Electrocardiographic Rhythms-Biomedical terminology of ECG

Normal sinus rhythm

This is a normal rhythm, and is not of diagnostic significance unless the rate, which ranges from 60 to 100 beats per minute, is not appropriate for the clinical setting.

Sinus tachycardia

This rhythm differs from normal sinus rhythm only in that the rate is above 100 beats per minute. The differential diagnosis is extensive. Common causes are anxiety; physiological stress such as hemorrhage, dehydration, sepsis, and fever; and hyperthyroidism. Correction of the underlying cause, if necessary, is recommended.

Sinus bradycardia

This rhythm differs from normal sinus rhythm only in that the rate is below 60 beats per minute (bpm). This can be a normal finding in young patients, particularly in athletes. It can be caused by medications, including as beta blockers, some calcium blockers such as diltiazem, aldomet, and perhaps digitalis. If there is any concern about this rhythm, consultation with a Cardiologist is recommended.

Hidden Atrial Activation

Activation of the atrium by the sinus node can be inferred from surrounding sinus P waves. For example, if the P wave following a ventricular premature complex occurs at the time that would have been expected had the premature complex not occurred, then in can be inferred that the atrium was not activated retrogradely by the premature complex and that a hidden, or obscured, P wave did occur. Such an inference can be confirmed during invasive electrophysiologic study.

Sinus arrhythmia

This rhythm is usually a benign finding. It is characterized by variations in the heart rate from cycle to cycle that are greater than would be expected from normal respiratory variation. When pronounced, it can be symptomatic. If there is any concern about this rhythm, consultation with a Cardiologist is recommended.

Sinus arrest

This rhythm results from failure of the sinus node to activate the atria. When it is of short duration (less than one to two seconds), it is usually benign. When it is of long duration (greater than or equal to three seconds), it can be life-threatening because of the potential for longer periods of sinus arrest with asystole. It can be caused by medications, including as beta blockers, some calcium blockers such as diltiazem, aldomet, and perhaps digitalis. It can also be part of the sick sinus (“tachy-brady“) syndrome, which is one of the leading indications for implantation of permanent pacemakers in this country. If there is any concern about this rhythm, consultation with a Cardiologist is recommended.

Atrial premature complex

This is a P wave that occurs earlier than would be expected from the sinus rate, and that usually has an abnormal morphology. It can fail to conduct through the atrioventricular node, in which case it will not result in a QRS complex. As Dr. Marriott observes, “the commonest causes of pauses are non-conducted atrial premature complexes.” When it does conduct through the atrioventricular node, it can be conducted aberrantly if it traverses the bundle branches of the His-Purkinje system while one or both is in its relatively refractory period. Aberrantly conducted QRS complexes are wider than normal, and have the morphology of bundle branch block pattern.

Atrial premature complexes are a normal finding in adults of all ages. The frequency can be increased during stress, with ingestion of caffeine, and with sympathomimetic drugs such as some over-the-counter cold remedies.

Atrial couplet

This is a pair of atrial premature complexes in a row. While it is less common in normal subjects than are atrial premature complexes, it can still be benign. The appearance of atrial couplets should also raise the index of suspicion for susceptibility to atrial fibrillation, atrial flutter, and supraventricular tachycardia.

Atrial multiform couplet

This is a pair of atrial premature complexes, with differing P wave morphologies, in a row.

This is unusual in normal subjects, but is itself benign. The appearance of multiform atrial couplets, especially in patients with pulmonary disease, should raise the index of suspicion for susceptibility to multifocal atrial tachycardia, atrial fibrillation, and atrial flutter.

Nonconducted atrial premature complex

See atrial premature complexes.

Atrial escape complex

This is a P wave that occurs later than would be expected from the sinus rate. Like all escape complexes, it can occur only when the normal cardiac pacemaker does not function, as is sinus arrest.

