M ODULE 7 – N ON - U RBAN C ARDIAC A RREST M ANAGEMENT P ROTOCOL (NUCAM) 1

M ODULE 7

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PEAK Emergency Response Training Advanced Protocol Training Program 2 M ODULE 7 – N ON - U RBAN C ARDIAC A RREST M ANAGEMENT P ROTOCOL (NUCAM)

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PEAK Emergency Response Training Advanced Protocol Training Program M ODULE 7 – N ON - U RBAN C ARDIAC A RREST M ANAGEMENT P ROTOCOL (NUCAM) 3

O VERVIEW AND L IABILITY

This ‘ Non - Urban Cardiac Arrest Management Protocol (NUCAM ) Tra ining M odule ’ i s not exhaustive. It is designed to be used in conjunction with an extensive practical and theoretical training program, which includes a written an d prac tical examination. Annual recertification is required for maintenance of PEAK’ S ‘Non - Urban Cardiac Arrest Management Protocol (NUCAM)’ certification. ‘90 - day S kills R efreshers’ are strongly encouraged.

This ‘ Non - Urban Cardiac Arrest Management Pro tocol Training Module’ is intended to be utilized by professional (paid & volunteer) n o n - u rb an r esponders such as ski/bike patrollers , s earch and r escue technicians, guides and other n on - u rban f i rst r esponders that are tasked with providing advanced emerge ncy medical care .

Candidates must hold, at a minimum, a current certification in at least one of the following programs (or equivalent): Non - Urban Occupational First Aid (NUOFA 3), Non - Urban Emergency Care (NUEC 3), Outdoor Emergency Care (OEC), Occupat ional First Aid Level 3 (OFA Level - 3) or the Canadian Ski Patrol First Aid Course (CSP) . Po tential candidates mu st also hold a current (within one y ear) CPR certification.

This ‘ Non - Urban Cardiac Arrest Management Protocol Training M odule ’ is as printed and carries no g uarantee whatsoever. PEAK assumes no responsibility to any party for lo ss or damage alleged to be caused by the information contained or by any alleged omission in this ‘ Non - Urban Cardiac Arrest Management Protocol Training M odule ’ .

Furt hermore, PEAK pr ohibits any individual, corporation or entity from copying, altering, l oanin g or using this manual in full or in part without prior express written permission of PEAK .

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S UDDEN C ARDIAC A RREST (SCA)

Sudden Cardiac Arrest (SCA) is the lead ing cause of death among adults striking nearly 45,000 Canadian s ann ually. The Canadian Heart and Stroke Foundation support implementing the “ Chain of Survival ” to assist people who suffer a cardiac arrest in the community. The ad ult chain consists of:

► Early Recognition and Activation of EMS ► Early CPR ► Rapid Defibr illat ion ► Effective Advanced Life Support Care ► Integrated Post - Cardiac Arrest Care

It is estimated that for every minute a person remains in cardiac arrest, surv ivability is reduced by 7 - 10%. The definitive treatment for Ventricular Fibrillation ( VF ), the most common ‘treatable’ type of cardiac arrest , or Ventricular Tachycardia (VT) , is defibrillation. Early defibrillation, in conjunction with cardiopulmonary re suscitation (CPR), incre ases survival rates by nearly 50%.

What is Sudden Cardiac Ar rest (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 6 5 years old; however, ma ny victims are in their 40’s and even younger. Very often, the re 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 S CA occur when the electr ical impulses in the diseased heart become too rapid ( Ventricul ar Ta chycardia ) or chaotic ( Ventricular Fibrillation ) – originating from incorrect parts of the heart. These irregular heart rhythms ( arrhythmias ) produce ineffective or absent contractions res ulting in the cessation of blood flow and ultimately death.

C PR / AED – Survival Rates

Early CPR CPR Delayed Defibrillation Defibrillation 2 - 8% survive

Early CPR Defibril l ation 2 0 % surv iv e 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 - exi sting heart abnormalitie s and/or respiratory compromise is likely the cause. Adrenalin e rel eased during intense physical or athletic activity often acts as a trigger for sudden death when these abnormalities are present.

Also, under certain conditions s ome heart medications an d other drugs (as well as recreational drugs) can lead to abnor mal h eart 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 fr o m a prior heart attack (often presented as a ‘silent’ attack), is o bserved 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 o ur knowledge of the anat o my and physiology (‘meat and motion’) of the respiratory and c ardia c systems.

