This ECG (11) shows a narrow complex tachycardia at a rate of 143 per minute- Deep

negative atrial waves are seen in the inferior leads, one in the usual position of the P wave and another just following the ORS complex-

The negative nadirs have a regular rhythm with a rate of 286 per minute- Small upright

atrial waves are seen in V1, one just preceding the QRS and the other closely

following the previous ORS, also having a regular rhythm at a rate of 286 per minute.

This pattern is typical of atrial flutter with 2:1 conduction ratio.

Atrial flutter with 2:1 conduction ratio is often misdiagnosed because it is somewhat

difficult to appreciate the atrial waveform when most of the atrial activity is superimposed on either the ORS complex or the T wave. Slowing the ventricular rate

transiently with carotid sinus pressure or adenosine administration reveals the typical

continuous atrial waveform

Atrial flutter is characterized by an atrial waveform that is regular in rhythm. constant

in waveform. and is a continuous undulation in the inferior Iimb leads rather than discrete P waves- ln V1 on the other hand. there are discrete waves separated by isoelectric periods. The atrial rate may vary widely. But is often very close to 300 per minute.

Three types of atrial flutter have been described. The common form of classical

atrial flutter usually has an atrial rate in the range of 260 to 320 per minute. unless slowed by antiarrhythmic drugs or by marked enlargement of the right atrium. The atrial waveform features sharp negative nadirs in the inferior leads and resembles a sawtooth. or a picket fence. The mechanism of the common form of classical flutter is a macro reentrant circuit around virtually the entire right atrium. in a counterclockwise direction-

A critical part of the circuit is a zone of slow conduction in the isthmus area of the low

right atrium. between the inferior vena caval orifice and the tricuspid annulus.

An uncommon form of classical flutter exists. in which the waveform appears to have

predorninantly positive waves in the inferior leads but is otherwise similar to the common form. The uncommon form usually has a circuit in the clockwise direction.

The third form of atrial flutter (Type II flutter) is characterized by faster atrial rates. in the range of 340 to 440 per minute and also by an inability to be terminated by atrial overdrive pacing.

Classical atrial flutter can usually be controlled by radio frequency catheter

ablation. which produces a block in the slowly conducting isthmus-

References:

Puech P. Latour H. Grolleau R. Le flutter et ses lirnits- Arch Mal Coeur Vaiss

1970:61}:116-44-

Schwartzman D. Callans DJ. Gottlieb CD. Dillon SM. Movsowitz C. Marchlinski FE-

Conduction block in the inferior vena cavaltricuspid valve isthmus: association with

outcorne of radiofrequency ablation of type l atrial flutter- J Am Coll Cardiol

1996:23:1519-31-

Waldo AL- Atrial flutter. ln: Podrid PJ. Kowey PR. eds. Cardiac Arrhythmia Mechanisms- Diagnosis and management- Baltimore

Williams & Wilkins: 1995:p. 791 -802- WeIIs JL. MacLean WA- James TN- Waldo AL- Characterization of atrial flutter- Studies in rnan after open heart surgery using fixed atrial electrodes- Circulation 1979:60:665-73

The ECG shows:

• Atrial fibrillation with a ventricular rate of

60-65/min

• Normal axis

• Normal QRS complexes

• Prominent U wave in lead V2

• Downward-sloping ST segments, best seen in leads V5—V6

Clinical interpretation

The downward-sloping ST segments (the ’reverse tick’) indicate that digoxin has been given. The ventricular rate seems well-controlled. The prominent U waves in lead V2 could indicate  hypokalemia.

Answer 4

The ECG shows:

• Sinus rhythm

• Normal axis

- Q waves in leads V2—V4

• Raised ST segments in loads V2-V4

•Inverted T waves in leads I., VL, V2—V6

Clinical inferpretation

This is a classic acute anterior myocardial

infarction.

ANSWER 3

The ECG shows:

• Complete heart block

• Ventricular rate 45/min

Clinical interpretation

In complete heart block there is no relationship between the P waves (here with a rate of 70 lat / min) and the QRS complexes. The ventricular ’escape’ rhythm has wide QRS cornplexes and abnormal T waves. No further interpretation of the ECG is possible.

