ECG Interpretation Course - Nursing Continuing Education

ECG Interpretation Course - Nursing Continuing Education (CE) - Nurse ...
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ECG Interpretation
Author: Donna Thomas
ECG Interpretation | Copyright 2010 CEUFast.com
Course Contents
Purpose Objectives Anatomy and Physiology Function Electrical Activity of the Heart Electrophysiological Properties of a Cardiac Cell Electrical Events of Depolarization and Repolarization Properties of the Heart Conduction System Determining Rate and Rhythm Calculating the Heart Rate Analyzing a Rhythm Strip Using the Eight Step Approach Naming the Rhythm Escape Pacemakers Reentry Lead Placement Normal Sinus Rhythm Sinus Bradycardia Sinus Tachycardia Sinus Arrhythmia Sinus Arrest or Sinus Pause
Pacemakers Pacemaker Terminology Pacemaker Malfunctions Assessing Pacemaker Function Diagrams of C Rhythms Ventricular Pacemaker Ventricular Pacing in Atrial Fibrillation References
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Sinus Exit Block (Sinoatrial Block) Premature Atrial Complexes (PACs) Supraventricular Tachycardia (SVT, PSVT, PAT, Atrial Tachycardia) Wandering Pacemaker Atrial Flutter -12 lead ECG Atrial Fibrillation Junctional Bradycardia Junctional Rhythms Wolff-Parkinson-White Syndrome (WPW) Ventricular Rhythms Accelerated Idioventricular Rhythm (AIVR) Premature Ventricular Complexes (PVCs) Ventricular Tachycardia (VT) Monomorphic Ventricular Fibrillation (VF) Atrial Ventricular Blocks (AV Blocks)
Click any section in the index above to browse to the corresponding course section
Purpose
This course prepares healthcare professional to identify and respond to abnormal ECG rhythms.
Objectives
At the completion of this course the participant will be able to: 1. Describe the normal cardiac anatomy and physiology and normal electrical conduction through the heart. 2. Identify and relate waveforms to the cardiac cycle. 3. Understand the different lead placements and purpose of each placement. 4. Utilize a systematic process when approaching the interpretation of the ECG. 5. Identify normal and abnormal components on ECG. 6. Recognize sinus, atrial, junctional and ventricular dysrhythmia on ECG and relate cause, significance, symptoms and treatment. 7. Identify three pacemaker malfunctions. The primary purpose of the cardiovascular system is to supply an adequate amount of blood to peripheral tissues to meet their metabolic demands at all times. The arterial system supplies tissues and organs throughout the body with oxygen, nutrients, hormones, and immunologic substances. Through venous return it removes wastes from tissues, routing deoxygenated blood through the lungs for excretion of metabolic wastes. The heart is the size of a fist and as small as it is it carries an impressive workload over a lifetime. It beats 60 to 100 times per minutes without resting. The heart must be flexible and able to adjust to changes in the body's metabolic demands, often in a matter of seconds. Vigorous exercise can increase metabolic requirements of muscles as much as 20 times over their needs during rest. To meet these demands the heart accelerates it rate to increase cardiac output. Vessels must redistribute blood flow, shunting a greater proportion of blood to muscle tissues and away from internal organs. The heart is unique and possesses several properties. It works as a pump by expanding and contracting without placing added stress on the cardiac muscle and without developing muscle fatigue. The heart pumps 4 to 8 liters per minute. This is equivalent to 6,000 liters per day. It has
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an inherent capability to generate electrical impulses that maintain proper rhythm regardless of other factors, such as heart rate, and ignores inappropriate electrical signals that might over stimulate the cardiac muscle. The ECG is a valuable diagnostic tool for the healthcare provider whether they are a doctor, nurse, or specialist in cardiac rehabilitation. Understanding the ECG enables the healthcare provider to respond correctly and to treat dangerous and potential deadly arrhythmias as quickly and efficiently as possible. It is important to understand the mechanisms, cutting edge treatments and to know exactly what needs to be done to treat these deadly arrhythmias. New drugs and high tech equipment which can cardio-vert, defibrillate, and serve as a pace maker are constantly being evaluated and introduced into the healthcare system.
Anatomy and Physiology

The heart is a hollow, muscular organ located in the middle of the thoracic cavity, cradled in a cage of bone cartilage, and muscle. It lies left of the midline of the mediastinum and just above the diaphragm. The heart is protected anteriorly by the sternum and posteriorly by the spine. Lungs are located on either side. The entire heart is enclosed in the fluid-filled pericardial sac. This sac helps to shield the heart against infection and trauma, prevents friction, and aids cardiac function by helping with the free pumping action of the heart. The heart consists of three layers; Epicardium, Myocardium, and Endocardium.
Function
Activities of the right side of the heart and the left side of the heart occur simultaneously.
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The right side of the heart receives impure blood from the body via the vena cava into the right atria. Blood is ejected from the right atria into the right ventricle. Blood is pumped to the lungs from the right ventricle via the pulmonary artery. The left side of the heart receives oxygenated blood from the lungs via the pulmonary vein into the left Atria. Blood is ejected from the left atria to the left ventricle. Blood is pumped to the body from the left ventricle via the aorta. Briefly the Right side of the heart pumps blood into the lungs. The Left side pumps blood into the body. The two atria and two ventricles of the heart are separated by atrioventricular valves. The action of the Right tricuspid and left Mitral (Diastole) represent the ventricle filing phase. AV-valves open during Systole; while the ventricle is in the contracting phase (empty) then the AV valves close. The Semilunar valves separate the ventricles from the arteries. The pulmonic valve separates the right ventricle, and the pulmonary artery. The Aortic valve separates the left ventricle from the Aorta, during systole, allowing blood to be ejected from the heart to the rest of the body.
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Coronary Arteries
Right Coronary Artery Supplies: Right Atrium, Anterior Right Posterior and Papillary Muscle Wall Ventricle Posterior Aspect of Septum (90% of population) Sinus and AV Nodes (80-90% of population) Inferior aspect of Left Ventricle
Left Coronary Arteries Left Anterior descending (LAD) Supplies: Anterior Left Ventricular Anterior Interventricular Septum Septal branches supply conduction system, Bundle of HIS, and Bundle branches Anterior papillary muscle Left ventricular apex
Circumflex Supplies: Left Atrium Posterior surfaces of Left ventricle Posterior aspect of septum
Electrical Activity of the Heart

