Fluid, Electrolyte, and Acid-Base Balance Flashcards
Exam I
Renal control of sodium
Via aldosterone
- RAAS: Decreased renal perfusion is sensed by the juxtaglomerular cells in the kidney, resulting in increased renin secretion and the activation of the renin-angiotensin-aldosterone system
-Angiotensin II causes vasoconstriction and stimulates the release of aldosterone by the adrenal cortex
-Aldosterone promotes sodium retention in the distal nephron - Volume receptors: Volume receptors in the great veins and atria are sensitive to small changes in venous and atrial filling
-Increased atrial filling stimulates volume receptors and results in the release of atrial natriuretic factor/peptide (ANF/ANP) and brain natriuretic factor/peptide (BNF/BNP), which promote sodium excretion - Baroreceptors: Pressure receptors in the aorta and carotid sinus are stimulated by volume depletion and subsequently active the sympathetic nervous system, leading to renal retention of sodium
Renal control of water
Via ADH
Two stimuli for ADH secretion:
- Osmotic stimulus: changes in plasma osmolality stimulate osmoreceptors in the hypothalamus
- Osmoreceptor stimulation results in:
1) an increase or decrease in thirst
2) an increase or decrease in ADH secretion - Volume/pressure stimulus: Changes in circulating blood volume/pressure are sensed by volume-sensitive receptors and baroreceptors:
-Volume/baroreceptors stimulate an increase or decrease in ADH secretion
*If both the osmolality AND the volume/pressure decrease, the volume/pressure stimulus will be most significant
Osmolality
a value determined by the total solute concentration in a fluid compartment
Tonicity
The ability of the combined effect of all the solutes to generate an osmotic driving force that causes water movement from one compartment to another
Solutes capable of changing the tonicity (i.e., translocating water from one body fluid compartment to another) are effective osmoles
Examples of effective osmoles
sodium, glucose, mannitol, and sorbitol
Urea osmolality
Contributes to the osmolality, but easily crosses cell membranes and distributes evenly throughout total body fluids
An ineffective osmole
Serum osmolality calculation
2 X [sodium concentration] + [glucose concentration/18] + [BUN/2.8]
Normal body fluid osmolality
280-294 mOsm/Kg (milliosmoles per kilogram)
Isotonic alterations
volume depletion or volume excess with a normal osmolality
Hypertonic alterations
volume depletion or volume excess with an increased osmolality
Causes of hypertonic alterations
increase in sodium or loss of free water
Outcomes of hypertonic alterations
Intracellular dehydration, and if untreated, extracellular dehydration
This is often seen first in signs and symptoms of brain cell shrinkage
These patients are usually hypernatremic
Hypotonic alterations
normal volume, volume depletion, or volume excess with a decreased osmolality
Causes of hypotonic alterations
May be related to a decrease in sodium, but more commonly, by impaired renal water excretion or free water excess
Outcomes of hypotonic alterations
Intracellular swelling (fluid shifts into the cell where there are more solutes)
This is often seen first in signs and symptoms of brain cell or cerebral swelling and/or pulmonary edema
These patients are usually hyponatremic and hypotonic
○ The most common form of hyponatremia
○ Usually caused by impaired renal water excretion in the presence of continued water intake
Psuedohyponatremia
a rare condition in which serum sodium concentration is low, but serum osmolality and tonicity is normal or above normal
A low sodium concentration with normal osmolality may be an artifact due to the accumulation of other plasma constituents (triglycerides or proteins) in plasma
Severe hypertriglyceridemia, severe hyperproteinemia [multiple myeloma]
Hyponatremia with hyperosmolality
Usually due to severe hyperglycemia
Increase in glucose in the extracellular fluid moves water from the cells to extracellular compartment and dilutes the sodium concentration
The sodium concentration falls about 1.6 mEq/L for every increase of 100 mg/dl in glucose concentration over normal (100 mg/dl)
Water deficit calculation
Current TBW = weight in kg x (0.4 for women/0.5 for men/0.6 for infants)
Ideal TBW = (Na (current) X TBW)/140 (ideal sodium concentration)
Water deficit = (Na (current) X TBW)/140) - TBW
Water excess calculation
Current TBW = weight in kg x (0.5 for women/0.6 for men/0.7 for infants)
Water excess = TBW x (1 – (Na/125))
TBW composition in fluid compartments
2/3 of TBW is intracellular (28 L) and 1/3 of TBW is extracellular [(3/4 interstitial (11 L) and 1/4 intravascular (3 L)]
Causes of edema
1) Increased capillary venous hydrostatic pressure
2) decreased capillary oncotic pressure
3) lymphatic obstruction/dysfunction
4) increased capillary permeability
5) sodium and water retention
Pitting edema
If the fluid contains few proteins, it will be pitting
Caused by increased capillary venous hydrostatic pressure or decreased capillary oncotic pressure
Non-pitting edema
If the fluid contains a lot of protein, it will be non-pitting
Caused by increased capillary permeability or lymphatic obstruction
Spurious hypokalemia
The serum potassium is not really low, but appears so due to insulin administration
A dose of insulin right before blood drawing can cause temporary movement of potassium into cells in the blood tube and a falsely lower serum potassium
Decrease of about 0.3 mEq/L
Pseudohyperkalemia
