Fluids, Electrolytes, and Acid

Electrolytes, Nutrition,
Acid-Base Disturbances
Geoff Vana
Loyola University Medical Center
General Surgery
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
Composition of
• Sodium – principle cation
• Chloride and Bicarbonate – principle anions
• Potassium and Magnesium – cations
• Phosphate and Proteins – anions
• Water diffuses freely according to sodium content
• Expands intravascular volume
• Expands interstitial volume 3x plasma
• 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
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 (<20mEq/L)
Volume Control
• Osmoreceptors and Baroreceptors
• Osmoreceptors in paraventricular and supraventricular nuclei in
hypothalamus – control thirst and ADH secretion from posterior
• 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
Volume Control
• Renin-Angiotensin
• Renin: released from juxtaglomerular cells of afferent arterioles in
kidney ( BP, NaCl)
• Cleaves angiotensinogen (α-2 globulin produced by liver) to angiotensin
• 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
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
Volume Replacement
• Lactated Ringer’s 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)
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
• 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
• Hyponatremia
• Sodium depletion or dilution
• Dilution:
• SIADH, anti-psychotics, tricyclics, ACE-Is
• Depletion:
• Low-sodium diet, GI losses (emesis, NG, diarrhea), renal d/t
• Pseudohyponatremia
• Elevated glucose level causes influx of H2O
• Na + (gluc-100) x .016
• Headache, confusion, N/V, seizures, fatigue, increased ICP,
HTN, bradycardia, oliguria
• Hypernatremia
• Loss off free water or gain of sodium
• Iatrogenic administration of sodium-rich fluids
• Mineralocorticoid excess (hyperaldosteronism, Cushing’s syndrome,
• Hypotonic skin losses from fever or tracheostomies during
• Urine Na > 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]
• 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
• Hyperkalemia
• Excessive intake, increased cellular release, impaired excretion from
• 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
• 1/3 bound to albumin – plasma level poor indicator with
• 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
• CNS hyperactivity, hyperactive DTRs, muscle tremors, ST depression,
torsades de pointes
• Can produce hypocalcemia and persistent hypokalemia
• Replace magnesium
• 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
• Hypercalcemia
• Primary hyperparathyroidism, malignancy (bone metastasis,
• 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,
• Parastheias of face, muscle cramps, carpopedal spasm, stridor, tetany,
seizures, hyperreflexia, heart block, prolonged QT
Vitamin Deficiency
Hyperglycemia, encephalopathy, neuropathy
Cardiomyopathy, weakness, hair loss
Hair loss, poor healing, rash
Trace elements
Poor wound healing
Weakness (fail to wean vent), encephalopathy, decreased phagocytosis
Thiamine (B1)
Wernicke’s, cardiomyopathy, peripheral neuropathy
Pyridoxine (B6)
Sideroblastic anemia, glossitis, peripheral neuropathy
Cobalamin (B12)
Megaloblastic anemia, peripheral neuropathy, beefy tongue
Megaloblastic anemia
Pellagra (diarrhea, dermatitis, dementia)
Essential Fatty Acids
Dermatitis, hair loss, thrombocytopenia
Vitamin A
Night Blindness
Vitamin K
Vitamin D
Rickets, Osteomalacia
Vitamin E
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
Respiratory Acidosis
• pH < 7.35, pCO2 > 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
Respiratory Alkalosis
• pH > 7.45, pCO2 < 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
Metabolic Acidosis
• pH < 7.35, HCO3 < 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 > 12: Methanol, Uremia, DKA, Paraldehyde, INH, Lactic acidosis,
Ethanol, Salicylates
• AG < 12: RTA, Carbonic anhydrase inhibitor, GI losses
Metabolic Alkalosis
• pH > 7.45, HCO3 > 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
• Pre-operative Evaluation
• Albumin: 20 days
• Transferrin: 10 days
• Pre-albumin: 2 days
• Poor nutrition:
• Weight loss >10% in 6 months
• Albumin < 3.0
• Weight = <85% IBW
• 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,
• Trauma/Surgery/Sepsis: increase 20-40%
• Pregnancy: increase by 300 kcal/day
• Lactation: increase 500 kcal/day
• Burns:
• Calories:25 kcal/kg/day + (30kcal/d X %burn)
• Protein: 1-1.5g/kg/day + (3g X %burn)
• 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
• 3-1 mixture of protein (AA), carbohydrate (dextrose), and fat (lipid
• 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
• Ratio of CO2 produced to O2 consumed
• RQ = CO2 produced / O2 consumed
• Energy expenditure
• Fat = 0.7
• Protein = 0.8
• Carbohydrate = 1
• RQ >1 = lipogenesis (overfeeding)
• Decrease carbohydrates and caloric intake
• High cholesterol can inhibit ventilator weaning
• RQ < .7 = ketosis and fat oxidation (starvation)
• Increase carbohydrates and calories
• Catabolic: POD 0-3
• Negative nitrogen balance
• Diuresis: POD 2-5
• Anabolic: POD 3-6
• Positive nitrogen balance
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
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]
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
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.
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
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.
Question 4
The primary substrate for starvation-induced
gluconeogenesis is
A. Liver glycogen
B. Organ protein
C. Skeletal muscle protein
D. Free fatty acids
E. Keto acids
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
Question 5
Enterocytes energy requirements are provided by:
A. Arginine
B. Alanine
C. Glutamine
D. Glycine
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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