An ectopic pacemaker, also known as ectopic focus or ectopic foci, is an excitable group of cells that causes a premature heart beat outside the normally functioning SA node of the heart. It is thus a cardiac pacemaker that is ectopic, producing an ectopic beat. Acute occurrence is usually non-life-threatening, but chronic occurrence can progress into tachycardia,[1] bradycardia or ventricular fibrillation.[2] In a normal heart beat rhythm, the SA node usually suppresses the ectopic pacemaker activity due to the higher impulse rate of the SA node. However, in the instance of either a malfunctioning SA node or an ectopic focus bearing an intrinsic rate superior to SA node rate, ectopic pacemaker activity may take over the natural heart rhythm.[3] This phenomenon (an intrinsically slower pacemaker activity being unmasked by failure of faster pacemaker tissue 'upstream') is called an escape rhythm, the lower rhythm having escaped from the dominance of the upper rhythm. As a rule, premature ectopic beats (i.e. with a shorter than the prevailing preceding R-R' interval) indicate increased myocyte or conducting tissue excitability, whereas late ectopic beats (i.e. with a prolonged preceding R-R' interval) indicate proximal pacemaker or conduction failure with an escape 'ectopic' beat.
| Ectopic pacemaker | |
|---|---|
| Other names | Ectopic focus, ectopic foci |
 | |
| An illustration of ectopic foci near papillary muscles in the left ventricle | |
| Specialty | Electrophysiology, Cardiology |
| Symptoms |
|
Signs and symptoms
edit- Isolated ectopic beats frequently cause no symptoms, although the most common symptom is the perception of a 'missed beat'. This occurs because the person notices the prolonged gap between the early (ectopic) beat and the next normal beat.
- Palpitations
- Feeling faint[4]
Cause
editEctopic pacemakers can occur within healthy hearts in response to various stimulating events, they can be caused by automaticity or triggered activity, such as:
- Increased local parasympathetic nervous system activity[3]
- Elevated sympathetic nervous system output[3]
- Overstimulation from drugs such as caffeine,[5] digitalis, and catecholamines[6]
- Cardiac Ischemia (particularly ventricular ischemia) – the membranes of apoptotic (dying) cells become "leaky" and cause surrounding tissue to become hyperkalemic or hypercalcemic (high concentration of potassium/calcium), causing random excitation.[7]
They can also occur within unhealthy hearts, caused by:
- Infection
- Disease, such as sinus venosus and atrial defects[8][9]
- SA node dysfunction (1st degree block) which can cause the rate of impulse to slow[1]
- SA node blockage so that impulses never leave the atria[1]
- AV node blockage (3rd degree block) prevents normal conduction across ventricles[1]
Physiology
editAn ectopic pacemaker can reside within a part of the electrical conduction system of the heart, or within the muscle cells of the atria or ventricles. When an ectopic pacemaker initiates a beat, premature contraction occurs. A premature contraction will not follow the normal signal transduction pathway, and can render the heart refractory or incapable of transmitting the normal signal from the SA node. Location of the pacemaker can also change its effect on the SA node and its rhythm. An ectopic pacemaker located in the atria is known as an atrial pacemaker and can cause the atrial contraction to be faster.[10] An ectopic pacemaker situated near the AV node and the septum is known as a junctional pacemaker.[11] The pacemaker that is operating in the ventricles is known as the ventricular.[12] Other such ectopic pacemakers can even lie within the pulmonary vein and thoracic vein walls.[13][14]
Diagnosis
editOn an ECG, the QRS complex will be abnormally shaped when looking at ventricular ectopic activity, often it occurs earlier with an absent P wave. It can be perceived as a skipped beat on both the ECG and through normal pulse-taking.[12] During atrial ectopic activity where the P wave is normally rounded can be inverted or peaked. However the QRS complex and T waves appear relatively normal.[10] Conversely, during junctional ectopic activity the P wave is frequently absent or can be hidden in the QRS complex.[11]
See also
editReferences
edit- ^ a b c d Phibbs, B. (1963). "Paroxysmal Atrial Tachycardia with Block Around the Ectopic Pacemaker: Report of a Case". Circulation. 28 (5): 949–50. doi:10.1161/01.CIR.28.5.949. PMID 14079200.
