a 68-year - old female presented to the emergency department with progressive weakness involving the upper and lower extremities and subsequent difficulty with ambulation for 1 week . she was unable to get out of bed and walk on the day of presentation . past medical history was significant for gitelman 's syndrome , with very labile , but generally very low , potassium levels being maintained on potassium sparing diuretics ( eplerenone ) and supplemental potassium 300 meq / day . on presentation , she was afebrile with blood pressure , 106/51 mm of hg ; heart rate , 96 beats / min ; respiratory rate , 16/min ; and normal oxygen saturation on room air . motor exam was significant for reduced power of 60 percent in both upper and lower extremities with flaccidity and diminished reflexes bilaterally . initial labs were as follows : sodium 131 meq / l ( range 135153 meq / l ) , potassium 9.9 meq / l ( range 3.55.3 meq / l ) , blood urea nitrogen 41 mg / dl ( range 526 mg / dl ) , and creatinine 2.1 mg / dl with baseline of 1.0 mg / dl ( range 0.501.50 mg / dl ) . 1 ) . emergent therapy for hyperkalemia was started with 1 g of intravenous calcium gluconate , 10 units of regular insulin with 50 g of dextrose , and 100 meq of sodium bicarbonate . a dialysis line was placed and emergent dialysis was done with improvement of her potassium to 4.8 meq / l post - dialysis . diuretics ( torsemide , zaroxolyn , and eplerenone ) were stopped and she was discharged on potassium chloride 60 meq three times daily for maintenance . she shortly thereafter became profoundly hypokalemic and her maintenance dose of potassium was increased to 300 meq / day . electrocardiogram ( ekg ) at presentation showing dramatically widened qrs complex and tall broad t waves . potassium ( k + ) is a very tightly regulated cation present ubiquitously inside and outside all living cells . it is responsible for maintaining the cell membrane potential required for physiological functioning . as significant k+ gradient exists between inside and outside of cells , even a slight change in extracellular k+ level has a significant physiologic impact . the changes in k+ ( hyper- or hypo- ) have significant effect on heart muscle and its conduction system . although absolute serum k+ level usually correlates with clinical symptoms , the rate of change is more important . it is not very sensitive ( 0.340.43 ) but the changes , if present , are specific ( 0.850.86 ) ( 2 , 3 ) . the most widely used reference range for normal serum k+ level is 3.55.5 meq / l . any value > 6.5 meq / l is an important cause of morbidity and mortality ( 4 ) . 3 ) due to differences in sensitivity of cardiac tissues ( in decreasing order  atria , ventricle , his cells , atrial nodes , and inter - atrial pathways ) to the change in serum k+ level . the earliest change is peaking of symmetric t waves with narrow base in precordial ( v2v4 ) leads , defined as any t wave taller than the corresponding r wave ( fig . meq / l ) manifesting as lengthening of pr interval followed by flattening and subsequent loss of p waves . this transforms the ekg pattern into development of  nodal  rhythm with absent p waves . by this time if hyperkalemia sustains or worsens , conduction system is also affected . at levels between 7.0 and 8.0 meq / l , qrs continues to widen and can merge with t wave to form a  sine wave  pattern ( fig . 5 ) , which is an indicator of impending ventricular fibrillation and cardiac arrest ( 5 ) . ekg showing tall peaked symmetric t waves with narrow base ( ekg courtesy , www.lifeinthefastlane.com/hyperkalemia/ ) . management of hyperkalemia involves addressing three different aspects : ( 1 ) preventing immediate complications ; ( 2 ) correcting the serum k+ level to a physiologically stable level ; and ( 3 ) elimination of excess potassium from the body . this is controlled with infusion of calcium in the form of calcium gluconate or chloride , which stabilizes the cardiac membrane potential . immediate correction of serum k+ levels can be achieved with medications that affect the transcellular shift of k+ . bicarbonate infusion , although less effective , may be used if there is co - existing non - gap metabolic acidosis . next , the elimination of elemental k+ from the body can be achieved via the kidneys or dialysis ( 2 ) . chelating agents , such as sodium polystyrene , are not recommended now because of delayed action , questionable efficacy , and a serious side - effect profile , including intestinal necrosis and undesirable sodium load ( 3 , 5 , 6 ) . recent clinical trials have shown promise for two different oral medications with more selective k+ binding . patiromer in patients with chronic kidney disease ( 7 ) and sodium zirconium cyclosilicate in patients with varying causes of hyperkalemia ( 8) have been shown to be effective in the reduction and maintenance of normokalemia in these patients . however , these medications have only been studied in the outpatient population with mild to moderate hyperkalemia ( < 6.5 meq / l ) and no ekg changes . hence , their efficacy in the acute emergency setting as a substitute for sodium polystyrene remains debatable . similarly , loop diuretics can be used for the elimination of k+ via kidneys if renal function is intact . dialysis can be used as a last resort for reduction of total body potassium ( 2 ) . although no formal guidelines exist as to when to initiate treatment for hyperkalemia , it is generally recommended in clinically symptomatic patients with or without ekg changes . authors pk , drp , and rp conceived , designed , and participated in literature review and drafting of the initial manuscript . ar and ra provided intellectual content , edited subsequent draft , and approved the final manuscript . the authors have not received any funding or benefits from industry or elsewhere to conduct this study .
hyperkalemia can present with a spectrum of clinical manifestations with progressive ekg changes and life - threatening arrhythmias . 
 although no formal guidelines exist as to when to initiate treatment for hyperkalemia , it is generally recommended in clinically symptomatic patients with or without ekg changes . 
 timely diagnosis and reversal can relieve symptoms and prevent life - threatening arrhythmias . 
 we review the ekg changes associated with hyperkalemia and management principles along with an example of a case of severe hyperkalemia resulting in arrhythmia and flaccid paralysis .