1. Chapter 11 Interpretation of Electrocardiogram Tracings

2. Introduction
RTs observing the onset of an ischemic cardiac event may be the first link in the chain of survival
Early recognition of a serious cardiac problem may minimize cardiac damage or prevent death
Given the hands-on nature of respiratory care, the likelihood of a respiratory therapist (RT) observing a patient during the acute onset of an ischemic cardiac event or lethal dysrhythmia is high . Thus, it is vital for RTs to have basic knowledge in electrocardiogram (ECG) interpretation. The RT may serve as the first link in the chain of survival for a patient experiencing a cardiac arrest and represent an important part of the medical team providing management of the patient once stabilized. Early recognition of a serious cardiac problem may potentially minimize cardiac damage or prevent death due to a myocardial infarction. In addition, understanding the significance of the subtle and often progressive aspects of ECG changes enhances the RT’s assessment of a patient’s cardiopulmonary health and may help optimize interdisciplinary care planning.
 This chapter describes the electrophysiology of normal and abnormal ECG tracings. Ultimately, it is intended to explain how to recognize basic and life-threatening ECG patterns that may be observed while performing respiratory care. After a review of cardiac physiology related to the production of electrical activity within the heart, numerous abnormal rhythms (dysrhythmias) are described. Criteria for recognition and possible causes are reviewed for each abnormality presented.
An ECG (also called an EKG) is an indirect measurement of the electrical activity within the heart. A recording of the electrical currents within the heart is obtained by placing electrodes containing a conductive media to each extremity and to numerous locations on the chest wall to create a 12-lead ECG. Each specific position of an electrode provides a tracing referred to as a lead. The purpose of using 12 leads is to obtain 12 different views of the electrical activity in the heart and therefore a more complete picture.
Current standard of practice in most hospitals calls for patients at risk for cardiac events or dysrhythmias to be placed on continuous ECG monitoring using the three-lead or five-lead system. These systems use only three or five leads, placed on the patient’s chest, which is less cumbersome and allows for more patient mobility than the 10 leads placed on the chest and extremities for a 12-lead ECG. Although these modified systems do not provide the overview that a 12-lead ECG does, they do allow for the recognition of gross abnormalities in the electrical conduction of the heart. Identification of a rhythm abnormality on a three-lead or five-lead tracing often indicates the need to obtain a more detailed 12-lead view of the heart.
<1>WHAT IS THE VALUE OF AN ECG?
The ECG provides valuable information about the cardiac status of a patient presenting with signs and symptoms suggestive of heart disease. For example, if a patient presents with dyspnea and chest discomfort, an ECG can aid in the diagnosis of an ischemic cardiac event. In addition, the ECG may indicate an increased workload on the myocardium as a compensatory response to the chronic dysfunction of another body system, such as the respiratory system. Both acute and chronic conditions may have adverse effects on the heart. The severity of such effects (e.g., myocardial infarction, ventricular hypertrophy, or abnormal heart rhythms known as dysrhythmias) may be assessed on interpretation of the ECG. The ECG may also be used to monitor the heart’s response to treatment of an event that causes changes in the ECG. Therefore, several ECGs may be needed over the course of treatment.
It is important to note that the ECG tracing does not measure the pumping ability of the heart. It is not unusual for a patient with a low cardiac output to have a normal ECG tracing. This is because the ECG does not directly depict abnormalities in cardiac structure such as defects in the heart valves or interventricular septum. Another limitation worth noting is that the probability of any patient having an acute problem such as myocardial infarction generally cannot be predicted from a resting ECG tracing.

3. Introduction ECG reflects electrical activity of the heart
12-lead ECGs provide 12 different views of that activity
Diagnostic tool to detect abnormalities such as:
Myocardial infarctions
Ventricular hypertrophy
Dysrhythmias

4. When Should an ECG Be Obtained?
Obtain an ECG when there are signs/symptoms of acute or chronic cardiac disorders
CHF
Angina
Acute myocardial infarction
Prior to surgery as a screening tool
<1>WHEN SHOULD AN ECG BE OBTAINED?
Because an ECG is noninvasive and does not present a risk to the patient, it is reasonable to obtain an ECG whenever the patient has signs and symptoms suggestive of an acute or chronic cardiac disorder such as myocardial infarction or congestive heart failure (Box 11-1). Of course, the process of obtaining the ECG should never delay the initiation of critically needed care such as oxygen therapy, airway placement, or cardiopulmonary resuscitation (CPR).
An ECG is often used as a screening tool to determine the patient’s health status before major surgery. An ECG is especially helpful in this situation if the patient is older or has a history of heart disease. If an abnormality is identified, it may need to be treated before the operation is performed.

6. Cardiac Anatomy and Physiology
The heart is composed of 4 chambers
2 upper chambers: atria
2 lower chambers: ventricles
Heart divided down the middle to form the right and left side
CARDIAC ANATOMY AND PHYSIOLOGY
Before discussing the interpretation of ECGs, it is important to review the cardiac anatomy and physiology related to electrical activity within the heart. The heart is made up of four chambers: two upper chambers called atria and two lower chambers called ventricles (Figure 11-1). The heart typically is described as having two sides, the right and the left. The right atrium receives deoxygenated blood from the venae cavae and directs the blood into the right ventricle. Right ventricular contraction ejects blood into the pulmonary artery, which carries blood to the lungs for oxygenation. The oxygenated blood returns to the left atrium of the heart via the pulmonary veins, where it is directed into the left ventricle. Left ventricular contraction ejects blood into the aorta, which branches off into the systemic circulation. Since the left side of the heart pumps blood throughout the entire body, it normally has a significantly larger muscle mass than the right side.
Cardiac muscle is referred to as the myocardium. Myocardial contraction occurs as a response to electrical stimulation. For the heart to move blood effectively, stimulation of the myocardium must be coordinated. Initiating and coordinating the electrical stimulation of the myocardium is the responsibility of the electrical conduction system, which is made up of special pacemaker and conducting cells (Table 11-1).

