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Surgery > Fluids, Electrolytes, Nutrition > Flashcards

Fluids, Electrolytes, Nutrition Flashcards

1
Q

Total Body Water

A

50-70% total body weight

Greater in lean individuals bc fat doesn’t have much water. Avg 60%.

Newborns 70%. Decreases with age to around 50%.

1L water = 1kg

2 compartments. ICF and ECF

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2
Q

ICF

A

mostly in skeletal muscle mass, thus a little lower in females (50%) than males (60%)

Cell wall separates ICF and ECF and acts as semipermeable membrane

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3
Q

ECF

A

Plasma and interstitial fluid

Capillary membrane separates plasma and interstitial fluid and acts as a semipermeable membrane

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4
Q

Fluid totals

A

ICF = 67% Total body water

ECF = 33% Total body water

  • Interstitial = 25% total body water (75% of ECF)
  • Plasma = 8% Total body water (25% of ECF)
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5
Q

Normal plasma osmolality

A

285-295 mmol/L

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6
Q

Calculated plasma osmolality

A

2[Na] + [gluc]/18 + [BUN]/2.8

Na is mmol/L

The others are mg/dL

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7
Q

Osmolar gap

A

Measured osmolality - calculated plasma osmolality

Normal gap 10 = lactic acid, ketones, methanol, ethanol

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8
Q

How much fluid can you lose through a trach?

A

1500ml/day if unhumidified and hyperventilation

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9
Q

Renal control of fluids/lytes

A

Distal tubules - reabsorption of Na in exchange for K and H secretion

Affected by ACTH and aldosterone

Aldosterone directly stimulates K secretion and Na reabsorption from distal tubule

Low Extracellular volume leads to low renal perfusion. This increases renin from JGA. Angiotensin 1 increases. Then Angio 2. Then aldosterone.

Aldosterone also released when low volume receptors in R atrium activated or from ACTH which is released in response to high K.

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10
Q

Causes of volume deficit (dehydration)

A

Mimics ECF loss:

Hemorrhage

Loss of GI fluid - vomit, NG suction, diarrhea, fistula

PostOp fluid sequestration - 3rd spacing: intestinal obstruction

Intra-abdominal and retroperitoneal inflammation (pancreatitis, peritonitis)

SIRS, burns, sepsis, pancreatitis

Losses that are mostly water:

  • Fever
  • Osmotic diuresis
  • DI
  • Prolonged water deprivation
  • Inadequate input during procedure
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11
Q

Judging degree of dehydration

A

Mild = 3% (adults) or 5% (kids) loss of body weight

Mod = 6% or 10%

Severe = 9% or 15%

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12
Q

Treatment of dehydration

A

Initial intervention is to give a large bolus as a volume expander: 20 ml/kg of NS or LR

During the next 8 hrs, expected maintenance fluid given plus 1/2 of remaining calculated loss.

Over next 16 hrs, the other 1/2 of remaining loss is given along with the assumed maintenance fluid

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13
Q

Crystalloid

A

Dextrose is used to deliver free water to body (dextrose quickly metabolized)

0.9% NaCl quickly adds volume to intravascular space

Goal is to expand intravascular space

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14
Q

Colloids

A

pRBCs, FFP, albumin

Stay mainly within intravascular space if the capillary membranes are intact

Possible increased incidence of pulm embolism and respiratory failure

Expensive

Indications:

  • Patients with too much Na and water but hypovolemic - ascites, CHF, postcardiac bypass
  • Patients unable to make enough albumin or other proteins to exert enough oncotic pressure - liver disease, transplant recipients, resections, malnutrition
  • Severe hemorrhage or coagulopathy
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15
Q

Isotonic causes of volume excess

A

Iatrogenic - intravascular overload of IVFs with lytes

Increased ECF without equilibration with ICF - esp postop or trauma when hormonal responses to stress are to decrease Na and H2O excretion by kidney

Often secondary to renal insufficiency, cirrhosis, CHF

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16
Q

Hypotonic causes of volume excess

A

Inappropriate NaCl-poor solution as a replacement for GI losses (most common)

Third spacing (shift of ECF from plasma to elsewhere like interstitial or transcellular spaces)

Increased ADH with surgical stress, inappropriate ADH (SIADH)

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17
Q

Hypertonic causes of volume excess

A

1 = excessive Na load without adequate water intake

  • water moves out of cells bc of increased ECF osmolarity
  • Causes increase in intravascular and interstitial fluid
  • Worse when renal tubular excretion of water and/or Na is poor
  • Can also be caused by rapid infusion of nonelectrolyte osmotically active solutes like glucose and mannitol
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18
Q

What can NS cause?