The human heart is a remarkable organ. The human heart beats 80,000 to 100,000 times and pumps approximately 2,000 gallons a day. The heart will have beat 2-3 billion times and pumped 50-65 million gallons of blood over a 70-90 year lifespan. The human heart is made of specialized muscle capable of sustaining continuous beating. This muscle is different than skeletal muscle that powers the arms and legs. Specialized areas of the myocardium exert electrical control over the cardiac cycle. These areas exhibit physiologic differences from the rest of the myocardium, forming a pathway for electrical impulses which energize the heart muscle. The two types of cardiac cells are contractive and conductive. When the cells are at rest, they are electrically more negative on the inside with respect to the outside of the cell. Charged particles
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(ions) of sodium and potassium move in and out of the cell causing changes that are sensed by electrodes on the skin. The electrical action will show as a tracing on the ECG. The sinoatrial (SA), or sinus node initiates a self-generating impulse and is the primary pacemaker which sets a rate of 60 to 100 beats per minute (bpm). The SA node is located at the border or junction of Superior Vena Cava and Right Atrium. Once generated, the electrical impulse sets the rhythm of contractions and travels through both atria over a specialized conduction network to the Atrioventricular (AV) Node. The AV node is located in the floor of the Right Atrium and receives the impulse and transmits to the Bundle of His. The Bundle of His then divides into a right bundle branch and two left bundle branches. These terminate in a complex network called the Purkinje Fibers, which spread throughout the ventricles. When the impulse reaches the ventricles, stimulation of the myocardium causes depolarization of the cells, and contraction occurs. The AV node serves as a gate to delay electrical conduction and in this way prevents an excessive number of atrial impulses from entering the ventricles. The SA node and AV Nodes are supplied with sympathetic and parasympathetic fibers. This enables nearly instantaneous changes in the heart rate in response to physiologic changes in oxygen demand. The normal cardiac conduction system occurs in this sequence: Sinoatrial node initiates electrical impulse and sends this impulse thru the atrium >lower section whereby an Atrial Kick occurs >AV node >Bundle of His thru ventricles via > Right Bundle & Left Bundle Branches>Purkinje fibers If the SA node falters, a hierarchy of pacemakers are able to take over. Atrial, AV node, and ventricular escape pacemakers can function as subsidiary pacemakers, however they generated impulses at a much slower rates. The AV node generates rates between 40 to 60 bpm and the Purkinje fibers at 20 to 40 bpm. Electrical impulse does not always equal contraction of the heart. Accessory pathways play a role in re-entry tachydysrhythmias, providing a detour for electrical impulses to circle through the heart. Mahaim: Short, direct connections from the AV node (or the Bundle of His or bundle branches) to muscle fibers in the interventricular septum. Mahaim fiber conduction, a type of accessory AV conduction with abnormal beats originating below the region of normal delay in the AV-conducting system, causes an arrhythmia
Components of the Electrical System
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Sinoatrial node (SA Node) Internodal Pathways Bundle of James Fascicle
Bundle of Kent Bundle of Mahaim Right Bundle Branch Purkinje fibers
Bachman's Bundle Atrioventricular node (AV) Left Anterior Fascicle Accessory Pathways
Atria Ventricles Bundle of His Right Posterior AV node/His Atria
There are two myocardial cell types. 1. Myocardial (working) cells (mechanical cells) which are located in the myocardium. These contain contractile filaments that contract when the cells are electrically stimulated. Their primary function is contraction and relaxation. Their primary property is contractility. 2. Electrical cells (pacemaker cells). These electrical conduction cells are found in the electrical conduction system. They conduct impulses very rapidly and their primary property is automaticity and conductivity.
Electrophysiological Properties of a Cardiac Cell
Cardiac cells are surrounded by and filled with a solution that contains ions. Three key ions are sodium (Na+), potassium (K+), and calcium (Ca++). In the resting period of the cell, the inside of the cell membrane is considered negatively charged and the outside of the cell membrane is positively charged. The movement of these ions inside and across the cell membrane constitutes a flow of electricity that generates the signal on an ECG.
Electrical Events of Depolarization and Repolarization

