Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

Fluid & Electrolytes COPY Flashcards

1
Q

Fluid Compartments

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

FLUID MOVEMENT

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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-)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Hydrostatic

A

PUSH
Opposes osmotic pressure
Determinant: water pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Oncotic

A

(colloid osmotic)
MAJOR determinant: ALBUMIN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

3 types of tonicity

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Fluid Balance

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Electrolyte Chart

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Effectors of Volume Change
Renin-angiotensin aldosterone Atrial natriuretic peptide Brain natriuretic peptide Sympathetic Nervous system Glomerular filtration rate and plasma sodium Tubuloglomerular balance ADH
26
Anesthesia Considerations
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
Chloride
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
Chloride - abnormal values
**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
POTASSIUM
**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
NA-K pump
Sodium-potassium pump Activated by catecholamines and insulin
31
HyperKalemia - values, manifestations, diagnosis
**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
Hyperkalemia EKG changes
33
Hyperkalemia - treatment
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
Hypokalemia
**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
Hypokalemia - Causes
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
Hypokalemia - treatment
Electrolyte repletion Oral replacement if mild IV replacement (SLOW) if moderate-severe
37
Calcium - where is it found
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
Calcium - absorb / excretion
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
Calcium - Regulated by:
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
HYPERCALCEMIA - value and causes
**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
Hypercalcemia - manifestations, diagnosis
Manifestations: Decreased cell membrane excitability (cardiac, nervous, musculoskeletal, and GI) Renal problems and aggravated hypertension Diagnosis: Exam, chem panel, 12-lead EKG
42
Hypercalcemia - treatment
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
HYPOCALCEMIA - value and causes
**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
Hypocalcemia - manifestations, diagnosis
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
Hypocalcemia - treatment
Oral/IV replacement Vitamin D supplement Supplemental PTH
46
PHOSPHOROUS - key roles, source
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
Phosphorus - Regulation
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
PHOSPHOROUS - manifestations, diagnosis
Manifestations like those of calcium imbalances Hyperphosphatemia mimics hypocalcemia Hypophosphatemia mimics hypercalcemia Diagnostics Physical exam, chem panel, identification of underlying causes
49
Treatment of hyperphosphatemia
Aluminum hydroxide and aluminum carbonate bind phosphorous and promote elimination via GI tract
50
Treatment of hypophosphatemia
Oral supplements and IV potassium phosphate
51
MAGNESIUM - abundance, storage, functions
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
Mg - source, elimination
Diet as main source Nuts, seeds, greens, legumes Primary renal elimination
53
Hyper Mg
HYPERmagnesemia, levels above 3.0 mg/dL Renal failure or excessive intake
54
HypoMg
HYPOmagnesemia, levels under 1.8 mg/dL Inadequate intake or decreased absorption Diuretics GI losses
55
Mg - clinical manifestations & diagnostics
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
Mg - treatments
Hypermagnesemia: Diuretics, IV fluids administration, dialysis Hypomagnesemia: PO/IV repletion

Anesthesia Concepts 4 (Butera) (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions