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QT Interval
Chapter 15
QT Interval Richard A. Harrigan
The QT interval reflects the systolic phase for the ventricles, and includes ventricular activation (QRS complex) as well as recovery. It is measured from the beginning of the QRS complex until the end of the T wave. Within any 12-lead tracing, there is lead-to-lead variation in QT interval duration (see Chapter 73, QT Dispersion); in general, the longest measurable QT interval is regarded as determining the overall QT interval for a given tracing. QT interval varies with age (increases slightly with age), sex (slightly longer in women than men), and heart rate (the higher the rate, the shorter the QT interval). The QT interval is also usually longer during the night. A correction factor for rate is automatically included on most tracings with computer printouts across the top of the tracing; this corrected QT interval (QTC) is determined by dividing the QT interval by the square root of the R-R interval. QTc = QT/√RR
Estimating the QT interval is difficult at times. If U waves occur, T-U wave fusion may make determination of the cessation of the T wave difficult. Similarly, T-P wave fusion may occur at higher heart rates, creating a similar dilemma. In such cases, the onset (of the U wave) or termination (of the P wave) should serve as markers of the terminus of the QT interval.
ELECTROCARDIOGRAPHIC DIAGNOSIS Short QT interval It is difficult to find universal agreement on what constitutes a short QT interval, especially in light of the coincident effects of age, sex, rate, and diurnal variation, as well as the lack of pathologic processes associated with short QT intervals. A short QT interval for normal sinus rates would be
QT Interval
70
Short
Long
• Digitalis effect • Hypercalcemia
• Congenital long QT syndromes – Jervell and Lange-Nielsen syndrome – Romano-Ward syndrome • CNS system disease – Subarachnoid hemorrhage – Cerebral hemorrhage – Thromboembolic stroke • Metabolic syndromes – Hypokalemia – Hypocalcemia – Hypothyroidism – Hypothermia • Pharmacologic agents
CHAPTER 15: QT Interval
71
FIGURE 15-1 • Digitalis effect. Shown here in lead V6, scooped ST seg-
FIGURE 15-3 • Long QT interval. The QT interval seen here in lead V3
ment depression includes the T wave and demonstrates a short QT interval.
exceeds 0.70 sec; the T wave nearly merges with the P wave from the following complex. ST segment depression is also evident. Serum potassium was 1.6 mEq/L.
roughly in the range of 0.28 to 0.33 sec. A very short QT interval may appear to encroach on the ST segment. Digitalis Effect. Among the earliest findings seen on the electrocardiogram exhibiting digitalis effect is a shortening of the QT interval, due to earlier repolarization of myocardial cells. QT interval shortening may or may not be seen with digitalis therapy (not related to toxicity), as well as PR interval prolongation, “scooped” ST segment depression, and diminished T wave amplitude (Fig. 15-1). Hypercalcemia. Serum calcium levels are inversely related to QT interval. The T wave in hypercalcemia may abruptly rise out of the ST segment, which itself may or may not be evident (Fig. 15-2).
Long QT interval A long QT interval at normal sinus rates is, conservatively, greater than 0.44 sec, whereas others have advanced 0.46 sec in men and 0.47 sec in women as sex-specific upper limits of normal. QT interval differences due to sex have not been observed in infants and children younger than 14 years of age. A rule of thumb for individuals with heart rates within normal limits (60 to 100 bpm) is that the QT interval should be less than half the preceding R-R interval. QT interval prolongation is seen in a variety of metabolic, toxicologic, and noncardiac diseases, as well as in primary cardiac diseases (see Chapter 47, Long QT Syndromes). Congenital Long QT Syndromes. Familial QT interval prolongation associated with syncope, sudden death, and congenital deafness, and transmitted through an autosomal
recessive pattern, is referred to as the Jervell and LangeNielsen syndrome. A similar syndrome lacking the hearing loss and transmitted in an autosomal dominant fashion is the Romano-Ward syndrome. These syndromes can show marked variability in QT interval within an individual at different points in time, and thus present randomly and unpredictably. Mitral Valve Prolapse. The relationship between mitral valve prolapse and QT interval prolongation is not clear; however, QT interval prolongation may occur in this population, and has been suggested as a marker of ventricular dysrhythmia. Central Nervous System Disease. A number of disorders of the central nervous system can present with QT interval prolongation, including subarachnoid hemorrhage, intracerebral hemorrhage, and thromboembolic cerebrovascular stroke. A marked increase in T wave amplitude, frequently with deep, symmetric T wave inversion (so-called roller coaster T waves), is another characteristic of these syndromes. Metabolic Syndromes. Hypokalemia and hypocalcemia are known to cause QT prolongation. Hypomagnesemia is not known directly to prolong the QT interval; however, effects on the QT interval seen in its presence may be mediated by associated low levels of potassium or calcium. Whereas hypokalemia also can cause ST segment depression (Fig. 15-3), T wave flattening, and U waves, hypocalcemia does not displace the ST segment or affect the T wave.
