Fluids, Fluids, Electrolytes, Nutrition,Electrolytes, Nutrition,

and and Acid-Base DisturbancesAcid-Base Disturbances

Geoff VanaGeoff Vana

Loyola University Medical CenterLoyola University Medical Center

General SurgeryGeneral Surgery

PGY-1PGY-1

Total Body WaterTotal Body Water

• 50-60% of total body weight50-60% of total body weight• 50% in males, 60% in females50% in males, 60% in females• Reflection of body fat – lean tissues = high water Reflection of body fat – lean tissues = high water

contentcontent

• Adjust down for obesity (10-20%)Adjust down for obesity (10-20%)

• Highest in newborns ~80%Highest in newborns ~80%

• Compartments:Compartments:• 2/3 (40%) – Intracellular (skeletal muscle)2/3 (40%) – Intracellular (skeletal muscle)• 1/3 (20%) – Extracellular1/3 (20%) – Extracellular

• 2/3 (15%) – Interstitial2/3 (15%) – Interstitial• 1/3 (5%) - Plasma1/3 (5%) - Plasma

Composition of FluidComposition of Fluid

• ECFECF• Sodium – principle cationSodium – principle cation• Chloride and Bicarbonate – principle anionsChloride and Bicarbonate – principle anions

• ICFICF• Potassium and Magnesium – cationsPotassium and Magnesium – cations• Phosphate and Proteins – anionsPhosphate and Proteins – anions

• Water diffuses freely according to sodium Water diffuses freely according to sodium contentcontent• Expands intravascular volumeExpands intravascular volume• Expands interstitial volume 3x plasmaExpands interstitial volume 3x plasma

Fluid Secretion/LossesFluid Secretion/Losses

• SecretionSecretion• Stomach: 1-2LStomach: 1-2L• Small Intestine: 2-3LSmall Intestine: 2-3L• Pancreas: 600-800ccPancreas: 600-800cc• Bile: 300-800ccBile: 300-800cc

• HH22O lossesO losses

• Urine: 800-1200ccUrine: 800-1200cc• Stool: 250ccStool: 250cc• Insensible: 600ccInsensible: 600cc

• Increased by fever, hypermetabolism, hyperventilationIncreased by fever, hypermetabolism, hyperventilation

• To clear metabolites: 500-800cc urine per dayTo clear metabolites: 500-800cc urine per day

Volume ControlVolume Control• Extracellular volume deficit – most commonExtracellular volume deficit – most common

• Loss of GI fluids (suction, emesis, diarrhea, fistula)Loss of GI fluids (suction, emesis, diarrhea, fistula)

• Acute – CV and CNS signsAcute – CV and CNS signs• Chronic – decreased skin turgor, sunken eyes, CV and Chronic – decreased skin turgor, sunken eyes, CV and

CNS signsCNS signs

• Urine osmolality is higher than serumUrine osmolality is higher than serum

• Urine sodium is low (<20mEq/L)Urine sodium is low (<20mEq/L)

Volume ControlVolume Control

• Osmoreceptors and BaroreceptorsOsmoreceptors and Baroreceptors• Osmoreceptors in paraventricular and supraventricular Osmoreceptors in paraventricular and supraventricular

nuclei in hypothalamus – control thirst and ADH nuclei in hypothalamus – control thirst and ADH secretion from posterior pituitarysecretion from posterior pituitary• Increased free water or decreased osmolality = Increased free water or decreased osmolality =

decreased ADH and water reabsorptiondecreased ADH and water reabsorption• Fine tuning day-to-dayFine tuning day-to-day

• Baroreceptors in cardiac atrium, aortic arch and Baroreceptors in cardiac atrium, aortic arch and carotid sinusescarotid sinuses• Neural and hormonal feedbackNeural and hormonal feedback

