Ch 7.1: Fluids, Electrolytes Flashcards
1
Q
Water
A
50-60% total body weight
2
Q
TBW
A
Total body water
Function of weight, age, sex, relative amount of body fat (least hydrated)
3
Q
TBW distribution:
A
- ICF (intracellular) = 2/3 of TBW
- ECF (extracellular) = 1/3 of TBW
- TCF (transcellular) = 3% of TBW
4
Q
Why is ECF the most clinically important fluid department?
A
it contains intravascular and interstitial spaces
5
Q
Major extracellular osmole holding water in the extracellular space
A
Sodium
6
Q
Major intracellular osmole holding water within the cells
A
Potassium
7
Q
Na-K-ATPase pumps
A
Maintenance of ECF/ICF compositions
Key role in regulating cell volume
8
Q
D5W-IVF effect on ECF/ICF
A
Dextrose metabolized
Water distributed proportionally to all fluid compartments:
* ICF: 2/3 (667 mL)
* ECF: 1/3 (333 mL)
Within the ECF:
* Intravascular space: 25% (83 mL)
* Interstitial fluid: 75% (250 mL)
9
Q
0.9% NaCl-IVF effect on ECF/ICF
A
0.9% NaCl is an isotonic saline
Distributed completely to ECF (sodium is major extracellular osmole)
* ICF: 0 mL
* ECF: 1000 mL
* 25% (250 mL) remains in intravascular space
* 75% (750 mL) - interstitial space
10
Q
Which is more efficient at expanding the intravascular (plasma) space?
D5W or 0.9%-NaCl
A
Isotonic saline is 3x more efficient than 5% dextrose in water at expanding the intravascular space (plasma)
11
Q
What effect does a hypertonic saline (3% NaCl) have?
A
Establishes osmotic gradient that results in movement of water out of the cells and into the ECF until osmotic equilibrium is obtained
Osmolality increases in both spaces:
* ECF – addition of NaCl
* ICF – water loss
12
Q
Osmotic forces
A
determine the distribution of water between ICF and ECF spaces
13
Q
Plasma oncotic and hydrostatic pressures
A
manage movement of fluid between plasma and interstitial fluid
14
Q
Third spacing:
A
Caused by a disruption in oncotic and/or hydrostatic pressure → net flow of fluid from one compartment to another
Plasma-to-interstitial fluid shift → accumulation of excess fluid:
* Edema: interstitial space
* Effusion: potential fluid spaces
15
Q
What can an acute reduction in blood volume cause?
During third-spacing
A
Can lead to severe volume depletion if not replaced
16
Q
Third spacing in critical illness
A
- Capillary permeability increases → leakage of albumin from plasma to interstitial space → reduced plasma oncotic pressure
- Favors movement of fluid from intravascular → interstitial space
17
Q
Third spacing can occur in the following scenarios:
A
- Intestinal obstruction
- Ileus
- Pleural effusions or ascites
- Severe acute pancreatitis
- Peritonitis
- Trauma
- Bleeding
- Obstruction of a major venous system
18
Q
On average, healthy adults require _ _ _ mL/kg/d of fluid
A
30-40 mL/kg/d
19
Q
Fluid losses - sensible vs insensible
A
- Sensible (easily measurable) losses from GI tract and kidneys account for most fluid loss
- Insensible losses from lungs/skin can contribute up to 1L/day
20
Q
Additional fluid required in:
A
- Severe diarrhea or emesis
- Large draining wounds
- Excessive diaphoresis
- Constant drooling
- Paracentesis losses
- Persistent fevers
- Drains
- High gastric, fistula, and ostomy outputs
- Lactation
21
Q
Strategies to measure outputs that may otherwise not be collectable:
A
- Weigh wound dressings before and after placement to determine losses from open wounds
- Excessive diaphoresis that soaks the bed is usually = 1 liter of fluid
22
Q
Heart failure
A
- 20-25 mL/kg of estimated dry weight
- Should take into consideration edema, fatigue, SOB
- 2g sodium restriction (83 mEq/d)
**HF patients with significant overload should initially be treated with loop diuretics and sodium/fluid restrictions **
23
Q
