George Nikolić

The Bix rule

The patient was a 64-year-old man with a history of myocardial infarction and subsequent episodes of atrial fibrillation and sinus bradycardia. A permanent ventricular inhibited rate responsive pacemaker was inserted 6 months before the outpatient visit, during which the electrocardiogram (ECG) shown in Figure 1 was recorded. He had been taking sotalol 160 mg twice per day for maintenance of sinus rhythm. The patient was asymptomatic apart from somewhat reduced exercise tolerance. His pacemaker was functioning as originally programmed. No changes were made, and he was sent home with instructions for routine follow-up. The cardiogram was originally thought to show sinus rhythm 67 beats/min with marked (0.44 sec) first-degree arteriovenous block and an appropriate paced escape beat at the end of the recording; deep symmetric T-wave inversion in multiple leads re

Tachycardia in ebstein’s anomaly

The patient was a 19-year-old girl with known Ebstein’s anomaly. She was on flecainide 100 mg bd for recurrent, long-standing attacks of palpitations. She presented to the emergency department during one of those attacks. The physical examination was unremarkable apart from tachycardia of 140 beats per minute. A 12-lead electrocardiogram (ECG) was obtained (Fig 1) and adenosine, 12 mg intravenously, was administered. The ECG changed immediately (Fig 2). As its lower strip shows, the tachycardia returned and adenosine was given one more time. No further therapy was required. Another ECG was taken (Fig 3). She was reassured and sent home on flecainide. The initial ECG was thought to represent an atrial tachycardia with left bundle branch block (LBBB) aberrancy. This impression appeared to be confirmed by the response to adenosine. However, there are problems with this interpretation: 1) aberrancy comprising LBBB with right axis deviation has not been reported to date, and 2) the LBBB itself is very broad and has an unusual slurred S wave descent in lead V1. Morphologically, the QRS complex (0.20 sec in the precordial leads) would be typical of ventricular tachycardia, even allowing for the intraventricular conduction delay possibly contributed by flecainide. Yet it cannot be ectopic venFrom the Intensive Care Unit, Canberra Hospital Canberra, Australia. Reprint requests: George Nikolic, MB, BS, FRACP, FACC, Canberra Hospital, PO Box 11, Woden, ACT 2606, Australia. Copyright

Cardiographic conundrum: Adding insult to injury

The patient was a 78-year-old woman monitored for carbon dioxide retention after laparotomy. She was admitted a day earlier with bowel obstruction due to adhesions. Her rhythm on admission was coarse atrial fibrillation with ventricular response of 100 beats/min, which reverted spontaneously to sinus rhythm. Her postoperative trace is shown in Figure 1. The trace shows sinus tachycardia 100 beats/min with 3 atrial ectopic beats and 1 ventricular ectopic beat; the tachycardia is conducted in Wenckebach sequences. There is also well-marked left atrial abnormality, small frontal leads voltage, and nonspecific T-wave changes. Sinus P waves are conducted with PR intervals of 0.24 to 0.48 seconds, inscribing typical Wenckebach sequences, with acceleration of the distal chamber due to decremental increases in the conducted PR intervals. There are no “dropped beats” because atrial premature waves, P’s, are in front of the last QRS before the pause.

Ventricular tachycardia: How many beats?

Cite this article: Nikoli c, G. (2012, SEPTEMBER/OCTOBER). Ventricular tachycardia: How many beats? Heart & Lung, 41(5), 507-508. doi:10.1016/j.hrtlng.2012.04.003. The strip below (Figure 1) belongs to a 46-year-old man receiving streptokinase infusions for an acute myocardial infarction. On the morning round, the Attending Physician remarked that runs of ventricular tachycardia (VT) such as these are generally discounted, and may in fact be a signal of successful reperfusion. His Fellow, looking at the strip, said that he could see only one run, the four-beat run in the first half of the strip. “Well,” said the Attending Physician, moving to the next patient, “Most of the beats here are of ectopic ventricular origin.” Some shaking of heads followed: a conundrum. First of all, does the broad-complex rhythm qualify for a designation of VT? It does. A rate of 100/minute or more defines it, provided that its complexes are of ectopic ventricular provenance. To say ectopic ventricular rather than merely ventricular is important, because all QRS complexes are ventricular. The evidence for their ectopic origin in this strip relies heavily on atrioventricular (AV) dissociation: a sinus BS, FRACP, FACC, 11 Bird ikoli c). er Inc. All rights reserved P wave can be mapped out to the onset of the first broad complex, and another is seen at the end of the first complex of the second run. But should we say “run” or “runs”? The second group of broad complexes is not just a couplet. In addition to the AV dissociation of the first beat, the strip shows an AV association of the second beat: a retrograde P wave precedes a normal QRS complex. In fact, both episodes of ventricular ectopic activity are terminated by echo beats, marked by inverted P waves and a QRS morphology identical to that of the sinus beats. Thus more QRS complexes of ventricular than of supraventricular origin occur here, i.e., 8 vs. 7. The echo (reentry) beats are surely of ventricular ectopic origin. Sinus captures should be mentioned in the differential diagnosis of VT terminated by a narrow complex. The polarity of P waves can be difficult to ascertain when the P waves are superimposed on T waves or sloping ST segments. In this case, not only are the wood Street, Hughes, Australian Capital Territory 2605, Australia.

An unusual conduction.

T he patient was an 89-year-old woman with a history of hypertension and strokes. Her medication consisted of aspirin and dipyridamole. The cardiovascular examination was unremarkable. A routine 12-lead electrocardiogram was obtained on the patient’s admission to the rehabilitation ward (Fig 1). This seemingly unprepossessing trace passed, to most observers, for intermittent, probably ratedependent, left bundle branch block (LBBB). They were not wrong. What they missed, however, is the progressive LBBB, best seen in lead aVL and further defined in the simultaneous leads below.

Two aberrancies for the price of one.

T he patient was a 29-year-old woman with unexplained persistent vomiting and mild (3.4 mEq/L) hypokalemia. Except for a regularly irregular pulse, there were no other abnormalities. A 12-lead electrocardiogram was obtained (Fig 1). The allorhythmia accounting for her pulse consists of repetitive triplets comprising a sinus beat and supraventricular ectopic beat followed by a junctional escape beat. Three premature supraventricular ectopic beats are probably present, judging from the P’ shape and the longer-than-sinus PR interval of atrial origin. The first beat has incomplete

Cardiovascular Effects of Cimetidine

Excerpt To the editor: The cardiovascular effects of Cimetidine have never been documented through organized studies addressing this problem; the number of case reports describing them may merely r...