Fluids, Electrolytes, and Acid-Base Disorders Flashcards
1
Q
What factors affect the percentage of total body water (TBW)?
A
Weight, age, sex, and relative amount of body fat
2
Q
Equation for calculating Free Water Deficit
A
Free Water Deficit = TBW x [1 - (140/Serum Sodium in mEq/L)]
3
Q
Which body tissue is the least hydrated?
A
Adipose tissue
4
Q
What are the 3 compartments of TBW distribution?
A
Intracellular fluid, extracellular fluid, and transcellular fluid
5
Q
Which fluid compartment is the most clinically important?
A
Extracellular fluid because it contains the intravascular and interstitial spaces
6
Q
What is osmotic pressure and why is it of clinical importance?
A
The pressure required to maintain equilibrium with no net movement of solvent. Prime importance in determining the distribution of water between the extracellular and intracellular spaces
7
Q
Equation for calculating lean body weight (LBW) for males and females
A
LBW (women) = 1.07 x weight (kg) - 148 x [weigh (kg)/height (cm)]^2
LBW (men) = 1.1 x weight (kg) - 128 x [weight (kg)/height (cm)]^2
8
Q
Describe the composition of D5W (5% dextrose) including its tonicity
A
Provides 50 g dextrose per liter
Hypotonic
No electrolytes
1000 ml/L free water
9
Q
Describe the composition of 0.225% NaCl (1/4 normal saline) including its tonicity
A
Hypotonic
Provides 38.5 mEq/L Na, 38.5 mEq/L Chloride
10
Q
Describe the composition of 0.45% NaCl (1/2 normal saline) including its tonicity
A
Hypotonic
Provides 77 mEq/L Na, 77 mEq/L Chloride
500 ml/L free water
11
Q
Describe the composition of 0.9% NaCl (normal saline) including its tonicity
A
Isotonic
Provides 154 mEq/L Na, 154 mEq/L Chloride
0 ml/L free water
12
Q
Describe the composition of 3% NaCl (hypertonic saline) including its tonicity
A
Hypertonic
Provides 513 mEq/L Na, 513 mEq/L Chloride
-2331 ml/L free water
13
Q
Describe the composition of Lactated Ringers (LR) including its tonicity
A
Isotonic
Provides 130 mEq/L Na, 109 mEq/L Chloride, 4 mEq/L K+, 3 mEq/L Calcium
0 ml/L free water
14
Q
Describe the composition Albumin in 0.9% NaCl including its tonicity
A
Isotonic
Provides 154 mEq/L Na and 154 mEq/L Chloride
15
Q
Describe the water distribution of 1 L IV Dextrose in water to extracellular fluid and intracellular fluid
A
333 mL ECF (250 mL interstitial fluid + 83 mL intravascular fluid)
667 mL ICF
16
Q
Describe the water distribution of 1 L IV 0.9% NaCl (normal saline) to extracellular fluid and intracellular fluid
A
1000 mL ECF (750 mL interstitial fluid + 250 mL intravascular fluid)
0 mL intracellular fluid
17
Q
What fluid requirement calculations are recommended in individuals age 65 years or older to prevent dehydration?
A
- An adjusted Holliday-Segar formula (1500 mL for the first 20 kg body weight + 15 mL/kg for remaining body weight)
- 30 mL/kg with a minimum of 1500 mL
- 1500-2000 mL/day
18
Q
List some clinical conditions which would require the addition of fluid
A
Patients with severe diarrhea or emesis; large draining wounds; excessive diaphoresis; constant drooling; paracentesis losses; drains; high gastric fistula and ostomy outputs; persistent fevers; lactation
19
Q
Explain the 2 equations some clinicians have success using for fluid requirements when the average between the 2 formulas is used
A
Equation 1 (based on body weight and age):
Age 18-55: 35 mL x body weight (kg)
Age 56-75: 30 mL x body weight (kg)
Age >75: 25 mL x body weight (kg)
Fluid-restricted adults (kidney/cardia disease or fluid overload states) </= 25 mL x body weight (kg)
Equation 2 (Holliday-Segar formula adjusted for age)
Age </=50 years: 1500 mL for first 20 kg body weight + [20 mL x remaining body weight (kg)]
Age >50 years: 1500 mL for first 20 kg body weight + [15 mL x remaining body weight (kg)]
20
Q
What is the calculation for obesity-adjusted weight?
A
Obesity-Adjusted Body Weight (lb) = [(Actual Weight - IBW) x 0.25] + IBW
21
Q
When is an obesity-adjusted weight often used?
A
When an individual’s weight is equal to or greater than 125% IBW unless the excess weight is due to muscle mass
22
Q
Calculate the fluid requirements for a 61 year old woman who is 5’4” tall and weighs 160 lb
A
BMI is 27.5, patient is 133% IBW
1. Calculate IBW: 100 lb + (5x4 lb) = 120 lb
2. Calculate obesity-adjusted weight: [(160-120)] x 0.25] + 120 = 130 lb (59 kg)
3. Calculate fluid requirements using Equation 1: 30 mL x 59 kg = 1770 mL/day
4. Calculate fluid requirements using Equation 2: 1500 mL + [15 x (59kg - 20kg)] = 2085 mL/day
5. Calculate the mean of the results from steps 3 and 4: (1770 + 2085)/2 = ~1900 mL/day
23
Q
How would you manage maintenance fluids for a patient with heart failure?
