In the electrocardiogram illustrated here (Figure), the ventricular rhythm is irregularly irregular with baseline undulation but no definite P waves; thus, the rhythm is atrial fibrillation. No time lines are visible on the tracing, but it was recorded at 25 mm per second and is 250 mm, or 10 seconds, long. Nineteen QRSs occur in the 10 seconds, making the ventricular rate 114 beats per minute. The fourth QRS is wide and unlike the other QRSs. It is not typical of right or left bundle branch block and therefore is more likely to be a ventricular premature complex than an aberrantly conducted supraventricular impulse. The calibration signals on the left side of the electrocardiogram are 10 mm/mV, and the R waves in V6 are 34 mm tall (3.4 mV), exceeding the 26 mm (2.6 mV) upper limit of normal for V5 or V6 (1). Likewise, the S wave in V1 plus the R wave in V6 equals 41 mm (4.1 mV), exceeding the 35 mm (3.5 mV) upper limit of normal for SV1 plus RV5 or V6 (2). In addition to meeting these two voltage criteria for left ventricular hypertrophy, the repolarization change in V6 is typical of the condition: depressed ST segment with asymmetric inversion of the T wave (3).
Figure.
Electrocardiogram recorded during the last month of the patient's life. See text for explication.
Perhaps the most interesting and least appreciated aspect of the electrocardiogram is the low QRS voltage in the limb leads in the presence of high QRS voltage in the precordial leads. This pattern was recognized as a clue to a dilated cardiomyopathy in 1985 by Goldberger et al (4), and others subsequently have confirmed it (5, 6). A less common, but perhaps more specific, electrocardiogram pattern indicating a dilated cardiomyopathy is left bundle branch block with right axis deviation (6–8).
This electrocardiogram was recorded in the last month of life of a 40-year-old man who died of cardiac failure. At necropsy, he had four-chamber cardiac dilatation. His valves and coronary arteries were normal, and his left ventricular wall was hypertrophied and the cavity dilated. He had never been hypertensive. Thus, he had an idiopathic dilated cardiomyopathy.
References
- 1.Milliken JA, MacFarlane PW, Veitch Lawrie TD. Enlargement and hypertrophy. In: MacFarlane PW, Veitch Lawrie TD, editors. Comprehensive Electro-cardiohgy: Theory and Practice in Health and Disease. New York: Pergamon Press; 1989. pp. 631–670. [Google Scholar]
- 2.Sokolow M, Lyon TP. The ventricular complex in left ventricular hypertrophy as obtained by unipolar precordial and limb leads. Am Heart J. 1949;37:161–186. doi: 10.1016/0002-8703(49)90562-1. [DOI] [PubMed] [Google Scholar]
- 3.Devereux RB, Reichek N. Repolarization abnormalities of left ventricular hypertrophy. Clinical, echocardiographic and hemodynamic correlates. J Electrocardiol. 1982;15(1):47–53. doi: 10.1016/s0022-0736(82)80044-7. [DOI] [PubMed] [Google Scholar]
- 4.Goldberger AL, Dresselhaus T, Bhargava V. Dilated cardiomyopathy: utility of the transverse: frontal plane QRS voltage ratio. J Electrocardiol. 1985;18(1):35–40. doi: 10.1016/s0022-0736(85)80032-7. [DOI] [PubMed] [Google Scholar]
- 5.Wellens HJ. Recognizing those electrocardiograms that distinguish you as a smart clinician. ACCEL. 2006;38(1):5. [Google Scholar]
- 6.Glancy DL, Jones BP, Raven MC, Fitz Patrick JA. Repeated hospitalizations for dyspnea and edema. J La State Med Soc. 2006;158(4):165–167. [PubMed] [Google Scholar]
- 7.Nickolic G, Marriott HJL. Left bundle branch block with right axis deviation: a marker of congestive cardiomyopathy. J Electrocardiol. 1985;18(4):395–404. doi: 10.1016/s0022-0736(85)80022-4. [DOI] [PubMed] [Google Scholar]
- 8.Childers R, Lupovich S, Sochanski M, Konarzewska H. Left bundle branch block and right axis deviation: a report of 36 cases. J Electrocardiol. 2000;33(Suppl):93–102. doi: 10.1054/jclc.2000.20326. [DOI] [PubMed] [Google Scholar]