User:BChinphmd/Hyperkalemia

Diagnosis
An ECG of a person with a potassium of 5.7 showing large T waves and small P waves

To gather enough information for diagnosis, the measurement of potassium must be repeated, as the elevation can be due to hemolysis in the first sample. The normal serum level of potassium is 3.5 to 5 mmol/L. Generally, blood tests for kidney function (creatinine, blood urea nitrogen), glucose and occasionally creatine kinase and cortisol are performed. Calculating the trans-tubular potassium gradient can sometimes help in distinguishing the cause of the hyperkalemia.[medical citation needed]

Also, electrocardiography (ECG) may be performed to determine if there is a significant risk of abnormal heart rhythms. Physicians taking a medical history may focus on kidney disease and medication use (e.g. potassium-sparing diuretics), both of which are known causes of hyperkalemia.

Definitions
Normal serum potassium levels are generally considered to be between 3.5 and 5.3 mmol/L. Levels above 5.5 mmol/L generally indicate hyperkalemia, and those below 3.5 mmol/L indicate hypokalemia. Hyperkalemia can be further classified into mild, moderate, and severe hyperkalemia. Mild hyperkalemia has serum potassium levels of 5.5-6.0 mmol/L, moderate hyperkalemia has serum potassium levels of 6.0-6.5 mmol/L and severe hyperkalemia has serum potassium levels exceeding 6.5 mmol/L.

ECG findings
With mild to moderate hyperkalemia, there is prolongation of the PR interval and development of peaked T waves. Severe hyperkalemia results in a widening of the QRS complex, and the ECG complex can evolve to a sinusoidal shape. There appears to be a direct effect of elevated potassium on some of the potassium channels that increases their activity and speeds membrane repolarisation. Also, (as noted above), hyperkalemia causes an overall membrane depolarization that inactivates many sodium channels. The faster repolarisation of the cardiac action potential causes the tenting of the T waves, and the inactivation of sodium channels causes a sluggish conduction of the electrical wave around the heart, which leads to smaller P waves and widening of the QRS complex.[medical citation needed] Some of potassium currents are sensitive to extracellular potassium levels, for reasons that are not well understood. As the extracellular potassium levels increase, potassium conductance is increased so that more potassium leaves the myocyte in any given time period. To summarize, classic ECG changes associated with hyperkalemia are seen in the following progression: peaked T wave, shortened QT interval, lengthened PR interval, increased QRS duration, and eventually absence of the P wave with the QRS complex becoming a sine wave. Bradycardia, junctional rhythms and QRS widening are particularly associated with increased risk of adverse outcomes

The serum potassium concentration at which electrocardiographic changes develop is somewhat variable. Although the factors influencing the effect of serum potassium levels on cardiac electrophysiology are not entirely understood, the concentrations of other electrolytes, as well as levels of catecholamines, play a major role.[medical citation needed]

ECG findings are not a reliable finding in hyperkalemia. In a retrospective review, blinded cardiologists documented peaked T-waves in only 3 of 90 ECGs with hyperkalemia. Sensitivity of peaked-Ts for hyperkalemia ranged from 0.18 to 0.52 depending on the criteria for peak-T waves.[medical citation needed]