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POS Flashcards - Box 2 > Fluid and Electrolytes > Flashcards

Fluid and Electrolytes Flashcards

1
Q

What are the insensible losses and water requirements for a neonate?

A

Insensible losses = 30-35mL/kg/day

H2O requirements = 150ml/kg/day, reduce to 4:2:1 rule when > 10kg

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2
Q

What is the type and rate of maintenance fluids in a neonate?

A
  • D10/0.25% NS
  • May add 10-20mEq/L of KCl on 2nd or 3rd day of life
  • May change to D5/0.25% NS in 2-3 weeks
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3
Q

What are the K+ and Na+ requirements for a neonate?

A

2 -3 mEq/kg/day

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4
Q

How do you estimate fluid requirements for a child?

A
  • 0 - 10 kg = 150mL/kg/day
  • 10 - 20 kg = 1000 + 50mL/kg/day over 10
  • > 20 kg = 1500 + 20mL/kg/day over 20
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5
Q

Where is the best location for trauma IV access in kids?

A
  • saphenous veins

- antecubital veins

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6
Q

How do you calculate the blood volume of a baby?

A

80cc/kg

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7
Q

How do you calculate transfusion amount for a baby?

A
  • blood = 10cc/kg

- platelets = 10cc/kg

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8
Q

How do you calculate a bolus for a child?

A

10 - 20 mL/kg of RL over 30 minutes

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9
Q

How does SV, CO and HR relate in infants?

A
  • SV is fixed

- only way to increase CO is to increase HR

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10
Q

How do you replace enteral losses in children?

A

Source = Replacement

  • Gastric = 1/2NS + 10mEq/L KCL
  • Pancreatic = RL or 1/2NS + 50mEq/L NaHCO3
  • Bilious = RL or 1/2NS + 50mEq/L NaHCO3
  • Ileostomy = RL or 1/2NS + 25mEq/L NaHCO3
  • Diarrhea = RL or 1/2NS + 25mEq/L NaHCO3
  • Pleural or peritoneal = RL + 5% albumin
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11
Q

What metabolic derangements occur in pyloric stenosis?

A
  • dehydration
  • hypoCl-
  • hypoK+
  • metabolic alkalosis
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12
Q

How do you replace the metabolic derangements caused from pyloric stenosis?

A
  • D5 + 1/2 NS until they void, then D5 + 1/2 NS + KCl
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13
Q

How are pharmacokinetics different in children?

A
  • decreased protein binding
  • decreased hepatic glucuronidation > slow clearance rate
  • decreased GFR in newborns until 2yrs > adult values
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14
Q

What is the calculation for osmolality?

A

2Na + Urea + Glucose + EtOH

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15
Q

How do you calculate TBW in adults?

A
  • 600cc/kg

- 60% of body weight

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16
Q

Hoe much whole blood is in an adult?

A

60cc/kg

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17
Q

How much plasma is in an adult?

A

40cc/kg

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18
Q

How much erythrocyte volume is in an adult?

A

26cc/kg

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19
Q

What is the ideal fluid for replacing losses?

A
  • RL

- some ionic concentration as plasma

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20
Q

What is the disadvantage of replacing losses with RL?

A

Low Na+ content > hyponatremia with long term use or in those who can’t excrete free H2O

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21
Q

What can happen with replacement of a large volume of normal saline?

A
  • total body Na+ overload and hyperCl-

- added Cl- > hyperCl- > overwhelms kidneys > metabolic acidosis

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22
Q

What are ion concentrations in common replacement fluids?

A

ECF = Na-142, K-4, Ca-5, Mg-3, Cl-103, HCO3-27, Osm-295
NS = Na-154, Cl-154, Osm-308
RL = Na-130, K-4, Ca-2.7, Cl-109, HCO3-28, Osm-273
D5/NS = Na-154, Cl-154, Osm-560
D5/0.45%NS = Na-77, Cl-77, Osm-406
2/3 & 1/3 = Na-56, Cl-56, Osm-?271
D5W = Osm-252

Albumin 5% = Na-145, Cl-145, Osm-300
Albumin 25% = Na-145, Cl-145, Osm-1500
Pentastarch 10% = Na-154, Cl-154, Osm-326

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23
Q

What salts are commonly lost in various bodily secretions?S

A
  • Salivary = Na-50, K-20, Cl-40, HCO3-30
  • Basal gastric = Na-100, K-10, Cl-140, H-30
  • Stimulated gastric = Na-30, K-10, Cl-140, H-100
  • Bile = Na-140, K-5, Cl-100, HCO3-60
  • Pancreatic = Na-140, K-5, Cl-75, HCO3-100
  • Duodenum = Na-140, K-5, Cl-80
  • Ileum = Na-140, K-5, Cl-70, HCO3-50
  • Colon = Na-60, K-70, Cl-15, HCO3-30
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24
Q

What are the best replacement fluid for various enteral losses?