Patient info: 65 y/o male, current weight 75 kg (IBW 66 kg), admit w/ 3+ pitting edema BLE receiving 8L/min O2, given 0.9% NaCl at 125 ml/hr, O2 requirements subsequently increased
A
Heart failure pt with evidence of fluid overload should be treated with loop diuretics and sodium and fluid restrictions. Start this patient on IV furosemide and change IV fluids to 0.45% NaCl at 10 mL/hr to maintain IV access. For pt with heart failure, fluid intake should be approximately 20-25 mL per kg estimated dry weight and clinical symptoms of fluid overload should be taken into account. Sodium intake restricted to <2000 mg/day (87 mEq). This patient received 3 L maintenance IV fluids which contributed to further respiratory decompensation requiring aggressive diuresis
24
Q
List the volume and average electrolyte composition of saliva
A
1.5 L/day, 10 mEq/L Na, 26 mEq/L K+, 10 mEq/L Chloride, 30 mEq/L bicarbonate (HCO3-)
25
List the volume and average electrolyte composition of the stomach
1.5 L/day, 60 mEq/L Na, 10 mEq/L K+, 130 mEq/L Chloride, 0 bicarbonate
26
List the volume and average electrolyte composition of the duodenum
Variable volume, 140 mEq/L Na, 10 mEq/L K+, 80 mEq/L Chloride, 0 bicarbonate
27
List the volume and average electrolyte composition of the ileum
3 L/day, 140 mEq/L Na, 5 mEq/L K+, 104 mEq/L Chloride, 30 mEq/L bicarbonate
28
List the volume and average electrolyte composition of the colon
Variable volume, 60 mEq/L Na, 30 mEq/L K+, 40 mEq/L Chloride, 0 bicarbonate
29
List the volume and average electrolyte composition of the pancreas
Variable volume, 140 mEq/L Na, 5 mEq/L K+, 75 mEq/L Chloride, 115 mEq/L bicarbonate
30
List the volume and average electrolyte composition of bile
Variable volume, 145 mEq/L Na, 5 mEq/L K+, 100 mEq/L Chloride, 35 mEq/L bicarbonate
31
What are the treatment considerations in general if the electrolyte level is below normal range?
Consider available administration routes (IV access peripheral vs central), GI tract function, renal function, fluid status, concurrent electrolyte abnormalities, product availability
32
What are general potential treatments if an electrolyte level is above normal range?
Remove exogenous sources, discontinue offending agents or medications, facilitate elimination of electrolyte, treat other conditions that may be contributing to disorder
33
Normal sodium level?
Mild hyponatremia:
Moderate hyponatremia:
Severe hyponatremia:
Normal range 135-145 mEq/L
Mild: 130-135 mEq/L
Moderate: 125-129 mEq/L
Severe: <125 mEq/L
34
Difference between osmolality and osmolarity?
Osmolality is a measurement of concentration per weight (mOsm/kg H2O)
Osmolarity is a measurement of concentration per volume (mOsm/L)
Serum osmolality and osmolarity are used interchangeably since 1 L of H2O weighs 1 kg
35
Clinical manifestations of hyponatremia related to central nervous system dysfunction are more likely when the serum sodium concentration drops below ___, gradually or rapidly?
Below 120 mEq/L, rapidly
36
How does the rate of correction differ between acute vs chronic hyponatremia?
Acute hyponatremia correction can occur at the same rate of onset of hyponatremia (patients are often symptomatic)
Chronic hyponatremia requires slow correction because these patients have adapted to lower serum sodium levels
37
What is the recommended rate of correction for acute and chronic hyponatremia?
10-12 mEq/L per day for acute
6-8 mEq/L per day for chronic or unknown duration
38
Explain hypertonic hyponatremia
Caused by the presence of osmotically active substances other than sodium in the ECF (hyperglycemia and hypertonic infusions such as dextrose and mannitol)
39
What are the 3 main types of hypotonic hyponatremia?
Hypovolemic, euvolemic, and hypervolemic
40
What are the treatment goals for hypovolemic hyponatremia? Euvolemic? Hypervolemic?
Hypovolemic: volume expansion (for both urine Na < or > 20 mEq/L) with isotonic fluids to expand the ECF volume
Euvolemic: water restriction (500-1000 ml/day)
Hypervolemic: sodium and water restriction
41
Explain hypovolemic, euvolemic, and hypervolemic hyponatremia
Hypovolemic: losing more sodium than water
Euvolemic: urine osmolality is always greater than serum osmolality and urine sodium is >20 mEq/L, stable sodium intake/output but retain additional amounts of water, kidneys are inappropriately concentrating urine and volume status is adequate
Hypervolemic: have some element of end-organ damage (renal failure, liver failure with ascites, heart failure), resulting in fluid retention or third spacing; retain more water than sodium
42
What are the extrarenal loss causes of hypovolemic hypotonic hyponatremia?
Fluid losses from excessive sweating, GI loss (vomiting, diarrhea, fistula drainage, NG suction, ostomy drainage), open wounds, fluid drains or third spacing/sequestration (burns, effusions, peritonitis, ascites, pancreatitis, intestinal obstruction)
43
What are the renal loss causes of hypovolemic hypotonic hyponatremia?
Fluid loss from the use of diuretics, osmosis diuresis, salt-wasting nephropathy, mineralocorticoid deficiency, pseudohypoaldosteronism, bicarbonaturia
44
What are the causes of euvolemic hypotonic hyponatremia?
SIAD (syndrome of inappropriate antidiuresis), hypothyroidism, drug induced, reset osmostat, hypopituitarism, psychogenic polydipsia
45
What are the edema-forming state causes of hypervolemic hypotonic hyponatremia? What is the other cause?
Disorders associated with edema: heart failure/CHF, nephrotic syndrome, hepatic cirrhosis
Acute and chronic renal failure
46
Describe hypovolemic hypernatremia and the treatment
Deficit of both sodium and water but water losses exceed sodium losses; need to determine source of fluid loss; treatment involves volume expansion by replacing hypotonic fluids (isotonic saline) via enteral or parenteral route
47
What are the extrarenal and renal fluid loss causes of hypovolemic hypernatremia?
