![]() ![]() Normal (Repolarization ) Variant - Suspect when T wave peaking has a more rounded summit with assymetric ascent and descent and a broader base – especially IF the patient is otherwise healthy and without any apparent reason to have hyperkalemia ( We saw this in Figure 1 of ECG Review #6 ).Hyperkalemia - Suspect as the cause of T wave peaking when the clinical setting is one likely to produce hyperkalemia ( ie, renal failure, volume depletion, acidosis, potassium-retaining drugs ) – and – when T waves are tall, pointed with steep ascent and near equally steep descent with a narrow base ( as seen in Figure 2 ).Thus, the Tee‐pee sign must be a manifestation of multiple electrolyte imbalances rather than a product of a single disturbance.Final Point: All that produces tall, peaked T waves is not necessarily hyperkalemia! Instead, the finding of Twave peaking should prompt one to consider a differential diagnosis of 3 possible causes – with the clinical situation ( as well as specific ECG features ) providing KEY clues as to which of the 3 is likely to be present. Have described that the QTc interval in hypocalcemia seldom exceeds 140% of normal otherwise, an additional electrolyte abnormality is probably present and if a QT interval is prolonged, it may in fact be a QU interval. However, the prolongation of the QT interval is in fact due to an increase in the duration of the ST segment, and not due to prolongation of the T‐wave duration. Usually, hypocalcemia manifests as prolongation of the QTc interval on the ECG. Nor can it be attributed to the concomitant hypocalcemia. This appearance has not been described previously in association with hyperkalemia or hypomagnesemia. The term also refers to the unusual relationship between the T and P waves. We have proposed that this unusual “tenting” of the descending limb of the T wave be termed the “tee‐pee sign” as its outline is reminiscent of the conical dwellings (teepees or tipis) made of animal skins or birch bark and constructed by Native North Americans of the Great Plains ( Fig. Instead, the descending limb of the T wave appears prolonged, and continues to merge into the subsequent P wave. Following the U wave, we would have expected the ECG signal to return to the isoelectric line. The ECG presented in this case has an additional interesting feature in the precordial leads occurring after the U wave. ![]() When measured to the point at which this tangent crossed the isoelectric line, the QT interval was found to be within normal limits ( Fig. To determine the QT interval in this case, we used the slope intercept technique to identify the end of the T wave as the intercept of an isoelectric level and a line tangential to the point of maximum T‐wave slope. However, we note that the QT initially appeared prolonged and difficult to quantify because of a prominent U wave-findings distinctly unlike those typical of hyperkalemia. In the case presented here, the serum potassium was found to be significantly elevated and serves to explain the peaked T waves that normalized upon correction of the hyperkalemia. The corrected QT interval is either normal or shortened. These changes are often seen when the serum potassium exceeds 5.5 mEq/L. Tall, narrow, and peaked T waves are the earliest ECG sign of hyperkalemia. The classic descriptions of hyperkalemia and hypocalcemia are listed in Table 1. Part of this prolongation was due to a prominent U wave. ![]() The appearance of the T waves was unusual with a prolongation of the descending limb of the T wave, merging into the next P wave. There were peaked T waves in the precordial leads. He was admitted to the intensive care unit for management of sepsis and initiation of chemotherapy.Ī 12‐lead ECG showed normal sinus rhythm at 80 beats/min ( Fig. Computed tomography of his abdomen revealed Richter's transformation of his CLL. His abdomen was tender, distended, and the skin was mottled. His temperature was 37.9☌ and he required a FIO 2 of 60% to maintain a SaO 2 greater than 92%. On examination his blood pressure was 94/62 mmHg, his heart rate was 111 beats/min, and his respiratory rate was 22/min. ![]() He had recently been treated with prednisone for warm autoimmune hemolytic anemia. A 62‐year‐old man with a history of chronic lymphocytic leukemia (CLL) presented to the Emergency Department complaining of a 4‐day history of vomiting and abdominal pain. ![]()
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