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U wave
U wave
U wave
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A 'U' wave as seen on Electrocardiogram (ECG)
An electrocardiogram of an 18-year-old male showing 'U' waves, most evident in lead V3.

The U wave is a wave on an electrocardiogram (ECG). It comes after the T wave of ventricular repolarization and may not always be observed as a result of its small size. 'U' waves are thought to represent repolarization of the Purkinje fibers.[1][2] However, the exact source of the U wave remains unclear. The most common theories for the origin are:

  • Delayed repolarization of Purkinje fibers
  • Prolonged re-polarisation of mid-myocardial M-cells
  • After-potentials resulting from mechanical forces in the ventricular wall
  • The repolarization of the papillary muscle.[3]

Description

[edit]

According to V. Gorshkov-Cantacuzene:

"The U wave is the momentum carried by the blood in the coronary arteries and blood vessels".[4][5][6]

The resistivity of stationary blood is expressed as , where is a coefficient, and is the hematocrit; at that time, as during acceleration of the blood flow occurs a sharp decrease in the longitudinal resistance with small relaxation times.

However, multiple factors affect blood resistivity. Erythrocyte aggregation occurs at low shear rates and implies that to all vessels (with the exception of large veins) the effect of aggregation is irrelevant. The interior of a blood vessel includes a near-wall layer of plasma (referred to as lubricant), the size of which strictly depends on Reynold's criterion and the shear rate of the flowing blood. Given that the thickness of this layer in all blood vessels (except capillaries) is less than 5 microns, and the resistivity of the plasma is half as much as in blood, then according to the scheme of parallel insertion, the contribution of this layer to the resistivity is negligible. By reducing the speed of blood flow profiles the dependence of Ht on the radius of the vessel becomes more elongated. However, at normal values of Ht, the effect is also insignificant. With high enough shear rates, the red blood cells become susceptible to deformation. The contribution of this phenomenon is difficult to assess because it is present in the background of all the above effects. However, even the sum of all these factors has little effect on blood resistivity.

It follows that at the time of ejection of blood from the left ventricle, part of the pulse is carried away, because there is no electrical resistivity of blood, which gradually increases high up in the coronary arteries and blood vessels. The U wave is the momentum carried by the blood in the coronary arteries and blood vessels. It is possible to take this momentum back to Purkinje fibers along the vessels of the myocardium. This idea is also proved by the fact that hypertrophy of the left ventricle, myocardial ischemia, coronary and insufficiency have momentum there is no possibility to move to the Purkinje fibers, therefore, the ECG recorded a negative U wave.

Interpretation

[edit]

According to many studies[which?], U waves often register in all leads except V6, most frequently in V2 and V3 when the heart rate is greater than 96 beats per minute. Its amplitude is often 0.1–0.33 mV. Particularly difficult is the allocation of the boundaries of the U wave on the background of the T wave and R wave, which may partial or complete (in the case of T wave) the merger. Higher values of heart rate or hypocalcemia U wave are superimposed on the T wave and in tachycardia — merges with the R-wave of the next cardiac cycle.

Prominent U waves (U waves are described as prominent if they are more than 1-2 mm or 25% of the height of the T wave.) are most often seen in hypokalemia but may be present in hypercalcemia, thyrotoxicosis, or exposure to digitalis, epinephrine and Class 1A and 3 antiarrhythmics, as well as in congenital long QT syndrome, and in the setting of intracranial hemorrhage.

An inverted U wave may represent myocardial ischemia (and especially appears to have a high positive predictive accuracy for left anterior descending coronary artery disease[7] ) or left ventricular volume overload.[8]

A U-wave can sometimes be seen in normal younger, athletic individuals.[9] The U-wave increases in adults that are older and less athletic.[10]