Volume ControlVolume Control• Renin-AngiotensinRenin-Angiotensin

• Renin: released from juxtaglomerular cells of afferent Renin: released from juxtaglomerular cells of afferent arterioles in kidney (arterioles in kidney ( BP, BP, NaCl)NaCl)• Cleaves angiotensinogen (Cleaves angiotensinogen (αα-2 globulin produced by liver) to -2 globulin produced by liver) to

angiotensin 1angiotensin 1• Angiotensin: cleaved by ACE which is produced by vascular Angiotensin: cleaved by ACE which is produced by vascular

endothelial cellsendothelial cells• Increases vascular tone, stimulates catecholamine release from Increases vascular tone, stimulates catecholamine release from

adrenal medulla and sympathetic nerve terminalsadrenal medulla and sympathetic nerve terminals• Decreases RBF and GFR – increases sodium reabsorption by Decreases RBF and GFR – increases sodium reabsorption by

indirect and direct effect (aldosterone release from adrenal indirect and direct effect (aldosterone release from adrenal cortex)cortex)

• AldosteroneAldosterone• Produced in zona glomerulosa of adrenal cortexProduced in zona glomerulosa of adrenal cortex• Increased absorption of sodium in CD & DCT– stabilizing Na Increased absorption of sodium in CD & DCT– stabilizing Na

channel in open state, increases number of channels in apical channel in open state, increases number of channels in apical membranemembrane• Increases Na/K activityIncreases Na/K activity• Increases sodium reabsorption and potassium excretionIncreases sodium reabsorption and potassium excretion

Volume ControlVolume Control

• Natriuretic PeptideNatriuretic Peptide• Brain and RenalBrain and Renal

• Released by atrial myocytes from wall distensionReleased by atrial myocytes from wall distension• Inhibitory effect on renal sodium absorptionInhibitory effect on renal sodium absorption• Urodilatin – ANP-like substance, synthesized by Urodilatin – ANP-like substance, synthesized by

cortical collecting tubulecortical collecting tubule• Released by kidney tubules in response to atrial Released by kidney tubules in response to atrial

distension and sodium loadingdistension and sodium loading

• Twice as potent as ANP, increases cGMP = Na, Cl, Twice as potent as ANP, increases cGMP = Na, Cl, water diuresiswater diuresis

Volume ReplacementVolume Replacement• Lactated Ringer’s solutionLactated Ringer’s solution

• Blood loss, edema fluid, small bowel lossesBlood loss, edema fluid, small bowel losses• Ideal when electrolytes are normalIdeal when electrolytes are normal• Na 130mEq/L – hyponatremia can occur with extended useNa 130mEq/L – hyponatremia can occur with extended use• Lactate converted to bicarbonate – no contribution to acidosisLactate converted to bicarbonate – no contribution to acidosis

• Normal SalineNormal Saline• Useful for hyponatremia and hypochloremia (154mEq/L)Useful for hyponatremia and hypochloremia (154mEq/L)• Can lead to increased electrolyte concentrationsCan lead to increased electrolyte concentrations• Hyperchloremic metabolic acidosisHyperchloremic metabolic acidosis• pH between 4-5pH between 4-5

• Hypotonic solutions (1/2 or ¼ NS)Hypotonic solutions (1/2 or ¼ NS)• Hypoosmotic and hypotonicHypoosmotic and hypotonic• Can result in RBC lysisCan result in RBC lysis• D5 added to prevent (200 kcal/L)D5 added to prevent (200 kcal/L)

Volume ReplacementVolume Replacement

• Hypertonic Saline SolutionsHypertonic Saline Solutions• 3% NaCl, 5% NaCl, 7.5% NaCl3% NaCl, 5% NaCl, 7.5% NaCl• Resuscitation for head trauma, hemorrhagic shock, Resuscitation for head trauma, hemorrhagic shock,

burnburn• Increases intravascular volume quickerIncreases intravascular volume quicker• Increases cerebral perfusion and reduces cerebral Increases cerebral perfusion and reduces cerebral

edemaedema• Decreases volume requirementDecreases volume requirement

• 4-2-1 rule4-2-1 rule

• Monitor UOPMonitor UOP

ColloidsColloids• Albumin (5%, 25%)Albumin (5%, 25%)

