dysrhythmia interpretation modules 1-6 june 2012

8/16/2019 Dysrhythmia Interpretation Modules 1-6 June 2012

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Dysrhythmia Interpretation &

Therapeutic ModalitiesModules I-VI

3340 Riverside Drive, Suite FChino, Ca. 91710

(909) 464-2299

Provider approved by the California Board of Registered Nursing, Provider Number 08593, And by the Nevada Board of Registered Nursing, Provider Number NV000556,

For 13.0 contact hours

You are required to maintain Continuing Education records for four (4) years.

Revised: 9/20/10


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Things to keep in mind when submitting a FLEX ED Home Study…

According to the appropriate board policies:

For complete details and specific polices for your license type, you will want to contact your board for any other

restrictions or requirements.

Students may not retake the same home study topic within 2 years of completion for

CEU credit.

California CNA’s are ineligible to complete home studies for CEU credit.

According to Flex Ed policies:

Home studies must be submitted no later than 30 days after completion date.Home Studies cannot be faxed or copied; the office must receive the original answer

sheet. ( You may want to use colored ink, to ensure your answer sheet is not flagged as

a copy, as some pens make it difficult to decipher)

Please fill out all information completely. (Full name, employer, address, etc.)

To ensure your credit is given quickly and efficiently be sure to PRINT as clearly as

possible.

All answers are to be filled out on answer sheet provided.

(Double check to ensure the answer sheet is fully completed before submitting)

Employees of contract facilities will have all certificates mailed directly to their hospitalsfor employment verification purposes.

Please keep in mind certificates take approximately 3-4 weeks to arrive.

A Passing Score is 80% or higher.

If you have any further questions regarding your home study please call the FLEX ED office at 909-464-2299

(Monday-Friday 9:00am-5:00pm)


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Dysrhythmia Interpretation & Therapeutic ModalitiesModules I-VI

Table of Contents

Objectives 4 - 7 Modules I-VI

Module I 8 - 49 Cardiovascular Structure and Function, Electrocardiography Monitoring,Introduction to Dysrhythmias, & Sinus Rhythms

Module II 50 – 65 Atrial Dysrhythmias

Module III 66 – 74 Junctional Rhythms

Module IV 75 – 91Ventricular Rhythms

Module V 92 – 100 Atrioventricular Blocks

Module VI 101 – 110Pacemakers

References 111

Post Test 112 – 125


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Dysrhythmia Interpretation & Therapeutic ModalitiesObjectives:

Module I: Cardiovascular Structure and Function, Electrocardiography Monitoring, Introduction toDysrhythmias, & Sinus Rhythms

1. Describe the anatomy of the heart.

2. Discuss preload, afterload, and components of cardiac output.

3. Discuss how atrial kick contributes to cardiac output.

4. Differentiate the effects of the sympathetic and parasympathetic nervous systems on the heart.

5. Be able to identify horizontal and vertical measurements on the ECG paper.

6. Name at least two methods for calculating heart rate.

7. Identify correct measurement for PR interval, QRS duration, and QT duration.

8. Be able to identify artifact on the ECG.

9. Describe the ECG characteristics of a sinus rhythm.

10. Describe the ECG characteristics, possible causes, signs and symptoms, and emergency

management of each of the following dysrhythmias that originate in the sinoatrial node :

a. Sinus bradycardia

b. Sinus tachycardia

c. Sinus arrhythmia

d. Sinus block

e. Sinus arrest

Module II: Atrial Dysrhythmias

1. Describe how atrial kick affects cardiac output.

2. Determine the etiology, identifying characteristics, significance and treatment for the following

groups of dysrhythmias:

a. Premature Atrial Contraction (PAC) and blocked PAC’s

b. Atrial fibrillation

c. Atrial Flutter


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d. Atrial Tachycardia

- Paroxysmal Atrial Tachycardia (PAT)

- Paroxysmal Supraventricular Tachycardia (PSVT)

e. Wandering Atrial Pacemaker

3. Describe the actions, uses, and adverse effects of the most commonly used drugs for the following

types of dysrhythmias:

a. Premature Atrial Contraction (PAC) and blocked PAC’s

b. Atrial fibrillation

c. Atrial Flutter

d. Atrial Tachycardia

- Paroxysmal Atrial Tachycardia

- Paroxysmal Supraventricular Tachycardia (PSVT)

e. Wandering Atrial Pacemaker

Module III: Junctional Rhythms


junctional rhythms:

a. Premature junctional contraction (PJC)

b. Junctional escape beat

c. Junctional Rhythm

d. Accelerated Junctional Rhythm

e. Junctional tachycardia

2. Describe the most commonly used drugs for the following types of dysrhythmias:

a. Premature junctional contraction (PJC)

b. Junctional escape beat

c. Junctional Rhythm

d. Accelerated Junctional Rhythm

e. Junctional tachycardia


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Module IV: Ventricular Rhythms


ventricular rhythms:

f. Premature Ventricular Complex/ Contraction (PVC)g. Ventricular Escape beats

h. Idioventricular Rhythm (Ventricular Escape Rhythm, IVR)

i. Accelerated Idioventricular Rhythm (AIVR)

j. Ventricular Tachycardia (VT)

- Monomorphic VT vs. Polymorphic VT

- Torsades de Pointes

k. Ventricular Fibrillation

l. Pulseless Electrical Activity (PEA)

m. Ventricular Standstill/ Agonal

n. Asystole

2. Describe the most commonly used drugs for the following types of dysrhythmias:

a. Premature Ventricular Complex/ Contraction (PVC)

b. Ventricular Escape beats

c. Idioventricular Rhythm (Ventricular Escape Rhythm, IVR)

d. Accelerated Idioventricular Rhythm (AIVR)

e. Ventricular Tachycardia (VT)

- Monomorphic VT vs. Polymorphic VT

- Torsades de Pointes

f. Ventricular Fibrillation

g. Pulseless Electrical Activity (PEA)

h. Ventricular Standstill/ Agonal

i. Asystole


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Module V: Atrioventricular Blocks


atrioventricular blocks:

a. First-degree AV Blockb. Second-degree AV Block- Type I (Wenckebach or Mobitz I)

c. Second-degree AV Block- Type II (Mobitz II)

d. Third-degree AV block (Complete Heart Block)

2. Describe the most commonly used drugs for the following types of atrioventricular blocks:

a. First-degree AV Block

b. Second-degree AV Block- Type I (Wenckebach or Mobitz I)

c. Second-degree AV Block- Type II (Mobitz II)

d. Third-degree AV block (Complete Heart Block)

Module VI: Pacemakers

1. Identify the primary indications and possible complications of pacemaker therapy.

2. Describe the various methods for pacing (transcutaneous, transvenous, epicardial).

3. Explain the difference between fixed-rate and demand pacemakers.

4. Identify the appearance of pacemakers spikes and the waveform on the ECG produced as a result

of:

a. Atrial pacing

b. Ventricular pacing


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Module I: Cardiovascular Structure and Function,Electrocardiography Monitoring, Introduction to

Dysrhythmias, & Sinus Rhythms

Important Terms- Cardiovascular Structure and Function

Afterload Affected by pressure and preload. What heart has to pumpagainst with each contraction.

Aortic Valve The valve between the left ventricle and the aorta.

Apex The bottom portion of the heart.

Arteriole Smaller arteries located between arteries and capillaries.

Artery A vessel carrying blood away from the heart. With theexception of the pulmonary artery, carries oxygenated blood.

Atrial Kick The amount of blood contributed by atrial contraction into theventricles. Accounts for 20 - 25 percent of cardiac output.

Capillary The area in the circulatory system where the exchange ofnutrients takes place.

Cardiac Output Hemodynamic calculation of heart rate X stroke volume.

Coronary Sinus Located at the base of the right atrium. It is the area where thecoronary veins return venous blood from the coronary arteries.

Coronary Arteries Supply the heart muscle with oxygenated blood.

Deoxygenated Venous blood is deoxygenated.The venous blood carries 70-75% oxygen, while the arterieshave 95% or greater oxygen.


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Diastole The relaxation phase of the cardiac cycle.

Mitral Valve The valve located between the left atrium and left ventricle.

Oxygenated With oxygen. Arteries carry 95% or greater oxygen.

Parasympathetic Part of the autonomic nervous system. Stimulation slowsNervous System heart rate. Associated with the vagus nerve.

PMI Point of maximal impulse where the apical pulse can bepalpated. The PMI is normally at the 5th intercostal space,midclavicular line.

Preload Amount of fluid coming into the ventricular chambers duringdiastole.

Pulmonary Artery Carries deoxygenated blood from right ventricle to the

pulmonary capillary membrane in the lungs.

Pulmonary Vein Carries oxygenated blood from the lungs to the left atrium.

Pulmonic Valve Valve located between the right ventricle and the pulmonaryartery.

Sinus of Valsalva Located at the base of the aorta on top of the aortic valve.Is the location where the left and right coronary arteries arise.

Sympathetic Part of the autonomic nervous system. Stimulation increasesNervous System heart rate and strength of contraction.