Extrarenal: profuse sweating, severe diarrhea, respiratory losses
Renal: diuretics, glycosuria, obstructive uropathy, acute/chronic renal failure
48
Describe euvolemic hypernatremia, common causes, and treatment
Decrease in total body water, but total body sodium remains normal; commonly caused by diabetes insipidus (central or nephrogenic); treated by replacing water deficit and removing and/or treating the underlying cause; desmopressin challenge to determine if central or nephrogenic
49
What is the difference between central and nephrogenic diabetes insipidus?
Central is an impairment of ADH secretion; nephrogenic occurs when kidneys cannot respons to ADH circulating in the serum
50
Describe hypervolemic hypernatremia, common causes, and treatment
An increase in total body sodium and total body water may be normal or increased. Common causes are iatrogenic (overadministration of sodium-containing IV fluids) and mineralocorticoid excess (Cushing's syndrome, adrenal hyperplasia). Treated by correcting underlying disorder, administering diuretics (furosemide), and replacing water deficit
51
How do you calculate free water deficit for the initial replacement volume?
Free water deficit = TBW (total body water in L) x [1 - (140/serum Na)]
52
Correction rate for chronic and acute hypernatremia
Due to risk of cerebral edema. Should not exceed 10 mEq/L/day in chronic or unknown duration; may correct at a rate of 2 mEq sodium per L per hour until serum sodium reaches 145 mEq/L
53
Calculate free water deficit for a 78 year old woman (60 kg) with serum sodium level 165 mEq/L
TBW for women = LBW x 0.5
LBW for women = 1.07 x weight in kg - 148 x (weight in kg/height in cm)^2
Free water deficit = TBW x [1 - (140/serum sodium)]
54
Mainstay treatment for SIAD?
Restrict fluids to 500-1000 ml/d. If symptomatic, administer exogenous salt. If refractory to conventional treatment, may require pharmacologic therapy with loop diuretics and/or vasopressin-2 receptor antagonists (conivaptan, tolvaptan)
55
Normal potassium concentration?
3.5-5 mEq/L
56
Where is most of the body's potassium located?
Inside the cells
57
What are normal daily potassium requirements?
0.5-2 mEq/kg
1 gm of potassium = 25 mEq of potassium
adequate potassium intake is 40-50 mEq (1600-2000 mg/day)
58
Which factors are the most important in the influence of the regulation of the internal distribution of potassium?
The Na-K-ATPase pump and the plasma potassium concentration
59
Range for mild, moderate, and severe hypokalemia
Mild: 3-3.5 mEq/L
Moderate: 2.5-2.9 mEq/L
Severe: <2.5 mEq/L
60
Drug-induced causes of hypokalemia occur in what 3 ways?
Increased renal potassium loss/excretion, excess/increased loss in stool, and transcellular shift (potassium shift from ECF to ICF)
61
When are patients with hypokalemia more likely to be symptomatic?
Commonly asymptomatic in mild disorders, symptoms occur with more severe cases
62
Symptoms of moderate and severe hypokalemia?
Nausea, vomiting, lassitude, constipation, generalized weakness, cardiac arrhythmias, rhabdomyolysis, paralysis leading to respiratory compromise, death
63
Nonmedication causes of hypokalemia from loss in stool?
Infectious diarrhea, tumors, jejunoileal bypass, enteric fistula, malaborption, intestinal ion-transport defects, cancer therapy, geophagia
64
Nonmedication causes of hypokalemia from loss in urine?
Mineralocorticoid excess, primary hyperaldosteronism, congenital adrenal hyperplasia, renin-secreting tumors, extopic corticotrophin syndrome, Cushing's syndome, glucocorticoid-responsive aldosteronism, renovascular hypertension, malignant hypertension, vasculitis, apparent mineralocorticoid excess, Liddle's syndome, 11beta-hydroxysteroid hydrogenase deficiency, impaired chloride-associated sodium transport, Bartter's syndrome, Gitelman's syndrome
65
Describe the treatment options for the following scenario: 78 year old woman (60 kg) w/ h/o uncontrolled hypertension presents with 5 day history of N/V, fever, fatigue. BP low, unable to keep food down, decreased skin turgor and dry mucous membranes. Na level 165 mEq/L, BUN 26, creatinine 0.86, urine sodium <5 mEq/L, all other labs WNL
Vital signs reflect hypovolemia, urine sodium level is consistent with sodium conservation and hypovolemia, differential diagnosis includes extrarenal losses from history of vomiting and high fevers. Treatment options include correction of water deficit slowly over a period of at least several days bc hypernatremia is likely chronic based on the onset of vomiting. Calculate water deficit (= 5.3 L). Administer hypotonic fluids IV to correct half of the water deficit (2.65 L) in the first 24 hours.
0.45% NaCl (1/2 normal saline): 1L only contributes 500 mL toward the water deficit so approximately 5.3L will be needed in the first 24 hours.
Dextrose 5% in water: 1L contributes 1000mL toward the water deficit so approximately 2.65L will be needed in the first 24 hours
66
Potential causes of transcellular shifts of potassium into the cells?
Metbolic alkalosis and increases in insulin and catecholamiones (epinephrine or norepinephrine)
67
Hypokalemia is often refractory to treatment in the setting of what other electrolyte deficiency?
Hypomagnesemia
68
What are the goals of therapy for hypokalemia?
Avoidance or resolution of symptoms, restoring the serum potassium concentration to normal, and preventing hyperkalemia
69
IV replacement dosing guidelines for hypokalemia in patients with normal renal function
Serum potassium 3-3.5 mEq/L: IV not recommended 20-40 mEq
Serum potassium 2.5-2.9 mEq/L: IV potassium 40-80 mEq
Serum potassium <2.5 mEq/L: IV potassium 80-120 mE
70
What are the available variations of IV potassium supplements?