FIGURE 15-2 • Short QT interval. These complexes from lead V3 in a man with bladder cancer and an elevated serum calcium of 14.8 mEq/L demonstrate a short QT interval and the virtual disappearance of a distinct ST segment before the T wave.
FIGURE 15-4 • Long QT interval. The slightly prolonged QT interval (0.49 sec) shown here in lead V5 is secondary to hypothermia (rectal temperature was 26.5°C [81°F]); note the Osborn wave (arrow).
72
SECTION II: THE ABNORMAL ELECTROCARDIOGRAM
Hypothyroidism may cause QT interval prolongation, as well as bradycardia, low voltage, and T wave changes. Hypothermia may cause prolongation of all intervals in the cardiac cycle; the characteristic notched J waves (Osborn waves) after the QRS complexes should be sought (Fig.15-4), as well as bradydysrhythmias (e.g., sinus bradycardia, atrial fibrillation with slow ventricular response). Drug Effects. An increasing number of pharmaceutical agents have been linked with varying degrees of certitude to QT interval prolongation. Some general rules are helpful in remembering drugs with a propensity to prolong the
QT interval. Potassium channel blocking agents prolong the QT interval, but are not a class of drugs readily familiar to most physicians for that effect. Some antidysrhythmics are classically linked to QT interval prolongation, including Vaughan Williams class Ia, Ic, and III agents, and as such may prolong the QT interval with or without widening the QRS complex, depending on the drug. Various psychotropic medications may prolong the QT interval. Several antibiotics (e.g., sparfloxacin, erythromycin, clarithromycin, pentamidine) also can lengthen the QT interval (see Chapters 49 through 57, on toxicology).
Chapter 16
U Wave Theodore C. Chan
The U wave follows the T wave and is the last deflection seen in the normal cardiac cycle. The U wave is the most inconspicuous deflection and is often not well visualized or is misinterpreted as part of the T wave on the electrocardiogram (ECG). The exact mechanism of the U wave is unclear. Theories as to the source of the U wave include repolarization of Purkinje fibers or some other portion of the ventricular myocardium, afterpotentials generated by mechanicoelectrical coupling during ventricular relaxation, longer duration of the action potential of conduction myocytes, and repolarization of the papillary muscle cells.
usually monophasic (positive or negative), but rarely can be biphasic. The upright U wave is best seen in leads II and V2 to V4. The U wave can have a negative deflection in lead aVR, and occasionally in leads III and aVF. The U wave can appear inconspicuous, particularly at higher heart rates. In addition, it can be mistaken as part of the T wave, erroneously suggesting a prolonged QT interval on ECG. U Wave
ELECTROCARDIOGRAPHIC DIAGNOSIS Increased Amplitude
Abnormal Inversion
Normal U wave The normal U wave is a small, rounded deflection occurring just after the T wave. The ascent of the wave is usually shorter than the descent, although the U wave can appear symmetric in morphology. The amplitude is usually less than 1 mm. At normal heart rates, the duration from the apex of the T wave to the apex of the U wave is approximately 0.1 sec. The normal U wave axis is directed anteriorly and to the left at approximately +60 degrees, and is similar to that of the T wave. That is, for a given lead, the U wave is directed similar to the T wave. The amplitude of the U wave varies, but is no more than 25% of the T wave amplitude. The U wave is
• Exercise-induced tachycardia • Athlete’s heart • Post-extrasystole • Bradycardia • Hypokalemia • CNS event • Medications • Hypertension • Pheochromocytoma
• • • •
Ischemia LV overload RV overload Pulmonary embolus
QT Interval Richard A. Harrigan
The QT interval reflects the systolic phase for the ventricles, and includes ventricular activation (QRS complex) as well as recovery. It is measured from the beginning of the QRS complex until the end of the T wave. Within any 12-lead tracing, there is lead-to-lead variation in QT interval duration (see Chapter 73, QT Dispersion); in general, the longest measurable QT interval is regarded as determining the overall QT interval for a given tracing. QT interval varies with age (increases slightly with age), sex (slightly longer in women than men), and heart rate (the higher the rate, the shorter the QT interval). The QT interval is also usually longer during the night. A correction factor for rate is automatically included on most tracings with computer printouts across the top of the tracing; this corrected QT interval (QTC) is determined by dividing the QT interval by the square root of the R-R interval. QTc = QT/√RR
Estimating the QT interval is difficult at times. If U waves occur, T-U wave fusion may make determination of the cessation of the T wave difficult. Similarly, T-P wave fusion may occur at higher heart rates, creating a similar dilemma. In such cases, the onset (of the U wave) or termination (of the P wave) should serve as markers of the terminus of the QT interval.