Systole The contractile phase of the cardiac cycle.

Tricuspid Valve The valve located between the right atrium and right ventricle.

Vein Vessel carrying blood to the heart. Carries deoxygenated blood,in exception to the pulmonary veins.

Venule A smaller vein. Part of the circulatory system locatedbetween the capillary and the vein


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CARDIOVASCULAR STRUCTURE AND FUNCTION

The purpose of the heart is to pump oxygenated blood to body tissues. Oxygen iscarried on the hemoglobin of the red blood cell. The blood carries oxygen via the arteries tocapillaries where all body tissues are perfused with oxygen. When tissues are not perfused,

they simply die. The heart has the job of pumping blood to all body tissue.

Anatomy

The heart is a four chambered muscular pump. These chambers are the right atrium,right ventricle, left atrium, and left ventricle. The right side of the heart pumps deoxygenatedblood to the lungs, and the left side of the heart pumps oxygenated blood to the peripheraltissues via the vasculature. Since the left side of the heart has to pump blood to entire body,the muscles of the left side are much thicker than the right. To put it simply, the heart is onehuge plumbing system. The heart, or pump, has to be strong enough to get blood through the

blood vessels (pipes). The pump and the pipes have to be in good working order for the tissuesto receive blood. This blood carries oxygen that provides nutrition to the tissues of the body.There are four valves located within the heart: the tricuspid valve, pulmonic valve, mitral valve,and aortic valve. The tricuspid valve is located on the right side of the heart between the rightatrium and right ventricle- Think “Tri (try) to be Right!” The pulmonic valve lies between theright ventricle and pulmonary artery. The mitral valve is on the left side of the heart between theleft atrium and left ventricle, and the aortic valve lies between the left ventricle and the aorta.


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Systemic Circulat ion

The circulation of the body is a closed system which carries blood to and from bodytissues. There are approximately 5 liters of blood circulating through the body at one time. Thepulmonary circulation takes blood to the lungs, while the central and peripheral circulation takesblood to the rest of the body. The functional units of the circulatory system are arteries,

arterioles, capillaries, venules, and veins. An artery is a vessel that goes away from the heartwhile a vein returns blood to the heart.

arteries: large, highly elastic vessels that transport oxygenated blood, with the exceptionof the pulmonary artery.

arterioles: small and controlled for release of blood into the capillaries.

capillaries: are the exchange point for nutrients, fluids, and other substances to the tissues.

venules: collect deoxygenated blood from the capillaries.

veins: transport deoxygenated blood back to the vena cava, with the exception of thepulmonary veins.

It is best to think of the circulatory system as a closed circuit. The lungs deliver oxygento the blood where the oxygen attaches to the hemoglobin of the red blood cell. As theoxygenated blood travels to the left ventricle, it is then pumped by the heart to the systemiccirculation via arteries, then arterioles. It is at the capillary level of the tissues that perfusion oroxygenation of body tissues occurs. The tissues then release carbon dioxide and return thedeoxygenated blood via venules and veins to the right side of the heart. The right ventricle thenpumps blood to the alveoli of the lungs to pick up more oxygen. Thus this cycle, via thecirculatory system maintains oxygenation of tissues. If the tissues do not get oxygen, they will

die. An analogy to the circulatory system is that the oxygen delivered to the alveoli of the

lungs are like passengers at a bus stop. The oxygen waits for the hemoglobin to give it a ride.There are four receptor sites for oxygen to attach the hemoglobin. The hemoglobin is like aHonda Accord (a four-seater). The passengers (oxygen) jump onto the Accords (hemoglobin).The oxygenated blood is then transported via the arteries (freeways), arterioles (side streets) tothe capillary systems throughout the body (your driveway —you eat at home). When theoxygen is used, the deoxygenated blood (empty Accords with waste products) returns via the


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venules (side streets) and veins (freeways) to the lungs to expel the waste product as carbondioxide. The lungs then pick up more oxygen which is inhaled to continue the cycle.

There are a number of situations that can be applied to this analogy. For example, anembolus is a road block, while hypertension could be a narrowed road. Hemorrhage could be abunch of vehicles driving off a bridge. I’m sure you can come up with more of your own!

In order for the cycle to continue, circulation must continue intact, promoting flow from

the lungs, to the left side of the heart, then the systemic circulation and back to the right side ofthe heart. The circulatory system diagram on the next page depicts the flow of blood throughoutthe body to the various tissues.

Flow of Bloo d Through th e Cardiovascular System

It is best to think of the right and left sides of the heart as separate. Although both sidesof the heart pump together, each ventricle pumps blood to different destinations. The rightventricle pumps blood to the lungs, while the left ventricle pumps to the systemic circulation.

Deoxygenated blood comes from the systemic circulation after oxygen has beendelivered to the tissues. This blood returns via the venous system to the right atrium via theinferior and superior vena cava and the coronary sinus. As the blood enters the right atrium, ittravels through the tricuspid valve to the right ventricle. The valves of the heart are one-wayvalves that allow blood to pass through them. As the right ventricle fills, the pressure of blood inthe right ventricle closes the tricuspid valve. When the right ventricle contracts,


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blood then passes through the pulmonic valve into the pulmonary artery. An artery is anyvessel carrying blood away from the heart. The pulmonary artery is the only artery in the bodythat carries deoxygenated blood. The pulmonary artery branches to pulmonary arterioles, thenbranches to capillaries. They branch to millions of capillaries, where each capillary ‘hugs’ analveolus (air sac). It is at the alveolar-capillary membrane that the exchange of gases takesplace. We have been told many times that we inhale oxygen and exhale carbon dioxide. The

oxygen we inhale at room air is 21% oxygen. Although we do exhale carbon dioxide, includedin this exhaled gas is approximately 16 to 17% oxygen. If you think about it, if we did not exhaleoxygen, CPR would not work.

Once the carbon dioxide and oxygen is exhaled, oxygen is inhaled and an exchange ofgases or diffusion occurs at the millions of alveolar capillary membranes in the lungs. It is atthis location that oxygen attaches to the hemoglobin receptor sites on the red blood cell. Theoxygenated blood is carried by the pulmonary vein to the left atrium. From the left atrium, bloodpasses through the mitral valve into the left ventricle. When the left ventricle fills with blood, themitral valve closes. As the left ventricle contracts, blood flows through the aortic valve, to theaorta.

At the base of the aorta, positioned on top of the aortic valve, is an area called the Sinusof Valsalva. The Sinus of Valsalva provides the opening to the coronary arteries which supplies

the heart muscle itself with blood. The aorta carries blood via the vasculature to the capillarieswhich provide nutrients to the body tissues. At the capillary level, oxygen is delivered to thetissues and carbon dioxide is picked up. The blood then travels through the venous systemback to the right side of the heart.

Coronary Art eries

The coronary arteries supply the heart muscle with blood. This is not the circulation thatflows through the heart, but is the blood supply that feeds the heart muscle. The coronaryarteries arise at the base of the aorta directly above the aortic valve. At the Sinus of Valsalvathe right and left coronary arteries arise. As a result of the structural location of the coronaryarteries on top of the aortic valve, filling occurs during diastole, or the backflow of the coronaryarteries. Systolic contraction of the ventricles is too strong for filling to occur during systole.


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The right coronary artery feeds the right side of the heart while the left coronary arterydivides into the left anterior descending and the circumflex branches. The circumflex branchwraps around the back of the heart. The heart muscle receives oxygen and nutrients viacapillaries. Venous blood from the coronary arteries returns via the coronary veins to thecoronary sinus, located at the base of the right atrium. It is blockage of these coronary arteriesfrom emboli, atherosclerosis or spasm that causes a heart attack or myocardial infarction.

Coronary arteries

The right and left coronary arteries each feed or perfuse different areas of the heart.Blockage of a specific area may predispose the patient to different types of dysrhythmias. Thefollowing table outlines the possible effects of blockage of each of the coronary arteries:

Right Coronary Artery Left Anterior Descending Left Circumflex

Right Atrium

Right Ventricle

Sinoatrial Node

Atrioventricular Bundle

Posterior Portion of the Left

Ventricle

Inferior Wall of the left ventricle

in 9 out of 10 people

Anterior 2/3 of the Septum

Anterior Left Ventricle

Lateral Left Ventricle

Apex

Left Atrium

Posterior Left Ventricle

Inferior Wall of the left ventricle

in one out of ten people

An important concept to understand is that people differ anatomically. As a result, noteveryone’s coronary arteries predictably feed the same portion of the heart.


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Posit ion o f the Heart

The heart is located in the center of the chest, and is tilted toward the left side. Thebase (top) of the heart is directed upward, back and to the right, while the apex (bottom) isdirected down, forward, and to the left. The PMI is the point of maximal impulse. Duringventricular contraction, the apex moves forward striking the left chest wall which can be

palpated as a light tap. The PMI is normally palpated at the left 5th intercostal space, mid-clavicular line. The significance of the PMI is that the normal position of the PMI may changewith certain conditions such as obesity, enlargement of the heart, or myocardial infarction.