Following this review, we must understand the electrical anatomy and physiology (electro - physiology) of the heart in order that we can understand how i t is that arterial block a ges lead to d eath of heart muscle tissue and interrupted elect rical cardiac signals. Subsequently this may lead to malfunctioning cardiac muscle, decreased blood flow and ultimately SCA.

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R ESPIRATORY / C ARDIAC A NATOMY & P HYSI OL OGY

► T HE R ESPIRATORY S YSTEM

We already know that our Primary Assessment includes making sure the patient has a clear airway and effective breathing, or by providing the necessary critical interventions. To ensure that we have a firm foundation upon whi ch to add the NUCAM Protocol , should it be 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 air way is composed of the mouth, nose, pharynx and epiglottis . The tongue is located in the upper airway and is the most common source of airway obstruction in an unresponsive patient (GCS < 8) . The lower airway is made up of the larynx, trachea, bronchi, br onchioles and alveoli .

Air Flow Through the Respiratory 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 no se), and the oropharynx (located behind the mouth).

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 t he 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. T he cricoid cartilage makes up the bottom portion of the larynx, and the trac hea lies just below the larynx.

Air passes through the trachea , which branches 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 alveo lar sacs located in the lung tissue.

Once the air reaches the capillaries surrounding 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 AND 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 (one fist for children) . It is composed of car diac muscle, called myocardium , and it is responsible for pumping Oxygen - rich blood to the body (including its own heart tissue) and Oxygen - depleted blood back to the lungs.

The heart is divided into four chambers, with the septum separating the left an d right sides. Each side is further divided in half with the atria being the upper chambers and the ventricles being the lower.

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’ right atrium , which, when the atria contract, expels the blood through a one - way valve (the tricuspid valve) into the right ventricle. T his creates the ‘ l ub’ of the familiar ‘ l ub - d ub ’ sound associated with a heart beat.

While the atria are contracting, the ventricles are ‘relaxing’ or re - expanding allowing them to refill with the next influx of blood.

Immediately after the atria contra ct, contraction of the ventricles occurs (‘ d ub’) and the blood is delivered into the pulmonary arteries via the pulmonary valve . ( S ee l ub - d ub in the Glossary for an in - depth explanation)

Now, 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 agai n the atria contract, the blood in the left atrium then passes through the bicuspid valve (also known as the mitral valve) to the most muscular chamber, the left ventricle.

Contraction of the ventricles occurs again, and the oxygenated blood is then pus hed through the aortic valve , to the aorta and then on to the entire body – including the coronary arteries . It is important 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 AND P HYSIOLOGY ( CONT ’ D )

► C ARDIAC S YSTEM – E LECTRICAL A & P (Electrophysiology)

Now that we’ve reviewed the A&P we can start to build on that foundation by exploring the electrical aspect of the hear t – that aspect which the AED addresses so effectively.

The heart has its own intrinsic electrical system which controls the sequencing , rate and rhythm of the contractions of the heart.

Heart Contraction Sequencing

The heart’s electrical system contro l s the timing or sequencing of the separate contractions of the upper and lower pairs of chambers. Think of it this way: if the whole heart muscle contracted at the same time, there would be no effective pumping, because the chambers wouldn’t be able to e f fectively pump and refill at the same time. Therefore, the timing of the contractions of the two pairs of chambers are slightly offset (‘ l ub - d ub’ = 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 pathways to ensure the coordinated pumping of blood through the heart and on to the lungs and the body.

The heart muscle n e eds electricity running through it in order to contract. T he heart has built - in pacemaker tissue (instead of a battery) located in the area of the heart that contracts first – the atria.

This pacemaker tissue is called the sinoatrial node (the word ‘si n o’ refers to an opening or hole – think of your sinuses), and in this case refers to the opening in the right atrium through which the inferior and superior vena cava e deliver the blood from the body.

Th is pacemaker tissue , called the sinoatrial n ode (or SA n ode), sends out an electrical impulse across the tissues closest to it (both atria). This jolt or impulse causes the atria to contract which pumps the blood down into the ventricles.

What prevents the ventricles contracting at the same time as the a t ria? That’s where the signal retarding tissue comes in.

As that electrical signal from the SA node follows the electrical pathways around and through the contracting atria, the pathways gather together again just above the right ventricle at the retardi n g atrioventricular node (or AV node obviously named for its location between the atria and the ventricles). The signal takes about 0.08 seconds to reach the AV node.

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R ESPIRATORY / C ARDIAC A NATOMY AND P HYSIOLOGY ( CONT ’ D )

Although the AV node can se rv e as a secondary, slower pacemaker if the SA node fails, its primary function is to slow the SA node’s signal momentarily before it electrifies the ventricles.

