► Female (50+) ► Hypertension ► Smoking ► Genetics ► Diabetes Mellitus ► Elevated cholesterol ► Sedentary lifestyle ► Prolonged excessive use of stimulants
What is the extent of the problem? (2010, Canada)
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► Over 70,000 – 85,000 heart attacks per year (1 every 7 seconds) ► Greater tha n 16,000 deaths due to heart attacks per year (prehospital) ► 45,000 – 55,000 prehospital cardiac arrests (SCAs)
A NGINA P ECTORIS
Angina Pectoris ( pain in the chest ) is the result of a reduced oxygen supply to the heart muscle ( myocardium ). This lack of oxygen to the heart muscle is known as myocard ial ischemia . Angina Pectoris is a common symptom of myocardial ischemia most commonly caused by a spasming or narrowing of a coronary artery due to coronary artery disease ( atherosclerosis) . Epis odes of Angina are typically brought on by exertion or high levels of stress. They are typically relieved with rest , and often, a Nitroglycerin Protocol initiation within 1 to 5 minutes of the episode occurring. Angina episodes may involve any one or all of the following symptoms:
► Chest Discomfort / Pain ▪ Feeling of fullness ▪ May mimic indigestion ▪ Pressure or weight - like ▪ Substernal & often radiates to jaw, arms, shoulders, neck & back
► Shortness of Breath ► Nausea & Vomiting ► Anxiety ► Pale, Cool, Clamm y = LLS ► Symptoms typically resolve with rest & Nitroglycerin
M YOCARDIAL I NFARCTION (M.I.)
M yocardial Infarction (M.I.) ( heart attack ) is caused by an obstruction of a coronary artery and thus severe myocardial ischemia. The infarction is nearly alway s the result of a clot that blocks the artery at an atherosclerotic narrowing. M.I. ’ s may have no obvious precipitating events and often occur while the patient is at rest.
► Chest Discomfort / Pain ▪ May mimic indigestion ▪ Pressure or vise - like ▪ Substernal & often radiates to jaw, arms, shoulders, neck & back
► Shortness of Breath ► Palpitations / Irregular Pulse ► Nausea & Vomiting ► Anxiety / Fear / Denial ► Pale, Cool, Clammy = LLS ► Symptoms don’t resolve PEAK E MERGENCY R ESPONSE T RAINING P ROVIDED FOR US E BY THE C ORPORATION OF D ELTA C ARDIAC A RREST M ANAGEMENT : AED P ROTOCOL T RAINING M ANUAL 19 with rest & Nitroglycerine
Note: The signs & symptom s (S&S) above typically describe what males tend to complain of when experiencing an M.I.; this is largely due to muscle mass & location. Females may or may not present with the S&S listed above and often complain of discomfort across the back and shoulde rs. It is imperative that all patients that complain of chest pain or the other symptoms listed, are treated as a probable M.I.; always err on the side of caution!
MI I NDUCED SCA
► A coronary artery is occluded (blocked) Damage and death to heart tissue shown as shaded area ► Perfusion ceases in: ▪ Myocardiu m (area weakens & dies) ▪ Electrical conduction tissues are damaged ▪ Pacing impulses are interrupted / redirected / disorganized ► Contractions become less effective & eventually absent
► Patient loses responsiveness & expires
Now that we have reviewed CAD and have seen how coronary artery blockages lead to tissue damage electrical signal interruption, we can now learn how these electrical signal interruptions lead to abnormal heart rhythms which lead to SCA.
SCA – S IGNS & S YMPTOMS
► Loss of Responsiveness (LOR) ► Non - Breathing / Agonal ► No Signs of Life . No Chest Mov ement . No Coughing or Movement ► Pale / Cool / Cold / Profuse Sweating (diaphoresis) / Cyanosed (bluish skin)
H EART R HYTHMS
Before learning about ‘abnormal rhythms’, it’s necessary to review the ECG of a normal sinus rhythm:
Normal Sinus Rhythm A heart i s said to be in a normal sinus rhythm when uniform heartbeats occur at regularly spaced PEAK E MERGENCY R ESPONSE T RAINING P ROVIDED FOR USE BY THE C ORPORATION OF D ELTA 20 C ARDIAC A RREST M ANAGEMENT : AED P ROTOCOL T RAINING M ANUAL intervals. This normal rhythm indicates that the SA node is acting as the primary pacemaker, and that the heart is beating between 60 - 100 times/minute. This rhythm is made up of many single ECG complexes wherein each complex signifies a single effective heart beat.