• Increases plasma oncotic pressure – reversing diffusion of Increases plasma oncotic pressure – reversing diffusion of water into interstitial spacewater into interstitial space

• ARDS, Burns, Infections, SepsisARDS, Burns, Infections, Sepsis• Can extravasate into tissues – worsening edemaCan extravasate into tissues – worsening edema

• HetastarchHetastarch• Synthetic plasma expanderSynthetic plasma expander• Coagulopathy and bleeding from reduced factor VIII and von Coagulopathy and bleeding from reduced factor VIII and von

Willebrand factor, prolonged PTT and impaired platelet Willebrand factor, prolonged PTT and impaired platelet functionfunction

• Hextend (6% in LR)Hextend (6% in LR)• Plasma expander with no effect on coagulationPlasma expander with no effect on coagulation• Reduce fluid requirement, eliminate need for mannitol, Reduce fluid requirement, eliminate need for mannitol,

improves neurologic outcomeimproves neurologic outcome• No inhibition of plateletsNo inhibition of platelets

SodiumSodium

• HyponatremiaHyponatremia• Sodium depletion or dilutionSodium depletion or dilution• Dilution:Dilution:

• SIADH, anti-psychotics, tricyclics, ACE-IsSIADH, anti-psychotics, tricyclics, ACE-Is

• Depletion:Depletion:• Low-sodium diet, GI losses (emesis, NG, diarrhea), renal Low-sodium diet, GI losses (emesis, NG, diarrhea), renal

d/t diureticsd/t diuretics

• PseudohyponatremiaPseudohyponatremia• Elevated glucose level causes influx of HElevated glucose level causes influx of H22OO

• Na + (gluc-100) x .016Na + (gluc-100) x .016

• Headache, confusion, N/V, seizures, fatigue, Headache, confusion, N/V, seizures, fatigue, increased ICP, HTN, bradycardia, oliguriaincreased ICP, HTN, bradycardia, oliguria

SodiumSodium

• HypernatremiaHypernatremia• Loss off free water or gain of sodiumLoss off free water or gain of sodium

• Iatrogenic administration of sodium-rich fluidsIatrogenic administration of sodium-rich fluids• Mineralocorticoid excess (hyperaldosteronism, Cushing’s Mineralocorticoid excess (hyperaldosteronism, Cushing’s

syndrome, CAH)syndrome, CAH)• Hypotonic skin losses from fever or tracheostomies during Hypotonic skin losses from fever or tracheostomies during

hyperventilationhyperventilation• Urine Na > 20mEq/LUrine Na > 20mEq/L

• Ataxia, tonic spasms, delirium, weakness, Ataxia, tonic spasms, delirium, weakness, tachycardia, hypotension, syncope, red swollen tachycardia, hypotension, syncope, red swollen tongue, decreased saliva/tears, fevertongue, decreased saliva/tears, fever

• Free Water Deficit = TBW x [(Na/140) – 1]Free Water Deficit = TBW x [(Na/140) – 1]

PotassiumPotassium

• Hypokalemia – more common than hyperkalemiaHypokalemia – more common than hyperkalemia• Caused by poor intake, excess renal excretion, Caused by poor intake, excess renal excretion,

diarrhea, fistulas, emesis, high NG output, intracellular diarrhea, fistulas, emesis, high NG output, intracellular shifts from metabolic alkalosis or insulinshifts from metabolic alkalosis or insulin

• Decreases 0.3 mEq/L for every 0.1 increase in pHDecreases 0.3 mEq/L for every 0.1 increase in pH• Amphotericin, aminoglycosides, foscarnet, cisplatin, Amphotericin, aminoglycosides, foscarnet, cisplatin,

ifosfamide – induce magnesium wastingifosfamide – induce magnesium wasting• Correct magnesiumCorrect magnesium