The AV node tissue has a slightly higher electrical resistance than the atrial tissue above i t. So, as the signal is gathered in the AV node, this resistant tissue holds the impuls e back very briefly (about 0.12 seconds) before allowing it to race on at its previous speed down through and around the ventricular tissues. An analogy we can use to de scribe 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 temporarily before continuing on as before. As this electrical signal races on from the AV node , it follows the long v entricular pathways – the right and left bundle branches and the purkinje fibres , and, in doing so, causes the respective ventricles to contract simultaneously.

To summarize, the SA node or pacemaker sends an electrical signal through the atria – causing t hem 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 after their last contraction and refill with blood from the atria. The signal then races on throug h 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 cycl e.

Heart Rate

The SA node is the primary rate - setter or ‘pacemaker’ in a healthy heart. It generates electrical impulses (and therefore contractions) 60 - 100 times/minute, thereby establishing a healthy, perfusing heart rate. It is important to note, ho we ver, that any of the electrical conductive tissue s of the heart ha ve the ability to act as the heart’s pacemaker. The SA node generates an electrical impulse faster than any other tissue, which is why it is typically in control. However, if the SA node s hould 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 / min Pacemaker Rates of Fire AV node: 40 - 50 times / m in Purkinje fibr e s : 30 - 40 times / min

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 AND P HYSIOLOGY ( CONT ’ D )

A healthy heartbeat for an adult is 60 - 100 beats per/ min. 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 no t healthy for your heart to beat out of rhythm. This arrhythmia will compromise the blood flow to the rest of your body.

The ECG Before w e discuss the rhythm of a heart beat, it is important to understand the graphical measurement or representation of t he heart’s electrical activity – the electrocardiograph – (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 provid ing training in ECG In terpretation . )

The following ECG strip example reflects 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 ra te , sequencing and rhythm. That is – it shows a rate between 60 - 100 times per/ m inute ( normal), an impulse starting in the SA n ode ( sinus ) and recurring regularly ( rhythm). This would be referred to as a ‘Normal Sinus Rhythm’ or NSR.

(ECG) Example

Note: In the diagram above, the 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 pat te rns 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 If we knew the time frame represented by the vertical li nes, we’d be able to calculate that these patterns repeated approximately 60 times per minute.

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R ESPIRATORY / C ARDIAC A NATOMY AND P HYSIOLOGY ( CONT ’ D )

Evaluating for Regularity It is easy to recognize that these patterns repeat regularly - approximate ly once every 4 vertical lines.

Evaluating 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 re fer red to as the P - wave. It represents 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 t o a s the QRS complex. It represents 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 . The ventricles are recovering and refilling before they must contract again ( repolarization is occurring).

2. QRS complex

1. P - wave

3. T - wave = r epolarization / r elaxation

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R ESPIRATORY / C ARDIAC A NATOMY AND P HYSIOLOGY ( CONT ’ D )

These recurring patterns (the P - QR S - T patterns) on this strip have a structure revealing that the sequencing of the electrical signal is healthy – the signal begins at the SA node , cross es the atria, slow s at the AV node , and then quickly cross es the ventricles.

In a very simplistic way t his ECG strip example reveals similarly structured, healthy patterns, recurring regularly at a rate of approximately 60 - 100 beats per/ min ute .

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……

Which in turn results in the:

► Delivery of blood to the lungs for cleaning and oxygenation; and ► Delivery of oxygenated blood back to the coro nary arte rie s, tissues and body

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 can result in SCA.

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C ORONARY A RTERY D ISEASE

Coronary Arter y Di sease (CAD) occurs when the arteries 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 coron ary arteries, blood flow to the heart 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 c ontr ibute to the development of coronary artery disease and atherosclerosis:

► Age ► Male ► Female (50+) ► Hypertension ► Smoking ► Genetics ► Diabetes Mellitus ► Elevated cholesterol ► Sedentary lifestyle ► Stress ► Sleep apnea ► Prolonged excessive use of stimulants

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A NG INA P ECTORIS

Angina Pectoris ( pain in the chest ) is the result of a reduced Oxygen supply to the hea rt muscle ( myocardium ) . This lack of Oxygen to the myocardium is known as myocardial ischemia . Angina Pectoris is a common symptom of myocardial ischemia most commonly caused by a ‘ s pasming ’ or narrowing of a coronary artery due to coronary artery disease ( atherosclerosis ). Episodes of a ngina are typically brought on by exertion or high levels of stress. They are relieved with rest and , often, with Nitroglycerin Protocol initia tion , 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, a rms, shoulders, neck & back