- ^ Tveito, Aslak; Lines, Glenn T. (2008). "A condition for setting off ectopic waves in computational models of excitable cells". Mathematical Biosciences. 213 (2): 141–50. doi:10.1016/j.mbs.2008.04.001. PMID 18539188.
- ^ a b c Rozanski, GJ (1991). "Atrial ectopic pacemaker escape mediated by phasic vagal nerve activity". The American Journal of Physiology. 260 (5 Pt 2): H1507–14. doi:10.1152/ajpheart.1991.260.5.H1507. PMID 2035673.
- ^ Abbott, Louise (December 2012). "Atrial Fibrillation – information, symptoms and treatment". Bupa. Archived from the original on 2009-01-24. Retrieved 2009-02-04.
- ^ Port, Carol Mattson (2005). Pathophysiology: Concepts of Altered Health States (7th ed.). Lippincott Williams & Wilkins. p. 588. ISBN 978-0-7817-4988-6.
- ^ Maupoil, V; Bronquard, C; Freslon, J-L; Cosnay, P; Findlay, I (2007). "Ectopic activity in the rat pulmonary vein can arise from simultaneous activation ofα1- andβ1-adrenoceptors". British Journal of Pharmacology. 150 (7): 899–905. doi:10.1038/sj.bjp.0707177. PMC 2013875. PMID 17325650.
- ^ Keller-Wood, Maureen. "Electrical Activity in the Heart." Lecture at the University of Florida College of Pharmacy, 23-Oct-2007.[verification needed]
- ^ Hamilton, S. D.; Bartley, T. D.; Miller, R. H.; Schiebler, G. L.; Marriott, H. J. L. (1968). "Disturbances in Atrial Rhythm and Conduction Following the Surgical Creation of an Atrial Septal Defect by the Blalock-Hanlon Technique". Circulation. 38 (1): 73–81. doi:10.1161/01.CIR.38.1.73. PMID 11712295.
- ^ Hoogaars, Willem M.H.; Engel, Angela; Brons, Janynke F.; Verkerk, Arie O.; de Lange, Frederik J.; Wong, L.Y. Elaine; Bakker, Martijn L.; Clout, Danielle E.; et al. (2007). "Tbx3 controls the sinoatrial node gene program and imposes pacemaker function on the atria". Genes & Development. 21 (9): 1098–112. doi:10.1101/gad.416007. PMC 1855235. PMID 17473172.
- ^ a b "Wandering pacemaker". ECG Interpretation: An Incredibly Easy! Pocket Guide (4th ed.). Lippincott Williams & Wilkins. 2007. pp. 116–18. ISBN 978-1-58255-701-4.
- ^ a b "Junctional escape rhythm". ECG Interpretation: An Incredibly Easy! Pocket Guide (4th ed.). Lippincott Williams & Wilkins. 2007. pp. 125–28. ISBN 978-1-58255-701-4.
- ^ a b "Atrial tachycardia". ECG Interpretation: An Incredibly Easy! Pocket Guide (4th ed.). Lippincott Williams & Wilkins. 2007. pp. 96–98. ISBN 978-1-58255-701-4.
- ^ Haghjoo, Majid (2007). "Efficacy, safety, and role of segmental superior vena cava isolation in the treatment of atrial fibrillation". Journal of Electrocardiology. 40 (4): 327.e1. doi:10.1016/j.jelectrocard.2007.04.003. PMID 17599474.
- ^ Tan, Alex Y.; Zhou, Shengmei; Jung, Byung Chun; Ogawa, Masahiro; Chen, Lan S.; Fishbein, Michael C.; Chen, Peng-Sheng (2008). "Ectopic atrial arrhythmias arising from canine thoracic veins during in vivo stellate ganglia stimulation". AJP: Heart and Circulatory Physiology. 295 (2): H691–98. doi:10.1152/ajpheart.01321.2007. PMC 2519231. PMID 18539751.