Phases of the Cardiac Cycle

The heart also has phases of contraction and relaxation or filling that occur in the atriaand ventricles. The contractile or pumping phase is called systole, while the relaxation or fillingphase is called diastole. During diastole, blood enters the atria and flows passively into therelaxed ventricles. Remember, the valves of the heart are one-way valves allowing the blood toflow passively. When atrial systole occurs and the atria contract, blood is pumped into theventricles allowing for better filling of the ventricles. As the ventricles fill they begin to contract.This pressure causes the tricuspid and mitral valves to close. As the ventricles contract, blood

is pushed out of the pulmonic and aortic valves. Therefore, blood flows into the ventricles in twophases; the passive ventricular filling phase (75 - 80% of blood) and the contraction of the atria(20 - 25% of blood). The contribution of the atrial contraction to ventricular filling is called atrialkick.

PMI is normally palpated at the 5th ICS,

Midclavicular line.


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Hemodyn amic Parameters

Knowledge of hemodynamic parameters in the heart is important to understandingdisease processes, interventions, and drug treatments. Hemodynamics is the movement of theblood and the forces involved. To understand this concept, you need to know about preload,afterload, and cardiac output. These concepts are probably very new to you, yet understanding

them will help you in your care of patients.Preload is what comes to the heart before contraction. Preload is the fluid or filling of the

chamber before contraction. The heart muscle is much like a rubber band. The more youstretch it, the better it will contract. This stretch is accomplished in the heart through filling of thechambers with blood. Therefore, preload is related to the amount of blood in the ventriclebefore contraction. If a person is overhydrated, preload will increase. If a person is dehydrated,preload will decrease.

Afterload is what comes after ventricular contraction or the resistance against which theheart must pump blood. Afterload is determined by two conditions; the blood volume ejectedfrom the ventricle and the compliance of the vascular space into which the blood is ejected.Think of afterload as a hose nozzle. If the hose nozzle is wide open, afterload is decreased dueto increased compliance and decreased resistance. If the hose nozzle is almost closed,

afterload will increase because the water has so much resistance to push against. Now, if youincrease or decrease the amount of water that comes from the nozzle, there will be a furthereffect on the afterload. Think of afterload of the left ventricle as blood pressure. Increasedblood pressure is increased afterload, while decreased blood pressure is decreased afterload.

Each side of the heart has its own preload and afterload. Preload is the filling of eachchamber while afterload is the pressure and volume of blood the chamber has to pump against.Most of the time these measurements are obtained via the use of a pulmonary artery (Swan-Ganz) catheter which is placed in the right side of the heart. The preload of the right side of theheart is reflected as the central venous pressure (CVP) and the afterload of the right side isreflected as the pulmonary vascular resistance (PVR). The preload of the left ventricle is thepulmonary capillary wedge pressure (PCWP) and the afterload is the systemic vascularresistance (SVR).

The body is constantly trying to maintain cardiac output. Cardiac output is affected bythe heart rate and stroke volume. Heart rate is the pulse, or the number of ventricularcontractions per minute. Stroke volume is the amount of blood ejected by the heart with eachbeat. The formula for cardiac output is:

Cardiac Output = Heart Rate X Stroke Volume

The body is always trying to keep in balance with this formula. For example, if someonehad a Myocardial Infarction (heart attack), the stroke volume would decrease because of theweakened heart muscle’s inability to pump out enough blood. To keep in balance, the heartrate would have to increase. On the other hand, the person who is athletic has built up theheart muscle so well that the stroke volume increases. As a result, he/she can manage well,

with a slow heart rate, to meet the cardiac output.


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Review of Hemodynamic Parameters

PARAMETER WHAT IS MEASURED

C.O. – cardiac output How much blood is ejected by the heart each

minute

CVP – central venous pressure The amount of volume returning to the rightside of the heart (Right Ventricular preload)

PCWP – pulmonary capillary wedge pressure The amount of volume returning to the left sideof the heart (Left Ventricular preload)

PVR – pulmonary vascular resistance The resistance the right ventricle has to pumpagainst to eject blood into the pulmonaryartery (Right Ventricular afterload)

SVR – systemic vascular resistance The resistance the left ventricle has to pumpagainst to eject blood into the aorta (LeftVentricular afterload)

Cardiac Muscle

Most of the heart has heart muscle tissue. This muscle tissue is involuntary, meaningwe cannot control its contractions. The heart muscle cells have the ability to lengthen andshorten, much like a rubber band. The heart muscle has interconnecting, overlapping bandsthat can shorten and lengthen The more the heart muscle is stretched, to a certain point, the

better contraction will occur. In other words, like a rubber band, the further you stretch it thebetter is will shoot. With the heart muscle, this stretching is achieved with the filling of theventricle with blood. As a result, the more blood that enters the chamber, the better stretch, andthus better contraction. This concept, called Starling’s Law of the Heart helps explain theimportance of adequate blood volume to create better stretch then contraction.


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Cardiac Muscle Propert ies

The heart muscle has properties which allow for conduction of electrical impulses.These properties of the heart muscle are:

Automaticity: the ability to generate an impulse

Excitability: the ability to respond to stimulation

Conductivity: the ability to transmit impulse

Contractility: the ability to respond with pump action (pulse)

As a result of these properties the heart spontaneously and rhythmically initiatesimpulses that are transmitted through the conduction system to excite the heart muscle andstimulate muscular contraction. Electrical activity precedes contraction. Once the heart hasbeen stimulated, contraction occurs which is validated by a pulse. It is possible to haveelectrical activity occurring without pump action. At times, especially during a cardiac arrestsituation, many drugs are given to the patient to enhance the electrical activity of the heart.These drugs make the heart muscle especially excitable. The electrical activity that occursshows on the ECG. When the heart muscle cannot respond with pump action, the patientessentially has no pulse and CPR must be initiated. This situation is called PEA or pulselesselectrical activity. Remember to always validate what you see on an ECG by assessing yourpatient and checking the pulse.

Conduc tion System of th e Heart

The heart has its own conduction system which is able to function as a result of thecardiac muscle properties listed above. The electrical impulses of the heart usually begin in thesinoatrial node (SA), an area located in the upper part of the right atrium. From the SA node,the impulse travels via interatrial tracts to the left atrium and through internodal tracts to theatrioventricular node (AV). At this point, the impulse pauses to allow time for the ventricles to fillwith blood. The impulse then travels to the Bundle of His, then to the right and left bundlebranches. From the bundle branches, the impulse goes to the Purkinje fibers which line theinside of the ventricular musculature. After the Purkinje fibers are innervated, contractionshould occur. As a result, electrical conduction of the heart precedes contraction.


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To review, the conduction system of the heart proceeds in the following order:

Sinoatrial (SA) node

Internodal and Interatrial tracts

Atrioventricular (AV) node

Bundle of His

Right & Left bundle branches

Purkinje fibers

Ventricular muscleUnder normal circumstances, the SA node is the pacemaker. The reason the SA node

is usually the pacemaker is because it has a leakier cell membrane that allows cells todepolarize spontaneously without waiting for an outside source. Sinus node cell membranesare more leaky to sodium ions, therefore activate more rapidly to pace the heart. The rule ofthum b is th at the part of the heart that beats the fastest wil l be the pacemaker of th e

heart. For example, if the ventricles beat faster than the SA node, the ventricles will becomethe pacemaker of the heart, as happens in ventricular tachycardia. Other areas of the heart,besides the SA node have the property of automaticity and can be the pacemaker of the heart.The SA node is usually the pacemaker of the heart because it beats the fastest. The part of theheart that beats the fastest will be the pacemaker for the time being. Each area of the heart hasinherent rates for initiating impulses:

Inherent Rates

Sinus Node (pacemaker): 60 to 100 times/minute AV Junctional Tissue (1° backup pacemaker): 40 to 60 times/minuteHis Purkinje System in Ventricles (2° backup pacemaker): 20 to 40 times/minute

Internodal Tracts

InteratrialTracts


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The pacemaker sites other than the SA node are backup systems for the heart. If theSA node were to fail for some reason, the AV nodal area could take over as the pacemaker. Ifthe AV nodal area were to fail, the ventricles could pace the heart at 20 to 40 times per minute. These areas can be enhanced or suppressed by the Autonomic Nervous System whichinnervates the heart.

Autonom ic Nervous System

The rate of impulse formation is determined by the autonomic nervous system, whichbranches into the sympathetic and parasympathetic nervous systems. The sympathetic branchspeeds the rate of impulses, while the parasympathetic branch slows the rate of impulseformation. The heart actually functions best as a balance of these two systems. Whensympathetic innervation to the heart is excessive, the heart rate increases. Whenparasympathetic innervation to the heart is excessive, the heart rate decreases. There areexamples of this occurring in our own body. When we are frightened, we release epinephrine, asympathetic substance which results in an increased heart rate. The parasympathetic nervoussystem is associated with the vagus nerve. The vagus nerve can be stimulated by the Valsalva

Maneuver, which may be caused by excessive straining as in a bowel movement. This resultsin the release of acetylcholine, which slows the heart.

