John D. Wofford
Cedric Lefebvre
Normal cardiac conduction follows a precisely coordinated pattern from the initiation of an electrical impulse to myocardial repolarization after ventricular contraction. Under normal conditions, the electrical cardiac cycle begins at the sinoatrial (SA) node—a collection of pacemaker cells located at the junction of the superior vena cava and the right atrium. These cells possess an intrinsic ability to initiate electrical impulses spontaneously. This is achieved by the depolarization of a polarized cell membrane, primarily from the flow of ions (Na+, K+, and Ca2+) through ion channels embedded in the membrane. The term “action potential” is used to describe the depolarization–repolarization cycle of a cell.
The SA node is the dominant pacemaker of the cardiac cycle and typically fires at a rate of 60–100 action potentials per minute. The rate is influenced by sympathetic and vagal stimulation. The action potential of one cell triggers the action potentials in adjacent cells. Thus, the impulse initiated by the SA node is propagated through nearby cells. This causes both contraction of the atrial myocardium (atrial systole) and further electrical impulse propagation through the cardiac conduction system. Specialized conducting cells are responsible for delivering this electrical signal to the remainder of the myocardium. Long, thin, and efficient in relaying electrical impulses, these cells are similar to wires carrying electricity. Once an electrical impulse reaches a myocardial cell, calcium ions are released within the cell causing contraction. This contraction, known as excitation–contraction coupling, is achieved through the coupling of actin and myosin molecules, which are abundant within the myocardial cell.
Starting at the SA node, an electrical impulse travels through internodal atrial pathways to the atrioventricular (AV) node. The AV node acts as a relay site by connecting atrial electrical impulses with the ventricular conducting system. Conduction through the AV node, which is located at the base of the atrial septum, is slowed momentarily, allowing for ventricular filling of blood prior to ventricular systole. Signal conduction is then accelerated rapidly through the bundle of His and its right and left bundle branches. The right bundle branch continues toward the apex of the right ventricle (RV), whereas the left bundle branch splits into left anterior superior and left posterior inferior fascicles. Electrical impulses progress through the fibers of the Purkinje system and are ultimately delivered to the ventricular myocardium that causes ventricular contraction (ventricular systole).
FIGURE 2.1
Action potentials in cardiac myocytes produce local currents that depolarize the membranes of adjacent cells and propagate electrical signals. Cell-to-cell conduction is also achieved by end-to-end connections called gap junctions. Reproduced, with permission, from Chapter 2. Characteristics of cardiac muscle cells. In: Mohrman DE, Heller LJ. eds. Cardiovascular Physiology. 7th ed. New York, NY: McGraw-Hill; 2010.
FIGURE 2.2
The cardiac conduction system propagates electrical signals that originate from the SA node (under normal conditions) to myocytes in the atria and ventricles to stimulate sequential contraction of these chambers. Reproduced, with permission, from Fauci AS, Kasper DL, Braunwald E, et al. Harrison’s Principles of Internal Medicine. 17th ed. New York, NY: McGraw-Hill; 2008.
Through the coordinated propagation of electrical impulses throughout the entirety of the myocardium, the heart is able to provide a coordinated contraction that is necessary to pump blood throughout the pulmonary and systemic circulation. Electrolyte disturbances, myocardial ischemia, medications, structural abnormalities, and other factors can result in alterations of electrical conduction. Disruption of this highly coordinated system can lead to various electrocardiac pathologies and is the basis of several cardiovascular emergencies.
Nicholas E. Kman
Daniel P. Zelinski
An electrocardiogram (ECG) is a graphic representation of the electrical events of the cardiac cycle. The normal ECG waveform results from an electrical current that originates in the SA node in the right atrium and is propagated through healthy myocardial tissue. The electrical current is transmitted from the atria to the ventricles via the AV node where it spreads throughout the ventricular myocardium.
A standard ECG records the heart’s electrical cycle across 12 channels simultaneously. Waveforms are printed on a special grid depicting amplitude and duration of electrical events. Electrical data are collected from electrodes applied to 12 distinct anatomical locations on the human torso and limbs. Abnormalities in ECG waveform morphology can indicate several clinical conditions including arrhythmias, myocardial ischemia/infarction, peridarditis/myocarditis, chamber hypertrophy, electrolyte disturbances, and drug toxicity.
FIGURE 2.3
Normal resting ECG. The ECG is recorded on graph paper divided into 1 mm × 1 mm squares. With a paper speed of 25 mm/s, each square represents 40-millisecond duration along the horizontal axis and 0.1 mV amplitude along the vertical axis. Darker lines mark 5 mm × 5 mm squares, or 0.2 seconds and 0.5 mV.
Normal sinus rhythm depicts a normal electrical cardiac cycle. It is characterized by regular P waves followed by normal QRS complexes at a rate of 60 to 100 beats per minute. P waves represent atrial depolarization. Inverted or larger amplitude P waves can indicate atrial enlargement. The PR interval is measured from the beginning of the P wave to the start of the QRS complex. The QRS complex represents ventricular depolarization. Widening of the QRS complex is caused by a delay in intraventicular conduction. Immediately following the P wave, any downward deflection is a Q wave, and any upward deflection is an R wave. Small Q waves can be seen in leads I, aVL, V5, and V6 and represent septal activation. Pathological Q waves (>¼ R-wave amplitude, >0.04 seconds) can signal old myocardial infarction (MI) or septal hypertrophy. An increase in R-wave amplitude from lead V1 to its maximum amplitude in V5 is considered normal R-wave progression. The S wave represents late ventricular depolarization. The ST segment, or interval, begins at the end of the QRS complex. Depression or elevation of the ST segment can represent myocardial ischemia or infarction. The T wave represents ventricular repolarization. Normally, T waves are upright in every lead except aVR and V1. Inverted or broad T waves can indicate myocardial ischemia or infarction. Peaked T waves can signal hyperkalemia. The QT interval is primarily a measure of ventricular repolarization. The QT interval varies with heart rate and its measurement can be adjusted accordingly using the corrected QT interval (QTc). A prolonged QTc interval can be a marker for ventricular arrhythmia and a risk factor for sudden cardiac death. U waves are small waves following T waves and may be normal in some leads, especially the precordial leads V2 to V4. U waves can also signal hypokalemia and other metabolic conditions. See Table 2.1 for normal ECG waveform and interval measurements.
