Fluids & Electrolytes Flashcards
Intracellular fluid: How much of total body fluid + Electrolyte concentrations
(2/3rds of all body fluid)
- Large amounts of K+
- Moderate amounts of Mg2+
- Small amounts of Na+, Cl-, HCO3-, PO3-
- Almost no Ca2+
Extracellular fluid: How much of total body fluid?, how much plasma vs interstitial fluid? what form is IF fluid and why? Electrolyte concentrations in ECF?
- Plasma: 1/4 of ECF
- Interstitial fluid (IF) 3/4 of ECF. Most IF fluid is in gel form. This cushions cells, and opposes outflow of water from capillaries, preventing accumulation of free water in interstitial spaces.
- Large amounts of Na+ and Cl-
- Moderate amounts of HCO3-
- Small amounts of K+, Mg2+ Ca2+ and PO3-
5 places of 3rd space transcellular compartment. How much of ECF is 3rd space
CSF, peritoneal cavity, joint spaces, pleural space, pericardial space.
1% of ECF.
How does ADH work?
Baroreceptors present in vascular system sense changes in pressure, prompting hypothalamus to send impulse to posterior pituitary
Pituitary sends ADH to collecting duct of kidney, which prompts kidney to retain water
How does RAAS work?
- When there is a decrease in blood, the pressure-sensitive receptors in kidney prompts it to secrete renin.
- In the bloodstream renin meets angiotensinogen which comes from the liver. When they meet, they make angiotensin I. Angiotensin I will meet angiotensin-converting enzyme (ACE) in the lungs, which turns it into angiotensin II.
- Angiotensin II is a potent vasoconstrictor and also acts directly on renal tubules to increase sodium reabsorption.
- This increases BP in the kidney, prompting less renin to be released, and maintaining homeostasis.
- Angiotensin II also goes to adrenal cortex, causing it to secrete aldosterone.
- Aldosterone goes to the kidney and causes sodium and water to be reabsorbed in the distal convoluted tubule. This also causes increased blood volume and pressure.
Aldosterone also causes potassium and magnesium to leave the blood stream due to ionic exchange.
How do natriuretic peptides work?
- Baroreceptors in the atria of the heart senses increases in stretch and blood volume, and releases ANP and BNP.
ANP causes kidney to excrete more sodium (natriuresis means diuresis of sodium), reducing the blood volume.
4 Physiologic mechanisms that contribute to edema formation
- Increased hydrostatic pressure
- Decreased colloidal osmotic pressure
- Increased capillary permeability
Obstruction to lymph flow
Causes of increased hydrostatic pressure
○ Increased vascular volume or venous congestion
○ Heart disease
○ Pregnancy
Kidney disease
Causes of Decreased colloidal osmotic pressure
○ Increased loss of plasma proteins
○ Malnutrition
○ Kidney disease
○ Burns
Liver disease
Causes of increased capillary permeability
○ Inflammation
○ Allergic reaction
○ Tissue injury/burns
Malignancy
Generalized vs localized edema
- Localized edema occurs in a limited anatomic site, often from tissue injury, local inflammation, etc.
- Generalized edema is frequently the result of increased vascular volume common in congestive heart failure.
- Edema resulting from increased capillary pressure commonly causes fluid to accumulate in dependent parts of the body like the ankles and feet, called dependent edema.
- Right sided heart failure causes blood to pool throughout the venous system causing organ congestion and edema of dependent extremities.
Complications of edema
- Makes it difficult for O2, CO2 and nutrients to be transported to cells
- Can separate tight junctions making it easier for microbes to enter cells
Interstitial edema can be life threatening in the brain, throat, and inside lungs
- Can separate tight junctions making it easier for microbes to enter cells
3rd space accumulation: 5 names for different places, most common cause, what can effusion fluid contain
- Usually due to lymph obstruction
- Pericardial effusion, pleural effusion, joint effusion, hydrocephalus in arachnoid space, ascites in pericardial space.
Effusion can contain blood, plasma proteins, inflammatory cells, and ECF.
- Pericardial effusion, pleural effusion, joint effusion, hydrocephalus in arachnoid space, ascites in pericardial space.
Hypovolemia: Isotonic fluid volume deficit: general description and physiology
Loss of water and sodium in equal proportions, concentrations of sodium in ECF remain normal. Vasculature shrinks, poor perfusion, BP decreases.