ELECTROCARDIOGRAPHIC DIAGNOSIS Short QT interval It is difficult to find universal agreement on what constitutes a short QT interval, especially in light of the coincident effects of age, sex, rate, and diurnal variation, as well as the lack of pathologic processes associated with short QT intervals. A short QT interval for normal sinus rates would be
QT Interval
70
Short
Long
• Digitalis effect • Hypercalcemia
• Congenital long QT syndromes – Jervell and Lange-Nielsen syndrome – Romano-Ward syndrome • CNS system disease – Subarachnoid hemorrhage – Cerebral hemorrhage – Thromboembolic stroke • Metabolic syndromes – Hypokalemia – Hypocalcemia – Hypothyroidism – Hypothermia • Pharmacologic agents
CHAPTER 15: QT Interval
71
FIGURE 15-1 • Digitalis effect. Shown here in lead V6, scooped ST seg-
FIGURE 15-3 • Long QT interval. The QT interval seen here in lead V3
ment depression includes the T wave and demonstrates a short QT interval.
exceeds 0.70 sec; the T wave nearly merges with the P wave from the following complex. ST segment depression is also evident. Serum potassium was 1.6 mEq/L.
roughly in the range of 0.28 to 0.33 sec. A very short QT interval may appear to encroach on the ST segment. Digitalis Effect. Among the earliest findings seen on the electrocardiogram exhibiting digitalis effect is a shortening of the QT interval, due to earlier repolarization of myocardial cells. QT interval shortening may or may not be seen with digitalis therapy (not related to toxicity), as well as PR interval prolongation, “scooped” ST segment depression, and diminished T wave amplitude (Fig. 15-1). Hypercalcemia. Serum calcium levels are inversely related to QT interval. The T wave in hypercalcemia may abruptly rise out of the ST segment, which itself may or may not be evident (Fig. 15-2).
Long QT interval A long QT interval at normal sinus rates is, conservatively, greater than 0.44 sec, whereas others have advanced 0.46 sec in men and 0.47 sec in women as sex-specific upper limits of normal. QT interval differences due to sex have not been observed in infants and children younger than 14 years of age. A rule of thumb for individuals with heart rates within normal limits (60 to 100 bpm) is that the QT interval should be less than half the preceding R-R interval. QT interval prolongation is seen in a variety of metabolic, toxicologic, and noncardiac diseases, as well as in primary cardiac diseases (see Chapter 47, Long QT Syndromes). Congenital Long QT Syndromes. Familial QT interval prolongation associated with syncope, sudden death, and congenital deafness, and transmitted through an autosomal
recessive pattern, is referred to as the Jervell and LangeNielsen syndrome. A similar syndrome lacking the hearing loss and transmitted in an autosomal dominant fashion is the Romano-Ward syndrome. These syndromes can show marked variability in QT interval within an individual at different points in time, and thus present randomly and unpredictably. Mitral Valve Prolapse. The relationship between mitral valve prolapse and QT interval prolongation is not clear; however, QT interval prolongation may occur in this population, and has been suggested as a marker of ventricular dysrhythmia. Central Nervous System Disease. A number of disorders of the central nervous system can present with QT interval prolongation, including subarachnoid hemorrhage, intracerebral hemorrhage, and thromboembolic cerebrovascular stroke. A marked increase in T wave amplitude, frequently with deep, symmetric T wave inversion (so-called roller coaster T waves), is another characteristic of these syndromes. Metabolic Syndromes. Hypokalemia and hypocalcemia are known to cause QT prolongation. Hypomagnesemia is not known directly to prolong the QT interval; however, effects on the QT interval seen in its presence may be mediated by associated low levels of potassium or calcium. Whereas hypokalemia also can cause ST segment depression (Fig. 15-3), T wave flattening, and U waves, hypocalcemia does not displace the ST segment or affect the T wave.