Atrial tachycardia

This is a supraventricular rhythm resulting from either an atrial automatic focus or a reentrant circuit that lies entirely within the atrium. It is characterized by a rate more than 100 beats per minute, and a P wave morphology that is usually different from that of the sinus P wave. It can be intermittent or incessant (present more than 50% of the time). When it is incessant, it can cause symptomatic dilated cardiomyopathy that is reversible with control of the tachycardia.

This is an abnormal rhythm that can result from digitalis toxicity, particularly when it occurs in combination with Atrioventricular nodal block, second degree, Mobitz type I (Wenckebach).

For emergency treatment of this rhythm, when the patient has hypotension, angina, or acute congestive heart failure, synchronized cardioversion with appropriate anesthesia is indicated. For short-term pharmacologic control of this rhythm, drugs that decrease AV nodal conduction (beta blockers, calcium blockers, and diltiazem) may be considered. For long-term treatment of this rhythm, consultation with a Cardiac Electrophysiologist is recommended.

Atrial flutter

This is a supraventricular rhythm resulting from a reentrant circuit that lies within the right atrium. It is characterized by an atrial rate of 250 to 350 beats per minute, and a ventricular response that is usually about 75, 150, or 300 beats per minute. Flutter waves are best found in ECG leads II, III, aVF, and V1. Sometimes they are located at the onset or offset of the QRS complex, and are best found by comparison with the QRS morphology in a 12-lead ECG recording obtained during sinus rhythm. Even if flutter waves are not found, this rhythm should be suspected when the ventricular rate ranges from 140 to 160 beats per minute and there is no clear evidence of atrial activity.

It can occur alone, but is usually associated with hypertensive cardiomyopathy, COPD, or congestive cardiomyopathy. The new onset of either rhythm is seen in about 5% of cases of acute myocardial infarction. The clinician may also want to check for congestive heart failure, since worsening CHF can present with these rhythms.

For emergency treatment of this rhythm, when the patient has hypotension, angina, or acute congestive heart failure, synchronized cardioversion with appropriate anesthesia is indicated. For short-term pharmacologic control of this rhythm, drugs that decrease AV nodal conduction (beta blockers, calcium blockers, and digoxin) may be considered. For long-term treatment of this rhythm, consultation with a Cardiologist is recommended.

Atrial fibrillation

This is a supraventricular rhythm resulting from multiple reentrant circuits within either the right or left atria, or both. It is characterized by an irregularly irregular ventricular rate that is usually rapid in young patients, but may be normal or even bradycardic in elderly patients or patients taking medications that can cause atrioventricular nodal blockade.

It can occur alone, but is usually associated with hypertensive cardiomyopathy, COPD, or congestive cardiomyopathy. The new onset of either rhythm is seen in about 5% of cases of acute myocardial infarction. The clinician may also want to check for congestive heart failure, since worsening CHF can present with these rhythms.

Digitalis toxicity is suggested by a regular ventricular response (Accelerated junctional rhythm) in combination with atrial fibrillation.

In the presence of an accessory atrioventricular pathway, atrial fibrillation can manifest as a rapid, irregularly irregular wide complex tachycardia that can resemble ventricular tachycardia closely. It should be suspected particularly in young patients with very rapid tachycardia that is well tolerated hemodynamically. Close examination of the ECG will reveal irregularly irregular RR intervals. In this case:

  • It is important to obtain a 12-lead ECG before cardioversion because the location of the pathway, and therefore the risks of a subsequent curative catheter-mediated radiofrequency ablation procedure, can be estimated fairly accurately from the 12-lead ECG.
  • DO NOT give digitalis or verapamil to try to slow ventricular response if an accessory pathway is suspected. These drugs can accelerate conduction over accessory pathways, resulting in even more rapid ventricular activation which can, in turn, induce ventricular fibrillation.

There are four issues related to care of patients with this rhythm:

  • control of the rate of the ventricular response,
  • conversion of the atrial rhythm to sinus rhythm,
  • maintenance of sinus rhythm following conversion, and
  • prevention of embolic stroke from thrombi that form in the fibrillating left atrium.

