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A 53-year-old woman first had a heart murmur noted at age 3. She was symptom free until age 47 but since then has had repeated episodes of cardiac failure. On this occasion she noted increasing shortness of breath, bilateral leg edema up to her knees, and a 10-lb weight gain over a week's time. Increasing her furosemide from 20 to 40 mg daily did not relieve her symptoms. On physical examination, this small, slender woman had a blood pressure of 140/84 mm Hg, bilateral expiratory wheezes, and crackles at both lung bases. Neck veins were elevated to 15 cm above the angle of Louis, and there was 1–2+/4+ edema up to her knees. A 2+/4+ right ventricular lift was felt at the left sternal edge. A hyperdynamic 4+/4+ left ventricular impulse was felt and a third heart sound was heard in the anterior axillary line. A 4+/6+ continuous murmur peaked at the second heart sound and was best heard in the second left intercostal space. There are many causes of continuous murmurs. When the intensity of the murmur peaks at the second heart sound and the murmur is loudest in the second left intercostal space or just below the medial portion of the left clavicle, the cause is almost always a patent ductus arteriosus. When the murmur is maximal elsewhere, the cause usually is not a ductus. An electrocardiogram (Figure) recorded at half standard, i.e., 1 mV = 5 mm, showed sinus rhythm with atrial premature complexes, biatrial enlargement, left axis deviation of the QRS complex (−35°), and left ventricular hypertrophy with repolarization abnormality, including a long QT interval (405 ms with a QTc of 473 ms). Although left ventricular hypertrophy with repolarization abnormality, i.e., a wide angle between the QRS and the ST-T vectors, is classically seen with pressure overload of the left ventricle, such as occurs with systemic hypertension or aortic stenosis, this repolarization change may occur whenever left ventricular hypertrophy is severe, no matter the cause (1). Figure. Electrocardiogram recorded in a 53-year-old woman with a continuous murmur and congestive heart failure. See text for explication. The chest radiograph demonstrated a huge cardiac silhouette, prominent pulmonary vasculature, bilateral pulmonary edema, and scoliosis of the spine, which is more common in patients with congenital heart disease than in the general population. In the past, patients with patent ductus arteriosus occasionally have lived to be far older than our patient (2), but for 75 years now closure of the arterial duct, first by surgical ligation (3) and more recently by catheter-delivered closure devices (4), has been available as a highly effective and relatively low-risk cure for the malformation. Consequently most arterial ducts are now closed in infancy or early childhood. Our patient, however, has always refused any invasive treatment. In her, the duct is large enough to allow a moderately large left-to-right shunt that over time has produced severe left atrial and left ventricular enlargement. Although her left ventricular ejection fraction 18 months ago was 50% as judged by echocardiogram, the left ventricle clearly is failing and the resulting pulmonary arterial hypertension has caused right ventricular and right atrial enlargement. This has been accentuated by chronic obstructive pulmonary disease caused by her smoking 1½ packs of cigarettes per day for 25 years and manifested by a forced expiratory volume in 1 second of 35% and wheezing even when she is not in overt cardiac failure, and by a hemoglobin of 17 g/dL and a hematocrit of 53% on the current admission. The patient responded to medical treatment for congestive heart failure but was lost to follow-up after discharge.