H EART R HYTHMS ( CONT ’ D )
A single ECG complex is regarded as having three sections: P, QRS and T, each representing a different stage in a single heart beat. The P wave is only evident when the SA node is the primary pacemaker. It represents the contraction of both atria of the heart. It also indicates that depolarization is occurring. The QRS wave signifies the contraction of the ventricles. The T wa ve occurs when both ventricles of the heart are relaxing. The ventricles are recovering and refilling before they must contract again (repolarization is occurring).
A BNORMAL H EART R HYTHMS – A RRHYTHMIAS As discussed, abnormal heart rhythms generally a rise from damaged conduction pathways in heart tissue. When coronary arteries become blocked, this stops the flow of oxygenated blood to distal heart tissue. This reduced perfusion leads to ischemia and heart tissue damage/death. In this tissue are nerve pathways which ordinarily conduct the signal from the SA node.
When this tissue dies, the electrical signal (which previously caused healthy contractions and pumping) no longer gets through. Many different results can occur – depending on the location, size and degree of damage – and most of these results will cause rhythm and ECG changes.
In some cases (inferior / ventricular blockages), the tissue below the blockage will receive but not be able to respond to the signal and therefore not contract adeq uately, leading to reduced cardiac output.
In other cases (superior / atrial blockages), major conduction pathways are damaged and the SA node won’t be able to fire, or its signal won’t get far. As a result, the task of pacemaker will relocate to the AV node – or even more inferiorly – in the ventricles resulting in a ‘ventricular rhythm’ wherein the atria are not receiving impulses at all. Therefore, they are not contracting, nor are they filling the ventricles. The pacemaker in the ventricles will fir e faster and faster trying to feed its starving muscle, but without adequate preload, there can be no cardiac output. This is a description of the pathophysiology of ventricular tachycardia – see below.
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H EART R HYTHMS ( CONT ’ D )
Often, this rhy thm will continue to accelerate and, as the tissues become more hypoxic , the electrical organization will begin to break down further. Many sites within the ventricles will begin acting as pacemakers resulting in uncoordinated, chaotic electrical and mech anical activity – continuing a state in which there is no cardiac output. This is a description of the pathophysiology of ventricular fibrillation – see below.
H EART R HYTHMS R ESULTING IN SCA
Although there are many different abnormal heart rhythms, there are only four which result in cardiac arrest. These four are: ventricular tachycardia (VT), ventricular fibrillation (VF), asystole (flat - line) and pulseless electrical activity (PEA). Of these four, only two are shockable rhythms: VT and VF .
Ventricular Tachycardia VT occurs when there is one site in the heart (in the ventricles) that takes over as the primary pacemaker. Because the electrical impulse isn’t traveling its normal route, it does not stop to pause at the AV node. The AV node is where the signal typically pauses to allow the ventricles to fill with blood and, without this pause and refilling, the heart begins to pump an inadequate amount of blood. Initially, a patient may be responsive while in VT, but as their blood pres sure steadily drops the patient will quickly lose responsiveness and develop pulseless ventricular tachycardia. VT is often seen before a patient falls into VF.
Ventricular Fibrillation VF occurs when there are many different tissues in the heart (in the ventricles) that are trying to act as the pacemaker. Therefore, the heart PEAK E MERGENCY R ESPONSE T RAINING P ROVIDED FOR USE BY THE C ORPORATION OF D ELTA 22 C ARDIAC A RREST M ANAGEMENT : AED P ROTOCOL T RAINING M ANUAL seems to be constantly firing and is very disorganized. The heart appears to be quivering when it is in VF and the disorganized contractions do not circulate the blood. In adequate circulation causes hypoxia and will quickly cause a patient to lose responsiveness. A normal heart rhythm must be established quickly to prevent irreparable damage to the heart muscle. VF is the most common rhythm associated with SCA.