► Shortness of Breath ► Nausea & Vomiting ► Anxiety ► Pale, Cool, Clammy = LLS ► Symptoms typically resolve with rest & Nitroglycerin

M YOCARDIAL I NFARCTION (M I )

M yocardial Infarction (heart attack) is caused by an obstruction of a coro nary artery and thus severe myocardial ischemia. The infarction is nearly always the result of a clot that blocks the artery a t an atherosclerotic narrowing. M yocardial infarctions m ay have no obvious precipitating events and often occur while the p atien t 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 ► Anxie ty / Fear / Denial ► Pale, Cool, Clammy = LLS ► Symptoms don’t resolve with rest & Nitroglycerin

Note: The signs & symptoms (S / S x ) above typically describe what males tend to complain of when experiencing a myocardial infarction ; this is largely due to muscl e mass and location. Females may or may not present with the S / S x listed above and often complain of discomfort across the back and shoulders. It is imperative that all patients that complain of chest pain , or the other symptoms listed, are treated as a probable myocardial infarction.

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M YOCARDIAL I NFARCTION I NDUCED S UDDEN C ARDIAC A RREST

► A coronary artery is occluded (blocked) Damage and death to heart ► Perfusion ceases in: tissue shown as shaded area ▪ Myocardium (area weakens & dies) ▪ Electrical conduction tissues are damaged ▪ Pacing impulses are inte rrupte d / 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 inter ruptio n, 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 Consciousness (LO C ) ► Non - Breathing (Apneic) / Agonal / Gasping ► No Signs of Life or Circulation . Pulsel ess (a dult - carotid, child - carotid or femoral, infant - brachial) . No Chest Movement , c oughing or m ovement ► Pale / Cool / Cold / Diaphoretic (profuse sweating) / Cyanotic (bluish skin)

H EART R HYTHMS

Before learning about ‘abnormal rhythms’, it’s necessary t o revi ew the ECG of a normal sinus rhythm:

Normal Sinus Rhythm (NSR) A heart is said to be in a normal sinus rhythm when uniform heartbeats occur at regularly spaced intervals. This normal rhythm indicates that the SA node is acting as the primary pacema ker, a nd that the heart is beating between 60 - 100 times per/minute . This rhythm is made up of many single ECG complexes wherein each complex signifies a single effective heart beat.

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H EART R HYTHMS ( CONT ’ D )

A single ECG complex is regarded as having thr ee sec tions: 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 occ urring. The QRS wave signifies the contraction of the ventricles. The T - wave occurs when both ventricles of the heart are relaxing. The ventricles are recovering and refilling before they must contract again (repolarization is occurring).

A BNORMA L H EAR T R HYTHMS – A RRHYTHMIAS As discussed above, abnormal heart rhythms generally arise from damaged conduction pathways in heart tissue. When coronary arteries become blocked, this stops the flow of oxygenated blood to distal heart tissue. This reduce d perf usion leads to ischemia and heart tissue damage / death. In this tissue there are nerve pathways which ordinarily conduct the signal from the SA n ode.

When this tissue dies, the electrical signal (which previously caused healthy contractions and p umping ) 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 distal to the bl ockage will receive but not be able to respond to the signal and therefore not contract adequately, 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 fir e, 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 a re not contracting, nor are they filling the ventricles. The pacemaker in the ventricles will fire 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 pathophysi ology of ventricular tachycardia – see below.

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H EART R HYTHMS ( CONT ’ D )

Often, this rhythm will continue to accelerate and, as the tissues become more hypoxic, the electrical organization will begin to break down further. Many sites within th e ventr icles will begin acting as pacemakers resulting in uncoordinated, chaotic electrical and mechanical activity – continuing a state in wh ich there is no cardiac output. This is a description of the pathophysiology of ventricular fibrillation – see be low.

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 and puls eless e lectrical activity (PEA). Of these four, only two are shockable rhythms: VT and VF .

Ventricular Tachycardia (VT) VT occurs when there is one site in the heart (in the ventricles) that takes over as the primary pacemaker. Because the electrical impuls e 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 pressure 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) 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 seems to be constantly firing and is very disorganized. The heart appears to be q uivering when it is in VF and the disorganized contractions do not circulate the blood. Inadequate circulation causes hypoxia and will quickly cause a patient to lose responsiveness. A normal heart rhythm must be established quickly to prevent irr epara bl e damage to the heart muscle. VF is the most common rhythm associated with SCA.