A

hypercholemic metabolic acidosis

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19
Q

What can LR cause?

A

When patient is hypovolemic and in metabolic alkalosis (from NG tube or vomiting), may worsen the alkalosis when lactate is metabolized

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20
Q

Treating hypervolemia

A

Restrict Na and fluids for isotonic

Free water replacement for hypertonic (will correct hypertonicity which should result in diuresis)

Saline for hypotonic (same as above)

Diuresis with furosemide 10-50mg

  • replete K as needed
  • don’t overdiuresis

Cardiogenic drugs, O2, artificial vent as needed (heart failure or resp failure)

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21
Q

Causes of ongoing fluid loss

A

Fever - each degreeC above 37 adds 2-2.5ml/kg/day of insensible water loss

Loss of body fluids (vomit, NG suction, fistulas)

3rd space losses

Burns

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22
Q

How much fluid does an average adult patient need?

A

About 2.5L/day… about 100ml/hr

unless other factors warrant higher rate

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23
Q

Calculating free water deficit

A

FWD = normal body water - current body water

NBW = 0.6 x body weight in kg

CBW = NBW (normal serum Na/measured serum Na)

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24
Q

How can labs show hypovolemia?

A

BUN/Cr > 20

FeNa

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25
Q

Working up hyponatremia

A

True hyponatremia = excess ingestion of water that overwhelms the kidneys (either normal or diseased) or due to increased ADH. It is NOT due to increased excretion of Na.

1) Determine plasma osmolality

  • Normal: pseudohyponatremia. Lab artifact due to high lipids or plasma proteins. Check a lipid profile or possible Multiple Myeloma
  • High - pseudohyponatremia. Due to increase of osmotically active molecules like glucose*** or mannitol
  • Low - true hyponatremia

2) Assess volume status
- hypovolemia
- euvolemia
- hypervolemia

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26
Q

Account for glucose in hyponatremia

A

For every 100 mg/dl increment in plasma glucose above normal (normal = 100), plasma Na should decrease by 1.6 mEq/L

“sweet 16”

Glucose of 500 should have decrease of 6.4. 140-6.4 = 133.6

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27
Q

Hyponatremia with hypotonicity (true hyponatremia) and hypovolemia

A
  • Renal cause = diuretics
  • Extrarenal = vomit, diarrhea, burns, pancreatitis

Differentiate using urine Na. Urine Na 20 indicated renal cause.

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28
Q

True hyponatremia with euvolemia

A

SIADH = #1

Increased vasopressin release from posterior pit or ectopic source causes decreased renal free water excretion

Signs:

  • hypo-osmotic hyponatremia (hypotonicity)
  • Inappropriately concentrated urine (urine osmolality > 100)
  • Normal renal, adrenal, thyroid function

Causes:

  • neuropsych disorders, malignancies (esp lung), and head trauma
  • glucocorticoid deficiency (Addison’s) - cortisol deficiency causes hypersecretion of ADH
  • hypothyroidism - causes decreased CO and GFR which leads to increased ADH release
  • primary polydipsia - usually in psych patients who compulsively drink massive volumes of water
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29
Q

True hyponatremia with hypervolemia

A

May be from CHF, cirrhosis, nephrotic syndrome

Increased thirst and ADH

Edematous state

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30
Q

Signs/symptoms of true hyponatremia in general and tx

A

Decreased reflexes, respiratory depression, seizures, coma

N/v, HA, lethargy, muscle cramps

For hypovolemic: Give 0.9% NaCl. Na repletion with saline isotonic to patient in order to avoid rapid changes in ICF volume.