SYMPATHETIC NERVES PARASYMPATHETIC NERVES (Vagu s)

Supply both atria and ventricles

Stimulation causes release of the hormoneNorepinephrine which causes:

Increased rate of SA node discharge

Increased excitability

**Enhances Automaticity

TOTAL EFFECT – increased overall activity ofthe heart

Supplies mainly the SA and AV nodes withlittle effect on the atrial muscle and no effecton ventricular muscle

Stimulation causes release of the hormoneacetylcholine which causes:

Slowing of SA node

Slows rate of conduction through the AV node

**Suppresses Automaticity

TOTAL EFFECT – decreased overall activityof the heart


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REVIEW OF AUTONOMIC NERVOUS SYSTEM

Excitabi l i ty and Conduc tiv i ty

All areas of the heart have the ability to respond to and transmit electrical impulses.They respond to and transmit electrical impulses by the process of DEPOLARIZATION. At rest

cardiac cells are negatively charged on the inside and are POLARIZED. Once depolarized thecell returns to its normal electrical state through a process called REPOLARIZATION.

a. The cell is POLARIZED when it is in a resting state. Potassium is in the inside andsodium is on the outside.

Electroloytes are positively charged but cell wall is negatively charged.

b. A stimulus to the cell, such as the electrical current from the SA node changes thepermeability of the cell membrane. The cell membrane becomes leaky andDEPOLARIZATION occurs. The leaky cell membrane allows sodium, potassium andcalcium to cross the cell membrane. Depolarization is the stimulation of the cell.

c. The cells have to get back to their initial resting state to prepare for another electricalimpulse. The cells get back to their original states passively through a processcalled REPOLARIZATION ; a relaxation of the cells.

This process of going from a polarized state to a depolarized state and thenrepolarization happens from cell to cell in rapid succession. This is called CONDUCTION .

Na + Ca ++


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Actio n Potentia l

The action potential is the process of depolarization and repolarization of a singlemyocardial cell. The action potential has various phases that indicate the stages ofdepolarization and repolarization. These phases correlated to the electrocardiogram (ECG)waveform and cycle.

ACTION POTENTIAL OF A SINGLE MYOCARDIAL CELL

If you were to look at the horizontal portion of the action potential as a time line, youwould see that depolarization (0) occurs very rapidly, while repolarization (1, 2,&3) takes a verylong time.

Phases of the Actio n Potentia l

0 = rapid depolarization of the cell

1 = initial stage of repolarization

2 = slowing down of repolarization to allow the cardiac muscle a more sustained contraction

3 = sudden acceleration of rate of repolarization. Inside of the cell becomes negative again

4 = resting membrane potential, or polarized state

Refractory Periods

During repolarization, the individual cardiac cells regain normal excitability, and duringthis process go through varying periods of excitability known as refractory periods. Therefractory periods represent times when the cells are partially or completely resistant to anystimuli, or when another beat could occur. Later in the book, this concept will be presented inmore depth.


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Review of Structu re and Function

Basically, the heart is a muscular pump. The left side of the heart is thicker than theright side since it has to pump to a large area of peripheral tissues via the vasculature. Theright side of the heart pumps blood only to the lungs, where carbon dioxide and oxygen isexhaled. Through the lungs oxygen is inhaled and attaches to the hemoglobin of the red bloodcell. The left side of the heart then pumps oxygenated blood to the capillaries of the body. Thecoronary arteries arise from the Sinus of Valsalva off of the aorta and supply the heart musclewith oxygenated blood. Blockage of these arteries is the cause of a myocardial infarction. Thecardiac muscle has specific properties of automaticity, excitability, conductivity, and contractilitythat allows for the integration of electrical activity then contraction of the heart muscle. Theheart, with this electrical activity has its own conduction system. The impulse begins at the SAnode, through interatrial and internodal tracts to the AV node, Bundle of His, bundle branches,then to the Purkinje’s fibers in the ventricles. Once the Purkinje fibers are innervated,ventricular contraction occurs. The autonomic nervous system divides into the sympathetic andparasympathetic branches. The sympathetic speeds the heart rate while the parasympatheticbranch slows the heart rate. The cardiac cycle is divided into systole, the contraction phase,and diastole, the filling phase.

Hemodynamic parameters of preload, afterload, and cardiac output are important tounderstand. Preload is what comes before ventricular contraction and is directly related to fluidvolume. Afterload is what comes after ventricular contraction and is related to the vascularresistance and the volume of blood to be ejected from the ventricle. Afterload of the rightventricle is reflected as pulmonary vascular resistance, or pulmonary artery pressure, whileafterload of the left ventricle is reflected as systemic vascular resistance or as blood pressure.Lastly, the formula for cardiac output is heart rate x stroke volume. Our body strives to keep thecardiac output in balance either by changing the heart rate or adjusting the stroke volume.

The systemic circulation includes the blood vessels of the body. The arteries and

arterioles transport oxygenated blood to the capillaries. The venules and veins then transportthe deoxygenated blood back to the right side of the heart. It is at the capillary level that theexchange of oxygen and nutrients occur.


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Important Terms

Antegrade conduction Conduction that occurs in a downward mannerfrom atria to ventricles.

Automaticity Quality of the conduction system thatautomatically initiates a stimulus.

Block Impulse is prevented from continuing onthe conduction pathway.

Re-entry When an impulse re-enters the conductionsystem in a retrograde manner ratherthan terminating.

Retrograde conduction Conduction that returns backwards throughthe conduction system.

Usurpation When a lower pacemaker takes over.

Vagal stimulation Stimulation of the parasympathetic nervoussystem resulting in a decrease in heart rate.

Normally, the heart is paced by the spontaneous activity of the sinus node at a regularrate consistent with the physiological demands of the body. The automatic impulses generatedin the sinus node normally dominate all the fibers of the heart. When this rhythm is disturbed orits conduction is interfered with, the term arrhythmia or dysrhythmia is used. The termarrhythmia actually means “without rhythm” while the term dysrhythmia means “difficult ordisturbed rhythm”. These terms are generally used interchangeably, although dysrhythmia isthe more accurate term.

SA Node

60-100 bpm

AV Junction

40-60 bpm

Purkinje system20-40 bpm


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Normal Mechanism of Rhythm Formation

The area of th e heart that b eats the fastest will p ace the heart. 1. The sinus node is the pacemaker of the heart because its cell membrane leaks Na+ ions

more readily and therefore, the sinus node is the first to reach an action potential and

depolarize the rest of the heart.

2. Other areas of the conduction system such as the AV node or the ventricles are merelypotential pacemakers that become active solely in the case of emergency.

3. The sinus node may DEFAULT as pacemaker due to DECREASED AUTOMATICITY.This sinus slowing allows the escape of lower pacemaker centers which are now firingfaster than the SA node.

a. Junctional rhythms - escape rhythms from the junction or AV nodal areab. Idioventricular - escape rhythms from the ventricles

Even though these rhythms are abnormal, the escape mechanism that takes over isnormal, thus placed under normal mechanisms of rhythm formation.

4. Causes of decreased automaticity and depression of cardiac cells leading to bradycardiaand possible escape rhythms are:

a. Vagal stimulation c. Electrolyte imbalance as hyperkalemia & hypercalcemiab. Hypothermia d. Drugs such as digoxin and Inderal

Abnorm al Rhythm Format ion 1. The sinus node may lose its job as the pacemaker due to INCREASED AUTOMATICITY

of other myocardial cells that now beat faster than the sinus node. Both escape beats and

premature beats are considered ECTOPIC BEATS.

2. The sinus node pacemaker loses its function because the other area of the heart beatfaster, shutting off the sinus node mechanism. This is called USURPATION of thepacemaker function. This is not because the SA node failed; another pacemaker firedfaster.

3. May be seen as PREMATURE BEATS or tachycardia from the atria, junction, or ventricles.

4. Causes of increased automaticity leading to premature beats or tachycardia rhythms:a. sympathetic stimulationb. hyperthermiac. electrolyte imbalance such as hypokalemia and hypocalcemia

d. hypoxia and hypercapniae. cardiac dilatationf. ischemia and injuryg. drugs - toxinsh. stimulants as caffeine, alcohol, or tobaccoi. metabolic diseases (hyperthyroidism)

j. mechanical stimulation (Swan-Ganz & pacemaker placement)k. acquired damage (trauma)l. diseases of the heart itself such as valve disease, hypertrophy, and aneurysms


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m. congenital abnormalitiesNormal Imp ulse Conduc tion

The conduction system is one continuous electrical system. Impulses will travel in eitherdirection depending upon where the stimulation occurs. If the impulse starts at the SA node,impulses will travel downward or antegrade. However, if the impulse starts at the AV node theimpulse will travel down to the ventricle and back or retrograde up to the atria.