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H EART R HYTHMS R ESULTING IN SCA ( CONT ’ D )

Asystole (Flat - Line) An AED will not advise a shock when the patient is in asystole . In an asystolic heart, there is absolut ely no e lectrical 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. Th is is do ne in the hope that the natural pacemaker will then resume it s electrical control of the heart – thereby restarting regular contractions. However, in the case of asystole, no pacemaker sites are firing at all, and no application of an electrical s hock can revive this tissue – the heart and its electrical system are already dead. The responder(s) will the refore have to rely on CPR as the treatment for this patient.

Pulseless Electrical Activity (PEA) During P EA the primary pacemaker keeps firing ; howeve r , the heart muscle is so damaged that it is not capable of contracting . The electrical signal flows normally down across the heart (resulting in a normal ECG), but the heart muscle cannot respond. An AED will not be beneficial with this rhythm b ecause t he problem is not so much an electrical one (the electrical system does not need t o be stopped and reorganized – it i s working fine); rather, it’s a mechanical problem . An AED will simply recognize this as a normal perfusing (non - shockable) rhythm and ind icate “No Shock Advised” . The r esponder will therefore have to rely on CPR as the treatment for this patient.

AED U SE AND D EFIBRILLATION

When a person collapses and is found to be in cardiac arrest as a result of VF or VT the definitive treat ment for this person is defibrillation .

The purpose of CPR is to artificially circulate a victim’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. Effec tive che st compressions can supply up to 25 - 30% of the typical cardiac output. It is not a corrective treatment; at best, it may keep the heart muscle alive while waiting for the AED and Advanced Cardiac Life Support (ACLS) – which is the definitive treat ment for SCA.

Studies conducted at cardiac rehabilitati on cent r e s have shown that when SCA victims in VF receive defibrillation 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 victims do not have immediate access to prompt, definitive treatment. Typically too much time elapses before CPR and an AED is applied.

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AED U SE AND D EFIBRILLATION ( CONT ’ D )

How Does De fibrillat ion 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 a re design ed for use by people who may not have the extensive training required to use a manual defibrillator. AEDs are very simple to operate as responder s 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 advise the Responder to administer a ‘shock’.

The purpose of the AED is to deliver an electric shock to the myocardium; momentarily terminati ng all el ectrical 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 n ode. This intrinsic ability is termed ‘ automaticity ’.

P URPOSE AND B ENEFITS

The extended response times by Paramedics can have a significant impact on patient outcomes. It is clear that a victim of SCA has little or no chance of surviving without immediate advanced treatment (less than 10 minutes). This i s the mai n 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 tra ining 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 S F OR U SE

The NUCAM Protocol is initiated for : ► Patients greater than 1 year of ag e; AND / OR ► Patients in cardiac arrest ( unresponsive, apneic or near apneic, and pulseless )

C ONTRAINDICATIONS

The NUCAM Protocol is contraindicated for : ► Patients that are less than 1 year of age; AND / OR ► Patients that are not in cardiac arrest

S A FETY , S TO RAGE AND D ELIVERY P RECAUTIONS

► Medication patches should be removed when they interfere with electrode placement. Any residual glue or medication should b e wiped off the patient’s chest

► Supplemental oxygenation devices (e.g. BVMs or pocket - face - masks) s hould 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 ignite

► Minimize excess movement during analysis as this m ovement may cause the AED to incorrect ly diagnose a shockable rhythm

► Patients should be extricated from wet environments. This does not pertain to wet surfaces or clothing ; however, rather only in cases where a patient is found in pools of standi ng water where one can make a splash in the puddle

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P OST - T REATMENT – T ERMINATION OF U SE

Participating in the restoration of spontaneous circulation and respirations in a patient of SCA is an enormous accomplishment. However, restorin g vital si gns is one challenge, maintaining a post - cardiac arrest patient is another thing altogether. Following successful resuscitation, the rate at which responsiveness and normal respirations return depends upon the duration of time the patient was wi thout circ ulation.