Major complication from rapid correction of chronic hyponatremia is central pontine myelinolysis

For hypervolemic: Correct underlying disorder - CHF, liver or renal failure

For euvolemic: Raise plasma Na (lower ICF volume) - restrict water intake

31
Q

Hypernatremia causes and signs

A

ALWAYS with hyperosmolarity

Causes:

  • Loss of water (dehydration!): DI, diuretics, sweating, GI loss, burns, fistulas
  • Gain of Na due to excess mineralocorticoid activity: Primary hyperaldosteronism, Cushing’s, renal artery stenosis (hyperreninism), congenital adrenal hyperplasia (will also cause hypoK)
  • If thirst mechanism is intact and water is available, hypernatremia will not persist. Suspect hypernatremia in young, elderly, and patients with AMS who may not have access to water

Symptoms

  • thirst
  • restlessness, weakness, delirium
  • hypotension and tachycardia
  • decreased saliva and tears
  • red, swollen tongue
  • Oliguria

Tx

  • Calculate free water deficit
  • If euvolemic - replace water deficit as D5W
  • if hypovolemic- use NS. Correct 1/2 of water deficit in first 24h then remaining over next 1-2days
32
Q

K balance

A

99% of K is in ICF so small changes in ECF K has clinical effects - impaired electrical signaling in heart, muscle, nerve.

Proper proportion of K and Ca must exist for their exchange across membrane channels that allow electrical conduction to occur

Cells act as rapid K buffer. Kidney regulates long term K control

33
Q

Too much K clinical

A

n/v, colic, diarrhea

Weakness, paralysis, resp failure

Arrhythmia, arrest

34
Q

Too much Mg clinical

A

N/v

Weakness, lethargy, decreased reflexes

Hypotension, arrest

35
Q

Too much Ca clinical

A

Anorexia, n/v, abdominal pain

Weakness, confusion, coma, bone pain

Hypertension, arrhythmia, polyuria, polydipsia

36
Q

Too little K clinical

A

Ileus, constipation

Decreased reflexes, fatigue, weakness, paralysis

Arrest

37
Q

Too little Mg clinical

A

Hyperactive reflexes, muscle tremors, tetany, seizures

Arrhythmia

38
Q

Too little Ca clinical

A

Hyperactive reflexes, paresthesias, carpopedal spasm, seizures

HF

39
Q

Causes of hypokalemia

A

Usually too much renal secretion

Loss of K due to excess mineralocorticoid activity - Primary hyperaldosteronism, Cushing’s, renal artery stenosis, congenital adrenal hyperplasia (will also cause hyperNa)

Movement of K into cells due to insulin, catecholamines, alkalemia

Prolonged administration of K-free parenteral fluids

Total parenteral hyperalimentation with inadequate K replacement

Loss of excessive lower GI secretions like diarrhea, colonic fistulas, VIPoma

Diuretics

40
Q

Signs/symptoms of hypokalemia

A

ECG - flattened T waves, ST depression, U wave

Arrhythmias, signs of low voltage

41
Q

Treating hypoK

A

Check Mg level first as hypomagnesiemia is commonly associated with hypoK and must be corrected before/along with hypoK.

Amount of K to be replaced can be estimated as 4-current K x 100, in mEq (if current K is 3.1, give 90 mEq)

If asymptomatic patient with K > 3, oral K may be enough

No more than 40 mEq should be added to a liter of IVF since rapid infusion causes fatal arrhythmias

Rate should not exceed 40 mEq/hr

May cause burning sensation if given in PIV. Using low flow of 10 mEq/hr or adding a small amount of lidocaine to solution can lower discomfort

42
Q

Causes of hyperK

A

Usually renal failure

Rarely found when renal function is normal and usully causes a transient hyperK due to cellular shifts: K spills from cells in severe injury; cells take up H ions in exchange for intracellular K, acting as a buffer in state of acidosis

Drugs - ACE inhibitors, K sparing diuretics

Iatrogenic - Penicillin G has 1.7 mEq of K per 1M units, KCl added to maintenance fluids, blood transfusions with old batch of pRBCs where K may have leaked out of cells, overtreatment of hypoK

Digoxin - blocks Na-K-ATPase pump

Hypoaldosteronism

PseudohyperK: Can result when RBCs lyse in test tube and release K. This is lab error. Repeat test.