7. Cardiac Anatomy and Physiology
Right atria and ventricle receive venous blood and circulate it to the lungs for gas exchange
Left atria and ventricle receive oxygenated blood from lungs and circulate it to entire body

9. Conduction Pathway in the Heart
Electrical activity starts in the sinoatrial (SA) node because it has the greatest level of automaticity
Signal travels throughout atria and via internodal pathways to atrioventricular (AV) node
Normally, the electrical activity of the heart is initiated in the sinus or sinoatrial (SA) node located in the right atrium (Figure 11-2). The SA node is a collection of specialized cells capable of spontaneously generating electrical signals. Cells that have the ability to generate electrical activity spontaneously are said to have automaticity. Because the SA node normally has the greatest degree of automaticity of all the cardiac cells, it usually controls the rate at which the heart beats. In this way, the SA node serves as the primary pacemaker of the heart, discharging at about 60 to 100 beats/min at rest.
The SA node is strongly influenced by the autonomic nervous system. For this reason, the rate at which the SA node fires can vary significantly. Increased activity of the sympathetic system increases the heart rate. Stimulation of the sympathetic ­system occurs with stress, anxiety, exercise, hypoxemia, and the administration of certain medications. On the other hand, slowing of the heart rate occurs due to vagal stimulation, which is a parasympathetic response.
Once the SA node initiates the electrical signal, the impulse spreads across the atria in a wavelike fashion. The electrical impulse travels through the atria by way of the internodal pathways, causing depolarization and then contraction. Contraction of the atria just before ventricular contraction (systole) aids in filling the ventricles with blood and accounts for about 10% to 30% of subsequent stroke volume. This atrial contraction is often referred to as the atrial kick.
After the electrical impulse passes through the atria, it reaches the atrioventricular (AV) junction. This junction acts as an electrical bridge between the atria and the ventricles. The AV junction contains the AV node and the bundle of His (see Figure 11-2). Once the electrical impulse reaches the AV node, it is delayed for approximately 0.1 second before passing on into the bundle of His. The delay is believed to serve the purpose of allowing more complete filling of the ventricles before ventricular contraction. In addition, the AV node can protect the ventricles from excessively rapid atrial rates that the ventricles could not tolerate. Damage to the AV junction, as may occur with a myocardial infarction, usually leads to excessive delays of the electrical impulse passing into the ventricles. This causes a condition known as heart block.
The AV junction normally guides only the electrical impulse from the atria into the ventricles. Under certain circumstances, however, it can also serve as the backup pacemaker. The AV junction has automaticity qualities similar to those of the SA node. If the SA node fails to function properly and does not pace the heart, the AV junction can serve as the pacemaker for the ventricles. When this occurs, the ventricular rate is usually between 40 and 60 beats/min and the ECG reveals a distinct pattern, described later in this chapter (Figure 11-3).
After the electrical impulse leaves the AV node, it travels rapidly through the bundle of His and then into the left and right bundle branches (see Figure 11-2). The stimulus travels simultaneously through the bundle branches into the myocardium. At the end of the bundle branches are countless fingerlike projections called Purkinje fibers. The Purkinje fibers pass the electrical impulse rapidly throughout the myocardium to create a coordinated contraction of the left and right ventricles.
Because most of the cardiac cells have automaticity characteristics, the heartbeat may be paced by heart tissue other than the SA node. When this occurs, it often indicates that the SA node is not functioning normally or that myocardial tissue is irritated. Any impulse that originates outside the SA node is called an ectopic impulse, and the site from which the ectopic impulse originates is called the focus. Ectopic impulses can originate from foci in either the atria or the ventricles. When the ectopic impulse results from depression of the normal impulse origin, it is called an escape beat.
The myocardium must receive a constant supply of oxygen and nutrients to pump blood effectively. Oxygen and nutrients are supplied to the myocardium via the left and right coronary arteries and their branches. The main coronary arteries arise from the ascending aorta and direct arterial blood into branches that feed various regions of the heart. Blockage of one or more of the coronary vessels leads to regionalized ischemia and tissue death (infarction). The size and location of the region affected by the coronary vessel blockage determines the resulting physiologic and clinical impact. Infarction of a major portion of the left ventricle is likely to cause significant arterial hypotension, abnormal sensorium, and a backup of blood into the pulmonary circulation. Infarction of the tissues associated with pacing the heart (e.g., the SA or AV junction) can lead to significant dysrhythmias and diminished blood flow to all regions of the body.

10. Conduction Pathway
Signal delayed in AV node to allow atrial contraction prior to ventricular contraction
Then travels through right and left bundle branches and to Purkinje fibers of the ventricles

12. Basic ECG Waves
Depolarization: sudden loss of negative charge in polarized cells when stimulated
Repolarization: return of the negative charge within the cell

13. Basic ECG waves
ECG tracings record the waves of depolarization and repolarization traveling across the myocardium
Each wave can be identified and analyzed

14. ECG Waves P wave: atrial depolarization
PR interval: time for impulse to travel to ventricles:
Normally 0.12 to 0.20 second
Allows atrial contraction and “priming of the pump” to precede ventricular contraction

15. Basic ECG Waves QRS complex: ventricular depolarization
Normally occurs in <0.12 second
ST segment: between QRS and T wave
T wave: ventricular repolarization

16. Basic ECG Waves
Depolarization of the atria creates the initial wave of electrical activity detected on the ECG tracing, known as the P wave (Figure 11-5). Because the atria usually are small, the atria generate less voltage than the ventricles and the resulting P wave is small. Repolarization of the atria is not seen on the ECG because it usually is obscured by the simultaneous depolarization of the ventricles.
Depolarization of the ventricles is represented by the QRS complex. Because the ventricular muscle mass is larger than the atria and produces more voltage during depolarization, the QRS complex is normally taller than the P wave in most cases (see Figure 11-5). Ventricular repolarization is seen as the T wave. The T wave is normally upright and rounded.
Just after the T wave but before the next P wave, a small deflection known as the U wave is sometimes seen. The U wave is thought to represent the final phase of ventricular repolarization. In most cases the U wave is not seen. The clinical significance of its presence or absence is not known.

17. Evaluating heart rate (HR)
If HR regular, count number of large boxes (0.2 sec) between QRS complexes and divide this number into 300
300: number of large boxes occurring in 1 minute
1 box between QRS would be rate of 300
2 boxes between would be rate of 150 etc.

