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 relatively 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 caused by a myocardial infarction. In addition, understanding the significance of the subtle and often progressive aspects of ECG changes enhances the RT’s or other clinician’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 initially placed on continuous ECG monitoring using the 3-lead or 5-lead system. These systems use only 3 or 5 leads, placed on the patient’s chest, which is less cumbersome and allows for more patient mobility than a 12-lead ECG. Although 3- and 5-lead systems do not provide the level of detail that a 12-lead ECG does, they may help faciliate a rapid assessment of gross abnormalities in the electrical conduction system of the heart. Identification of a rhythm abnormality on a 3-lead or 5-lead tracing often indicates the need to obtain a more detailed 12-lead view of the heart.
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.
Because an ECG is noninvasive and does not present a risk to the patient, it is reasonable to obtain an ECG when the patient has signs and symptoms suggestive of an acute or chronic cardiac disorder such as myocardial infarction or congestive heart failure (CHF) (Box 11-1). An ECG is often used as an assessment tool to help determine the patient’s general health status or as a screening tool 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 early, treatment can be promptly started, thus potentially improving the longer term prognosis. 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).
It should also be noted that different clinical situations dictate whether a 3-, 5- or 12-lead ECG is warranted. Suffice to say that 3- or 5-lead ECG’s may be adequate for more routine monitoring such as ongoing telemetry or for initial preliminary cardiac screening. However, the most diagnostic value can be gathered from a standard 12-lead ECG. In essence, a 12-lead ECG provides a more complete assessment of the electrical activity of the heart by viewing it from 12 different angles. As a result, the focus of this chapter is the 12-lead ECG.
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 (Fig. 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).
|Pacemaker cells||Specialized cells that have an extensive ability to generate their own electrical activity (automaticity) and provide the electrical power for the heart|
|Conducting cells||Cells that conduct the electrical impulse throughout the heart|
|Myocardial cells||Cells that contract in response to electrical stimuli and pump the blood|
Normally, the electrical activity of the heart is initiated in the sinus node, also known as the sinoatrial (SA) node located in the right atrium (Fig. 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 as a result of 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 also known as interatrial 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 Fig. 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, further adding to the atrial kick. 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 (Fig. 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 Fig. 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.
Disturbances in cardiac conduction are called dysrhythmias. Dysrhythmias can occur even in healthy hearts. Often, minor dysrhythmias produce no symptoms and resolve without any treatment. More serious dysrhythmias indicate significant acute or chronic heart disease. When serious dysrhythmias occur, medication or electrical therapy often is required to increase or decrease the ventricular rate or to suppress an irritable area within the myocardium. Occasionally, surgical intervention or thrombolytic therapy is needed to prevent the progression of injury or infarct, thereby salvaging viable tissue. The application and improved delivery of oxygen often is a key factor in reducing or eliminating cardiac irritability. Causes of dysrhythmias include the following:
• Hypoxia: Hypoxia results from inadequate delivery of oxygen to the heart muscle or myocardium, and may be caused by hypoxemia or low blood flow known as ischemia. Inadequate delivery may be caused by reduced arterial oxygen levels, reduced hemoglobin levels, reduced perfusion (blood flow), or a combination of such factors.
• Ischemia: Ischemia is low blood flow, which can lead to cardiac tissue hypoxia further resulting in myocardial injury and infarction. Myocardial cells deprived of oxygen do not conduct nor contract well.
• Sympathetic stimulation: Physical or emotional stress from fear or anxiety and conditions, such as hyperthyroidism and CHF, can elicit dysrhythmias. Sympathetic stimulation can also result in cardiac ischemia caused by an increased workload on the myocardium without concurrent increase in blood flow such as in the case of diseased coronary arteries.
• Drugs: Many prescribed medications taken in nontherapeutic ranges or in the presence of inadequate biotransformation or clearance may produce dysrhythmias. Illegal use of sympathomimetic agents, such as cocaine or methylphenidate (Ritalin), may cause myocardial irritability and even infarction.
• Electrolyte imbalances: Electrical activity in the heart results from the exchange of electrolytes within cardiac tissue, known as the action potential. As a result, abnormal serum concentrations of electrolytes, such as potassium, magnesium, and calcium, can cause dysrhythmias.
• Hypertrophy: Overdevelopment of the heart muscle due to a genetic disorder or a consequence of increased workload on the myocardium (e.g., pulmonary and/or systemic vaso-constriction), resulting in smaller heart chambers and/or abnormal pumping action.