A

Source = Replacement

  • Gastric = 1/2NS + 10mEq/L KCL
  • Pancreatic = RL or 1/2NS + 50mEq/L NaHCO3
  • Bilious = RL or 1/2NS + 50mEq/L NaHCO3
  • Ileostomy = RL or 1/2NS + 25mEq/L NaHCO3
  • Diarrhea = RL or 1/2NS + 25mEq/L NaHCO3
  • Pleural or peritoneal = RL or 1/2 NS + 5% albumin
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25
Q

Albumin

A
  • main determinant of plasma oncotic pressure
  • half-life = 20 days
  • on electrophoresis, it accounts for 52 - 66% of protein
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26
Q

How do you calculate maintenance fluid in adults?

A
  • Insensible H2O losses = 8 - 12 mL/kg/day (increases 10% for every degree > 37.2 celsius)
  • 4:2:1 rule
  • Na = 1 - 2 mEq/kg/day
  • K = 0.5 - 1 mEq/kg/day
  • 0.33% NaCl + 20 - 30 mEq/L LCl best fits daily requirements
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27
Q

What are predisposing conditions to HypoCa2+?

A
  • hypoparathyroidism
  • PTH resistance
  • vit D deficiency
  • vit D resistance
  • acute hypocalcemic syndromes
  • tumor lysis syndrome
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28
Q

How does tumor lysis syndrome affect body ions?

A
  • hypocalcemia
  • hyperphosphatermia (chelates Ca > hypoCa)
  • hyperuricemia
  • hyperkalemia
  • due to massive tumor death
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29
Q

How can hypocalcemic syndromes occur?

A
  • when there is acute chelation or precipitation of Ca2+
  • happens when lots of citrate is infused: large volumes of fluid in resuscitation, large transfusions, rapid infusion of phosphate, acute pancreatitis when Ca2+ is saponified
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30
Q

What are the manifestations of hypoCa?

A

Neuromuscular excitability

  • paresthesias
  • hyperreflexia & laryngospasm
  • seizures
  • tetany
  • chvostek’s sign
  • trousseau’s sign
  • paralytic ileus

Cardiac Dysfunction

  • direct suppression of contractility
  • hypotension
  • decreased pulse pressure
  • delayed repolarization
  • heart block
  • long S/QT segment
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31
Q

What is the management of hypoCa?

A
  • PO maintenance for 0.65 - 0.8 mmol/L
  • IV replacement only when symptomatic or < 0.65 mmol/L
  • correct hypoMg first
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32
Q

What are the predisposing conditions to hyperCa?

A
  • primary hyperparathyroidism
  • malignancy
  • drugs (thiazides, lithium, tamoxifen)
  • immobilization
  • familial hypocalciuric hypercalcemia
  • granulomatous disease (sarcoid, TB)
  • thyrotoxicosis
  • milk alkali syndrome
  • malignant hyperthermia
  • paget’s disease of the bone
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33
Q

What are the manifestations of hyperCa?

A
  • CNS: decreased LOC
  • Neuromuscular: proximal muscle weakness, hyporeflexia
  • GI: A/N/V, constipation, paralytic ileus, PUD, pancreatitis
  • Renal: polyuria (nephrogenic DI), nephrocalcinosis, nephrolithiasis
  • CVS: HTN, short QT, exacerbates digoxin toxicity
  • MSK: bone pain
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34
Q

What is the management of hyperCa?

A
  • diuretics + isotonic saline + lasix (standard tx)
  • bisphosphonates
  • calcitonin
  • mithramycin
  • IV phosphates (absolute last resort)
  • corticosteroids (in sarcoidosis)
  • chloroquine phosphate (in sarcoidosis)
  • gallium nitrate
  • surgical excision (of excess functioning tissue)
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35
Q

How do you diagnose Paget’s Disease of the bone?