Available as chloride, acetate, and phosphate salts
71
When is potassium acetate use as an alternative to potassium chloride?
In the presense of a metabolic acidosis because acetate is converted to bicarbonate by a normally functioning liver
72
Why is oral correction of hypokalemia generally safer than IV correction?
Reduces the risk of overcorrection and rebound hyperkalemia
73
What dosage of oral potassium is generally sufficient to prevent hypokalemia? What dosage may be required to treat hypokalemia?
10-30 mEq/day for prevention, 40-100 mEq/day for treatment
74
How are potassium supplements best administered orally?
In a moderate dosage over a period of several fays to 1 week to achieve complete potassium repletion
75
When is IV potassium supplementation reserved for?
For the treatment of severe hypokalemia or when the condition of the GI tract precludes the use of oral agents
76
What precaution should be taken if potassium infusion exceeds 10 mEq/hour?
Continuous cardiac monitoring to detect any signs of hyperkalemia
77
Total daily potassium supplementation in most cases should not exceed:
40-100 mEq/day (or 0.5 to 1.2 mEq/kg/day)
78
Potential complications of peripheral potassium infusion?
Phlebitis and burning
79
Caveats to consider when replacing a potassium deficit
Consider the dilutant (dextrose versus saline) and the presense of hypomagnesemia
80
Why should dextrose solutions be avoided when replacing a potassium deficit?
May worsen the hypokalemia by stimulating insulin release that promotes an intracellular shift of potassium
81
How would hypomagnesemia result in refractory hypokalemia?
Related to accelerated renal potassium loss or the impairment of Na-K-ATPase pump activity
82
Patients with hyperkalemia are often asymptomatic until levels exceed what value?
>5.5 mEq/L
83
Signs and symptoms of hyperkalemia
Muscle twitching, cramping, weakness, ascending paralysis, electrocardiogram changes, and arrhythmias
84
How does metabolic acidosis result in an extracellular potassium shift?
Some of the excess hydrogen ions are buffered intracellulary
85
In general, for every 0.1 decrease in pH, potassium will increase by an average of:
0.6 mEq/L (but the increase can range from 0.3-1.3 mEq/L)
86
What are the various mechanisms for drug-induced hyperkalemia?
Impaired renal potassium excretion, increased potassium input, potassium shift from ICF to ECF
87
Goals of therapy for treating hyperkalemia
Antagonizing the cardiac effects of potassium, reversing symptoms (if present), and returning the serum potassium concentration to normal. All sources of exogenous potassium and other medications that can cause hyperkalemia should be discontinued if feasible.
88
When should IV Calcium gluconate be given to treat hyperkalemia?
When patient is symptomatic and those with electrocardiogram changes to restore membrane excitability to normal.
89
Which medication treatments for hyperkalemia cause potassium to move intracellularly?
Insulin and dextrose, sodium bicarbonate, and beta2-adrenergin agonists
90
Which treatments for hyperkalemia facilitate potassium removal?
Loop and thiazide diuretics, cation-exchange resins (sodium polystyrene sulfonate), and dialysis
91
Normal magnesium concentration
Normal serum concentration = 1.5-2 mEq/L (or 1.8-2.4 mg/dL)
92
Total body magnesium content and distribution throughout the body
Total body magnesium content is 25 gm (2000 mEq). 50-60% is in bone, the rest is located in cardiac muscle, skeletal muscle, and the liver. 2% in the ECF
93
Mg absorptive capacity may be as low as __% on a high Mg diet, and as high as __% on a low Mg diet
25%
75%
94
What factors may impair intestinal absorption of Mg?
High phosphate diets and high fiber foods containing phytate
95
Concomitant electrolyte abnormalities in the setting of Mg deficiency that are refractory to treatment until Mg deficit is corrected?
Hypokalemia and hypocalcemia
96
General etiologies of hypomagnesemia?
Decreased intake or absorption, excessive losses, or redistribution into the ICF
97
What are common causes of reduced Mg intake or absorption?
Protein-energy malnutrition, prolonged administration of Mg-free IV fluids or PN, alcoholism, presence of an ileostomy or colostomy, malabsorption syndromes, short bowel syndrome, and intestinal bypass operations
98
Non-medication related renal loss causes of hypomagnesemia?
Acute tubular necrosis, renal tubular acidosis, Barter syndrome, hyperaldosteronism, hypercalcemic states including malignancy, post-obstructive diuresis, renal transplant, glucosuria-induced osmotic diuresis in DM
99
Drug-induced renal loss causes of hypomagnesemia?
Thiazide and loop diuretics, cisplatin, cyclosporine, amphotericin B, aminoglycosides, foscarnet, PPIs, digoxin, alcohol
100
When might intracellular shifts of Mg be seen?
During refeeding, DKA, hyperthyroidism, acute MI
101
Why might serum Mg levels not correlate with intracellular concentrations or total body Mg levels?
Because only 1-2% of total body Mg is located in the ECF
102
Why is IV administration of Mg preferred over oral?
Issues with oral administration, slow onset of action, GI intolerance
103
What is the maximum infusion rate of magnesium sulfate and why?
Should not exceed 1gm/hr (8 mEq/hr) in asymptomatic patients because more than 50% of the dose may be lost in the urine as renal magnesium reabsorption is exceeded
104
Expected serum Mg changes with IV treatment of hypomagnesemia?