Maintenance Fluid Requirements
Weight and Age Based Formula
A
- 18-55 years: 35 mL/kg/day
- 56-75 years: 30 mL/kg/day
- > 75 years: 25 mL/kg/day
- Fluid-restricted adults: < 25 mL/kg/day
Based on 2023 NFM course
24
Q
Maintenance Fluid Requirements
Energy based Formula
A
1 mL/kcal consumed or required
Not encouraged in >65 YOA
Based on 2023 NFM course
25
# Maintenance Fluid Requirements
Holliday-Segar Formula
1500 mL for the first 20 kg of body weight, then ADD
* 20 mL/kg remaining kg of BW
## Footnote
Based on 2023 NFM course
26
# Maintenance Fluid Requirements
Adjusted Holliday-Segar Formula
1500 mL for the first 20 kg of body weight, then ADD
* **< 50 YOA: 20 mL/kg** of remaining BW
* **> 50 YOA: 15 mL/kg** of remaining BW
## Footnote
Based on 2023 NFM course
27
# Disorders of Fluid Balance - Disturbance of Volume
Hypervolemia
Volume overload
Excessive gain of fluid
28
# Disorders of Fluid Balance - Disturbance of Volume
Hypovolemia & Causes
Volume depleton
Excessive fluid loss
* Often follows GI hemorrhage, vomiting, diarrhea, and diuresis
29
# Disorders of Fluid Balance - Disturbance of Concentration
What is recognized by a change in serum sodium concentration and plasma osmolality?
* Overhydration - Gain of water alone
* Dehydration - Loss of water only
30
# Disorders of Fluid Balance - Composition
Disturbance of Composition
Gain or loss of potassium, magnesium, calcium, phosphate, chloride, bicarbonate, or hydrogen ions
31
# Electrolytes
Acute abnormality –
developed < 48 hours
Associated with symptoms requiring immediate treatment
* Ex: AMS with acute hyponatremia
32
# Electrolytes
Chronic abnormality –
pt often asymptomatic
Patient may be harmed if disorder is corrected too rapidly
* Ex: chronic hyponatremia
33
What should you do if labs are inconsistent with trends?
Validate accuracy of specimen prior to treatment
34
Electrolyte above normal level – Potential treatments
* Consider removing electrolyte supplementation from IVF or PN
* Changing an enteral formulation containing the electrolytes to something else
* D/c’ing medications that could contribute to electrolyte disorder
* Manage acid-base abnormalities (e.g., metabolic acidosis)
* Inducing renal or GI elimination of the electrolyte
35
How should patients with volume overload receive electrolyte repletions?
Patients with volume overload should receive volume-restricted electrolyte replacement, or PO therapy when able
36
# Electrolytes
Why does peripheral administration have limits for volume and rate of administration?
* Potassium/calcium especially
* Exceeding limits can → tissue damage and potential patient harm
37
# Sodium
Sodium disorders are a result of:
Alterations in water balance
38
# Sodium
Adequate intake of sodium is
_ _ _ mg (_ _ mEq)
daily
Adequate intake (AI) is 1500 mg (65 mEq) daily
39
# Sodium
Clinically relevant hyponatremia:
| Lab value & what do you do in response?
* Serum sodium <130 mEq/L
* Determine serum sodium concentration and volume status
40
Role of sodium in the body
* Major osmotic determinant in regulating ECF volume and water distribution in the body
* Determines membrane potential of cells
* Active transport of molecues across cell membranes (Na-K-ATPase pumps)
41
# Sodium
When are clinical manifestations of hyponatremia more likely to occur?
| Lab value
Na <125 mEq/L
42
# Sodium
Hypertonic hyponatremia
* Serum osmolarity >295 mOsm/L
* Caused by presence of osmotically active substances other than sodium in the ECF
* Common causes: hyperglycemia, mannitol
43
# Sodium
Formula to correct serum sodium in setting of hyperglycemia
Corrected Na = serum Na + 0.016 (serum glucose – 100)
| Hypertonic hyponatremia
44
# Sodium
Why do you not want to correct sodium too quickly?