• Disorders of muscle contractility in GI smooth Disorders of muscle contractility in GI smooth muscle, cardiac muscle, skeletal musclemuscle, cardiac muscle, skeletal muscle• Ileus, constipation, weakness, fatigue, dec DTR, Ileus, constipation, weakness, fatigue, dec DTR,

paralysis, cardiac arrestparalysis, cardiac arrest

PotassiumPotassium

• HyperkalemiaHyperkalemia• Excessive intake, increased cellular release, impaired Excessive intake, increased cellular release, impaired

excretion from kidneysexcretion from kidneys• PO/IV supplementation, post-transfusion RBC lysis, acidosis, PO/IV supplementation, post-transfusion RBC lysis, acidosis,

rapid rise in extracellular osmolalityrapid rise in extracellular osmolality• K-sparing diuretics, ACE-Is, NSAIDsK-sparing diuretics, ACE-Is, NSAIDs

• Spironolactone and ACE-Is inhibit aldosterone (renal excretion)Spironolactone and ACE-Is inhibit aldosterone (renal excretion)

• N/V, intestinal colic, diarrhea, weakness, ascending N/V, intestinal colic, diarrhea, weakness, ascending paralysis, peaked T-waves, wide QRS, sine wave paralysis, peaked T-waves, wide QRS, sine wave formation, V-fibformation, V-fib

MagnesiumMagnesium• 1/3 bound to albumin – plasma level poor indicator with 1/3 bound to albumin – plasma level poor indicator with

hypoalbuminemiahypoalbuminemia

• HypermagnesemiaHypermagnesemia• Severe renal insufficiency, magnesium-containing Severe renal insufficiency, magnesium-containing

antacids/laxatives, TPN, massive trauma, severe acidosisantacids/laxatives, TPN, massive trauma, severe acidosis• N/V, neuromuscular dysfunction, weakness, lethargy, N/V, neuromuscular dysfunction, weakness, lethargy,

hyporeflexia, impaired cardiac conduction, elevated T waveshyporeflexia, impaired cardiac conduction, elevated T waves

• HypomagnesemiaHypomagnesemia• Regulated by calcium/magnesium receptors in tubular cellsRegulated by calcium/magnesium receptors in tubular cells• Starvation, EtOH, prolonged IVF therapy, TPN, diuretic use, Starvation, EtOH, prolonged IVF therapy, TPN, diuretic use,

amphotericin B, Primary aldosteronism, diarrhea, amphotericin B, Primary aldosteronism, diarrhea, malabsorption, acute pancreatitismalabsorption, acute pancreatitis• CNS hyperactivity, hyperactive DTRs, muscle tremors, ST CNS hyperactivity, hyperactive DTRs, muscle tremors, ST

depression, torsades de pointesdepression, torsades de pointes• Can produce hypocalcemia and persistent hypokalemiaCan produce hypocalcemia and persistent hypokalemia

• Replace magnesium Replace magnesium

PhosphorusPhosphorus

• HyperphosphatemiaHyperphosphatemia• Decreased urinary excretion, increased intake, impaired Decreased urinary excretion, increased intake, impaired

renal function, hypoparathyroidism, hyperthyroidism, renal function, hypoparathyroidism, hyperthyroidism, rhabdomyolysis, tumor lysis syndrome, sepsis, rhabdomyolysis, tumor lysis syndrome, sepsis, hemolysishemolysis• Metastatic deposition of soft tissue calcium-phosphorus Metastatic deposition of soft tissue calcium-phosphorus

complexescomplexes

• HypophosphatemiaHypophosphatemia• Decreased intake, intracellular shift (alkalosis, insulin, Decreased intake, intracellular shift (alkalosis, insulin,

refeeding), decreased GI uptake from phosphate refeeding), decreased GI uptake from phosphate bindersbinders