1. Antegrade Conduction - normal impulses proceed downward from the sinus node to thePurkinje system.

2. Retrograde Conduction - reverse conduction is possible from the Purkinje system to theatria. Premature ventricular contractions (PVCs) may conduct through the system in aretrograde manner and activate the atria. In this situation, the P wave may appearinverted or may be seen following the QRS.

Abnorm al Impulse Conduct ion 1. Conduction disturbances and dysrhythmias occur if there is a delay or block somewhere

in the conduction system.

a. A block in the sinus node would not allow the impulse to progress to the atria(no P wave, no QRS, no T wave).

b. With a block in the AV node, the impulse may have trouble getting from the atria tothe ventricles (1st, 2nd, 3rd degree block).

c. A block in the bundle branches causes abnormal ventricular conduction (a wide,bizarre QRS).

2. Conduction disturbance in a small area can develop into a unidirectional block and maycause re-entry dysrhythmias. Re-entry occurs when an impulse is able to re-enter an

area that was just recently depolarized and repolarized. Conduction occurs in a circuit.Re-entry phenomena usually allow for faster depolarization and is the cause of manytachycardias.

CONDUCTION AND DEFECTS

A - impulse travels down the Purkinje fiber and terminates at the ventricular muscle.

B- impulse travels down the Purkinje fiber but is blocked before reaching the ventricularmuscle

C - impulse travels down the Purkinje fiber, reaches the ventricular muscle, but does notterminate there. The impulse re-enters the conduction system, permitting re-excitationof the ventricular muscle.


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Important Terms- Electrocardiography, Monitorin g, and ECG

12-lead ECG Views the heart from 12 angles to help in determining infarction,hypertrophy, axis deviation, and bundle branch blocks.

Acute MI Blockage of the coronary artery from atherosclerosis, spasm,

or embolus results in death of heart muscle.

Artifact Extra events recorded on the ECG that do not relate to actualelectrical activity of the heart.

Depolarization The electrical stimulation of cells.

Isoelectric line The flat horizontal line on the ECG that represents noelectrical activity (the base line).

J point The location at the end of the QRS complex which indicates thechange from the QRS complex to the ST segment.

Large box method A method for determining heart rate on regular rhythms. Thenumber of large boxes between two QRS complexes is dividedinto 300 to obtain the minute heart rate.

P wave Wave representing atrial depolariztion.PR interval Time interval from the beginning of the P wave to the

beginning of the QRS complex. Represents atrial firing to thebeginning of ventricular depolarization. Normal range is 0.12 -0.20 seconds.

Q-T interval Interval from the beginning of the QRS to the end of the T wave.

QRS duration Interval from the beginning of the QRS to the end of the QRSwave. Normal range is below 0.12 seconds.

Refractory Periods Various periods in the ECG complex where the heart can orcannot accept a new impulse.

Repolarization The passive recovery phase of the ECG which occurs afterdepolarization.

S-T segment Interval from end of the QRS complex to the beginning of the Twave.

Six-second method A method for determining heart rate with regular or irregularrhythms. The number of QRS complexes in 6 seconds ismultiplied by 10 to calculate minute heart rate.

Small box method A method for calculating heart rate for regular rhythms. Thenumber of small boxes between two QRS complexes is dividedinto 1500 to obtain minute heart rate.


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Somatic tremor Electrical artifact that results from muscle shaking; seizures.

T wave Repolarization of the ventricle.

Time Measured on the horizontal plane of the ECG.

U wave At times is seen after the T wave. May be indicative ofIschemia, hypokalemia, or incomplete repolarization.

Voltage Measured on the vertical plane of the ECG.

Vulnerable period The area from the peak of the T wave back to the baseline. Earlybeats hitting on this area may result in Ventricular Tachycardia orVentricular Fibrillation.

ELECTROCARDIOGRAPHY, MONITORING AND ECG

The electrocardiogram or ECG (EKG) represents electrical activity of the heart. Thisbook provides methods to learn to read the ECG. ECG or EKG may be used interchangeably,since they both represent the electrocardiogram.

The electrocardiogram only measures electrical activity of the heart. The ECG does notverify contraction of the heart. This can be determined only by pulse or blood pressure.

The wave of depolarization and repolarization spreading through the heart can berecorded on paper through the use of the ECG. The ECG waveform has specific names thatcorrelate with various activities occurring in the heart.

Definit ion of comp onents of the ECG configurat ion

Isoelectric line - baseline that indicates no electrical activity is occurring

P wave - represents depolarization of the atria or the spread of electrical activity

through the atria. The P wave is normally upright in Lead II. If the P wave is of normalsize and shape, it may be assumed that the stimulus began in the SA node.

PR Interval - the period from the start of the P wave to the beginning of the QRScomplex. It is the time taken for the original impulse to reach the ventricles,including the delay at the AV node.

J- oint


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Normal = 0.12 - 0.20 seconds. A prolonged PR interval indicates a longer than normal delay inthe impulse getting through the AV node.

QRS Complex - represents depolarization of the ventricles.

Q wave - first negative wave (in front of a positive wave) Q waves that are at

least 1/4 the depth of the R wave are abnormal and may be indicativeof a myocardial infarction.

R wave - positive wave (above the isoelectric line)

S wave - negative wave after a positive wave

**Note: Not al l ECG complexes wil l have all of the components of the QRS.Some may on ly have an R, or an R and an S.

Others may only have a QS wave.

QRS Duration - measured from the beginning of the QRS to the end of the QRS.

Normal Range = < 0.12 seconds. A prolonged QRS duration may indicate a blockin the bundle branches.

Q-T Interval - includes the QRS complex and T wave. Normal ranges will vary withage and heart rate.

Normal = 0.36 - 0.44 seconds

T wave - represents repolarization or recovery of the ventricles. The T wave is normallyupright in lead II. Inversion of the T wave may indicate ischemia occurring inthe heart. Flat T waves may be an indication of potassium deficiency, while

tall, peaked T waves may indicate hyperkalemia or early ischemia.

S-T segment - the interval between the completion of depolarization & repolarizationof the ventricular muscle. The S-T segment seen from the end of the QRS tothe beginning of the T wave. Elevation of the S-T segment may indicate aninjury pattern occurring in the heart.

U wave - comes after the T wave. May be seen as normal, or may be indicative ofpotassium deficiency or ischemia or incomplete repolarization of the ventricles.

J point - the point on the QRS complex where a distinct change is seen in direction, fromthe QRS to the ST segment. It is important to identify the J point to determine

accurate measurement of the QRS duration and as a reference to calculate STelevation or depression .


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Configur at ions of the QRS Complex

Not all components of the QRS complex are present on each person’s ECG. In fact, alarge Q wave is abnormal and may indicate that an MI has occurred in the past. Below aresome examples of variations of the QRS complex. Even though parts of the QRS may not bepresent, it is still referred to as the QRS complex.

The prime (‘) indicates a second wave of the same. The second R wave is termedprime. The capital letter or lower case letter of the Rr’ indicates which peak is the tallest. If thefirst R is taller, it gets the capital. If the second R is taller, it gets the capital letter.

As you can see, the QRS complex can have many different shapes. It is important tounderstand this so that you can correctly measure intervals such as the PRI and the QRSduration.


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The ECG paper that comes out of the cardiac monitor is a graph paper that comes out at aspeed of 25 mm/Sec. Some machines can have a paper speed of 50 mm/Sec. or othervariations, but the standard is 25 mm/Sec.

Rule #1: Horizontal measurement on the paper = TIME

1 small box = 0.04 seconds1500 small boxes = 60 seconds or 1 minute

1 large box = 0.20 seconds5 large boxes = 1 second

300 large boxes = 60 seconds or 1 minute

1 inch on the ECG paper = 1 second of time6 inches on the ECG paper = 6 seconds

The ECG paper will usually have some sort of marking on the paper to indicate a 1

second, 3 second or 6 second period of time. This paper has markings in 1 second intervals onthe top of the page.

Rule #2: Vertical measurement on the paper = VOLTAGE

1 small box = 1 mm (millimeter) or .1 mV (millivolt)1 large box = 5 mm .5 mV

10 small boxes = 10 mm 1 mV

LEAD SYSTEMS Leads are a method of recording electrical activity within the heart. It takes two wires,

one positive (+) and one negative (-) to make a lead. The leads view the heart from differentangles. There are 12 established leads, each viewing the heart from a different angle. Theelectrical field extends to the body surface where it is measured by electrodes and thenwaveforms on paper. Electrodes are patches that the wires attach to and measure the voltagedifference between two electrodes. There are 4 principles of electrocardiography that youmust know to understand lead systems:


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1. No electrical current flowing yields no voltagedifference shown as an ISOELECTRIC LINE

2. Current flowing towards a (+) electrode willrecord a positive or upright wave.

3. Current flowing away from a (+) electrode, or toa (-) electrode records a negative or downwardwave.

4. Current flowing perpendicular to the lead’s axis will record a biphasic wave.

Remember, the leads only view the heart from different angles. The electrical forces ofthe heart progress from the SA node down to the ventricles. That is saying that the electricalforces go down and to the left of the heart. This is called the mean cardiac vector . Any leadwith its positive electrode down at the left or at the foot area should record an upright P waveand QRS complex. This is because the electrical current (of the heart) is flowing toward apositive electrode.

