Delta wave

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12 lead EKG shows typical Delta waves in a patient with WPW syndrome.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

In both cardiology and neurology, there are references to the "Delta wave".


A delta wave can be observed in patients with Wolff-Parkinson-White syndrome.

Wolff-Parkinson-White syndrome (WPW) is a syndrome of pre-excitation of the ventricles of the heart due to an accessory pathway known as the Bundle of Kent. This accessory pathway is an abnormal electrical communication from the atria to the ventricles.

The incidence of WPW syndrome is between 0.1 and 3% of the general population.[1][2][3]

While the vast majority of individuals with WPW syndrome remain asymptomatic throughout their entire lives, there is a risk of sudden death associated with the syndrome. Sudden death due to WPW syndrome is rare (incidence of less than 0.6%[3][4]), and is due to the effect of the accessory pathway on tachyarrhythmias in these individuals.


In normal individuals, electrical activity in the heart is initiated in the sinoatrial (SA) node (located in the right atrium), propagates to the atrioventricular (AV) node, and then through the bundle of His to the ventricles of the heart. (See electrical conduction system of the heart).

The AV node acts as a gatekeeper, limiting the electrical activity that reaches the ventricles of the heart. This function of the AV node is important, because if the signals generated in the atria of the heart were to increase in rate (as they do during atrial fibrillation or atrial flutter), the AV node will limit the electrical activity that conducts to the ventricles. For instance, if the atria are electrically activated at 300 beats per minute, half those electrical impulses are blocked by the AV node, so that the ventricles are activated at 150 beats per minute (giving a pulse of 150 beats per minute). Another important property of the AV node is that it slows down individual electrical impulses. This is manifest on the ECG as the PR interval, the time from activation of the atria (manifest as the P wave) and activation of the ventricles (manifest as the QRS complex).

Individuals with WPW syndrome have an accessory pathway that connects the atria and the ventricles, in addition to the AV node. This accessory pathway is known as the bundle of Kent. This accessory pathway does not share the rate-slowing properties of the AV node, and may conduct electrical activity at a significantly higher rate than the AV node. For instance, in the example above, if an individual had an atrial rate of 300 beats per minute, the accessory bundle may conduct all the electrical impulses from the atria to the ventricles, causing the ventricles to activate at 300 beats per minute. Extremely fast heart rates are potentially dangerous, and can cause hemodynamic instability. In some cases, the combination of an accessory pathway and cardiac arrhythmias can trigger ventricular fibrillation, a leading cause of sudden cardiac death.


One beat from a rhythm strip in V2 demonstrating characteristic findings in WPW syndrome. Note the characteristic delta wave (subtler here than in some cases), the short PR interval of 0.08 seconds, and the long QRS complex at 0.12 seconds.

WPW syndrome is commonly diagnosed on the basis of the surface ECG in an asymptomatic individual. In this case it is manifested as a delta wave, which is a slurred upstroke in the QRS complex that is associated with a short PR interval. The short PR interval and slurring of the QRS complex is actually the impulse making it through to the ventricles prematurely (across the accessory pathway) without the usual delay experienced in the AV node.

If the patient experiences episodes of atrial fibrillation, the ECG will show a rapid polymorphic wide-complex tachycardia (without turning of the points). This combination of atrial fibrillation and WPW is considered dangerous, and most antiarrhythmic drugs are contraindicated.

When an individual is in normal sinus rhythm, the ECG characteristics of WPW syndrome are a short PR interval, widened QRS complex (greater than 120 ms in length) with slurred upstroke of the QRS complex, and secondary repolarization changes reflected in ST segment-T wave changes.

In individuals with WPW syndrome, electrical activity that is initiated in the SA node travels through the accessory pathway as well as through the AV node to activate the ventricles via both pathways. Since the accessory pathway does not have the impulse slowing properties of the AV node, the electrical impulse first activates the ventricles via the accessory pathway, and immediately afterwards via the AV node. This gives the short PR interval and slurred upstroke to the QRS complex known as the delta wave.

Patients with WPW often exhibit more than one accessory pathway, and in some patients as many as eight additional abnormal pathways can be found. This has been seen in individuals with Ebstein's anomaly.

Wolff-Parkinson-White syndrome is sometimes associated with Leber's hereditary optic neuropathy (LHON), a form of mitochondrial disease.[5]


Delta waves

A delta wave is a large, slow (2 Hz or less) brain wave recorded with an EEG and is usually associated with deep sleep.

Delta activity is characterized by frequencies under 3 Hz and is absent in awake healthy adults, but is physiological and normal in awake children under the age of 13. Delta waves are also naturally present in stage three and four of sleep (deep sleep) but not in stages 1, 2, and rapid eye movement (REM) of sleep. Finally, delta rhythm can be observed in cases of brain injury and comatic patients.

Human non-rapid eye movement (NREM) sleep is divided in the categories 2, 3, and 4 by the percentage of slow waves.


  1. Rosner MH, Brady WJ Jr, Kefer MP, Martin ML. (1999). "Electrocardiography in the patient with the Wolff-Parkinson-White syndrome: diagnostic and initial therapeutic issues". American Journal of Emergency Medicine. 17 (7): 705–14. PMID 10597097.
  2. Sorbo MD, Buja GF, Miorelli M, Nistri S, Perrone C, Manca S, Grasso F, Giordano GM, Nava A. (1995). "The prevalence of the Wolff-Parkinson-White syndrome in a population of 116,542 young males". Giornale Italiano di Cardiologia (in Italian). 25 (6): 681–7. PMID 7649416.
  3. 3.0 3.1 Munger TM, Packer DL, Hammill SC, Feldman BJ, Bailey KR, Ballard DJ, Holmes DR Jr, Gersh BJ. (1993). "A population study of the natural history of Wolff-Parkinson-White syndrome in Olmsted County, Minnesota, 1953-1989". Circulation. 87 (3): 866–73. PMID 8443907.
  4. Fitzsimmons PJ, McWhirter PD, Peterson DW, Kruyer WB (2001). "The natural history of Wolff-Parkinson-White syndrome in 228 military aviators: a long-term follow-up of 22 years". American Heart Journal. 142 (3): 530–6. PMID 11526369 doi:10.1067/mhj.2001.117779.
  5. Mashima Y, Kigasawa K, Hasegawa H, Tani M, Oguchi Y. (1996). "High incidence of pre-excitation syndrome in Japanese families with Leber's hereditary optic neuropathy" (subscription required). Clinical Genetics. 50 (6): 535–7. PMID 9147893.

See also


de:Deltawelle (EEG)

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