**To prevent osmotic demyelination**
Target rate of sodium correction for hyponatremia should not exceed
* Acute: 10-12 mEq/L/d
* Chronic/unknown duration: 6-8 mEq/L/d
45
# Sodium
Isotonic hyponatremia
* Serum osmolarity in normal range: 280-295 mOsm/L
* Rarely observed with recent advances in lab analysis
* Fraction of serum that is composed of water is reduced = excess of plasma proteins or lipids
* Isotonic infusions: dextrose, mannitol
46
# Sodium
What is pseudohyponatremia caused by?
hypertriglyceridemia; hyperproteinemia
47
# Sodium
Hypotonic hyponatremia:
* serum osmolarity <280 mOsm/L
* Requires detailed assessment of volume status and urine sodium osmolality
* Check urine osmolality: >100 mOsm/kg = inappropriate renal dilution
48
# Sodium
Hypovolemic hypotonic hyponatremia
| Include sodium / TBW
**↓↓ total body Na; ↓ TBW**
* Patients lose more sodium in relation to water
* Critical to identify source of fluid loss
* Urine osmolality > serum osmolality = concentrated urine + body’s attempt to retain fluid
49
# Sodium
What can cause hypovolemic hypotonic hyponatremia?
Cerebral salt wasting 2/2 SAH can → hypovolemic hyponatremia
Extrarenal losses:
Diarrhea, GI fistula output, excessive sweating, burns, open wounds, and fluid drains (peritoneal, pleural, biliary, or pancreatic)
Renal losses:
Diuretics, osmosis diuresis,
50
# Sodium
Hypovolemic state:
Determine ECF volume & treatment
* ECF volume status: Tachycardia, low BP, poor skin turgor
* Treatment: isotonic fluids to expand ECF volume
51
# Sodium
Euvolemic hypotonic hyponatremia
| Include sodium / TBW
**+/= total body Na; ↑ TBW**
* Urine osmolality > serum osmolality & Urine Na+ > 20 mEq/L
* Indicates kidneys are inappropriately concentrating urine (would be dark urine)
* Volume status is adequate
* Urine osmolality > serum osmolality AND urine Na >20 = kidneys inappropriately concentrating urine
52
# Sodium
What can cause euvolemic hypotonic hyponatremia?
**Commonly associated with SIADH**
* Hypothyroidism
* Drug-induced
53
# Sodium
Euvolemic state
Determine ECF volume & treatment
* ECF volume status: Normal pulse, BP, skin turgor; no edema
* Treatment (additional causes): correct the underlying disorder + fluid restriction
SIADH
* Fluid restriction 500-1000 mL/d
* Concentrate PN
* Ensure at least isotonic fluids (PN concentration = 154 mEq Na/L)
* NaCl tablets
* Urea
* Vaptan
Deficiency
* Glucocorticoids
Hypothyroid
* Thyroid hormone replacement
54
# Sodium
Hypervolemic hypotonic hyponatremia
| Include sodium / TBW
**↑ total body Na; ↑↑ TBW**
* Pts have some element of end-organ damage (renal failure, hepatic failure w/ ascites, HF)
→ fluid retention or third spacing
* Patients retain more water > sodium
55
# Sodium
Hypervolemic state
Determine ECF volume & treatment
* ECF volume status: Edema
* Treatment: fluid and sodium restrictions; concentrate PN, diuretics, vaptans
56
# Sodium
SIADH
| Cause, what happens, what contributes to it, what does pt present w/?
