Potassium A NNA VINNIOVA, M. D. DIVISION OF NEPHROLOGY Graphics by permission from The Fluid, Electrolyte and Acid-Base Companion, S. Faubel and J. Topf, http://www.pbfluids.com
Do you want to hear a Sodium joke?
Do you want to hear a Sodium joke? Na
Do you want to hear a Sodium joke? Na Do you want to hear a Potassium joke?
Do you want to hear a Sodium joke? Na Do you want to hear a Potassium joke?!
POTASSIUM Main intracellular cation Cl
POTASSIUM Main intracellular cation Cl since first organisms
Potassium: basics 60 meq 4000 meq
Potassium: physiologic roles 1. Cell volume maintenance 2. Resting potential E m =-61 log r[ + ] c +0.01 [Na + ] c r[ + ] e +0.01 [Na + ] e 3. Action potential
Q1: Match EG with an electrical event 1 2 A. Depolarization of resting potential in pacemaker cells and slowed conduction B. Hyperpolarization of resting potential in pacemaker cells and increased automaticity
Pacemaker action potential
Hypokalemia Hyperpolarization
Normokalemia: pacemaker cells
Hypokalemia: pacemaker cells Hyperpolarization
Hypokalemia: pacemaker cells Hyperpolarization
Hypokalemia: pacemaker cells Brisk action potential Hyperpolarization
Hypokalemia: pacemaker cells Brisk action potential Enhanced excitability/ectopy Hyperpolarization
Hypokalemia: cardiac myocytes U-wave Delayed repolarization
Hypokalemia: hyperpolarization of resting potential, enhanced excitability/ectopy, delayed repolarization
Life-threatening hypokalemia: prolonged QT/torsades/reentrant arrhythmias
Hyperkalemia Depolarization
Normokalemia
Hyperkalemia Depolarization
Hyperkalemia Depolarization
Hyperkalemia Slowed conduction Depolarization
Cardiac cycle effect of hyperkalemia Peaked T wave Decreased automaticity, slowed conduction Brisk repolarization
Hyperkalemia and EG changes, the Fisherman
Life-threatening hyperkalemia: heart blocks, sine wave, VT/Vfib/asystole
Hyperkalemia: depolarization of resting potential, slowed conduction, brisk repolarization
Q1: Match EG with an electrical event 1 2 A. Depolarization of resting potential in pacemaker cells and slowed conduction B. Hyperpolarization of resting potential in pacemaker cells and increased automaticity
Q1: Match EG with an electrical event 1 2 A. Depolarization of resting potential in pacemaker cells and slowed conduction B. Hyperpolarization of resting potential in pacemaker cells and increased automaticity 1-A, 2-B
Potassium balance Internal External
Potassium balance _cells How much potassium is outside and inside the cell? Why?
Potassium balance _cells _Na,-ATPase
Potassium balance _cells _Na,-ATPase What regulates Na, -ATPase?
Potassium balance _cells _Na,-ATPase Digoxin is a classic blocker of Na, -ATPase
Potassium balance _cells _Na,-ATPase α-adrenergic stimulation inhibits and β2-adrenergic stimulation activates Na, -ATPase
Q2 Which pressor is most likely to cause hyperkalemia? A. Epinephrine B. Levophed C. Neosynephrine
Q2 Which pressor is most likely to cause hyperkalemia? A. Epinephrine: α1 α2 β1 β2 - least B. Levophed: α1 α2 β1 C. Neosynephrine: α1 - most
Potassium balance _cells _Na,-ATPase
Potassium balance _cells _Na,-ATPase Why should insulin stimulate Na, -ATPase?
Potassium balance _cells _Na,-ATPase Why should insulin stimulate Na, -ATPase? Let s take a standard breakfast:
Potassium balance _cells _Na,-ATPase
Potassium balance _cells _Na,-ATPase
Potassium balance _cells _Na,-ATPase
Potassium balance _cells _Na,-ATPase
Potassium balance _cells _Na,-ATPase This is more than in our entire blood volume!
Q3 A 28 year old patient with DM I presents to ER with N/V. Na 132, 5.8, Cl 100, bicarb 12, BUN 30, cr 1.0, glucose 612 What is the cause of patient s hyperkalemia? A. Metabolic acidosis B. Insulin deficiency C. Hypertonicity D. B and C E. All of the above
Q3 A 28 year old patient with DM I presents to ER with N/V. Na 132, 5.8, Cl 100, bicarb 12, BUN 30, cr 1.0, glucose 612 What is the cause of patient s hyperkalemia? A. Metabolic acidosis B. Insulin deficiency C. Hypertonicity D. B and C E. All of the above
Potassium balance _cells _changes in ph
Potassium balance _cells Rhabdomyolysis Tumor lysis Dead tissue Treatment of megaloblastic anemia
Potassium balance _kidney Glomerulus filters potassium
Potassium balance _kidney_distal nephron
Potassium balance _kidney_ increased distal flow
Hypokalemia
Q4 A 26-year-old Asian male presents to the emergency room with flaccid muscle weakness. He denies diarrhea or vomiting. Na 138 meq/l, 1.8 meq/l, Cl 104 meq/l HCO3 26 meq/l, Glucose 97 mg/dl, BUN12 mg/dl Which of the following would be most appropriate : A. Cl, 200 meq po daily B. Serum thyroid-stimulating hormone level C. Acetazolamide D. None of the above
