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Fluids, Electrolytes, Nutrition, and Acid-Base Disturbances

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Fluids, Electrolytes, Nutrition, and Acid-Base Disturbances Geoff Vana Loyola University Medical Center General Surgery PGY-1 Decrease minute ventilation * Answer 2 E ... – PowerPoint PPT presentation

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Title: Fluids, Electrolytes, Nutrition, and Acid-Base Disturbances


1
Fluids, Electrolytes, Nutrition,and Acid-Base
Disturbances
  • Geoff Vana
  • Loyola University Medical Center
  • General Surgery
  • PGY-1

2
Total Body Water
  • 50-60 of total body weight
  • 50 in males, 60 in females
  • Reflection of body fat lean tissues high
    water content
  • Adjust down for obesity (10-20)
  • Highest in newborns 80
  • Compartments
  • 2/3 (40) Intracellular (skeletal muscle)
  • 1/3 (20) Extracellular
  • 2/3 (15) Interstitial
  • 1/3 (5) - Plasma

3
Composition of Fluid
  • ECF
  • Sodium principle cation
  • Chloride and Bicarbonate principle anions
  • ICF
  • Potassium and Magnesium cations
  • Phosphate and Proteins anions
  • Water diffuses freely according to sodium content
  • Expands intravascular volume
  • Expands interstitial volume 3x plasma

4
Fluid Secretion/Losses
  • Secretion
  • Stomach 1-2L
  • Small Intestine 2-3L
  • Pancreas 600-800cc
  • Bile 300-800cc
  • H2O losses
  • Urine 800-1200cc
  • Stool 250cc
  • Insensible 600cc
  • Increased by fever, hypermetabolism,
    hyperventilation
  • To clear metabolites 500-800cc urine per day

5
Volume Control
  • Extracellular volume deficit most common
  • Loss of GI fluids (suction, emesis, diarrhea,
    fistula)
  • Acute CV and CNS signs
  • Chronic decreased skin turgor, sunken eyes, CV
    and CNS signs
  • Urine osmolality is higher than serum
  • Urine sodium is low (lt20mEq/L)

6
Volume Control
  • Osmoreceptors and Baroreceptors
  • Osmoreceptors in paraventricular and
    supraventricular nuclei in hypothalamus control
    thirst and ADH secretion from posterior pituitary
  • Increased free water or decreased osmolality
    decreased ADH and water reabsorption
  • Fine tuning day-to-day
  • Baroreceptors in cardiac atrium, aortic arch and
    carotid sinuses
  • Neural and hormonal feedback

7
Volume Control
  • Renin-Angiotensin
  • Renin released from juxtaglomerular cells of
    afferent arterioles in kidney (? BP, ?NaCl)
  • Cleaves angiotensinogen (a-2 globulin produced by
    liver) to angiotensin 1
  • Angiotensin cleaved by ACE which is produced by
    vascular endothelial cells
  • Increases vascular tone, stimulates catecholamine
    release from adrenal medulla and sympathetic
    nerve terminals
  • Decreases RBF and GFR increases sodium
    reabsorption by indirect and direct effect
    (aldosterone release from adrenal cortex)
  • Aldosterone
  • Produced in zona glomerulosa of adrenal cortex
  • Increased absorption of sodium in CD DCT
    stabilizing Na channel in open state, increases
    number of channels in apical membrane
  • Increases Na/K activity
  • Increases sodium reabsorption and potassium
    excretion

8
Volume Control
  • Natriuretic Peptide
  • Brain and Renal
  • Released by atrial myocytes from wall distension
  • Inhibitory effect on renal sodium absorption
  • Urodilatin ANP-like substance, synthesized by
    cortical collecting tubule
  • Released by kidney tubules in response to atrial
    distension and sodium loading
  • Twice as potent as ANP, increases cGMP Na, Cl,
    water diuresis

9
Volume Replacement
  • Lactated Ringers solution
  • Blood loss, edema fluid, small bowel losses
  • Ideal when electrolytes are normal
  • Na 130mEq/L hyponatremia can occur with
    extended use
  • Lactate converted to bicarbonate no
    contribution to acidosis
  • Normal Saline
  • Useful for hyponatremia and hypochloremia
    (154mEq/L)
  • Can lead to increased electrolyte concentrations
  • Hyperchloremic metabolic acidosis
  • pH between 4-5
  • Hypotonic solutions (1/2 or ¼ NS)
  • Hypoosmotic and hypotonic
  • Can result in RBC lysis
  • D5 added to prevent (200 kcal/L)

10
Volume Replacement
  • Hypertonic Saline Solutions
  • 3 NaCl, 5 NaCl, 7.5 NaCl
  • Resuscitation for head trauma, hemorrhagic shock,
    burn
  • Increases intravascular volume quicker
  • Increases cerebral perfusion and reduces cerebral
    edema
  • Decreases volume requirement
  • 4-2-1 rule
  • Monitor UOP

11
Colloids
  • Albumin (5, 25)
  • Increases plasma oncotic pressure reversing
    diffusion of water into interstitial space
  • ARDS, Burns, Infections, Sepsis
  • Can extravasate into tissues worsening edema
  • Hetastarch
  • Synthetic plasma expander
  • Coagulopathy and bleeding from reduced factor
    VIII and von Willebrand factor, prolonged PTT and
    impaired platelet function
  • Hextend (6 in LR)
  • Plasma expander with no effect on coagulation
  • Reduce fluid requirement, eliminate need for
    mannitol, improves neurologic outcome
  • No inhibition of platelets

12
Sodium
  • Hyponatremia
  • Sodium depletion or dilution
  • Dilution
  • SIADH, anti-psychotics, tricyclics, ACE-Is
  • Depletion
  • Low-sodium diet, GI losses (emesis, NG,
    diarrhea), renal d/t diuretics
  • Pseudohyponatremia
  • Elevated glucose level causes influx of H2O
  • Na (gluc-100) x .016
  • Headache, confusion, N/V, seizures, fatigue,
    increased ICP, HTN, bradycardia, oliguria

13
Sodium
  • Hypernatremia
  • Loss off free water or gain of sodium
  • Iatrogenic administration of sodium-rich fluids
  • Mineralocorticoid excess (hyperaldosteronism,
    Cushings syndrome, CAH)
  • Hypotonic skin losses from fever or
    tracheostomies during hyperventilation
  • Urine Na gt 20mEq/L
  • Ataxia, tonic spasms, delirium, weakness,
    tachycardia, hypotension, syncope, red swollen
    tongue, decreased saliva/tears, fever
  • Free Water Deficit TBW x (Na/140) 1

14
Potassium
  • Hypokalemia more common than hyperkalemia
  • Caused by poor intake, excess renal excretion,
    diarrhea, fistulas, emesis, high NG output,
    intracellular shifts from metabolic alkalosis or
    insulin
  • Decreases 0.3 mEq/L for every 0.1 increase in pH
  • Amphotericin, aminoglycosides, foscarnet,
    cisplatin, ifosfamide induce magnesium wasting
  • Correct magnesium
  • Disorders of muscle contractility in GI smooth
    muscle, cardiac muscle, skeletal muscle
  • Ileus, constipation, weakness, fatigue, dec DTR,
    paralysis, cardiac arrest

15
Potassium
  • Hyperkalemia
  • Excessive intake, increased cellular release,
    impaired excretion from kidneys
  • PO/IV supplementation, post-transfusion RBC
    lysis, acidosis, rapid rise in extracellular
    osmolality
  • K-sparing diuretics, ACE-Is, NSAIDs
  • Spironolactone and ACE-Is inhibit aldosterone
    (renal excretion)
  • N/V, intestinal colic, diarrhea, weakness,
    ascending paralysis, peaked T-waves, wide QRS,
    sine wave formation, V-fib

16
Magnesium
  • 1/3 bound to albumin plasma level poor
    indicator with hypoalbuminemia
  • Hypermagnesemia
  • Severe renal insufficiency, magnesium-containing
    antacids/laxatives, TPN, massive trauma, severe
    acidosis
  • N/V, neuromuscular dysfunction, weakness,
    lethargy, hyporeflexia, impaired cardiac
    conduction, elevated T waves
  • Hypomagnesemia
  • Regulated by calcium/magnesium receptors in
    tubular cells
  • Starvation, EtOH, prolonged IVF therapy, TPN,
    diuretic use, amphotericin B, Primary
    aldosteronism, diarrhea, malabsorption, acute
    pancreatitis
  • CNS hyperactivity, hyperactive DTRs, muscle
    tremors, ST depression, torsades de pointes
  • Can produce hypocalcemia and persistent
    hypokalemia
  • Replace magnesium