18. Evaluating HR
If HR irregular, average obtained by counting QRS complexes in a 6-sec strip times 10

19. ECG Leads 12-lead ECG provides different views of same event
6 limb leads:
I, II, III, aVR, aVL, aVF
View heart on frontal plane used to determine axis
6 chest leads:
V1, V2, V3, V4, V5, V6
View the heart on the horizontal plane
Overlie the RV (V1, V2), ventricular septum (V3, V4) and LV (V5, V6 )
ECG LEADS
Because the heart is a three-dimensional organ, a more complete picture of the electrical activity in the heart will be obtained if it is viewed from several different angles. The standard ECG uses 12 different leads to provide 12 different views from different angles of the heart. Interpretation of the 12 leads is a little more difficult, but the information obtained is more complete and abnormalities are not likely to be missed.
The 12 leads can be subdivided into two groups: six extremity (limb) leads and six chest leads. To obtain the six limb leads, two electrodes are placed on the patient’s wrists and two on the patient’s ankles. The ECG machine can vary the orientation of these four electrodes to one another to create the six limb leads. The chest leads are created by attaching six electrodes across the patient’s chest. The chest leads are discussed after the limb leads are reviewed.
Limb Leads
The six limb leads are called leads I, II, III, aVR, aVL, and aVF. Leads I, II, and III are bipolar. Each lead is created by comparing the difference in electrical voltage between two electrodes. For lead I, the ECG machine temporarily designates the electrode on the left arm as a positive lead and the electrode on the right arm as negative. The measured difference in voltage between these two leads results in lead I. For lead II, the right arm electrode remains negative and the left leg electrode is positive. Lead III is created by making the left arm negative and the left leg positive.
The other three limb leads (aVR, aVL, and aVF) are called augmented leads because the ECG machine must amplify the tracings to get an adequate recording. This is because the augmented leads are created by measuring the electrical voltage at one limb lead, with all other limb leads made negative. For the augmented leads, the ECG machine must augment the recorded voltages by about 50% to get an adequate recording. Lead aVR is created by making the right arm positive and all the others negative. Lead aVL calls for the left arm to be positive, and lead aVF is created by making the left leg positive.
The six limb leads view the heart in a vertical plane called a frontal plane. Any electrical activity that is directed up, down, left, or right is recorded by the limb leads (Figure 11-10). The frontal plane can be envisioned as a giant circle that surrounds the patient and lies in the same plane as the patient. This circle can be marked off in 360 degrees, as shown in Figure
The angle of orientation for each of the bipolar limb leads can be determined by drawing a line from the designated negative lead to the designated positive lead. For lead I, the angle of orientation is 0 degrees; for lead II, +60 degrees; and for lead III, +120 degrees. For the augmented leads, the angle of orientation can be determined by drawing a line from the average of the other three limb leads to the one that is designated as the positive lead. The angle of orientation is -150 degrees for lead aVR, -30 degrees for lead aVL, and 90 degrees for lead aVF.
In review, the limb leads consist of three bipolar leads and three unipolar leads. The three bipolar leads are called leads I, II, and III. The three unipolar leads are called aVR, aVL, and aVF. The abbreviation a refers to augmented, V to voltage, and R, L, and F to right arm, left arm, and left leg, respectively. The limb leads measure the electrical activity in the heart that occurs in the frontal plane, and each lead has its own specific view or angle of orientation to the heart (Table 11-2).
Chest Leads
The six chest leads, or precordial leads, are called leads V1, V2, V3, V4, V5, and V6. The chest leads are unipolar leads that are placed across the chest in a horizontal plane (Figure 11-11). The chest leads define a horizontal or transverse plane and view electrical voltages that move anteriorly and posteriorly. Like the limb leads, each chest lead has its own view or angle of orientation. Under normal conditions, leads V1 and V2 lie directly over the right ventricle, V3 and V4 lie over the interventricular septum, and V5 and V6 lie over the left ventricle. In addition, leads V1through V4 often are called the anterior leads because they view the anterior portion of the heart. Leads V5 and V6 view the left lateral portion of the heart and are therefore called the left lateral leads (see Table 11-2).

20. Steps of ECG Interpretation
First evaluate patient’s overall condition
Clinical signs and symptoms may aid in identifying the dysrhythmia
Interpretation can be done on three levels
Ventricular response
Origin of the impulse
Electrophysiology
Ectopic beats or rhythms, escape beats or rhythms
AV blocks or bundle branch blocks
First and most importantly, the patient’s condition must be evaluated. All dysrhythmias should be interpreted and evaluated in accordance with the patient’s clinical presentation and medical history. Important signs and symptoms that may be associated with dysrhythmias may include:
Chest pain
Dyspnea
Fine, inspiratory crackles in the lower lobes
Palpitations
Nausea
Pale, cool clammy skin
Dizziness or syncope
Sense of impending doom
Hypotension
Altered level of consciousness
Interpretation of dysrhythmias can be accomplished on three levels. The first level is simply identifying ventricular response. The contraction of the ventricles determines the majority of the cardiac output and perfusion of blood to the tissues. The ventricular response is determined by evaluating the QRS complexes and subsequent pulse strength.
Second, dysrhythmias can be placed into categories based on the origin of the impulse formation, which may include:
Atrial
Junctional
Ventricular
Third, dysrhythmias can be evaluated based on the electrophysiology (or pathway) of the conduction disturbance. These can be categorized as:
Ectopic beats or rhythms
Escape beats or rhythms
AV blocks
Bundle branch blocks