Serum Mg change of 0.1 mg/dL for each gram (8 mEq) administered, although the plasma concentration typically takes up to 48 hours after the bolus to equilibrate
105
Guidelines for treatment in the first 24 hours of hypomagnesemia according to severity:
Mild (1.3-1.5 mEq/L [1.5-1.8 mg/dL])
Moderate (0.8-1.2 mEq/L [1-1.4 mg/dL])
Severe (<0.8 mEq/L [<1 mg/dL])
Mild = 0.5 mEq/kg
Moderate = 1 mEq/kg
Severe = 2 mEq/kg
106
Clinical presentation/manifestation of hypomagnesemia?
Primarily associated with other electrolyte abnormalities. Neuromuscular symptoms (muscle fasciculations, tremors, hyperreflexia, paresthesias, positive Chvostek's and Trousseau's signs, myalgias, tetany, myoclonic jerk); Cardiac (V.fib, ventricular tachycardia, PR prolongation, QT prolongation, torsades de pointes); Metabolic (hypokalemia, hypocalemia); CNS (nystagmus, seizures, depression, agitation, psychosis, disorientation, confusion, hallucinations, irritability, restlessness)
107
Define hypermagnesemia
Serum Mg level >2.8 mg/dL
108
Etiology and symptoms of hypermagnesemia?
Occurs in the setting of CKD in combination with Mg intake. Generally well tolerated but can affect neurological, neuromuscular, and cardiac function when levels exceed 4.8 mg/dL. Symptoms include nausea, vomiting, diaphoresis, flushing sensation of heat, depressed mental functioning, drowsiness, muscular weakness, loss of deep tendon reflexes, hypotension, bradycardia
109
Treatment for symptomatic and asymptomatic hypermagnesemia?
Symptomatic: IV calcium (chloride or gluconate) administered to reverse cardiac and neuromuscular effects
Asymptomatic: removal of exogenous sources of Mg (PN and IV fluids), Mg restriction, loop diuretics
110
Normal serum calcium (Ca2+) level?
8.6-10.2 mg/dL
111
Low serum calcium concentrations stimulate which functions?
Release of PTH which increases bone resorption, augments renal conservation of calcium, and activate vitamin D, which in turn increases intestinal calcium absorption
112
What is the purpose of calcitonin and when is it released?
Released by the thyroid gland in response to elevated serum calcium concentrations and acts to inhibit bone resorption and increase urinary calcium excretion
113
What 3 forms does serum calcium exist in and which is the metabolically active form that is of greatest physiological importance?
Complexed, protein bound, and ionized. Ionized
114
Normal range of ionized calcium?
1.12-1.3 mmol/L
115
What is the equation for adjusting total calcium with hypoalbuminemia?
Corrected Total Serum Calcium = Measured Total Serum Calcium + [0.8 x (4 - serum albumin)]
116
True or False: Hypoalbuminemia decreases total serum calcium and ionized calcium levels
False. Does not affect ionized calcium levels
117
Range for hypocalcemia and its most frequent cause?
Total serum calcium <8.6 mg/dL or ionized calcium less than 1.12 mmol/L
Hypoalbuminemia
118
Causes of hypocalcemia?
Decreased vitamin D activity (vitamin D deficiency, hyperphosphatemia, pseudohypoparathyroidism), decreased PTH activity (acute pancreatitis, hypomagnesemia, hypoparathyroidism), citrate anticoagulation during CRRT, hungry bone syndrome (can occur after total parathyroidectomy or thyroidectomy)
119
Conditions in critical illness that are associated with hypocalcemia?
Sepsis, rhabdomyolysis, massive blood transfusion (secondary to citrate preservative in the blood bank binding with serum calcium)
120
What are some drugs implicated in the etiology of hypocalcemia?
Biphosphonates, calcitonin, furosemide, foscarnet, and long-term therapy with phenobarbital and phenytoin
121
Clinical manifestations of hypocalcemia?
Cardiovascular: hypotension, decreased myocardial contractility, or prolonged QT interval
Neuromuscular: distal extremity paresthesias, Chvostek sign, Trousseau sign, muscle cramps, tetany, seizures
122
What is the empirical treatment for acute hypocalcemia?
Serum ionized calcium 1-1.2 mmol/L = 1-2 gm (4.65-9.3 mEq) calcium gluconate over 1-2 hours
Serum ionized calcium <1 mmol/L = 2-4 gm (9.3-18.6 mEq) calcium gluconate over 2-4 hours
123
What is the limiting factor for using calcium chloride to correct acute symptomatic hypocalcemia even though it contains 3 times more elemental calcium than an equivalent amount of calcium gluconate?
It may cause tissue necrosis if extravasation occurs
124
How can chronic or asymptomatic hypocalcemia be treated?
With oral calcium supplements and vitamin D
125
Range for hypercalcemia and its most frequent causes?
Total serum calcium >10.2 mg/dL or ionized calcium >1.3 mmol/L
Most often occurs with hyperparathyroidism and cancer with bone metastases (primarily breast cancer, lung cancer, and multiple myeloma)
126
Name some causes for hypercalcemia?
Hyperparathyroidism, cancer with bone metastases, toxic levels of vitamin A or D, chronic ingestion of milk and/or calcium carbonate-containing antacids in the setting of renal insufficiency (milk-alkali syndrome), adrenal insufficiency, immobilization, TB, and use of various medications (thiazide diuretics and lithium)
127
Describe some early clinical manifestations of hypercalcemia?
Fatigue, nausea, vomiting, constipation, anorexia, and confusion. Cardiac arrhythmia (bradycardia) in more severe cases
128
Treatment of mild hypercalcemia (total serum calcium 10.3-11.9 mg/dL)?
Usually responds well to hydration and ambulation
129
Range for severe hypercalcemia and potential consequences if not treated immediately?
Total serum calcium greater than or equal to 14 mg/dL. Can lead to acute renal failure, obtundation, ventricular arrhythmias, coma, death
130
What is the treatment for severe hypercalcemia?
