Management of severe hyperkalemia - EMCrit Blog

1 R. Phillip Dellinger, MD, FCCM, Section EditorConcise Definitive ReviewManagement of severe hyperkalemiaLawrence S. Weisberg, MDHyperkalemia is common inhospitalized patients, andmay be associated with ad-verse clinical outcomes (1,2). Its prevalence and clinical impact incritically ill patients are unknown. Thereis no doubt, however, that severe hyper-kalemia can be fatal. Proper treatment ofhyperkalemia depends on an understand-ing of the underlying ratio of extracellular to intracel-lular potassium (K) concentration largelydetermines the cell membrane restingelectrical potential that, in turn, regu-lates the function of excitable tissues(cardiac and skeletal muscle, and nerve)(1).

2 Small absolute changes in the extra-cellular K concentration will have largeeffects on that ratio, and consequently onthe function of excitable tissues. Thus, itis not surprising that the plasma K con-centration (PK) normally is maintainedwithin very narrow limits. This tight reg-ulation is accomplished by two coopera-tive systems. One system defends againstshort-term changes inPKby regulatinginternal balance: the equilibrium of Kacross the cell membrane. This equilib-rium is modulated by insulin (3 5), cat-echolamines (6, 7) and, to a lesser extent,by acid-base balance (8 10), plasma to-nicity, and several other factors (3).

3 Theother system governs K homeostasis overthe long-term by regulating external bal-ance: the parity between K intake andelimination. In individuals with normalrenal function, the kidneys are responsi-ble for elimination of about 95% of thedaily K load with the remainder exitingthrough the gut. External K balance ismaintained largely by modulating renal all the K excreted by the kid-ney comes from K secreted in the distalnephron (connecting tubule and collect-ing duct) (11). Virtually all regulation ofK excretion takes place at this site in thenephron, under the influence of two prin-ciple factors: the rate of flow and solute(sodium and chloride) delivery throughthat part of the nephron; and the effect ofaldosterone (11).

4 K secretion is directlyproportional to flow rate and sodium de-livery through the lumen of the distalnephron, and to circulating aldosteronelevels in the setting of an aldosterone-sensitive epithelium. This explains, inpart, why the use of diuretic drugs thatwork proximal to the K secretory site(loop and thiazide diuretics) often is ac-companied by hypokalemia. K secretionis inversely proportional to the chlorideconcentration of the luminal fluid and isstimulated, for example, by luminal deliv-ery of sodium bicarbonate (12).

5 Con-versely, hyperkalemia commonly accom-panies acute kidney injury, particularly inthe setting of mineralocorticoid defi-ciency (13 15). Such mineralocorticoiddeficiency is often induced by drugs thatinterfere with the renin-angiotensin-aldosterone axis and commonly causeshyperkalemia in patients with chronickidney disease, as well (16, 17). Sustainedhyperkalemia is always attributable to in-adequate renal K elimination. A detaileddiscussion of the causes of hyperkalemiain critically ill patients is beyond thescope of this article, but may be found ina recent review (18).

6 Clinical Manifestations ofHyperkalemiaAlterations inPKhave a variety of ad-verse clinical consequences, the expres-sion of which may be magnified in thecritically ill patient. The most serious ofthese manifestations are those involvingexcitable depo-larizes the cell membrane, slows ventric-ular conduction, and decreases the dura-tion of the action potential. Thesechanges produce the classic electrocar-diographic (EKG) manifestations of hy-perkalemia including (in order of theirusual appearance) peaked T waves, wid-ening of the QRS complex, loss of the Pwave, sine wave configuration, or ven-tricular fibrillation and asystole (19, 20).

7 These EKG changes may be modified by amultitude of factors such as extracellularfluid pH, calcium concentration, sodiumconcentration, and the rate of rise ofPKFrom the Division of Nephrology, Department ofMedicine, UMDNJ-Robert Wood Johnson MedicalSchool, Cooper University Hospital, Camden, author has not disclosed any potential con-flicts of information regarding this article, 2008 by the Society of Critical CareMedicine and Lippincott Williams & WilkinsDOI: and Objectives: hyperkalemia is one of the fewpotentially lethal electrolyte disturbances.

8 Prompt recognition andexpeditious treatment of severe hyperkalemia are expected tosave lives. This review is intended to provide intensivists andother interested clinicians with an understanding of the patho-physiology that underlies hyperkalemia , and a rational approachto its :This article reviews and analyzes literature relevantto the pathophysiology and Management of severe include search of MEDLINE, and bibliographic search ofcurrent textbooks and journal and Conclusions:A more complete understanding ofpotassium homeostasis in recent years has led to new ap-proaches to the Management of severe hyperkalemia .

9 The phys-iologically based sequential approach still applies. The efficacy,pitfalls, and risks of the agents available for use at each step inthe sequence are critically reviewed. Rational use of the availabletools will allow clinicians to successfully treat severe hyperkale-mia. (Crit Care Med 2008; 36:3246 3251)KEYWORDS: hyperkalemia ; treatment; critical illness3246 Crit Care Med 2008 Vol. 36, No. 12(19). Hospitalized patients with hyperka-lemia are reported to have a higher mor-tality rate than those without hyperkale-mia (21, 22), but the high prevalence ofcoexistent renal insufficiency in this pop-ulation is a significant confounding vari-able that prevents attribution of the in-creased mortality to the changes may not accompanychanges inPK.

10 The sensitivity of the elec-trocardiogram to reveal changes of hy-perkalemia is quite low (23). It does in-crease in proportion to the severity of thehyperkalemia (23), but normal electro-cardiograms have been seen even withextreme hyperkalemia (24) and the firstcardiac manifestation of hyperkalemiamay be ventricular fibrillation (25). (Theexplanation for a normal electrocardio-gram in the setting of extreme hyperka-lemia is not entirely clear, but may relateto a slow rate of rise in thePK 20, 24 ).Given this insensitivity of the electrocar-diogram, EKG changes should not beconsidered necessary for the emergencytreatment of severe result in paraesthesias and weaknessprogressing to a flaccid paralysis, whichtypically spares the diaphragm.