17
Phosphorus
  • Hyperphosphatemia
  • Decreased urinary excretion, increased intake,
    impaired renal function, hypoparathyroidism,
    hyperthyroidism, rhabdomyolysis, tumor lysis
    syndrome, sepsis, hemolysis
  • Metastatic deposition of soft tissue
    calcium-phosphorus complexes
  • Hypophosphatemia
  • Decreased intake, intracellular shift (alkalosis,
    insulin, refeeding), decreased GI uptake from
    phosphate binders

18
Calcium
  • Hypercalcemia
  • Primary hyperparathyroidism, malignancy (bone
    metastasis, PTHr)
  • Neurologic impairment, muscle weakness/pain,
    renal dysfunction, n/v, abdominal pain, worsening
    of Digitalis toxicity, short QT interval, flat T
    waves, AV block
  • Hypocalcemia
  • Pancreatitis, soft tissue infection, renal
    failure, small bowel fistulas, hypoparathyroidism,
    TSS, abnormal magnesium, tumor lysis syndrome,
    post-parathyroidectomy, breast/prostate cancer,
    alkalosis
  • Parastheias of face, muscle cramps, carpopedal
    spasm, stridor, tetany, seizures, hyperreflexia,
    heart block, prolonged QT

19
Vitamin Deficiency
Deficiency Effect
Chromium Hyperglycemia, encephalopathy, neuropathy
Selenium Cardiomyopathy, weakness, hair loss
Copper Pancytopenia
Zinc Hair loss, poor healing, rash
Trace elements Poor wound healing
Phosphate Weakness (fail to wean vent), encephalopathy, decreased phagocytosis
Thiamine (B1) Wernickes, cardiomyopathy, peripheral neuropathy
Pyridoxine (B6) Sideroblastic anemia, glossitis, peripheral neuropathy
Cobalamin (B12) Megaloblastic anemia, peripheral neuropathy, beefy tongue
Folate Megaloblastic anemia
Niacin Pellagra (diarrhea, dermatitis, dementia)
Essential Fatty Acids Dermatitis, hair loss, thrombocytopenia
Vitamin A Night Blindness
Vitamin K Coagulopathy
Vitamin D Rickets, Osteomalacia
Vitamin E Neuropathy
20
Acid-Base Disorder
  • Disorder of balance between HCO3- and H
  • Blood pH 7.35 7.45
  • Arterial PCO2 35 45mmHg
  • Plasma HCO3- 22 26mEq/L
  • Lungs compensate for metabolic abnormalities
  • Quick
  • Kidneys compensate for respiratory abnormalities
  • Delayed, up to 6 hours
  • Acute before compensation
  • Chronic after compensation

21
Respiratory Acidosis
  • pH lt 7.35, pCO2 gt 45
  • Decreased ventilation
  • BiPAP, intubation to increase minute ventilation
  • Chronic form pCO2 remains constant and HCO3
    increases as compensation occurs
  • Narcotics, Atelectasis, Mucus plug, pleural
    effusion, pain, limited diaphragmatic excursion

22
Respiratory Alkalosis
  • pH gt 7.45, pCO2 lt 35
  • Most cases acute from hyperventilation
  • Pain, anxiety, neurologic disorders, CNS injury,
    hypoxemia
  • Salicylates, fever, Gram Neg bacteria,
    thyrotoxicosis
  • Acute hypocapnia uptake K and phosphate into
    cells, increased Ca binding to albumin
  • Symptomatic hypokalemia, hypophosphatemia,
    hypocalcemia