Polarized - Cardiac cells that are in a resting state are negative. The sodium ions are outside of the cell and the potassium ions are inside the cell. Both ions carry a positive charge however; the sodium ion has a stronger charge than the potassium. Thus the inside of the ion electrically is weaker than the outside so it is negative. The polarized state is a "ready state". When the cell is ready to accept and electrical impulse, a large amount of potassium leaks out. This causes a discharge of electricity. The cell becomes positively charged. This is called depolarization. The electrical wave then travels from cell to cell throughout the heart. Now there is cell recovery, sodium and potassium ions are shifted back to their original place by the sodium-potassium pump. This is called repolarization.
Action Potential of a Myocardial Working Cell

1. Electrical impulses are the result of brief, but extremely rapid flow of positively charged ions (mainly Na+) back and forth across the cell membrane. 2. Cardiac action potential illustrates the changes in the membrane potential of a cardiac cell during depolarization and repolarization.
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There a five phases starting with the following: Phase O Rapid Depolarization also called "upstroke", "overshoot", or "spike" Begins when cell receives an impulse Sodium moves quickly into the cell through the fast sodium channels Potassium then leaves the cell Calcium moves slowly into the cell through calcium channels This is about +20 mV Cell depolarizes and cardiac contraction begins Phase 1 Early Repolarization The Rapid flow of sodium into the cell is stopped as the fast sodium channels close Potassium begins to reenter the cell and sodium begins to leave This is about 0mV and is therefore neutrally charged, neither positively or negatively charged This is the absolute refractory period Phase 2 Plateau Phase (slow repolarization, part of absolute refractory period) Slowly repolarization continues Calcium continues to flow into the cell through slow calcium channels Phase 3 Final Rapid Repolarization Rapidly the cell completes repolarization Calcium channels close Potassium rapidly flows out of the cell Active transport via the potassium-sodium pump begins restoring potassium to the inside of the cell and sodium to the outside of the cell Cell now in negative state due to the outflow of potassium Gradually the cell becomes very sensitive to external stimuli until its original sensitivity has been restored; called the relative refractory period. Phase 4 Return to Resting Stage Corresponds to diastole Calcium and sodium remain outside the cell Potassium remains inside the cell During this phase the heart is "polarized" and getting ready for discharge Once another stimuli occurs the cell will reactivate
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Depolarization Discharge, excited, active stage. Depolarization of the myofibril releases energy stored in the cell. This energy pulls the "contractile" proteins actin and myosin closer together, thus shortening the myofibril. This action immediately precedes mechanical systole. Repolarization - Recharge, return to the resting stage. This is the longer portion of the action potential. Energy is reincorporated into the cell to restore the resting transmembane potential. Repolarization of the myofibril is the process that prepares the cell for another action potential and contraction and occurs during mechanical diastole. Absolute Refractory Period During depolarization, the cell cannot accept another stimulus
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Relative Refractory Period During repolarization the cell may be stimulated by only a strong stimulus
Keys to Remember:
1. Electrical events show as tracings on the ECG 2. Depolarization and Repolarization are Electrical Events 3. Contraction and Relaxation are Mechanical Events
Properties of the Heart

Automaticity is the ability of the heart to initiate an electrical impulse. The heart can begin and maintain rhythmic activity without the aid of the nervous system. A heart removed from the body has the ability to beat on its own for a limited period of time. The highest degree of automaticity is found in the pacemaker cells of the sinus node. The atria, atrioventricular (AV) Node, Bundle of His, bundle branches, Purkinje Fibers, and the ventricular myocardium have a lesser degree of automaticity. Excitability is the ability of the heart to respond to an electrical impulse. A cardiac cell will respond to an electrical stimulus with an abrupt change in its electrical potential. Each cardiac cell that receives an electrical impulse will change its ionic composition and its respective polarity. Once an electrical potential begins in a cardiac cell it will continue until the entire cell is polarized. Conductivity is the ability of the heart to conduct an electrical impulse. All areas of the heart appear to depolarize at the same time because a cardiac cell transfers an impulse to a neighboring cell very rapidly.
The velocity of the transfer varies in the different cardiac tissues:

200mm/second in the AV node 400mm/second in the ventricular muscle 1000mm/second in the atrial muscle 4000mm/second in the Purkinje fibers
Contractility is the ability of the heart to respond by contracting.
Conduction System
The normal cardiac impulse arises in the specialized pacemaker cells of the SA node, located about 1 mm beneath the right atrial epicardium at its junction with the superior vena cava. The impulse then spreads over the atrial myocardium to the left atrium via Bachmann's bundle and to the region of the AV node via the anterior, middle, and posterior internodal tracts connecting the sinus and AV nodes. These represent the usual routes of spread, but are not specialized tracts analogous to the Purkinje system. When the impulse reaches both atria, they depolarize electrically, producing a P wave on the electro cardiogram (ECG), and then contract mechanically, producing the A wave of the atrial pressure pulse and propelling blood forward into the ventricles. Conduction slows when the impulse reaches the AV node, allowing sufficient time for blood to flow from the atria into the ventricles. After the impulse emerges from the AV node, conduction resumes it rapid velocity through the Bundle of HIS to the Right and Left Bundle Branches, and terminates in the Purkinje Fibers in the ventricular muscle. Stimulation of the myocardium causes progressive contraction of the myocardial cells. Therefore, wave deflections correspond to the mechanical events in the cardiac cycle which include contraction and relaxation of the cardiac chambers. Repolarization is only electrical and the heart is at rest. Three major waves of electric signals appear on the ECG. Each one shows a different part of the heartbeat. The first wave is called the P wave. It records the electrical activity of the atria.
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The second and largest wave, the QRS wave, records the electrical activity of the ventricles. The third wave is the T wave. It records the heart's return to the resting state.
The P wave represents atrial activation; the PR interval is the time from onset of atrial activation to onset of ventricular activation. The QRS complex represents ventricular activation; the QRS duration is the duration of ventricular activation. The ST-T wave represents ventricular repolarization. The QT interval is the duration of ventricular activation and recovery. The U wave probably represents "after depolarization" in the ventricles. Baseline is a bioelectric line; neutral usually without any deflections; flat line
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"P" wave represents atrial depolarization. This represents one electrical activity associated with an impulse from the S-A node and its spread through the atria. "P-R" Interval represents the time from the start of atrial depolarization, P-wave to the beginning of the QRS, or ventricular depolarization. Normal P-R interval is .12 to .20 seconds. "QRS" represents ventricular depolarization (phase 0 of the action potential) until the end of ventricular depolarization. "Q" = initial downward or negative deflection The normal Q wave is less than 25% of the amplitude of the R wave The Q wave does not exceed 0.04 sec in duration "R" = first upward or positive deflection after the P wave "S" = first downward or negative deflection after the R wave Normal QRS complex is 0.04 to 0.10 seconds in adults. "ST segment" is the electrical resting period after ventricular depolarization. Represents early repolarization of the left and right ventricles. Begins with the end of the QRS complex and ends with the onset of the T wave. It is usually not depressed more than 0.5 mm in any lead. "T Wave" ventricular repolarization and is not usually greater than 5 mm in amplitude. Peaked T waves are seen in hypercalcemia. "QT" interval represents total ventricular activity which is the time required for ventricular depolarization and repolarization. Measured from the beginning of the QRS complex to the end of the T wave Normally measures 0.36 -0.44 sec. This can vary with the patient's heart rate. Slower heart rates tend to have a longer QT interval and fast heart rates tend to have a shorter QT interval. Prolonged QT intervals indicate a lengthened relative refractory period (vulnerable period). In the vulnerable period critical, life threatening rhythms may occur (Premature Ventricular Contractions Torsades de Pointe, "T" wave represents ventricular repolarization Normally not greater than 5mm in amplitude Peaked T waves are seen in patients with hyperkalemia
Determining Rate and Rhythm

Dr. Ken Grauer (2008) stresses that the real key to rhythm interpretation is to utilize a Systematic Approach. 1. First ask yourself are there P waves? 2. What is the QRS width? 3. Is it a Regular rhythm? 4. Are P waves related to the QRS? 5. What is the Heart Rate?
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The Graphing Paper

The horizontal lines measure time Vertical lines measure amplitude of voltage Records at 25mm/sec Width of each small square = 0.04 seconds Width of one large square = 0.20 seconds Five large boxes = one second One large box = 5 mm high = 0.5 millivolts
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Calculating the Heart Rate

There are several methods for calculating the heart rate. 1. Rule of 300: If the rhythm is regular, the heart rate can be "estimated" by using the "Rule of 300". Count the number of large squares between two R waves and divide this number into 300. ( There are 300 boxes, or 1500 tiny boxes, in a one minute strip) 2. The Six-Second Method: Count the number of complete R waves within a period of 6 seconds and multiply that number by 10. This is the one minute heart rate. This method can be used when the rhythm is "regular or irregular". 3. The Three-Second Method: Count the number of complete QRS complexes in a period of three seconds and multiply that by twenty. This is the one minute heart rate. 4. The Block Method: Find a QRS complex that hits exactly on a vertical line. The next block The second block The third block The fourth block The fifth block 300 150 100 75 60
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The sixth block The seventh block The eight block The ninth block The tenth block
50 43 37 30 prayers are needed
Analyzing a Rhythm Strip Using the Eight Step Approach

Step One: Determine the Rate: What is the atrial rate? To determine the atrial rate, measure the distance between P-P. What is the ventricular rate? To determine the ventricular rate, measure the distance between R-R. Note: The rate of a Normal Sinus Rhythm is 60-100 beats per minute Step Two: Determine the Rhythm Is the rhythm is regular or irregular? To determine if the atrial rate is regular or irregular, measure the distance between two consecutive P-P intervals. Use a point from one P wave to the same point on the next P wave. Then compare this with another P-P interval. If the atrial rate is regular, the P-P interval will measure the same. Determine if the ventricular rate is regular or irregular, measure the distance between two consecutive R-R intervals Use a point from one R wave to the same point on the next R wave. Then compare this with another R-R interval. If the atrial rate is regular, the R-R interval will measure the same. Is the rhythm regular? Basically regular? Regularly irregular? Irregularly irregular? Step Three: Evaluate P Waves Are P waves present and uniform in appearance? Are P waves upright (positive) in Lead II? Do P waves appear regularly before each QRS complex or is there More than one P wave before a QRS complex? If irregular is there an associated beat? Step Four: Evaluate the P-R interval If the P-R interval is less than 0.12 or more than 0.20 second, conduction follows an abnormal pathway or the electrical impulse was delayed at the AV node. The normal P-R interval is 0.12 to 0.20 second.
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Is the P-R interval consistent? Step Five: Evaluate the QRS complex Do the QRS complexes occur uniformly and look the same throughout the strip? If the QRS measures .10 second or less it is considered narrow and is presumed to be supraventricular in origin. If the QRS complex is greater than .12 second or more it is considered wide, and presumed to be ventricular in origin until proven otherwise. The QRS normally measures 0.04 to 0.10 seconds in duration. Determine if they are married to the P waves. Step Six: Evaluate T Wave Are T waves present? Are T waves smooth and rounded? Do they have normal amplitude of 0.5 mV or less? Is the deflection the same as the preceding QRS? Is there a relationship between any ectopy to the T wave? Step Seven: Evaluate the QT Interval Is the duration from 0.36 to 0.44 seconds? Step Eight: Evaluate other components Is the ST segment elevated? Depressed? Sloping or scooped? Are U waves present? Prominent? Are there other (funny little beats) FLB's detected?
Naming the Rhythm

