Chapter 27 ST-Segment and T-Wave Changes ECG changes involving the ST segment and the T wave are common in adults but relatively rare in children, This is because ofa high incidence of ischemic heart disease, bundle Branch block, myecarialinfaeton, and other myocardial disorders in adults Nonpathologic ST-Segment Shift Not all STacgment shits ac abnormal, Sigh shit ofthe ST segment is common in ‘ommal cilren, Elevation or depression of upto I mm inthe limb leads and upto 2 nm inthe precordial leads is within normal lis “Two common types of nonpathologic ST-segment sbifls are J-deprssion and ealy repolarization, The T veto remain norma in these condion. J-DEPRESSION ‘E-depression isa sift ofthe junction between the QRS complex and the ST segment (- point) without sustained ST-segment depression (Fig. 27-1A). IL is a normal ST-segment Shift, The J-deprestion is seen moce often inthe precordial leads than in the limb leads (and therefore is best shown in an ECG recorded during an exercise test). Figure 27 shows both the J-depression (seen in most of the precortial leads) and early repolariza- tion (Seen in the limb leads; see later discussion), EARLY REPOLARIZATION In early repolarization, all leads with upright T waves have elevated ST segments, and leads with inverted T waves have depressed ST segmen's (see Fig. 27-2). The T vector Depression [Abnormal ST-Segments oy aS Figure 27-1, Nonpathologic (nonischemlc) and pathologie ‘schemic) STsegment and Twave ‘changes. Characteristic nonischemic ST segment change called -lepression: note tat the ST Slope ts upward B and C, Examples of pathologic STsegmert changes; noe that the downward Slope of the ST segment (B) or the horizontal segment 1s sustained (C). (From Pork MK. ‘Guntherh WG! How to Read Pediaric ECGs, Ine. St. Las, Mosby, 192.)VaR Figure 27-2. Tracing from a healthy 16yearold boy that exis early repolarization and J ‘depression. The ST segment i shed towar’ the diection ofthe T wave and i most marked in Ml and aVE. depression ts sen in most ofthe precordial lead ‘remains normal. Ths condition, seen in tealthy adolescents and young adults, resembles the ST-segment shift seen in acute pericarditis; inthe former, the ST segment is stable, and in te later the ST segment returns to the isoelectric line. Pathologic ST-Segment Shift [Abnormal shits of the ST segment ofen ae accompanied by T-vave inversion, A trthologie ST-segment shit assumes onc of the following forms 1, Downvard sian followed by a phasic or inverted T wave (ee Fig. 7-1B). 2. Horizontal elevation or depression sisttined for >008 second (se Fig. 27-10. Pathologic ST-segment site are seein left or right ventricular hypertrophy with “sin” (ee Chaper 3); digitalis effet pecadits, including posoperstve ste; myocarditis; myocardial infarction; and some eleclyte disturbances (hypokalemia and igpatalenay T-Wave Changes ‘T-wave changes usually are associated with the same conditions related to ST-segment shift Other conditions associated with Tswave changes with or without ST-segment shift, discussed in previous chapters, include bundle branch block and. ventricular arzhythmias, Only conditions not covered previously are discussed briefly inthis chapter. PERICARDITIS “The ECG changes seen in pericarditis are the result of subepicardial myocardial damage ‘or pericardial effusion and consist ofthe following: 1. Pericardial effusion may produce low QRS voltages (QRS voltages <5 mm in ‘every one ofthe limb lead). 2, Subepicardial myocardial damage produces the following time-dependent changes in the ST segment and T wave (Fig. 27-3) ‘4 ST-segment elevation occurs in the leads representing the left ventricleReturn of ST segment B foward normal Figure 27-2. Time-dependent changes ofthe ST se ‘nent and T wave in pericarditis (From Park MK, Gantheroh WG: How to Read Pedic ECC, 3nd C ‘T.wave aversion fl St Lous, Mosby. 1992.) The ST-segment shift returns to normal within 2to 3 days. €. Frwave inversion (with isoelectris ST segment) occurs 2 to 4 weeks after the ‘onset of pericarditis MYOCARDITIS ECG findings of myocaritis (rheumatic or viral) ate relatively nonspecific and may include changes in all phases of the cardiac cycle. Various arrhythmias also have been associated with myocarditis. One or more of the following changes are seen in myocarditis 1. Disturbances in atrioventricular (AV) conduction (fist- or second-degree AV block, Low QRS voltages (=5 mm th all $x limb leads). Decreased amputude of the T wave. Prolongation of the QT interval. Amhythmias or ectopic beats MYOCARDIAL INFARCTION ‘Myocardial infarction is rare in infants and children, but comectly diagnosing the condition is important for proper care. All conditions that have been associated with myocardial infarction in adults have beon described as causing myocardial infarction in children, such as atherosclerosis, inflammatory disease of the myocardium, lupus erythematosus, syphilis, olyartertis nod>sa, hypertension, and diabetes mellitus. Un- tonmon causes of myocardial infarction in pediatric patients include anomalous origin ff the left coronary artery fom the pulmonary artery, endocardial fibroclatosis, coronary frtery embolization resulting from infective endocarditis or ftom diagnostic procedures performed on the left side of the heart, and inadvertent surgical interruption of the Coronary. artery during cardiac surgery. In rocent years, early