WHEN PLACING THE LEADS, THINK “WHITE ON THE RIGHT, SMOKE OVE R FIRE!”

LEAD II

The most common monitoring lead is lead II since it produces an upright P wave andQRS that are easy to see.


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SUMMARY OF ECG CHANGES THAT OCCUR WITH ACUTE MI

THE THREE I’S The “road” to an MI (myocardial infarction) includes 3 predictable changes on the ECG. These changes will show only on the leads that view the part of the heartwhere the injury occurs.

I. Ischemia = ST depression and/or T wave inversionII. Injury = ST elevationIII. Infarct = Q waves

NORMAL EKG COMPLEX

ISCHEMIA (inverted T waves) - The first change to occur.

INJURY (elevated ST segments) - The second change to occur.


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INFARCTION (development of Q waves) - The last and permanent change.

As mentioned before, Q waves are abnormal if they are ¼ (25%) the depth of the Rwaves height and at least 0.04 seconds wide. During the acute phase of a myocardialinfarction, T waves will initially invert, then ST segments will elevate. Q waves may not show upfor over a day. Eventually, the ST segments will return to normal, T waves will return to an

upright position, but the Q waves will remain forever as the wave of depolariztion passesthrough dead or infarcted tissue. The location of an MI is determined by analyzing the 12 leadEKG. Changes will be seen in the leads that correlate with the infarction in that area, and mustbe visualized in 2 or more leads of the same group to be considered significant.

ARTIFACT

Artifact is extraneous electrical activity that shows up on the EKG that is not occurringwith the patient’s heart. Artifact can sometimes be confused with a number of

dysrhythmias and must be differentiated by physical assessment of the patient. Goodelectrode contact is essential to obtaining a picture without artifact.

Suggestions for good electrode placement:

1. Place on a stable part of the body. For example, do not place electrode onthe clavicle where there may be a lot of movement with respirations. Or donot place under pendulous breasts, where each time the person breathes ittaps against the electrode

2. Place on a smooth part of the skin. You may need to shave the area wherethe electrode is attached.

3. Assure that the electrode has adequate amounts of conductive gel on theinside. If the gel is dried out, a poor reading may occur.

4. Make sure the wires are in good working order for continuous monitoring.

5. Electrodes need to be affixed firmly to the skin. If the patient is perspiring,you may need to change the electrodes often. Tincture of Benzoine on theskin may help the leads stay on.

Q-Wave


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Types of artifact that can occur are:

60 cycle interference - interference from electrical equipment and may be caused fromimproper grounding of equipment. A magnifying glass will show exactly sixty even, regular,spikes in a 1 - second interval on the ECG tracing. Check all the equipment to see what may be

causing the interference and have the equipment replaced or repaired. Prehospital causes maybe electric blankets or heating pads,

60 cycle interference shows as thick lines of up and down spikes.

Wandering Baseline - the baseline of the EKG will wander with the person’s respirations.Changing the electrode to a different position may help. This artifact is sometimes unavoidable.


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Somatic or Muscle Tremor - can occur with chilling, seizures or tension. This will show as agrossly uneven, tremulous baseline. Artifact will continue until the condition stops.

CPR Artifact - when CPR is done, compressions show up on the ECG tracing.


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Calculatin g Heart Rates

Each time an ECG strip is analyzed, the heart rate must be calculated. Since we don’talways have a full minute strip, we need to determine ways to calculate the heart rate with asmaller strip. Before determining the method for calculating heart rate, it is important to know ifthe heart rhythm is regular or irregular. A regular heart rhythm is one that has an equal

distance from one QRS complex to the next QRS complex. An irregular rhythm would not havethe same distance from one QRS complex to the next.

R R R R R R These R’s are regular r r r r r r r r These r’s are irregular

One method that can aid in determining regularity is to take a blank piece of paper andmark a line for 3 QRS complexes in a row on the blank sheet of paper. Then take the 3 lines ofthe paper and move them to the next set of QRS complexes. Another method is to use acaliper to march out the regularity of a strip. If the lines match up or “march out” with the newQRS’s, the rhythm is regular. If they do not match, the rhythm is irregular. If less than threesmall boxes difference between the narrowest and widest R-R interval on 6 second strip, thanthe strip is regular. Look at the rhythm strips below and determine if they are regular or irregular:

Strip A

Strip B


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You should have said that Strip A was regular and Strip B was irregular, since the QRS complexes in Awere equal distance apart and the QRS complexes in B were not equal.

Methods f or Calculat ing Heart Rate

A. Six Second Method - approxim ate

1. Take six seconds on the ECG paper2. Count the number of QRS complexes in the six seconds3. Multiply this number by 10 to give the minute heart rate4. Accuracy

a. Safe to use with irregular rhythmsb. May also be used with regular rhythms

B. Large Box Method

1. One large box on the ECG paper equals 0.20 seconds, so there are 300

large boxes in a minute or 60 seconds2. Count the number of large boxes between 2 QRS complexes.3. Divide this number into 300

For Example:a. if there are 3 large boxes between two QRS complexes,

divide 3 into 300 = rate of 100 per minuteb. if there are 5 large boxes between two QRS complexes,

divide 5 into 300 = rate of 60 per minute4. Accurate for regular rhythms only

C. Small Box Method

1. One tiny box on the ECG paper equals 0.04 seconds, so there are 1500small boxes in 60 seconds

2. Count the number of small boxes between two QRS complexes3. Divide this number into 1500

For Example:a. if there are 15 small boxes between two QRS complexes

then divide 15 into 1500 for a rate of 100b. if there are 25 small boxes between two QRS complexes

then divide 25 into 1500 for a rate of 604. Accurate for regular rhythms only

he most accurate method for regular rhythms other than taking a full minute strip


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Table for Large Box Method

To calculate the heart rate, count the number of 0.20 squares (or large boxes)between two QRS complexes (300 divided by X = HR)

1 box = 300 3 boxes = 100 5 boxes = 60

2 boxes = 150 4 boxes = 75 6 boxes = 507 boxes = 43

Table for Small Box Method

To calculate the heart rate, count the number of 0.04 squares (or small boxes)between two QRS complexes (1500 divided by X = HR)

Number of Squares = Heart Rate of X

4----------------375 20---------------75 36---------------425----------------300 21---------------72 37---------------416----------------250 22---------------68 38---------------407----------------214 23---------------65 39---------------388----------------188 24---------------63 40---------------379----------------168 25---------------60 41---------------3710---------------150 26---------------58 43---------------3511---------------136 27---------------56 44---------------3412---------------125 28---------------54 45---------------3313---------------115 29---------------52 46---------------3314---------------107 30---------------50 47---------------3215---------------100 31---------------48 48---------------31

16----------------94 32---------------47 49---------------3117----------------88 33---------------45 50---------------3018----------------83 34---------------4419----------------79 35---------------43

You really only need to know 1 or 2 methods for calculating heart rate. The importantfactor is to know that in the absence of a full minute strip to count heart rate, you may use anyof these methods for regular rhythms. For irregular rhythms, the six-second method is the onlymethod that can be used.

MEASURING THE PRI (PR Int erval)

The P wave represents atrial depolarization. The PR interval is measured from the beginningof the P wave to the beginning of the QRS. Normal PRI is 0.12- 0.20 seconds. A prolongedPRI indicates that the impulse is delayed as it passes through the atria or AV Node.


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MEASURING THE QRS DURATION

The QRS represents ventricular depolarization and is measured from the beginning of the QRSto the end of the QRS. Normal QRS duration is < 0.12 seconds. A wide QRS that follows a Pwave indicates that the impulse was delayed as it traveled down the bundle braches.

MEASURING THE QTI (QT Int erval)

The QT interval represents total ventricular activity (the time from ventricular depolarization toventricular repolarization) and is measured from the beginning of the QRS to the end of the Twave. The duration of the QT interval varies according to age, gender, and heart rate. Toquickly determine if the QTI is normal or prolonged, measure the interval between twoconsecutive R waves and divide by two. Measure the QT interval. If the QT interval is lessthan half of the R-R interval, it is probably normal. If the QT interval is more than half of theR-R interval, it is considered prolonged. A prolonged QT interval puts the patient at risk fordeveloping life threatening dysrhythmias because this prolongs the vulnerable period during theventricular refractory period.


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Refractory Periods

During repolarization, the individual cardiac cells regain normal excitability, and duringthis process go through varying periods of excitability known as refractory periods. There aretimes in these periods when the cells are partially or completely resistant to any stimuli, whenanother beat could not occur.

1. Absolute Refractory Period - Cardiac cells are unable to respond to any stimulusregardless of strength.

This area extends from the Beginning of the QRS to the initial part of the T wave.

2. Relative Refractory Period - A strong stimulus can cause an impulse.

This area is on the T wave.