Origin of the Impulse plus the Cardiac Activity = rhythm name. Origin of the Impulse: Is it sinus, atrial, junctional, or ventricular? Cardiac Activity: Normal (In rhythm), bradycardic (slow), accelerated (Faster than normal), or Tachycardic (Greater than 100/min)? For example: sinus bradycardia, sinus tachycardia, accelerated junctional, or ventricular tachycardia.
Escape Pacemakers
The normal electrical flow through the heart originates in the SA node>AV node>Bundle of His> left and right bundle branches> Purkinje fibers where the mechanical cells are stimulated. The primary pacemaker therefore is the SA node and has an inherent rate of 60-100 beats/minute. The SA node has the highest level of automaticity, but escape pacemakers can exist. Common escape pacemakers exist in the Atrio-Ventricular (AV) junction and in the Ventricles. The AV junction is the AV node and the nonbranching portion of the Bundle of His. The pacemaker cells in the AV junction are located near the nonbranching portion of the Bundle of His. The AV node only generates an impulse if the SA node does not function at its normal rate. The AV node fires electrical impulses at a rate of 40-60 beats/ minute.
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The Ventricular pacemakers located in the bundle branches and the Purkinje network will become the initiating pacemaker if the AV node is not able to function at its normal rate. The inherent ventricular rate is 20-40 beats/minute.
Reentry
This occurs when an electrical impulse is delayed, blocked or both in one or more portions of the electrical conduction system while the impulse is conducted normally through the rest of the conduction system. The end results are a delayed impulse entering cardiac cells which have been depolarized by the normally conducted impulse. If they have repolarized sufficiently, depolarizing them prematurely, produces ectopic beats and rhythms.
Lead Placement
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Lead I: Positive electrode is placed just below the left clavicle Negative electrode place just below the right clavicle Provides information about the left lateral wall of chest.
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Lead II: Positive electrode just below the left pectoral muscle Negative electrode just below the right clavicle Provides information about the inferior wall of the heart Very common in cardiac monitoring because position of this lead is close to actual conduction pathways. Lead III: Positive electrode is at the left pectoral muscle, and negative is below the left clavicle. Provides information about the inferior wall of the heart MCL I Negative electrode is below the left clavicle and positive is at the right of the sternum at the fourth intercostals space. Useful in assessing the anterior wall of the heart (LV) and the conduction through the ventricles. This lead is useful in assessing the width of the QRS complex to differentiate supraventricular tachycardia (SVT) from ventricular tachycardia (VT). Disorders of the Heartbeat are caused by: 1. Defects in impulse formation 2. Defects in impulse conduction 3. Combinations of above
Arrhythmogenic Mechanisms Reentry Altered automaticity- enhanced or depressed
Normal Sinus Rhythm
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Sinus Bradycardia
May be due to: a normal response to sleep or in well conditioned athlete, abnormal drops in rate could be caused by diminished blood flow to S-A node, vagal stimulation, hypothyroidism, increased intracranial pressure, or pharmacologic agents, such as digoxin, propranolol, quinidine, or procainamide.
Sinus Tachycardia
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May be the result of stress, exercise, pain, fever, pump failure, hyperthyroidism, drugs-caffeine, nitrates, atropine, epinephrine, and isoproterenol, nicotine
Sinus Arrhythmia
Rate: Usually 60-100 beats/min but may be either faster or slower Commonly seen in the elderly and the young and usually does not require treatment. Heart rate increases with inspiration and decreases with expiration.
Sinus Arrest or Sinus Pause
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Rate: Usually 60-100 beats/min but may be either faster or slower Rhythm: Irregular The SA node initiates and impulse, but the impulse is blocked before leaving the node itself. This results in an absent PQRST complex. In sinus arrest, the pause is not a multiple of other P-P interval and can be due to multiple problems. Treatment may include Atropine or a pacemaker if symptomatic.
Sinus Exit Block (Sinoatrial Block)

