What percentage of body weight is total body water? What is the amount in liters in the average 70 kg patient?
What percent of total body water is intracellular fluid? What is the amount in liters in the average 70 kg patient?
What percent of total body water is extracellular fluid? What is the amount in liters in the average 70 kg patient?
What are the 2 components of ECF?
interstitial fluid and plasma
What is the average amount (in liters) of interstitial fluid?
What is the average amount (in liters) of plasma?
True / False- proteins are confined to the plasma
true! they create osmotic pressure (pulling force that keeps fluid in the intravascular space)
What is the "equivalent weight of a substance"?
=gram molecular weight / # of charges -used for electrolytes or ions -this value equals "equivalents," get meq by multiplying by 1000
What regulates the composition of the ECF?
What are the ECF electrolytes?
Na, Cl, Ca, bicarb
What are the major ICF components?
K, Mg, Phos, organic acid anions (lactate and pyruvate), and protein
Which electrolytes are anions?
Phosphate, Cl, bicarb, proteins, organic anions (lactate and pyruvate)
Which electrolytes are cations?
Na, K, Ca, Mg
What is the Donnan Effect?
-total colloid osmotic pressure is on avg 28 mmHg -plasma proteins contribute 19 mmHg to colloid osmotic pressure -cations (Na+ and K+) held in the plasma by proteins contribute the remaining 9 mmHg
What non electrolytes exist in the plasma?
phospholipids, cholesterol, neutral fat (triglycerides), glucose, urea, lactic acid, uric acid, creatinine, bilirubin, bile salts (listed from most to least)
How does the hypothalamus help in the regulation of fluid balance?
it has osmoreceptors that can sense a very small change (1-2%) in osmolality and can adjust ADH accordingly - increased osmolality would result in increased ADH -decreased osmolality would result in decreased ADH
What are the ways in which body fluid is lost and how much is lost daily on average?
Urine- 60% Sweating- 100 ml (but up to 5L with heavy exercise) Insensible losses- 1L GI tract losses- 100-150 ml
What hormones contribute to regulation of fluid balance? How?
ADH- hypothalamus senses increase in osmolality and increases the number of aquaporins to allow more water reabsorption (or opposite) ANP- atrial naturitic peptide, causes renal excretion of Na and water aldosterone- increased aldosterone causes increased water reabsorption
What is tonicity?
Compares osmotic pressure of IV solution to that of plasma
What happens to a cell in a HYPERtonic solution?
cell shrinks as water leaves the cell
What happens to a cell in a HYPOtonic solution?
cell swells as water enters
What makes a solution isotonic?
What does an isotonic solution do to ECF and ICF?
Isotonic = 250-375 mosm / L Isotonic solution expands ECF volume (plasma and ISF) No change to osmolarity
What makes a solution HYPERtonic?
What does it do to ECF and ICF?
Hypertonic= >375 mosm/L Hypertonic solution causes water to leave ICF, increases volume of ECF to a greater extent than the volume administered Increases osmolarity of both ECF and ICF Pulls fluid out of cells
What makes a solution HYPOtonic? What does it do to ECF and ICF?
Hypotonic= <250 mosm/L Increases volume of both ICF and ECF but increases ICF more than ECF Decreases osmolarity of both ICF and ECF ECF enters cells
How is D5W classified in terms of tonicity? What is its osmolarity?
Osmolarity = 278 mosm/L = isotonic, BUT... Acts isotonic at first, dextrose is absorbed by cells and used for energy, then water is left Water dilutes ECF, cells end up in a HYPOtonic environment, ICF increases as cells swell as water enters 2/3 goes to ICF, 1/3 to ECF
What are benefits to using LR? When might you want to avoid it?
Benefits- near physiologic, balanced electrolyte solution, isotonic, good to replace surgical losses Caution- contains K, caution in renal failure, can also get metabolic alkalosis from metabolism of lactate to bicarb
What's the max dose of dextrose? What happens if you give too much dextrose?
0.5 g / kg/ hr 700 ml D5W for avg 70 kg patient Glucosuria
How do you calculate the fluid volume needed to infuse?