4 categories of causes of hypovolemia
-1. Inadequate fluid intake
- 2. GI loss of sodium containing fluid
○ Emesis, Diarrhea, Gastric suction, Fistula drainage
- 3. Polyuria
○ Adrenal insufficiency (aldosterone insufficiency), Sodium-wasting renal disorders, Extensive diuretic use
- 4. Other body fluid loss
Hemorrhage, Massive diaphoresis, Third-space fluid accumulation, Paracentesis and similar procedures (fixing 3rd space fluid accumulation), Burns
Clinical manifestations of hypovolemia
- Vitals: Thready, rapid pulse, Orthostatic hypotension, Increase cap refill time
- Signs: Sudden weight loss 3-4lbs in a day, Tenting of skin, Decreased urine output & increased concentration, Sunken eyes, sunken fontanelles
- Symptoms: Thirst, Dizzy, faint
Labs: Increased RBC, hematocrit, Blood Urea Nitrogen
Hypervolemia: Isotonic fluid volume excess: 2 main mechanisms
Inadequate Na and H2O elimination
○ CHF, renal disease/failure
○ Hyperaldosteronism
○ Cushings, corticosteroids (cortisol causes Na+ retention)
Cirrhosis
Excess intake of Na and water
○ Excess dietary intake/OTC meds plus water
- Excessive IV infusion of isotonic solutions
Clinical manifestations of hypervolemia
- Vitals: Fast & bounding pulse
- Signs: Sudden weight gain, Edema, Bulging neck veins, Crackles in lungs, Cough, Bulging fontanelles
- Symptoms: Dyspnea, Orthapnea
- Labs: Decrease in BUN and hematocrit
Related conditions: Ascites and pleural effusion
Complications of hypervolemia
Pulmonary edema
Hyponatremia: general physiology and vulnerable population
Serum sodium <135. Water flows into cells to equalize concentration & cells become swollen
Older populations more vulnerable to hyponatremia due to decreased renal function
Causes of hyponatremia: 3 main physiologic processes
Gain of relatively more water than salt (euvolemic hypotonic hyponatremia)
Loss of relatively more salt than water (hypovolemic hypotonic hyponatremia)
Fluids shift (hypertonic hyponatremia)
Specific causes of gaining relatively more water than salt
○ Dilute infant formula
○ Excessive SIADH
○ Excessive IV dextrose
○ Hypotonic irrigating solutions
○ Tap water enemas
○ Psychogenic polydipsia (mental illness)
○ Beer potomania
○ Ecstasy
○ Near-drowning in fresh water
○ SSRIs
Specific causes of losing relatively more salt than water
○ Diuretics esp thiazides
○ Salt-wasting renal disease
Replacing fluid losses from emesis, diarrhea, gastric suction, diaphoresis or burns with pure water
Mechanism for fluid shift process causing hyponatremia
Sodium in ECF becomes diluted as water moves out of cells in response to the osmotic effects of elevated blood glucose (Hyperglycemia)
Clinical manifestations of hyponatremia
- Anorexia, nausea/vomiting,
- Malaise, weakness, fatigue, Headache
- Muscle cramps,
- Fingerprint edema on sternum,
Seizures, coma (CNS symptoms d/t swelling of brain cells)
Hypernatremia: characteristics
Characterized by hypertonicity of ECF and almost always causes cellular dehydration.
Causes of hypernatremia: 2 main mechanisms
Gain of relatively more salt than water
Loss of relatively more water than salt
Causes of gaining relatively more salt than water
○ Tube feeding
○ IV infusion of hypertonic solution
○ Near-drowning in salt water
○ Overuse of salt tablets
○ Food intake w reduced fluid intake
○ Difficulty swallowing liquids
○ No access to water
Inability to respond to thirst
Causes of losing relatively more water than salt
○ Diabetes insipidus (deficient ADH)
○ Osmotic diuresis
Prolonged diarrhea or diaphoresis w/o water replacement
Clinical manifestations of hypernatremia
- Thirst, dry mouth
- Rapid, thready pulse, decreased BP
- Elevated body temp
- Dry skin and mucous membranes
- Oliguria (decreased urine output)
CNS symptoms–confusion, agitation
Clinical dehydration
hypernatremia + fluid volume deficit
Potassium: why is it important, main regulatory mechanisms, intake & output
- Second most abundant cation in the body (after Na+), major cation in ICF
- Normal range is very narrow, thus must be monitored closely as small changes can be significant
- Important for transmission of nerve impulses, cardiac, smooth, & skeletal muscle contractions, cell metabolism, acid-base balance
- Largely regulated through renal mechanisms and transcellular shift between ICF and ECF
○ Aldosterone plays an essential role in regulating K+ via Na+/K+ exchange mechanism in distal and cortical collecting tubules. Presence of aldosterone causes retention of Na+ and K+ to be secreted - Normally derived from dietary sources
- Excreted by kidneys, feces, sweat
Causes of hypokalemia
Potassium wasting diuretics
Decreased intake of K+
Alkalosis
Insulin administration
Excess beta-adrenergic stimulation (stress)
Adrenal overstimulation
Drugs
Loss of K+ containing fluids
Causes of decreased intake of K+
NPO, alcoholism, eating disorders, GI surgery, IV solutions w/o K+, fad diets
Mechanism of hypokalemia secondary to alkalosis
H+ leaves the cell to neutralize the pH and K+ replaces it
Mechanism of hypokalemia secondary to insulin administration
Insulin pushes K+ as well as glucose into cells
Causes of adrenal overstimulation that may cause hypokalemia
Hyperaldosteronism, cushings, corticosteroids
Causes of hypokalemia related to fluid loss
Diarrhea, diaphoresis, emesis, gastric suction, fistula, burns
Clinical manifestations of hypokalemia
Vitals: shallow respirations, thready pulse
Alkalosis
Dilute urine, polyuria
Nausea, vomiting, decreased GI motility
Cramps, weakness, lethargy
Arrhythmias, dysrhythmias, increased sensitivity to digoxin
Mechanism of alkalosis secondary to hypokalemia
K+/H+ exchange mechanism in cortical collecting tubules–when K+ is low, K+ is reabsorbed and H+ eliminated, increasing pH
Hyperkalemia causes
Potassium sparing diuretics
Renal failure
Increased intake of K+ (rarely from diet alone, but w/ supplements)
Lethal injection
Acidosis (H+ goes into cells to compensate & is exchanged w K+)
Diabetes mellitus
Adrenal insufficiency (addison’s)
Drugs: ACE inhibitors, ARBs, beta blockers
Crushing or burning injury (cells break open and release K+ into blood stream)
Clinical manifestations of hyperkalemia
Muscle cramps
Respiratory distress
Decreased cardiac contractility
Nausea/vomiting, intestinal cramps
Cardiac dysrhythmias
One of the most life-threatening electrolyte imbalances, especially for children
Hypo and hyperkalemia affect on nerves and muscles
Hypokalemia: Membrane potential becomes more negative, moving it further from the threshold and requiring a greater stimulus to open Na+ channels for an action potential
Hyperkalemia: Resting membrane potential is more positive, moving it closer to the threshold and making it easier to excite. However, severe hyperkalemia may cause prolonged depolarization which decreases excitability
Muscle cramps is a symptom of both hyper and hypokalemia
Why is calcium important
Important for neuromuscular transmission, cardiac skeletal, & smooth muscle contraction, role in clotting cascade, bone and tooth structure
Where is calcium found, what forms exist in the ECF
99% of calcium in the body is in bone, only 0.1-0.2% is in the ECF
In ECF Ca2+ is found in three forms: protein (albumin) bound (40%), complexed (10%), and ionized/free(50%).
Mechanism for calcium regulation
Decrease in Ca2+ causes increase in parathyroid hormone (PTH). PTH does two things:
- Moves Ca2+ from bone to blood
- Activates vitamin D
Vitamin D, once activated, does two things:
- Increases absorption of Ca2+, Phos, and Mg2+ in intestine
- Increases Ca2+ reabsorption and phos secretion in kidney
When Ca2+ is high, PTH is inhibited, causing Ca2+ to be deposited in bone
Calcitonin comes from the thyroid and brings Ca2+ levels down
Calcium and phosphorous
Calcium and phosphorus have an inverse, see-saw relationship
Causes of hypocalcemia
○ Decreased intake of Ca2+ or vit D
○ Malabsorption issues
○ Hypoparathyroidism
○ CKD
○ Drugs
○ Excess phosphate intake
○ Hyperphosphatemia
○ Tumor lysis
○ Pancreatitis
Preterm infancy
Clinical manifestations of hypocalcemia
○ Spasms, cramps, tetany, convulsions, paresthesia
○ Stridor, laryngospasm
○ Increased reflexes
○ Positive trousseau (hand closing) or chvostek (mouth twitch) sign
Cardiac dysrhythmias
Hypercalcemia causes
- Increased intake of Ca2+ or vit d
- Hyperparathyroidism
- Drugs
- Hypophosphatemia
- Malignant tumors, bone tumors
- Immobility
- Leukemia
- Milk–Alkali syndrome
Clinical manifestations of hypercalcemia
○ Renal or biliary stones
○ Nausea/vomiting, constipation, anorexia
○ Bone pain, fracture, osteopenia, osteoporosis
○ Muscle weakness/atrophy
○ Depression, anxiety, cognitive/behavioral changes
○ Lethargy, stupor, coma
○ Polyuria
Cardiac dysrhythmias, HTN
Phosphorous: why is it important?