3. Vulnerable Period - A stimulus hitting at this time is sensitive and vulnerable to

electrical chaos such as ventricular tachycardia or ventricular fibrillation.

This area is located at the peak of the T wave and back to the baseline.

4. Supernormal Period - A weak stimulus can initiate the heart.

This occurs after the T wave.

ARP (absolute refractory period)

RRP (relative refractory p eriod )

V (vul nerable period)

SN (supernormal period)


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SYSTEMATIC APPROACH FOR ANA LYZING CARDIAC RHYTHMS

When analyzing an individual ECG, it is essential that the analysis be done in a standard, sequentialmanner. Failure to analyze the strip systematically can result in missing important details and drawingincorrect conclusions.

Each and every time you analyze a str ip, fol low t his step-by -step approach.

1. Determine the regulari ty of th e QRS complexes (rhythm). This allows you to determine themethod for obtaining rate.

REGULAR? - use any methodIRREGULAR? - use the six second method or obtain a full minute strip

2. Calculate the heart rate .a. Determine the atrial rate (P) b. Determine the ventricular rate (QRS)

3. Examine the P waves.a. First, determine if P waves are present.

b. Examine the contour.1. P waves should be upright in leads II.2. Each P wave should be similar shape.

c. Observe the position of the P waves in respect to the QRS’s. Normally each P waveshould be followed by a QRS, and each QRS should be preceded by a P wave.

4. Measure the QT Interval .

5. Measure the PR Inter val .

6. Measure the QRS Duration.

7. Measure the ST Segment.

8. Identify the T-Wave. a. Upright?b. Inverted?c. Flat?d. Peaked?e. Biphasic?

9. Search for any ectopic beats. Are the premature or escape beats?

10. Determine the or ig in of the rhythm : a. Sinus?b. Atrial?c. Junctional?d. Ventricular?e. Pacemaker (artificial)?

**Fol low this procedure for analyzing al l rhythm s.


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Sinus Rhythms

IMPORTANT TERMS- SINUS RHYTHMS

Arrhythmia “Without rhythm”; A rhythm that is disturbed.

Aberrant Conduction Conduction that takes a different pathway through the Atria orventricles. Usually results in a wider QRS complex.

Asymptomatic Patient is free of symptoms even though an abnormal rhythm ispresent.

Bradycardia In general, a heart rate below 60.

Dysrhythmia A rhythm that is disturbed.

Etiology The cause of a problem.

Symptomatic When the patient has symptoms such as hypotension,dizziness, or chest pain.

Tachycardia In general, a heart rate above 100 in the adult patient.

Sinus rhythms originate in the sinoatrial (SA) node. Normal Sinus rhythm is the mostdesired rhythm and will comprise most of the rhythm strips that you will see in the clinicalsetting. There are other rhythms that originate in the sinus node and differ in rate or rhythm.They will be discussed in this section.


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NORMAL SINUS RHYTHM

A. EtiologySince sinus rhythm is normal, there is no etiology.

B. Identifying Characteristics

1. Rhythm - Regular

2. Rate - 60 to 100/min

3. P Waves - Normal in size and shape. Upright and before each QRS

4. P-R Interval - Normal (0.12 to 0.20 seconds)

5. QRS Duration - Normal (< 0.12 seconds) unless there is a right or leftbundle branch block or aberrant conduction

C. Significance -1. There are no signs and symptoms since it is a normal rhythm.

2. In children the rate may vary from 90 in a 3-year old to 150 in an infant.

D. Treatment - None


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SINUS BRADYCARDIA

A. Etiology1. Damage to the SA node2. Normal in athletes and sleep3. Physiologic response to increased vagal tone from the Valsalva maneuver,

coughing, suctioning or carotid massage.4. Pathologic response to increased intracranial pressure, glaucoma, hypothermia,

hypothyroidism, or M.I.5. Drug response to Digoxin, Inderal or Morphine Sulfate

B. Identifying Characteristics1. Rhythm - Regular2. Rate - < 60 (40 – 59 is the most common)3. P Waves - Normal in size and shape4. P-R Interval - Normal (0.12 to 0.20 seconds)5. QRS Duration - Normal (< 0.12 seconds)

C. Significance1. Potential dangers are that slow rate may lead to blocks or escape rhythms2. May allow for an irritable focus to take over3. May cause a decrease in cardiac output and decreased level of consciousness4. May develop congestive heart failure post-M.I.

D. Treatment

1. If asymptomatic - none2. If symptomatic- Bradycardia Algorithm (AHA)IV/ O2/ 12-lead ECG/ Differential Diagnosis (treat cause)a. Atropine 0.5 mg IV q 3-5 min, max 3 mgb. Pacing (Transcutaneous, Transvenous)c. Dopamine 2 - 20 mcg/kg per mind. Epinephrine Drip at 2 - 10 mcg/min


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SINUS TACHYCARDIA

A. Etiology1. Physiologic response to exercise, excitement, and anxiety.2. Stimulants such as coffee, tea, alcohol, and nicotine.3. Response to sympathomimetic medications such as Epinephrine (Adrenalin)

4. Pathologic response to fever, shock, CHF, MI, chronic lung disease, hypotension,thyrotoxicosis, anemia, pain or hypoxemia.

B. Identifying Characteristics1. Rhythm - Regular2. Rate - 100 - 150 / min3. P Waves - normal in size and shape4. P-R Interval - Normal (0.12 to 0.20 seconds)5. QRS Duration - Normal (< 0.12 seconds)

C. Significance1. In the presence of an MI (myocardial infarction) may lead to ischemia and or CHF.2. May cause a decreased filling time in the ventricles. If the diastolic filling time is

short (i.e. tachycardia), the ventricles don’t have time to fill with blood. Decreased fil l in g = decreased stretch = decr eased C.O.

3. Impaired filling of the coronary arteries with oxygenated blood. The coronaryarteries arise from the Sinus of Valsalva on top of the aortic valve. They fillduring diastole. Tachycardias may prevent complete filling of the coronary arterieswhich may lead to myocardial ischemia.

D. TreatmentTreat the underlying cause of the tachycardia, not the rhythm itself. For example,

if the person has a fever, decrease the fever. If the person is hypoxemic, treat theHypoxemia.


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SINUS ARRHYTHMIA

A. Etiology1. Common in children2. Considered benign3. Can be from drugs which influence vagal tone such as digoxin and morphine

4. Rate varies with respirations from vagal influences:a. Rate increases with inspiration (decreased vagal tone)b. Rate decreases with exhalation (increased vagal tone)

B. Identifying Characteristics1. Rhythm - Irregular . This rhythm is cyclically irregular, speeding and slowing with each

Respiratory cycle.

2. Rate - usually normal at 60 - 100/min3. P Wave - normal in size and shape4. P-R Interval - Normal (0.12 to 0.20 seconds)5. QRS - Normal (< 0.12 seconds)

C. Significance1. Usually not symptomatic

2. Pulse will be irregular so the rhythm is sometimes confused with other dysrhythmias

D. Treatment – None, unless the overall rate is too slow or too fast then treat as bradycardia ortachycardia.


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SINUS ARREST and SINUS BLOCK

A. Etiology1. Failure of the SA node to fire resulting in the absence of an entire PQRST

sequence for one or more cardiac cycles. The SA node “takes a rest”. 2. Pathologic causes are MI, hypersensitive carotid sinus, overdose of digoxin or

quinidine, and hyperkalemia.3. Physiologic response to increased vagal tone.

B. Identifying Characteristics1. Rhythm - Irregular 2. Rate - Usually Slow3. The entire PQRST sequence is absent for one or more cardiac cycles.4. To calculate the length of the pause that occurs, measure the number of small

boxes from the R wave before the pause to the next R wave. Multiply the numberof small boxes by 0.04 seconds to calculate how many seconds long the pause is.

Sinus Arrest Since the SA node fails to initiate an impulse for a time, the node has to reset itself.

a. the rhythm before and after the pause is sinus rhythm.b. the next beat that comes in has a P wavec. P- P interval is disturbed . The next P wave after the pause returns off cycle.

P P P P P P P

SA node fails tofire


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Sinus Block The impulse originates in the SA node but is blocked within the sinus node.The SA node continues to fire regularly, even though some are blocked.

a. the rhythm before and after the pause is sinus rhythm.b. the next beat that comes in has a P wavec. P- P interval is undisturbed. The next P wave after the pause returns

on cycle.

P P P P P P P P

C. Significance of Sinus Arrest and Sinus Block1. These rhythms are not significant if backup pacemakers take over to keep the heart

rate adequate to prevent complete asystole.2. They are dangerous if ectopic rhythms such as ventricular tachycardia or

ventricular fibrillation take over as a result of irritability that may occur from theslow rate..