Rate: Usually 60-100 beats/min but may be either faster or slower Rhythm: Irregular The SA node initiates and impulse, but the impulse is blocked before leaving the node itself. This results in an absent PQRST complex. The pause is the same as the distance between two P-P intervals of the underlying rhythm. Uniform and upright in appearance P waves: One P wave precedes each QRS complex that is present PRI: .12-.20 sec QRS: <.10 May be due to: Myocardial Infarction, drug effect, Coronary Artery Disease, etc. Treatment may include Atropine or a pacemaker if symptomatic.
Premature Atrial Complexes (PACs)
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Rate: Usually normal, but depends on underlying rhythm Rhythm: Irregular due to PACs. Irregular since the impulse occurs early. Premature beats are identified by their site of origin (atrial, junctional, and ventricular). PAC occurs when an irritable site within the atria discharges before the next SA node is due to discharge. PAC's with a wide complex are called aberrantly conducted PAC's. May occur in pairs (couplet), burst (Premature Atrial Tachycardia) PAT, every other beat (bigeminy). P waves: P wave of the early beat differs from sinus P waves and is premature. P waves may be flattened or notched. May be lost in the preceding T wave. PRI: Varies from .12- .20 when the pacemaker site is near the SA node, to .12 sec when the pacemaker site is nearer the AV node. QRS: Usually <.10 but may be prolonged May be due to normal response to sleep or in well conditioned athlete; Abnormal drops in rate caused by diminished blood blow to S-A node, vagal stimulation, hypothyroidism, increased intracranial pressure, or pharmacologic agents such as digoxin, propranolol, quinidine, or procainamide. May be associated with signs of impaired CO; symptoms: dizziness, syncope, chest pain.
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(Lead II )PACs marked by green arrow.
In this rhythm the atrial rate from an ectopic focus is 160 bpm. Atrial activity can be seen on top of T waves, and before QRS's. Careful observation reveals a 3:2 Wenckebach relationship between P waves and QRS's. Atrial tachycardia with block is often a sign of digitalis intoxication.
Supraventricular Tachycardia (SVT, PSVT, PAT, Atrial Tachycardia)

Rate: 150-250/min Rhythm: Regular P waves: Atrial P waves differ from sinus P waves originating in the SA node. P waves are usually identifiable when there is a low rate and seldom identifiable at rates >200. PRI: Usually not measurable because the P wave is difficult to distinguish from the preceding T wave; if measurable, is .12-.20. QRS: <.10 sec If an event is documented, usually a PAC that continues into SVT, it is termed PAT. May be the result of stress, caffeine, nicotine, or heart disease. Treatment consists of oxygen, vagal maneuvers, or possibly adenosine. Unstable patients may receive a counter shock to allow the SA node to recapture.
Wandering Pacemaker
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Rate: Could be fast or slow depending upon the cause Rhythm: Irregular because the stimulus originates in different sites P waves: May look different in the same lead QRS: QRS duration is usually normal (0.10 seconds or less) May be due to COPD, Heart Disease or Digitalis toxicity. Wandering atrial pacemaker is a benign rhythm change where the pacemaker site shifts from the sinus node into the atrial tissues. P-wave morphology varies with the pacemaker site.
Atrial Flutter -12 lead ECG
Atrial flutter with 2:1 AV block is one of the most frequently missed ECG rhythm diagnoses because the flutter waves are often hard to find. In this example two flutter waves for each QRS are best seen in lead III and V1. The ventricular rate at 150 bpm should always prompt us to consider atrial flutter with 2:1 conduction as a diagnostic consideration Rate: Atrial rate 250-350/ min Rhythm: Atrial rhythm regular, Ventricular rhythm usually regular, but may be irregular. If the AV node blocks the same number of impulses, and only allows a certain amount of impulses to be conducted to the ventricles, the ventricular rate will be constant (such as 3:1 or 4:1). P waves: Saw-toothed, "flutter waves are buried in the QRS complex PRI: Not measurable QRS: Usually <. 10 but may be widened if flutter waves are buried in the QRS complex
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May be due to: ischemia, MI valvular disease, hypoxia, or drug effects. If ventricular response is less than 100, and the patient is asymptomatic, the condition is treated medically. If the ventricular response is more than 100, and the patient shows symptoms of heart failure, treatment may consist of countershock.
The basic rhythm is atrial flutter with variable AV block. When 2:1 conduction ratios occur there is a rate-dependent LBBB. Do not be fooled by the wide QRS tachycardia on the bottom strip. It is not ventricular tachycardia, but atrial flutter with 2:1 conduction and LBBB. Lidocaine is not needed because there is no ventricular ectopy.
Atrial Fibrillation
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Diagram of Atrial Fibrillation Rate: Atrial rate usually > 400, Ventricular rate variable Rhythm: Atrial and ventricular very irregular (regular, bradycardic ventricular rhythm may occur as a result of digitalis toxicity) P waves: No identifiable P waves, Erratic, wavy baseline PRI: None QRS: Usually <.10 Rapid impulses originating in multiple sites in the atria cause the atrium itself to "quiver". This is ineffective in allowing for an effective atrial kick. The AV node protects the patient from having too high a ventricular response, and blocks the majority of the impulses. Blood may pool or stagnate in the atria and the patient is at risk for clot formation. May be due to: ischemia, Myocardial Infarction hypoxia, or drug therapy. Treatment may consist of beta-blockers (Inderal), calcium blockers (verapamil), or synchronized cardioversion in an attempt to restore the patient to a sinus rhythm.
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Junctional Bradycardia
The ladder diagram illustrates the PJC with retrograde atrial capture
Junctional Rhythms
Impulses coming from the Junction (AV node). The inherent rate of the junction is 40-60/min. Characteristics: Rate: Junctional bradycardia - < 40 Junctional rhythm norm 4 - 60/ min Accelerated junctional rhythm 61-10 Junctional tachycardia - > 100 Rhythm: regular P waves: inverted before or after the QRS, or absent PRI: not measurable if no P wave or if P wave occurs after QRS QRS: normal
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Wolff-Parkinson-White Syndrome (WPW)

