Acute and chronic cardiovascular effects of hyperkalemia: new insights into prevention and clinical management.
The plasma pool of potassium is a partial reflection of the overall body, transient cellular shifts, and potassium elimination regulated by the kidneys. Potassium concentrations elevating above the upper limit of normal (> 5.0 mEq/L) have become more common in cardiovascular practice due to the growing population of patients with chronic kidney disease and the broad applications of drugs that modulate potassium excretion by either reducing production of angiotensin II (angiotensin-converting enzyme inhibitors, direct renin inhibitors, beta-adrenergic receptor antagonists), blocking angiotensin II receptors (angiotensin receptor blockers), or antagonizing the action of aldosterone on mineralocorticoid receptors (mineralocorticoid receptor antagonists). In addition, acute kidney injury, critical illness, crush injuries, and massive red blood cell transfusions can result in hyperkalemia. Progressively more severe elevations in potassium are responsible for abnormalities in cardiac depolarization and repolarization and contractility. Untreated severe hyperkalemia results in sudden cardiac death. Traditional management steps have included reducing dietary potassium and discontinuing potassium supplements; withdrawal of exacerbating drugs; acute treatment with intravenous calcium gluconate, insulin, and glucose; nebulized albuterol; correction of acidosis with sodium bicarbonate for short-term shifts out of the plasma pool; and, finally, gastrointestinal ion exchange with oral sodium polystyrene sulfonate in sorbitol, which is mainly used in the hospital and is poorly tolerated due to gastrointestinal adverse effects. This review explores hyperkalemia as a complication in cardiovascular patients and highlights new acute, chronic, and preventative oral therapies (patiromer calcium, cross-linked polyelectrolyte, ZS-9) that could potentially create a greater margin of safety for vulnerable patients with combined heart and kidney disease.
Baylor University Medical Center, Baylor Heart and Vascular Institute, Baylor Jack and Jane Hamilton Heart and Vascular Hospital, Dallas, TX, and The Heart Hospital, Plano, TX.
Peter A
PA
McCullough
University of Florida College of Medicine, Gainesville, FL.
Thomas M
TM
Beaver
Duke Clinical Research Institute, Durham, NC.
Elliott
E
Bennett-Guerrero
Baylor University Medical Center, Dallas, TX.
Michael
M
Emmett
Ahmanson-UCLA Cardiomyopathy Center, Los Angeles, CA.
Gregg C
GC
Fonarow
Emory University School of Medicine, Atlanta, GA.
Abhinav
A
Goyal
Hennepin County Medical Center, University of Minnesota, Minneapolis, MN.
Charles A
CA
Herzog
Mid-America Heart Institute, St. Lukes Hospital, University of Missouri-Kansas City School of Medicine, Kansas City, MO.
Mikhail
M
Kosiborod
University of Texas Southwestern Medical Center, Dallas, TX.
Biff F
BF
Palmer
D000208:Acute Disease; D015415:Biomarkers / Q000097:blood; D002318:Cardiovascular Diseases / Q000209:etiology* / Q000401:mortality / Q000628:therapy; D002908:Chronic Disease; D016757:Death, Sudden, Cardiac / Q000209:etiology / Q000517:prevention & control; D006801:Humans; D006947:Hyperkalemia / Q000097:blood / Q000209:etiology* / Q000401:mortality / Q000628:therapy; D007674:Kidney Diseases / Q000097:blood / Q000150:complications* / Q000401:mortality / Q000628:therapy; D011188:Potassium / Q000097:blood*; D011379:Prognosis; D012307:Risk Factors; D013997:Time Factors; D015854:Up-Regulation
D015415:Biomarkers; D011188:Potassium