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 outcomesThe 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.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. Prevention
Preventing recurrence of hyperkalemia typically involves reduction of dietary potassium, removal of an offending medication, and/or the addition of a diuretic (such as furosemide or hydrochlorothiazide). Sodium polystyrene sulfonate and sorbitol (combined as Kayexalate) are occasionally used on an ongoing basis to maintain lower serum levels of potassium though the safety of long-term use of sodium polystyrene sulfonate for this purpose is not well understood.High dietary sources include vegetables such as avocados, tomatoes and potatoes, fruits such as bananas, oranges and nuts. Treatment
Emergency lowering of potassium levels is needed when new arrhythmias occur at any level of potassium in the blood, or when potassium levels exceed 6.5 mmol/L.
Transfusional hemosiderosis is the accumulation of iron in the body due to frequent blood transfusions. Iron accumulates in the liver and heart, but also endocrine organs. Frequent blood transfusions may be given to many patients, such as those with thalassemia, sickle cell disease, leukemia, aplastic anemia, or myelodysplastic syndrome, among others. It is diagnosed with a blood transferrin test and a liver biopsy. It is treated with venipuncture, erythrocytapheresis, and iron chelation therapy. Signs and symptoms
Transfusional hemosiderosis can cause cardiac arrhythmia and cardiomyopathy. Causes
Transfusional hemosiderosis is a potential side effect of frequent blood transfusions. These may be given for a number of conditions, including:

thalassemia. sickle cell disease. leukemia. aplastic anemia. myelodysplastic syndrome. Mechanism
Hemoglobin, the oxygen-carrying molecule in a red blood cell, contains iron. The body has limited ways to store and remove iron. When red blood cells (RBCs) die, they are consumed by macrophages. Transfused RBCs have shorter lifespans that native ones, so they die and are consumed more frequently by the macrophages, which causes the latter to die from excess iron which is then released into the blood. Therefore, with frequent blood transfusions, iron builds up in the body over time. This can enter the liver, heart, pancreas, and endocrine organs. Free iron increases the production of oxygen radicals (mostly hydroxyl radicals) that cause damage to cells (particularly their DNA). Diagnosis
Transfusional hemosiderosis can be inferred with a blood transferrin test. Blood ferritin may be increased with a number of other conditions, so is less reliable for diagnosis.