23
Metabolic Acidosis
  • pH lt 7.35, HCO3 lt 22
  • Increased acid intake, increased generation of
    acids, increased loss of bicarbonate
  • Response increase buffers (bone/muscle),
    increase respiration, increased renal
    reabsorption and generation of bicarbonate and
    excretion of hydrogen
  • Calculate Anion Gap (Na) (Cl HCO3)
  • Corrected AG AG 2.5(4.5-albumin)
  • AG gt 12 Methanol, Uremia, DKA, Paraldehyde, INH,
    Lactic acidosis, Ethanol, Salicylates
  • AG lt 12 RTA, Carbonic anhydrase inhibitor, GI
    losses

24
Metabolic Alkalosis
  • pH gt 7.45, HCO3 gt 26
  • Loss of fixed acids, gain of bicarbonate
    (worsened by potassium depletion), pyloric
    stenosis and duodenal ulcer disease
    (hypochloremic, hypokalemic)
  • Increased urine bicarbonate, reabsorption of
    hydrogen and potassium excretion
  • Aldosterone causes Na reabsorption and increased
    K excretion H/K interchange results in
    paradoxical aciduria

25
Nutrition
  • Pre-operative Evaluation
  • Albumin 20 days
  • Transferrin 10 days
  • Pre-albumin 2 days
  • Poor nutrition
  • Weight loss gt10 in 6 months
  • Albumin lt 3.0
  • Weight lt85 IBW

26
Nutrition
  • Caloric Need 20-25 kcal/kg/day
  • Fat 9kcal/g
  • Carbohydrate 4kcal/g
  • Dextrose 3.4kcal/g
  • Protein 4kcal/g
  • Requirements
  • Normal 1-1.5g/kg/d protein, 20 AA, 30 calories
    from fat, carbohydrates
  • Trauma/Surgery/Sepsis increase 20-40
  • Pregnancy increase by 300 kcal/day
  • Lactation increase 500 kcal/day
  • Burns
  • Calories25 kcal/kg/day (30kcal/d X burn)
  • Protein 1-1.5g/kg/day (3g X burn)

27
Starvation
  • Brain glucose
  • Colonocytes Short-chain fatty acids
  • Enterocytes glutamine
  • Glycogen stores converted to glucose
  • 24-36 hours of starvation
  • Low insulin, high glucagon
  • Lipolysis into glycerol and FFA gluconeogenesis
  • 2-3 days
  • Amino acids from protein (glutamine and alanine)
    converted to glucose
  • Muscle breakdown
  • Ketones from fatty acids
  • Brain utilization
  • Resumption of glucose intake can reverse

28
TPN
  • 3-1 mixture of protein (AA), carbohydrate
    (dextrose), and fat (lipid emulsion)
  • Fat can be separate piggy-back
  • Standard Solution 50-60 dextrose, 24-34 fat,
    16 protein
  • Additives
  • Electrolytes adjusted daily for pt needs
  • Na 60-80mEq/day
  • K 30-60mEq/day
  • Cl 80-100mEq/day
  • Ca 4.6-9.2mEq/day
  • Mg 8.1-20mEq/day
  • PO4 12-24mmol/day
  • Anions and Cations must balance
  • Use chloride and acetate
  • Low bicarbonate, increase acetate
  • Trace elements and multivitamins added as
    prepared mixture
  • Vitamin K not included

29
RQ
  • Ratio of CO2 produced to O2 consumed
  • RQ CO2 produced / O2 consumed
  • Energy expenditure
  • Fat 0.7
  • Protein 0.8
  • Carbohydrate 1
  • RQ gt1 lipogenesis (overfeeding)
  • Decrease carbohydrates and caloric intake
  • High cholesterol can inhibit ventilator weaning
  • RQ lt .7 ketosis and fat oxidation (starvation)
  • Increase carbohydrates and calories

30
Post-Operative
  • Catabolic POD 0-3
  • Negative nitrogen balance
  • Diuresis POD 2-5
  • Anabolic POD 3-6
  • Positive nitrogen balance

31
Question 1
  • A 72-year-old man from a nursing home is admitted
    to the hospital with severe volume depletion. Her
    serum sodium is 180 mEq/L and she weighs 45 kg.
    Her estimated relative free water deficit is
  • A. 4L
  • B. 5L
  • C. 7.2L
  • D. 6L
  • E. 3L