H EART R H YTHMS R ESULTING IN SCA ( CONT ’ D )
Asystole An AED will not advise a shock when the patient is in asystole . In an asystolic heart, there is absolutely no electrical activity in the tissues. Therefore, defibrillation will be of no value. This is because – as you will shortly learn – the purpose of defibrillation is actually to shock the heart so that all electrical activity is completely stopped. This is done in the hope that the natural pacemaker will then resume its electrical control of the heart – th ereby restartin g regular contractions. However, in the case of asystole, no pacemaker sites are firing at all, and no application of an electrical shock can revive this tissue – the heart and its electrical system are already dead. The responder will the refore have to rely on CPR as the treatment for this patient.
Pulseless Electrical Activity During PEA the primary pacemaker keeps firing; however, the heart muscle is so damaged that it is not capable of contracting. The electrical signal flows normal ly down across the heart (resulting in a normal ECG), but the heart muscle cannot respond. An AED will not be beneficial with this rhythm because the problem is not so much an electrical one (the electrical system does not need to be stopped and reorganiz ed – its working fine); rather, it’s a mechanical problem. An AED will simply recognize this as a normal perfusing (non - shockable) rhythm and indicate “No Shock Advised”. The responder will therefore have to rely on CPR as the treatment for this patient.
AED U SE & D EFIBRILLATION
When a person collapses and is found to be in cardiac arrest as a result of VF or VT the definitive treatment for this person is defibrillation .
The purpose of CPR is to artificially circulate a patient’s blood by performing chest compressions. This pressure on the heart can make the ventricles contract and thus push blood to some of the vital organs. Effective chest compressions can supply up to 25 - 30% of the typical cardiac output. It is not a corrective treatment; at be st, it may keep the heart muscle alive while waiting for the AED and Advanced Cardiac Life Support (ACLS) – which is the definitive treatment for SCA.
PEAK E MERGENCY R ESPONSE T RAINING P ROVIDED FOR US E BY THE C ORPORATION OF D ELTA C ARDIAC A RREST M ANAGEMENT : AED P ROTOCOL T RAINING M ANUAL 23 Studies conducted at cardiac rehabilitation cent res have shown that when SCA victims in VF receive defib rillation within the first minute or two after collapse, more than 90% survive to be discharged from hospital. In more typical community settings, victims of SCA rarely survive. Why? This is because most patients do not have immediate access to prompt, de finitive treatment. Typically , too much time elapses before CPR and an AED is applied.
AED U SE & D EFIBRILLATION ( CONT ’ D )
How Does Defibrillation Work?
An AED is a small, compact device that interprets heart rhythms and can deliver electrical shocks to treat SCA. The main difference between AEDs and the manually operated defibrillators often used by medical professionals is that AEDs are designed for use by people who may not have the extensive training required to use a manual defibrillator. AEDs a re very simple to operate as responders do not need to recognize or interpret heart rhythms – the AED does this automatically.
The AED is capable of recognizing whether the patient has a ‘shockable abnormal rhythm’ (i.e. VT or VF), and if so, it will adv ise the responder to administer a ‘shock’.
The purpose of the AED is to deliver an electric shock to the myocardium; momentarily terminating all electrical activity, thus allowing the heart’s intrinsic ability to re - establish a coordinated and organized electrical impulse from the heart’s natural pacemaker – the SA node. This intrinsic ability is termed ‘ automaticity ’.
P URPOSE & B ENEFITS
The extended response times by p aramedics can have a significant impact on patient outcomes. It is clea r that a victim of SCA has little or no chance of surviving without immediate advanced treatment (less than 10 minutes). This is the main reason that AEDs are becoming an integral part of a responder’s tool kit, and they are saving lives.
The following pages present some of the basic concepts that you need to understand before being trained in how to operate an AED. The goal of this training module is to provide responders with a systematic approach to optimize patient survival; this includes CPR, AED, and post resuscitation management.
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I NDICATION F OR U SE
T HE AED P ROTOCOL IS INITIATED FOR :
► Patients that are unresponsive; ► Patients that are not breathing.
C ONTRAINDICATIONS
T HE AED P ROTOCOL IS CONTRAINDICATED FOR :
► Patients that are res ponsive; ► Patients that are breathing.
S AFETY , S TORAGE & D ELIVERY P RECAUTIONS
► Medication patches should be removed when they interfere with electrode placement. Any residual glue or medication should be wiped off the patient’s chest.
► Supplemental o xygenation devices (i.e. BVMs or pocket - face - masks) should be removed from the patient’s face. Canada’s Health Protection Branch recommends that oxygen delivery devices should be removed as there is a slight risk that during defibrillation, they may ignit e.