References

[edit]
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U wave

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from Grokipedia
The U wave is a small positive deflection in the electrocardiogram (ECG) that follows the and precedes the next , typically representing the delayed of or papillary muscles in the heart. First described by in the early 20th century, it is a normal feature of the , visible in up to 70% of healthy adults but often inconspicuous due to its low amplitude. In a standard ECG, the U wave shares the same polarity as the preceding , with an amplitude usually less than one-third that of the in the same lead, and it is most prominent during and best visualized in the right precordial leads (V2-V3). Its physiological origin is attributed to delayed afterdepolarizations—small depolarizing after-potentials that follow —potentially triggered by myocardial stretch, as proposed in mechano-electrical theories. Clinically, prominent or inverted U waves can signal electrolyte imbalances such as , or underlying conditions including ischemia, , or arrhythmogenic disorders like and right . Abnormal U wave changes, such as augmentation during exercise or , may serve as early markers for myocardial stress or instability, though interpretation requires correlation with patient history and other ECG findings.

Anatomy and Physiology

Cardiac Electrophysiology Basics

The cardiac action potential in ventricular myocytes consists of five phases (0 through 4), which govern depolarization and repolarization processes essential for coordinated heart contraction. Phase 0 represents rapid depolarization, driven by the influx of sodium ions through voltage-gated sodium channels, shifting the membrane potential from approximately -90 mV to +50 mV. This phase occurs similarly in Purkinje fibers, which exhibit faster conduction velocities due to their specialized structure, enabling rapid signal propagation across the ventricles. Phase 1 involves early repolarization, marked by sodium channel inactivation and a transient outward potassium current (Ito), causing a brief drop in potential. Phase 2, the plateau phase, maintains the potential near 0 mV through a balance of inward calcium currents via L-type calcium channels and outward potassium currents, prolonging contraction time. In M-cells, located in the midmyocardium, this phase is extended due to reduced potassium currents, leading to longer action potential durations compared to epicardial or endocardial myocytes. Phase 3 entails final repolarization, where calcium channels close and delayed rectifier potassium currents dominate, restoring the potential to -90 mV. Phase 4 is the resting state, stabilized by inward rectifier potassium currents (IK1) with minimal ion flux. Ventricular repolarization, primarily during phase 3, underlies the on the electrocardiogram (ECG), which reflects the vectorial summation of gradients across the myocardium. This ensures sequential recovery of excitability, setting the stage for subsequent electrical events in the . Key channels, particularly channels, are pivotal in repolarization and maintaining normal ECG patterns by regulating duration and preventing arrhythmias. Voltage-gated channels, including the rapid delayed rectifier (IKr) and slow delayed rectifier (IKs), facilitate outward efflux during phase 3, shortening the and contributing to the on ECG. The inward rectifier IK1 stabilizes the in phase 4 and aids terminal repolarization, while transient outward channels (Ito) initiate phase 1, with expression varying across cell types—higher in epicardial myocytes and than in M-cells. Disruptions in these channels can prolong repolarization, altering ECG waveforms, but under normal conditions, they ensure efficient recovery and rhythmic stability. The comprises specialized tissues that propagate electrical impulses from the atria to the ventricles, including the , , , bundle branches, , and associated structures like papillary muscles. form a subendocardial network branching from the bundle branches, distributing impulses rapidly across the ventricular myocardium with conduction velocities up to 4 m/s, far exceeding that of ordinary myocytes. These fibers are larger, glycogen-rich cells embedded in the inner ventricular walls and extend into papillary muscles, which are conical projections from the ventricular walls that anchor the atrioventricular valves via ; the papillary muscles themselves contain to synchronize contraction with valve function. This anatomy ensures synchronous ventricular activation, optimizing ejection efficiency.