CalciumCalcium

• HypercalcemiaHypercalcemia• Primary hyperparathyroidism, malignancy (bone Primary hyperparathyroidism, malignancy (bone

metastasis, PTHr)metastasis, PTHr)• Neurologic impairment, muscle weakness/pain, renal Neurologic impairment, muscle weakness/pain, renal

dysfunction, n/v, abdominal pain, worsening of Digitalis dysfunction, n/v, abdominal pain, worsening of Digitalis toxicity, short QT interval, flat T waves, AV blocktoxicity, short QT interval, flat T waves, AV block

• HypocalcemiaHypocalcemia• Pancreatitis, soft tissue infection, renal failure, small Pancreatitis, soft tissue infection, renal failure, small

bowel fistulas, hypoparathyroidism, TSS, abnormal bowel fistulas, hypoparathyroidism, TSS, abnormal magnesium, tumor lysis syndrome, post-magnesium, tumor lysis syndrome, post-parathyroidectomy, breast/prostate cancer, alkalosisparathyroidectomy, breast/prostate cancer, alkalosis• Parastheias of face, muscle cramps, carpopedal spasm, Parastheias of face, muscle cramps, carpopedal spasm,

stridor, tetany, seizures, hyperreflexia, heart block, stridor, tetany, seizures, hyperreflexia, heart block, prolonged QTprolonged QT

Vitamin DeficiencyVitamin DeficiencyDeficiency 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) Wernicke’s, 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

Acid-Base DisorderAcid-Base Disorder

• Disorder of balance between HCODisorder of balance between HCO33- - and Hand H++

• Blood pH: 7.35 – 7.45Blood pH: 7.35 – 7.45

• Arterial PCO2: 35 – 45mmHgArterial PCO2: 35 – 45mmHg

• Plasma HCO3-: 22 – 26mEq/LPlasma HCO3-: 22 – 26mEq/L

• Lungs compensate for metabolic abnormalitiesLungs compensate for metabolic abnormalities• QuickQuick

• Kidneys compensate for respiratory abnormalitiesKidneys compensate for respiratory abnormalities• Delayed, up to 6 hoursDelayed, up to 6 hours

• Acute – before compensationAcute – before compensation• Chronic – after compensationChronic – after compensation

Respiratory AcidosisRespiratory Acidosis

• pH < 7.35, pCO2 > 45pH < 7.35, pCO2 > 45• Decreased ventilationDecreased ventilation• BiPAP, intubation to increase minute ventilationBiPAP, intubation to increase minute ventilation• Chronic form: pCO2 remains constant and HCO3 Chronic form: pCO2 remains constant and HCO3

increases as compensation occursincreases as compensation occurs

• Narcotics, Atelectasis, Mucus plug, pleural effusion, Narcotics, Atelectasis, Mucus plug, pleural effusion, pain, limited diaphragmatic excursionpain, limited diaphragmatic excursion

Respiratory AlkalosisRespiratory Alkalosis

• pH > 7.45, pCO2 < 35pH > 7.45, pCO2 < 35

• Most cases acute from hyperventilationMost cases acute from hyperventilation• Pain, anxiety, neurologic disorders, CNS injury, Pain, anxiety, neurologic disorders, CNS injury,

hypoxemiahypoxemia• Salicylates, fever, Gram Neg bacteria, thyrotoxicosisSalicylates, fever, Gram Neg bacteria, thyrotoxicosis

• Acute hypocapnia: uptake K and phosphate into Acute hypocapnia: uptake K and phosphate into cells, increased Ca binding to albumincells, increased Ca binding to albumin• Symptomatic hypokalemia, hypophosphatemia, Symptomatic hypokalemia, hypophosphatemia,

hypocalcemiahypocalcemia

Metabolic AcidosisMetabolic Acidosis

• pH < 7.35, HCO3 < 22pH < 7.35, HCO3 < 22

• Increased acid intake, increased generation of Increased acid intake, increased generation of acids, increased loss of bicarbonateacids, increased loss of bicarbonate• Response: increase buffers (bone/muscle), increase Response: increase buffers (bone/muscle), increase

respiration, increased renal reabsorption and respiration, increased renal reabsorption and generation of bicarbonate and excretion of hydrogengeneration of bicarbonate and excretion of hydrogen• Calculate Anion Gap = (Na) – (Cl + HCO3)Calculate Anion Gap = (Na) – (Cl + HCO3)• Corrected AG = AG – [2.5(4.5-albumin)]Corrected AG = AG – [2.5(4.5-albumin)]