► Minimize excess movement during analysis as this movement may cause the AED to incorrectly diagnose a shockable rhythm.
► Patients should be extricated from wet environments. This does not pertain to wet surfaces; however, rather only in cases where a patient is found in pools of standing water where one can make a splash in the puddle.
► Ensure that the Corporation of Delta’s ‘Post AED Procedure’ is immediately implemented following an AED use.
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P OST T REATMENT – T ERMINATION OF U SE
P articipating in the restoration of spontaneous circulation and respirations in a patient of SCA is an enormous accomplishment. However, restoring vital signs is one challenge, maintaining a post - cardiac arrest patient is another thing altogether. Followi ng successful resuscitation , the rate at which consciousness and normal respirations return depends upon the duration of time the patient was without circulation.
Management of the post - arrest patient should be focused on:
► Maintaining a clear airway ; ► E nsuring effective ventilation with high - flow supplemental oxygen; if appropriate and trained to do so, provide assisted ventilations if the respiratory rate is less than 10 - breaths per - minute ;
► Continually assess for signs of life (circulation) and breathi ng which includes continuous observation and recording of the patient’s vital signs .
T RANSFER OF C ARE
When transferring care of the patient to the p aramedics, you must provide the following:
1. A brief history of the incident, including mechanism of inju ry or nature of illness.
2. Patient ’s chief complaint, past medical history, medications, and allergies.
3. What injuries were found, the treatment provided and vital signs.
4. Number of ‘shocks’ delivered or number of ‘no shock advised’ messages received.
D OCUMENTATION
It is essential that each AED incident response be thoroughly documented. This is to ensure that paramedics and hospital staff have complete patient information so that appropriate and timely patient care can be rendered. In addition, be cause our society is becoming more litigious, responders must protect themselves legally by properly documenting what they do and don’t do for the patient. Immediately following a deployment of an AED Protocol , the responder(s) are required to:
1. Imple ment the Corporation of Delta’s ‘Post AED Procedure’ immediately following an AED use incident.
2. Notify the ‘On - Call Manager’; the AED Go Responder will be notified.
PEAK E MERGENCY R ESPONSE T RAINING P ROVIDED FOR USE BY THE C ORPORATION OF D ELTA 26 C ARDIAC A RREST M ANAGEMENT : AED P ROTOCOL T RAINING M ANUAL 3. The ‘ AED Go Responder ’ will attend the scene and direct post - AED activities which will include: AED device maintenance, facility needs, and assistance with the completion of the PEAK ’ S report forms; ‘Protocol Initiation Report’ and ‘Post AED Incident Report’.
Electronic Data Retrieval / Post Incident Review – The ‘ AED Go Responder ’ will notify PEAK of an AED Protocol deployment and will provide the electronic incident data from the AED device so that a post - incident review can be conducted by PEAK .
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E A K PP E A K EE MM EE RR GG EE NN CC YY RR EE SS PP OO NN SS EE TT RR AA II NN II NN GG
A LGORITHMS
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CPR / AED A LGORITHM – 1 R ESCUER
A LGORITHM D ESCRIPTION : One rescuer responding to or coming across a patient; no back - up available and no communications av ailable at scene.
S C E N E A S S E S S M E N T
C O N F I R M E D
U N R E S P O N S I V E Yes Yes
ADULT PATIENTS (8+) PAEDIATRIC P ATIENTS (1 - 7)
Place in r ecovery p osition Quickly a ctivate EMS Retrieve AED Breathing?
No Yes
Breathing? Perform CPR for 2 - mi nutes (30:2) Place in r ecovery p osition Place in r ecovery p osition
Yes Quickly a ctivate EMS Quickly a ctivate EMS No Retrieve AED Retrieve AED Perform critical interventions Complete p atient a ssessment while awaiting EMS arrival Perform critical interventions while awaiting EMS arrival
R E A D Y A E D D E V I C E ( 3 S t e p s )
Step 1 : Press On/Off Button Step 2 : Apply Pads Step 3 : Plug in Pads Connector
CLEAR PATIENT
ANALYZE
OR PEAK E MERGENCY R ESPONSE T RAINING SHOCK NO - SHOCK P ROVIDED FOR USE BY THE C ORPORATION OF D ELTA 30 C ARDIAC A RREST M ANAGEMENT : AED P ROTOCOL T RAINING M ANUAL
CPR (2 - MINUTES) (30:2) Initiated immediately after shock is delivered Time is Muscle!