- Important for ATP formation, cell membrane integrity, O2 delivery, muscle and nerve function, bone and tooth structure, acid-base balance
Causes of hypophosphatemia
○ Hypercalcemia
○ Hyperparathyroidism
○ Lack of vit d
○ Chronic alcoholism, alcohol withdrawal
○ Chronic diarrhea, emesis, diuresis, malabsorption
○ Insulin administration
○ Long term antacid use
○ Refeeding syndrome–always check phosphate before feeding a starving patient (long-term phosphate deficiency coupled with sudden surge of insulin causing sudden increase in phosphate use for cell metabolism)
Alkalosis
Clinical manifestations of hypophosphatemia
○ Intention tremor
○ Ataxia, paresthesia, seizures, confusion, stupor, coma
○ Weak muscles, stiff joints, bone pain, osteomalacia,
Platelet/RBC dysfunction
Causes of hyperphosphatemia
Hypocalcemia: Hypoparathyroidism,
Renal disease
Diabetic ketoacidosis
Excessive vit d
Overzealous phosphate administration
Excessive laxatives/enemas containing phosphate
Tumor lysis
Crushing injury, Rhabdomyolysis (cells break down and release phosphate)
Clinical manifestations of hyperphosphatemia
○ Paresthesia, cramps, tetany, seizure
○ Cardiac dysrhythmias
Decrease BP
Why is magnesium important
Important for producing ATP, protein and DNA synthesis, vasodilation, muscle contraction, nerve transmission, Na+/K+ pump, cardiac muscle/rhythm
Causes of hypomagnesemia
- Decreased intake
- Malnutrition, starvation, chronic alcoholism, diarrhea
- Malabsorption, ileal resection, prolonged GI suction
- Diabetic ketoacidosis (DKA) w/ polyuria
- Long term IV w/o Mg2+
- Renal disease
- Hyperaldosteronism
Drugs
Clinical manifestations of hypomagnesemia
- Increased reflexes
- Positive trosseau or chvostek
- Paresthesias, cramps, tetany, seizure, nystagmus, personality change
Cardiac dysrhythmias, HTN, increased HR
Causes of hypermagnesemia
- Increased intake of Mg2+
- Long term IV w Mg2+
- Renal disease
- Renal compromise and Mg2+ containing meds
- Milk of magnesia
- Adrenal insufficiency
- Mother/newborn can become hypermagnesemic after treatment
Clinical manifestations of hypermagnesemia
- Lethargy, decreased reflexes, confusion, coma
- Decreased BP, HR, resp
- Vasodilation
Cardiac dysrhythimas, cardiac arrest
9 rules: sodium and water
Where sodium goes, water follows
9 rules: albumin
Albumin pulls water towards it and provides osmotic pressure
9 rules: glucose
High glucose will pull water to itself through osmosis
9 rules: ADH and Na+ relationship
When ADH increases, Na+ decreases, and vice versa
9 rules: RAAS, blood volume, K+, Mg+ relationship
When Renin Angiotensin Aldosterone System (RAAS) kicks in, blood volume increases, and K+ and Mg2+ concentrations decrease
9 rules: ANP and blood volume relationship
Increased Atrial Natriuretic Peptide (ANP) causes blood volume to decrease
9 rules: K+ storage
The body cannot store potassium
9 rules: Ca2+ and phosphate relationship
Inverse: When Ca2+ increases, phosphate decreases, and vice versa
9 rules: Mg2+, K+, Ca2+ relationship
Hypomagnesia, hypokalemia and hypocalcemia often occur together