• AG > 12: Methanol, Uremia, DKA, Paraldehyde, INH, Lactic AG > 12: Methanol, Uremia, DKA, Paraldehyde, INH, Lactic acidosis, Ethanol, Salicylatesacidosis, Ethanol, Salicylates

• AG < 12: RTA, Carbonic anhydrase inhibitor, GI lossesAG < 12: RTA, Carbonic anhydrase inhibitor, GI losses

Metabolic AlkalosisMetabolic Alkalosis

• pH > 7.45, HCO3 > 26pH > 7.45, HCO3 > 26

• Loss of fixed acids, gain of bicarbonate (worsened Loss of fixed acids, gain of bicarbonate (worsened by potassium depletion), pyloric stenosis and by potassium depletion), pyloric stenosis and duodenal ulcer disease (hypochloremic, duodenal ulcer disease (hypochloremic, hypokalemic)hypokalemic)• Increased urine bicarbonate, reabsorption of hydrogen Increased urine bicarbonate, reabsorption of hydrogen

and potassium excretionand potassium excretion• Aldosterone causes Na reabsorption and increased K Aldosterone causes Na reabsorption and increased K

excretion – H+/K+ interchange results in paradoxical excretion – H+/K+ interchange results in paradoxical aciduriaaciduria

NutritionNutrition

• Pre-operative EvaluationPre-operative Evaluation• Albumin: 20 daysAlbumin: 20 days• Transferrin: 10 daysTransferrin: 10 days• Pre-albumin: 2 daysPre-albumin: 2 days

• Poor nutrition:Poor nutrition:• Weight loss >10% in 6 monthsWeight loss >10% in 6 months• Albumin < 3.0Albumin < 3.0• Weight = <85% IBWWeight = <85% IBW

NutritionNutrition• Caloric Need – 20-25 kcal/kg/dayCaloric Need – 20-25 kcal/kg/day

• Fat: 9kcal/gFat: 9kcal/g

• Carbohydrate: 4kcal/gCarbohydrate: 4kcal/g• Dextrose: 3.4kcal/gDextrose: 3.4kcal/g

• Protein: 4kcal/gProtein: 4kcal/g

• RequirementsRequirements• Normal: 1-1.5g/kg/d protein, 20% AA, 30% calories from fat, Normal: 1-1.5g/kg/d protein, 20% AA, 30% calories from fat,

carbohydratescarbohydrates• Trauma/Surgery/Sepsis: increase 20-40%Trauma/Surgery/Sepsis: increase 20-40%• Pregnancy: increase by 300 kcal/dayPregnancy: increase by 300 kcal/day• Lactation: increase 500 kcal/dayLactation: increase 500 kcal/day• Burns: Burns:

• Calories:25 kcal/kg/day + (30kcal/d X %burn)Calories:25 kcal/kg/day + (30kcal/d X %burn)• Protein: 1-1.5g/kg/day + (3g X %burn)Protein: 1-1.5g/kg/day + (3g X %burn)

StarvationStarvation• Brain: glucoseBrain: glucose• Colonocytes: Short-chain fatty acidsColonocytes: Short-chain fatty acids• Enterocytes: glutamineEnterocytes: glutamine

• Glycogen stores converted to glucoseGlycogen stores converted to glucose• 24-36 hours of starvation24-36 hours of starvation