IV hydration using 0.9% NaCl should be started promptly at 200-300 ml/hr to reverse the volume depletion caused by hypercalcemia. After adequate hydration is achieved, 40-80mg IV furosemide may be used to enhance renal calcium excretion if the patient is vigilantly monitored to avoid further volume depletion. Calcitonin can be used but tachyphylaxis often limits its usefulness after 48 hours. Hemodialysis may be necessary in life-threatening hypercalcemia or in patients with CKD
131
Normal serum phosphorus concentration?
2.7-4.5 mg/dL
Reflects <1% of total body phosphorus, most found in bones and soft tissue
132
What functions is adequate total body phosphorus needed for?
Necessary for carbohydrate use, glycolysis, maintenance of normal pH, 2,3-diphosphoglycerate synthesis and function (necessary for oxygen release from hemoglobin and ultimately tissue oxygenation), neurologic function, and muscular function
133
What determines serum phosphorus concentration?
Intake, intestinal absorption, renal excretion, hormonal regulation of bone resorption and deposition, and distribution between intracellular shifts of phosphorus
134
What can result in the release of phosphorus from the cell to the ECF?
Cellular destruction and acidosis
135
Define hypophosphatemia and manifestations of it?
Serum phosphorus concentration <2.7 mg/dL
Neurologic: ataxia, confusion, paresthesias
Neuromuscular: weakness, myalgia, rhabdomyolysis
Cardiopulmonary: cardiac and ventilatory failure
Hematologic: reduced 2,3-diphosphoglycerate concentration, hemolysis
136
Conditions in which hypophosphatemia is common
Chronic alcoholism, critical illness, respiratory and metabolic alkalosis, following the treatment of DKA, patients receiving phosphate binders
137
What are limitations of oral phosphate supplementation?
Diarrhea and unreliable absorption
138
Empirical treatment (intravenous) for mild, moderate, and severe hypophosphatemia?
Mild (2.3-2.7 mg/dL) = 0.08-0.16 mmol/kg
Moderate (1.5-2.2 mg/dL) = 0/16-0.32 mmol/kg
Severe (<1.5 mg/dL) = 0.32-1 mmol/kg
139
When should patients receive IV potassium phosphate or sodium phosphate to correct phosphorus levels?
Patients with symptomatic, moderate or severe hypophosphatemia as well as those that cannot tolerate oral phosphate formulations
140
Where is phosphorus actively absorbed and what enhances its absorption? Diminishes it?
2/3 of phosphate is actively absorbed from the proximal small intestine (predominately jejunum). Absorption increased by the presence of vitamin D- and moderate amounts of calcium. Absorption diminished in the presence of a large amount of calcium or aluminum in the intestine (antacids) due to formation of soluble phosphate compounds
141
IV potassium phosphate is preferred for phosphorus replacement except when:
Unless the potassium concentration is >4 mEq/L or renal insufficiency exists
3 mmol potassium phosphate = 4.4 mEq potassium
142
Why should infusion rates of phosphorus not exceed 7 mmol/hour?
Because faster infusion rates can often cause thrombophlebitis and soft tissue calcium-phosphate deposition
143
Hypophosphatemia secondary to intracellular shifts is more likely to occur under what circumstances?
Respiratory alkalosis, after a carbohydrate load, with PN containing inadequate phosphorus, in nutrition recovery, and during androgen therapy
144
General treatment for mild hypophosphatemia?
Can usually be treated by increasing dietary intake or giving an oral supplement
145
Treatment for moderate hypophosphatemia?
Usually can be treated with dietary/oral supplement but may require IV replacement. IV replacement indicated when symptomatic, according to severity of illness, and underlying cause of depletion
146
Scenario: How can complications be prevented when providing nutrition support therapy to a malnourished esophageal cancer patient?
Patient info: 37 y/o M 68 kg, 6', esophageal cancer s/p chemoradiation and esophagectomy admit with progressive wt loss (-10 kg in 2 months) and FTT. J-tube placed hospital day 2, on day 4 pt falls getting out of bed with weakness and pain. EN support was advanced to goal within 24 hours. From hospital day 1 to 4, Na increased, K+ decreased, Mg decreased, Phos decreased
Nutrition support therapy should be advanced cautiously for patients at risk for refeeding. Goal EN rate for scenario patient was 70 ml/hr of a 1.5 kcal/ml formula. Rate was decreased to 20 ml/hr and IV electrolyte replacement ordered, serum chemistry ordered q 12 hours, daily administration of 100mg thiamin added. Scenario patient started on aggressive feeding regimen with no titration which resulted in massive intracellular shift of K+, Mg, Phos that caused symptomatic hypokalemia, hypomagnesemia, hypophosphatemia. Decrease nutrition support therapy to safe rate of 500 kcal/day before further advanced
147
Range for hyperphosphatemia and 3 primary mechanisms for its occurrence?
Serum phosphorus concentration >4.5 mg/dL
Increased phosphorus load, primary increase in renal phosphate reabsorption, and decrease in renal excretion
148
What is the most serious complication of hyperphosphatemia?
Soft tissue and vascular calcification
149
Name some causes of endogenous release of phosphorus into the ECF:
Cellular destruction from massive trauma, cytotoxic agents, neoplastic disease (leukemia and lymphoma), chemo, hypercatabolism, hemolysis, rhabdomyolysis, malignant hyperthermia
150
What causes transcellular shifts of phosphorus from the ICF to the ECF?
Respiratory or metabolic acidosis
151
Recommended dietary phosphorus restriction with hyperphosphatemia?