Proposed Origins of the U Wave

One leading hypothesis attributes the U wave to the delayed of , which exhibit a longer duration compared to surrounding ventricular myocardium, resulting in a secondary deflection following the that represents ventricular completion. This theory posits that the subendocardial location and slower phase 3 of generate a distinct electrical gradient after the primary myocardial , supported by transmembrane potential recordings in canine hearts showing Purkinje action potentials outlasting those in adjacent muscle by 50-100 ms. Experimental evidence from isolated Purkinje fiber preparations further demonstrates that their repolarization timing aligns with U wave onset in surface ECGs. Another prominent theory links the U wave to prolonged repolarization in mid-myocardial M cells, a subpopulation of specialized cardiomyocytes located in the midmyocardial region of the ventricular wall. These cells display action potentials extended by up to 200 ms relative to epicardial or endocardial cells due to reduced outward currents, contributing to transmural dispersion of that manifests as a late positive deflection after the . In canine left ventricular preparations, selective prolongation of M-cell action potentials correlated with increased U wave , though human validation remains limited and controversial, with some studies on tissue samples suggesting heterogeneous properties. A third hypothesis proposes that the U wave arises from mechanical after-potentials induced by ventricular wall stretch or delayed in papillary muscles during early , with hemodynamic factors such as momentum in coronary vessels amplifying these effects. Stretch-activated channels in ventricular myocytes can trigger delayed after-depolarizations following , leading to a small electrical signal recorded as the U wave; this is evidenced by studies where mechanical deformation of isolated ventricular tissue produced after-potentials timed to U wave position. Additionally, Gorshkov-Cantacuzene suggested that the U wave reflects momentum transfer from ejected through low-resistivity to , disrupted in conditions like ischemia, based on biophysical modeling of flow dynamics. Despite these explanations, no single theory has achieved consensus, with evidence varying in strength across models. The Purkinje hypothesis faces challenges from observations in species lacking prominent Purkinje networks, such as amphibians, yet it benefits from direct electrophysiological correlations in mammalian hearts; the M-cell model is bolstered by robust animal data from wedge preparations showing dispersion gradients, though validation remains limited to tissue slices. Mechanical theories align with timing to diastolic events but lack specificity, as signal-averaged ECGs in patients with mutations implicate inward rectifier potassium currents (I_K1) over stretch alone. Isolated tissue and canine studies provide key support for all, but integrative data underscore ongoing debate.

Characteristics on ECG

Waveform Morphology

The U wave appears as a small deflection immediately following the within the ST-T-U complex on the electrocardiogram. It is typically most visible in the precordial leads V2 and V3, where it manifests as a low-amplitude wave that aligns in direction with the preceding . Morphologically, the U wave is characterized by its upright, positive deflection in most cases, often presenting a rounded contour or, less commonly, a notched appearance that may blend seamlessly with the in certain tracings. Unlike the , which exhibits a more symmetric or slowly ascending shape, the U wave is asymmetric, with a steeper ascending limb compared to its descending portion. This distinct shape aids in its identification on standard ECG diagrams, particularly in examples from precordial leads showing the ST-T-U complex. Differentiation of the U wave from artifacts or other ECG features is essential for accurate interpretation; artifacts typically lack consistency across beats and do not align with the T wave's polarity, whereas the U wave maintains a reproducible position post-T wave. It must also be distinguished from misinterpreted components of a prolonged , where fusion with the T wave can create an illusion of T wave extension, or from superimposed P waves, which occur earlier in the cycle and exhibit different profiles. In standard ECG examples, the U wave's prominence is gauged by exceeding 1-2 mm or surpassing 25% of the T wave height, thresholds commonly used to identify prominent U waves, which may suggest underlying clinical abnormalities requiring further evaluation.

Normal Variations and Measurement

The U wave on an electrocardiogram (ECG) is measured by evaluating its , from the isoelectric baseline to its peak, and its duration, from onset to return to baseline. Typical ranges from 0.05 to 0.2 mV (0.5 to 2 mm at standard calibration of 10 mm/mV), rarely exceeding one-third of the T wave in the same lead. Duration in healthy individuals varies from approximately 160 to 300 ms, depending on . The U wave is most visible and prominent in the precordial leads V2 and V3, where it appears as a small positive deflection following the , while it is less conspicuous or absent in limb leads. Normal does not typically exceed 1-2 mm, and the wave's size is inversely related to heart rate, becoming more apparent during (heart rates below 65 bpm) and diminishing or disappearing with . Duration may prolong slightly with slower rates. In healthy populations, the U wave is observed in up to 70% of adults and is a common normal finding in children, often more prominent during relative and due to immature conduction patterns. Among young athletes, positive U waves in precordial leads are frequently noted as physiological adaptations to , without . With aging and reduced , U wave prominence tends to increase, reflecting changes in dynamics. Factors such as maintained electrolyte balance within normal ranges (e.g., serum potassium 3.5-5.0 mEq/L) support consistent U wave appearance without exaggeration. Standard supine positioning during ECG acquisition minimizes artifacts and ensures reliable measurement, as postural shifts can subtly alter wave visibility in some individuals.