Management of the post - arrest patient should be focused on:

► Maintaining a clear airway while e nsuring effective ventilation with high flow supplemental Oxygen ; patie nt s with respiratory rates of less than 10 per /min should have their respirati ons assisted

► Continually assess for signs of life / circulation which includes continuous observation and recording of the patient’s vital signs

T RANSFER OF C ARE

When transferring care of a p atient to Paramedics you must provide the followin g: 1. A brief summary of the incident, including mechanism of injury or nature of illness

2. Patient’s chief complaint, past medical his tory, medications and allergies

3. What injuries were found, the treatment provided, vital and diag nostic signs

4. Number of ‘shocks’ d elivered , the time(s) they were delivered and/ or number of ‘no s hock advised’ messages received

D OCUMENTATION

It is essential that each protocol initiation be thoroughly documented. This is to ensure that Paramedics and hospital staff have complete patient information . In addition, because our society is becoming more litigious, Responders must protect themselves against potential legal action by properly documenting what they do and don’t do for the patient. The NUCAM Responder is requir ed to comp lete a ‘Post - AED Incident Report’ (PAIR) (see page 132 or 133 ) in addition to the ‘Protocol Initiation Report’ (PIR) (see page 134 ) . Specifically, the following information should be documented:

1. AED Use – in dicate that an AED was applied 2. Number of ‘ Shocks ’ delivered and time(s) they were deliver or number of ‘ No Shock Advised ’ messages received

Post Incident Reporting – Immediately following the implementation of a NUCAM Protocol, fax or scan the completed PAIR and PIR to PEAK .

Data Tra nsmission / Post Incident Review – incident data from the AED device may be retrieved for post - incident review by PEAK’s Medical Direction Team .

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P OST - AED I NCIDENT R EPORT (PAIR) – G ENERIC

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P OST - AED I NCIDENT R EP ORT (PAIR) – A VALANCHE S PECIFIC

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D OCUMENTATION – P ROTOCOL I NITIATION R EPORT (PIR)

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SPECIFIC CARDIAC ARREST PROTOC OL S

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CPR / AED A LGORITHM F LOWCHART

S C E N E A S S E S S M E N T

P R I M A R Y A S S E S S M E N T

C O N F I R M E D P A T I E N T : U n r e s p o n s i v e ; & A p n e i c o r n e a r - a p n e i c ; & P u l s e l e s s

R A D I O C O M M U N I C A T I O N

I N I T I A T E C P R W I T H O U T D E L A Y

LEVEL OF RESPONSE AIRWAY ADJUNCT COMPRESSIONS SINGLE RESPONDER NO ADJUNCT / OPA / NPA 30:2 SYNCHRONOUS VENTILATIONS MULTIPLE RESPONDERS NO ADJUNCT / OPA / NPA 30:2 SYNCHR ONOUS VENTILATIONS MULTI PL E RESPONDERS KING - LT / ETT CONTINUOUS CARDIAC COMPRESSIONS WITH ASYNCHRONOUS VENTILATIONS

W H E N A E D D E V I C E A R R I V E S A T S C E N E

R E A D Y A E D D E V I C E ( 3 S t e p s )

S TEP 1 : P RESS O N /O FF B UTTON S T EP 2 : A PPLY P ADS S TEP 3 : P LUG IN P ADS C ONNECTOR

C L E A R P A T I E N T

A N A L Y Z E

S H O C K OR N O - S H O C K

C P R (2 - MINUTES) Initiated immediately after the advisory - Ti me is M uscle!

INITIATE TRANSPORT FOLLOWING 6 - CYCLES or IMMEDIATALY FOLLOWING A RETURN OF SPONTANEOUS CIRCULATION (ROSC)

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C ARDIAC A RREST T RANSPORT P ROTOCOL

This protocol outlines the actions to be taken when Responders are tasked to extricate and transport the patient using an e mergency t ransport v ehicle (ETV) , helicopter or any another fo rm of conveyance (e .g. T - bog) directly to a health care facility or to meet th e BCEHS ambulance en route.

PROCEDURE ► A sudden cardiac arrest patient should be classified as Critical T ransport Category (CTC)

► Patients without signs of circulation/life should be transported (if logistically possible) immediately following: Completion of 6 cycles of ‘CPR (2 minutes) ; Analyze; Shock/No - Shock’

► Patients who regain spontaneous signs of circulation/life should be transported immediately with the AED remainin g att ached until ar rival at hospital

T RAUMATIC C ARDIAC A RREST P ROTOCOL

This protocol outlines the actions to be taken when NUCAM Responders are confronted with an unresponsive patient with significant blunt or penetrating trauma.