CONTINUE CYCLE UNTIL EMS ARRIVES or SIGNS OF LIFE PRESENT
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CPR / AED A LGORITHM – 2+ R ESCUERS
A LGORITHM D ESCRIPTION : 2 or more rescuer s re sponding to a cardiac arrest patient.
S C E N E A S S E S S M E N T
C O N F I R M E D
U N R E S P O N S I V E Yes Yes
RESCUER #1 RESCUER #2
Quickly a ctivate EMS Retrieve AED & CODE 3 Pack CPR (30:2) Breathing? No Time is Muscle!
Yes
Complete p atient a ssessment Perform critical interventions while awaiting EMS arri val
R E A D Y A E D D E V I C E ( 3 S t e p s )
Step 1 : Press On/Off Button Step 2 : Apply Pads Step 3 : Plug in Pads Connector
CLEAR PATIENT
ANALYZE
SHOCK OR NO - SHOCK
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CPR (2 - MINUTES) (30:2) Rotate Rescuers Initiated immediately after shock delivered Every 2 - Minutes Time is Muscle!
CONTINUE CYCLE UNTIL EMS ARRIVES or SIGNS OF LIFE PRESENT
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CPR / AED ( WITH BVM / OPA) A LGORITHM – OFA L EVEL 2/3 A TTENDANTS
A LGORITHM D ESCRIPTION : 2 or more rescuer s responding to a cardiac arrest patient u tilizing a BVM and OPA.
S C E N E A S S E S S M E N T
C O N F I R M E D
U N R E S P O N S I V E Yes Yes
RESCUER #1 RESCUER #2
Quickly a ctivate EMS Retrieve AED & CODE 3 Pack CPR (30:2) Breathing? Time is Muscle! No Yes
Complete p atient a ssessment Perform critical interventions while awaiting EMS arrival
R E A D Y A E D D E V I C E ( 3 S t e p s )
Step 1 : Press On/Off Button Step 2 : Apply Pads Step 3 : Plug in Pads Connector
CLEAR PATIENT
ANALYZE
SHOCK OR NO - SHOCK
CPR (2 - MINUTES) (30:2) Rotate Rescuers Initiated immediately after a shock is delivered Every 2 - Minutes Time is Muscle!
Rescuer not performing CPR: If 2 n d Attendant Measures & insert s OPA a vailable u se BVM (if trained) PEAK E MERGENCY R ESPONSE T RAINING Attach es BMV to O 2 @ 15LPM flow P ROVIDED FOR USE BY THE C ORPORATION OF D ELTA 34 C ARDIAC A RREST M ANAGEMENT : AED P ROTOCOL T RAINING M ANUAL
CONTINUE CYCLE UNTIL EMS ARRIVES or SIGNS OF LIFE PRESE N T
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C HILD / A DULT C ONSCIOUS C HOKING
S C E N E A S S E S S M E N T
No Assess Degree of Are you Obstruction choking ? End
Yes
No Wait for implied consent Can I Help ? (unresponsiveness)
Yes Yes
MILD OBSTRUCTION SEVERE OBSTRUCTION Encourage patient to cough Activate EMS Provide reassurance Administer 5 abdominal - thrusts (patient dependent – see below) Administer oxygen 1 0 LPM (if appropriate) After 5 failed attempts deliver 5 back - blows if unsuccessful
Activate EMS (if appropriate – see below) Alternate until airway is cleared or the patient becomes unresponsive
Post Obstruction Management: Post Obstruction Management: Conduct a thorough patient assessment Conduct a thorough patient assessment Administer oxygen 1 0 LPM (i f appropriate) Administer oxygen 1 0 LPM Update EMS if activated Update EMS Record vital signs Record vital signs Treat for shock Treat for shock
Notes:
- Should a patient become unresponsive at any point , manage patient according to the ‘Unresponsive Choking’ algorithm.
- Activation of EMS should not be disco uraged; when in doubt activate EMS.
- Abdominal - Thrusts may be replaced with Chest - Thrusts if the patient is pregnant or obese.
- For ‘back - blows’ patient should be encouraged to rest their hands on their knees (or a table) to help support themselves. The b ack of the patient should be as horizontal as possible.
- Implied Consent: A pplies to unresponsive patients .
