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Fluid and Electrolyte Imbalance Jianzhong Sheng MD, PhD.

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Presentation on theme: "Fluid and Electrolyte Imbalance Jianzhong Sheng MD, PhD."— Presentation transcript:

1 Fluid and Electrolyte Imbalance Jianzhong Sheng MD, PhD

2 Water

3 Body fluids Extracellular fluids (ECF) –Interstitial fluid - fills the spaces between most cells of the body –Intravascular fluid - plasma (WBC, RBC and platelets in this fluid)

4 Body fluids Intracellular fluids (ICF) –Liquids within cell membranes –40% of body weight

5 Components in body fluids Electrolyte –an element that when dissolved can carry an electrical current –Cations - (+) ; Anions - (-) –neuromuscular function –acid-base balance –ingested compounds –serve as catalysts in nerve response, muscle contraction, and metabolism of nutrients in foods, regulate electrolyte balance

6 Movement of body fluids Diffusion –Area of higher concentration to an area of lower concentration till even distribution Osmosis –Movement of a pure solvent, e.g. water through a semipermeable membrane from a solution that has a lower solute concentration to one that has a higher solute concentration

7 Osmotic pressure Drawing power of water (dependent on the number or molecules in solution) –Isotonic –Hypotonic –Hypertonic

8 Movement of body fluids Filtration –Water and diffusible substances move together in response to fluid pressure Active transport –Requires energy –Able to move larger molecules and go from less to greater concentration

9 Transmembrane water permeability All biological membranesRenal tubules, secretory glands, red cells Low capacityHigh capacity for H 2 O, not H 3 O + Bi-directionalDirected by osmotic gradients Unknown inhibitorsReversibly inhibited by Hg ++ Bilayer DiffusionAquaporin Water Channels Hard to explain

10 Discovery of Aquaporin-1 A serendipitous observation Contaminant in 32 kDa Rh preparations Simple purification Atypical staining Insoluble in N-lauroylsarc. 200,000 copies per red cell Channel-like homotetramer Protein sequence 1-35 aa Denker et al., J Biol Chem, 1988 Smith & Agre, J Biol Chem, 1991

11 Discovery of Aquaporins-AQP1 Functional expression (with Wm. Guggino at JHMI) Hypo-osmolar swelling Hg ++ inhibited, no currents Xenopus oocyte, CHIP28 Preston et al., Science 1992

12 Peter Agre & Roderick MacKinnon Nobel Prize December 2003


14 Structure of AQP1 Hg ++ inhibitory site

15 Fluid Intake Hypothalamus - thirst control center Oral fluid intake - requires an alert state Osmoreceptors - monitor osmolality

16 Fluid Output Loss through the kidneys and GI tract Insensible Sensible

17 Cations Sodium (Na+) –Most abundant in the extracellular fluid –Maintains water balance, transmits nerve impulses, contracts muscles –Values mEq/L

18 Potassium (K+) –Major intracellular cation –Regulates neuromuscular excitability, muscular contraction, and acid-base –Value mEq/L Cations

19 Calcium (Ca2+) –Cardiac conduction, blood coagulation, bone growth and formation, & muscular relaxation –Value mEq/L Cations

20 Magnesium (Mg2+) –Second most important of intracellular fluids –Enzyme activities, muscular excitability –Value mEq/L Cations

21 hypertonic hypertonic Dehydration isotonic water excess isotonic hypotonic hypotonic Extracellular fluid deficit 1. Hypotonic dehydration sodium loss > water loss serum sodium < 130mmol/L plasma osmotic pressure < 280mOsm/L Water (and sodium) disorders

22 1) Cause and Pathogenesis Excessive loss of water Sodium replaced with water only. Vomiting, diarrhea; burn; diuretics; Addison’s disease (ADS ) ; Chronic renal failure; renal tubular acidosis 2) Adaptive response and effect on body ① movement of body fluid ECF ICF Cellular swelling Blood volume Extracellular fluid Shock Dehydrated signs Brain and lung edema

23 ② urinary alteration urine specific urine volume gravity [Na + ] Early ADH ±or stage ADS Late ADH stage ADS

24 3) principles of treatment ① treating primary disease ② 0.9%NaCl 2. Hypertonic dehydration ① water loss > sodium loss ② serum sodium > 150mmol/L ③ plasma osmotic pressure > 310mOsm/L

25 1) Cause and pathogenesis lack of water (desert; sea) ① intake to drink inability (coma; baby) lung: hyperpnea (hypoxia; acidosis) skin: fever; hyperthyroidism; sweat; exposure to hot environment digestive tract: vomiting; diarrhea; ② loss baby diarrhea ([Na + ]: 60mmol/L) kidney: diabetes (ketosis); diabetes insipidus diuretic (mannitol; hypertonic glucose)

26 2) Effect on body ① hypertonic of ECF thirst ② movement of the body fluid ICF ECF cell dehydration Brain dehydration Sleepiness subarachnoid bleeding Dehydrated fever

27 ③ urinary alteration urine specific urine volume gravity [Na + ] Early ADH stage ADS± Late ADH stage ADS ) principles of treatment Water > NaCl

