Fluids/Electrolytes/Acid-Base Flashcards
(138 cards)
1
Q
What is the maintenance of normal blood volume and serum osmolality essential for?
A
proper cell function
-adequate blood volume is required for tissue perfusion
-serum osmolality is an important determinant of intracellular fluid volume (cell size) which is important in the brain
2
Q
What is serum osmolality determined by?
A
serum sodium concentration
3
Q
What do the homeostatic mechanisms for controlling blood volume focus on?
A
controlling sodium balance
4
Q
What do the homeostatic mechanisms for controlling serum osmolality focus on?
A
controlling water balance
5
Q
Provide an overview of body water composition.
A
total body water = 50-60% body weight
2/3 = intracellular fluid
1/3 = extracellular fluid
-3/4 = interstitial fluid
-1/4 = plasma
6
Q
How is ECF osmolality maintained?
A
maintained primarily by sodium
-and its anion counterparts (chloride and bicarbonate)
7
Q
How is ICF osmolality maintained?
A
potassium concentrations
-and its accompanying anion proteins and phosphate
8
Q
What is required for movement of electrolytes?
A
active transport
9
Q
Which fluid compartment are proteins found in?
A
proteins are present within cellular ICF and within blood vessels (albumin) but not in the interstitial ECF
-helps maintain an osmotic gradient between the interstitial fluid and intravascular space of the ECF –> oncotic pressure
10
Q
What can low albumin states lead to?
A
decreased oncotic pressure in blood vessels –> increased fluid in interstitial spaces (ascites, leg swelling, pulmonary edema, etc.)
11
Q
What can rapid and/or extreme changes in osmolality lead to?
A
cell swelling and shrinkage
-plasma hyper-osmolality –> brain cell shrinkage –> somnolence, confusion –> if severe enough –> cerebral bleeding, death
-plasma hypo-osmolality –> brain cell swelling –> HA, NV, gait, instability –> seizures, coma, death
12
Q
What is plasma osmolality?
A
concentration of effective solutes in plasma (relative to water)
13
Q
What is the role of osmoreceptors?
A
sense and respond to changes in plasma osmolality
-specialized cells that recognize changes in plasma osmolality and initiate corrective actions by the release of hormones
-key to regulating water homeostasis
14
Q
What are the important hormones in sodium/water balance?
A
vasopressin (antidiuretic hormone)
aldosterone
natriuretic peptides (ANP and BNP)
15
Q
What can cause the release of vasopressin?
A
increased plasma osmolality (as sensed by osmoreceptors)
non-osmotic stimuli when osmoreceptors in the brain detect decreased circulating blood volume or decreased BP
-volume depletion, poor kidney perfusion, BP maintenance, pain, hypoxia, acidosis
16
Q
What are the results of vasopressin release?
A
increased plasma osmolality:
-water reabsorption in the distal tubule/collecting duct –> excretion of a more concentrated urine
-stimulates thirst
-increase amount of water in circulation, restoring plasma osmolality to normal
non-osmotic stimuli:
-water conservation restores circulating blood volume at the expense of decreased serum osmolality –> dilutional hyponatremia
17
Q
What stimulates release of aldosterone?
A
decreased blood volume or decreased blood pressure
increased serum K+ or decreased serum Na+
18
Q
What is the role of aldosterone?
A
stimulates reabsorption of Na+ from the distal convoluted tubule of the kidney –> increased serum Na+ (and therefore water because water follows Na+) and decreased serum K+
19
Q
What stimulates release of natriuretic peptides?
A
released by the atria/ventricles in response to increased blood pressure and/or increased blood volume
20
Q
What is the role of natriuretic peptides?
A
inhibit the activity of aldosterone by decreasing sympathetic nervous system activity (decrease RAAS activation)
-also increase vasodilation
-have opposite effects of ADH and aldosterone
21
Q
What is the role of the kidneys in serum osmolality?
A
kidney regulates water excretion to keep serum osmolality relatively constant despite variability in water intake
22
Q
How is serum osmolality primarily determined?
A
by sodium concentration
- ~ 90% of the bodys Na+ is extracellular
-sodium is the predominant solute in the ECF
also affected by glucose and urea
23
Q
What is the goal of fluid/electrolyte administration?