- Expressed Consent: Applies to a patient who grants consent verbal ly or who d oes not refuse assistance .
PEAK E MERGENCY R ESPONSE T RAINING P ROVIDED FOR USE BY THE C ORPORATION OF D ELTA 36 C ARDIAC A RREST M ANAGEMENT : AED P ROTOCOL T RAINING M ANUAL - Observe ‘mildly obstructed’ patients for signs of deterioration to include: cyan osis, inability to move air, or high - pitched wheezing. If these signs are present , treat patient according to severe obstruction.
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C HILD / A DULT U NRESPONSIVE C HOKING – 1 R ESCUER
S C E N E A S S E S S M E N T
C O N F I R M E D
U N R E S P O N S I V E P A T I E N T Yes
ADULT PATIENTS (8+) PAEDIATRIC PATIENTS (0 - 7)
Place in r ecovery p osition Perform 30 c hest - c ompressions Quickly a ctivate EMS Attempt to Ventilate: Retrieve AED if available - If unsuccessful: reposition head & r eattempt ventilation
Continue CPR for 2 - m inutes
Perform 30 Chest Compressions Place p atient in r ecovery p osition Quickly a ctivate EMS Retrieve AED if a vailable Yes Continue C PR & refer Air goes in? to AED algorithm
No
Reposition the Yes Continu e C PR & airway & reattempt refer to AED ventilation algorithm Air goes in?
No
Chest compressions Ye s Continue C PR & Foreign body check refer to AED Attempt to ventilate and/or algorithm reposition the airway and reattempt ventilation Continue cycle or until patient show signs of life
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EE AA KK PP EE MM EE RR GG EE NN CC YY RR EE SS PP OO NN SS EE TT RR AA II NN II NN GG
A PPENDICES
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A PPENDIX 1 U SE OF A B AG - V ALVE - M ASK D EVICE
Used mainly on patients that are not breathing (can be used for those having trouble breathing)
Three parts - 1. A bag 2. A valve 3. A mask
Is located in the “Code 3” bag
One - way valve allows air to move from the bag to the patient, but prevents the patient’s exhaled air from entering the bag
Child and infant BVM have release valves to prevent over inflation
Use: Wherever possible the BVM should be used by 2 rescuers. An Oropharyngeal Airway (O PA) is to be inserted prior to setting up the BVM.
One - Rescuer – With one hand make a “C - clamp” with the index finger and thumb, placed around the mask. Using the rest of the fingers, form a letter “E” to open the airway ( k nees can be used to hold patie nt’s head in a head tilt position if patient is not considered a spinal patient ). Use the other hand to gently squeeze the bag smoothly, just until the patient’s chest starts to rise.
Two - Rescuer – One rescuer uses two hands to hold the mask to the pati ent’s face using two “C - clamps” with their index finger and thumb and opening the airway by forming a letter “E” with their remaining fingers of each hand. The second rescuer provides the ventilations for the patient by gently squeezing the bag smoothly, just until the patient’s chest starts to rise.
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A PPENDIX 2 U SE OF A S UCTION D EVICE
Used to clear the airway of a patient that is regurgitating (fluids without chunks)
Parts – 1. Rubber hose 2. Fluid holding tank 3. Trigger mechanism 4. Cap (for tank)
Is located in the “Code 3” bag
Hose may need to be attached to the trigger mechanism
Bio - Hazard bag is in the same pocket as the suction
Use: The suction is manual to allow for control of suction. Second or third rescuer to assemble if needed. Using both hands; one to insert the hose (only as far as the tip can be seen) into the corner of the mouth and hold the hose and the other hand to squeeze the suction. Pull back as suction action i s started and repeat until airway is cleared. If possible, patient to be rolled to the side.