A 19-year-old woman with congenital HIV infection was admitted to the hospital after experiencing nausea, vomiting, diarrhea, and fatigue for 1 week. Her CD4 count was 27. She had undergone percutaneous endoscopic placement of a gastrostomy tube for feeding 5 months earlier. In addition, she had extensive genitoanal ulceration due to infection with herpes simplex virus complicated by secondary bacterial infection. Her home medications included tenofovir disoproxil fumarate, sulfamethoxazole and trimethoprim, lamivudine, lopinavir/ritonavir, duloxetine hydrochloride, Nystatin, azithromycin, hydromorphone, and lorazepam. An electrocardiogram 11 months earlier had been normal except for sinus tachycardia, but in addition to sinus tachycardia the electrocardiogram recorded soon after the current admission showed changes suggestive of severe hypokalemia (Figure ​(Figure11): sagging ST segments, low T waves, and prominent U waves (which because of the tachycardia fuse with the subsequent P waves). Serum electrolyte concentrations in mEq/L were potassium, 1.4; sodium, 139; chloride, 119; and bicarbonate, 14. Her serum calcium concentration was 7.8 mg/dL, and the creatinine and urea nitrogen concentrations were 1.9 mg/dL and 6 mg/dL, respectively. Urinalysis at that time showed a glucose concentration of >1000 mg/dL while her serum glucose was only 90 mg/dL. Her serum uric acid concentration was 0.8 mg/dL, and serum phosphorus was 1.4. The hypercholemic, hypokalemic, metabolic acidosis was thought to be due to therapy with tenofovir. In addition to this, her metabolic acidosis was certainly exacerbated by recent diarrhea. The tenofovir was discontinued because of the suspected Fanconi syndrome. Figure 1 Electrocardiogram recorded soon after admission. See text for explication. After 5 days of aggressive fluid therapy and electrolyte replacement, her serum potassium concentration increased to 4.4 mEq/KL, and the tenofovir was restarted because of her serious HIV infection. After 5 weeks in the hospital, the patient had improved; her electrocardiogram was normal except for sinus tachycardia (Figure ​(Figure22), and she was discharged to inpatient hospice care on numerous medications, including electrolyte replacement. Figure 2 Electrocardiogram recorded shortly before discharge. See text for explication. Six days after discharge, the patient was readmitted with confusion and profound weakness. The admission electrocardiogram, seen in Figure ​Figure33, showed sinus tachycardia at a rate of 153 beats/minute, right axis deviation, and an intraventricular conduction defect (QRS duration, 0.20 seconds) that suggested hyperkalemia. Serum electrolyte concentrations in mEq/L at this time were potassium, 10.5; sodium, 135; chloride, 120; and bicarbonate, 12. The serum calcium level was 14.5 mg/dL despite a serum albumin level of only 2.2 gm/dL, the highest albumin level recorded during either admission. Her serum creatinine and urea nitrogen concentrations were 2.5 mg/dL and 41 mg/dL, respectively. As the hyperkalemia was treated with oral sodium polystyrene sulfonate, insulin, 50% dextrose solution, and emergent hemodialysis, the QRS duration shortened to 0.12 seconds, and T waves became more peaked and “typical” of hyperkalemia (Figure ​(Figure44). In addition, the QT interval was noticeably short considering the intraventricular conduction defect (QT interval, 0.25 seconds; QT interval corrected for heart rate, 0.40 seconds), a feature consistent with hypercalcemia. Figure 3 Electrocardiogram recorded on the second admission. See text for explication. Figure 4 Electrocardiogram recorded an hour after the electrocardiogram in Figure ​Figure3.3. See text for explication. One of the patient's discharge medications on her previous admission was potassium chloride, 60 mEq three times per day by mouth, and that dosage in the presence of her renal dysfunction undoubtedly caused the hyperkalemia that occasioned the second admission. She improved, but never sufficiently to leave the hospital. Her stay was complicated by multiple nosocomial infections, pressure sores, and worsened debilitation, and she eventually developed gram-negative sepsis and died 6 weeks after admission.

(2011). Electrocardiogram of a Man with a Single-Chamber Cardioverter/Defibrillator. Baylor University Medical Center Proceedings: Vol. 24, No. 4, pp. 348-349.

A 49-year-old man complained of worsening headaches after using crack cocaine a week earlier. He had a slow heart rate (32 beats per minute) and high blood pressure (174/90 mm Hg), and an electrocardiogram recorded on admission showed sinus bradycardia with junctional escape complexes (Figure).