800-1000 mg/day
152
Describe clinical manifestations of hyperphosphatemia
Anorexia, nausea, vomiting, muscle weakness, hyperreflexia, tetany, tachycardia
153
When does calcification occur in the setting of hyperphosphatemia?
When the calcium-phosphorus product exceeds 55 mg^2/dL
154
Describe consequences of hyperphosphatemia?
Secondary hyperparathyroidism, renal osteodystrophy
155
How can hyperphosphatemia be treated?
Removing or limiting exogenous sources of phosphorus (dietary sources, PN, phosphate-containing enemas or laxatives), Aluminum- and calcium-based phosphate binders, dialysis, volume repletion with normal saline IV, loop diuretic
156
Name potential disadvantages of using an aluminum-based phosphate binder
Risk of bone, hematological and neurological toxicity, constipation
157
Definition of an acid? A base?
A substance that can donate hydrogen ions (H+); A substance that can accept or combine with hydrogen ions
158
Normal range for pH of arterial blood?
7.35-7.45
159
pH below 7.35 is called ___ and a pH greater than 7.45 is called ___
Acidemia; alkalemia
160
Processes that tend to raise or lower the H+ concentration are called ___ and ___ respectively
Acidosis; alkalosis
161
Metabolism of carbohydrates and fats alone results in the daily production of approximately how many mmols of CO2
15,000 mmol
162
Protein metabolism accounts for how many mEqs of daily acid production?
50-100 mEq
163
Name the 3 sequential steps required in the process of H+ regulation
1. Chemical buffering by extracellular and intracellular mechanisms
2. Control of the partial pressure of CO2 in the blood by alterations in the rate of alveolar ventilation
3. Control of the plasma bicarbonate concentration by change in renal H+ excretion
164
What is the principle buffer system? Name other buffer systems
The carbonic acid/bicarbonate system (H2CO3/HCO3-)
Proteins, phosphate, and hemoglobin
165
What is the principle role of the lungs in maintaining acid-base balance?
To regulate the pressure exerted by dissolved CO2 gas in the blood (PCO2)
166
Which chemical is the most powerful respiratory stimulant?
CO2
167
What are the 2 processes that alter renal H+ excretion?
1. Reabsorption of filtered HCO3-
2. Excretion of the H+ produced daily as a result of protein metabolism
168
What is the only organ that is able to regulate levels of alkaline substances in the blood and eliminate acids from the body?
Kidneys
169
Difference between ABG and VBG
ABG (arterial blood gas) reflects the ability of the lungs to oxygenate blood
VBG (venous blood gas) reflects tissue oxygenation
170
Increases in PCO2 represent ___ and decreases in PCO2 represent ___
Acidosis
Alkalosis
171
Increases in HCO3- represent ___ and decreases is HCO3- represent ___
Alkalosis
Acidosis
172
Define the stepwise approach to evaluating acid-base disorders
1. Assess pH of blood to determine whether pt is acidemic (pH <7.4) or alkalemic (pH >7.4). If pH is 7.4, an acid-base disorder cannot be ruled out; a mixed acid-base disorder or compensation may be present
2. Assess PCO2 to determine whether a respiratory process may be contributing. If PCO2 is elevated, patient has respiratory acidosis; if low, patient has respiratory alkalosis
3. Assess serum HCO3- to determine whether metabolic process may be contributing. If HCO3- is elevated, patient has metabolic alkalosis; if low, patient has metabolic acidosis
4. Calculate anion gap to determine whether metabolic acidosis is present. Calculation is critical to determine the etiology of the acid-base disorder and select the appropriate treatment
5. Determine whether acid-base disorder is acute or chronic; determine whether they are appropriately compensated and if not, then patient has mixed acid-base disorder
173
Define PCO2
Provides information on the lungs' ability to excrete CO2
174
Name the blood gas measurements
pH, PCO2, PO2 (partial pressure of oxygen in the blood), SaO2 (oxygen saturation), calculated HCO3-, base excess
175
Define respiratory acidosis
Clinical disorder characterized by a reduced pH, an elevation in the PCO2, and a variable increase in the serum HCO3- concentration. Almost always results from decreased effective alveolar ventilation, not an increase in CO2 production
176
Define respiratory alkalosis
Clinical disturbance characterized by an elevated pH, a decrease in PCO2, and a variable reduction in serum HCO3-. Occurs when effective alveolar ventilation is increased beyond the level necessary to eliminate metabolically produced CO2 (hyperventilation)
177
List common causes of respiratory acidosis
Medications: opioids, anesthetics, sedatives, neuromuscular blockers
Neuromuscular: Guillain-Barre, Myasthenia gravis, MS, ALS, central respiratory depression, head/spinal cord/brainstem/cervical cord injury, stroke, hypophosphatemia
Metabolic: PN or EN overfeeding
Pulmonary/Thoracic disease/complications: massive PE, ARDS, interstitial lung disease, flail chest, pleural disease, pneumothorax, severe pulmonary edema, severe pneumonia, smoke inhalation, COPD, emphysema, bronchitis, asthma, sleep apnea, obesity hypoventilation, hypoxemia, mechanical ventilator hypoventilation
Airway obstruction: foreign body, severe asthma attack/bronchospasm, aspiration, malignancy
Perfusion abnormalities
Cardiac arrest
178
List common causes of respiratory alkalosis
Medications (stimulate CNS respiration): xanthine derivatives, nicotine, catecholamines (epinephrine, norepinephrine, dopamine), salicylate overdose
CNS stimulation of respiration: brain tumors, encephalitis/meningitis, head trauma, vascular accidents, anxiety, pain, fever, pregnancy
Hypoxia: high altitudes, hyperventilation, hypoxemia, pneumonia, pulmonary edema, severe anemia
Peripheral stimulation of respiration: pulmonary embolus, asthma
Other: thyrotoxicosis, cirrhosis, hepatic encephalopathy, mechanical ventilator hyperventilation
179
Define metabolic acidosis
Clinical disturbance characterized by a reduced pH, reduced serum HCO3- concentration, and compensatory hyperventilation resulting in a decrease in PCO2
180
What are the 2 fundamental mechanisms that can induce metabolic acidosis?