• Rate: Rhythms that are too slow or too fast result in inadequate cardiac output. Cardiac output is a product of stroke volume and cardiac rate. Stroke volume is the volume of blood pumped by one ventricle during one beat. Therefore, if the heart rate is too slow and the stroke volume is not increased proportionally, the cardiac output will be reduced. On the other hand, if the heart rate is too fast, the ventricles do not have enough time to fill with blood and stroke volume may be significantly reduced, resulting in poor cardiac output.
• Stretch: How much the atrium or ventricle stretches open so it can fill and then contract. With all else equal, greater stretch is associated with more stroke volume according to Frank Starling’s Law.
Before coming in contact with a patient, the RT will receive a verbal report from the RT from the preceding shift regarding the patient’s clinical status and notable aspects of their medical record (see Chapter 21). It is important to understand the meaning of descriptive terms, abbreviations, and acronyms related to cardiology and ECG interpretation that may be presented while receiving a report or reviewing the medical record. Table 11-2 provides a list of some of the most common cardiology abbreviations and acronyms that may assist in the assessment of the patient’s underlying disease process or cardiac conduction abnormalities.
|AIJR||Accelerated idiojunctional rhythm|
|AIVR||Accelerated idioventricular rhythm|
|ARP||Absolute refractory period|
|BBB||Bundle branch block|
|bpm||Beats per minute|
|CABG||Coronary artery bypass graft|
|CAD||Coronary artery disease|
|CK-MB||Creatine kinase-myocardial band|
|EKG||Electrocardiogram (German abbreviation)|
|EMD||Electromechanical dissociation (see PEA)|
|f wave||Fibrillatory wave|
|F wave||Flutter wave|
|LAE||Left atrial enlargement|
|LAP||Left atrial pressure|
|LBBB||Left bundle branch block|
|LVH||Left ventricular hypertrophy|
|MAT||Multifocal (or multiformed) atrial tachycardia|
|MCL||Modified chest lead|
|NSR||Normal sinus rhythm (see RSR)|
|PAC||Premature atrial contraction|
|PEA||Pulseless electrical activity|
|PJC||Premature junctional contraction|
|PJT||Paroxysmal junctional tachycardia|
|PMI||Point of maximal impulse|
|PSVT||Paroxysmal supraventricular tachycardia|
|PTCA||Percutaneous transluminal coronary angioplasty|
|PVC||Premature ventricular contractions|
|PVR||Pulmonary vascular resistance|
|QTc||QT interval corrected for heart rate|
|RAE||Right atrial enlargement|
|RBBB||Right bundle branch block|
|RVH||Right ventricular hypertrophy|
|SVR||Systemic vascular resistance|
|SSS||Sick sinus syndrome|
|TdP||Torsades de pointes|
|VSD||Ventral septal defect|
|WAP||Wandering atrial pacemaker (multifocal atrial rhythm)|
|1° AVBL||First-degree AV block|
|2° AVBL||Second-degree AV block types I or II|
|3° AVBL||Third-degree AV block|
The spread of electrical stimuli throughout the heart by way of the action potential initially causes depolarization of the myocardial cells. Depolarization occurs when a polarized cell is stimulated. Polarized cells carry an electrical charge on their surface; the inside of the cell is more negatively charged than the outside of the cell. The sudden loss of the negative charge within the cell is called depolarization, which is a result of potassium moving out of the cell and sodium moving into the cell. The return of the negative electrical charge is called repolarization (Fig. 11-4) and is a result of potassium moving back into the cell and sodium moving out of the cell. This process of depolarization and repolarization produces waves of electrical activity that travel back and forth across the heart. These waves of electrical activity are represented by waves detected by the ECG electrodes. The magnitude or amplitude of each wave is determined by voltage generated by depolarization of a particular portion of the heart.
Depolarization of the atria corresponds with atrial contraction and creates the initial wave of electrical activity detected on the ECG tracing, known as the P wave (Fig. 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 corresponds with the ventricular contraction and 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 Fig. 11-5). Ventricular repolarization corresponds to ventricular relaxation between contractions and 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.
QRS complexes usually consist of several distinct waves, each of which has a letter assigned to it as a label. This labeling system is needed because the precise configuration of the QRS complex can vary from one lead to the next and from one patient to the next. To establish a standardized labeling system, several guidelines have been developed. If the first deflection of the QRS complex is downward (negative in lead II), it is labeled a Q wave. The initial upward (positive) deflection is called an R wave. The first negative deflection following an R wave is called an S wave (Fig. 11-6). If the QRS complex has a second positive deflection, it is labeled R′ (R prime), and if a second S wave is also present it is called S′ (S prime). A negative deflection can be called a Q wave only if it is the first wave of the complex. In clinical practice, each ventricular depolarization complex is called a QRS complex whether it has all three waves or not.
