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Anesthesia Concepts 4 (Butera) > Fluid & Electrolytes > Flashcards

Fluid & Electrolytes Flashcards

1
Q

Fluid Compartments

A

**ICF: 67%; 25L **
ECF: intravascular (plasma) 7% & Interstial 26%, transcellular 2.5%

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2
Q

Fluids breakdown

A

60/40/20 (16/4)
TBW = 42L and weights 42kg or 92lbs, 60%
Intracellular fluid: 28L = 40%
Extracellular fluid = 14L = 20%
Divided into:
Interstitial fluid 11L, 16% &
Plasma vol 4L, 4%

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3
Q

Fluid Distribution

A

Consist of solvent or medium (water) and solutes (charged particles, electrolytes)
Intracellular (ICF) and extracellular fluid (ECF)

TBW varies by age and gender
Higher total body water: men, infants
Lower total body water: women, obese, elderly
Furthermore affected by muscle mass (more TBW) and fat composition (less TBW)

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4
Q

FLUID MOVEMENT

A

Dependent on pressures
1. Osmotic
2. Hydrostatic
3. Oncotic

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5
Q

Osmotic

A

PULL
ECF determinants: Sodium (Na+), Chloride (Cl-), and bicarbonate (HCO3-), urea and glucose
ICF determinants: Potassium (K+), adenosine triphosphate (ATP), phosphate (PO4-)

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6
Q

Hydrostatic

A

PUSH
Opposes osmotic pressure
Determinant: water pressure

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7
Q

Oncotic

A

(colloid osmotic)
MAJOR determinant: ALBUMIN

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8
Q

TONICITY

A

Determined by difference in osmotic pressure between two solutions across a semipermeable membrane

The effect of osmotic pressure or tension on the cell

Describes cell response to an external solution

Classification method for sodium and water imbalances between ICF and ECF compartments

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9
Q

3 types of tonicity

A

Isotonic: equal exchange of water
Hypertonic: water movement out of cell
Hypotonic: water movement into cell

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10
Q

Fluid Balance

A

Fluid regulation
Water balance is equated with volume
Serum sodium concentration is equated with osmolality/tonicity

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11
Q

Homeostasis Parts

A

Compensatory mechanisms maintain homeostasis
1. Volume receptors
Heart (atria), kidneys, vasculature (aorta, carotid arteries)
Provide feedback to the CNS regarding volume status
2. Osmoreceptors
Anterior hypothalamus
Trigger thirst mechanism if ↑ serum osmolality
3. Hormone regulation of water and sodium

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12
Q

Electrolytes

A

Minerals with electrical charges
Found in blood, urine, and other body fluids
Cations are positively (+) charged
Anions are negatively (-) charged
Homeostasis = net neutrality between ECF and ICF
Near equal osmolality as well

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13
Q

Electrolyte Chart

A
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14
Q

Water, Sodium, & Chloride

A

Intricately linked based on electrical charge and polarity
Sodium is the most abundant solute in the ECF (135-145mEq/L)
Major determinant of volume
Levels closely mirror chloride
Key determinant of isotonic, hypertonic, or hypotonic fluid shifts
Intravascular compartment volume may shift as a result of tonicity
Euvolemic, hypervolemia, and hypovolemia
Considerations for determining cause of Na/Cl/H2O disorders
Most likely inappropriate sodium or water control

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15
Q

Sodium

A

Most significant cation
Most prevalent electrolyte within ECF
Controls serum osmolality and water balance
Helps maintain acid-base balance when combined with
bicarbonate
Regulated by:
1. Kidneys
2. Sympathetic nervous system
3. Renin-angiotensin-aldosterone system (RAAS)
Primarily dietary intake
Primarily renal excretion
Other losses: GI, burns, sweating

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16
Q

HYPERNATREMIA - value and osmolality

A

Serum sodium (Na+) level > 145 mEq/L (Ref: 135-145 mEq/L)
Leads to HIGH serum osmolality > 295 mOsm/kg (Ref: 285-295 mOsm/kg)
Hypertonicity leads to** cellular dehydration**

Causes:
Primarily water imbalances due to excessive loss without adequate hydration
* Impaired thirst mechanism or lack of water intake
* Extrarenal vs. renal losses
* Hyperglycemia, mannitol administration, parenteral nutrition, diabetes insipidus