A 51-year-old security officer had an electrocardiogram recorded because of a strong family history of coronary arterial disease (Figure ​(Figure11). His medical history was significant for a gunshot wound to the left side of his chest in the line of duty 25 years earlier. Figure 1 Electrocardiogram. See text for explication. The electrocardiogram shows sinus rhythm and prominent R waves in leads V1 to V3 and otherwise is normal. The Table lists many of the causes of tall R waves in the right precordial leads and confirming clues to their diagnoses (1). Table Causes and diagnosis of tall R waves in lead V1∗ In this patient, the chest radiograph makes the diagnosis (Figure ​(Figure22). Eventration of the left hemidiaphragm, the result of left phrenic nerve damage from the gunshot, allows upward displacement of the gut that pushes the heart far enough to the right that leads V1 to V3 lie over the left ventricle and record complexes resembling those usually recorded from the left precordial leads. A similar appearance may occur when atelectasis of the right lung causes a rightward displacement of the heart (2). Figure 2 Anteroposterior chest radiograph showing eventration of the left hemidiaphragm. Much of the gut is at the level of the heart and pushes it toward the right side of the chest.

The simultaneously recorded lead II and lead V1 electrocardiographic rhythm strips show a narrow QRS followed by a wide QRS and then by a pause (Figure ​(Figure11). The cycle then recurs repeatedly. Superficially, this sequence suggests sinus rhythm with ventricular premature complexes occurring in a bigeminal pattern. Closer observation, however, reveals P waves in front of the wide QRSs as well as in front of the narrow ones. This raises the possibility of atrial bigeminy with the atrial premature complexes being conducted to the ventricles with aberration of the left-bundle-branch-block type. Even closer inspection shows that each cycle contains a third P wave, which is best seen as a negative deflection at the end of each second T wave in lead V1. In lead II this third P wave appears as minimal widening, occasionally with a slight notch on the downslope, of the second T wave. Furthermore, the P-P intervals are regular. Thus, the rhythm is sinus tachycardia (rate = 118 beats/min), and second-degree atrioventricular block is present with a conduction ratio of 3:2. Figure 1 Initial electrocardiogram. See text for explication. Two questions remain. First, is this type I or type II atrioventricular block? Because the P-R intervals of all conducted P waves appear to be the same, this is type II block. Second, why is the first QRS of each cycle narrow while the second QRS is wide ? There is rate-related left bundle branch block; the interval preceding the first QRS is long, allowing normal intraventricular conduction, but the interval preceding the second QRS is shorter than the refractory period of the left bundle branch. An electrocardiogram recorded a day later further clarifies the rhythm (Figure ​(Figure22). The sinus rate has slowed to 98 beats per minute, and more P waves are conducted. The slower rate allows separation of the P waves from the preceding T waves. All QRSs except the one following the pause show left bundle branch block that is clearly rate related. In each group of beats, the first P-R interval is approximately 0.02 seconds shorter than all of the subsequent P-R intervals, which are identical at 0.16 seconds as measured in lead II. Pick and Langendorf have pointed out that the constancy of the P-R intervals after the first one is what establishes the diagnosis of type II atrioventricular block (1). The first P-R of each cycle may be shorter because the first QRS is actually a junctional escape beat. In addition, when the QRS morphology changes as in this case, the second QRS may have a longer initial isoelectric period, making the P-R interval appear slightly longer. Figure 2 Electrocardiogram recorded the following day. See text. Bigeminal rhythms are common and have many causes (2). High on the list is 3:2 atrioventricular block, in this case type II block. This and the even more common rate-related bundle branch block are the salient features of this electrocardiogram.

A 62-year-old diabetic, hypertensive woman with prior stenting of her dominant right coronary artery underwent coronary arteriography because of an abnormal stress test. A 90% narrowing of the left circumflex coronary artery beyond the second obtuse marginal branch was stented with a 3 × 18-mm drug-eluting stent. She went to the recovery room in good condition, and an electrocardiogram was recorded (Figure).