Q4 A 26-year-old Asian male presents to the emergency room with flaccid muscle weakness. He denies diarrhea or vomiting. Na 138 meq/l, 1.8 meq/l, Cl 104 meq/l HCO3 26 meq/l, Glucose 97 mg/dl, BUN12 mg/dl Which of the following would be most appropriate : A. Cl, 200 meq po daily B. Serum thyroid-stimulating hormone level C. Acetazolamide D. None of the above
Hypokalemia
Hypokalemia
Case 1 32 year old wf w h/o GI motility disorder s/p multiple surgeries, with short bowel syndrome Has h/o hypokalemia with low-normal BP, carries diagnosis of Bartter s syndrome from outside institution Presented to ED c/o abdominal pain
Case 1 Labs: 137 84 16 1.7 >40 0.7 Patient admitted to floor w tele
EG 1 Case 1
EG 2 Case 1
Case 1 Labs 5 days later. Still with nausea, diarrhea, requiring TPN 138 97 23 3 34 0.9 U 222, U Na 83
EG 3 Case 1
Case 1 Labs in 2011: 140 106 12 3.6 27 0.6 U 163, U Na 23 Plasma aldosterone 250 Labs in 2009 (had ileostomy at that time): 140 106 12 3.6 27 0.6 U Cl <15, U Na <10, U 107
Hypokalemia Ethiologies_increased loss_renal_non-reabsorbable anions_hypokalemia in vomiting is due to renal loss of
Hypokalemia Cl HCO 3 - Na +
Case 2 47 yo bf w h/o HTN since age 20 and chronic hypokalemia (on thiazide), as well as DMII and mild obesity. She was seen in renal clinic in 2004, BP 160/100 BMP 141 99 10 3.1 32 0.8 Plasma aldosterone 12, plasma renin <0.15 (PA/PRA >80) Started on eplerenone, but later lost to renal f/u
Case 2 I saw patient in 2010, at that time BP 170/91 on eplerenone 25, chlorthalidone 25, lisinopril 40, atenolol 50 and amlodipine 10. She is also on Cl 40 bid Labs: 140 98 10 3.2 35 0.5 Plasma aldosterone 34, plasma renin 0.4 (PA/PRA 85)
Case 2 Inspra increased to 50 mg and chlorthalidone changed to maxzide (triamterene/hctz) F/u BP 120/80 and labs: 137 101 16 4.0 24 0.7 In 2012 pt developed worsening glycemic control (A1C 8) Is her metabolic syndrome worsened by aldosterone excess?
Case 2 Decision to pursue hyperaldosteronism w/u: Abd CT showed a Rt adrenal adenoma Adrenal Vein Sampling lateralized overproduction of aldosterone to Rt adrenal Pt underwent Rt adrenalectomy
Case 2 After adrenalectomy, hypertension controlled on 3 meds: atenolol, lisinopril and chlorthalidone A1C down to 6
Hypokalemia Ethiologies_increased loss_renal_hypomagnesemia
Hypokalemia Ethiologies_increased loss_renal_hypomagnesemia Mg 2+
Hypokalemia
Hypokalemia
Hypokalemia
Hypokalemia
Hyperkalemia
Hyperkalemia
Hyperkalemia
Hyperkalemia: high diet
Hyperkalemia
Hyperkalemia
Hyperkalemia Cyclosporine, Tacrolimus Heparin
Hyperkalemia
Hyperkalemia eplerenone
Q5 A 39-year-old male with AIDS is admitted with pneumocystis pneumonia and treated with prednisone and intravenous trimethoprim-sulfamethoxazole. On examination, BP is 125/77, HR 98, RR 22. He appears tachypneic with diffuse rales on chest auscultation. Laboratory Studies Na 138 meq/l, 6.0 meq/l, Cl 99 meq/l HCO3 28 meq/l, BUN 10 mg/dl, Scr 0.9 mg/dl Which of the following would be the most appropriate: A. Discontinue trimethoprim-sulfamethoxazole and start pentamidine B. Discontinue trimethoprim-sulfamethoxazole and start atovaquone C. Fludrocortisone D. Sodium bicarbonate
Q5 A 39-year-old male with AIDS is admitted with pneumocystis pneumonia and treated with prednisone and intravenous trimethoprim-sulfamethoxazole. On examination, BP is 125/77, HR 98, RR 22. He appears tachypneic with diffuse rales on chest auscultation. Laboratory Studies Na 138 meq/l, 6.0 meq/l, Cl 99 meq/l HCO3 28 meq/l, BUN 10 mg/dl, Scr 0.9 mg/dl Which of the following would be the most appropriate: A. Discontinue trimethoprim-sulfamethoxazole and start pentamidine B. Discontinue trimethoprim-sulfamethoxazole and start atovaquone C. Fludrocortisone D. Sodium bicarbonate
Treatment of hyperkalemia www.lightersideofdialysis.com
Treatment of hyperkalemia
Treatment of hyperkalemia
Hyperkalemia Depolarization
Hyperkalemia IV Ca raises threshold potential Depolarization
Q6 A 57-year-old female with ESRD secondary to diabetic nephropathy maintained on chronic hemodialysis is seen on a non-dialysis day. Na 134 meq/l, 7.3 meq/l, Cl 102 meq/l HCO3 19 meq/l, BUN 22 mg/dl, Cr 6 mg/dl All of the following would lower the serum potassium EXCEPT: A. Insulin and glucose B. Albuterol C. Sodium bicarbonate D. Sodium polystyrene sulfonate E. Hemodialysis
Q6 A 57-year-old female with ESRD secondary to diabetic nephropathy maintained on chronic hemodialysis is seen on a non-dialysis day. Na 134 meq/l, 7.3 meq/l, Cl 102 meq/l HCO3 19 meq/l, BUN 22 mg/dl, Cr 6 mg/dl All of the following would lower the serum potassium EXCEPT: A. Insulin and glucose B. Albuterol C. Sodium bicarbonate D. Sodium polystyrene sulfonate E. Hemodialysis
Treatment of hyperkalemia
Treatment of hyperkalemia
Treatment of hyperkalemia www.lightersideofdialysis.com