Clinical Relevance

Physiological and Benign Associations

The U wave becomes more prominent and separable from the T wave in states of bradycardia, where heart rates below 65 beats per minute allow for prolonged repolarization phases that enhance its visibility on the electrocardiogram (ECG). In such conditions, U waves are observed in approximately 90% of cases, often appearing as small positive deflections in the precordial leads, reflecting normal Purkinje fiber repolarization without pathological implications. This separation is particularly evident during sinus bradycardia at rest, where the slower rhythm prevents fusion with the preceding T wave. In athletes, benign prominence of the U wave is frequently noted due to enhanced vagal tone, which induces physiological bradycardia and alters repolarization dynamics. Well-trained individuals commonly exhibit positive U waves following the T wave, especially in precordial leads, as part of adaptive cardiac changes from endurance training without signifying disease. Similarly, younger individuals may display more visible U waves owing to higher baseline vagal activity, which prolong the QT interval and accentuate these deflections in asymptomatic ECGs. Normal physiological states, such as post-exercise recovery, can influence U wave through transient heart rate changes and autonomic shifts, with deflections becoming more discernible as rates slow despite overall stability in healthy individuals. The U wave also plays a role in , a benign variation driven by respiratory-linked vagal modulation, where cyclic slowing in patients allows intermittent prominence of the wave, often seen in ECG tracings of healthy young adults or athletes during rest. In these contexts, the U wave typically remains within normal ranges of less than 1 mm in precordial leads, underscoring its non-pathological nature.

Pathological Conditions and Abnormalities

Prominent or exaggerated U waves are a key electrocardiographic finding in , where low serum potassium levels delay ventricular , particularly in , leading to after-potentials that manifest as increased U-wave amplitude following T-wave . This abnormality often appears alongside ST-segment depression and flattened T waves, forming a characteristic triad that predisposes patients to ventricular arrhythmias. In hypercalcemia, severe elevations in serum calcium can also produce prominent U waves, attributed to shortened duration and altered calcium-dependent currents that affect stability. Thyrotoxicosis, particularly in , is associated with exaggerated U waves due to hypokalemia-induced intracellular potassium shifts, exacerbating heterogeneity. Similarly, in , giant T-U waves—where the U wave fuses with and amplifies the —signal early afterdepolarizations during prolonged , often preceding . Inverted U waves, typically observed as negative deflections opposite the T wave polarity, indicate underlying structural or ischemic cardiac pathology. In myocardial ischemia, especially involving the , inverted U waves in precordial leads V2-V3 serve as an early marker of or evolving , reflecting subendocardial changes. often presents with inverted U waves in right precordial leads, linked to increased myocardial strain and altered gradients. states, such as in or valvular regurgitation, can similarly cause U-wave inversion due to ventricular dilation and heterogeneous , though less commonly emphasized than in ischemic conditions. U-wave abnormalities also arise in central nervous system events and from certain medications. frequently features large U waves exceeding 1 mm in , peaking 48-72 hours post-event, likely mediated by hypothalamic stimulation and catecholamine surges that disrupt autonomic balance and . Drug effects, such as those from , can superimpose prominent U waves on biphasic T waves by shortening refractory periods and inducing secondary shifts, particularly in leads with dominant R waves. Quinidine administration may accentuate upright U waves through prolongation of the action potential and , altering dynamics in susceptible patients. Diagnostic criteria for pathological U waves include an amplitude exceeding 25% of the preceding or any inversion in leads where the T wave is upright, serving as red flags for further evaluation. For instance, in , prominent U waves greater than one-third of T-wave height in precordial leads V2-V3, combined with , warrant immediate correction to prevent arrhythmias. Inverted U waves in ischemia may appear as deep negative deflections (>0.5 mm) in V2-V3, prompting , while giant T-U fusion in exhibits amplitudes up to 6 mm, signaling high torsades risk. These patterns underscore the U wave's role in identifying vulnerabilities across diverse pathologies.