1. An inability of the kidneys to excrete the dietary H+ load
2. An increase in the generation of H+ either by the addition of H+ or the loss of HCO3-
181
What is the anion gap?
Represents unmeasured serum anions (proteins, phosphate, sulfate, and organic ions) and unmeasured serum cations (potassium, calcium, magnesium). Useful in the diagnosis of metabolic acidosis. It is equal to the difference between the serum concentrations of the major measured cation and the major measured anions
182
What is the equation for calculating the anion gap?
Anion Gap = (Serum Na) - ([Serum Cl] + [Serum HCO3-])
All values measured in mEq/L
183
What is a normal anion gap?
9 mEq/L (range from 3-11 mEq/L)
184
List common causes of normal (non-) anion gap metabolic acidosis
GI loss of HCO3-: obstructed ileal loop conduit, ketoacidosis, ureterosigmoidostomy, anion-exchange resins, cholestyramine, diarrhea, high output (>1L/day) ostomy, pancreatic/biliary/small bowel fistula
Excessive ingestion of acidic/chloride-based substances: ammonium chloride, overuse of chloride salts in PN
Renal loss of HCO3-: carbonic anhydrase inhibitors, hyperparathyroidism, hypoaldosteronism, type 2 renal tubular acidosis (spironolactone, amiloride)
185
List common causes of increased anion gap metabolic acidosis
Failure to excrete acids: acute and chronic renal failure
Increased production of endogenous acid: ketoacidosis (diabetic, alcohol, starvation), inborn errors of metabolism, lactic acidosis: tissue hypoxia (shock/sepsis), Propofol (doses >80 mcg/kg/min for >48 hr), Metformin use in renal failure, Nitroprusside use, Nucleoside-analog reverse transcriptase inhibitors, carbon monoxide poisoning, liver disease, rhabdomyolysis, seizures, thiamine deficiency
Toxins/overdoses: salicylate, propylene glycol, propyl alcohol, methanol, ethylene glycol
186
Scenario: How would you alter the electrolyte composition of a PN formulation for a patient with an elevated end ileostomy output?
Patient info: 54 y/o F with 30 yr h/o Crohns, multiple small bowel resections with creation of end ileostomy. Admit w/ progressive wt loss and fatigue, elevated ostomy OP (3-4.5 L/day), ARF 2/2 volume depletion. Albumin/Prealbumin 2.1g/dL and 18.6 mg/dL. IV NaCl (0.9%) started @ 125 ml/hr + oral diet. Developed severe metabolic acidosis on day 3 with continued ostomy OP >3L/day. Primarily consuming high fat foods. Na increase, K+ increase, Cl increase, HCO3- decrease, BUN decrease, Creatinine decrease.
PN formulation for high-output ileostomy should contain maximum amounts of acetate salts to prevent and/or correct a hyperchloremic metabolic acidosis. PN started at 50% of estimated energy needs to reduce risk of refeeding and acetate salts maximized. Acetate additives include sodium and potassium and should be tailored for individual needs/tolerance. Sodium concentration of PN should be equal to that of 0.9% NaCl (normal saline) to approximate the sodium concentration of ileostomy fluid. Pt with high OP ileostomies are at risk for acid-base disturbances 2/2 anatomical changes. Management should include fluid replacement that approximates the electrolyte composition of ileal fluid
187
Define metabolic alkalosis
An elevation in the pH, an increase in serum HCO3- concentration, and compensatory hypoventilation resulting in a rise in the PCO2
188
Most commonly observed acid-base disorder in hospitalized patients (33-55% of hospitalized patients with acid-base disturbances)?
Metabolic alkalosis
189
What is saline-responsive metabolic alkalosis?
Urine chloride <20 mEq/L
The increase in HCO3- reabsorption that maintains the alkalosis can be reversed by the administration of half-isotonic or isotonic saline
190
What is saline-resistant metabolic alkalosis?
Urine chloride >20 mEq/L
Characterized by high urinary chloride concentration
191
List causes of saline-responsive metabolic alkalosis
Cystic fibrosis (loss of Cl- in sweat)
Diuretic therapy: loop and thiazide
Excessive HCO3- administration: sodium bicarbonate, citrate, antacids, overuse of acetate salts in PN
GI losses: vomiting, NG suction, gastric fistula, villous adenoma
Rapid correction of hypocapnia
Renal loss
192
List causes of saline-resistant metabolic alkalosis
Cushing's syndrome
Excess mineralocorticoids
Hyperaldosteronism
Profound hypokalemia (serum potassium <2 mEq/L)
Excessive licorice ingestion (chewing tobacco)
Renal artery stenosis
Laxative abuse
Clay ingestion
193
Simple review of the characteristics of the primary acid-base disorders (name the disorder, pH, primary disturbance, and compensatory response)
Metabolic acidosis: pH ↓ , HCOs- ↓ , PCO2 ↓
Metabolic alkalosis: pH ↑, HCO3- ↑, PCO2 ↑
Respiratory acidosis: pH ↓ , PCO2 ↑, HCO3- ↑
Respiratory alkalosis: pH ↑ , PCO2 ↓ , HCO3- ↓
194
With metabolic alkalosis induced by moderate/severe hypokalemia, what is the only way to reverse the metabolic alkalosis?
Administration of potassium chloride. Although adequate NaCl repletion with usually normalize the plasma HCO3- concentration, it will not reverse the metabolic alkalosis