PROCEDURE ► A traumati c cardiac arrest pa tient should be classified as Critical Transport Category (CTC) and transport should not be delayed unless to perform critical interventions

► Patients without signs of circulation/life should be transported (if logistically possible) imm ediately following: Completion of 6 cycles of ‘CPR (2 minutes); Analyze; Shock/No - Shock’

► Responders should conduct an RBS as soon as practical or followi ng 3 cycles of 2 minutes of CPR

► Patients who regain spontaneous signs of circulation should be transported immedia tely with the AED remaining att ached until arrival at hospital

► If ALS is readily available , Responders should consider transporting traumatic cardiac arrest patients before the completion of 6 cycles of CPR/AED as th ese patients may hav e a correctable cau se of the cardiac arrest . Correctible causes of traumatic cardiac arrest include ( but not limited to ) tension pn eum othorax, airway collapse, failed airway, hypovolemia, etc.

In the event of cardiac arrest in combination with catastro phic injuries (disr upted head or chest injuries, etc.), refer to the ‘Termination of Resuscitation Protocol’ .

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H YPOTHERMIC C ARDIAC A RREST P ROTOCOL

D E T E R M I N E D P A T I E N T I S S E V E R E L Y H Y P O T H E R M I C & I N C A R D I O P U L M O N A R Y A R R E S T

A B S E N T C A R O T I D P U L S E S ( C H E C K F O R 6 0 S E C )

INDICATIONS FOR WITHHOLDING OR TERMINATING RESUSCITATION Yes INDICATIONS FOR WITHHOLDING  Unacceptable risk to responders RESUSCITATION  Responder exhaustion  Extreme envir onments; CPR not possible ? No  Ca rdiac Arrest – Mass Casualty Incident  Avalanche Burial ; see specific protocol  D R I E D F P R E V E N T F U R T H E R D Decapitation , Dependant Lividity, H E A T L O S S Drowning >90 minutes R Rigor Mortis I Incinerated E Evisceration WITNESSED D Decompos ition F Body Frozen Solid (not compressible) ARR EST ? P E R F O R M C P R 2 M I N U T E S No NOTE: Fixed and dilated pupils or stiffness INSERT ADVANCED AIRWAY that resembles rigor mortis are not reliable indicators of death in IF AVAILBLE Yes hypothermia. Yes C O N N E C T A E D / A N A L Y Z E DELIVER 1 - SHOCK I F INDICATED WITHHOLD OR TERMINATE

RESUSCITATION I N I T I A T E T R A N S P O R T IF LOGISTICALLY POSSIBLE

C O N T I N U E R E S U S C I T A T I O N DELIVER MAXIMU M 3 - SHOCKS

I N I T I A T E I M M E D I A T E T R A N S P O R T

IF APPLICABLE TRANSPORT AS PER  Minimize movements to prevent arrhythmias

‘ NON - URBAN CRITICAL PATIENT  Arrange for ALS if applicable  Transport T ime > 6 hours : TRANSPORTATION PROCEDURE ’ T ransport to closest hospital  Transport time < 6 hours : If logistically possible & ALS is avai lable consider transp or ting directly to ECMO/CPB*

* If logistically possible, severe hypothermic patients should be transported to a hospital that has Cardiopulmonary Bypass (CPB) and/or Extracorporeal Membrane Oxygenation (ECMO) capabilities.

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A VALANCHE B URIAL (< 60 MINUTES ) C ARDIAC A RREST

This protocol outlines the actions to be taken when Responders are confronted with a single cardiac arrest patient who has been buried in an avalanch e for < 60 minutes .

PRO CEDURE BUR TIME < 60 MINUTES; CONFIRMED ► C onfirm cardiopulmonary arrest for 15 seconds ► Initiate critical interventions without delay; a large percentage of patients that fall into this category are ‘asphyxial cardiac arrest s’ ; ther efore primary critica l i nterventions should focus on establishing a patent airway and rescue breathing with high - concentration Oxygen

AED DEVICE WITH ECG CAPABILITY AIRWAY ECG RESPONDER ACTION STATUS

Patent or Asystole, - Ini tiate resuscitation a ccording to Traumatic C ardiac A rrest Protocol Obstructed VT, VF, PEA - Prevent further heat loss and provide active rewarming if applicable

AED DEVICE WITHOUT ECG CAPA B ILITY AIRWAY RESULT OF RESPONDER ACTION STATUS ANALSYIS

Patent or Shocka ble or - Initiate resuscitation according to Traumatic C ardiac A rrest Protocol Obstructed Non - Shockable - Prevent further heat loss and provide active rewarming if applicable

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A VALANCHE B URIAL (> 60 MINUTES ) C ARDIAC A RREST

This protocol outlines the actions to be taken when Responders are confronted with a single cardiac arrest patient who has been buried in an avalanche for > 60 minutes .

