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66 Cards in this Set
- Front
- Back
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M&M Ch. 28
what does one mole of a substance represent |
6.02 x 10 to 23rd degree molecules
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what is molarity
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the standard SI unit of concentration that expresses the number of moles of solute per liter of solution
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what is molality
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an alternative term that expresses moles of solute per kilogram of solvent
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what is osmotic pressure generally dependent on
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only on the number of nondiffusable solute particles. because the average kinetic energy of particles in solution is similar regardless of their mass
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how much weight is water in the average male and female
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male: 60%
female: 50% |
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how much fluid is in the intracellular compartment
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*40% of body weight
*67% of total body water *28L of fluid volume |
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how much fluid is in the interstitial compartment
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*15% of body weight
*25% of total body water *10.5L of fluid volume |
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how much fluid is in the intracellular compartment
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*40% of body weight
*67% of total body water *28L of fluid volume |
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how much fluid is in the intravascular compartment
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*5% of body weight
*8% of total body water *3.5L of flud volume |
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what is the volume of water within a compartment determined by
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its solute composition and concentrations
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how much fluid is in the intravascular compartment
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*5% of body weight
*8% of total body water *3.5L of flud volume |
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how much fluid is in the interstitial compartment
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*15% of body weight
*25% of total body water *10.5L of fluid volume |
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what is the most important determinant of intracellular osmotic pressure
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potassium
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what is the most important determinant of extracellular osmotic pressure
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sodium
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what is the volume of water within a compartment determined by
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its solute composition and concentrations
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what is the principal function of extracellular fluid
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provide medium for cell nutrients and electrolytes and for cellualr waste products
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what is the most important determinant of intracellular osmotic pressure
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potassium
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maintenance of which extracelluar volume is critical to keep normal
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intravascular volume
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what is process to cause edema
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the gelatinous interstitial fluid pressure is normally negative and as the volume increases, insterstitial pressure rises and eventually becomes positive. The free fluid in the gel increases rapidly and appears clincally as edema
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what is intravascular fluid commonly referred to
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plasma
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how are increases in extracellular fluid volume normally relfected
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proportionately between intravascular and interstitial volume
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what does the rate of diffusion of a substance across a membrane depend on
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1. permeability of that substance through that membrane
2. concentration difference for that substance between two sides 3. the pressure difference between either side becasue pressure imparts greater kinetic energy 4. the electrical potential across the membrane for charged substances |
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what are the mechanisms by which diffusion can occur between interstitial and intracellular fluid
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1.directly through the lipid bilayer of the cell membrane
2.through protein channels within the membrane 3.by reversible binding to a carrier protein that can traverse the membrane |
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what is the fluid exchange between intracellular and interstitial spaces governed by
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the osmotic forces created by differences in nondiffusable solute concentrations
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what does the plasma sodium concentration generally reflect
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total body osmolality
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what is the normal plasma osmolality value
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280-290 mOsm/L
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what do significant osmolal gaps indicate
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high concentration of an abnormal osmotically active molecule in plasma such as, ethanol glycol
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what patients may osmolal gaps may be seen in
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CRF
ketoacidosis pts receiving lg amounts of glycine (TURP) Hyperlipidemia Hyperproteinemia |
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major causes of hypernatremia
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impaired thirst
coma essential hypernatremia solute diuresis osmotic diuresis: DKA, nonketotic hyperosmolar coma, mannitol admin excessive water losses renal neurogenic diabetes insipidous nephrogenic DI extrarenal sweating combined disorders coma plus hypertonic nasogastric feeding |
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what is the most common cause of hypernatremia with a normal total body sodium content
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diabetes insipidus (in conscious patients)
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what is diabetes insipidus characterized by
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marked impairment in renal concentrating ability that is due either to ecreased ADH secretion (central diabetes insipidus) - OR-
failure of the renal tubules to respond normally to circulating ADH (nephrogenic diabetes insipidus) |
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causes of central diabetes insipidus
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*lesions in or around he hypothalamus and the pituitary stalk
*following neurosurgical procedures and head trauma |
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diagnosis of central diabetes insipidus
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history of
polydipsia polyuria (>6L/d) absence of hyperglycemia confirmed by an increase in urinary osmolality following administration of exogenous ADH |
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treatment of central diabetes insipidus
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aqueous vasopressin 5U SC Q4
DDAVP intranasal spray QD-BID |
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causes of nephrogeic diabetes insipidus (DI)
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congenital
CRF hypokalemia hypercalcemia sickle cell hyperproteinemias SE of drugs: amphotericin B, lithium, ifosfamide, mannitol ADH secretion normal but kidneys fail to respond |
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diagnosis of nephrogenic DI