Historical Development and Research

Discovery and Early Observations

The U wave was first identified by in 1903 during his pioneering work on standardizing electrocardiographic recordings using the string galvanometer, where it appeared as a small deflection following the in human ECG tracings. Einthoven described this feature in his seminal publication, extending the conventional P-QRS-T nomenclature to include the U wave as the sixth component of the ventricular complex, though its physiological significance remained unclear at the time. In the ensuing decades, the U wave gained wider recognition through systematic observations in clinical and experimental settings. Notably, Sir Thomas Lewis and M.D.D. Gilder conducted a detailed analysis of ECGs from healthy young male adults in , reporting the U wave in approximately 75% of records, most prominently in lead II, where it typically measured about 0.1 mV in and 0.16 seconds in duration. Their study established baseline characteristics of the U wave in normal physiology, emphasizing its consistency as a post-T wave deflection without attributing a specific mechanism. By , further investigations into ventricular deflections, such as those exploring ECG variations in and early states, reinforced its presence as a recurring feature in standard leads, though interpretations varied. Early researchers interpreted the U wave as an extension of ventricular , akin to the but delayed, based on its temporal position and polarity alignment in normal tracings. Clinical observations in the began linking exaggerated U waves to disturbances, such as those seen in cases of metabolic imbalance, providing initial evidence of its sensitivity to physiological perturbations without deeper mechanistic insight. These pre-1950 accounts, drawn from Einthoven's foundational 1903 paper and subsequent studies like Lewis and Gilder's analysis, laid the groundwork for understanding the U wave amid the absence of contemporary knowledge on ion channels.

Modern Theories and Ongoing Debates

Since the , theories on the U wave's origin have evolved from dismissing it as a recording artifact to recognizing it as a reflection of delayed ventricular , with a primary focus shifting toward the role of and mid-myocardial M-cells. Early post-1950 investigations, such as those by in the 1970s, proposed that the U wave arises from prolonged duration in compared to ventricular myocardium. This view gained traction in the 1980s and 1990s through studies by Antzelevitch and colleagues, who demonstrated that M-cells in the deep layers of the ventricular wall exhibit intrinsically prolonged , contributing to transmural dispersion of (TDR) that manifests as the U wave on the surface ECG. These findings, based on isolated canine ventricular preparations and computational models, highlighted how M-cell lags behind epicardial and endocardial cells, producing a secondary deflection after the . Debates persist between mechanical and electrical origins of the U wave, with electrical theories emphasizing dynamics and gradients, while mechanical hypotheses invoke stretch-activated currents during . A notable mechanical model by Gorshkov-Cantacuzene posits that the U wave represents the of blood flow from the left ventricle transmitted through coronary vessels to , without significant electrical resistivity from blood. This 2016 proposal links negative U waves to impaired transmission in conditions like ischemia or . Critiques of mechanical models, including this one, argue they fail to account for the U wave's consistency across heart rates and its absence in some stretch-sensitive preparations, favoring electrical explanations supported by wedge preparations showing U waves tied to TDR rather than mechanical feedback alone. Post-2010 has bolstered electrical theories through advanced and modeling in animal models, confirming dispersion as key to U wave genesis. In human subjects, high-resolution body surface potential mapping has revealed U waves with spatial patterns mirroring T waves, supporting a ventricular origin and enabling discrimination of arrhythmic risk via U-wave integrals. Computational models incorporating dynamic coupling further show that M-cell delays produce realistic U waves only when intercellular conductance varies during , aligning with observed ECG morphologies. Ongoing debates highlight significant gaps in U wave research, including the absence of definitive cellular-level proof isolating its generators in intact hearts. Longitudinal studies tracking U wave changes in aging populations are lacking, despite evidence of progressive T-U fusion with age potentially masking abnormalities. Integration with genetic (LQTS) research remains incomplete, as prominent U waves in LQTS may reflect amplified TDR but require clearer mechanistic links to mutations like KCNQ1. These unresolved issues underscore the U wave's status as an enigma, limiting its routine clinical use beyond ischemia detection. As of 2025, recent studies have further explored U wave changes in conditions like for diagnostic reliability.

