Fluids, Electrolytes, and Acid

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Transcript Fluids, Electrolytes, and Acid

Fluids, Electrolytes, Nutrition, and Acid-Base Disturbances

Geoff Vana Loyola University Medical Center General Surgery PGY-1

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 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

Fluid Secretion/Losses

• Secretion • Stomach: 1-2L • • • Small Intestine: 2-3L Pancreas: 600-800cc Bile: 300-800cc • H 2 O 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 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

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 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

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

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 diuretics • Pseudohyponatremia • Elevated glucose level causes influx of H 2 O • 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, CAH) • Hypotonic skin losses from fever or tracheostomies during hyperventilation • 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 arrest


• 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


• 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


• 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, 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

Vitamin Deficiency


Chromium Selenium Copper Zinc Trace elements Phosphate Thiamine (B1) Pyridoxine (B6) Cobalamin (B12) Folate Niacin Essential Fatty Acids Vitamin A Vitamin K Vitamin D Vitamin E


Hyperglycemia, encephalopathy, neuropathy Cardiomyopathy, weakness, hair loss Pancytopenia Hair loss, poor healing, rash Poor wound healing Weakness (fail to wean vent), encephalopathy, decreased phagocytosis Wernicke’s, cardiomyopathy, peripheral neuropathy Sideroblastic anemia, glossitis, peripheral neuropathy Megaloblastic anemia, peripheral neuropathy, beefy tongue Megaloblastic anemia Pellagra (diarrhea, dermatitis, dementia) Dermatitis, hair loss, thrombocytopenia Night Blindness Coagulopathy Rickets, Osteomalacia Neuropathy

Acid-Base Disorder

• Disorder of balance between HCO 3 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, carbohydrates • • • • 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 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


• Ratio of CO2 produced to O2 consumed • RQ = CO 2 produced / O 2 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 NaHCO 3 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 gluconeogenesis.

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