A 64-year-old woman had been experiencing short episodes of rapid regular heart beating for nearly a year. The bouts became frequent and lengthy, resulting in a hospital admission a month earlier when intravenously administered adenosine terminated an episode. She was discharged on diltiazem, but the bouts of tachycardia continued and were accompanied by light-headedness and sometimes nausea. When she returned to the hospital with one of these episodes, a narrow QRS complex tachycardia again was documented and again was terminated by adenosine (Figures ​(Figures11 and ​and22). Figure 1 Electrocardiogram recorded in the emergency department on the patient's second admission shows a regular tachycardia at a rate of 143 beats/minute. The QRS complexes are narrow (0.08 seconds) but in some leads appear wider because of retrograde P waves ... Figure 2 Electrocardiogram recorded after intravenously administered adenosine terminated the tachycardia seen in periods. In addition, many Figure ​Figure1.1. There is now sinus rhythm at a rate of 88 beats/minute with frequent multiform ventricular premature ... In the hospital, episodes of tachycardia continued, but adenosine frequently was ineffective; the episodes would end spontaneously after varying periods. In addition, many of the episodes were now wide QRS complex tachycardias (Figure ​(Figure33), and the patient became dyspneic for the first time. Amiodarone was given, first intravenously and then by mouth, and in time all episodes of tachycardia ceased and dyspnea disappeared. Figure 3 Electrocardiogram recorded 2 days after those shown in Figures ​Figures11 and ​and2.2. A regular wide QRS complex (0.13 seconds) tachycardia has a rate of 138 beats/minute. The wide QRS complexes are not characteristic of either right bundle ... Regular wide QRS complex tachycardias often are difficult to diagnose. Brugada et al (1) and Vereckei et al (2) each have used stepwise approaches, incorporating four somewhat different criteria, with high rates of accuracy as judged by electrophysiological studies. Both groups found A-V dissociation to be 100% specific for ventricular tachycardia. However, A-V dissociation could be identified in fewer than 25% of patients with ventricular tachycardia, and most diagnoses were made from various morphologic characteristics of the QRS complexes (1, 2). Both A-V nodal reentrant tachycardia and A-V reciprocating tachycardia usually occur in patients with so-called structurally normal hearts, but ventricular tachycardia rarely does so. Our patient has had systemic arterial hypertension since she was a young woman and has known of a heart murmur for many years. She never had symptoms, however, until the tachycardias began. Echo-Doppler studies obtained during her recent admissions have shown left ventricular hypertrophy and dilatation with a reduced ejection fraction of 40% and a restrictive filling pattern, biatrial dilatation, severe mitral regurgitation with morphologically normal leaflets and annular dilatation, and an elevated pulmonary arterial systolic pressure of 40 mm Hg. She has been scheduled for mitral valvular repair.

The salient features of the electrocardiogram in Figure ​Figure11 are sinus bradycardia, low QRS voltage, flat T waves in all leads in the absence of ST-segment depression, and a long QT interval. Each of these findings is typical of hypothyroidism, and the combination of all four in the same electrocardiogram has a high positive predictive value (1, 2). Indeed, the patient's serum levels of thyroid-stimulating hormone (183.71 μIU/mL; reference range, 0.50–5.00) and free thyroxine (

A 67-year-old radiologist had a routine electrocardiogram before arthroscopic surgery (Figure). The computer interpreted it as normal. In fact, the electrocardiogram is normal except for an infrequently diagnosed pattern: the T wave in lead V1 is taller than that in V6. Figure A 67-year-old man's preoperative electrocardiogram was read by the computer as normal, but the T wave in lead V1 is taller than the T wave in V6. French and Russian articles initially recognized the TV1-taller-than-TV6 pattern as abnormal. In the first English- language article on the subject, Weyn and Marriott found this pattern and no other abnormality in approximately 1% of hospital electrocardiograms (1). Diagnoses in their 80 patients were coronary heart disease in 25%, systemic hypertension in 24%, lung disease in 11%, miscellaneous conditions in 23%, and no apparent disease in 17%. Perhaps because of the large hypertensive patient population, high blood pressure appears to be the most common disorder associated with isolated TV1 taller than TV6 at the Medical Center of Louisiana. Indeed, the patient whose electrocardiogram is shown in the Figure had long-standing, untreated high blood pressure averaging 155/95 mm Hg, a value he believed to be at the upper limit of normal. An echocardiogram revealed concentric left ventricular hypertrophy (wall thickness = 1.3 cm) in the absence of other abnormalities. With advanced left ventricular hypertrophy due to systemic