43
Q

Signs/symptoms of hyperK

A

Cardiac effects most significant. Confirm hyperK and get ECG

ECG

  • early: Peaked T waves, wide QRS, ST depression
  • late: disappearance of T waves, heart block, sine wave (ominous for impending fatal arrhythmia), cardiac arrest

GI
- n/v, intermittent intestinal colic, diarrhea

44
Q

Tx for hyperK

A

10% CaGluconate 1g IV - monitor ECG. Ca temporarily suppresses cardiac arrhythmias by stabilizing the cardiac membrane and should be given first. Does not effect K load. The membrane of cardiac muscle would abnormally fire in presence of high K.

Lower extracellular K (acute treatment): Albuterol, insulin with glucose, or sodium bicarb promote cellular reuptake of K

Kayexalate - cation exchange resin. As opposed to above measures, which immediately protect against dangers of high K, this actually removes the K from the body

Dialysis (last resort)

45
Q

Calcium balance

A

Normal: 1,000 - 1,200 mg. Most in bone in form of phosphate and carbonate

Normal daily intake = 1-3g

Most excreted via stool

Normal serum 8.5-10.5 - half of this is nonionized and bound to plasma protein

Ionized calcium is the most accurate measure of calcium, but labs report total calcium

An additional nonionized fraction (5%) if bound to other substances in ECF

Ratio of ionized to nonionized Ca is related to pH

Acidosis causes increase in ionized fraction and alkalosis causes decrease in ionized fraction

46
Q

First thing you do when you notice hypoCa

A

Correct for low albumin

Corrected Ca = 0.8 (Normal albumin - observed albumin) + observed calcium

If corrected Ca is within normal range, do nothing

47
Q

Causes of hypoCa

A
  • Acute pancreatitis
  • Massive soft-tisse infections (nec fasc)
  • Acute/chronic renal failure
  • Pancreatic/small bowel fistuals
  • Hypoparathyroidism (common after parathyroid or thyroid surgery)
  • Hypoproteinemia
  • Severe depletion of Mg
  • Severe alkalosis may elicit symptoms with normal serum levels bc there is a decrease in ionized fraction of total serum Ca
48
Q

Signs/symptoms of hypoCa

A

Numbness and tingling of fingers, toes, and around mouth

Increased reflexes

Chvostek’s sign: tapping over facial nerve in front of tragus of the ear causes ipsilateral twitching

Trousseau’s sign: Carpopedal spasm following inflation of sphygmomanometer cuff to above systolic blood pressure for several minutes

Muscle and abdominal cramps

Convulsions

ECG - prolonged QT interval

49
Q

Tx for hypoCa

A

IV Ca Gluconate or CaCl2

Monitor QT interval on ECG

50
Q

Causes of hyperCa

A

Hyperparathyroidism
Cancer (esp breast, MM)
Drugs (thiazides)

51
Q

Signs/symptoms of hyperCa

A

Fatigue, weakness, anorexia, weight loss, n/v

Somnambulism (sleepwalking), stupor, coma

Severe HA, pain in back and extremities, thirst, polydipsia, polyuria

Death

52
Q

Tx for hyperCa

A

Vigorous volume repletion with salt solution - dilutes Ca and increases urinary Ca excretion

  • can be augmented with furosemide
  • definitive tx of acute hypercalcemic crisis in patients with hyperparathyroidism is immediate surgery

Treat underlying cause

53
Q

Indications for enteral nutritional support

A

Gut works but oral intake not possible - AMS, ventilator, oral/pharyngeal/esophageal disorders

Oral intake not sufficient for metabolic requirements - anorexia, sepsis, severe trauma/burns

Presence of malnutrition and wasting

54
Q

Indications for TPN

A

Enteral feeding not possible - GI obstruction, ileus

Enteral intake not enough for metabolic requirements - chronic diarrhea/emesis, malabsorption, fistulas, chemo, irradiation therapy

Biggest danger of TPN is infection (organic products in TPN can become infiltrated with bacteria and sent right into the blood)

Adjunctive support needed for managing disease - pancreatitis, hepatic failure, renal failure, chylothorax

55
Q

Basal energy expenditure for males

A

25 kcal/kg/day

56
Q

Basal energy expenditure for females

A

22 kcal/kg/day

57
Q

Calorie requirements for nonstressed patient

A

BEE x 1.2

58
Q

Calorie requirements for postsurgery

A

BEE x 1.3 - 1.5

59
Q

Calorie requirements for trauma/sepsis/burns

A

BEE x 1.6 - 2

60
Q

Calorie requirements for fever

A

12% increase per degree C over 37

61
Q

Important to keep in mind for calorie requirements

A

must be met with non-protein calories. 70% carbs. 30% fat

62
Q

Respiratory quotient

A

ratio of CO2 released to O2 consumed per unit metabolism of a substrate (VCO2/VO2)

