Disorders: Is it Just Salt and Water? Mark L. Zeidel, M.D Herrman - - PowerPoint PPT Presentation

▶
disorders is it just salt and water
SMART_READER_LITE
LIVE PREVIEW

Disorders: Is it Just Salt and Water? Mark L. Zeidel, M.D Herrman - - PowerPoint PPT Presentation

Feb 15, 2023 250 likes •638 views

Managing Electrolyte Disorders: Is it Just Salt and Water? Mark L. Zeidel, M.D Herrman L. Blumgart Professor of Medicine Harvard Medical School Chair, Department of Medicine Physician-in-Chief, BIDMC Boston, Massachusetts Each of these

slide-1
SLIDE 1

Managing Electrolyte Disorders: Is it Just Salt and Water?

Mark L. Zeidel, M.D Herrman L. Blumgart Professor of Medicine Harvard Medical School Chair, Department of Medicine Physician-in-Chief, BIDMC Boston, Massachusetts

slide-2
SLIDE 2

2

Each of these creatures survives by highly effective management

  • f salt and

water

slide-3
SLIDE 3

Case 1 Case 2

slide-4
SLIDE 4

Case 1

A 56 year old man discovers that he has hypertension when he uses a blood pressure machine in a pharmacy. He is seen by his PCP, who notes a blood pressure of 155/95 on multiple readings. After salt restriction fails to alter the blood pressure, the patient is started on hydrochlorothiazide, 25 mg/day. His blood pressure is 140/85 on follow-

  • up. Routine electrolytes reveal:

Na+ 135; K+ 3.0; Cl- 96; HCO3

  • 29, BUN 32 and Cr 0.9.

1

4

How does thiazide lower BP? Since he continues the thiazide, why does he not go into shock? Why is he now alkalotic, hypokalemic, with a high BUN/Cr ratio? Why do some patients receiving thiazides become hyponatremic?

slide-5
SLIDE 5
slide-6
SLIDE 6

Defense Against Volume Depletion

Sensors of Volume Depletion Extrarenal Renal Effector Mechanisms Sympathetic Outflow Renin-Angiotensin Aldosterone Anti-Diuretic Hormone Effectors act on the kidney.

slide-7
SLIDE 7

Extrare rarenal nal volu lume e senso sors rs

slide-8
SLIDE 8

Rena nal l sensor nsors s of volume lume depletion pletion  renin nin release lease

  • Barorec

ecep eptors tors in the affere rent nt arterio riole

  • Sympa

pathe theti tic input t to the JG apparatus atus

  • Macul

ula densa feedbac ack (fall in tubular r flow in dista tal nephron

  • n eithe

her r becaus use of  GFR or  proxima mal reabsor

  • rpti

ption

  • n)
slide-9
SLIDE 9

Defense Against Volume Depletion

Sensors of Volume Depletion Extrarenal Renal Effector Mechanisms Sympathetic Outflow Renin-Angiotensin Aldosterone Anti-Diuretic Hormone Salt Hunger and Thirst

slide-10
SLIDE 10

Sympa pathet thetic ic Effec ector tor Mech chanism anisms

Cardiac Output Preload Increased Venous Return Renal Salt Retention Direct, R-A-A system Increased Cardiac Performance Increased Contractility Increased Heart Rate Peripheral Arterial Resistance Circulating Catecholeamines, Angiotensin II

slide-11
SLIDE 11
slide-12
SLIDE 12

What at does es Renin nin do?

slide-13
SLIDE 13

Angiot iotens ensin in II

  • Potent

nt syste temi mic vasoc

  • cons

nstric tricto tor

  • Retenti

tion n of sodium m and water through ghou

  • ut

t the nephron (espec ecially in proximal mal tubule) e)

  • Regulati

tion

  • n of glomeru

erular ar filtration tration rate

  • Stimul

mulates ates releas ase of aldoste teron rone

slide-14
SLIDE 14

Aldos

  • steron

terone

Primary mary effect t is to increase rease sodium m reabsorp rpti tion n in the distal tal nephron

slide-15
SLIDE 15

Na+ transport along the nephron

Hoenig and Zeidel CJASN 2014;9:1272-1281

Filter 180l/d PNa = 140 FL = 25,200 mEq/d

NaCl 60-80% NaCl 25%

NaCl 3%

NaCl 5% NaCl 5%

slide-16
SLIDE 16
slide-17
SLIDE 17

Angiotensin II and increased sympathetic tone increase sodium reabsorption in proximal tubule

  • L. Lee Hamm et al. CJASN 2015;10:2232-2242
  • NB. sodium and bicarbonate reabsorption

are intimately linked! Angiot iotensin sin Cate techo cholami lamines

slide-18
SLIDE 18

Aldosterone paradox: Volume Depletion: Kidney augments NaCl retention with minimal K+ secretion Hyperkalemia: Kidney wastes K+ without Na+ retention

