Potassium A NNA VINNIKOVA, M. D.

Transcription

1 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,

2 Do you want to hear a Sodium joke?

3 Do you want to hear a Sodium joke? Na

4 Do you want to hear a Sodium joke? Na Do you want to hear a Potassium joke?

5 Do you want to hear a Sodium joke? Na Do you want to hear a Potassium joke?!

6 POTASSIUM Main intracellular cation Cl

7 POTASSIUM Main intracellular cation Cl since first organisms

8 Potassium: basics 60 meq 4000 meq

9 Potassium: physiologic roles 1. Cell volume maintenance 2. Resting potential E m =-61 log r[ + ] c [Na + ] c r[ + ] e [Na + ] e 3. Action potential

10 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

11 Pacemaker action potential

12 Hypokalemia Hyperpolarization

13 Normokalemia: pacemaker cells

14 Hypokalemia: pacemaker cells Hyperpolarization

15 Hypokalemia: pacemaker cells Hyperpolarization

16 Hypokalemia: pacemaker cells Brisk action potential Hyperpolarization

17 Hypokalemia: pacemaker cells Brisk action potential Enhanced excitability/ectopy Hyperpolarization

18 Hypokalemia: cardiac myocytes U-wave Delayed repolarization

19 Hypokalemia: hyperpolarization of resting potential, enhanced excitability/ectopy, delayed repolarization

20 Life-threatening hypokalemia: prolonged QT/torsades/reentrant arrhythmias

21 Hyperkalemia Depolarization

22 Normokalemia

23 Hyperkalemia Depolarization

24 Hyperkalemia Depolarization

25 Hyperkalemia Slowed conduction Depolarization

26 Cardiac cycle effect of hyperkalemia Peaked T wave Decreased automaticity, slowed conduction Brisk repolarization

27 Hyperkalemia and EG changes, the Fisherman

28 Life-threatening hyperkalemia: heart blocks, sine wave, VT/Vfib/asystole

29 Hyperkalemia: depolarization of resting potential, slowed conduction, brisk repolarization

30 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

31 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

32 Potassium balance Internal External

33 Potassium balance _cells How much potassium is outside and inside the cell? Why?

34 Potassium balance _cells _Na,-ATPase

35 Potassium balance _cells _Na,-ATPase What regulates Na, -ATPase?

36 Potassium balance _cells _Na,-ATPase Digoxin is a classic blocker of Na, -ATPase

37 Potassium balance _cells _Na,-ATPase α-adrenergic stimulation inhibits and β2-adrenergic stimulation activates Na, -ATPase

38 Q2 Which pressor is most likely to cause hyperkalemia? A. Epinephrine B. Levophed C. Neosynephrine

39 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

40 Potassium balance _cells _Na,-ATPase

41 Potassium balance _cells _Na,-ATPase Why should insulin stimulate Na, -ATPase?

42 Potassium balance _cells _Na,-ATPase Why should insulin stimulate Na, -ATPase? Let s take a standard breakfast:

43 Potassium balance _cells _Na,-ATPase

44 Potassium balance _cells _Na,-ATPase

45 Potassium balance _cells _Na,-ATPase

46 Potassium balance _cells _Na,-ATPase

47 Potassium balance _cells _Na,-ATPase This is more than in our entire blood volume!

48 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

49 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

50 Potassium balance _cells _changes in ph

51 Potassium balance _cells Rhabdomyolysis Tumor lysis Dead tissue Treatment of megaloblastic anemia

52 Potassium balance _kidney Glomerulus filters potassium

53 Potassium balance _kidney_distal nephron

54 Potassium balance _kidney_ increased distal flow

55 Hypokalemia

56 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

57 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

58 Hypokalemia

59 Hypokalemia

60 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

61 Case 1 Labs: > Patient admitted to floor w tele

62 EG 1 Case 1

63 EG 2 Case 1

64 Case 1 Labs 5 days later. Still with nausea, diarrhea, requiring TPN U 222, U Na 83

65 EG 3 Case 1

66 Case 1 Labs in 2011: U 163, U Na 23 Plasma aldosterone 250 Labs in 2009 (had ileostomy at that time): U Cl <15, U Na <10, U 107

67 Hypokalemia Ethiologies_increased loss_renal_non-reabsorbable anions_hypokalemia in vomiting is due to renal loss of

68 Hypokalemia Cl HCO 3 - Na +

69 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 Plasma aldosterone 12, plasma renin <0.15 (PA/PRA >80) Started on eplerenone, but later lost to renal f/u

70 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: Plasma aldosterone 34, plasma renin 0.4 (PA/PRA 85)

71 Case 2 Inspra increased to 50 mg and chlorthalidone changed to maxzide (triamterene/hctz) F/u BP 120/80 and labs: In 2012 pt developed worsening glycemic control (A1C 8) Is her metabolic syndrome worsened by aldosterone excess?

72 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

73 Case 2 After adrenalectomy, hypertension controlled on 3 meds: atenolol, lisinopril and chlorthalidone A1C down to 6

74 Hypokalemia Ethiologies_increased loss_renal_hypomagnesemia

75 Hypokalemia Ethiologies_increased loss_renal_hypomagnesemia Mg 2+

76 Hypokalemia

77 Hypokalemia

78 Hypokalemia

79 Hypokalemia

80 Hyperkalemia

81 Hyperkalemia

82 Hyperkalemia

83 Hyperkalemia: high diet

84 Hyperkalemia

85 Hyperkalemia

86 Hyperkalemia Cyclosporine, Tacrolimus Heparin

87 Hyperkalemia

88 Hyperkalemia eplerenone

89 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

90 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

91 Treatment of hyperkalemia

92 Treatment of hyperkalemia

93 Treatment of hyperkalemia

94 Hyperkalemia Depolarization

95 Hyperkalemia IV Ca raises threshold potential Depolarization

96 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

97 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

98 Treatment of hyperkalemia

99 Treatment of hyperkalemia

100 Treatment of hyperkalemia