28 3. isotonic dehydration ① water loss ≈ sodium loss ② serum sodium = mmol/L ③ plasma osmotic pressure: mOsm/L 1) cause and pathogenesis ① vomiting; diarrhea; gastrointestinal suction; biliary fistula; intestinal fistula ② ascitic fluid; pleural effusion

29 2) effects on body ① slight thirst ② blood volume dehydrated signs; BP ③ urinary alteration urine specific urine volume gravity [Na + ] Early ADH stage ADS Late ADH stage ADS ) principles of treatment 补偏低渗液;先补 0.9%NaCl

30 Extracellular fluid excess 1. Water intoxication water intake, total sodium ±; ECF, ICF ; hyponatremia; Serum sodium < 130mmol/L 1) Causes excessive water intake renal loss (acute renal failure; acute congestive heart failure) 2) effects on body brain cells swelling water moves into cells pulmonary edema 3) principles of treatment diuresis

31 2. Edema interstitial fluid fluid in the body cavities hydrops fluid in the cells cellular edema (1) pathogenesis 1) imbalance of exchange between intra- and extra-body fluid (retention of water and sodium) basic mechanism: glomerular-tubular imbalance ① GFR acute glomerulonephritis heart failure ② reabsorption of proximal tubule sympathetic nerve filtration fraction ANP reabsorption of water and sodium

32 Electrolyte Imbalances

33 Hyponatremia Defined as serum [Na+] less than 136 mEq/L Water shifts into cells causing cerebral edema 125 mEq/L – nausea and malaise 120 mEq/L – headache, lethargy, obtundation 115 mEq/L – seizure and coma

34 Hyponatremia (cont) 1. Assess plasma osmolality 2. Assess volume status of patient –Hypervolemic, Euvolemic, Hypovolemic 3. Assess Urine Sodium Concentration –Needed for definitive diagnosis, not needed for treatment purposes 4. Calculate Na+ Deficit –0.6 x weight (kg) x (130 – plasma [Na+]) 5. Correct at no more than 0.5mEq/L per hour or 12 mEq/L per 24 hours

35 Isosmotic and Hyperosmotic Hyponatremia –Iso and Hyperosmotic hyponatremia are due to excessive solutes in plasma. –Isosmotic Pseudohyponatremia – No treatment necessary –Hyperlipidemia –Hyperproteinemia Isotonic Infusions –Glycine –Mannitol –Hyperosmotic – Treat underlying cause Hyperglycemia –Each 100 mg/dl of glucose reduces [Na+] by 1.6 mEq/l Hypertonic Infusions –Glycerol –Mannitol –Glycine

36 Hyposmotic Hyponatremia 1. Assess volume status –Hypervolemic – cirrhosis, heart failure, nephrotic syndrome –Euvolemic – polydipsia, SIADH –Hypovolemic – most common cause Excessive renal (diuretic) or GI (emesis, diarrhea) losses

37 Treatment of Hyponatremia Iso or Hyperosmotic –Correct underlying disorder Hyposmotic –Iso or hypervolemic – fluid restriction –Hypovolemic Asymptomatic – fluid resuscitate with isotonic saline Symptomatic or plasma [Na+] less than 110 mEq/L –Calculate Na+ deficit –Correct at a rate no greater than 0.5 mEq/L/hour or 12 mEq/L/day

38 Correction of Sodium Deficit Example: A 60 kg woman with a plasma sodium concentration of 120mEq/L: Sodium deficit = TBW x (130 – [Na+]p) Sodium deficit = 0.5 x 60 x ( ) = 300mEq 3% NaCl contains 513 mEq sodium/L Volume of 3% NaCl needed = 300/513 = 585 mL At 0.5 mEq/L/hr a correction of 10 mEq should be done over 20 hours So, 585 mL/20 hours = 29 mL/hour of 3% NaCl

39 Hypernatremia Defined as serum [Na+] greater than 146 mEq/L Lethargy, weakness, and irritability that progress to seizure, coma, and death Usually occurs in adults with altered mental status or no access to water

40 Hypernatremia (cont) 1. Assess volume status 2. Measure urine [Na+] 3. Calculate water deficit –0.6 x weight (kg) x ([Na+]/140 -1) 4. Correct with free water no faster than 0.5 mEq/L/hour or 12 mEq/L/day

41 Hypernatremia Hypovolemic – loss of hypotonic fluids –Diuresis, vomiting, diarrhea Isovolemic – loss of free water –Diabetes insipidus, hypodipsia Hypervolemic – gain of hypertonic fluids –Hypertonic saline administration

42 Treatment of Hypernatremia Hypovolemic –Replace the free water deficit Hypervolemic –Diuretics (lasix) to excrete sodium in urine combined with hypotonic saline for partial volume replacement

43 Treatment of Hypernatremia Isovolemic –Diabetes Insipidus –Loss of hypotonic urine secondary to lack of ADH production (central) or lack of response to ADH by kidney (nephrogenic) –Hallmark is hypotonic urine ( mOsm/L) with hypertonic plasma –Treat by correcting free water deficit –In central DI must also administer 5 – 10 units of DDAVP Q6H to prevent ongoing free water loss