ANSWER 2

The ECG shows:

• Sinus rhythm

• Normal axis

• Small Q waves in leads Il, III, VF

• Biphasic T waves in leads ll, V6; inverted T

waves in leads III , VF

• Markedly peaked T waves in leads V1—V2

Clinical interpretation

The Q waves in the inferior leads, together with inverted T waves, point to an old inferior myocardial infarction. While symmetrically peaked T waves in the anterior leads can be due to hyperkalaemia, or to ischaemia, they are frequently a normal variant.

The patient seems to have had a myocardial infarction at some point in the past, and by implication his vague chest pain may be due to cardiac ischaemia.

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Discussion ECG 5

In this ECG hypothermia is strongly suggested by a combination of findings. 1) Osborn waves (sometimes designated J waves) are present in leads V2-V6- 2) The QT is quite prolonged to 0.57 seconds- 3) The limb leads are almost obscured by a movement artifact typical of shivering with relative sparing of the precordial leads.

Osborn waves are deflections at the junction of the QRS and the ST segrnent which are positive in leads over the left ventricle. The waves are named for John J. Osborn (sometirne misspelled Osborne in current publications), who published his results in experimental hypothermia in dogs in 1953.

Osborn noted that others had Publisher similar ECG observations in 1950 and 1952: However, his name has remained attached to the finding. He interpreted the wave as “a current of injury”: however. The electrophysiologic mechanism remains unclear- The morphology resembles the type of deflection occasionally seen in young persons with ST segment elevation of early repolarization.

References:

Castellanos A. Kessler KM. Myerherg RJ. The resting electrocardiograrn. In Hurst’s The Heart. ed. Schlant RC. Alexander RW. New York: McGraw-Hill. 3th ed.. 1994. p 321.

Oshorn JJ. Experimental hypothermia: Respiratory and hlood pH changes in relation to cardiac function. Am J Physiol 1953:175: 339-98.

The ECG shows an irregular rhythm. that consists of one to three consecutive sinus beats at 88 per rninute. followed by runsof tachycardia of three to five beats in duration at approximately 150 per rninute.

The ORS complexes are the same in the sinus and tachycardia beats indicating that the tachycardia is supraventricular- The first beat of each run of tachycardia is initiated by a premature P wave (superimposed on the T wave} with a longer PR interval than that of the sinus beats. The second and subsequent beats during the tachycardia are preceded by P waves that have a different morphology than the initiating atrial premature beat- They are inverted in the inferior leads consistent with retrograde atrial activation- The retrograde P waves fall closer to the following ORS complex than to the preceding one. Thus. this is a long RP tachycardia.

This pattern is characteristic of a reentrant tachycardia in which the retrograde conduction is through a slowly conducting pathway- The mechanism is similar to that of atypical AV nodal reentrant tachycardia (AVNRT`)- The retrograde pathway is slow resulting in the long RP interval. Ectopic atrial tachycardia can also cause a long RP tachycardia with inverted P waves in the inferior leads. The mode of onset indicates the reentrant mechanism in the present case.

When a long RP tachycardia continually starts and stops and is present for rmuch of the 24 hours per day, it is usually designated as the perrnanent forrn of junctional reciprocating tachycardia (PJRT)- Typical and atypical AVNRT usually occur in discrete paroxysms lasting longer, but occurring at intervals more widely separated in time, than the nearly continuous runs of tachycardia seen in PJRT. The rate of PJRT is often in the range of 110 to 140 in adults, contrasted with the usually faster rates of 150 to 220 in AVNRT. The present case is intermediate with regard to the rate. PJRT is usually classified with the tachycardias caused by reentry via accessory pathways. However, the accessory pathway in PJRT is physiologically similar to AV nodal tissue. and is also usually located close to the AV node. Such pathways have even been termed “accessory AV nodes”. PJRT is particularly likely to induce the tachycardia-related reversible cardiomyopathy syndrorne, because it is often present nearly continuously for months or years. It can usually be cured by radiofrequency catheter ablation.

References:

Chien WW. Cohen TJ. Lee MA. et al. Electrophysiological findings and long-term follow-up of patients with the permanent form of junctional reciprocating tachycardia treated hy catheter ablation. Circulation 1992:85:1329-36.

Coumel P. Cahrol C. Fabiato A. Gourgon R. Slama R. Tachycardie permanente par rythme reciproque. Arch Mal Coeur \/aim; 1967: 60:1330.

Gallagher JJ. Sealy WC. The permanent form Of junctional reciprocating tachycardia: further elucidation of the underlying mechanism. Eur J Cardiol 1978:8:413-30.