Biff F. Palmer CJASN 2015;10:1050-1060

slide-19
SLIDE 19
slide-20
SLIDE 20

1 20

Case e 1

A 5 56 year old man discover ers that he has hypert erten ension

  • n when he uses a blood pressure

ure machine e in a p pharma macy. . He is seen by his PCP, who notes a b blood pressure ure of 155/95 5

  • n multiple

e readi ding ngs. After salt restr tricti tion

  • n fails to a

alter the blood pressure, ure, the patient t is starte ted d on hydrochl

  • chlorot
  • rothi

hiazi azide de, 25 mg/day. . His blood pressure ure is 140/85 5 on follow-up

  • up. Routine

ne electr trolytes tes reveal al: : Na Na+ 135; K+ 3.0; Cl- 96; HCO3

  • 29, BUN 32 and

Cr 0.9.

How does thiazide lower BP? Since he continues the thiazide, why does he not go into shock? Why is he now alkalotic, hypokalemic, with a high BUN/Cr ratio?

slide-21
SLIDE 21

So, we’ve explained why he does not go into shock.

  • ck. Why

hy does this is therapy rapy treat eat hypertens pertension ion?

  • BP is down, CO is the same

so SVR must st be decr crease sed. How does s this s happen?

Titze, J and Luft, F. Kidney Int 2017 91:1324-35.

slide-22
SLIDE 22

Salt load alters skin Na+ storage in rats and people.

slide-23
SLIDE 23

Peripheral Na+ storage might influence peripheral vascular tone

slide-24
SLIDE 24

Case 2

  • A 67 year old man suffers a major

MI, from which he recovers. One month later he notes increased edema, dyspnea on exertion, and 2 pillow orthopnea.

  • PE reveals P = 120, BP = 100/65,

RR = 22, afebrile. Exam notable for distended neck veins, rales 1/3 up, a palpable S3, and 2+ pitting edema to the mid calf.

  • Serum Na+ 125, K+ 3.0, HCO3
  • 32,

Cl- 81, BUN 36, Cr 1.1

  • Urine Na+ is 2. Urine osmolality is

685; Serum Osmolality is 262. Volume and Osmoregulation

slide-25
SLIDE 25

Extrare rarenal nal volu lume e senso sors rs

slide-26
SLIDE 26

Na+ transport along the nephron

Hoenig and Zeidel CJASN 2014;9:1272-1281

Filter 180l/d PNa = 140 FL = 25,200 mEq/d

NaCl 60-80% NaCl 25%

NaCl 3%

NaCl 5% NaCl 5%

slide-27
SLIDE 27

Lowell, BB NEJM 380:459-71, 2019

slide-28
SLIDE 28

Control of Salt Appetite

Resch, JM et al Neuron 96:190-206, 2017

slide-29
SLIDE 29

Case 2

  • A 67 year old man suffers a major

MI, from which he recovers. One month later he notes increased edema, dyspnea on exertion, and 2 pillow orthopnea.

  • PE reveals P = 120, BP = 100/65,

RR = 22, afebrile. Exam notable for distended neck veins, rales 1/3 up, a palpable S3, and 2+ pitting edema to the mid calf.

  • Serum Na+ 125, K+ 3.0, HCO3
  • 32,

Cl- 81, BUN 36, Cr 1.1

  • Urine Na+ is 2. Urine osmolality is

685; Serum Osmolality is 262. Volume and Osmoregulation

slide-30
SLIDE 30

Osmoreceptor functions of the OVLT nuclei and SON control thirst and vasopressin release, respectively.

Danziger J , and Zeidel M L CJASN

slide-31
SLIDE 31

Neurobi biol

  • logy

gy of Thirst t and ADH release

  • Nat. Rev Neurosci 18:459 2017
slide-32
SLIDE 32

Thirs rst adapt pts to antic icipat ipated d rather er than n real l changes nges in body fluid uid osmolalit

  • lality.
slide-33
SLIDE 33

Hyperosmolality: a major stimulus for ADH release

adapted from Robertson et al, Am J Med 1982

thirst

Hyperosmolality: a major stimulus for ADH release

adapted from Robertson et al, Am J Med 1982

thirst

slide-34
SLIDE 34

Volume Status Modulates ADH Release

Robertson, G. J Clin Endocrinol Metab. 1976;42:613–20

slide-35
SLIDE 35

ADH IS NOT PRESENT NT Large volume of dilute urine Small volume of concentrated urine* ADH IS PRESENT NT *provided the interstitium is concentrated (H2O moves along gradient with the help of aquaporins)

slide-36
SLIDE 36

Cellular action of vasopressin

Danziger J , and Zeidel M L CJASN

slide-37
SLIDE 37

Managing Electrolyte Disorders: Is it Just Salt and Water?

Mark L. Zeidel, M.D Herrman L. Blumgart Professor of Medicine Harvard Medical School Chair, Department of Medicine Physician-in-Chief, BIDMC Boston, Massachusetts