The electrical activity of the heart is recorded on paper that has gridlike boxes with light and dark lines running horizontally and vertically (Fig. 11-7). The light lines circumscribe small boxes (1 × 1 mm) and the dark lines circumscribe larger boxes (5 × 5 mm).
Time is measured on the horizontal axis of the ECG paper. The ECG paper moves through the electrocardiograph at a speed of 25 mm/sec. Therefore each small square (1 mm) represents 0.04 second and each larger square (5 mm) represents 0.2 second. Five large boxes represent 1.0 second.
On the vertical axis, voltage, or amplitude, of the ECG waves is measured. The exact voltage of any ECG wave can be measured because the electrocardiograph is standardized so that 1 mV produces a deflection 10 mm in amplitude. Therefore, the standard for most ECG recordings is 1 mV = 10 mm. Each small square represents 1 mm.
To measure the amplitude of a specific wave, the isoelectric baseline must be identified. This is the flat line seen just before the P wave or right after the T or U wave (Fig. 11-8). Any movement of the ECG stylus above this line is considered positive; any downward movement is considered negative. To measure the degree of positive or negative amplitude of a specific wave, the isoelectric line is used as a reference point marking zero voltage.
R waves are measured from the isoelectric line to the top of the R wave. Q and S waves are measured from the isoelectric line to the bottom of the wave (see Fig. 11-6). P waves can be either positive or negative and are also measured from the isoelectric line to the top (if positive) or bottom (if negative) of the wave.
In addition to the amplitude of any wave, the duration of waves, intervals, and segments can be measured. A segment is a straight line between two waves. An interval encompasses at least one wave plus the connecting straight line.
The normal P wave is less than 2.5 mm in height and not more than 0.11 second in length. The PR interval is an important measurement that provides information regarding conduction time. This interval is measured from the beginning of the P wave, where the P wave lifts off the isoelectric line, to the beginning of the QRS complex (see Fig. 11-5). The PR interval represents the time it takes for the electrical stimulus to spread through the atria and to pass through the AV junction to the ventricles. The normal PR interval is between 0.12 and 0.20 second (3 to 5 small boxes). If conduction of the impulse through the AV junction is abnormally delayed, the PR interval will exceed 0.2 second. A prolonged PR interval is called first-degree AV block and is discussed later in this chapter.
The duration of ventricular depolarization is determined by measuring the QRS interval. This interval is measured from the first wave of the QRS complex to the end of the last wave of the QRS complex. Normally the QRS interval does not exceed 0.10 seconds (2 1/2 small boxes). The amplitude of the QRS complex may range from 2 to 15 mm, depending on the lead and the size of the ventricular mass.
A very important segment to evaluate is the ST segment. This segment is the portion of the ECG cycle from the end of the QRS complex (even if no S wave is present) to the beginning of the T wave (see Fig. 11-5). It measures the time from the end of ventricular depolarization to the start of ventricular repolarization. The normal ST segment is isoelectric (no positive or negative voltage) or at least does not move more than 1 mm above or below baseline. Certain pathologic abnormalities, such as myocardial ischemia or injury, cause the ST segment to be elevated or depressed (Fig. 11-9). The duration of the ST segment is not as important as its configuration.
The RR interval is useful in identifying the rate and regularity of ventricular contraction. The distance in millimeters is determined from one R wave to the next in successive QRS complexes. This is done for several different RR intervals. ECG calipers can be helpful in making this measurement. The average of the measurements is determined and converted to time. Remember that each large box is equal to 0.2 second and 5 large boxes equal 1.0 second. If the RR interval is 1.5 seconds, the heart rate is 40 beats/min (60 seconds divided by 1.5 = 40). If the RR interval is 1.0 second, the heart rate is 60 beats/min. If the RR interval is 0.5 second, the heart rate is 120 beats/min. This method for determining the heart rate is easy to apply if the RR interval falls conveniently on one of the numbers just described. Unfortunately, this is not usually the case. Other methods for calculating the heart rate are described later. Marked variation in the RR interval from one interval to the next indicates that the heartbeat is irregular and may be a sign of sinus dysrhythmia, which is described in more detail in the section on dysrhythmia identification.
The QT interval is measured from the beginning of the QRS complex to the end of the T wave (see Fig. 11-5). This interval represents the time from the beginning of ventricular depolarization to the end of ventricular repolarization. The normal values for the QT interval depend on the heart rate. As the heart rate increases, the QT interval normally shortens; as the heart rate decreases, the QT interval increases. As a general rule, the QT interval that exceeds one half of the RR interval is prolonged if the heart rate is 80 beats/min or less. Common causes of an abnormally prolonged QT interval include hypokalemia (low potassium), hypocalcemia (low calcium), and the side effects of certain medications such as quinidine.