• Low insulin, high glucagonLow insulin, high glucagon

• Lipolysis into glycerol and FFA – gluconeogenesis Lipolysis into glycerol and FFA – gluconeogenesis • 2-3 days2-3 days

• Amino acids from protein (glutamine and alanine) converted to Amino acids from protein (glutamine and alanine) converted to glucose glucose • Muscle breakdownMuscle breakdown

• Ketones from fatty acidsKetones from fatty acids• Brain utilizationBrain utilization

• Resumption of glucose intake can reverseResumption of glucose intake can reverse

TPNTPN• 3-1 mixture of protein (AA), carbohydrate (dextrose), and fat 3-1 mixture of protein (AA), carbohydrate (dextrose), and fat

(lipid emulsion)(lipid emulsion)• Fat can be separate piggy-backFat can be separate piggy-back

• Standard Solution: 50-60% dextrose, 24-34% fat, 16% proteinStandard Solution: 50-60% dextrose, 24-34% fat, 16% protein

• Additives:Additives:• Electrolytes adjusted daily for pt needsElectrolytes 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

RQRQ

• Ratio of CO2 produced to O2 consumedRatio of CO2 produced to O2 consumed

• RQ = CORQ = CO2 produced 2 produced / O/ O2 consumed2 consumed

• Energy expenditureEnergy expenditure

• Fat = 0.7Fat = 0.7

• Protein = 0.8Protein = 0.8

• Carbohydrate = 1Carbohydrate = 1

• RQ >1 = lipogenesis (overfeeding)RQ >1 = lipogenesis (overfeeding)• Decrease carbohydrates and caloric intakeDecrease carbohydrates and caloric intake• High cholesterol can inhibit ventilator weaningHigh cholesterol can inhibit ventilator weaning

• RQ < .7 = ketosis and fat oxidation (starvation)RQ < .7 = ketosis and fat oxidation (starvation)• Increase carbohydrates and caloriesIncrease carbohydrates and calories

Post-OperativePost-Operative

• Catabolic: POD 0-3Catabolic: POD 0-3• Negative nitrogen balanceNegative nitrogen balance

• Diuresis: POD 2-5Diuresis: POD 2-5

• Anabolic: POD 3-6Anabolic: POD 3-6• Positive nitrogen balancePositive nitrogen balance

Question 1Question 1

A 72-year-old man from a nursing home is admitted A 72-year-old man from a nursing home is admitted to the hospital with severe volume depletion. Her to the hospital with severe volume depletion. Her serum sodium is 180 mEq/L and she weighs 45 kg. serum sodium is 180 mEq/L and she weighs 45 kg. Her estimated relative free water deficit is:Her estimated relative free water deficit is:

A. 4LA. 4L

B. 5LB. 5L

C. 7.2LC. 7.2L

D. 6LD. 6L

E. 3LE. 3L

Answer 1Answer 1

D. 6LD. 6L

Whenever hypernatremia develops, a relative Whenever hypernatremia develops, a relative free water deficit exists and must be free water deficit exists and must be replaced. The water deficit can be replaced. The water deficit can be approximated using the formula: approximated using the formula:

water deficit = 0.5 x wt(kg) × [(Na/140)-1]water deficit = 0.5 x wt(kg) × [(Na/140)-1]

Question 2Question 2

Which of the following statements regarding hypokalemia Which of the following statements regarding hypokalemia is correct?is correct?

A. Metabolic acidosis may contribute to renal potassium A. Metabolic acidosis may contribute to renal potassium wastingwasting

B. The degree of hypokalemia correlates very well with B. The degree of hypokalemia correlates very well with total body potassium deficittotal body potassium deficit

C. High levels of aldosterone stimulate potassium C. High levels of aldosterone stimulate potassium reabsorption in the distal tubulereabsorption in the distal tubule

D. Diuretics rarely cause hypokalemiaD. Diuretics rarely cause hypokalemia

E. Hypokalemia in patients who are vomiting is primarily E. Hypokalemia in patients who are vomiting is primarily due to renal potassium lossesdue to renal potassium losses