A
maintain homeostasis
-best way to do this is to continue eating and drinking normally if possible
24
Q
What are the different ways we lose fluids during a day?
A
fluid loss in urine
fluid loss in stools
insensible fluid loss from skin, respiratory tract
25
What is the minimum amount of fluids needed per day?
~1400 ml (or 60 ml/hr)
26
What does maintenance fluid therapy include?
water
electrolytes (usually 75-175 mEq Na+ and 20-60 mEq K+ per day)
dextrose 100-150 g/day to prevent protein catabolism and starvation ketoacidosis
27
What is volume depletion generally a result of?
generally results from decreased total body Na+ due to renal or extrarenal Na+ loss from the ECF
-renal losses can be due to increased diuresis, salt-wasting nephropathies, mineralocorticoid deficiencies
-extra-renal losses can be due to fluid loss from GIT (vomiting, diarrhea), skin losses (burns), hemorrhage, or increased capillary permeability
28
Why do we need to lose a lot of water to cause volume depletion?
because most of our water is in the ICF (volume contraction assesses ECF and specifically intravascular which only accounts for ~8.5% of total body water)
29
What are the signs and symptoms of hypovolemia?
mild volume depletion may be asymptomatic
severe volume depletion may lead to mental status changes, renal failure, and hypovolemic shock
symptoms: thirst, fatigue, muscle cramps, orthostasis
signs: decreased JVP, decreased sweat, postural hypotension and postural tachycardia
30
What are the lab values that might be seen for a hypovolemic patient?
urine sodium < 15 mEq
FeNa < 1%
urine chloride < 20 mEq confirms volume contraction
increased urine osmolality
*can be helpful but must be correlated with the clinical picture*
31
How can mild hypovolemia be corrected?
orally
32
When do we correct hypovolemia via IV?
symptomatic fluid loss, hemodynamic instability, or intolerance to oral administration necessitates IV therapy
-frequent reassessment of fluid status is required to prevent over-correction
33
What is the goal with hypovolemia treatment?
replenish intravascular volume by expanding ECF compartment (use Na+-based solutions because the Na+ will remain in the ECF)
34
What kind of fluids are used for hypovolemia?
isotonic fluids
-contain Na+ [ ] similar to that of the plasma fluid in the ECF --> therefore will remain in the ECF space
-normal saline (0.9%) generally preferred
35
How are fluids administered for hypovolemia?
as a bolus or at a steady infusion rate
-with symptomatic volume depletion, usually administer 1-2 L bolus to expand intravascular space more quickly
-caution with poor cardiac function or peripheral edema
-watch for volume overload
36
What causes hypervolemia?
may result from a surplus of total body Na+
-disorder of renal Na+ retention
may result from decreased effective circulating volume
-e.g. HF, cirrhosis, or profound hypoalbuminemia
37
Describe the clinical presentation of hypervolemia.
expansion of the interstitial fluid compartment of the ICF may result in peripheral edema, ascites, and pleural effusions
expansion of the intravascular compartment of the ECF may result in increased JVP, pulmonary rales, an S3 heart sound, and elevated BP
symptoms: dyspnea, orthopnea, leg swelling, abdominal distention
-signs and sx do not usually appear until ~ 3-4 L of fluid retention has occurred
38
What are the lab values seen in hypervolemia?
primarily a clinical diagnosis - lab values generally unremarkable
-CXR can help detect pleural effusions or pulmonary edema
39
How is hypervolemia managed?
address the underlying cause
Na+ excess can be managed with:
-dietary Na+ restriction
-diuretics
40
Describe the use of diuretics for hypervolemia.
thiazides:
-may work for mild Na+ retention; however, TZD diuretic use often results in compensatory increased Na+ and H20 reabsorption in the proximal tubule
loops:
-increase H20 excretion, and also loss of Ca and Mg
-preferred for brisk and immediate diuresis
K+ sparing:
-relatively small diuretic effect but may be useful adjunctive agents
41
What is the MOA of the different diuretics?
thiazides:
-block NaCl transporters in the distal convoluted tubule
loops:
-block Na/K/Cl transporter in the thick ascending loop of Henle
K+ sparing:
-decrease Na+ reabsorption in the collecting duct
42
What is the impact of thiazide diuretics on electrolytes?