Consultation with an Internist or Cardiologist is recommended for advice on these issues.

Wandering atrial pacemaker

This is a supraventricular rhythm resulting from multiple ectopic foci in the atria. It is characterized by three or more P wave morphologies and a rate less than 100 beats per minute. It itself is benign, but reflects electrical abnormalities in one or both atria that increase the likelihood of multifocal atrial tachycardia or other atrial arrhythmias.

Multifocal atrial tachycardia

This is a supraventricular rhythm resulting from multiple ectopic foci in the atria. It is characterized by three or more P wave morphologies and a rate greater than or equal to 100 beats per minute. It is seen most frequently in patients with severe pulmonary disease. The rapid ventricular rate can be symptomatic (hypotension, angina, congestive heart failure). Treatment includes improvement of the concommitant pulmonary disease, and consideration of adminstration of verapamil. Digoxin is not effective in treatment of this rhythm. Consultation with an Internist, Pulmonologist or Cardiologist is recommended for further advice.

Junctional escape complex

This is a QRS with normal morphology for the patient that is not preceded by a P wave and occurs later than would be expected from the sinus rate. Like all escape complexes, it can occur only when the normal cardiac pacemaker does not function, as is sinus arrest.

Junctional premature complex

This is a QRS complex that occurs earlier than would be expected from the sinus rate, and that usually has a normal morphology for the patient. It can fail to conduct retrograde through the atrioventricular node, in which case it results in a compensatory pause. That is, the next P wave occurs at the same time as would be expected had the VPC not occurred. More usually, it does conduct through the atrioventricular node, so that the following P wave may occur either sooner or later than would be expected.

Junctional premature complexes are relatively uncommon. They can be seen with increased frequency during stress, with ingestion of caffeine, and with sympathomimetic drugs such as some over-the-counter cold remedies. They can also be misdiagnosed when the P wave of an atrial premature complex is obscured by the preceding T wave.

Junctional premature couplet

See junctional premature complex. This is an unusual rhythm, and most likely represents two cycles of one of the supraventricular tachycardia.

Junctional rhythm

This is a slow rhythm, with rates ranging from 40 to 60 beats per minute, with QRS complexes that have the patient’s normal morphology. Usually, no P waves are seen. When P waves are present, they follow closely after the QRS complexes.

This rhythm results from the backup pacemaker capability of the atrioventricular node during sinus arrest.

Accelerated junctional rhythm

This is a supraventricular rhythm resulting from a focus in or near the atrioventricular junction. The rate ranges from 60 to 100 beats per minute.

This is an abnormal rhythm that can result from digitalis toxicity, particularly when it occurs in combination with atrial fibrillation. It can also result from physiologic stress and other causes of increased sympathetic nervous system tone.

Junctional tachycardia

This is a supraventricular rhythm resulting from a focus in or near the atrioventricular junction. The rate is greater than or equal to 100 beats per minute. See also Accelerated junctional rhythm.

This rhythm usually results from a primary arrhythmia rather than as a response to physiologic stimulation. The electrocardiogram usually cannot distinguish this rhythm from the more common types of Supraventricular tachycardia, for which different treatments may be appropritae. Consultation with a Cardiac Electrophysiologist is recommended for further evaluation.

Atrioventricular nodal block, first degree

This refers to an excessively long PR interval only. All P waves are conducted through the atrioventricular node to the ventricle. By itself, it is a benign condition, but may result from disease in the atrioventricular node, high vagal tone, or medication that reduces conduction through the atrioventricular node.

Atrioventricular nodal block, second degree, Mobitz type I (Wenckebach)

This refers to a gradual prolongation of the PR interval, with occasional failure to conduct a P wave through the atrioventricular node to the ventricle. By itself, it is a benign condition, but may result from disease in the atrioventricular node, high vagal tone, or medication that reduces conduction through the atrioventricular node. It is commonly seen in atheletic young patients, particularly during sleep.