hypertension, the T-wave vector is anteriorly directed and the QRS vector is large and posteriorly directed, giving deep S waves and positive T waves in lead V1 and tall R waves and inverted T waves in lead V6, the so-called left-ventricular-hypertrophy-with- strain pattern. Although the QRS changes often precede the T- wave changes, such is not always the case, and anterior rotation of the T-wave vector before significant QRS changes are seen accounts for the isolated TV1-taller-than-TV6 pattern in hypertensive patients. Dilaveris et al recently described a decrease in T-wave amplitude in the frontal plane as an early marker of altered ventricular repolarization that may occur before QRS voltage changes in patients with systemic hypertension (2). They did not comment on horizontal-plane changes, which account for the TV1-taller-than-TV6 pattern. Because positioning of the precordial leads may vary from one electrocardiogram to the next, occasionally the T in V1 is taller than that in V6 in one electrocardiogram but not another. Thus, the pattern of TV1 being taller than TV6 is more convincingly abnormal when seen in more than one electrocardiogram. Preoperative examination by an internist or cardiologist provides not only the opportunity to assess the risks of the procedure, but often the chance to evaluate and manage a variety of serious conditions not previously addressed. This patient now receives an angiotensin-converting enzyme inhibitor, and his blood pressure readings are consistently normal.

A 32-year-old echocardiographic technician was honing her skills by self-examination when she noted that her right ventricle was dilated. A cardiologist confirmed her finding and noted a left-to-right shunt across a 1-cm defect in the fossa ovalis region of the atrial septum. The patient was entirely asymptomatic and regularly engaged in an aerobic exercise program. Physical examination revealed mild pectus excavatum. The right ventricle was not palpable. The a wave in the jugular venous pulse was larger than the v wave. The second heart sound was of normal intensity, was persistently split, and moved physiologically with respiration. The only definite auscultatory abnormality was a third heart sound followed by a short diastolic rumble heard at the lower left sternal border. A chest roentgenogram showed mild enlargement of the cardiac silhouette and minimal prominence of the pulmonary trunk and vasculature. A normal electrocardiogram was recorded. The normal electrocardiogram, the inequality of the a and v waves in the jugular pulse, the respiratory movement of the second heart sound, the absence of a systolic ejection murmur, and the size of the defect measured echocardiographically all suggested that the defect was restrictive and the left-to-right shunt smaller than usual. On the other hand, the third heart sound and short diastolic rumble, the minor abnormalities on chest roentgenogram, and the dilated right ventricle on echocardiography indicated that the shunt was hemodynamically important, and operative closure was recommended. After collecting second opinions for over a year, the patient agreed, and the defect was closed by primary suture. This is the second of our patients whose fossa ovalis–type atrial septal defect was discovered in such a serendipitous fashion. The first was a 22-year-old echocardiographic repairman seen 28 years ago. When he finished repairing the echocardiograph, he was asked to volunteer for an echocardiogram to be sure the machine was working properly, and the defect was found. He also underwent primary suture closure despite being asymptomatic. Until the echocardiograph came into daily use in cardiologic practice, atrial septal defects were diagnosed on the basis of symptoms, sometimes subtle but unmistakable physical findings, distinctly abnormal chest roentgenograms, and abnormal electrocardiograms that typically showed incomplete right bundle-branch block, often with right axis deviation. Because symptoms developed in 70% of such patients by age 40 and in virtually all of them by age 60 (1), and because operative closure carried a low risk and improved prognosis when performed early (2–5), closure of fossa ovalis–type atrial septal defects was uniformly recommended in the absence of severe pulmonary arterial disease. Does this conventional wisdom apply to patients, such as ours, whose defects are smaller and probably would not have been discovered except for serendipitous echocardiography? Opinion is divided (6). The patient herself has had second thoughts post-operatively because of several bouts of postpericardiotomy syndrome, a common problem after operative closure of atrial septal defects. She has now been well for more than 3 years, and those doubts are receding. Our own view is that a left-to-right shunt large enough to cause right ventricular enlargement should be closed, even in the absence of symptoms. As catheter-delivered devices to close holes in the atrial septum are perfected (7), perhaps even smaller defects will be closed routinely, regardless of symptoms.