Volume needed to infuse = vol lost X volume of distribution (where does this sol'n go) / normal plasma volume
Where does D5W distribute to?
Total body water
Where does LR distribute to?
It's isotonic and distributes to ECF
What is the rule of thumb for replacing blood loss with fluids? With cells?
Replace every 1 ml blood loss with 3 ml isotonic crystalloid 1:1 replacement with PRBCs
What patients should probably get fluids containing dextrose?
Infants and people taking insulin as they are at risk for hypoglycemia
What is the "conventional management" for surgical fluid requirements?
Min. tissue trauma 4-6 ml / kg/ hr Mod. trauma 6-8 ml / kg / hr Extreme trauma 8-12 ml / kg/ hr
Also called 3rd space losses
How do you calculate maintenance fluid requirements?
Use 4-2-1 rule Replace 4 ml / kg for 1st 10 kg 2 ml / kg for next 10 kg replace rest at 1 ml / kg
How do you calculate NPO deficit?
Maintenance fluid requirement x # hours NPO
What are some of the risks associated with hetastarch and dextran?
Both interfere with clotting ability Hespan is associated with a prolonged PTT, decreased Plt function, and decrease in clotting factors Dextran interferes with Plt function, also associated with anaphylactic reactions due to IgG antibodies (?)
What is normal plasma osmolarity?
275-290 mosm/L (class) 280-295 mosm/L (study questions)
What is the normal sodium level? Does it reflect total body sodium or plasma sodium?
135-145 meq/L Plasma sodium
What organ typically controls ECF sodium levels?
What is hyponatremia and what is the most frequent cause?
Na < 135 meq/L Excess free water
What is hypernatremia and what are frequent causes?
Na > 150 meq/L Excess Na intake, excess water excretion (absence of ADH), inadequate water intake
DI, hypertonic fluids, osmotic diuresis, insensible losses
What is the sodium requirement for premature infants?
Infants 3 meq/ kg / day Adults 1.5 meq/ kg/ day
ADH, ANP, and aldosterone all play a role in regulating sodium levels, but how do they differ?
ADH regulates Na concentration ANP and aldosterone regulate total body sodium NOT concentration
What are examples of hyponatremic and hypovolemic states?
Vomiting, diarrhea, diuretic abuse, Addison's disease (decreased aldosterone secretion results in body being unable to reabsorb sodium) Hemorrhage, burns (edema), peritonitis, cerebral salt-wasting syndrome
What are examples of hyponatremic and hypervolemic states?
CHF, nephrotic syndrome, cirrhosis, TURP syndrome (absorb irrigant during surgery)
What is TURP syndrome?
Intravascular absorption of irrigant causes hypervolemic hyponatremia Also occurs in hysteroscopy
Why like to have these pts awake during surgery so can monitor for CNS changes
What are examples of hyponatremic and euvolemic states?
SIADH, pseudohyponatremia syndome
Which is more severe acute or chronic hyponatremia?
acute is more severe, no time for compensation to occur
What are s/sx of hyponatremia?
S/sx vary with rate of development and severity Loss of appetite, N/V, cramps, weakness, When Na < 125 meq/L see altered LOC, coma, seizures (brain over hydration)
Hyponatremia causes an _______ in brain volume.
Increase, causes brain swelling. Brain relatively impermeable to Na but very permeable to water.
Hyponatremia needs to be rapidly corrected. T of F and why?
FALSE! Rapid correction of hyponatremia causes osmotic injury in the brain.
What is central pontine myolinolysis? How does it occur?
Brain neurons become demyelinated due to osmotic injury. Occurs during rapid correction of hyponatremia.
How can one prevent central pontine myolinolysis?
Limit Na correction to LESS than 10-12 meq/ L in 24 hours OR 18 meq / L in 48 hours
What are s/sx of central pontine myolinolysis?
mild behavioral disturbances, seizures, quadraparesis
Hypernatremia is always a hypoosmolar state. T or F?
FALSE! It is always a HYPERosmolar state.
What are s/sx of HYPERnatremia?