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17
Q

HyperNatremia - manifestations, diagnosis

A

Manifestations
Chiefly neurologic in nature
Mild: lethargy, headache, confusion, irritability
Severe (>158 mEq/L): seizure, coma
Hypovolemia, hypotension, dry mucous membranes, thirst, ↓UOP
Diagnosis: serum/urine chemistry and osmolality

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18
Q

Hypernatremia - Treatment

A

Treatment of underlying cause
Correct water losses (PO if mild, IV if severe)
AVOID RAPID CORRECTION OF SODIUM
1mEq/L per hour and no greater than 12 mEq/L over 24 hours recommended

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19
Q

Hypernatremia Anesthesia Considerations

A

Hypernatremia increases MAC in animal studies

Consider hypovolemia and induction of anesthesia, decreased volume of distribution and decreased cardiac output

Postpone elective surgery for Na > 150mEq/L, establish cause and replace volume deficits

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20
Q

Hyponatremia - values and causes

A

Serum sodium (Na+) level < 135 mEq/L (Ref: 135-145 mEq/L)
Leads to **LOW serum osmolality < 280 **mOsm/kg (Ref: 285-295 mOsm/kg)
Hypotonicity leads to intracellular swelling
Nervous system impairment

Causes:
Primarily inadequate renal excretion of water
Renal failure, volume depletion, diuretics, SIADH, adrenal insufficiency/failure, lack of sodium intake, excess water ingestion, heart/liver/kidney failure

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21
Q

Hyponatremia - manifestations, diagnosis

A

Manifestations
Mild (< 130 mEq/L): GI symptoms (N/V/D)
Severe (< 125 mEq/L): Neurologic symptoms (lethargy, headache, confusion, seizure, coma)
Edema if hypervolemic, hypotension if hypovolemic
Diagnosis: serum/urine chemistry and osmolality

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22
Q

Hyponatremia - treatment

A

Treatment of underlying cause
AVOID RAPID CORRECTION OF SODIUM
May result in osmotic demyelination syndrome

Low total body sodium; replace isotonic deficit

Normal total body sodium; water restriction or hormone replacement

Increased total body sodium; restrict water and loop diuretic (CHF Cirrhosis, nephrotic syndrome) restrict water (renal failure)

Rapid correction of hyponatremia has been associated with demyelinating lesions in the pons resulting in permanent neurological sequelae

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23
Q

Hyponatremia Anesthetic Considerations

A

Sodium should be corrected to > 130mEq/L for elective procedures

Lower concentrations may result in significant cerebral edema

Post operatively as agitation, confusion or somnolence

TURP and hysteroscopy can absorb irrigation fluids as much as 20ml/min and risk for rapid development of acute water intoxication

24
Q

Control of Sodium Balance and ECF Volume

A

Baroreceptors; located in the carotid sinus modulate sympathetic stimulation and and non-osmotic ADH secretion.

The juxtaglomerular apparatus modulates the renin-angiotensin aldosterone system

Stretch receptors in both atria are affected by volume changes and modulate the release of atrial natriuretic peptide hormone and ADH

25
Q

Effectors of Volume Change

A

Renin-angiotensin aldosterone
Atrial natriuretic peptide
Brain natriuretic peptide
Sympathetic Nervous system
Glomerular filtration rate and plasma sodium
Tubuloglomerular balance
ADH

26
Q

Anesthesia Considerations

A

Hypovolemia (sodium deficit) or hypervolemia (sodium excess) should be corrected before elective surgery

Hypovolemia increases the negative inotropic effects of anesthesia

Hypervolemia increases extracellular volume can impair gas exchange due to pulmonary edema, or collections of ascitic or pleural fluid

27
Q

Chloride

A

Mineral electrolyte and major extracellular anion
Affects fluid distribution by attaching to sodium and water
Helps maintain acid-base balance when combined with hydrogen
- Found in gastric secretions, pancreatic juices, bile and stomach acids; also present in CSF
- Primarily dietary intake
Eggs, cheese, milk, fish, canned and preserved food (salt)
- Primarily renal excretion; secondary losses due to sweating

28
Q

Chloride - abnormal values

A

Hyperchloremia (> 108 mEq/L) and hypochloremia (< 98 mEq/L)
No distinct set of clinical manifestations
Tend to mirror sodium alterations
- Diagnosis:
History, physical examination, blood chemistry, urine analysis, ABGs measurement
Hyperchloremia and metabolic acidosis, hyperparathyroidism
Hypochloremia and metabolic alkalosis, hypoparathyroidism
- Treatment:
Underlying causes (usually sodium derangement)
Consider diuretics and/or bicarbonate