sodium: decrease
potassium: decrease
magnesium: decrease
calcium: increase
43
What is the impact of loop diuretics on electrolytes?
sodium: no change
potassium: decrease
magnesium: decrease
calcium: decrease
44
What is the impact of K+ sparing diuretics on electrolytes?
sodium: no change
potassium: increase
magnesium: no change
calcium: no change
45
What is sodium imbalance due to?
an initial challenge to water balance as well as a failure of adaptive responses to compensate for this
-hypo and hypernatremia are disorders of water balance or water distribution
46
What defines hyponatremia?
serum Na+ < 135 mEq/L
47
What is the most common electrolyte abnormality?
hyponatremia
48
What are the many different types and causes of hyponatremia?
excess free water consumption
hyperosmolar hyponatremia
hypovolemic hyponatremia
hypervolemic hyponatremia
euvolemic hyponatremia (e.g. SIADH)
49
How likely is excess water consumption to cause hyponatremia?
very rare - a lot of water must be consumed to overwhelm the kidneys ability to excrete it
-usually seen in combination with a solute-poor diet
50
What is hyperosmolar hyponatremia?
occurs when an osmotically active agent other than Na+ accumulates in the ECF, drawing H20 into the ECF and diluting Na+
-actual Na+ content is normal, but the concentration of Na+ is reduced (dilutional hyponatremia)
51
What is the most common cause of hyperosmolar hyponatremia?
hyperglycemia
-excessive blood glucose draws water from ICF --> ECF
-increased water in ECF dilutes Na+ --> relative hyponatremia
52
What is hypovolemic hyponatremia?
results from net sodium loss
-e.g. thiazide diuretics
53
True or false: hyponatremia is common with loop diuretics
false
54
What is hypervolemic hyponatremia?
occurs during fluid-overloaded states such as HF, cirrhosis with ascites, and severe nephrotic syndrome
fluid shifts from the intravascular to the interstitial space --> dilutional hyponatremia
55
What is euvolemic hyponatremia?
activation of water-conserving mechanisms (i.e. ADH) in the absence of osmotic or volume-related stimuli
-renal response to volume remains intact, so individuals are generally euvolemic
-however, due to increased total body water, serum Na+ concentration is decreased
56
What is the most common form of euvolemic hyponatremia?
syndrome of inappropriate antidiuretic hormone secretion (SIADH)
57
What is SIADH?
non-physiological release of ADH from the pituitary or an ectopic source
58
What are the many different causes of SIADH?
neurologic or psychiatric disorders
pulmonary diseases
malignant tumours
drugs
59
What are some drugs that can cause SIADH?
SSRIs
antipsychotics
narcotics
NSAIDs
60
What are the primary symptoms of hyponatremia?
symptoms are primarily neurologic
-due to osmotic intracellular water shift --> cell swelling and cerebral edema
61
What are the symptoms of hyponatremia proportional to?
magnitude and rapidity of sodium decline
62
What are normal sodium levels?
135-145 mEq/L
63
Describe acute hyponatremia.
sx may appear ~ 125 mEq/L and include nausea, malaise, headache
if Na + drop continues, sx progress to lethargy, confusion, decreased consciousness
seizures, coma if Na+ ~ 115 mEq/L
*developing over ~ 48h*
64
Describe chronic hyponatremia.
> 3 days duration
adaptive mechanisms kick in and help defend against cellular swelling, which minimizes symptoms
65
Describe the typical findings we would see in hyponatremia.
low plasma osmolality
-if not low --> hyperosmolar hyponatremia
low urine osmolality
-if not low --> SIADH
66
In what kind of manner should hyponatremia be corrected?
slowly
-cells gradually adapt to the hyponatremic state, and overly rapid correction can lead to rapid cell shrinkage and brain damage
-overly rapid correction can lead to central pontine myelinosis
67
What amount of sodium should not be exceeded per day when correcting hyponatremia?
total daily sodium correction should not exceed 8 mEq per day
68
How is treatment targeted in asymptomatic hyponatremia?
targeted to the underlying cause
69
Describe hypovolemic hyponatremia management.