A

X-Ray

  • increased bone density
  • cortical thickening
  • abnormal architecture
  • bowing
  • overgrowth

Labs

  • increased ALP
  • increased urinary excretion of pyridinoline crosslinks
  • Ca and PO4 levels usually normal

Bone Scan
- increased localization to affected sites

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36
Q

What causes hyperMg and what physiologic change does it cause?

A
  • seen in RF and Mg-containing antacid abuse

- high Mg blocks entrance of Ca into myocardial cells and causes heart failure

37
Q

What is the treatment for hypoMg2+?

38
Q

What is the etiology of hypoMg2+?

A
  • chronic diarrhea
  • prolonged aggressive diuresis
  • DM w/ persistent osmotic diuresis
  • heavy EtOH abuse
  • pancreatitis
  • hypoPO4
39
Q

What are the clinical manifestations of hypoMg2+?

A

Neuromuscular Manifestations

  • changes in mental status
  • seizures
  • tremors
  • hyperreflexia

Cardiac Manifestations

  • prolonged PR interval
  • prolonged QT
  • T-wave flattening
  • tachyarrhythmias
  • atrial fibrillation
  • torsades de pointes
  • digitalis toxicity enhanced as both inhibit the membrane pump
40
Q

What is the division of ECF and ICF in TBW?

A

ECF = 1/3

  • plasma 1/4
  • interstitial/lymphatic 3/4

ICF = 2/3

41
Q

How is osmolality regulated?

A
  • 285 - 295 mOsm range
  • ADH > regulates [Na+] via H2O reabsorption
  • aldosterone > regulates total body Na+
42
Q

What is ADH secretion stimulated by?

A
  • osmolality > 280 mOsm
  • decreased intravascular volume > 10%
  • decreased mean arterial pressure > 10%
  • pain + emotional stress
43
Q

What is aldosterone secretion stimulated by?

A
  • hypovolemia (via RAAS)

- hyperkalemia

44
Q

What can cause hypertonic hyponatremia?

A
  • hyperglycemia - decreased Na by 2.5 for every increased glucose by 10
  • mannitol
  • other effective osmole
45
Q

What can cause isotonic hyponatremia?

A
  • lab artifact from increased lipids or increased proteins

- absorption of glycine or sorbitol

46
Q

What are the various types of hypotonic hyponatremia?

A
  • hypovolemic hypotonic hyponatremia
  • hypervolemic hypotonic hyponatremia
  • euvolemic hypotonic hyponatremia
47
Q

What can cause hypovolemic hypotonic hyponatremia?

A
  • depletion of Na volume
  • loop diuretics
  • thiazides
  • Addison’s disease
  • osmotic diuresis
  • vomiting
  • diarrhea
  • fistualas
  • third spacing
  • weeping wounds
48
Q

What can cause hypervolemic hypotonic hyponatremia?

A
  • CHF
  • nephrotic syndrome
  • cirrhosis
  • psychogenic polydipsia
  • SIADH
49
Q

What can cause euvolemic hypotonic hyponatremia?

A
  • SIADH
  • adrenal insufficiency
  • hypothyroidism
  • psychogenic polydipsia
  • low solute intake (“tea and toaster”)
50
Q

How do you delineate extrarenal losses from renal losses in hypovolemic hypotonic hyponatremia?

A
  • UNa < 10 = kidney holding onto Na+ > extrarenal

- UNa > 20 = kidney not holding onto Na+ > renal

51
Q

How do you delineate extrarenal from renal in hypervolemic hypotonic hyponatremia?

A
  • UNa < 10 = kidney holding onto Na+ > extrarenal or nephrotic syndrome
  • UNa > 20 = kidney not holding onto Na+ > renal failure
52
Q

How do you delineate the various causes for euvolemic hypotonic hyponatremia?

A
  • UOsm > 110 = SIADH, adrenal insufficiency, hypothyroidism
  • UOsm < 100 = psychogenic polydipsia, low solute intake
  • UOsm variable = screwed up “osmostat”
53
Q

How do you treat hypovolemic hypotonic hyponatremia?

A
  • Na+ > 120 = NS

- Na+ < 120 = 3% hypertonic NS

54
Q

How do you treat hypervolemic hypotonic hyponatremia?