The short PR interval is due to a bypass track, also known as the Kent pathway. By bypassing the AV node the PR shortens. The delta wave represents early activation of the ventricles from the bypass tract. The fusion QRS is the result of two activation sequences, one from the bypass tract and one from the AV node. The ST-T changes are secondary to changes in the ventricular activation sequence.
Short PR intervals and delta waves are best seen in leads V1-5. Pseudo-Q waves, seen in leads II, III, and aVF, are actually negative delta waves. There is no inferior MI on this ECG. Wolff-Parkinson-White Syndrome (WPW) must be seen in more than one lead. The classical ECG features of the syndrome originally described are a short P-R interval and a broad QRS. Rate: Usually 60-100 beats/min but may be either faster or slowerWPW may be due to congenital pathways that allow rapid conduction of
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impulses. May predispose the patient to atrial tachycardia since there is no blocking of impulses at the AV node. PRI: If this interval is short, it is because the sinus impulse partially avoids its normal delay in the AV node by traveling rapidly down the accessory pathway. QRS: Often greater than 0.10 seconds since there is no delay in the AV node. Subsequent activation of the ventricles depends upon intra-atrial conduction time from sinus node to the accessory pathway plus conduction time down the accessory pathway, compared with the conduction time from sinus node to ventricles via orthodox conduction pathways. Delta Wave: Slurring occurs at the beginning of the QRS complex. Secondary T wave changes: Because ventricular depolarization is abnormal, repolarization will also be abnormal, causing ST and T wave changes secondary to the degree and area of pre-excitation. Abnormal Q waves: Q waves are considered abnormal when they have an amplitude 25% of the succeeding R wave and /or a duration of 0.04 second or greater. Such Q waves are often seen in the presence of an accessory AV pathway and may be misdiagnosed as Myocardial infarction. They are actually negative delta waves, reflecting pre-excitation and not myocardial necrosis.
Ventricular Rhythms
Ventricular impulses come from the ventricles. Inherent rate of ventricles is: 15 -40 Idioventricular Rhythm (IVR) or Ventricular Escape Rhythm Rate: Intrinsic rate is 20-40 beats per minute Rhythm: Atrial not discernible, ventricular essentially regular P waves: absent PRI: None QRS: >.12 May be due to: MI, metabolic imbalances, or severe hypoxia. Treatment includes activation of code/890, CPR given if patient is pulseless. Lidocaine is contraindicated since it may knock out the last available pacemaker.
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Accelerated Idioventricular Rhythm (AIVR)

Rate: Atrial not discernable, ventricular 40-100 beats/minute Rhythm: Ventricular rate regular, atrial rate not discernable P waves: Absent PRI: None QRS: > .12 May be due to: Heart disease (e.g., acute myocardial infarction, digitalis toxicity, at reperfusion of a previously occluded coronary artery), may occur During Resuscitation, Drugs (e.g., digoxin), dilated cardiomyopathy, and during Outpatient procedures (due to spinal anesthesia).
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Premature Ventricular Complexes (PVCs)

Rate: Atrial and ventricular rate dependent upon the underlying rhythm Rhythm: Irregular due to PVC. If PVC is sandwiched between two normal beats it is called interpolated and the rhythm will be regular P Waves: A P wave is not associated with the PVC PRI: None with the PVC because the ectopic originates in the ventricles QRS: .12 Wide and bizarre. T wave frequently in opposite direction of the QRS complex. If the QRS is negative, the T wave is usually upright; if the QRS is positive, the T wave is usually inverted. May be due to: stress, activity, valvular disease, CAD, or MI. PVC may produce a pulse and the patient should be treated, not the monitor.
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The main feature of this wide QRS tachycardia that indicates its ventricular origin is the concordance of QRS's in the precordial leads (all QRS's are in the same direction).
Ventricular Tachycardia (VT) Monomorphic

Rate: Ventricular rate 100-250 beats/minute, atrial not discernible Rhythm: Atrial not discernible, ventricular essentially regular P waves: May or may not be present, if present they have not set relationship to the QRS complexes. P waves may appear between the QRS at a rate different from that of the VT. PRI: None QRS: >.12 Often times difficult to differentiate between QRS and T wave. Three or more PVCs in a row at rate of 100 per minute are referred to as a "run" of VT. There may be a long or a short run. Patient may or may not have a pulse. If it is unclear as to where a regular, wide QRS tachycardia is VT or Supraventricular Tachycardia treat the rhythm as VT until proven otherwise. Note: Ventricular tachycardia can occur in the absence of apparent heart disease. May be due to: an early or a late complication of a heart attack, or during the course of cardiomyopathy, alveolar heart disease, myocarditis, and following heart surgery.
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Ventricular Fibrillation (VF)

Rate: rapid and disorganized Rhythm: irregular and chaotic P Wave: absent but can be recognizable PRI: not measurable QRS: fibrillatory waves; wide irregular oscillations of the baseline.
The normal PR interval (PRI) is 0.12 - 0.20 sec, or 120 -to- 200 ms. 1st degree AV block is defined by PR intervals greater than 200 ms. This may be caused by drugs, such as digoxin; excessive vagal tone; ischemia; or intrinsic disease in the AV junction or bundle branch system.
Atrial Ventricular Blocks (AV Blocks)