isotonic (0.9%) saline to restore the intravascular volume --> decreased renal water retention (turn off ADH) --> normalize serum Na+ [ ]
-avoid overcorrection
70
Describe hypervolemic hyponatremia management.
manage underlying condition
administration of fluids will worsen volume overload without changing serum Na+ [ ]
restricting water intake and salt intake
diuretics (loop) may help attenuate hypervolemia
71
How is euvolemic hyponatremia managed?
identify and correct underlying cause
if not effective:
-water restriction
-salt tablets to increase water excretion
-loop diuretics impair urine-concentrating mechanisms and increase water excretion
-if refractory: vasopressin antagonists
72
What are examples of vasopressin antagonists?
conivaptan
tolvaptan
72
What is the plasma sodium that indicates hypernatremia?
> 145 mEq/L
73
What does hypernatremia lead to?
state of hyperosmolality --> cellular dehydration
74
What is hypernatremia usually a result of?
water deficit
-rather than a net sodium gain
75
What does the hyperosmolar state of hypernatremia usually stimulate?
stimulates thirst and excretion of a maximally concentrated urine
-for hypernatremia to persist, one or both of these compensatory mechanisms must not be working
76
Describe fluid movement during hypernatremia.
hypernatremia --> movement of fluid from ICF to ECF --> brain cell shrinkage
77
Describe the clinical presentation of hypernatremia.
presence and severity of symptoms depends on both the acuity and magnitude of hypernatremia
diabetes insipidus generally presents with polyuria and polydipsia
severe or acute hypernatremia may present with altered mental status, weakness, focal neurological deficits --> coma, seizures, death
78
In what kind of manner should hypernatremia be corrected?
slowly
-overaggressive correction of hypernatremia can lead to brain cell swelling --> seizures, permanent neurological damage, death
79
Describe treatment of symptomatic and chronic hypernatremia.
symptomatic:
-correct Na+ lvls by no more than 10-12 mEq/L per day
chronic:
-correct Na+ lvls even more slowly (5-8 mEq/L per day)
80
How is hypernatremia managed if it is due to hypovolemia?
ECF volume should be restored
81
How is hypernatremia associated with central diabetes insipidus managed?
desmopressin
-synthetic analogue of ADH
82
How is hypernatremia associated with nephrogenic diabetes insipidus managed?
identify and correct concurrent hypercalcemia and hypokalemia
thiazide diuretic + Na+ restriction decrease urine volume and normalize Na+ levels
indomethacin may potentiate ADH in kidney
83
What are the usual causes of sodium overload?
usually iatrogenic (e.g. administration of too much Na+-containing fluids/medications in hospitalized patients)
84
How is hypernatremia associated with sodium overload managed?
administer D5W and loop diuretic
stop underlying cause
85
What is the most abundant cation in the body?
potassium
86
Where is the majority of potassium found?
98% intracellular
87
What are normal serum concentrations of potassium?
3.5-5 mmol/L
88
What are the roles of potassium in the body?
intracellular functions, such as protein and glycogen synthesis, cell growth and metabolism
determines resting membrane potential across the cell membrane
helps maintain blood pressure
89
What are potassium levels impacted by?
dietary intake
GI and urinary excretion
hormones
-insulin: drives K+ into liver, muscle, fat cells
-epinephrine/NE: stimulates K+ uptake by cells
-aldosterone: promotes urinary K+ excretion
acid-base balance
-excessive H+ ions --> increased acidity --> increased serum K+
-metabolic alkalosis --> decreased H+ ions in serum --> decreased serum K+
90
What are the levels that constitute hypokalemia?
serum K+ [ ] < 3.5 mmol/L
-mild: 3.1-3.5 mmol/L
-moderate: 2.5-3 mmol/L
-severe: < 2.5 mmol/L
91
What are the main causes of hypokalemia?
total-body K+ deficit or intracellular shift of K+
-deficit: diet, GI loss, renal loss
-excessive loss also due to thiazide or loop diuretics
92
Which electrolyte deficiency can contribute to hypokalemia?
hypomagnesemia
93
What are the symptoms of hypokalemia?
