Criterion Odds Ratio (95% CI) Score[*]
ST ≥1 mm and concordant (in the same direction) with QRS complex 25.2 (11.6–54.7) 5
ST ≥1 mm in lead V1, V2, or V3 6 (1.9–19.3) 3
ST ≥5 mm and discordant with QRS complex 4.3 (1.8–10.6) 2
Modified from Sgarbossa EB, Pinski SL, Barbagelata A, et al: N Engl J Med 334:481–487, 1996. MI, myocardial infarction.
* A score of ≥3 is required to reach a specificity of ≥90% and sensitivity ≥36%. Therefore the third criterion should not be used alone to diagnose acute MI, and the absence of Sgarbossa criteria cannot be used to rule out an acute MI.
B. WAVEFORM FEATURES OF OTHER CLINICAL DISORDERS
1. Electrolyte abnormalities result in alterations in depolarization and repolarization that produce characteristic waveform abnormalities. However, a normal ECG does not rule out a serious electrolyte
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a. Hyperkalemia ( Fig. 6-5 ). Acute hyperkalemia produces peaked T waves with a narrow base and may shorten the QT interval. Progressive hyperkalemia causes P wave flattening, PR prolongation, and widening of the QRS complex. Severe hyperkalemia can lead to advanced AV block, diffuse intraventricular conduction delay, precordial STE (pseudoinfarction pattern), and asystole.
b. Hypokalemia. Common findings include T wave flattening or inversion, increased U wave prominence, ST depression, increased P wave amplitude and duration, and QT interval prolongation that increases the risk for torsades de pointes.
c. Hypercalcemia. Hypercalcemia shortens the QT interval (beginning of the QRS complex to the beginning of the T wave) with little effect on the T wave duration itself. An abrupt T wave upstroke, biphasic T waves, increased QRS amplitude, PR prolongation, and Osborn waves have also been described in severe hypercalcemia.
d. Hypocalcemia prolongs the QT interval.
2. Wolff-Parkinson-White syndrome (WPW) is a preexcitation syndrome that is important to identify because patients are at risk for life-threatening paroxysmal tachycardia. The ECG in WPW is characterized by the classic triad of a short PR interval, widened QRS, and delta waves (see Fig. 6-2 ). See Chapter 15 for further discussion of WPW.
3. Pericarditis (See Chapter 13 ).
a. Diffuse STE is the earliest electrocardiographic manifestation of acute pericarditis. ST depression may be seen in aVR and V1. The STE typically is concave, present in both limb and precordial leads, and without reciprocal ST depression. These features can help distinguish pericarditis from ST elevation acute coronary syndrome.
b. PR depression (and PR elevation in aVR) is the most sensitive electrocardiographic feature for the diagnosis of pericarditis.
4. Pulmonary embolism.
a. Electrocardiographic findings in acute PE are insensitive and nonspecific.
b. A prospective study of 28 electrocardiographic abnormalities in 212 patients who were evaluated for PE found only tachycardia and incomplete right bundle branch block (RBBB) to occur
significantly more often in patients with than without PE.[12] See Chapter 86 .
5. Hypothermia. Pathologic J waves called Osborn waves, best seen in the precordial leads, may occur in severe hypothermia (see Fig. 6-2 ). Their amplitude corresponds with the degree of hypothermia, and they disappear with rewarming. QTc prolongation, sinus bradycardia, U waves, atrial fibrillation, and other arrhythmias may also occur during hypothermia.
6. Brugada's syndrome is a familial syndrome of sudden cardiac death with characteristic
electrocardiographic abnormalities during sinus rhythm in the right precordial leads, consisting of STE and a pseudo-RBBB pattern in V1. The electrocardiographic changes may be transient and may be elicited by sodium channel blockade.
7. Arrhythmogenic right ventricular dysplasia is a hereditary cardiomyopathy characterized by fibrofatty replacement of the right ventricular myocardium that predisposes to VT and sudden cardiac death. Classic electrocardiographic abnormalities include complete or incomplete RBBB, T wave inversion in V1 to V3, epsilon waves (terminal notch in the QRS complex), and QRS prolongation in the right precordial leads.
8. Digoxin. The digitalis effect consists of coved ST depression (occurring more commonly in the lateral precordial leads), T wave flattening, and decreased QT interval (see Fig. 6-2 ). Digoxin toxicity can result in any of a large number of bradyarrhythmias, tachyarrhythmias, and conduction blocks.
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FIG. 6-5 Electrocardiographic changes in progressive hyperkalemia. (Modified from Lobato E. In Kirby RR, ed. Critical Care. Atlas of Clinical Anesthesiology series, ed. Miller R. Philadelphia, 1997, Current Medicine.)