A 30-year-old woman (gravida 4, para 3) with full-term pregnancy presented in spontaneous labor. She had no significant medical history and was asymptomatic except for labor contractions. Her heart rate was 42 beats per minute, and her blood pressure was normal. Chest was clear to auscultation bilaterally. Her cardiac rhythm was regular with a varying first sound intensity. No murmurs were heard. Her extremities did not show significant edema. The electrocardiogram (Figure) demonstrated complete atrioventricular block with a junctional escape rhythm at a rate of 43 beats per minute. The atrial rhythm was sinus with ventriculophasic sinus arrhythmia: the P-P intervals were shorter (0.70 to 0.75 seconds; mean 0.727) when they contained QRS complexes and longer (0.76 to 0.81 seconds; mean 0.782) when they did not. The R-R intervals were quite regular at 1.38 to 1.39 seconds. The electrocardiogram was unchanged from one recorded a year earlier. A previous evaluation had not revealed any abnormality other than the arrhythmia, and the patient was presumed to have congenital complete heart block. She delivered vaginally a healthy baby and has remained asymptomatic. Figure Admission electrocardiogram in a 30-year-old pregant woman. See text for explication. Congenital complete atrioventricular block occurs in approximately 1 of 25,000 live births (1), and estimates based on fetal echocardiography are that nearly an equal number of fetuses die in utero. The great majority of these deaths, as well as deaths in the neonatal period, occur in the 50% of patients who have associated congenital malformations, most commonly left atrial isomerism, often coexisting with atrioventricular septal defect, and ventricular inversion (congenitally corrected transposition of the great arteries). Among live births, congenital complete atrioventricular block is isolated in some 70% of patients, and most of their mothers have evidence of systemic lupus erythematosus, especially SS-A (anti-Ro) antibodies. Evidence suggests that these antibodies cross the placenta and damage the fetal conduction tissue (1). Some of these mothers have yet to experience clinical manifestations of lupus. Blocked conduction may be due to an inadequate connection between the atria and the atrioventricular node, a defect in the node itself, or lack of connection between the node and the bundle of His (1). With rare exceptions, the escape rhythm arises above the His bifurcation, and the QRS complex is narrow. Although syncope and sudden death may occur, some 80% to 90% of patients with isolated congenital complete atrioventricular block survive to adulthood, and the majority are asymptomatic. Excessively slow ventricular rates or symptoms attributable to the bradycardia are indications for permanent pacemaker insertion (2). Ventriculophasic sinus arrhythmia is seen in up to 40% of cases of complete atrioventricular block and has been described in second–degree atrioventricular block, with ventricular premature complexes, and in pacemaker–induced ventricular rhythm (3–6). The possible mechanisms involved in this phenomenon include arterial baroreceptor-mediated changes in vagal tone, activation of the Bainbridge reflex by the ventricular contraction, mechanical traction on the atria, and perhaps an increase in blood flow to the sinoatrial node during ventricular systole.