NORMAL ECG WAVEFORM AND INTERVAL MEASUREMENTS
| Amplitude (mV) | Duration (s) | |
|---|---|---|
| P wave | <0.25 | <0.12 |
| PR interval | – | 0.12–0.20 |
| Q wave | <¼ R wave, usually ≤0.1 | <0.04 |
| QRS complex | Variable | <0.1 |
| QT interval | – | <½ R–R interval |
| QTc interval | – | ≤0.44∗ |
| T wave | Variable | 0.04–0.08 |
| U wave | ≤0.1 | – |
FIGURE 2.5
ECG waves are labeled alphabetically and begin with the P wave. Normal waveform and interval measurements are included in Table 2.1. Reprinted, with permission, from Chapter 29. Origin of the heartbeat & the electrical activity of the heart. In: Barrett KE, Boitano S, Barman SM, Brooks HL. eds. Ganong’s Review of Medical Physiology. 24th ed. New York, NY: McGraw-Hill; 2012.
Electrodes should be placed flat against the skin. When lead wires are attached, ensure lead wires are not pulling on the skin.
When interpreting an ECG, use a systematic approach to evaluate the rate, rhythm, axis, and waveforms.
Cedric Lefebvre
A key component of acute MI (AMI) management includes rapid acquisition of ECG on patients presenting with anginal symptoms and early reperfusion therapy for patients in whom ST-segment elevation is noted. Identifying ST-segment elevation on ECG in certain cases can be challenging. The use of ECG leads beyond the conventional 12-lead anatomic territory can supplement electrocardiographic evaluation for ST-elevation MI (STEMI).
Occlusion of the left circumflex artery causes infarction of the posterobasal wall of the left ventricle (LV), resulting in posterior AMI. Because conventional ECG leads are placed on the anterior chest wall, posterior AMI may escape detection by ECG. Although the true incidence of ST-segment elevation posterior AMI is unknown, studies have shown a 3.3% incidence of isolated posterior wall infarction among all cases of AMI and an incidence of 15% to 21% of posterior AMI associated with inferior and/or lateral AMI. Patients with posterior wall involvement during inferior or lateral AMI have a greater incidence of LV dysfunction and death.
In right dominant coronary circulations (most common), the inferior wall and RV receive vascular supply from branches of the right coronary artery (RCA). Occlusion of the right coronary circulation may cause inferior wall AMI with or without RV infarction. Although isolated RV infarctions are relatively rare, up to 30% to 40% of inferior wall infarctions are associated with RV infarction. Inferior AMI with RV involvement confers unique hemodynamic sequelae, has a relatively high rate of mortality, and requires a specific therapeutic approach. As RV infarction progresses, cardiac output decreases and cardiogenic shock may ensue. The clinical manifestations of RV infarction are elevated neck veins and hypotension. Although RV infarction may be suspected when these clinical findings are present or when ST-segment elevation is noted in the inferior leads, RV infarction can be missed because conventional 12-lead ECG is not sensitive for injury patterns in this region of the heart.
Indirect ECG changes associated with posterior AMI such as ST-segment depression and prominent R waves in the anterior precordial leads (V1–V3) may be evident on 12-lead ECG. If posterior AMI is suspected, the American College of Cardiology/American Heart Association (ACC/AHA) practice guidelines advise the use of posterior leads (V7–V9) to investigate the presence of this phenomenon (class IIa recommendation). Posterior leads are placed on the left posterior chest wall, just below the scapula. ST-segment elevation of ≥1 mm in leads V7–V9 is highly suggestive of posterior AMI. If such ECG changes are noted, AMI treatment should be expedited and immediate cardiology consultation should be obtained for consideration of reperfusion therapies.
The clinician should investigate the presence of RV infarction in cases of inferior AMI. A class I recommendation of the ACC/AHA practice guidelines on the management of STEMI is the use of right-sided ECG leads to screen for RV involvement in cases of inferior AMI. The addition of right-sided chest leads may improve the sensitivity of 12-lead ECG for the detection of RV infarction by up to 9%. Leads V1R–V6R are placed to the right of the sternum as a mirror image of the locations for V1–V6 on the left. ST-segment elevation in these leads, particularly V4R (mid-clavicular line, fifth intercostal space), is highly suggestive of RV infarction. If RV infarction is detected, therapy should include preload optimization, RV afterload reduction, inotropic support if necessary, and consideration of early reperfusion therapy. Nitrates, diuretics, morphine, and other agents that decrease preload should be avoided. Emergent cardiology consultation should be obtained and/or transfer to a medical center capable of percutaneous coronary intervention (PCI) should be arranged.
FIGURE 2.10
To investigate RV infarction, a right-sided ECG is obtained by placing leads V1R–V6R as a mirror image of the locations for V1–V6 on the left.
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