* A disorder of impaired water excretion caused by the inability to suppress the secretion of antidiuretic hormone (ADH)
* If water intake exceeds the reduced urine output, the ensuing water retention leads to the development of hyponatremia
* ADH: increases water reabsorption by the kidney
* Retain water (hypotonic hyponatremia); low UOP
* Presents with excessive thirst
57
SIADH essential diagnostic criteria:
| Includes lab value
* Serum osmolality = < 275 mOsm/kg
* Urine osmolality = double to serum osmolality
* Urine sodium = >20
* No adrenal, thyroid, pituitary or renal insufficiency
* No recent diuretic use
58
SIADH causes
Respiratory (small cell lung cancer, pneumonia, abscess, tuberculosis)
Neurologic (tumors, trauma, meningitis, abscess, subarachnoid hemorrhage, pain, anxiety, nausea)
Medications
* Anticancer agents: cyclophosphamide, ifosfamide, vincristine, cisplatin, carboplatin
* Anticonvulsants: carbamazepine, oxcarbazepine
* Antidepressants: SSRIs, TCADs, MAOI, venlafaxine
* Antidiabetic agent: chlorpropamide
* Antipsychotics: phenothiazines, haloperidol
* Miscellaneous: opiates, 3,4-methylenedioxy-methamphetamine, NSAIDs
* Vasopressin analogs: desmopressin, oxytocin, terlipressin, vasopressin
59
# Sodium
Hypernatremia - levels > _ _ _ mEq/L are associated with a significant increase in mortality
Levels >160 mEq/L associated with a significant increase in mortality
60
# Sodium
Symptoms of hypernatremia
* Lethargy
* Twitching
* Weakness
* Seizures
* Confusion
* Coma
* Restlessness
* Death
* Irritability
61
# Sodium
How to address hypernatremia:
1. Assess volume status
2. Correct water deficit: administer 50% within first 24 hours, remainder over next 24-48 hours
3. Limit serum Na correction to 8-10 mEq or mmol / Liter per day → prevention of cerebral edema
62
# Sodium
Equation for free water deficit
Water deficit (L) = TBW x [(serum Na – 140)/ 140]
TBW =
* 0.6 x weight (males)
* 0.5 x weight (females)
63
# Sodium
Hypovolemic hypernatremia & causes
**↓ Na / ↓↓ water**
* Above normal serum osmolality
Causes:
* Osmotic or solute diuresis
* Post-obstructive diuresis
* Vomiting
* Diarrhea or excess laxative use
* High insensible losses
64
# Sodium
Hypovolemic hypernatremia - treatment
* Replace free water deficit (oral water, enteral water flushes, dextrose 5% in water, 0.45% NaCl, addition of sterile water to PN)
* Insulin (hyperglycemia)
* Amino acid dose reduction (solute diuresis)
65
# Sodium
Euvolemic hypernatremia & causes
**WNL Na / ↓ water**
Water losses exceed sodium losses
Common causes:
* Central diabetes insipidus → impairment of ADH secretion
---- DI also presents with extreme thirst like SIADH; polydipsia
* Nephrogenic DI → kidneys cannot respond to ADH circulating in serum
---- Hypercalcemia, hypokalemia, amphotericin B, cidofovir, foscarnet, demeclocycline, lithium
66
# Sodium
Euvolemic hypernatremia- treatment
* Desmopressin (central diabetes insipidus)
* Remove offending agent, potassium replacement, thiazide diuretics, Na restriction (nephrogenic diabetes insipidus)
67
# Sodium
Hypervolemic hypernatremia
& causes
**↑↑ Na / ↑ water**
Common causes:
* Hypertonic saline or Na bicarbonate infusions
* Hyperaldosteronism
68
# Sodium
Hypervolemic hypernatremia - treatment
* Loop diuretic
* Hypotonic fluids (Na overload)
* Spironolactone/adrenalectomy (hyperaldosteronism)
69
What is the role of potassium in the body?
* Critical role in cell metabolism (protein and glycogen synthesis)
* Also maintains resting membrane potential with ratio between ECF and cell
70
What is the most important component in daily regulation of potassium balance?
Na-K-ATPase pump
impacts plasma potassium concentration
71
Additional impacts on potassium distribution:
* Insulin and catecholamines;
* exercise,
* extracellular pH,
* cellular breakdown
72
Symptoms of hypokalemia:
| mild, mod, severe
* Mild depletion (3.0-3.5) → asymptomatic
* Lower serum levels → nonspecific sx: generalized weakness, lethargy, constipation
* Severe deficiency/consequences → muscle necrosis, ascending paralysis, arrhythmias, and death
73
What is hypokalemia often the result of?
Abnormal losses via urine or stool
74
What are two additional causes of hypokalemia?
* Can develop from transcellular shift of potassium from ECF → cells,
* Inadequate PO intakes
75
What are potential causes of transcellular shifts of potassium into the cells?
