2 The largest U waves are usually seen in the precordial leads. Normal U wave amplitude rarely exceeds 0.2 mV, 3 11 though there are a few reports of amplitudes exceeding 1.0 mV in normal individuals. 3 12 Despite such a high common prevalence, clinicians often miss U waves in practice primarily due to their low amplitude, less familiarity with it and probable belief in its negligible clinical significance. It can be present in up to 90% of ECGs with heart rates, 65 bpm or lower, though the U wave is often hard to appreciate in the presence of tachycardia especially if the T wave abuts the P wave. A ‘physiological’ U wave is usually a small positive deflection and is concordant with its preceding T wave that occurs in the setting of normal serum potassium and an absence of cardiac pathology. The majority of clinicians believe that U waves only occur in association with hypokalaemia although that is untrue. 2–11 Identification of U waves and their clinical significance has been often underutilised in clinical practice by most physicians. The origin and clinical significance of U waves has remained an area of controversy. Her initial ECG revealed normal sinus rhythm, vertical frontal P-vector, large-amplitude peaked T waves and biphasic U waves (with predominant negative discordance in relation to T wave) 1 most prominently seen in the precordial leads ( figure 1). The patient showed moderate clinical improvement with intravenous steroids, nebulisations and intravenous hydration in the emergency room and was subsequently hospitalised on optimal medical management for emphysema exacerbation. Physical examination was remarkable for dry mucous membranes, wheezing and mildly rhonchorous breath sounds bilaterally. Vital signs were stable but pulse oximetry revealed oxygen saturations of 93% on 4 L oxygen by nasal cannula. Her current symptoms started 2 days previously and were preceded by a viral prodrome. We also describe a short review of the possible mechanisms of the U wave genesis and its importance in different clinical settings.Īn 81-year-old woman with home oxygen-dependent severe emphysema and end-stage renal disease (on haemodialysis thrice weekly) presented to the hospital with symptoms of shortness of breath, chronic cough with increased clear expectoration, anorexia and generalised weakness. Herewith, we report an unusual ECG of biphasic U waves with predominant negative discordance which were noted in association with large amplitude peaked T waves in the setting of hyperkalaemia. Hypokalaemia has a well-known association with pathological ‘U wave’ which actually combines with the T wave (TU complex) and results from slowing of phase 3 of the action potential with resultant electrical interaction between the three myocardial layers. Three main hypothesis regarding physiological U wave genesis have been proposed which include late repolarisation of Purkinje fibres, late repolarisation of some myocardial cells (M-cell hypothesis) and delayed after depolarisation of the ventricular wall occurring during ventricular filling (electrical diastole) (mechanoelectrical hypothesis). We also discuss the possible mechanisms of the U wave genesis and the importance of different U wave morphologies encountered in the real clinical practice.Įlectrophysiological basis for the genesis of the U wave has been a topic of debate for over a century since Einthoven first defined it in 1903. We believe that this may have occurred as a result of partial clinical adaptation of cardiac myocytes to the long-standing effects of hyperkalaemia as the patient had underlying history of chronic kidney disease. We report an unusual case where hyperkalaemia and discordant U waves coexisted.

U waves usually tend to disappear in the setting of hyperkalaemia. Physiological U wave genesis occurs likely secondary to either late repolarisation of Purkinje fibres, or late repolarisation of some myocardial cells and/or delayed after depolarisation of the ventricular wall occurring during ventricular filling.

Hyperkalemia ecg u wave