Why peaked t waves in hyperkalemia

The QRST is replaced by a smooth diphasic, sine wave. This finding is a pre-terminal event unless treatment is initiated immediately. The fatal event is either asystole, as there is complete block in ventricular conduction, or ventricular fibrillation. Almost any arrhythmia, axis deviation and degree of heart block can occur.

In patients with acutely elevated serum potassium levels, a pseudo myocardial infarction pattern has been reported to appear as massive ST-segment elevation that develops secondary to derangement in myocyte repolarization.

Interestingly, bypass tracts are more sensitive to delayed conduction secondary to hyperkalemia than the normal conductive system, which can result in normalization of the EKG changes and loss of the delta wave in patients with Wolff-Parkinson-White syndrome.

The above EKG progression is classic of but do not always accompany hyperkalemia. Metabolic alterations such as alkalosis, hypernatremia, or hypercalcemia can antagonize the trans-membrane effects of hyperkalemia and result in blunting of these EKG changes 9.

On the other hand, these EKG effects are enhanced by hyponatremia, hypocalcemia or both. This explains, in part, the significant inter-patient variability in the actual serum potassium level leading to specific ECG changes.

One problem with the assessment of plasma potassium is that it is often unclear whether the hyperkalemia represents a chronic or an acute condition in which the plasma potassium may still be rising.

A careful history to assess the probable etiology of the hyperkalemia is mandatory, and treatment should be adjusted accordingly.

Immediate therapy is warranted if EKG changes or peripheral neuromuscular abnormalities are present, regardless of the degree of hyperkalemia Parenteral calcium is indicated only for severe hyperkalemia manifested with widening of the QRS complex or loss of P-waves, but not peaked T-waves alone.

Intravenous calcium is effective in reversing the EKG changes and reducing the risk of arrhythmias but does not lower serum potassium. The membrane stabilizing protective effect of calcium begins within minutes after infusion; however, it is relatively short-lived, about 30 minutes. Calcium may be given as calcium gluconate or calcium chloride which contains three times the concentration of elemental calcium compared to the earlier. The dose of calcium gluconate is mg 10 mL of a 10 percent solution [calcium chloride: to mg 5 to 10 mL of a 10 percent solution ] infused slowly over two to three minutes, with constant cardiac monitoring.

Response to therapy is often prompt with visualization of changes being reversed on the EKG tracing or monitor. The dose of either formulation can be repeated after five minutes if the ECG changes persist.

Calcium can effectively block the effect of extracellular potassium elevation on cardiac myocytes by restoring a more appropriate electrical gradient across the cellular membrane. However, calcium may induce toxic dysrhythmias such as asystole in digitalis toxic patients. Extravasation of calcium salts can cause tissue necrosis. Measures aiming at shifting of potassium ions into the intra cellular compartment, transiently decreasing the extra cellular without affecting the total body levels, include: administration of intra venous insulin-glucose, intravenous sodium bicarbonate and inhaled B-2 adrenergic agonists eg, albuterol Oral Cation exchange resin eg, sodium polystyrene sulfonate , loop diuretics and hemodialysis are used to decrease total body potassium.

A low-potassium diet and avoiding medication-induced hyperkalemia are the most important prophylactic measures. Video Series. July 7, Feature extraction and time dependencies can be effectively captured by combining both models. If the deep learning-based model is used, more diverse and complex features can be extracted from ECG.

Our study has some limitations. First, T-amp and T-right slope were measured manually rather than automatically because there have been issues with determining the end of the T-wave. Because the end of the T-wave transits very slowly from around the signal, locating the end of the T-wave is one of the most challenging issues in the evaluation of the ECG waveform [ 23 — 25 ]. By having two independent evaluators perform the measurements and then using only accordant results, we attempted to ensure the reliability of our results.

Second, the length of the waveform used in the study was short about 3 seconds. Our data might be relatively limited and less tolerant of noise or artifacts. Finally, we did not consider other ECG patterns, such as QRS widening or P wave flattening, which can also be observed in hyperkalemia. However, T-wave change is known as the most representative and earliest sign of hyperkalemia. As shown by findings from previous research, our study also showed that T-wave-based features were not correlated with serum potassium levels in real-world clinical practice in the Korean population; even in the normal ECG subgroup, we could not detect any correlation.

Therefore, the use of these features in the estimation of serum potassium level in real clinical practice is very limited. Data of the measurement of T-wave-based features used to support the findings of this study are included in the supplementary information file.

Supplementary 1. Data S1. Values of T-wave-based features and the corresponding serum potassium values. Supplementary 2. Table S1. The detailed interpretation lists of otherwise normal ECG and the count per interpretation. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Article of the Year Award: Outstanding research contributions of , as selected by our Chief Editors. Read the winning articles. Journal overview. Special Issues. Academic Editor: Dirk Bandorski. Received 02 Sep Accepted 25 Nov Published 18 Dec Abstract Background. Introduction Hyperkalemia is an electrolyte derangement that can lead to fatal cardiac arrhythmia. Data Source We used a clinical research database that included patient demographics, diagnoses, drug prescriptions, and laboratory test results extracted from the electronic health records of a tertiary teaching hospital in Korea Ajou University Hospital between September and December Figure 1.

Figure 1. Overview of the study process. Three hundred and thirty manually reviewed electrocardiograms ECGs were used to evaluate the linear correlation between T-wave features and serum potassium level. Two hundred and thirty-one ECGs were independently analyzed to exclude bias due to abnormal heart rhythm.

ECG: electrocardiogram; no. Figure 2. Process and quality evaluation of T-amp and T-right slope measurements. ECG waveforms have been extracted and evaluated using web-based evaluation tools b. Measurements of T-amp c and T-right slope d between the two evaluators are well correlated. Measurements that have a discrepancy between the two evaluators marked with orange color are excluded from further analysis.

T-amp: amplitude; T-right slope: right slope of T-waves. Table 1. Table 2. Pearson correlation coefficients between T-wave features from each lead and serum potassium level. Figure 3. Linear correlations between features of T-norm and serum potassium level. Absolutely no correlation was found in all leads. T-norm: normalized feature. References N. Jain, S. Kotla, B. Little et al.

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