* Metabolic alkalosis
* Increases in insulin and catecholamines (epi, norepi)
76
# Potassium
What are potential causes of extracellular shift
* glucagon
* metabolic acidosis
* aldosterone (allows renal elimination)
77
Drug-induced hypokalemia - Increased renal potassium loss
**Diuretics**
* Acetazolamide (glaucoma tx)
* Thiazides (↑ excretion of Na/Cl; Increased reabsorption of calcium)
* Indapamide
* Metolazone (inhibits resorption of sodium and chloride in the proximal convoluted tubule)
* Bumetanide (loop; decreased reabsorption of Ca2+ and Mg2+)
* Furosemide (loop)
* Torsemide (loop)
Fludrocortisone
Hydrocortisone
**Drugs associated with magnesium depletion:**
* Aminoglycosides (antibiotics)
* Cisplatin (chemotherapy)
* Foscarnet (antiviral)
* Amphotericin B (antifungal)
* Posaconazole (antifungal; used in weakened immune states)
78
Drug-induced hypokalemia - Excess potassium loss in stool
* Patiromer (binds with potassium in the gut)
* Phenolphthalein (laxative; increased fecal sodium/potassium loss)
* Sodium polystyrene sulfonate (kayexelate, same as patiromer)
* Sorbitol
79
Drug-induced hypokalemia - Potassium shift from ECF to ICF
Beta-2 adrenergic agonists (respiratory dz: asthma, copd)
* Epinephrine
* Albuterol
* Terbutaline
* Pirbuterol
* Salmeterol
* Isoproterenol
* Ephedrine
* Pseudoephedrine
Theophylline (Bronchodilator)
Caffeine
Verapamil intoxication (calcium channel blocker)
Insulin (all types)
80
Generalized causes of losses
| body systems
* Kidney losses- diuretics, hyperaldosteronism, amphotericin, aminoglycosides
* GI tract losses
* --Diarrhea (10 mEq/L)
* --Emesis / NG losses (up to 50 mEq/L)
* Skin losses – burns, strenuous exercise on hot humid day
* Altered distribution – alkalosis, catecholamine surge, excessive insulin
* Dietary – inadequate intake, large volumes of IV saline, pica
81
Liquid and slow release potassium supplementation
82
At what rate of potassium infusion...
1) does a patient require cardiac monitoring
2) should a central line be used, and why?
If infusion >10 mEq/h → continuous cardiac monitoring required
* CVC to avoid phlebitis and burning
83
Empiric potassium dose in PN for normal renal function and impaired renal function?
* Empiric potassium dose in PN: 1-2 mEq/kg/day
* 10 mEq of K intravenously increases serum K by ~0.1 mEq/L
* Decrease dose by 50% in renal impairment
84
What type of solutions do you want to avoid in hypokalemia when repleting?
Avoid dextrose solutions; can worsen hypokalemia 2/2 insulin stimulation → ITC shift
85
What electrolyte can cause refractory hypokalemia?
Hypomagnesemia
Can result in refractory hypokalemia 2/2 accelerated renal potassium loss or impairment of Na-K-ATPase pump activity
86
Clinical manifestations of hyperkalemia:
* changes in neuromuscular and cardiac function
* Muscle weakness, paralysis
* ECG changes
* Arrhythmias
87
In hyperkalemia, pts are often asymptomatic until >_ _ _ mEq/L
>5.5 mEq/L
88
Etiology of hyperkalemia
* Traumatic blood draw – hemolyzed specimen
* Excessive intake – usually IV administration
* Altered distribution – acidosis, succinylcholine
* Massive cellular breakdown – intravascular hemolysis, burns, crush injuries, tumor lysis syndrome
Impaired renal excretion ** most often occurs in CKD **
* AKI, CKD 4/5
* ACEI, ARBs, K-sparing diuretics, aldosterone antagonists, NSAIDs, trimethoprim, tacrolimus
89
# Meds:
Treatment of hyperkalemia (>6) or changes in ECG:
Stabilize myocardium
Calcium gluconate
| Does NOT remove potassium
90
# Meds:
Treatment of hyperkalemia (>6) or changes in ECG:
Shift potassium intracellularly
* Insulin +/- 50% dextrose
* Sodium bicarb
* Albuterol
91
# Meds:
Treatment of hyperkalemia (>6) or changes in ECG:
Remove potassium
* Furosemide
* Sodium polystyrene sulfonate
* Patiromer (not for acute use)
* Sodium zirconium cyclosilicate (not for acute use)
* HD
92
Where is Magnesium found?