44 Hyperkalemia Defined as a serum [K+] greater than 4.6 mEq/L Changes in cellular transmembrane potentials can lead to lethal cardiac arrhythmias Most often associated with renal impairment coupled with exogenous K+ administration or drugs that increase K+ Transcellular shifts – acidosis, succinylcholine, insulin deficiency, massive tissue destruction Massive blood transfusions Pseudohyperkalemia - Thrombocytosis, hemolysis, leukocytosis Urine K+ excretion rate can be used to determine exact cause of hyperkalemia

45 Hyperkalemia Drugs causing hyperkalemia – K+ sparing diruetics, ACEI, NSAIDs, Heparin, Cyclosporin, Tacrolimus, Bactrim EKG Changes –5.5 – 6.5 mEq/L – peaked T-waves –6.5 – 7.5 mEq/L – loss of P-waves –> 8.0 mEq/L – widened QRS

46 Treatment of Hyperkalemia 1. If EKG changes administer 10 mL of 10% Calcium Gluconate 2. 1 amp D50 with 10 units IV insulin (onset minutes, duration 2-3 hours) 3. Albuterol mg (onset 4-5 hours, duration 2-3 hours) 4. Kayexalate g (oral onset 4-5 hours, enema onset 1 hour) Dialysis

47 Hypokalemia Defined as serum [K+] less than 3.6 mEq/L Occurs in up to 20% of hospitalized patients 2.5 mEq/L – muscular weakness, myalgia <2.5 mEq/L – cramps, parasthesias, ileus, tetany, rhabdomyolisis, PVCs, A-V block, V-tach, V-fib

48 Hypokalemia Inadequate intake Increased excretion – diarrhea, diuretics, alkalosis, glucocorticoids, RTA Transcellular shifts – beta-agonists, theophylline, insulin, hyperthyroidism, barium Replace no faster than 20 mEq/H peripherally and 100 mEq/H centrally

49 Hypercalcemia Excess calcium Needs vit D for efficient absorption; most of Ca is stored in the bones. Causes: bone tumors that cause bone destruction, chemo rx release Ca from the bones; immobilization causes loss from the bones (usually excreted) but if kidneys can’t clear it, hypercalcemia results, increased intake (milk- alkali syndrome).

50 Hypercalcemia (cont) Clinical manif: Ca imbalances alter neuromuscular irritability with non-specific symptoms –Constipation, anorexia, N/V, fatigue, skeletal muscle weakness, confusion, lethargy. –Renal calculi, cardiac arrhythmias –HyperCa increases Na and K excretion leading to polyuria and polydipsia. –Rx: serum Ca, Ionized Ca, fluids, Lasix, steroids, dialysis.

51 Hypocalcemia Decreased serum calcium Causes: decreased intake of Ca and/or Vit D (adolescents are vulnerable d/t fad diets and the deficit cannot be made up later, increasing risk for osteoporosis). –Limited exposure to sunlight, premature infants and dark skinned people at increased risk to inadeq. Vit D and therefore decreased Ca absorption. –Parathyroid dysfunction, multiple transfusion (Citrate binds Calcium), steatorrhea (as in pancreatitis and Cystic Fibrosis) binds Calcium in the stool.

52 Hypocalcemia (cont) Clinical Manif: acute situation related to increased muscular excitability: tetany. +Chvostek’s Sx, + Trousseau’s Sx. In children: Twitching, cramping, tingling around the mouth or fingers, carpal/pedal spasms. In infants: tremors, muscle twitches, brief tonic- clonic seizures, CHF. Laryngospasm, seizures and cardiac arrhythmias in severe situations.

53 Hypocalcemia (cont 2) In children and adolescents, chronic hypocalcemia more common, manif. By spontaneous fractures. Lab tests: serum Ca; bone density study Rx: oral and/or IV Ca, Ca rich diet

54 Hypermagnesemia Excess in Mg. Imbalances characterized by neuromuscular irritability Causes: impaired renal function, Mag Sulfate given perinatally to treat eclampsia, increased use of laxatives, enemas, antacids, IV fluid additives.

55 Hypermagnesemia (cont) Clinical Manif: decreased muscle irritability, hypotension, bradycardia, drowsiness, lethargy, weak or absent DTR’s. Rx: increase fluids, diuretics, dialysis.

56 Hypomagnesemia Decreased serum Mg. Stored in cells and bones Causes: prolonged NPO without replacement, chronic malnutrition, chronic diarrhea, short bowel syndrome, malabsorption syndromes, steatorrhea, multiple transfusions, prolonged NG Sx, some medications.

57 Hypomagnesemia (cont) Clinical manif: increased neuromuscular excitability (tetany). Hyperactive reflexes, skeletal muscle cramps, twitching, tremors, cardiac arrhythmias, seizures. Lab: serum Mg along with Ca and K. Rx: po/IV Magnesium admin and treating underlying cause of imbalance.

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