This is an abnormal rhythm that can result from digitalis toxicity, particularly when it occurs in combination with Atrial tachycardia.

It is distinguished from Second degree Atrioventricular nodal block, Mobitz type II by the fact that the PR interval of the P wave that follows the non-conducted P wave is at least 10 msec shorter than the PR interval of the P wave that precedes the non-conducted P wave. Typically, the QRS complex is unchanged from the patient’s normal QRS morphology. By contrast, the PR interval does not change in Mobitz type II block. Mobitz type II block is dangerous because it can progress to complete heart block and death without warning.

Atrioventricular nodal block, second degree, Mobitz type II

This refers to occasional failure to conduct a P wave through the atrioventricular node to the ventricle without a change in the PR interval after the nonconducted P wave compared with before the nonconducted P wave. This is a dangerous condition because it can progress to complete heart block and death without warning. Immediate consultation with a Cardiologist for placement of a temporary pacemaker is advisable. Placement of an external pacemaker may be lifesaving if a temporary pacemaker cannot be placed immediately.

This condition, while dangerous, is very unusual. The QRS complex is usually wide, due to extensive disease of the His-Purkinje system, although a narrow QRS complex does not exclude the diagnosis. The clinician should measure the change in PR interval carefully, as described for Second degree Atrioventricular nodal block, Mobitz type I.

2:1 Atrioventricular nodal block

This rhythm is diagnosed when the entire rhythm strip shows only conduction of every other P wave to the ventricle. Because the record does not show two consecutive P waves that conduct to the ventricle, it is not possible to measure prolongation of the PR interval, so that it is not possible to distinguish between Mobitz type I and the dangerous Mobitz type II Second degree Atrioventricular nodal block. By convention, recordings obtained at other recent times are used to make this distinction.

Third degree (complete) heart block

This rhythm is characterized by failure of conduction from the atria through the atrioventricular node to the ventricles. The atrial rhythm is independent of the ventricular rhythm, unless an accessory pathway that conducts antegrade is present. It is most easily distinguished from high-grade atrioventricular nodal block when the atrial and ventricular rhythms are regular but have different rates. Because of weak coupling between the chambers by the autonomic nervous system, these rates can be very close to each other and in fact can oscillate around each other.

Complete heart block is one of three forms of atrioventricular dissociation. The other two forms are

  • Sinus arrest or sinus bradycardia with junctional rhythm or Idioventricular rhythm.
  • Ventricular tachycardia.

Of these three forms, only Complete Heart Block results from antegrade conduction block from the atria to the ventricles.

Ventricular premature complex

This is a wide QRS complex that occurs earlier than would be expected from the sinus rate, and that almost always has an abnormal morphology. It fails to conduct retrograde through the atrioventricular node in half of patients, in which case it results in a compensatory pause. That is, the next P wave occurs at the same time as would be expected had the VPC not occurred. When it does conduct through the atrioventricular node, the following P wave may occur either sooner or later than would be expected.

Ventricular premature complexes are a normal finding in adults of all ages. The frequency can be increased during stress, with ingestion of caffeine, and with sympathomimetic drugs such as some over-the-counter cold remedies. The frequency is also increased in patients with a tendency to develop ventricular tachycardia.

Ventricular couplet

Two ventricular premature complexes  in a row. This can be a normal finding, but is more suggestive of electrical heart disease than are single ventricular premature complexes.

Ventricular escape complex

This is a QRS that is wide and occurs later than would be expected from the sinus rate. Like all escape complexes, it can occur only when the normal cardiac pacemaker does not function, as is sinus arrest.

Asystole, Ventricular standstill

This is diagnosed when only ventricular escape complexes are present, and they occur very slowly. This is an agonal rhythm that is not consistent with life. If you see this, you should initiate Cardiopulmonary Resuscitation immediately.