21. Steps of ECG Interpretation
Use a systematic method:
Identify the heart rate
Evaluate the rhythm
Note the presence of P waves
Measure the PR interval
Measure the width of the QRS complex
Inspect the ST segment in all leads
Identify the mean QRS axis
Assess the waveform morphology
Evaluate the Q wave
Look for signs of chamber enlargement
To make sure that all components of the ECG tracing are covered, use a systematic method. Read every strip from left to right and apply the stepwise process as described below. It is important to avoid assumptions as glancing at a strip may lead to misinterpretation. The steps are as follows:
1.Identify the heart rate. Most modern ECG monitors provide a display of the heart rate. Always take the patient’s pulse to verify that the monitor is calculating the heart rate correctly. Note that the monitor may not provide an accurate rate if the rhythm is irregular. If this is the case, a strip should be printed and calculation should be done as mentioned in the “Evaluating Heart Rate” section of this chapter. Rhythms are called bradycardia if the rate is below 60 beats/min and tachycardia if the heart rate is over 100 beats/min.
2.Evaluate the rhythm. Note whether the spacing between the QRS complexes is equal. Small variations of 0.04 second (40 msec) are considered normal. If the spaces are greater than 0.04 second, the rhythm is irregular. Irregularity may occur randomly or in patterns (e.g., occur every other beat or change with respirations). Irregular rhythms are present with the following dysrhythmias:
Ectopic beats
Escape beats
Second-degree AV blocks
Atrial fibrillation
Sinus dysrhythmia
3.Note the presence of P waves. A normal P wave generally is positive, depending on the lead, and round in shape. Normal P waves are less than 0.11 second (110 msec) wide and less than 2.5 mm (2 ½ small boxes) tall. Oddly shaped P waves may indicate atrial enlargement. Normal rhythms will only have one P wave preceding each QRS complex, and each P wave should have the same configuration as the others. If there appears to be more than one P wave preceding a QRS complex, the rhythm may be:
Atrial flutter
Atrial fibrillation (each P wave will have a different configuration)
Second-degree AV block
Third-degree AV block
4.Measure the PR interval. The normal PR interval is 0.12 to 0.20 second (120 to 200 msec) wide. A PR interval that is wider than 0.20 second indicates a delay in conduction through the AV node, indicating the possibility of a block (see Table 11-4).
5.Measure the width of the QRS complex. The normal QRS complex is less than 0.12 second (120 msec) wide. Wide QRS complexes can occur with:
Bundle branch blocks
Ectopic beats originating in the ventricles (premature ventricular contractions)
Ventricular dysrhythmias such as ventricular tachycardia, idioventricular rhythm, or premature ventricular complexes
6.Inspect the ST segment in all leads. ST segment elevation may indicate myocardial injury whereas ST segment depression may indicate myocardial ischemia. The portion or wall of the heart that is ischemic can be determined by identifying the leads looking at that portion of the heart (see Table 11-4). The ST segment is measured from the J point: the junction between the QRS complex and the ST segment (see Figure 11-8).
7.Identify the mean QRS axis. Most modern 12-lead ECG tracings indicate the QRS axis. Normal axis is 0 to +90 degrees. Left axis deviation is 0 to -90 degrees, and right axis deviation is +90 to 180 degrees (see Figure and Table 11-3). Box 11-3 lists causes of axis deviation.
8.Assess the waveform morphology. Some QRS complexes may have additional deflections. If there is a second deflection, the second portion is called prime (see Figure 11-6). For example, a second R wave would be labeled R’.
9.Evaluate the Q wave. A Q wave is considered normal (or physiologic) if it is less than 0.04 second (40 msec) wide and less than one third the amplitude of the R wave. Q waves that exceed either of these values are considered pathologic and indicate a new or possibly old infarction.
10. Look for signs of chamber enlargement. High-voltage R waves in the precordial leads indicate ventricular hypertrophy. Large or abnormally shaped P waves indicate atrial enlargement (see review later in this chapter).

22. Sinus Bradycardia Meets all the criteria for NSR but is too slow
Rate: less than 60 beats/min
Rhythm: regular
P waves: normal and followed by a QRS complex
PR interval: 0.12 to 0.2 second
QRS: less than 0.12 second in width

23. Sinus Tachycardia Meets all criteria for NSR but is too fast
Rate: 100 to 150 beats/min
Rhythm: regular
P waves: normal and followed by a QRS complex
PR interval: 0.12 to 0.2 second
QRS: less than 0.12 second in width
Sinus tachycardia is present when the heart rate is beats/min, the SA node is the pacemaker, and all the normal conduction pathways in the heart are followed. Sinus tachycardia may be well-tolerated by the patient; however, it increases myocardial oxygen demand and decreases the diastolic period, both of which can lead to myocardial ischemia. Sinus tachycardia results from sympathetic nervous system stimulation and may indicate a significant physiologic problem or be self-limiting and cease once the underlying cause is addressed. Fever, pain, hypoxemia, hypovolemia, hypotension, sepsis, and heart failure are causes of sinus tachycardia. Tracheal suctioning, especially if it is performed without adequate oxygenation before, during, and after each catheter insertion, can cause sinus tachycardia. In addition, many β-agonist bronchodilators and excessive intake of caffeine often increase heart rate.

24. Atrial Flutter Distinct rapid sawtooth pattern between normal QRS
Rate: atrial rates 180 to 400; ventricular rate is slower
Rhythm: regular
P waves: sawtooth and uniform
PRI: not measurable
QRS: less than 0.12 second in width
Atrial flutter is a dysrhythmia that produces a very distinctive ECG pattern, usually caused by a rapidly firing ectopic site in the atria that presents as a characteristic sawtooth pattern between normal-appearing QRS complexes. The sawtooth pattern of flutter waves (often referred to as F waves) represents the rapid flutter or contraction of the atria upon stimulation by a reentry circuit or accelerated automaticity. Atrial flutter results in diminished atrial “filling time,” which results in minimal atrial assistance in filling the ventricles. Recall that the term atrial kick refers to the contraction of the atria forcing out blood at the latter part of systole and results in about 10% to 30% of cardiac output in a healthy person, but will be diminished in atrial flutter. A secondary problem with atrial flutter is that the pattern of blood flow in the atria causes areas of diminished blood movement near the atrial walls. This stagnation of blood promotes the formation of thrombi, often referred to as mural thrombi, along the wall of the atria. The patient is then at risk for embolization caused by the migration of a mural thrombus.
Atrial flutter usually is a short-lived dysrhythmia; it usually deteriorates to atrial fibrillation or the patient’s previous rhythm returns spontaneously. Some possible causes of atrial flutter may include valvular heart disease, myocardial infarction, hypertensive heart disease, cardiomyopathy, myocarditis, and pericarditis.

25. Atrial Fibrillation Characterized by chaotic baseline between QRSs
Rate: variable (count QRSs in 6-second strip)
Rhythm: irregularly irregular
P waves: fibrillatory waves that all vary
PRI: not measurable
QRS: less than 0.12 second in width
In atrial fibrillation, the electrical activity of the atria is completely chaotic and without coordination because it is arising from multiple ectopic sites within the atria. This results in a quivering of the atrial myocardium and complete loss of atrial pumping ability. Because the atria provide useful assistance in filling the ventricles from the atrial kick, there is a decrease in ventricular filling during atrial fibrillation. In most cases, the reduction in cardiac output is not serious enough to produce symptoms, although it reduces cardiac reserve and may limit the normal activities of daily living. Atrial fibrillation carries an even higher risk of mural thrombi formation and embolization than atrial flutter. Some possible causes of atrial fibrillation include all of those mentioned under atrial flutter but may also include hyperthyroidism, pulmonary disease, and congenital heart disease.
The ECG tracing shows a chaotic baseline between QRS complexes, with no regular pattern or organization. This irregular baseline is composed of what are called fibrillatory waves (f waves) that all have a different configuration due to their origin from different ectopic sites in the atria.
Systematic Evaluation (Figure 11-18):
Atrial Rate: Difficult to determine
Ventricular Rate: Varies, but is always less than the atrial rate
Rhythm: Irregularly irregular
P Waves: Fibrillatory waves (f waves) all having a different configuration. The relationship between the fibrillatory waves and the QRS complexes is irregular.
PR Interval: Not measurable
QRS Complex: Less than 0.12 second in width

