The clinical surface ECG records the potential (voltage) differences between "neutral" ground and recording electrodes. The ECG is generated by the electrical activity of the heart and depicts the net sum of this activity recorded over time. By convention, a potential difference that points toward a recording electrode is assigned a positive deflection on the ECG, and a potential that points away from the recording electrode is assigned a negative deflection. Also by convention, routine ECG recordings are obtained with paper speed at 25 mm/s (2.5 cm/s) and signal calibration of 1.0 mV/10 mm (1.0 cm).
In Fig;.24:1, depolarization starts on the left side of the ventricular septum and initially proceeds to the right; this is recorded as a small negative deflection in the recording electrode. Subsequent depolarization involves the free walls of both ventricles, and since the left side has a much larger mass, the net sum of electrical activity is directed toward the recording electrode and a tall, positive deflection is recorded.
The P-QRS-T complex of the normal ECG represents electrical activity over one cardiac cycle ( Fig 24:2).
FIG. 24-2. Normal P-QRS-T ECG pattern.
FIG. 24-2. Normal P-QRS-T ECG pattern.
The P wave is caused by atrial depolarization. The QRS complex usually obscures atrial repolarization. The normal P wave duration is less than 0.10 s (2.5 mm), and normal amplitude is less than 0.3 mV (3 mm). A P wave originating from the SA node is directed inferiorly and to the left on the frontal plane.
The PR interval is the time between the onset of depolarization in the atria and the onset of depolarization in the ventricles. It is commonly used as an estimation of AV nodal conduction time because the AV node is the most likely site for delay in conduction. For adults in sinus rhythm, the PR interval is 0.12 to 0.20 s (3 to 5 mm) at 25 mm/s.
The QRS complex indicates ventricular depolarization. In general, depolarization starts on the endocardium and spreads outward to the epicardium. Despite the large amount of myocardium that must be depolarized, the specialized conducting system makes this a rapid process and the normal QRS duration is 0.06 to 0.10 s (1.5 to 2.5 mm). Any delay in intraventricular conduction results in a wide QRS. Ectopic impulses that originate below the bundle of His or that arrive prior to repolarization of the bundle branches also result in a widened QRS because they do not use the Purkinje network.
While small negative initial deflections (Q waves) are normal, large Q waves can be due to an electrically unexcitable area just under the recording electrode. An abnormal Q wave has a width of 0.04 s or greater and a height one-third that of the QRS complex.
The ST segment represents the plateau phase of ventricular depolarization. While the ST segment is usually isoelectric, a small deviation, less than 0.1 mV (1 mm), is not always pathologic.
The T wave is caused by ventricular repolarization. Depolarization is a rapid, near-simultaneous release of stored energy (like the release of a compressed spring); repolarization is a slow, asynchronous event where the metabolic machinery of each individual cell restores the transmembrane potential. Therefore, the T-wave duration is much longer and the amplitude much lower than those of the QRS complex. In general, repolarization starts on the epicardium and spreads to the endocardium. Many factors can influence this normal repolarization sequence: (1) metabolic factors (hypoxia, fever, drugs), (2) autonomic stimuli (abdominal pain, hyperventilation), (3) myocardial hypertrophy, (4) myocardial ischemia or inflammation, and (5) abnormal depolarization (Bundle branch block).
The QT interval represents ventricular depolarization and repolarization. While QT duration is commonly between 0.33 and 0.42 s, it does vary inversely with heart rate. The corrected interval is obtained by dividing the measured QT interval (in seconds) by the square root of the R-R interval (in seconds). The normal corrected QT interval is less than 0.47 s. This corrected QT should be checked prior to giving drugs such as ibutilide (Corvert), a recently released drug for the conversion of new onset atrial fibrillation. If Corvert is given in face of a prolonged correct QT, it may cause torsades de pointes.
The U wave may be seen as a normal component of the surface ECG. It is best seen in leads V! and V2. There is still some dispute as to the origin of the U wave. The classic explanation is that the U wave represents the delayed repolarization of the Purkinje network. More recent research has shown that the U wave can be seen at the same time as early afterdepolarizations (EADs) in patients with a prolonged QT interval and torsades de pointes.
Was this article helpful?
This guide will help millions of people understand this condition so that they can take control of their lives and make informed decisions. The ebook covers information on a vast number of different types of neuropathy. In addition, it will be a useful resource for their families, caregivers, and health care providers.