Mostly found in ICF (second most abundant intracellular cation)
93
Where is Magnesium absorbed?
Distal jejunum and ileum
94
How is magnesium regulated/excreted?
Regulated by GI tract, kidney, and bone
95
What are some of magnesium's functions?
* Enzyme cofactor: glucose metabolism, fatty acid synthesis and breakdown, and DNA and protein metabolism
* Maintenance of Na-K-ATPase pump / cell membrane action potential
* Neuromuscular transmission
* Cardiovascular tone
* Muscle contraction
96
Concomitant electrolyte abnormalities in hypomagnesemia:
**Potassium and calcium**
* Both refractory to treatment until magnesium deficit is corrected
97
How can hypomagnesemia impact insulin and glucose?
* May reduce insulin sensitivity and glucose cellular uptake
* Impair insulin secretion
* Reduce lipoprotein lipase
98
Etiology of hypomagnesemia:
* Poor PO intake
* Malabsorption or GI losses
* --Small bowel diseases, gastric bypass, alcoholism, laxatives, diarrhea
* Intracellular shift with insulin, refeeding, DKA, MI, hyperthyroidism
* Increased renal excretion
* CRRT
99
_ _ _ mEq of IV Mg increases serum Mg by _ _ _ mg/dL
8 mEq of Mg IV increases serum Mg by ~0.1 mg/dL
| In healthy individuals
100
Parenteral IV Magnesium:
what is the max rate and why?
* Do not exceed 1 g/hr (8 mEq/h)
→ 50% of dose can be lost in urine
* Adverse effects – phlebitis, injection site pain
101
How much should you reduce magnesium dosing in renal insufficiency?
Reduce empirical dose by 50% in renal impairment to avoid causing hypermagnesemia
102
What long term medication use may be associated with hypomagnesemia?
Long term PPI use may be associated with hypomagnesemia
* May not correct even with magnesium supplementation
* H2 blockers do not have this effect
103
Hypermagnesemia
Typically associated with renal dysfunction and Mg intake
104
Calcium is essential for;
* Normal muscle contraction
* Nerve function
* Blood coagulation
* Bone formation
105
Metabolically active form of calcium:
Iionized fraction of calcium
* Ionized calcium – most accurate method to assess calcium abnormalities
* Important in critical illness
106
How is calcium excreted?
Excess calcium is excreted in the urine
107
Calcium regulation:
* Vitamin D
* PTH
* Calcitonin
* Phosphorous
* pH
* Metabolic alkalosis
* Vitamin D (increases)
* Parathyroid hormone (increases)
* Calcitonin (decreases)
* Phosphorus (decreases ionized calcium level)
* pH (affects albumin binding)
* Metabolic alkalosis (decreases ionized calcium level)
108
Hypocalcemia occurrences:
**Frequently occurs 2/2 hypoalbuminemia**
Common in:
* Critically ill patients
* Sepsis
* Rhabdomyolysis
* Massive blood transfusions
109
How do massive blood transfusions affect calcium levels?
Xfusions 2/2 citrate preservative in blood bank binding with serum calcium
110
What is a side effect of PO calcium?
Constipation
111
Calcium chloride may cause:
Tissue necrosis if extravasation occurs
112
Management of hypocalcemia
* Correct **hypomagnesemia** if present (reduced parathyroid hormone)
* Hyperphosphatemia may require phos binders prior to calcium repletion to reduce the risk of soft tissue calcification
* Oral vitamin D therapy
* Parenteral calcium therapy
113
Causes of hypercalcemia:
acute vs chronic
* Acute > hypercalcemia of malignancy
* Chronic > primary hyperparathyroidism
114
Why does severe hypercalcemia (>14 mg/dL) require immediate treatment?
→ acute renal failure, obtundation, ventricular arrhythmias, coma, death
115
First step in treating hypercalcemia
Aggressive IV hydration – reverse volume depletion caused by hypercalcemia
116
Additional steps in treating hypercalcemia
* Calcitonin – rapid onset; tachyphylaxis ~ 48 hours
* HD – life threatening or in CKD
* Bisphosphonates – slower onset (4-10 days), longer duration / maintenance therapy
* Steroids – decreases calcitriol production and reduces intestinal calcium absorption
* Surgery (primary hyperparathyroidism)
| Tachyphylaxis: acute, sudden decrease in response to a drug after admin
117
What medication is controversial in tx of hypercalcemia?