Similar to HYPOnatremia: seizures, coma (but due to brain dehydration in this case)
polyurea due to inability of kidneys to concentrate urine
What are diagnostic criteria for DI?
large amounts of dilute urine increased serum osmolarity hypernatremia
How should hypernatremia be corrected?
SLOWLY! To prevent seizures and cerebral edema. Do not decrease serum Na by more than 1-2 meq / L/ hr
How should one treat hypernatremia with sodium depletion (hypovolemia)?
Correct hypovolemia with NS Treat hypernatremia with hypotonic fluids
How should one correct hypernatremia with sodium overload (hypervolemia)?
Enhance Na removal with HD or loop diuretics Replace water deficit with hypotonic fluids
How should one correct hypernatremia with normal total body sodium (euvolemia)?
Replace water deficit with hypotonic fluids Control DI -Central DI- give DDAVP -Nephrogenic- restrict water and sodium intake, thiazide diuretics
What causes K to move INTO the cell?
Insulin, beta agonists, alkalosis
Is K more prevalent in the ICF or ECF?
What can cause HYPERkalemia?
ACEI acidosis K sparing diuretics renal failure intracellular shift due to succ, dig, non selective beta blockers, or abx
What can cause HYPOkalemia?
certain antibiotics, diuretics, hormones (aldosterone, glucocorticoids), some chemo drugs, Mg deficiency
skeletal muscle weakness that can lead to paralysis, arrhythmias due to hyperpolarization of cardiac cells (need more energy to reach action potential), get pauses in normal firing, increased ectopic beats, depression of AV and SA node increased dig toxicity
What EKG changes might one notice with HYPOkalemia?
Flat or inverted T waves Prominent U waves ST depression
Does hyper or hypokalemia result in increased dig toxicity?
What drugs can cause HYPERkalemia?
Succinylcholine, ACEI, NSAIDs, K sparing diuretics Also people with denervation injuries (stroke or quads) or burns are at increased risk for hyperkalemia with succ and it is contraindicated in these patients
Ascending muscle weakness that can lead to resp or cardiac arrest, EKG changes
What EKG changes occur in hyperkalemia and when would you likely see them?
Peaked T waves As K rises, elongated PR interval Widened QRS - sine wave - asystole
What other factors can increase cardiac effects of hyperkalemia?
HYPOnatremia, HYPOcalcemia, acidosis
Treatment for severe HYPERkalemia?
Promote cellular reuptake with insulin and glucose, Nabicarb
Calcium chloride or gluconate to depress membrane potential and stabilize cardiac rhythm
Increase K elimination with lasix, HD, or kayexalate
What form of calcium is the physiologically active form?
The ionized form
How do acute acidosis and acute alkalosis effect ionized calcium levels?
acute acidosis increases ionized calcium levels and acute alkalosis decreases ionized calcium levels
Why is calcium such an important anion?
It contributes to the cardiac action potential, and excitation and contraction of the heart Also involved in skeletal muscle contraction, neurotransmitter release, secretion of enzymes and hormones, bone formation
What constitutes hypocalcemia?
Ionized Ca < 4 mg / dl (1 mmol/L, or 2 meq / L)
What are s/sx of hypocalcemia?
CV: Dysrhythmias, heart failure, hypotension, EKG changes Neuro: muscle spasms, tetany, seizures, weakness Resp: apnea, laryngospasm, bronchospasm Psych: anxiety, MS changes, depression, psychosis
What can cause hypocalcemia?
Most common: Parathyroid hormone failure (responsible for calcium homeostasis) due to surgical removal during thyroidectomy Massive blood transfusion- preservative citrate produces hypocalcemia by chelating calcium Hypomagnesemia Hyperphosphatemia Cell lysis due to chemo Cell destruction from rhabdo Hyperventilation
What are physical exam signs indicative of hypocalcemia?
Chvostek's sign (tap facial nerve see twitching) Trousseau's sign (inflate BP cuff see hand twitching)
What is the treatment for hypocalcemia?
Rule of 10's: give 10 ml of 10% calcium gluconate (or chloride) over 10 mins, followed by a continuous infusion Vitamin D (to increase enteric calcium uptake) Check other lytes
If a patient is hypocalcemic and is having arrhythmias and neuro changes what other lytes would you want to check?