PROCEDURE L TIME > 60 MINUTES; CONFIRMED OR UN KNOWN

► C onfirm ca rdio pulmonary arrest for 60 seconds

AED WITH ECG CAPABILITY AIRWAY ECG ACTION STATUS Obstructed Asystole - Consider withholding resuscitation ; consult a Physician if applicable

- Initiate resuscitation according t o Hypothermic C ard iac A rrest Protocol

Patent Asystole - Apply spinal motion restriction

- Prevent further heat loss and provide active rewarming

- Initiate resuscitation according to Hypothermic C ardiac A rrest Protocol Patent or VT, VF, PEA - Apply spinal motion rest riction Obstructed - Prevent further heat loss and provide active rewarming

- Initiate resuscitation according to Hypothermic C ardiac A rrest Protocol Avalung VT, VF, PEA - Apply spinal motion restriction Deployed - Prevent further heat l oss and provide ac tive rewarming

AED WITHOUT ECG CAPA B ILITY AIRWAY ECG ACTION STATUS Obstructed Non - Shockable - Consider withholding resuscitation; consult medical control if applicable

- Initiate resuscitation according to Hy pothermic C ardiac A rrest Protocol

Patent Non - Shockable - Apply spinal motion restriction

- Prevent further heat loss and provide active rewarming

- Initiate resuscitation according to Hypothermic C ardiac A rrest Protocol Patent or Shockable - Apply spinal motion restrictio n Obstructed - Prevent further heat loss and provide active rewarming

- Initiate resuscitation according to Hypothermic C ardiac A rrest Protocol Avalung Shockable or - Apply spinal motion restriction Deployed Non - Shockable - Prevent furt her heat loss and provide active rewarming

► Patients who regain circulation should be transported with high - concentration Oxygen and ventilations if applicable without delay . The AED must remain attached to the patient until arrival at a heath - care fac ility or until the patient is transferred to a higher level of care

► Avoid rough handling of hypothermic patients

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T ERMINATION OF R ESUSCITATION P ROTOCOL

INDICATIONS FOR P R I M A R Y A S S E S S M E N T WITHHOLDING OR TERMINATING RESUSCITATION

 Unacceptable risk to responders  Responder exhaustion INDICATIONS FOR  Extreme environments; CPR n ot possible Yes  Cardiac Arrest – Mass Casualty Incident WITHHOLDING  Avalanche Burial ; see specific protocol RESUSCITATION

 D R I E D F ? No D Decapitation , Dependent Lividity, Drowning > 90 minutes R Rigor Mortis I Incinerated E Evisceration COLD D Decompos ition ENVI RONMENT ? F Body Frozen Solid (not compressible) PATIENT COLD ?

Yes NOTE: Fixed and dilated pupils or stiffness No that resembles rigor mortis are not REFER TO reliable indicators of death in HYPOTHERMIC hypothermia. CARDIAC ARREST I N I T I A T E R E S U S C I T A T I O N Yes PROTOCOL 1 0 C Y C L E S C P R / A E D M I N I M U M 2 0 M I N U T E S WITHHOLD OR TERMINATE

RESUSCITATION A N Y O F T H E F O L L O W I N G P R E S E N T ?

RE - REFER TO ‘ INDICATIONS FOR  ROSC OR SIGNS OF LIFE PRESENT ? No WITHHOLDING OR TERMINATING AND / OR

RESUSCITATION ’  ARREST WITNESS ED BY RESPONDERS ?

AND / OR

 SHOCK ( S ) BEEN DELIVERED ?

Yes

C O N T I N U E R E S U S C I T A T I O N

IF APPLICABLE TRANSPORT AS PER ‘ NON - URBAN CRITICAL PATIENT

TRANSPORTAT ION PROCEDURE ’

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P ROTOCOL P RE - T EST ( Page 1 of 2 )

1. Define the term Sudden Cardi ac Arrest . ______

2. Define the term Coronary Artery Dis ease . ______

3. Describe in detail 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 use of an AED and what is the rationale? ______

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P ROTOCOL P RE - T EST ( 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 t he heart. ______

9. What are the 2 ‘ Shockable Rhythms ’ t hat an AED will treat with ‘ electrical medicine’? ______

10. Describe the differenc es between Angina and Myocardial Infarction . ______

11. Describe in detail the difference between a myocardial infarction induced SCA and cardia c arrest due to asphyxiation or hypoxia (other resources may be needed to answer this question) . ______

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