A
  • Na+ > 120 = volume restriction to as little as 10mL H20/kg/day
  • Na+ < 120 = small volume 3% NS +/- dialysis
55
Q

How does SIADH present?

A

euvolemia or hypervolemia + low plasma osmolality + high urine osmolality

renal & adrenal function normal
K+ normal

56
Q

What is the DDX for SIADH?

A
  • malignancy: SCLC, pancreatic, H&N epithelial carcinomas, hematological (hodgkin’s)
  • pulmonary disorders: bacterial, fungal, tuberculosis infections
  • CNS: infection, injury
  • medications: carbamazepine, clofibrate, clorpropramide, thiazides, cyclophosphamides, cisplatin, vinblastine, vincristine, NSAIDs, SSRIs
  • medical conditions: hypothyroid, renal impaiment with salt losing nephritis, mineralocorticoid deficiency, psychogenic polydipsia, EtOH withdrawal
  • other: pain, nausea, post-op state
57
Q

How is SIADH diagnosed?

A

urine Na+ > 20 mEq/L
+
urine osmolality > plasma osmolality

58
Q

How is SIADH managed?

A
  • Na < 120 = H2O restrict 7 - 10 mL/kg/day
  • malignancy: demeclocycline (antagonizes renal action of ADH), lithium
  • when H2O restriction inadequate: osmotic diuresis + furosemide
59
Q

What is the advised correction rate for sodium?

A

Chronic

  • 0.5 mEq/L.hr
  • don’t exceed 10 - 15 mEq over 24hrs

Acure
- don’t exceed 1 mEq/L/hr until Na+ of 120 reached

60
Q

What is the most common cause of hypertonicity?

A

Hypernatremia

61
Q

What are aetiologies of hypertonicity?

A
  • DI
  • burns
  • exfoliative dermatitis
  • vomiting
  • diarrhea
  • sweating
  • fever
  • resp losses
  • inadequate AVP secondary to EtOG
  • fistulas
  • endoluminal tubes
  • DKA
  • hyperglycemic induced diuresis
62
Q

What happens when hypertonic patients become hypotensive?

A

Kidneys can no longer produce hypertonic urine and thus they can’t achieve a net H2O balance

63
Q

What is the treatment for hypernatremia?

A
  • IV isotonic solution
  • DDAVP can be used for central DI patients. Desmopression is the preparation of choice given intranasally. Chlorpropramide can be used to enhance renal effects of DDAVP.
  • Thiazides can be used paradoxically
  • Carbamazepine and clofibrate can be used with caution
  • Indomethacin may be modestly effective
64
Q

What are the 2 types of diabetes insipidus?

A

Central
- endocrine disorder resulting from blunted or existent synthesis or release of AVP/ADH

Nephrogenic
- kidney doesn’t respond to AVP/ADH

65
Q

What is the etiology of central DI?

A
  • brain injury
  • brain surgery
  • brain tumor
  • SAH
  • Reset DI > osmoreceptors that trigger AVP release are reset to go off at an osmolality > 280
  • Idiopathic > autoimmune
66
Q

What is the etiology of nephrogenic DI?

A
  • renal disease: post-obstructive diuresis, sickle cell nephropathy, medullary cystic disease, ESRD
  • medications: lithium, glyburide, amphotericin B, foscarnet, demeclocycline, methoxyflurane
  • electrolyte disturbances: hyperCa, hypoK
67
Q

How does DI present clinically?

A

Sustained urine output > 100cc/hr + hyperNa

68
Q

How is DI diagnosed?

A

Urine osmolality < 300 + serum Na+ > 150

Increased AVP = nephrogenic
Decreased urine output in response to DDAVP = central

69
Q

What is the water deprivation test?

A

Patients with DI cannot concentrate their urine, event in the context of complete water deprivation

70
Q

What is the treatment for central DI?

A
  • rehydration with isotonic solution
  • DDAVP
  • chlorpropramide
71
Q

What is the treatment for nephrogenic DI?

A
  • rehydration with isotonic solution

- correct underlying renal disease

72
Q

What is the management of post-obstructive diuresis?