Idioventricular rhythm

This is diagnosed when only ventricular escape complexes are present, and they occur at 20 to 40 beats per minute. This rhythm is barely consistent with life. If you see this, you should consider initiating Cardiopulmonary Resuscitation immediately, and should move the patient to an intensive care unit as soon as possible.

DO NOT give lidocaine or any other antiarrhythmic medication for this rhythm. You could cause asystole and death by inhibiting the only spontaneous rhythm the patient’s heart is able to generate.

Accelerated ventricular rhythm

This is diagnosed when only ventricular escape complexes are present, and they occur at 60 to 100 beats per minute. This rhythm is usually seen in the setting of acute myocardial infarction. If the patient is in sinus rhythm, the rate of this rhythm tends to be about the same as the rate of the sinus rhythm. In this case, the two rhythms will speed up and slow down so that they alternately capture the ventricle, with characteristic periods of fusion QRS complexes during the changes in rate.

This rhythm is usually benign. Because it occurs in the setting of acute myocardial infarction, patients who exhibit it are already in an intensive care unit where any malignant sequellae can be treated readily.

Ventricular tachycardia, General

This rhythm is diagnosed when three or more premature ventricular complexes occur in a row at a rate of 100-120 beats per minute or faster. The major clinical distinctions are between hemodynamically unstable versus stable ventricular tachycardia and between sustained versus unsustained ventricular tachycardia.

Hemodynamically unstable ventricular tachycardia is a life threatening emergency for which the ACLS protocol should be initiated immediately. Synchronized cardioversion is usually the treatment of choice. Awake patients should be sedated heavily before cardioversion if at all possible.

Sustained ventricular tachycardia is defined as having a duration of 30 seconds or more, or being hemodynamically unstable. The immediate treatment is specified by the ACLS protocol. For long-term treatment, it is important to realize that these patients have a 20% to 40% sudden death mortality, when untreated, over the 12 months following initial presentation. Empiric treatment with antiarrhythmic drugs does not reduce this mortality. Effective treatment with drugs and/or an implantable cardioverter defibrillator reduces the sudden death mortality over the next 12 months to 0-2%. Therefore, consultation with a Cardiac Electrophysiologist is recommended during the initial hospital stay to ensure adequate evaluation and treatment before discharge from the hospital.

Ventricular tachycardia, polymorphic

This form of ventricular tachycardia is characterized by changing QRS morphology, sometimes accompanied by slight changes in the rate. It is a particularly malignant form of ventricular tachycardia that is thought to be intermediate between ordinary monomorphic ventricular tachycardia, and ventricular fibrillation. For etiology, think of proaarrhythmia , as from type IA antiarrhythmic medications, hypokalemia, hypomagnesemia, profound bradycardia, and idiopathic prolonged QT syndrome.

Ventricular fibrillation

This is a lethal rhythm, characterized by absence of both organized electrical and organized mechanical activity. This rhythm is equivalent to cardiac death. If you see this, you should initiate Cardiopulmonary Resuscitation immediately.

Bundle branch block

This term refers to the QRS morphology seen when either the right bundle branch or the left bundle branch fails to conduct from the His bundle to the ipsilateral ventricle. Right bundle branch block is characterized by an “M” pattern in V1 and wide S waves in the lateral leads (I, V6). Complete left bundle branch block is characterized by negative forces (QS or rS) in V1 and positive forces (monophasic R wave with no Q wave) in V6. Incomplete left bundle branch block can manifest as left anterior hemiblock or left posterior hemiblock. Consultation with Marriott’s “Practical Electrocardiology”, or the ECG textbook of your choice, is recommended for further information.

Atrioventricular nodal reentrant tachycardia

This is a reentrant supraventricular rhythm whose circuit is located in the region of the atrioventricular node. It is characterized by a QRS morphology that is normal for the patient. P waves may or may not be seen, but they follow closely after the QRS if they are seen.

Only about 60% of narrow-complex tachycardias have this mechanism. It is important to note that 20% of narrow-complex tachycardias are atrioventricular reentrant tachycardias, which use a concealed accessory pathway for retrograde conduction.