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EE AA KK PP EE MM EE RR GG EE NN CC YY RR EE SS PP OO NN SS EE TT RR AA II NN II NN GG
P OST C OURSE Q UIZ
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P OST C OURSE Q UIZ ( Page 1 of 2 )
1. Define the term Sudden Cardiac Arrest . ______
2. Define the term Coronary Artery Disease . ______
3. Describe in brief the flow of blood as it passes from the heart to the lungs and back. ______
4. Describe in detail the flow of air as it enters the respiratory system. ______
5. What are the indications for the use of an AED? ______
6. What is the contraindication against the us e of an AED and what is the rationale?
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P OST C OURSE Q UIZ ( Page 2 of 2 )
7. What are the precautions for the use of an AED? ______
8. Describe in detail the path of the normal conduction system of the heart. ______
9. What are the 2 ‘ Shockable Rhythms ’ that an AED will treat with ‘electrical medicine’? ______
10. Describe the differences between Angina and Myocardial Infarction (MI). ______
11. Describe in detail the difference between a MI induced SCA and cardiac arrest due to asphyxiation or hypoxia. (O ther resources may be needed to answer this question . )
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EE AA KK PP EE MM EE RR GG EE NN CC YY RR EE SS PP OO NN SS EE TT RR AA II NN II NN GG
GG LL OO SS SS AA RR YY
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G LOSSARY
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AED – Automated External Defibrillator is a portable LLS – A Peak© expression. Derived from the Latin: electrical devic e that is capable of analyzing heart “Resemblar Shock”, and the olde English: “Lukus lik shock”. rhythms (by way of an on - board computer) and of Meaning to have a poor, sickly appearance – shock - like. making the medical decision to deliver or withhold an Literally: “Looks like shock”. electrical shock capable of stopping the uncontrolled fibrillation of the heart muscle. LOR – Level of Responsiveness.
Agonal Breathing – Ineffect ive breathing (no actual air Lub - Dub – To be more accurate, we should note that these exchange) due to brain stem functioning and muscle sounds are actually made by the valves closing right after the memory. contraction completes. (i.e the “Lub” is the sound of the tricuspid & bicuspid valves closing after the atria contract, and Angina Pectoris – Chest pain caused by a reversible the “Dub” is the sound of the pulmonary & aortic valves closing narrowing of a coronary artery. after the ventricles contract)
Apnea / Apneic – Not breathing. Medical Direction – Authority or licensing body overseeing the use of restricted medical acts. Asystole (Flat - line) – A cardiac rhythm in which there is no electrical or mechanical activity in the heart. Myocardial Infarction (MI) – See Heart Attack.
Atrioventricular Node (AV - node) – A specialized Nitroglycerin (NTG) – Vasodilator used mainly for angina structure located in the atrial / ventricular junction of the pectoris. heart that slows electrical conduction through the AV junction; also serves as less effective back - up Necrosis – Tissue death. pacemaker if the SA node fails. Occlusion – A blockage; generally applies to a blockage or a Bradycardia – Slow heart - rate. coronary or cerebral blood vessel.
Bundle Branches (Left & Right) – Specialized Perfusion – Adequate blood flow to the tissues resulting in conductive tissue transmitting electrical impulses from effective delivery of oxygen and nutrients t o the cells, and also the AV node to the Purkinje fibers. effective removal and disposal of cellular waste products.
Contraindicated – A situation that prohibits the use of a Purkinje Fibers – Specialized conductive fibers located within medication. the walls of the ventricles.
Cyanosis – A bluish - grey skin colour that is caused by Sino - Atrial Node (SA - node) – Situated at the opening (Sino = reduced levels of oxygen in the blood. opening) of the supe rior vena cava into the right atrium. This
is the pacemaker in a healthy heart - the wave of myocardial Distal – The more (or most) distant of two (or more) contraction begins here then spreads over the heart. things.
Sudden Cardiac Arrest (SCA) – Unexpected sudden Dyspnea – Difficulty breathing. collapse, cardiac arrest with no pre - existing ter minal illness.
Embolic – Pertaining to emboli sm (traveling clot). Tachycardia – Fast heart - rate.
Ischemia – A lack of perfusion that deprives tissues of Ventricular Fibrillation (VF) – Disorganized, ineffective necessary oxygen, nutrients, and waste removal twitching of the ventricles, resulting in no blood flow and a resulting from partial or complete blockage of blood flow; state of cardiac arrest. potentially reversible since permanent injury has not yet
occurred. Ventricular Tachycardia (VT) – Rapid heart rhythm in which
t he electrical impulse begins in the ventricle (instead of the Hea rt Attack – (MI) A condition resulting from a blocked atrium), which may result in inadequate blood flow and may coronary artery with subsequent death of part of the eventually deteriorate into cardiac arrest. myocardium (heart muscle).
Hypotension – Low blood pressure.
Hypoxia – A dangerous condition in which the body tissues and cells do not have enough oxygen.
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