26. Premature Ventricular Contractions
Underlying rhythm is interrupted by wide QRS (>0.12 s) not preceded by a P wave, with an inverted T
Rate: that of the underlying rhythm
Rhythm: regular rhythm is interrupted by PVC
P waves: not associated with the PVC
PR interval: not measurable
QRS: >0.12 second, premature, abnormal configuration, followed by compensatory pause
Premature ventricular contractions (PVCs) represent ectopic beats originating in one of the ventricles due to enhanced automaticity. PVCs occur in both the normal and the diseased heart. PVCs commonly occur with anxiety or excessive use of caffeine, alcohol, or tobacco. Certain medications such as epinephrine and theophylline may also provoke PVCs in patients with normal hearts. Myocardial ischemia is a common cause of PVCs in patients with heart disease. Other causes may include acidosis, electrolyte imbalance, congestive heart failure, myocardial infarction, and hypoxia.
A single PVC poses no threat to the patient (Figure 11-19), but certain configurations of PVCs may signal a serious cardiac problem that may need immediate treatment. Although the idea that PVCs are “warning” dysrhythmias has not been proved by clinical research, the following conditions warrant further investigation and indicate the need for close monitoring of the patient:
Increased frequency: Multiple PVCs occur in 1 minute (Figure 11-20)
Multifocal PVCs: The QRS complexes of the PVCs have more than one configuration (Figure 11-21); this indicates that more than one area of the ventricles is irritated.
Couplets: Two PVCs occur in a row.
Salvos: Three or more PVCs occur in a row (sometimes called a short run of ventricular tachycardia).
R-on-T phenomenon: The PVC occurs during the T wave of the preceding beat; this poses a real danger because it can precipitate ventricular tachycardia (Figure 11-22).
Systematic Evaluation (see Figure 11-19):
Rate: That of the underlying rhythm
Rhythm: Underlying rhythm is usually regular but irregular with a PVC
P Waves: None associated with the PVC
PR Interval: Not measurable
QRS Complex: More than 0.12 second in width, abnormal configuration, and premature. T wave following the PVC is deflected in a direction opposite to that of the QRS complex. There is a full compensatory pause following the PVC confirmed by measuring the interval between the normal QRS complex immediately before the PVC and the normal QRS complex immediately after the PVC; it will be double the normal RR interval for that patient.

27. PVC

28. Ventricular Tachycardia
Wide QRSs occurring rapidly without P waves
Rate: 140 to 300 beats/min
Rhythm: regular
P waves: not associated with the QRS complexes
PR interval: not measurable
QRS: abnormal and >0.12 second
Ventricular tachycardia appears on the monitor as a series of broad QRS complexes, occurring at a rapid rate, without identifiable P. This condition originates from an ectopic focus in the ventricles associated with enhanced automaticity or reentry. By definition, ventricular tachycardia is a run of three or more consecutive PVCs. It may be classified as sustained which lasts more than 30-seconds and requires immediate medical attention or non-sustained ventricular tachycardia which terminates spontaneously after a short burst. The rhythm is regular, and the rate is usually in the range of 140 to 300 beats/min. The majority of patients deteriorate rapidly with this dysrhythmia; therefore, it must be treated as an emergency. Without appropriate treatment, sustained ventricular tachycardia may lead to ventricular fibrillation (described later). When ventricular tachycardia occurs, the patient may become hypotensive and be slow to respond. If cardiac output deteriorates significantly, the patient usually becomes unresponsive. Ventricular tachycardia is often caused by problems similar to those that cause PVCs. When the heart is hypoxic, as occurs with severe myocardial ischemia, ventricular tachycardia is common and is a sign that the patient needs ­immediate care.
Systematic Evaluation (Figure 11-23):
Rate: 140 to 300 beats/min
Rhythm: Regular
P Waves: None associated with the QRS complex. They may occasionally occur because the SA node is still functioning.
PR Interval: Not measurable
QRS Complex: Abnormal and greater than 0.12 second in width

29. V-Tach

30. Ventricular Fibrillation
Chaotic, characterized by wavy irregular pattern
Rate: none
Rhythm: irregular, chaotic waves
P waves: none
PRI: none
QRS: none or sporadic low-amplitude waves
Ventricular fibrillation is the presence of chaotic, completely unorganized electrical activity in the ventricular myocardial fibers. It produces a characteristic wavy, irregular pattern on the ECG monitor. Depending on the amplitude of the electrical impulses, it can be mistaken for asystole or ventricular tachycardia. Because the heart cannot pump blood when fibrillation is occurring, the cardiac output drops to zero and the patient becomes unconscious immediately. This dysrhythmia is life threatening and must be treated immediately in accordance with the Advanced Cardiovascular Life Support (ACLS) protocol including defibrillation. Ventricular fibrillation often is caused by the same factors that precipitate ventricular tachycardia.
Systematic Evaluation (Figure 11-24):
Rate: None
Rhythm: Irregular, chaotic waves
P Waves: None
PR Interval: None
QRS Complex: No waves appear with any regularity on the ECG tracing. There may be occasional low-amplitude waves that appear somewhat like ventricular-origin complexes, but they are sporadic in occurrence and totally irregular.

31. V-Fib

32. Asystole Characterized by a straight or almost flat line Rate: none
Rhythm: none
P waves: none
PRI: none
QRS: none
Asystole is cardiac standstill and is invariably fatal unless an acceptable rhythm is rapidly restored. In fact, asystole is one of the criteria used for the determination of clinical death. Asystole is recognizable on the ECG monitor as a straight or almost straight line. The bedside clinician must take care to assess the patient with what appears to be asystole before initiating therapy because a simple disconnection of the ECG leads can resemble asystole. Clinically, asystole is characterized by immediate pulselessness and loss of consciousness. The ECG tracing shows a line that is flat or almost flat, without discernible electrical activity (Figure 11-25).

33. AV Heart Block
General term: problems conducting impulses from the atrial to the ventricles
Blocks can occur at the AV node, bundle of His, or the bundle branches
Complete heart block may be associated with hypotension
Milder forms of heart block often cause no symptoms
 AV heart block is a general term that refers to a disturbance in the conduction of impulses from the atria to the ventricles through the AV node. However, the block may be at the level of the AV node or the bundle of His or in the bundle branches. Classification of the AV blocks is based on the site of the block and the severity of the conduction disturbance.
Disturbances in AV conduction can occur as an adverse effect of medications such as digitalis, or when damage to the conduction system occurs with myocardial infarction. In some cases of complete heart block, the patient may develop symptoms associated with hypotension (fainting and weakness) if the ventricles are beating too slowly. In milder forms of heart block, the patient often is asymptomatic.