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failure of kidneys to produce a hypertonic urine following the admin of exogenous ADH
Treatment is directed at treating underlying cause |
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clinical manisfestations of hypernatremia
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*restlessness
*lethargy *hyperreflexia *seizures *coma |
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treatment of hypernatremia
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aimed at restoring plasma osmolality to normal and correcting the underlying problem
*water deficits should be corrected over 48h with a hypotonic solution such a 5% dextrose in water *decreased total body sodium should be given isotonic fluids to restore plasma volume to normal prior to treatment with a hypotonic solution *increased total body sodium should be treated with loop diuretic along with IV 5%dextrose in water |
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how long should treatment proceed
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plasma sodium should not be decreased faster than 0.5 mEq/L/H
rapid corection could lead to siezures, brain edema, permanent neuro damage and even death |
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anesthetic considerations with hypernatremia
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*increases MAC for IA
*hypovolemia accentuates any vasodilation or cardiac depression from anesthetic agents and predisposes to hypotension and hypoperfusion of tissues *dose reduction b/c decreased volume distribution *elective surgery should postponed in pt with na >150 |
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causes of pseudohyponatremia
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with normal plasma osmolality
asymptomatic hyperlipidemia hyperproteinemia symptomatic marked glycine absorption during transurethral surgery elevated plasma osmolality hyperglycemia adminstration of mannitol |
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what is hyponatremia nearly always a result of
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defect in urinary diluting capacity
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how is hyponatremia classified
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according to total body sodium content
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what are the decreased total sodium content hyponatemias
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RENAL
*diuretics *mineralocorticoid deficiency *salt losing nephropathies *osmotic diuresis (glucose, mannitol) *renal tubular acidosis EXTRARENAL *vomiting *diarrhea *sweating, burns *third spacing |
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normal total sodium content hyponatremia
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*primary polydipsia
*SIADH *gluccocorticoid deficiency *hypotyroidism *driug-induced |
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increased total sodium content hyponatremia
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*CHF
*cirrhosis *nephrotic syndrome |
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clinical manifestations of
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mild to mod: asymptomatic
early: anorexia, NV and weakness severe:lethargy, confusion, seizures, coma, death |
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what are severe manifestation of hyponatremia usually associated with
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plasma sodium concentrations <120 MEq/L
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treatment of hyponatremia
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*isotonic saline is generally the treatment of choice for hyponatremic pts with decreased total body sodium content
*water restriction is treatment for pts with normal or increased total body sodium |
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what has very rapid correction of hyponatremia been associated with
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demyelinating lesions in the pons resulting in serious serious permanent neurological sequelae
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anesthetic consideration for hyponatremia
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plasma levels >130 mEq/L are generally considered safe
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what is the major hazard of increases in extracelllar volume
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impaired gas exchange due to pulmonary interstitial edema, alveolar edema, or large collections of pleural or ascitic fluid
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what pts should IV replacement of KCL be reserved for
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pts with or at risk for serious cardiac manisfestations or muscle weakness
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at what level should hyperkalemia always be treated
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>6 mEq/L
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what is the most effective treatment initial tratment of hypercalcemiaIV
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rehydration followed by a brisk diuresis (UO 200-300 mL/h) with IV saline infusion and a loop diuretic to accelerate calcium excretion
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how should symptomatic hypocalcemia be treated
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as medical emergency with IV CaCl 3-5 ml of 10% sol OR
Ca gluconate 10-20ml of 10% sol |
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anesthetic consideration of severe hypophophatemia
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may require mechanical ventilation postop
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what could severe hypermagnesemia lead to
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respiratory arrest
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anesthetic considerations of isolated hypomagnesemia
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should be corrected prior to elective procedures b/c of potential for causing cardiac dysrhythmias
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excess renal loss causes of hypokalemia
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*mineralocorticoid excess
*renin excess *barter's syndrome *liddle's syndrome diuresis *chronic metabolic acidosis *antibiotics (gent, amphotericin B) *renal tubular acidosis |
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what gastrointestinal losses lead to hypokalemia
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vomiting
diarrhea |
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what ECF to ICF shifts lead to hypokalemia
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*acute alkalosis
*hypokalemic periodic paralysis *barium ingestion *insulin therapy *vit B12 therapy *thyrotoxicosis (rare) |
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effects of hypokalemia
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cardio
EKG changes/arrythmias myocardial dysfinction neuromuscular skeletal muscle weakness tetany rhabdomyolysis ileus renal polyuria incrased ammonia production increased bicarbonate reabsorption hormonal decreased insulin secretion decreased aldosterone secretion metabolic negative ntrogen balance encephalopathy with liver disease |
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causes of hyperkalemia
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PSEUDOHYPERKALEMIA
*red cell hemolysis *marked leukocytosis/thrombocytosis INERCOMPARTMENTAL SHIFT *acidosis *hypertoncity *rhabdomyolosis *excessive exercise *periodic paralysis *succinylcholine DECREASED RENAL POTASSIUM EXCRETION *renal failure *decreased mineralocorticoid activity *AIDS *K sparing diuretics *ACE inhibitors *NSAIDs *pentamidine *trimethoprim ENHANCED CL REABSORPTION *gordon's syndrome *cyclosporine INCREASED K INTAKE *salt substitutes |
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causes of hypercalcemia
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*hyperparathyroidism
*malignancy *excessive vit D intake *pagets disease *granulomatous disorders *chronic immobilization *milk-alkali syndrome *adrenal insufficiency *drug-induced thiazide diuretics lithium |
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causes of hypocalcemia
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*hypoparathyroidism
*pseudohypoparatyroidism *Vit D deficiency (nutritional or malabsorption) *hyperphosphatemia *precipitation of clacium pancreatitis rhabdomyolosis fat embolism *chelation of calcium multiple rapid PRBC tranfusion or rapid infusion of lg amts of albumin |