C. DIFFERENTIAL DIAGNOSIS OF SELECTED ELECTROCARDIOGRAPHIC ABNORMALITIES
Numerous clinical disorders can result in similarly appearing waveform abnormalities. Taking into account the clinical context and the nuances of the specific waveform abnormality can help distinguish the cause. Table 6-1 lists
differential diagnoses of some common electrocardiographic abnormalities. PEARLS AND PITFALLS
▪
Always check the patient name, voltage standardization mark, and paper speed on each ECG. Conventional values are 1 mV for every 10-mm deflection for voltage standardization and 25 mm/s for paper speed (i.e., 0.04 seconds for each small, 1-mm box and 0.2 seconds for each large, 5-mm box).
▪ Suspect limb lead misplacement (or dextrocardia) when the P wave and QRS complex are negative in lead I. Precordial lead misplacement can cause abrupt changes in R wave progression.
▪ Whereas the electrocardiograph's rate, interval, and axis measurements generally are accurate, the diagnosis offered often is inaccurate or incomplete.
▪ Ischemia and infarction cause dynamic electrocardiographic changes. Therefore, obtaining serial ECGs is crucial in evaluating the patient with suspected acute coronary syndrome.
▪ The most common cause of left axis deviation is left anterior fascicular block.
▪ The specificity of LVH criteria that use voltage measurements in limb leads I or aVL is lower in younger patients or in the presence of LAD, as in left anterior fascicular block. In patients <40 years old, the diagnosis of LVH should be made by both voltage and nonvoltage abnormalities, such as left ventricular strain pattern (ST depression with asymmetric T wave inversions V4 to V6), LAD, left atrial abnormality, delayed R wave progression, U waves, intraventricular conduction delay, and delayed onset of intrinsicoid (beginning of QRS to peak of R wave more than 0.05 seconds).
▪ Q waves, STE, and hyperacute T waves localize to specific myocardial regions, whereas ST depressions and T wave inversions are less reliable for localizing ischemia.
▪ Always obtain an ECG with right-sided leads when evidence of inferior ischemia is present.
▪ ST depression in V1 to V3 in the patient with chest discomfort may represent nontransmural ischemia, but it may also reflect posterior transmural ischemia.
▪ STE that does not resolve within 4 weeks after an STEMI suggests the development of ventricular aneurysm.
▪ Electrocardiographic findings in acute PE are insensitive and nonspecific.
▪ Atrial fibrillation with a wide QRS and a very rapid ventricular response (>200 beats per minute) should raise concern for the presence of an accessory pathway, as in WPW syndrome.
▪ Consider digitalis toxicity in the patient with a history of atrial fibrillation who develops a regular, junctional tachycardia.
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▪ Digitalis toxicity does not necessarily correlate with the serum levels. Serious manifestations of digitalis toxicity include bradycardia, ventricular tachycardia, and ventricular fibrillation.
▪ Consider mitral stenosis in the patient with the triad of dyspnea, left atrial abnormality, and RVH.
REFERENCES
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2. Levy D, Labib SB, Anderson KM, et al: Determinants of sensitivity and specificity of electrocardiographic criteria for left ventricular hypertrophy. Circulation 1990; 81:815-820.
3. Alfakih K, Walters K, Jones T, et al: New gender-specific partition values for ECG criteria of left ventricular hypertrophy: recalibration against cardiac MRI. Hypertension 2004; 44:175-179.
4. Moon JC, De Arenaza DP, Elkington AG, et al: The pathologic basis of Q-wave and non–Q-wave myocardial infarction: a cardiovascular magnetic resonance study. J Am Coll Cardiol 2004; 44:554-560.
5. Bogaty P, Boyer L, Rousseau L, et al: Is anteroseptal myocardial infarction an appropriate term?. Am J Med 2002; 113:37-41.
6. Shalev Y, Fogelman R, Oettinger M, et al: Does the electrocardiographic pattern of “anteroseptal” myocardial infarction correlate with the anatomic location of myocardial injury?. Am J Cardiol 1995; 75:763-766.
7. Zehender M, Kasper W, Kauder E, et al: Right ventricular infarction as an independent predictor of prognosis after acute inferior myocardial infarction. N Engl J Med 1993; 328:981-988.
8. Yamaji H, Iwasaki K, Kusachi S, et al: Prediction of acute left main coronary artery obstruction by 12-lead electrocardiography. ST segment elevation in lead aVR with less ST segment elevation in lead V(1). J Am Coll Cardiol 2001; 38:1348-1354.
9. Barrabés JA, Figueras J, Moure C, et al: Prognostic value of lead aVR in patients with a first non–ST-segment elevation acute myocardial infarction. Circulation 2003; 108:814-819.
10. de Zwaan C, Bar FW, Wellens HJ: Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart
J 1982; 103(4 Pt 2):730-736.
11. Sgarbossa EB, Pinski SL, Barbagelata A, et al: Electrocardiographic diagnosis of evolving acute myocardial infarction in the presence of left bundle-branch block. N Engl J Med 1996; 334:481-487.
12. Rodger M, Makropoulos D, Turek M, et al: Diagnostic value of the electrocardiogram in suspected pulmonary embolism. Am J Cardiol 2000; 86:807-809.
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