Answer 2Answer 2

E. Hypokalemia in patients who are vomiting is primarily due to renal E. Hypokalemia in patients who are vomiting is primarily due to renal potassium lossespotassium losses

Hypokalemia can have profound physiologic consequences. Of Hypokalemia can have profound physiologic consequences. Of greatest clinical concern are cardiac arrhythmias and exacerbation greatest clinical concern are cardiac arrhythmias and exacerbation of digitalis toxicity. Muscle weakness, cramps, myalgias, paralysis, of digitalis toxicity. Muscle weakness, cramps, myalgias, paralysis, and when severe, rhabdomyolysis can result. Hypokalemia also and when severe, rhabdomyolysis can result. Hypokalemia also enhances renal acid excretion, which can generate and maintain enhances renal acid excretion, which can generate and maintain metabolic alkalosis. Potassium may be lost through the metabolic alkalosis. Potassium may be lost through the gastrointestinal (GI) tract, primarily in patients with diarrhea, and gastrointestinal (GI) tract, primarily in patients with diarrhea, and through the kidneys. The most important cause of renal potassium through the kidneys. The most important cause of renal potassium loss is diuretics. Metabolic alkalosis also contributes to renal loss is diuretics. Metabolic alkalosis also contributes to renal potassium wasting. Whenever large quantities of NaHCOpotassium wasting. Whenever large quantities of NaHCO33 transit transit the distal parts of the nephron, potassium secretion is stimulated. the distal parts of the nephron, potassium secretion is stimulated. High levels of aldosterone, whether due to volume depletion or High levels of aldosterone, whether due to volume depletion or autonomous secretion, also stimulate potassium secretion. When autonomous secretion, also stimulate potassium secretion. When hypokalemia develops in patients with vomiting or nasogastric hypokalemia develops in patients with vomiting or nasogastric suction, it is primarily caused by renal potassium losses, and not suction, it is primarily caused by renal potassium losses, and not the small amount of potassium lost in the vomitus. The high the small amount of potassium lost in the vomitus. The high aldosterone levels and metabolic alkalosis associated with the aldosterone levels and metabolic alkalosis associated with the gastric losses combine to stimulate renal potassium excretion. gastric losses combine to stimulate renal potassium excretion.

Question 3Question 3

All of the following are associated with All of the following are associated with hypomagnesemia except:hypomagnesemia except:

A. Previous treatment with cisplatinA. Previous treatment with cisplatin

B. AlcoholicsB. Alcoholics

C. Poor oral intakeC. Poor oral intake

D. DiureticsD. Diuretics

E. Oral potassium supplementsE. Oral potassium supplements

Answer 3Answer 3

E. Oral potassium supplementsE. Oral potassium supplements

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

Question 4Question 4

The primary substrate for starvation-induced The primary substrate for starvation-induced gluconeogenesis isgluconeogenesis is

A.A.Liver glycogenLiver glycogen

B.B.Organ proteinOrgan protein

C.C.Skeletal muscle proteinSkeletal muscle protein

D.D.Free fatty acidsFree fatty acids

E.E.Keto acidsKeto acids

Answer 4Answer 4

C. Skeletal muscle proteinC. Skeletal muscle protein

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

Question 5Question 5

Enterocytes energy requirements are provided Enterocytes energy requirements are provided by:by:

A. ArginineA. Arginine

B. AlanineB. Alanine

C. GlutamineC. Glutamine

D. GlycineD. Glycine

Question 6Question 6

Decreasing glucose and increasing fat in total Decreasing glucose and increasing fat in total parenteral nutrition will:parenteral nutrition will:

A. Increase respiratory quotientA. Increase respiratory quotient

B. Increase CO2 productionB. Increase CO2 production

C. Decrease minute ventilationC. Decrease minute ventilation

D. Delay weaning from mechanical ventilationD. Delay weaning from mechanical ventilation