34. First-Degree AV Block Rate: underlying rhythm rate Rhythm: regular
P waves: normal each preceding a QRS complex
PRI: >0.2 second* (Key Feature)
QRS: < 0.12 second in width
The mildest form of heart block is first-degree block, which is present when the PR interval is prolonged more than 0.2 second. In first-degree block, all the atrial impulses pass through to the ventricles but are delayed at the AV node. First-degree AV block may or may not compromise cardiac output. It is important to assess the patient as discussed earlier in the section on steps of ECG interpretation. Some potential causes of first-degree AV block include adverse effects of medications such as digitalis, increased vagal tone, hyperkalemia, myocarditis, and degenerative disease.
Systematic Evaluation (Figure 11-26):
Rate: Underlying rhythm rate
Rhythm: Regular
P Waves: Normal sinus configuration, each preceding a QRS complex
PR Interval: Greater than 0.20 second in length and constant
QRS Complex: Less than 0.12 second in width

35. Second-Degree AV Block Type I (Wenckebach)
Recurrent lengthening PRI followed by a dropped QRS
Rate: varies, ventricular rate less than atrial rate
Rhythm: irregular
P waves: normal not always followed by a QRS
PR interval: varies, lengthens, then none conducted
QRS: < 0.12 second in width
Second-degree AV block type I, also known as Wenckebach, is an intermediate form of heart block that presents with a PR interval that becomes ­progressively longer (changes in length) until the stimulus from the atria is blocked completely for a single cycle (dropped QRS complex). After the blocked beat, relative recovery of the AV junction occurs, and the progressive increasing of the PR interval starts all over again. The ventricular rhythm is almost always irregular. As with first-degree AV block, second-degree AV block type I may or may not compromise cardiac output; thus, it is important to assess the patient in conjunction with rhythm interpretation. Causes of second-degree AV block type I are similar to those of first-degree AV block.
Systematic Evaluation (Figure 11-27, A):
Rate: Varies, but ventricular rate is always less than the atrial rate
Atrial Rhythm: Regular
Ventricular Rhythm: Irregular
P Waves: Normal sinus configuration, not always followed by QRS complex
PR Interval: Varies, lengthening, and then dropping a QRS complex
QRS Complex: Less than 0.12 second in width

36. Second-Degree AV Block Type I (Wenckebach)
Second-degree AV block type I, also known as Wenckebach, is an intermediate form of heart block that presents with a PR interval that becomes ­progressively longer (changes in length) until the stimulus from the atria is blocked completely for a single cycle (dropped QRS complex). After the blocked beat, relative recovery of the AV junction occurs, and the progressive increasing of the PR interval starts all over again. The ventricular rhythm is almost always irregular. As with first-degree AV block, second-degree AV block type I may or may not compromise cardiac output; thus, it is important to assess the patient in conjunction with rhythm interpretation. Causes of second-degree AV block type I are similar to those of first-degree AV block.
Systematic Evaluation (Figure 11-27, A):
Rate: Varies, but ventricular rate is always less than the atrial rate
Atrial Rhythm: Regular
Ventricular Rhythm: Irregular
P Waves: Normal sinus configuration, not always followed by QRS complex
PR Interval: Varies, lengthening, and then dropping a QRS complex
QRS Complex: Less than 0.12 second in width 36

37. Second-Degree AV Block Type II
Characterized by nonconducted P waves followed by a P wave that is conducted thus has an associated QRS
Rate: varies, ventricular rate less than atrial rate
Rhythm: atrial rate is regular, ventricular rate may be regular or irregular
P waves: normal not always followed by a QRS
PR interval: normal or prolonged but constant
QRS: < 0.12 second in width
Second-degree AV block type II is a rarer but more serious form of second-degree AV block and is characterized by a series of nonconducted P waves followed by a P wave that is conducted to the ventricles. It is important to note that each time the P wave is followed by a QRS complex, the PR interval is always fixed (not changing in length). This will help differentiate between the two types of second-degree AV block. Sometimes the ratio of nonconducted to conducted P waves is fixed (at 3:1 or 4:1, for example). This block should be considered serious and treated promptly. Common causes of second-degree AV block type II include extensive damage to the bundle branches after an acute anteroseptal myocardial infarction or degenerative disease.
Systematic Evaluation (see Figure 11-27, B):
Rate: Varies, but ventricular rate is always less than the atrial rate
Atrial Rhythm: Regular
Ventricular Rhythm: May be regular if there is a constant conduction ratio or irregular if conduction is not constant
P Waves: Normal sinus configuration, not always  followed by QRS complex
PR Interval: Normal or prolonged but always constant
QRS Complex: Less than 0.12 second in width

38. Second-Degree AV Block Type II
Second-degree AV block type II is a rarer but more serious form of second-degree AV block and is characterized by a series of nonconducted P waves followed by a P wave that is conducted to the ventricles. It is important to note that each time the P wave is followed by a QRS complex, the PR interval is always fixed (not changing in length). This will help differentiate between the two types of second-degree AV block. Sometimes the ratio of nonconducted to conducted P waves is fixed (at 3:1 or 4:1, for example). This block should be considered serious and treated promptly. Common causes of second-degree AV block type II include extensive damage to the bundle branches after an acute anteroseptal myocardial infarction or degenerative disease.
Systematic Evaluation (see Figure 11-27, B):
Rate: Varies, but ventricular rate is always less than the atrial rate
Atrial Rhythm: Regular
Ventricular Rhythm: May be regular if there is a constant conduction ratio or irregular if conduction is not constant
P Waves: Normal sinus configuration, not always  followed by QRS complex
PR Interval: Normal or prolonged but always constant
QRS Complex: Less than 0.12 second in width 38