A
  • low risk = PO replacement
  • moderate risk = D5 1/2 NS + 20 KCl at 1/2 previous hours urine output rate when they have > 200cc/hr
  • increased Cr/CHF/metal obtundation/peripheral edema = replace urine output mL for mL with NS
73
Q

What are the mechanisms of post-obstructive diuresis?

A
  • volume overload
  • renal insensitivity to ADH
  • urea osmotic diuresis
  • elevated ANP
74
Q

How do beta-2 adrenergic agents affect extracellular K+?

A

Increased Na-K-ATPase activity = decreased extracellular K+

75
Q

Where is the majority of K+ absorbed and excreted?

A
  • reabsorbed in proximal tubules

- excretion carried out by cortical collecting ducts under the influence of aldosterone

76
Q

What are the signs and symptoms of hypokalemia?

A
  • arrhythmias: u-waves, flattened t-waves, inverted t-waves, prolonged QT
  • weakness
  • acute respiratory failure: if marginal respiratory function to begin with
  • worsening hepatic encephalopathy
  • nephrogenic DI
77
Q

What is the relationship between potassium and digoxin?

A
  • hypokalemia exacerbates digoxin toxicity

- use cholestyramine to decrease digoxin toxicity

78
Q

What is the etiology of hypokalemia?

A

Excessive renal loss

  • loop diuretics (lasix) - increased exchange of Na for K in distal convoluted tubule
  • barter’s syndrome and gitelman’s syndrome
  • primary hyperaldosteronism (adrenal cortex tumor)
  • excess renin production (renal a. stenosis)

Uncompensated GI losses
- villous adenoma

Medications
- salbutamol, insulin, cortisol, vit B12

79
Q

What is the distribution of potassium in the body?

A
  • ECF = 1 mmol/kg
  • ICF - 30 - 40 mmol/kg

small decrease in serum K+ = big decrease in total body K+

80
Q

What does refractory hypoK+ suggest?

81
Q

What are the various K+ salts and when should you use them?

A

KCl
- enables absorption of Na+ in proximal tubule therefore aids with volume expansion

KHCO3
- if diarrhea is cause therefore bicarb loss is present

KPO4

  • nutritional support of catabolic patients
  • recovery of DKA
82
Q

What is hypokalemic hypochloremic alkalosis?

A
  • litres of gastric juices lost (decreased HCl) > hypoCl + alkalemic > nephron decreases Cl- dependent reabsorption of Na+ in the proximal tubule > increased delivery of Na+ to distal tubule > aldosterone driven excretion of K+
  • urine K+ > 20 mEq/L & paradoxically acidic
  • treat wth KCl fluids
83
Q

What is the etiology of hyperkalemia?

A

PseudohyperK
- hemolyzed sample, leukocytosis, thrombocytosis, prolonged tourniquet, upstream IV with KCl

Redistributional
- acidosis, hypoinsulinism, tissue necrosis, reperfusion syndrome, digoxin poisoning, succinylcholine

Elevated total body K
- renal failure, excessive intake, aldosterone deficiency, DM, spironolactone use

Drugs
- trimethoprim, pentamidine, amlodipine, ACEi, succinylcholine

84
Q

What EKG changes can you see from hyperK?

A
  • prolonged PR interval
  • peaked T waves
  • loss of P waves
  • slurring of QRS
  • terminal, broad V tach
85
Q

What are the treatment options for hyperK?

A
  • Tx needed in mins: 10mL calcium gluconate over 3 - 5 mins then another 10mL over 10 min + 50 - 100 mEq NaHCO3 IV over 10 - 20 mins
  • Tx needed within in 1 hr: D50W 50 mL IV + 10 U insulin + hemodialysis
  • Tx needed within hours: rectal kayexalate + lasix
86
Q

What are the sign and symptoms of hypophosphatemia?

A
  • lassitude
  • fatigue
  • weakness
  • convulsions
  • death
  • RBC hemolysis
  • impaired O2 delivery
  • impaired WBC phagocytosis
87
Q

How do you treat hyperphosphotemia?

A

Diuresis + phosphate-binding antacids

88
Q

What are common diuretics?

A
  • CAI: acetazolamide
  • Loop: lasix
  • Thiazides: HCTZ, chlorthaladone, metolazone
  • K-sparing, blk-aldo: spironolactone
  • K-sparking, blk-Na: amiloride

POS Flashcards - Box 2 (3 decks)

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