mild:
-generally asymptomatic
moderate:
-muscle cramping, myalgias, weakness, malaise
severe:
-ECG changes, impaired muscle contraction, heart changes
94
What might be a reasonable treatment for mild, asymptomatic hypokalemia?
may respond to increased dietary K+ intake
95
What is the preferred treatment for moderate or refractory hypokalemia?
oral potassium
- ~ 10 mmol K+ should increase serum K+ by 0.1 mmol/L
-chronic loop or thiazide: 40-100 mmol K+ per day should correct mild-moderate hypokalemia
96
How should oral potassium be taken?
with food to decrease GI intolerance
divide total daily dose TID
97
What is an advantage and disadvantage of elixir potassium?
advantage: rapid increase
disadvantage: bitter taste
98
How is severe hypokalemia managed?
IV replacement
-caution: overly rapid admin cause cause cardiac conduction abnormalities = continuous ECG monitoring if giving high doses quickly
99
Which class of drugs might help prevent loop or thiazide associated hypokalemia?
potassium-sparing diuretics
-spironolactone especially effective with hyperaldosteronism
-amiloride or triamterene are 2nd line
100
What should be done if hypokalemia is refractory to usual management?
test for and manage hypomagnesemia
101
What are the K+ levels that constitue hyperkalemia?
serum K+ > 5 mmol/L
-mild: 5.1-5.9 mmol/L
-moderate: 6-7 mmol/L
-severe: > 7 mmol/L
102
True or false: hyperkalemia is more common than hypokalemia
false
103
What is the most common contributor to hyperkalemia?
renal disease
104
What are the many causes of hyperkalemia?
increased K+ intake
-rich foods, salt substitutes
decreased k+ excretion
-AKI/CKD, adrenal insufficiency, Addisons, drugs
tubular unresponsiveness to aldosterone
-autoimmune diseases
extracellular redistribution of K+
-acidosis, diabetes, CKD
105
What are some drugs that can contribute to hyperkalemia?
ACEI/ARB
K+ sparing diuretics
NSAIDs
TMP/SMX
cyclosporine
tacrolimus
106
What does the treatment of hyperkalemia depend on?
severity of hyperkalemia and how quickly it developed
107
How is hyperkalemia managed if it is moderate, symptomatic, severe, or there are ECG changes?
calcium gluconate 1 g IV to stabilize myocardium
promote intracellular K+ shift:
-insulin (+ dextrose to prevent hypo)
-beta 2 agonists via nebulizer or MDI
-sodium bicarbonate
eliminate excess K+ from body:
-loop diuretics
-oral cation exchange resins
-if severe --> hemodialysis
108
What is the role of magnesium?
cellular function
cofactor for numerous biochemical processes
109
Where is magnesium mainly found?
primarily intracellular
-67% in bone, 20% in muscle
110
What is the normal serum magnesium level?
0.7-0.95 mmol/L
111
What are the symptoms of hypomagnesemia?
neuromuscular: tetany, muscle twitches
cardiac: palpitations, ECG changes, arrhythmias
112
What are the causes of hypomagnesemia?
decreased intestinal Mg absorption
-ulcerative colitis
-chronic diarrhea
-pancreatic insufficiency
-chronic PPI use
renal magnesium wasting
-e.g. thiazide or loop diuretic
113
Which form of supplementation is preferred for hypomagnesemia?
oral
-except in severe deficiency
114
What is the most common adverse effect of magnesium?
diarrhea
115
True or false: hypermagnesemia is common
false
116
Which patients is hypermagnesemia generally seen in?
CKD with excess magnesium consumption
117
How is hypermagnesemia managed?
mild cases:
-identify and correct the cause
if severe:
-IV calcium to antagonize cardiac effects of hypermagnesemia
-loop diuretics to increase Mg+ elimination
118
What is our normal pH range?
normal pH = 7.4
-range 7.35-7.45
- < 6.7 or > 7.7 incompatibile with life
119
What is a frequent cause/contributor to acid-base abnormalities?
medications
120
What is the pH that signifies acidosis? What is the pH that signifies alkalosis?