Lipid = 0.7
Protein = 0.8
Carb = 1.0
Balanced diet = 0.83

63
Q

Protein requirement

A

0.8 - 1 g/kg body weight

Increases in illness and is maximal in burn patients

Avg surg patient needs 1.2-1.6 g/kg

Each gram of urinary nitrogen is equivalent to 6.25g of degraded protein

Nitrogen balance = (protein intake in g/6.25) - (Urinary urea nitrogen + 4)

Goal nitrogen balance should be positive 4-6

64
Q

Enteral vs parenteral

A

Enteral preferred. Reduces infection. May be continuous or intermittent.

Routes for GI feeding = PO, NG, gastrostomy, jejunostomy

Glutamine is the fuel for enterocytes

Short chain fatty acids serve as fuel for the colonocytes

Omega 3 fatty acids and arginine serve as immune modulating agents

Complications of enteral = diarrhea, aspiration, obstruction of tube

65
Q

Causes of elevated anion gap metabolic acidosis

A

AG > 12

MUDPILES + CAT

Methanol/Metabolism (inborn error)
Uremia
DKA
Paraldehyde/ Propylene glycol
Iron/Isoniazid/Isopropyl alcohol
Lactic acidosis
Ethylene glycol
Salicylates/strychnine

CO, CN-
Alcoholic ketoacidosis
Toluene

4 basic processes = ketoacidosis, lactic acidosis, renal failure, intoxication

66
Q

Causes of normal anion gap metabolic acidosis

A

HARDUPS + G

Hyperparathyroidism/Hyperalimentation (TPN), hyperparathyroid
Adrenal insufficiency/Acetazolamide, Addison's, Ammonium Chloride
Renal tubular acidosis***
Diarrhea***
Ureteroenteric fistula
Pancreatic fistulas
Sprionolactone, Saline
Glue sniffing
67
Q

Causes of respiratory alkalosis

A

MIS[HAP]3S

Mechanical overventilation/MI/Meningitis
Increased ICP
Sepsis
Hypoxemia/Hyperpyrexia/HF
Anxiety/Asthma/Ascites
Pregnancy/Pain/Pneumonia
Salicylates
68
Q

Figuring out acid/base disorders

A

1) pH in relation to 7.4
2) CO2 in relation to 40

Resp acidosis: pH 40

Metabolic acidosis: pH 7.4, CO2 7.4, CO2 > 40

69
Q

So you have resp acidosis, what now?

A

For every change in CO2 of 10, the pH should also change by 0.08 (acute) or 0.04 (chronic)

For every change in CO2 of 10, the HCO3 should change by 1 (acute) or 3 (chronic) in direction that brings pH back to normal

If we find there’s too much HCO3 (over corrected) = coexisting metabolic alkalosis

If we find there’s too little HCO3 = coexisting metabolic acidosis

70
Q

So you have metabolic acidosis, what now?

A

1) Is CO2 appropriate? Use Winter’s formula (1.5HCO3 + 8 +/- 2). If CO2 > expected from formula, there is also a respiratory acidosis. If CO2 2 = metabolic alkalosis
If 1-2, pure anion gap acidosis (lactic acidosis about 1.6, DKA around 1)
If

71
Q

So you have respiratory alkalosis, now what?

A

For every change in CO2 of 10, the pH should also change by 0.08 (acute) or 0.04 (chronic)

For every change in CO2 of 10, the HCO3 should change by 2 (acute) or 4 (chronic) in direction that brings pH back to normal

Too much HCO3? Coexisting metabolic alkalosis

Too little? Coexisting metabolic acidosis

72
Q

So you have metabolic alkalosis, now what?

A

1) Urine Cl > 10 = not volume responsive
- is there HTN? Yes = hyperaldosteronism, renal artery stenosis. No = Barter’s, Gittelman’s
2) Urine Cl

73
Q

Causes of respiratory acidosis

A

Hypoventilation
Opiate OD
Asthma/COPD with air trapping
Muscular strength (long-term ventilators or obese/OSA)

Surgery (27 decks)

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