39. Third-Degree AV Block (Complete Heart Block)
No association between P waves and QRS complexes
Rate: slow, ventricular rate less than atrial rate
Rhythm: atrial and ventricular rates are regular
P waves: normal not always followed by a QRS
PRI: varies, no relationship to QRS complexes
QRS: generally but not always >0.12 second
The most extreme form of heart block is third-degree AV block, which is caused by conduction disturbances below the AV node in the bundle of His (producing a narrow QRS complex) or bundle branches (producing a wide QRS complex). This block does not allow any conduction of stimuli from the atrium to the ventricles. In this situation, the ventricles and atria beat independently of one another. Thus there is no distinguishable pattern between the atria and ventricles. Third-degree AV block may be transient or permanent but is always considered serious and should prompt immediate intervention. Possible causes of transient third-degree AV block may include inferior myocardial infarction, increased vagal tone, myocarditis, and digitalis toxicity. Permanent causes may include degenerative disease or acute anteroseptal myocardial infarction.
Systematic Evaluation (Figure 11-28):
Rate: Usually less than 60 beats/min but may vary; ventricular rate is always less than the atrial rate
Rhythm: Both atrial and ventricular rates are regular
P Waves: Normal sinus configuration, not always followed by QRS complex
PR Interval: Varies, no relationship
QRS Complex: Usually greater than 0.12 second but may also be less than 0.12 second in width

41. Evidence of Cardiac Ischemia, Injury, or Infarction
Indicated by depressed ST segment (≥1 mm below baseline) or inversion of the T waves
Injury is potentially reversible at this point
Normally the ST segment is isoelectric, meaning that it is in the same horizontal position as the baseline, isoelectric line. Significant deviations (1 mm) of the ST segment from baseline, either up or down, suggest an abnormality in myocardial perfusion and oxygenation.
Cardiac ischemia is seen on the ECG as depression of the ST segment (Figure 11-31) or inversion of the T waves. At this point, there is no permanent damage to the heart, and proper therapy usually reverses any ECG abnormalities. In many cases of myocardial infarction, however, this pattern of ischemia may not be seen because the event has already progressed to the injury phase.
The typical pattern of acute myocardial injury is ST segment elevation in the leads that reflect electrical activity of the corresponding injured heart tissue (Figure 11-32). For example, an acute myocardial injury to the anteroseptal part of the heart will cause ST segment elevation in the leads that examine the anteroseptal portion of the heart (see Table 11-4; Figure 11-33). In general, the degree of damage to the heart caused by the ischemia determines the degree of ST segment elevation. The ST segment abnormality usually resolves when perfusion is restored. At some point after myocardial infarction, significant Q waves (0.04 second in length) will be seen on the ECG in the corresponding leads. Q waves may develop within hours of an infarction but may not evolve for several days in some patients. They persist for the remainder of the patient’s life.
It can be helpful to identify ST segment abnormalities by drawing a straight line over the imaginary isoelectric line. This will reveal whether ST segment elevation or depression is present and to what degree. If the deviation from the isoelectric line is greater than 1 mm, significant changes have occurred and further investigation is appropriate. The patient should be monitored closely when this abnormality is ­identified.

42. Evidence of Cardiac Ischemia, Injury, or Infarction
Acute myocardial injury
Noted by elevated ST segment changes over the affected myocardium
Generally indicates acute myocardial infarction
ST segment returns to baseline with restored perfusion
Normally the ST segment is isoelectric, meaning that it is in the same horizontal position as the baseline, isoelectric line. Significant deviations (1 mm) of the ST segment from baseline, either up or down, suggest an abnormality in myocardial perfusion and oxygenation.
Cardiac ischemia is seen on the ECG as depression of the ST segment (Figure 11-31) or inversion of the T waves. At this point, there is no permanent damage to the heart, and proper therapy usually reverses any ECG abnormalities. In many cases of myocardial infarction, however, this pattern of ischemia may not be seen because the event has already progressed to the injury phase.
The typical pattern of acute myocardial injury is ST segment elevation in the leads that reflect electrical activity of the corresponding injured heart tissue (Figure 11-32). For example, an acute myocardial injury to the anteroseptal part of the heart will cause ST segment elevation in the leads that examine the anteroseptal portion of the heart (see Table 11-4; Figure 11-33). In general, the degree of damage to the heart caused by the ischemia determines the degree of ST segment elevation. The ST segment abnormality usually resolves when perfusion is restored. At some point after myocardial infarction, significant Q waves (0.04 second in length) will be seen on the ECG in the corresponding leads. Q waves may develop within hours of an infarction but may not evolve for several days in some patients. They persist for the remainder of the patient’s life.
It can be helpful to identify ST segment abnormalities by drawing a straight line over the imaginary isoelectric line. This will reveal whether ST segment elevation or depression is present and to what degree. If the deviation from the isoelectric line is greater than 1 mm, significant changes have occurred and further investigation is appropriate. The patient should be monitored closely when this abnormality is ­identified.

43. Evidence of Cardiac Ischemia, Injury, or Infarction
Myocardial infarction
Noted early by elevated ST segments and T wave changes
Once fully evolved pathologic Q waves appear
Appear hours to days following AMI
Generally remain for the duration of patient’s life
Normally the ST segment is isoelectric, meaning that it is in the same horizontal position as the baseline, isoelectric line. Significant deviations (1 mm) of the ST segment from baseline, either up or down, suggest an abnormality in myocardial perfusion and oxygenation.
Cardiac ischemia is seen on the ECG as depression of the ST segment (Figure 11-31) or inversion of the T waves. At this point, there is no permanent damage to the heart, and proper therapy usually reverses any ECG abnormalities. In many cases of myocardial infarction, however, this pattern of ischemia may not be seen because the event has already progressed to the injury phase.
The typical pattern of acute myocardial injury is ST segment elevation in the leads that reflect electrical activity of the corresponding injured heart tissue (Figure 11-32). For example, an acute myocardial injury to the anteroseptal part of the heart will cause ST segment elevation in the leads that examine the anteroseptal portion of the heart (see Table 11-4; Figure 11-33). In general, the degree of damage to the heart caused by the ischemia determines the degree of ST segment elevation. The ST segment abnormality usually resolves when perfusion is restored. At some point after myocardial infarction, significant Q waves (0.04 second in length) will be seen on the ECG in the corresponding leads. Q waves may develop within hours of an infarction but may not evolve for several days in some patients. They persist for the remainder of the patient’s life.
It can be helpful to identify ST segment abnormalities by drawing a straight line over the imaginary isoelectric line. This will reveal whether ST segment elevation or depression is present and to what degree. If the deviation from the isoelectric line is greater than 1 mm, significant changes have occurred and further investigation is appropriate. The patient should be monitored closely when this abnormality is ­identified.