D. Treatment

1. If asymptomatic and infrequent - none2. If symptomatic- Bradycardia Algorithm

IV/ O2/ 12-lead ECG/ Differential Diagnosis (treat cause)a. Atropine 0.5 mg IV q 3-5 min, max 3mgb. Pacing (Transcutaneous, Transvenous)c. Dopamine 2 - 20 mcg/kg per mind. Epinephrine Drip at 2 - 10 mcg/min

Review of Sinus Rhythms

This completes the section on sinus rhythms. Remember that sinus rhythms originate inthe SA node. Normal Sinus Rhythm, sinus bradycardia, and sinus tachycardia are differentiatedby rate alone. Sinus arrhythmia has a varying rhythm that speeds and slows with respirations.Sinus arrest and sinus block are similar in that there is a pause with each, followed by aPQRST. The only difference is that sinus arrest has a disturbed P-P while sinus block has anundisturbed P-P.


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Module II: Atrial Dysrhythmias

IMPORTANT TERMS- ATRIAL DYSRHYTHMIAS

Atrial Kick Atrial filling of the ventricle which can account for 20 to 25% of cardiacoutput.

Ectopic/ectopy A beat occurring in the wrong place, not from the sinus node.

Fibrillation A quivering chamber resulting from multiple firings.

Flutter Rhythmic, rapid firing within a chamber.

Nonconducted A area in heart fired, but did not progress through the conduction

system.

Paroxysmal Referring to sudden start or stop.

Premature Occurring early.

Supraventricular Occurring above the ventricle. Can include rhythms that are sinus, atrial,and junctional.

Vagal maneuvers Intentional interventions to stimulate the vagus nerve.Examples are the Valsalva Maneuver, coughing, or carotid massage.


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ATRIAL DYSRHYTHMIAS

Normally rhythms originate in the SA node, the normal pacemaker of the heart.

Sometimes, the SA node loses its pacemaking role. As a result, the pacemaking function is

taken over by another site along the conduction system. The site with the fastest inherent rate

usually controls the pacemaking function.

Rhythms that originate in the atria are called ATRIAL DYSRHYTHMIAS. Atrial

dysrhythmias are caused when the atrial rate becomes faster than the sinus rate, either by

irritability (usurpation).

As with the sinus rhythms, impulses originating in the atria will travel through to the AV

junction, through the ventricles, to the Purkinje fibers. This mechanism will give atrial rhythms a

normal shaped, narrow QRS complex.

Since atrial rhythms originate in the atria, and not the SA node, the atrial conduction will be

faster and rougher than the sinus rhythms. Atrial dysrhythmias always produce

tachyarrhythmias, and will not produce bradyarrhythmias (unless induced by medication) or

escape beats/rhythms. The P waves in atrial rhythms will be atypical and can be:

flattened

notched

peaked

saw tooth

diphasic or biphasic

Common features of atrial dysrhythmias are:

narrow QRS - impulse originates above the ventricles

atypical P wave (usually not rounded)

Remember that in the cardiac cycle, about 75-80% of blood passively fills the ventriclesfrom the atria. Then, the atria contract causing the other 20-25% of blood to enter the

ventricles. This is called the “atrial kick.” When atrial dysrhythmias interrupt the normal

contraction of the atria, they can negatively impact cardiac output by affecting that additional 20-

25% of blood that would normally enter the ventricles.


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PREMATURE ATRIAL CONTRACTION (PAC)

A. Etiology

A PAC arises from the premature discharge of an atrial ectopic focus. PAC’s occur in

the presence of a sinus rhythm as the underlying rhythm.

A PAC is not a rhythm itself, but considered an ectopic beat.

Ectopic Focus - is a site of origin of a cardiac complex other than the normal SA node.

Ectopy - a conducted premature or escape complex from a site other than normal.

Can be caused from:

1. Stimulants such as caffeine, tobacco, or alcohol

2. Hypoxia

3. Digitalis toxicity

4. Ischemia/ Injury

B. Identifying Characteristics: When identifying a PAC, there are actually 2 jobs for you:

Identify the underlying rhythm

Locate the ectopic beats

For example, a person could be in: Sinus tachycardia (underlying rhythm) with

2 PAC’s (ectopy)

1. Rhythm – irregular

a. The basic underlying rhythm is regular, but is interrupted by a sudden, premature

beat. It is the premature beat that causes the rhythm to look irregular.

b. There may be a regularity to the irregularity

1. bigeminal PAC’s - every other beat a PAC

2. trigeminal PAC’s - every third beat a PAC

2. Rate - usually normal or tachycardic

3. P waves

a. Premature

b. Differently shaped from the sinus P wave. May be flattened, notched, peaked,

diphasic.

c. May be hidden in the preceding T wave if the P wave comes really early. The

preceding T wave will look different if there is a P wave hidden in it.

4. PR Interval - will generally be within normal range of 0.12 to 0.20 seconds, but

could be shorter or longer than the PR intervals seen in the underlying rhythm.

5. QRS - usually normal but can be prolonged if the impulse passes through an

aberrant pathway


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6. Usually non-compensatory or incomplete compensatory pause.

Note the second beat below that comes earlier than expected, followed by an incompletecompensatory pause.

NONCONDUCTED OR BLOCKED PAC Sometimes, a premature atrial contraction (PAC) may be completely blocked at the AV node.When this happens, you will see a premature P wave that is not followed by a QRS because itwas not conducted down to the ventricles.

DIFFERENTIATING PAC’S FROM SINUS ARRHYTHMIA

It is important to differentiate PAC’s from sinus arrhythmia. In sinus arrhythmia, the irregularityof the R-R will be cyclic with each cycle gradually prolonging then speeding up and isasscociated with the respiratory cycle. In PAC’s, the underlying rhythm will be regular with asudden, premature beat.


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Sinus Arrhythmia

PAC

C. Significance of PACs

1. May indicate an underlying problem such as CHF2. May be precursor to other atrial dysrhythmias

3. A PAC falling on the vulnerable period of atria may produce atrial fibrillation or atrial flutter

D. Treatment

1. Treat the underlying cause

2. Treat occasionally with amiodarone, beta blockers, or calcium channel blockers.


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ATRIAL TACHYCARDIASPAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA (PSVT) PAROXYSMAL ATRIAL TACHYCARDIA (PAT)

Atrial tachycardia occurs when there is a repetitive recycling of an ectopic atrial focus. In

PSVT the pacemaker is a single, irritable site that lasts seconds to hours. PSVT is usually

initiated by a PAC. This is thought to be a re-entry rhythm.

A. Etiology

1. Emotional stress, fatigue (mental or physical)

2. Caffeine, alcohol, tobacco

3. PSVT has a paroxysmal (sudden or abrupt) start or stop

4. Atrial Tachycardia is present and may have gradually reached the tachycardia range

B. Identifying Characteristics

1. Rhythm - regular

2. Rate - Atrial - 150 to 250 /min

Ventricular - 150 to 250

3. P wave - different from the sinus P wave, but is often buried in the preceding T wave.

4. PR Interval - may vary but is sometimes difficult to measure since the P waves are

obscured.

5. QRS - Usually normal (< 0.12 seconds) but may be wider than normal if

aberrant conduction is present.

6. Variations

a.Atrial Tachycardia - rhythm with rate 150 to 250 present on the paper

b.PSVT (paroxysmal supraventricular tachycardia) - paroxysmal means sudden

onset or sudden termination. The tachycardia begins abruptly with a PAC and may

end as suddenly as it started. The criteria is the same as atrial tachycardia but you

see it start or stop abruptly.

7. 3 or more PAC’s in a row is a run of Atrial Tach or SVT.

8. The difference between supraventricular tachycardia (SVT) and paroxysmal

supraventricular tachycardia (PSVT) is that PSVT had a sudden onset or abrupt stop.

Rhythms that are supraventricular were initiated above the ventricles.

This incudes sinus, atrial, or junctional tachycardias.


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Atrial Tachycardia

PSVT

C. Significance

1. Usually tolerated in young.

2. In the elderly may lead to myocardial ischemia, myocardial infarction (M.I.) or

pulmonary edema.

3. Person may feel short of breath and feel weak and dizzy depending upon how fast

the heart rate is.

4. PAT frequently occurs in people with normal hearts and is caused by stress or

anxiety, usually not causing any real problems in these individuals.

D. Treatment1. Vagal Maneuvers

a. Valsalva’s maneuver (bearing down as if you were having a bowel movement

while holding your breath or blow through an occluded straw). The increased

intrathoracic pressure stimulates the vagus nerve.


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b. Carotid sinus massage (use with caution)

Contraindications

Patient >50

History o f CVA or heart disease

Carotid bruit or thrills. Unequal carotids

Procedure

Begin with right carotid

Massage 15 to 20 seconds

Wait 2 to 3 minutes, go to left carotid. Only one carotid at a time

2. Asymptomatic or Hemodynamically Stable (BP in normal range):

a. Adenosine

6 mg RAPID IV push, may repeat in 1-2 minutes at 12 mg RAPID

IV push, then 12 mg RAPID IV push

follow each dose immediately with a 10-20 cc flush

Blocks conduction through AV node

May produce transient asystole

Short half-life (4-10 seconds)

Drug Int

dysrhythmia interpretation modules 1-6 june 2012

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