This electrocardiogram of a 90-year-old man shows repeating similar cycles, each consisting of 4 complexes (Figure). Every cycle begins with 2 sinus-initiated complexes followed by an early, wide QRS (ventricular premature complex) that has a right-bundle-branch-block configuration and precedes a pause that is terminated by a slightly different, wide QRS. The cycle then repeats itself. What is not readily apparent is that the interval between each ventricular premature complex and the following wide QRS (1.10 seconds) is exactly half the interval between this second wide QRS of each cycle and the ventricular premature complex of the next cycle (2.20 seconds). Furthermore, an interval of 1.10 seconds from the beginning of the last QRS of each cycle lies in the ventricular refractory period of the first sinus-initiated complex of the next cycle (vertical lines above the V1 rhythm strip). Thus, one can make a good case for a left ventricular, parasystolic focus discharging every 1.10 seconds, with every third impulse failing to capture the ventricles because it arrives in the absolute refractory period. Figure Electrocardiogram in a 90-year-old man shows a repetitive pattern, or group beating. See text for explication. Why is the second wide QRS complex of each cycle different from the first wide QRS? Close inspection again is the key and reveals that immediately following each premature wide QRS complex, there is a retrograde P wave that resets the sinus node and causes the ensuing P′-P interval to be longer than the usual P-P interval. Before the next sinus P wave can be conducted to the ventricles, the atrioventricular junction escapes, causing a fusion beat with the simultaneously discharging parasystolic focus. Parasystole results from a protected, spontaneously discharging focus in the atria, atrioventricular junction, or, as in this case, the ventricles. This protection from the dominant rhythm, here sinus rhythm, is demonstrated by interectopic intervals that are multiples of a common denominator (1.10 seconds in this patient) and by variable coupling of the ectopic impulses with the dominant rhythm (1). Fusion beats are seen frequently, and parasystolic complexes fail to appear when their exit from the parasystolic focus is blocked by refractoriness of the surrounding tissue, here ventricular refractoriness following the first sinusinitiated complex of each cycle. Although this electrocardiogram is too short to make a definitive determination, the first wide QRS complex of each cycle appears to have fairly constant coupling to the preceding sinus- initiated QRS: 0.41, 0.40, and 0.36 seconds for the 3 complexes seen. Even fixed coupling would not exclude parasystole in this case. Because the sinus rhythm is fixed to the parasystolic rhythm by the retrograde P waves that reset the sinus node, as long as the parasystolic rate and the sinus rate each remain constant, which is not unusual for short intervals, the parasystolic impulses will appear to be coupled to the sinus impulses (1). Other electrocardiograms in the same patient often answer many questions. This patient's prior and subsequent electrocardiograms frequently reveal ventricular parasystole of the more typical variety with the parasystolic QRSs not fixedly coupled to the sinus rhythm because no retrograde P waves couple the sinus rhythm to the parasystolic rhythm. Furthermore, the parasystolic QRS complexes in those electrocardiograms all have the identical right-bundle-branch-block morphology seen here. Parasystole usually is considered a rare phenomenon, but its prevalence depends on how it is sought and by whom. Routine electrocardiograms have yielded a prevalence of 0.13% (2), while the prevalence among patients, who may have >1 electrocardiogram to review, is greater (0.3%) (3). When Holter monitoring is used for the search, the prevalence is much higher (1). The parasystolic focus is more often in the ventricles (>50%) than in the atria (20%) or atrioventricular junction (20%) (2). Although most examples of parasystole have been reported in patients with heart disease, many persons with apparently normal hearts have these rhythms (1). Parasystolic rhythms per se appear to carry no significant risk. A repetitive pattern, or group beating, of which a bigeminal rhythm is the simplest example, has many causes, which include most of the abnormalities of impulse formation and impulse conduction (4). Because parasystolic rhythms usually are independent of the dominant cardiac rhythm, they do not often present as group beating. In this example, group beating occurs not because the parasystolic rhythm is coupled to the dominant rhythm, but because sinus rhythm is coupled to the parasystolic rhythm through the mechanism of ventriculoatrial conduction resetting the sinus node.