44. Assessing Chest Pain Assess S/S by asking the patient:
O: onset of pain
P: provoked by …
Q: quality of pain
R: radiation of pain to …
S: severity of pain between 0 and 10
T: time frame of symptoms (acute or chronic)
U: what do You perceive as wrong?
AHA says suspect AMI if nonresponsive to nitroglycerin
The significance of pain as a general clinical finding is discussed in Chapter 3 of this text. Pain and distress are subjective to the patient’s perception of his/her condition and may be difficult to assess. However, it is essential that signs and symptoms associated with cardiac events be accurately reported both verbally and on the patient’s chart. The following sequence
will provide you with a reference for assessing these signs and symptoms. Ask the patient:
O When and how abrupt was the onset of the symptoms?
P What provoked the symptoms? (e.g., exercise, sleep, emotional upset)
Q How would you describe the quality of the pain? (e.g., sharp, dull)
R Does the pain radiate anywhere?
Does anything provide relief from the pain?
In what region is the pain located?
Does the pain change with deep respiration?
S Placing severity on a scale of 0 to 10, how would you rate your pain?
T What is the time frame of your symptoms? Is this chronic or acute?
U What do you think is wrong? Is this different from any previous episodes?
The American Heart Association recommends that for chest pain or associated symptoms not relieved by nitroglycerin, a myocardial infarction should be suspected until proven otherwise. Remember that “time is muscle,” and treatment interventions such as thrombolytic therapy or surgical intervention should be implemented quickly to salvage as much viable myocardium as possible.
The role of an RT in such cardiac events is to notify the patient’s physician, evaluate and optimize oxygen delivery, obtain a 12-lead ECG, and stand by to participate as a member of the cardiac arrest team if needed.

45. ECG Patterns with Chronic Lung Disease
Multiple ECG changes with severe COPD
Right axis deviation is common
P waves larger due to right atrial enlargement
Leads II, III, and aVF
Prominent and negative P wave in lead I
May have changes associated with cor pulmonale
Increase R-wave size on leads V1, V2, and V3
Reduced size of QRS in leads I, II, III, V5, and V6
The majority of patients with chronic obstructive pulmonary disease (COPD) have ECG abnormalities. Hyperinflation of the lungs and flattening of the diaphragm are associated with a more vertical position of the heart. This causes a clockwise rotation and contributes to the right axis deviation associated with COPD. (For quick axis determination, see Table 11-3.) Additionally, chronic pulmonary hypertension is common in patients with COPD and causes an enlargement of the right side of the heart. Enlargement of the right atrium causes the following:
Rightward deviation of the P-wave axis
Enlarged positive P waves greater than 2.5 mm in leads II, III, and aVF
A prominent and negative P wave in lead I
This syndrome is called cor pulmonale. Right ventricular enlargement may be associated with this syndrome and is recognized by the following characteristics:
Right axis deviation of the QRS complex
Increased R-wave voltage in leads V1, V2, and V3
Reduced voltage in the limb leads (I, II, and III) is seen when severe pulmonary hyperinflation (emphysema) is present. This is seen as QRS complexes that are less than 5 mm tall in leads I, II, and III. Reduced voltage in precordial leads V5 and V6 may also be present. The reduced measured voltage appears to be caused by two factors:
Reduced transmission of electrical activity through hyperinflated lungs
A mean QRS axis directed posteriorly and perpendicular to the frontal plane of the limb leads, causing decreased voltage on the ECG
Dysrhythmias often are seen in patients with COPD and acute lung disease. Tachycardia, multifocal atrial tachycardia, and ventricular ectopic beats are some of the more common ECG abnormalities seen in COPD. Such dysrhythmias occur as the result of hypoxemia from lung disease and from adverse effects of medications (e.g., bronchodilators) used to treat the obstructed airways. Hypoxemia often worsens during sleep in patients with COPD and increases the prevalence of nighttime dysrhythmias.

46. Summary An ECG provides a picture of heart’s electrical activity
ECG can identify the condition of the heart’s electrical conduction system
The ECG can also identify abnormal rhythms that may be of little consequence or very serious and life threatening
ECG does not measure pumping ability of the heart
SUMMARY
An ECG is an indirect measurement of the electrical activity of the heart.
The normal electrical conducting pathway of the heart starts with the sinoatrial (SA) node, then travels through the atrioventricular (AV) junction, bundle of His, bundle branches, Purkinje fibers and finally through the heart muscle known as the myocardium.
The RT should recommend that an ECG be obtained whenever the patient has signs and symptoms (e.g., chest pain) of an acute cardiac disorder such as a myocardial infarction.
Disturbances in the cardiac conduction system are called dysrhythmias which can be detected with an ECG.
The RT should remember that dysrhythmias can occur for many reasons including hypoxemia, myocardial ischemia, sympathetic nerve stimulation and certain drugs.
In an ECG, the initial wave of electrical activity or P wave occurs with atrial depolarization; the QRS complex represents ventricular depolarization and the T wave occurs with ventricular repolarization.
On the graphical (paper) display of an ECG, time is measured on the horizontal axis and voltage or amplitude is measured on the vertical axis.
On ECG paper, each small square represents 0.04 seconds and each large square is 0.2 seconds. Therefore, if the interval between R waves (RR interval) is 5 large boxes (1 second) and the rhythm is regular, then the rate is 60 beats/min.
An ECG involves the placement of six leads on the extremities and another six chest leads across the chest to measure cardiac electrical activity from several different angles.
There are several steps involved in ECG interpretation including identifying the heart rate, evaluating the rhythm and presence of P waves and measuring both the PR interval and the QRS complex.
Sinus tachycardia in an adult is a common dysrhythmia characterized by a heart rate of beats/ min, a regular rhythm and normal P waves, PR interval and QRS complex. It may be caused by hypoxemia and selected respiratory medications such as certain β-agonist bronchodilators.
Sinus bradycardia in an adult is characterized by a regular rhythm and heart rate less than 60 beats/min, as well as normal P waves, PR interval and QRS complex. This dysrhythmia can be caused by vagal stimulation associated with suctioning or tracheostomy tube manipulation.
Premature ventricular contractions (PVCs) can occur in a normal heart due to such causes as hypoxemia or they can signal a diseased heart. PVCs occurring several times per minute, two or more in a row or are of different shapes tend to be considered more serious.
Dysrhthymias such as ventricular fibrillation characterized by chaotic electrical activity or asystole (cardiac standstill) should be considered medical emergencies by the RT and require immediate and aggressive intervention according to resuscitation protocols.
The role of the RT for a patient experiencing severe chest pain is to notify the physician, evaluate/optimize oxygen delivery, help ensure that a 12-lead ECG is quickly obtained and be ready to participate as part of the cardiac resuscitation team.