FIGURE 15-2 • Short QT interval. These complexes from lead V3 in a man with bladder cancer and an elevated serum calcium of 14.8 mEq/L demonstrate a short QT interval and the virtual disappearance of a distinct ST segment before the T wave.
FIGURE 15-4 • Long QT interval. The slightly prolonged QT interval (0.49 sec) shown here in lead V5 is secondary to hypothermia (rectal temperature was 26.5°C [81°F]); note the Osborn wave (arrow).
72
SECTION II: THE ABNORMAL ELECTROCARDIOGRAM
Hypothyroidism may cause QT interval prolongation, as well as bradycardia, low voltage, and T wave changes. Hypothermia may cause prolongation of all intervals in the cardiac cycle; the characteristic notched J waves (Osborn waves) after the QRS complexes should be sought (Fig.15-4), as well as bradydysrhythmias (e.g., sinus bradycardia, atrial fibrillation with slow ventricular response). Drug Effects. An increasing number of pharmaceutical agents have been linked with varying degrees of certitude to QT interval prolongation. Some general rules are helpful in remembering drugs with a propensity to prolong the
QT interval. Potassium channel blocking agents prolong the QT interval, but are not a class of drugs readily familiar to most physicians for that effect. Some antidysrhythmics are classically linked to QT interval prolongation, including Vaughan Williams class Ia, Ic, and III agents, and as such may prolong the QT interval with or without widening the QRS complex, depending on the drug. Various psychotropic medications may prolong the QT interval. Several antibiotics (e.g., sparfloxacin, erythromycin, clarithromycin, pentamidine) also can lengthen the QT interval (see Chapters 49 through 57, on toxicology).
Chapter 16
U Wave Theodore C. Chan
The U wave follows the T wave and is the last deflection seen in the normal cardiac cycle. The U wave is the most inconspicuous deflection and is often not well visualized or is misinterpreted as part of the T wave on the electrocardiogram (ECG). The exact mechanism of the U wave is unclear. Theories as to the source of the U wave include repolarization of Purkinje fibers or some other portion of the ventricular myocardium, afterpotentials generated by mechanicoelectrical coupling during ventricular relaxation, longer duration of the action potential of conduction myocytes, and repolarization of the papillary muscle cells.
usually monophasic (positive or negative), but rarely can be biphasic. The upright U wave is best seen in leads II and V2 to V4. The U wave can have a negative deflection in lead aVR, and occasionally in leads III and aVF. The U wave can appear inconspicuous, particularly at higher heart rates. In addition, it can be mistaken as part of the T wave, erroneously suggesting a prolonged QT interval on ECG. U Wave
ELECTROCARDIOGRAPHIC DIAGNOSIS Increased Amplitude
Abnormal Inversion
Normal U wave The normal U wave is a small, rounded deflection occurring just after the T wave. The ascent of the wave is usually shorter than the descent, although the U wave can appear symmetric in morphology. The amplitude is usually less than 1 mm. At normal heart rates, the duration from the apex of the T wave to the apex of the U wave is approximately 0.1 sec. The normal U wave axis is directed anteriorly and to the left at approximately +60 degrees, and is similar to that of the T wave. That is, for a given lead, the U wave is directed similar to the T wave. The amplitude of the U wave varies, but is no more than 25% of the T wave amplitude. The U wave is
• Exercise-induced tachycardia • Athlete’s heart • Post-extrasystole • Bradycardia • Hypokalemia • CNS event • Medications • Hypertension • Pheochromocytoma
• • • •
Ischemia LV overload RV overload Pulmonary embolus