and Tate sequelae of Kawasaki's disease, surgical complications ofthe arterial switch operation for tansposi- tion of the great arteries, and dilated cardiomyopathy have emerged as important causes ‘of myocardial infarction in the pediatie population. "The ECG findings of adult myocardial infarction ae ime dependent and ae illustrated in Figure 27-4. Changes seen during the hyperacute phase are short-lived. The more common ECG findings are those ofthe early evolving phase. These consist of patholosic {Q waves (abnormally wide and deep), STsegment elevation, and T-wave inversion. The ration ofthe Q wave is 0,04 second or greater in adults, and it shouldbe atleast 0.03 Second in children, Over the next few weeks, the elevated ST segment gradually returns towand the baseline, but inverted T waves persist (late evolving phase). The pathologic (Q waves persist for yeurs after myocardial infarction (see Fig. 27-4). Leads that show these abnormalities vary with the locaton of the infarction and are summarized in Table 27-1yporacte Phase Elevated ST Segment {e few hours) Deep and Wie Q Wave ary Evolving Phase Deep and Wide Q Wave "afew days) Elevated ST Segment Diphase T Wave Late Evolving Phare Deep and wide o Wave (23 weeks Sharply Inverted T Wave Resolving Phase ‘Beep and wide Q Wave (or yeas) ‘most Normal F Wave Figure 27-4, Sequential changes of the ST segment and T wave in myocardial infarction, (From ‘Park MK, Guntherth WG: How t0 Read Pediatric ECGs, 3 ed St Lous, Mosby. 1992) In most pediatric patients with myocarial infarction, the time of onset isnot clearly known, and the evolution ofthe different phases is difficult to document. Frequent ECG findings in children with acute myocardial infarction include the following, (Towbin et al, 1992) 1, Wide Q waves (0,035 second) veth or without Q-wave notching, 2. ST-segment elevation (>2 mm). 3. Pralongation of QTe interval (6.44 second) with accompanying abnormal Q ‘The width of the Q wave is more important than the depth; the depth of the Q wave varies widely in normal children (see Table 3-6). Figure 27-5 is an ECG of myocandial infarction in an infant with anomalous origin of the left coronary artery from the pulmonary artery. The most important abnormality is the presence of a deep and wide Q wave (0.04 second) in I, aVL, and V6. A. QS pattem appears in V2 through V5, indicating anterolateral myocardial infarction (see Table 27-1) Electrolyte Disturbances ‘Two important serum electrolytes that preduce ECG changes are calcium and potassium. “Although T-wave changes are not seen with hypocalcemia and hypercalcemia, these conditions ae discussed here because they change the relative postion of the T wave ‘lable 27-1, Leads Showing Abnormal ECG Findings in Myocardial Infarction Lint end Precordial Leads aca La V5.6 ‘terior Vi¥3, v3 ‘Ancol Lav vive Dirge tat ve oe ‘Nowe of th Kade i rend ward he postr ace ofthe eat. Ths, poche ncn ges tht woul! hve ben preset inthe serie sarc lene at se i these leas ‘minor image (ell sl apy wide R wate in V1 aad 2s ad lan! Wide symmetea T ware BVT antST-SEGMENT AND T-WAVE CHANGES 361 rece GEG Hi Figure 27-5. Tracing from a 2-nonth-ld infant wo has anomalous origin ofthe left coronary ‘ares from the pulmonary artery. An abnormally derp and wide Q wave (0204 second) seen inf GUL. and VO. and 0.08 puter seen in V2 thragh V6 are characteristic of anterolateral vacant infarction. ‘CALCIUM, Calcium fon affects the duration of the ST segment without producing ST-segment shift ‘or changes in the T vector. Hypocaleemia prolongs the ST segment and, as a result, prolongs the QTe interval (Fig, 27-6). The T-wave duration remains normal. Hypercalce- fia shortens the ST segment without affecting the T wave, resulting in shortening of the OTe interval (see Fig. 27-6), PoTassiuM Hypokalemia produces one ofthe least specific 3CG changes. When the serum potassium level is below 2.5 mEq/L, ECG changes consist of a prominent U wave with apparent prolongation of the QTe, Nat or diphasic T waves, and ST-segment depression (Fig. 21-7). With further lowering of serum potassium levels, the PR interval becomes prolonged, and sinoatial block may occur. “The earliest ECG abnormality scen in hyperkalemia is tall, peaked, symmetrical T waves with a narrow base-—the so-called tenled T wave. In hyperkalemia, sinoatrial biock, second-degree AV block (either Mobitz I or I), and passive or accelerated Jjunctional or ventricular escape rhythm may eccur. Severe hyperkalemia may resalt in ther ventricular fibrillation or arrest, The folowing ECG sequence is associated with f progressive increase in the serum potassium level (see Fig. 27-1) 1, Tall, tented T waves. 2. Prolongation of QRS duration (intraventicular block). 5. Prolongation ofthe PR interval (ist-degree AV block). ab tee Hypercalcemia Normal Hypocaeeia Figure 27-6 ECG findings of hypercalcemia and hypocalcemia. Hyperalcemia shortens and hypocalcemia lengthens the ST segment. (From Park MK, Guntheroth WG: How to Read Pediatric ECGs, Srl eS Lous, Mosby, 192.)‘SERUM K we a >90 meat Abn Wav Figure 27-7. ECG findings of hypokalemia and hyperkalemia. (From Park MK, Gutherth WO: How to Read Pediairie ECGs, Sn ed. St Lot, Mosby, 1992) 4, Disappearance ofthe P wave, 5. Wide, bizarre diphasic QRS complex (“sine wave"), 6, Eventual asystole ‘These ECG changes are usual) seen best in leds II and III and the left precordial leads