Loop diuretics
* Enhance renal calcium excretion
* Requires vigilant monitoring to avoid further volume depletion
118
Phosphorous funtions:
* Essential part of nucleic acids, phospholipid membranes and nucleoproteins
* Key role in macronutrient metabolism
* Provides energy-rich bonds in ATP
* Bone and cell membrane composition
* Muscular function – especially myocardium and diaphragm
119
Primary causes of ITC shifts of phos
CHO and insulin, catecholamines, alkalosis
120
Release of Phos from cell → ECF:
cellular destruction, and acidosis
121
Hypophosphatemia symptoms:
Symptoms: neurologic, neuromuscular, cardiopulmonary, hematologic
122
Etiologies of hypophosphatemia
* Poor PO intake
* Critical illness
* Alcoholism
* Respiratory and metabolic alkalosis
* Poor absorption
* Phosphate binders, vitamin D deficiency, laxatives, diarrhea
* Increased renal excretion
* RRT
* Intracellular shifts
123
Why are dosing recommendations of phosphorous empirical?
Because serum phosphorous concentrations may not accurately reflect total body stores
124
Infusion rate shouldn’t exceed _ _ _ mmol/hr
Why?
Infusion rate shouldn’t exceed 7 mmol/hr
Faster infusion rates can cause thrombophlebitis and soft tissue calcium-phosphate deposition
125
Hyperphosphatemia
Rare, typically associated with renal dysfunction / CKD
126
Additional causes of hyperphosphatemia
* Endogenous release of phos into ECF from cellular destruction
* Massive trauma
* Cytotoxic agents - esp in tx of lymphomas and leukemias with large tumor burden
* Hypercatabolism
* Hemolysis
* Rhabdomyolysis
* Malignant hyperthermia
* Transcellular shifts of phos from ICF to ECF 2/2 respiratory or metabolic acidosis
127
Respiratory or Metabolic **Acidosis** + Phosphorous
Hyperphosphatemia
shifts of phos from ICF to ECF
128
Respiratory or Metabolic **Alkalosis** + Phosphorous
Hypophosphatemia
shifts of phos from ECF → cell
129
Treatment of hyperphosphatemia:
Reduced intake, phosphate binders
130
Gastric fluid loss replacement
0.45% NaCl (1/2 Normal Saline) + 10-20 mEq KCl/L
131
**Stomach**
mEq/L
sodium, chloride, potassium, bicarb
* Na: 60 mEq
* Cl: 130 mEq
* K: 15 mEq
* HCO3: 0 mEq
132
**Duodenum**
mEq/L
sodium, chloride, potassium, bicarb
* **Na: 140 mEq**
* Cl: 80 mEq
* K: 5 mEq
* HCO3: 0 mEq
133
**Pancreas**
mEq/L
sodium, chloride, potassium, bicarb
* **Na: 140 mEq**
* Cl: 75 mEq
* K: 5 mEq
* **HCO3: 115 mEq**
134
**Bile**
mEq/L
sodium, chloride, potassium, bicarb
* **Na: 145 mEq**
* Cl: 100 mEq
* K: 5 mEq
* **HCO3: 35 mEq**
135
**Ileum**
mEq/L
sodium, chloride, potassium, bicarb
* **Na: 140 mEq**
* Cl: 104 mEq
* K: 5 mEq
* **HCO3: 30 mEq**
136
**Colon**
mEq/L
sodium, chloride, potassium, bicarb
* Na: 60 mEq
* Cl: 40 mEq
* K: 30 mEq
* HCO3: 0 mEq
137
Small bowel fluid loss replacement
* Balanced crystalloid (e.g., Ringers Lactate, Plasmalyte)
* Bicarbonate or acetate-based customized fluid
* 0.9% NaCl (Normal Saline)
138
Rapid infusion of phosphate can result in tetany due to
## Footnote
ASPEN self assessment - PN
an abrupt decrease in serum calcium concentration
139
Thiazide diuretics
* act solely in the distal tubules
* do not interfere with urinary concentration and the ability of antidiuretic hormone to promote water retention
* use can cause hyponatremia in older patients