29
Q

POTASSIUM

A

Major intracellular cation
Role in electrical conduction, acid-base balance, and metabolism
Serious issues from fluctuation!
Diet as main source of intake
Fruits and green leafy vegetables
Regulated by
Kidneys
Aldosterone
Promotes sodium retention and potassium excretion

30
Q

NA-K pump

A

Sodium-potassium pump
Activated by catecholamines and insulin

31
Q

HyperKalemia - values, manifestations, diagnosis

A

Serum levels over 5 mEq/L (Ref: 3.5-5mEq/L)
Medical emergency if greater than 6 mEq/L
Most common causes are disorders that
decrease excretion or conditions that cause
intracellular release
CKD, Diabetes, Dehydration, Trauma,
Excess dietary intake, Medications
Manifestations:
Nervous, cardiac, and GI HYPER-excitability
Diagnosis:
Physical exam, chem panel, EKG

32
Q

Hyperkalemia EKG changes

A
33
Q

Hyperkalemia - treatment

A

Treatments:
1. Insulin (10 units) and IV dextrose (25g)
Reduction = 1 mEq/L within 10-20 mins, DOA 4-6 hrs
2. Polystyrene sulfonate (Kayexelate)
3. Administration of albuterol
Mean reduction 0.4 mEq/L, DOA 60 mins
4. Correction of acidosis promotes H+/K+ exchange
5. Hyperventilation
6. Diuresis
7. Administration of calcium gluconate (PIV) or calcium chloride (CVC)-stabilizes the cardiac membrane
DOES NOT CORRECT HYPERKALEMIA – THIS IS PROTECTIVE MEASURE TO PREVENT CARDIAC DYSRHYTHMIAS!!!!
8. Hemodialysis
9. Discontinuation of attributing foods/medications

34
Q

Hypokalemia

A

**Serum levels under 3.5 mEq/L **
(Ref: 3.5-5 mEq/L)
Medical emergency if less than 2.5 mEq/L
Most common causes are excessive loss, decreased intake, or increased potassium cellular uptake
Drugs, Endocrine DX, Renal DX
Manifestations
Nervous, cardiac, GI HYPO-excitability
Diagnosis
Physical exam, chem panel, EKG

35
Q

Hypokalemia - Causes

A

Excessive renal/GI losses
Renal: diuretics (thiazide + loop), corticosteroids (secondary hyperaldosteronism)
GI: nausea, vomiting, NG suctioning, fistula
Decreased intake
Deficient diet
Limited intake
Inadequate IV supplementation
Increased cellular uptake from ECF
Alkalosis (H+/K+ pump)
Excess insulin (Na-K pump)

36
Q

Hypokalemia - treatment

A

Electrolyte repletion
Oral replacement if mild
IV replacement (SLOW) if moderate-severe

37
Q

Calcium - where is it found

A

Most found in bones and teeth (99%)
Remainder in blood (1%)
1. Ionized calcium (45%)
Used for several physiological processes
Serum measure represents level of functional calcium in the blood
2. Bound (40%) to albumin and chelated (15%) with phosphate, citrate, and sulfur
Inverse relationship with phosphorus
Phosphorous binds free calcium
Synergistic, direct relationship with magnesium
Mg required for production and release of parathyroid hormone

38
Q

Calcium - absorb / excretion

A

Dietary intake is absorbed primarily in the small intestine
Vitamin D aids absorption
Source: sunlight and fortified dairy products
Vitamin K regulates calcium and aids bone formation
Source: green leafy vegetables

Excreted normally in urine/feces

39
Q

Calcium - Regulated by:

A
  1. Parathyroid hormones (PTH)
    Activated in states of hypocalcemia: pulls calcium from bone and prevents renal excretion; activates vitamin D; increases elimination of phosphorous
    Release inhibited by hypomagnesemia
  2. Calcitonin
    Thyroid hormone: drives excess calcium into bone, decreases intestinal absorption, and increases renal elimination
40
Q

HYPERCALCEMIA - value and causes

A

Serum level > 10.3 mg/dL (Ref: 8.8-10.3 mg/dL)

Causes:
Decreased renal excretion
Renal failure
Thiazide diuretics
Increased GI intake/absorption OR increased bone resorption
Cancer
Excessive intake or excess vit D
PTH abnormalities (e.g. hyperparathyroidism)
Prolonged immobility
Medications (e.g. corticosteroids)
Hypophosphatemia

41
Q

Hypercalcemia - manifestations, diagnosis

A

Manifestations:
Decreased cell membrane excitability (cardiac, nervous, musculoskeletal, and GI)
Renal problems and aggravated hypertension

Diagnosis:
Exam, chem panel, 12-lead EKG

42
Q

Hypercalcemia - treatment

A

Medications: bisphosphonate and calcitonin inhibit osteoclast activity, corticosteroids, mithramycin, loop diuretics
Avoidance of thiazide diuretics
Increased mobility promotes osteoblast activity and reduces osteoclast activity
Increased hydration with IV fluids

43
Q

HYPOCALCEMIA - value and causes

A

**Serum level < 8.8 mg/dL (Ref: 8.8-10.3 mg/dL)
**
Causes:
1. Excess loss
- Renal failure, alkalosis, medications (i.e. diuretics, gentamicin), hyperphosphatemia, diarrhea, pancreatitis
- Massive blood transfusion binds calcium to citrate preservatives
2. Decreased intake/absorption OR decreased bone release
- Deficient diet, absorption disorders
- Vitamin D deficiency
- Excessive laxative use promotes phosphate binding
- PTH abnormalities/parathyroidectomy

44
Q

Hypocalcemia - manifestations, diagnosis

A

Manifestations:
Increased cell membrane excitability (CV, Neuro)
Respiratory impairment
Prolonged bleeding times
Tetany
+ Trousseau sign
+ Chvostek sign

Diagnosis:
Exam, chem panel, 12-lead EKG (prolonged QT)

45
Q

Hypocalcemia - treatment

A

Oral/IV replacement
Vitamin D supplement
Supplemental PTH

46
Q

PHOSPHOROUS - key roles, source

A

Key roles in:
Bone and tooth mineralization, cellular metabolism (ATP), acid-base balance (buffers H+ ions), cell membrane formation (phospholipids)

Diet as main source
Chicken, beef, fish, nuts

47
Q

Phosphorus - Regulation

A

Regulation and excretion is primarily renal
- Parathyroid hormone (PTH) promotes phosphorous reabsorption and prevents excretion

HYPERphosphatemia if levels** above 4.5** mg/dL (Ref: 2.5-4.5 mg/dL)
Decreased renal elimination OR increased intake OR ICF -> ECF fluid shift

HYPOphosphatemia if levels under 2.5 mg/dL
Increased renal elimination OR decreased intake OR ECF -> ICF fluid shift

48
Q

PHOSPHOROUS - manifestations, diagnosis

A

Manifestations like those of calcium imbalances
Hyperphosphatemia mimics hypocalcemia
Hypophosphatemia mimics hypercalcemia

Diagnostics
Physical exam, chem panel, identification of underlying causes

49
Q

Treatment of hyperphosphatemia

A

Aluminum hydroxide and aluminum carbonate bind phosphorous and promote elimination via GI tract

50
Q

Treatment of hypophosphatemia

A

Oral supplements and IV potassium phosphate

51
Q

MAGNESIUM - abundance, storage, functions

A

Second most abundant intracellular cation

50% stored in bone/muscle, 50% stored in cells, ~1% in intravascular space

Functions of magnesium include regulation of muscle/nerve/cardiac functions and reduced vascular tone

Direct relationship with Ca++, inverse relationship with Phosphorous

52
Q

Mg - source, elimination

A

Diet as main source
Nuts, seeds, greens, legumes
Primary renal elimination

53
Q

Hyper Mg

A

HYPERmagnesemia, levels above 3.0 mg/dL
Renal failure or excessive intake

54
Q

HypoMg

A

HYPOmagnesemia, levels under 1.8 mg/dL
Inadequate intake or decreased absorption
Diuretics
GI losses

55
Q

Mg - clinical manifestations & diagnostics

A

Clinical manifestations
Neuromuscular
Hypermagnesemia: decreased deep tendon reflexes
Hypomagnesemia: excitability, tremor, tetany
Cardiovascular
Hypermagnesemia: shortened QT interval
Hypomagnesemia: QRS widening

Diagnostic procedures
History, physical exam, blood chemistry

56
Q

Mg - treatments

A

Hypermagnesemia: Diuretics, IV fluids administration, dialysis

Hypomagnesemia: PO/IV repletion

Anesthesia Concepts 4 (Butera) (15 decks)

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