32
Answer 1
  • D. 6L
  • Whenever hypernatremia develops, a relative free
    water deficit exists and must be replaced. The
    water deficit can be approximated using the
    formula
  • water deficit 0.5 x wt(kg) (Na/140)-1

33
Question 2
  • Which of the following statements regarding
    hypokalemia is correct?
  • A. Metabolic acidosis may contribute to renal
    potassium wasting
  • B. The degree of hypokalemia correlates very well
    with total body potassium deficit
  • C. High levels of aldosterone stimulate potassium
    reabsorption in the distal tubule
  • D. Diuretics rarely cause hypokalemia
  • E. Hypokalemia in patients who are vomiting is
    primarily due to renal potassium losses

34
Answer 2
  • E. Hypokalemia in patients who are vomiting is
    primarily due to renal potassium losses
  • Hypokalemia can have profound physiologic
    consequences. Of greatest clinical concern are
    cardiac arrhythmias and exacerbation of digitalis
    toxicity. Muscle weakness, cramps, myalgias,
    paralysis, and when severe, rhabdomyolysis can
    result. Hypokalemia also enhances renal acid
    excretion, which can generate and maintain
    metabolic alkalosis. Potassium may be lost
    through the gastrointestinal (GI) tract,
    primarily in patients with diarrhea, and through
    the kidneys. The most important cause of renal
    potassium loss is diuretics. Metabolic alkalosis
    also contributes to renal potassium wasting.
    Whenever large quantities of NaHCO3 transit the
    distal parts of the nephron, potassium secretion
    is stimulated. High levels of aldosterone,
    whether due to volume depletion or autonomous
    secretion, also stimulate potassium secretion.
    When hypokalemia develops in patients with
    vomiting or nasogastric suction, it is primarily
    caused by renal potassium losses, and not the
    small amount of potassium lost in the vomitus.
    The high aldosterone levels and metabolic
    alkalosis associated with the gastric losses
    combine to stimulate renal potassium excretion.

35
Question 3
  • All of the following are associated with
    hypomagnesemia except
  • A. Previous treatment with cisplatin
  • B. Alcoholics
  • C. Poor oral intake
  • D. Diuretics
  • E. Oral potassium supplements

36
Answer 3
  • E. Oral potassium supplements
  • Hypomagnesemia is a less common and frequently
    overlooked electrolyte abnormality. It should be
    suspected in patients on an insufficient diet,
    especially alcoholics, or in patients chronically
    using diuretics. Both alcohol and most diuretics
    increase renal magnesium excretion.
    Hypomagnesemia is clinically important not just
    because it has direct effects, but also because
    it can produce hypocalcemia and contribute to the
    persistence of hypokalemia. Magnesium deficiency
    will cause renal potassium wasting. When
    hypokalemia and hypomagnesemia coexist, magnesium
    should be aggressively replaced to restore
    potassium balance. The same is true for
    hypocalcemia. The level of plasma magnesium is a
    poor indicator of the degree of total body
    magnesium stores. Magnesium should be replaced
    until the plasma level returns to the upper
    normal range. Magnesium can be replaced either
    intravenously or, in less acute circumstances,
    through oral supplements. Gastrointestinal
    absorption of this cation, which occurs with
    greatest facility in the duodenum, is variable.
    In addition, all magnesium salts have a laxative
    effect when taken by mouth.

37
Question 4
  • The primary substrate for starvation-induced
    gluconeogenesis is
  • Liver glycogen
  • Organ protein
  • Skeletal muscle protein
  • Free fatty acids
  • Keto acids

38
Answer 4
  • C. Skeletal muscle protein
  • Following a few days of starvation, the body
    begins a period of catabolism in which muscle is
    broken down in order to use the protein found
    therein. The protein is subsequently converted
    to glucose by gluconeogenesis.

39
Question 5
  • Enterocytes energy requirements are provided by
  • A. Arginine
  • B. Alanine
  • C. Glutamine
  • D. Glycine

40
Question 6
  • Decreasing glucose and increasing fat in total
    parenteral nutrition will
  • A. Increase respiratory quotient
  • B. Increase CO2 production
  • C. Decrease minute ventilation
  • D. Delay weaning from mechanical ventilation
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