< 7.4 = acidosis
> 7.4 = alkalosis
121
What are the main organs involved in acid-base homeostasis?
lungs
-regulate pH via CO2, which is acidic
kidneys
-regulate pH via HCO3, which is basic
122
How are acid-base abnormalities categorized?
respiratory (lung/CO2 problem)
-when increased CO2 is primary abnormality --> respiratory acidosis
-when decreased CO2 is the primary abnormality --> respiratory alkalosis
metabolic (kidney/HCO3 problem)
-when decreased HCO3 is the primary abnormality --> metabolic acidosis
-when increased HCO3 is the primary abnormality --> metabolic alkalosis
123
Which body system compensates when there is a respiratory abnormality? What about if it were a metabolic abnormality?
respiratory abnormality:
-kidneys compensate by adjusting HCO3 concentration
metabolic abnormality:
-lungs compensate by adjusting CO2 concentrations
124
Describe the role of the lungs in acid-base balance.
sense alterations in blood pH
adjust breathing rate to increase or decrease PaCO2
-acidosis --> increase RR --> decreased PaCO2 --> increased pH toward normal
-alkalosis --> decrease RR --> increase PaCO2 --> decrease pH toward normal
the lungs are able to make adjustments to RR (and PaCO2) relatively quickly (within minutes-hours)
125
Describe the role of the kidneys in acid-base balance.
sense alterations in blood pH
adjust rate of HCO3 excretion to increase or decrease HCO3
-acidosis --> decrease HCO3 excretion --> increase serum HCO3 --> increase pH toward normal
-alkalosis --> increase HCO3 excretion --> decrease serum HCO3 --> decrease pH toward normal
kidney response to acid-base balance change is slower (2-3 days)
126
Where is blood drawn from to assess acid-base balance?
arterial blood
127
Describe the steps to take in assessing acid-base balance.
1. evaluate the "emia" (acidic or basic disturbance?)
-acidemia = pH < 7.4
-alkalemia = pH > 7.4
2. evaluate the "osis" (metabolic or respiratory?)
-metabolic: increased/decreased HCO3
-respiratory: increased/decreased PaCO2
3. evaluate whether appropriate compensation has occurred
-lungs compensate quickly
-renal compensation takes 2-3 days
128
Provide an interpretation of the acid-base disorders.
respiratory acidosis:
-decreased pH
-increased PaCO2
-increased HCO3
metabolic acidosis:
-decreased pH
-decreased HCO3
-decreased PaCO2
respiratory alkalosis
-increased pH
-decreased PaCO2
-decreased HCO3
metabolic alkalosis
-increased pH
-increased PaCO2
-increased HCO3
129
How is metabolic acidosis treated?
identify and correct cause
administer bicarbonate
130
What might metabolic acidosis be due to?
accumulation of acidic anions
-lactic acidosis (metformin), ketoacidosis, intoxications
disturbances of endogenous H+/HCO3
-renal tubule acidosis, diarrhea, drugs (ex: lithium)
131
What are the most common causes of metabolic alkalosis?
loss of gastric acid due to persistent vomiting
loss of intravascular volume and chloride due to diuretics
iatrogenic
132
How is metabolic alkalosis managed?
correct underlying factors
-e.g. anti-emetics, stop or reduce diuretics
volume repletion with normal saline
carbonic anhydrase inhibitors
-increase serum carbonic acid levels
133
When will we see metabolic compensation for respiratory alkalosis?
if acute (< 24h): serum HCO3 will still be normal
if chronic (> 24h): serum HCO3 will be decreased to compensate
134
Which patients is respiratory alkalosis seen in?
occurs physiologically in pregnancy and individuals living at high altitudes
also commonly seen in hospitalized patients
135
How is respiratory alkalosis managed?
identify and correct underlying cause
-manage pain, decrease anxiety, correct hypoxemia, oxygen if necessary
136
When will metabolic compensation be seen for respiratory acidosis?
if acute (< 24h), serum HCO3 will still be normal
if chronic (> 24h), serum HCO3 will be increased to compensate
137
Describe management of respiratory acidosis.
assess whether the disturbance is acute or chronic
chronic, compensated respiratory acidosis may not require treatment
-supplemental O2, supportive care
acute respiratory acidosis
-severe hypoxia present and is the immediate threat - increase tissue oxygenation
-treat underlying cause and the acidosis will correct rapidly