K and Mg HYPERkalemia and HYPOmagnesemia will potentiate cardiac and neuro changes seen in hypocalcemia
What constitutes HYPERcalcemia?
Ionized calcium greater than 1.5 mmol / L or 3meq/ L) Total serum Ca > 10.5 mg /dl
What are causes of HYPERcalcemia?
HYPERparathyroidism, malignancy, bone lysis
What is a major effect of HYPERcalcemia?
Impairs kidneys ability to concentrate water
What symptoms are you likely to see with a calcium level of 11.5 -13 mg / dl?
lethargy, anorexia, nausea, polyuria
At what level is HYPERcalcemia a medical emergency?
How should you treat it?
> 14 mg / dl NS (dilute out Ca), lasix (promote excretion, goal UO 200-300 ml/ hr), correct other lyte abnormalities
Hydration with NS to dilute calcium Give Lasix to promote calcium excretion
Can also give calcitonin (opposes effects of PTH) but takes 24 - 48 hours to work, give with glucocorticoids
Where is the majority of phosphate stored in the body?
90% in the bones 10% ICF 1% ECF
(Adds up to more than 100, but that's what's on the slides...)
What is phosphate's role in the body?
Forms AT P 2nd messenger systems (cAMP) Nucleic acids, cell membranes (phospholipids) Part of 2,3 DPG Urinary buffer
How does PTH effect phosphate levels?
PTH controls the reabsorption of Phos in the kidneys, PTH causes more Phos to be excreted in the urine
Normal phosphate level
2.7 - 4.5 mg / dl
Causes of hypophosphatemia
common in post-op and trauma pts decreased absorption from GI tract hyperventilation
Severe organ dysfunction with levels < 1 mg/dl Neuro: paresthesias, myopathy, encephalopathy, delirium, coma, seizures Heme: dysfunction of RBC, WBC, Plt Resp muscle weakness Rhabdo Cardiac issues
Moderate Hypophosphatemia: 15 mmol bolus over 2 hours Chronic Hypophosphatemia: 0.2-0.68 mmol / kg/ or 5-16 mg / kg over 12 hours
Causes of hyperphosphatemia
Renal failure (most common) Rapid lysis of cells (chemo)
Correct underlying cause Correct associated HYPOcalcemia Restrict Phos intake Increase Phos excretion with NS and acetazolamide (diamox), Al hydroxide, HD
Magnesium normal lab value
1.8 - 2.5 mg / dl
Co-factor in enzymatic reactions (DNA and protein synthesis, energy metabolism) Endogenous calcium antagonist Partially regulates PTH secretion Regulates and stabilizes membranes, regulates membrane excitability Prevents vasospasm Maintains end organ sensitivity to PTH and vitamin D
Membrane irritability and tetany (similar to hypocalcemia), muscle spasms, paresthesias, depression, weakness, fatigue, HF, coronary spasms, hypotension, dysrhythmias SEVERE: seizures, coma, confusion
Causes of hypomagnesemia
ETOH Usually not due to inadequate intake but to increased losses (NGT, drains, kidneys fail to conserve Mg) aminoglycosides, cardiac glycosides, chemo, diuretics
T or F hypomagnesemia worsens CHF and digoxin toxicity?
IV Mg! 8-16 meq bolus over 1 hour
HYPERmagnesemia- therapeutic uses
premature labor, pre-eclampsia, eclampsia, arrhythmias
When would one normally see symptoms of HYPERmagnesemia?
>5 mg/dl Pts usually asymptomatic between 2.5 - 5 mg/dl
Causes of HYPERmagnesemia
iatrogenic- due to antacids, enemas, renal failure, parenteral nutrition and RF, hypothyroidism, Addison's disease, lithium toxicity
Decreased deep tendon reflexes, somnolence, flushing, hypotension, N/V EKG changes and neuro changes progress as Mg level increases and can lead to cardiac arrest, coma, and paralysis
What 2 lytes are most important for cardiac function?
K and Mg