References

  1. https://www.ncbi.nlm.nih.gov/books/NBK549803/
  2. https://pmc.ncbi.nlm.nih.gov/articles/PMC6932552/
  3. https://pmc.ncbi.nlm.nih.gov/articles/PMC1513620/
  4. https://ecg.utah.edu/lesson/3
  5. https://ecg.utah.edu/lesson/12
  6. https://www.ncbi.nlm.nih.gov/books/NBK537194/
  7. https://www.ahajournals.org/doi/10.1161/circep.108.789081
  8. https://www.ncbi.nlm.nih.gov/books/NBK526089/
  9. https://www.ahajournals.org/doi/10.1161/circep.113.001622
  10. https://my.clevelandclinic.org/health/body/21648-heart-conduction-system
  11. https://emedicine.medscape.com/article/1922987-overview
  12. https://www.vhlab.umn.edu/atlas/conduction-system-tutorial/overview-of-cardiac-conduction.shtml
  13. https://pmc.ncbi.nlm.nih.gov/articles/PMC7509993/
  14. https://cyberleninka.ru/article/n/to-the-question-of-the-etiology-and-clinical-significance-of-the-u-wave-of-the-ecg
  15. https://litfl.com/u-wave-ecg-library/
  16. https://ecgwaves.com/topic/ecg-normal-p-wave-qrs-complex-st-segment-t-wave-j-point/
  17. https://www.researchgate.net/publication/23275778_The_enigmatic_sixth_wave_of_the_electrocardiogram_The_U_wave
  18. https://litfl.com/qt-interval-ecg-library/
  19. https://pmc.ncbi.nlm.nih.gov/articles/PMC6932608/
  20. https://academic.oup.com/cardiovascres/article/53/1/202/431093
  21. https://www.rch.org.au/clinicalguide/guideline_index/Basic_Paediatric_ECG_interpretation/
  22. https://www.ahajournals.org/doi/10.1161/circulationaha.110.013078
  23. https://pmc.ncbi.nlm.nih.gov/articles/PMC9301030/
  24. https://www.uptodate.com/contents/ecg-tutorial-basic-principles-of-ecg-analysis
  25. http://www.scielo.org.mx/scielo.php?script=sci_arttext&pid=S2954-38352021000400197
  26. https://www.ahajournals.org/doi/10.1161/01.cir.51.6.1030
  27. https://pubmed.ncbi.nlm.nih.gov/6239355/
  28. https://pmc.ncbi.nlm.nih.gov/articles/PMC11508899/
  29. https://www.mdpi.com/1424-8220/20/14/4029
  30. https://www.ahajournals.org/doi/10.1161/circulationaha.108.191096
  31. https://pmc.ncbi.nlm.nih.gov/articles/PMC6931435/
  32. https://pmc.ncbi.nlm.nih.gov/articles/PMC8881231/
  33. https://www.jacc.org/doi/10.1016/j.jacc.2009.03.043
  34. https://www.amjmed.com/article/S0002-9343(06)00886-2/fulltext
  35. https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/u-wave
  36. https://pmc.ncbi.nlm.nih.gov/articles/PMC3077842/
  37. https://litfl.com/digoxin-effect-ecg-library/
  38. https://pmc.ncbi.nlm.nih.gov/articles/PMC1502069/
  39. https://royalsocietypublishing.org/doi/10.1098/rstb.1912.0011
  40. https://www.ahajournals.org/doi/pdf/10.1161/01.cir.7.2.205
  41. https://pubmed.ncbi.nlm.nih.gov/1132093/
  42. https://pmc.ncbi.nlm.nih.gov/articles/PMC1952680/
  43. https://pmc.ncbi.nlm.nih.gov/articles/PMC2842929/
  44. https://www.sciencedirect.com/science/article/abs/pii/S0022073623000353
  45. https://pubmed.ncbi.nlm.nih.gov/41080383/
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