The clinical significance of this rhythm depends on the rate. It stops abruptly with effective treatment. The usual initial treatments are the Valsalva maneuver, then intravenous adenosine. If these are unsuccessful, one can try medication that reduces conduction through the atrioventricular node. Consultation with a Cardiac Electrophysiologist is recommended for follow-up because this rhythm can now be cured by catheter-mediated radiofrequency ablation.

Atrioventricular reentrant tachycardia (AVRT)

This is a reentrant supraventricular rhythm whose circuit includes both the atrium and the ventricle, and that uses an accessory atrioventricular pathway for at least one limb of the circuit. “Orthodromic” AVRT, which is the most common form, proceeds antegrade (from atrium to ventricle) over the AV node, and retrograde over an accessory pathway. “Antedromic” AVRT proceeds in the reverse direction, and has is a wide QRS tachycardia except when the accessory pathway is located in the right anteroseptal location very close to the His bundle. When multiple pathways are present, it is also possible for the circuit to use two pathways as a circuit.

P waves may or may not be seen, but they usually do not follow closely after the QRS if they are seen.

The clinical significance of this rhythm depends on the rate. It stops abruptly with effective treatment. The usual initial treatments are the Valsalva maneuver, then intravenous adenosine. If these are unsuccessful, one can try medication that reduces conduction through the atrioventricular node, except that verapamil and digitalis SHOULD NOT BE GIVEN. Consultation with a Cardiac Electrophysiologist is recommended for follow-up because this rhythm can now be cured by catheter-mediated radiofrequency ablation.

Supraventricular tachycardia

This is a generic name for a variety of specific supraventricular rhythms, including Atrioventricular Reentrant Tachycardia, Atrioventricular Nodal Reentrant Tachycardia, and Atrial Tachycardia. It is also used in reference to any narrow complex rhythm to distinguish it from wide-complex rhythms that could arise in the ventricle. In addition to the specific rhythms mentioned above, this use of the term includes atrial fibrillation, atrial flutter, junctional tachycardia, accelerated junctional rhythm, and multifocal atrial tachcyardia,

Parasystole

The rhythm that results from intermittent capture of the ventricle by a ventricular focus that has entrance block. That is, it is not depolarized when the remainder of the ventricle is activated. The rhythm is characterized by premature ventricular complexes with variable coupling intervals (intervals from the preceding normal QRS complex to the premature complex) and with constant intervals between the premature complexes. Detection of the latter constancy usually requires finding the least common denominator of the intervals between premature complexes, because of the intermittency of ventricular capture by the focus.

This rhythm is rare. It is usually considered benign, although any premature ventricular activation can induce malignant ventricular rhythms in the ischemic myocardium or in the presence of a suitable myocardial subtrate.

Wolff-Parkinson-White syndrome

The term used to describe the presence of one or more accessory atrioventricular pathways that conduct in the antegrade direction, with or without retrograde conduction. Patients with this syndrome are susceptible to atrioventricular reentrant tachycardia and atrial fibrillation.

Reciprocal complex

A QRS complex that is caused by activation of a reentrant circuit rather than by the sinus node. This can be harbinger of atrioventricular nodal tachycardia or atrioventricular tachycardia.

Retrograde atrial activation

A P wave that occurs because of activation of a portion of the heart below the sinus node, including elsewhere in the atrium, the atrioventricular node (via the fast or a slow AV nodal pathway) or the ventricle (via an accessory pathway). Retrograde P waves typically are inverted in the inferior and right precordial ECG leads (II, III, aVF, and V1), in which the normal sinus P wave is upright.

Atrioventricular dissociation

This term refers to a group of three categories of rhythms in which the atrial and ventricular rhythms are unrelated to each other. The three categories are:

  • Third degree (complete) heart block.
  • Sinus arrest or sinus bradycardia with junctional rhythm or Idioventricular rhythm.
  • Ventricular tachycardia.
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