First Degree:
PRI longer than .20 sec There is No Block at all just a delay in conduction. Every P wave is married to a QRS; no missed beats.
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Second Degree:
Type I (Mobitz I or Wenckebach) The 3 rules of "classic AV Wenckebach" are: 1. decreasing RR intervals until pause; 2. the pause is less than preceding 2 RR intervals; and 3. the RR interval after the pause is greater than the RR interval just prior to pause. There is a gradual and progressive increase in the PR interval (PRI) with successive beat, until finally the QRS is dropped. Unfortunately, there are many examples of atypical forms of Wenckebach where these rules do not hold.
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The QRS morphology in lead V1 shows LBBB. The arrows point to two consecutive nonconducted P waves, most likely hung up in the diseased right bundle branch. This is classic Mobitz II 2nd degree AV block.
Mobitz II 2nd degree AV block is usually a sign of bilateral bundle branch disease. One of the two bundle branches should be completely blocked; in this example the left bundle is blocked. The nonconducted sinus P waves are most likely blocked in the right bundle which exhibits 2nd degree block. Type II (Mobitz II) PRI is fixed (no progressive increase in PRI) QRS is dropped without warning; there will always be more P Waves than QRS The P waves are married to the QRS The level of conduction problem is usually lower than the AV node, often involving the Bundle of His
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Diagram is Third Degree with Junctional Rhythm
Third Degree (Complete Heart Block)

There is complete heart block so that none of the impulses from above are conducted to the ventricles The atria and the ventricles are controlled independently by separate pacemakers P Waves are NOT married to the QRS The level of the complete block is High, when the AV node takes control of the ventricles. The QRS will therefore be narrow and the junctional rate will be between 40-60. If the level of the block is Low, a ventricular pacemaker will control the ventricles. The QRS will therefore be wide and the rate is slower.
Asystole is synonymous with Ventricular Standstill and death. This is usually associated with prolonged circulatory insufficiency and cardiogenic shock. This could also be drug related and at times reversible.
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Pacemakers
The following are indications for a Pacemaker: Symptomatic Sinus Bradycardia 2:1 AVB Junctional rhythms Idioventricular rhythms Dying heart Asystole Overdrive suppression of tachycardias Second degree AVB Type II Third degree AVB
Pacemaker Terminology
Firing refers to the pacemaker's generation of electrical stimuli. This is seen as a pacemaker spike on the ECG. Capture refers to the presence of a P or QRS or both after a pacemaker spike. This indicates that the tissue in the chamber being paced has been depolarized. The term is that the pacemaker has "captured" the chamber being paced. Paced QRS are wide, bizarre and resemble PVCs. Sensing refers to the pacemaker's ability to recognize the patient's own intrinsic rhythm in order to determine if it needs to fire. Most pacemakers function in the demand mode and fire when needed.
Pacemaker Malfunctions
Failure to Fire: When a pacemaker fails to send an impulse when it should it is said to malfunction. Usually this means a dead battery or that the connecting wires are at fault. At time artifact can fool the pacemaker and it will not fire. This is displayed as no pacer spike where there should be one. Loss of Capture: When loss of capture exists there is no P or QRS after the pacer has fired; just a spike. The pacer needs to be adjusted to allow detection of the heart's need to be paced. It is possible the pacing wire has lost contact with the chamber wall which can occur when the heart is too damaged to respond. Under-sensing: This occurs when the pacemaker fires too soon after an intrinsic beat and there are pacer spikes where there should not be. These can appear in the T wave, on the QRS or anywhere on the heart rhythm's tracing. This requires adjustment with the wires or battery replacement.
Assessing Pacemaker Function

Classification: Pacemaker function is usually identified by 3 letters which indicate the cardiac chambers paced, sensed, and the mode of pacing. First letter (A, V or D) refers to the chamber(s) paced (Atria, Ventricles, Dual both atria and ventricles). Second letter (A, V or D) refers to the chamber(s) sensed (Atria, Ventricles, Dual both the atria and ventricles). Third letter mode of pacing (Inhibited or Triggered or Demand). Examples: DDD, VVI, VVD Pacemaker function is judged by its ability to Sense the patient's underlying rhythm and Pace or Capture the ventricles when needed. Capture is confirmed when a QRS complex follows a Pacemaker Spike. (A Spike is a vertical line on the ECG which indicates the pacemaker has fired. A QRS after a spike means there is ventricular capture).
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Three questions to ask when analyzing an ECG strip with pacemaker spikes are: 1. Is the chamber being paced capturing? 2. Is the pacemaker sensing the patient's inherent rhythm? 3. Is there a pulse with each the pacer rhythm?
Diagrams of C Rhythms
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Ventricular Pacemaker
Observe the small pacemaker spikes before the QRS complexes in many of the leads. In addition, the QRS complex in V1 exhibits ventricular ectopic morphology. There is a slur or notch at the beginning of the S wave.
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AV Sequential Pacing
In this ECG both atria and ventricles are being paced. Two pacemaker spikes are seen before each QRS, one for the atria and one for the ventricles (best seen in lead V1).
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Ventricular Pacing in Atrial Fibrillation
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References
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American Heart Association Advanced Cardiac Life Support. (2006). CD ECG Image Index. ECG Learning Center (2008). Retrieved April 16, 2008 from http://library.med.utah.edu/kw/ecg/image_index/index.html#Sinus Fussell, D. (2008). Telemetry Study Guide. Lake City VA Medical Media, January 2008. Grauer, Ken, MD. ACLS: Practice Code Scenarios. (2008). Retrieved April 16, 2008 from ekgpress@mac.com 12 Lead ECG. (2008) Retrieved April 16, 2008 from http://www.sh.lsuhsc.edu/fammed/OutpatientManual/EKG/ecghome.html
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