The serum potassium is not really high, but appears so due to:
· 1) Hemolysis during blood draw
· 2) Platelets > 1,000,000
· 3) WBC > 200,000
· 4) Mononucleosis
· 5) Familial pseudohyperkalemia
Serum K+ response in alkalosis
Serum potassium falls about 0.3 mEq/L for each 0.1 increase in pH (alkalosis)
Serum K+ response in respiratory acidosis
Serum potassium rises about 0.3 mEq/L for each 0.1 decrease in pH in respiratory acidosis
Serum K+ response in metabolic acidosis
Serum potassium rises about 0.7 mEq/L for each 0.1 decrease in pH in metabolic acidosis
Serum ical response in alkalosis
Decrease
In metabolic alkalosis, bound hydrogen ions dissociate from albumin, which increases the amount of albumin available to bind ionized calcium
Serum ical response in acidosis
Increase
Causes of metabolic acidosis
- A primary loss of bicarbonate from the body (usually GI or renal)
- An increase in the production or addition of metabolic, nonvolatile acids (in other words, NOT carbonic acid [carbon dioxide])
- A decrease in acid excretion
The last 2 mechanisms lead to “using up” bicarbonate stores (as opposed to “losing” bicarbonate from the body)
Anion gap calculation (without K)
Anion gap = Na - (Cl + HCO3)
Normal anion gap (without K+)
12 ± 2
(10-14)
Causes of normal anion gap metabolic acidosis
Loss of bicarbonate (usually from the GI tract or kidneys)
GI: diarrhea or diarrheal equivalents
Renal: renal tubular acidosis
Type 1 RTA
Distal RTA
Involves a decrease in the ability of the distal nephron to produce new bicarbonate (or secrete hydrogen ions into the tubular fluid)
Can be caused by a defect in any step in the production of bicarbonate
Classic distal RTA can result in hypokalemia
Type 2 RTA
Proximal RTA
Involves a decrease in the ability of the proximal tubule to reabsorb filtered bicarbonate
Type 4 RTA
Hyperkalemic RTA
Involves a lack of aldosterone activity at the distal nephron
A hallmark of type 4 RTA is hyperkalemia
Causes of elevated anion gap metabolic acidosis
Retention or addition of acid
Retention: renal failure (GFR <25% normal)
Addition: via derangements in metabolism or exogenous ingestions
You’re doing great sweetie
Derangements in metabolism causing elevated anion gap metabolic acidosis
Ketoacids and lactic acidosis
Ketone bodies: 2 organic acids (acetoacetic acid and beta-hydroxybutyric acid) and acetone (ketone) produced by the liver from triglycerides
Lactic acid: a byproduct of anaerobic metabolism
Type A lactic acidosis
Results from tissue hypoxia, leading to increased anaerobic metabolism (e.g., all types of shock, respiratory failure, severe anemia, carbon monoxide poisoning)
Type B lactic acidosis
Results from a mitochondrial defect in oxygen utilization (e.g., cyanide toxicity, malignancies [leukemia, lymphoma, sarcoma], medications [isoniazid, phenformin, salicylates, AZT])
Causes of ketoacidosis
DKA
Starvation
Alcoholism
Exogenous ingestions causing elevated anion gap metabolic acidosis
Their metabolism produces toxic acids and other products that can cause severe acidosis
PLUMSEEDS:
Paraldehyde
Lactic acidosis
Uremia
Methanol
Salicylates
Ethanol
Ethylene glycol
DKA
Starvation
K+ and Ca2+ levels in metabolic acidosis
hyperkalemia and hypercalcemia
Acidosis is associated with an increase in the ionized calcium and hypercalcemic effects
Causes of metabolic alkalosis
Addition of bicarbonate to the body, loss of hydrogen ions, or contraction alkalosis
Contraction alkalosis
Involves the loss of fluids from the body that are low in bicarbonate (and usually high in chloride)
The fluid losses “contract” the vascular/blood volume
There is decreased water content, but because the loss of bicarbonate is slight, the bicarbonate concentration increases
Vomiting, GI suction, and the administration of thiazide or loop diuretics can result in contraction alkalosi
H+ loss causing metabolic alkalosis
For every hydrogen ion lost, one bicarbonate ion is added
Extrarenal or renal
Extrarenal hydrogen ion loss: Usually results from GI losses (vomiting, GI suction) or a shift of hydrogen ions from the extracellular to the intracellular compartment
Renal loss of hydrogen ions: Usually occurs due to increased mineralocorticoid (aldosterone) activity (primary hyperaldosteronism, Cushing’s, congenital adrenal hyperplasia, renal artery stenosis
K+ and Ca2+ levels in metabolic alkalosis
hypokalemia and hypocalcemia
Causes of inability to excrete bicarb
- Excessive mineralocorticoid activity
- Increased hydrogen ion excretion and increased bicarbonate retention - Hypovolemia
-Stimulates aldosterone secretion –> increased hydrogen ion excretion and increased bicarbonate retention - Hypokalemia and hypochloremia:
-Both stimulate renal secretion of hydrogen ions and retention of bicarbonate ions (These two abnormalities, because they tend to maintain a state of metabolic alkalosis, must be corrected before acid base imbalances from any cause can be successfully treated)
Saline-responsive metabolic alkalosis
Associated with hypovolemia and is corrected when the ECF is expanded with a solution of sodium chloride and potassium (as above the chloride and potassium levels must be corrected)
Saline-resistant metabolic alkalosis
Associated with excessive mineralocorticoids (aldosterone)
Corrected sodium in hyperglycemia
The sodium concentration falls about 1.6 mEq/L for every increase of 100 mg/dl in glucose concentration over normal (100 mg/dl)
Corrected sodium = Na+ + ( [BGL-100]/100 x 1.6)
Normal serum calcium
8.5-10.5 mg/dL
