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Fluid & Electrolytes

QuestionAnswer
normal sodium 135-145 mEq/L
normal potassium 3.5-5 mEq/L
normal BUN 7-20 mg/dl
normal hematocrit 40-50%
normal urine specific gravity 1.002-1.030
normal glucose 60-110 mg/dl
normal osmolality 275-295
FVD classic sign dry mucous membranes, comes later
FVD late sign hypotension
FVD, temp changes decreased temp, blood shunted to central area
FVD, respiratory increased respiratory rate bc acidotic, blowing of CO2; thick and sticky secretions
anasarca severe, generalized third spacing
most common site, 3rd spacing abdomen (ascites, in peritoneal cavity?)
primary mediator of fluids hypothalamus
2nd spacing stage where fluid moves from one space to another
3rd spacing fluid in interstitial compartments
FVD sodium normal to high (hemoconcentration)
FVD potassium normal to high (is intracellular, if enough cell death --or sodium levels -- could be high)
FVD BUN high (hemoconcentration); in children may be low but not pathologic
FVD glucose normal to high (stress response, >120)
FVD urine specific gravity high >1.030
FVD osmolality (serum) >300, more particles ↑ number of particles, concentration
FVE hemodynamic signs full bounding pulses, hypertension, increased CVP, neck vein distension, CHF
cerebral edema seen with FVE, Confusion, dizziness, convulsions, coma
pulmonary edema seen with FVE, Dyspnea, tachypnea, hacking cough, crackles, o2 sat down
FVE general signs weight gain, nonpitting interstitial edema, hepatomegaly/splenomegaly
FVE first sign seen pulmonary edema
neck vein distension sign of FVE but not seen in kids, make sure know baseline for adults
goal of Rx for FVE prevent cerebral edema
>>> causes of FVE (10) renal failure, heart failure, excess fluid intake (without electrolytes), high corticosteroids, high aldosterone, plain water enema, NG irrigations, excess hypotonic IV fluids, SIADH, inappropriately prepared formula (dilute formula)
>>> excess fluid intake examples excessive hypertonic fluids, binge drinking contest, psych disorders, drowning in fresh water, inappropriate dialysis
FVE, potassium normal to high (potassium shift out of cells, rasing levels)
FVE, sodium very low, <125
FVE, BUN low (hemodilution)
FVE, urine spec gravity low, <1.005
FVE, glucose normal to high (stress response, >120)
decreased sodium and potassium signs lethargy, weakness
increased sodium and potassium signs increased excitability
acid releases H+ ions in water
base binds to H+ ions in water
buffers prevent major acid-base changes; carbonic acid-bicarbonate, protien, and phosphate buffer system
carbonic acid measured as CO2
acid-base homeostasis bicarb: carbonic acid = 20:1
carbonic acid-bicarb system primary system, 50% of activity, to maintain balance l/t have to also use protein and phosphate buffer systems, 1-2 hours to kick in, bicarb is the major ECF buffer
alkaline environment hard for cells to grow
>>> Respiratory buffer system, carbonic acid carbonic acid compensates and dissociates into CO2 and H20, CO2 exhaled by lungs, system activates rapidly but exhausted quickly
respiratory buffer system, breathing changes changes in depth/rate of resp alters it: hypoventilation retains CO2/carbonic acid and causes acidosis, hyperventilation loses CO2 and causes alkalosis
renal buffer system: time and effectiveness works w/in hours/days, more efficient than respiratory can go for longer periods of time
renal buffering system, bicarbonate primary renal component, can be absobed as needed, combines HCl with ammonia to make ammonium, which is easily excreted by kidneys into urine
compensation regulatory mechanism to return pH to normal level by transforming acids and bases within the body
primary metabolic disturbance causes a respiratory compensation
acute primary respiratory disturbance causes an acute metabolic response
complete compensation pH is fully corrected (normal)
partial compensation buffers are in the process of working; pH is low but the bicarb is elevating to compensate (or pH is high but CO2 is elevating to compensate)
pH *negative logarithm of H+ ion concentration in mEq/L (as H+ ion concentration increases, pH decreases)*normal values 7.35 -7.45 (less is acidotic, more is alkalotic)
HCO3- (bicarb) *normal 22-26 mEq/L (decreased in acidosis, increased in alkalosis)
BE "base excess" indicates the amount of bicarb available in the ECF normal value: +/- 2 mEq/L
serum anion gap *Concentration of anions (HCO3- , Cl-, protein, phosphate, & sulfates) and cations (Na+, K+, MG++, & Ca++) | *10-12 mEq/L normal | *increased in metabolic acidosis (but can be normal) | *calculated by Na - Cl + bicarb
SaO2 the percent of Hb saturated with O2, a calculated value (indirect measurement), calculated with pH and PaO2 (combination of O2 sat, PaO2, and Hb), indicates tissue oxygenation
PaO2 amount of oxygen available to bind with hemoglobin, amount of pressure exerted on O2 by plasma
the lower the PaO2 pressure, the .... less oxygen available to bind with Hb
dramatic drops in PaO2 correlate with dramatic drops in oxygen saturation
PaO2 normal values 75-100 mmHg (for every year above 60 drop 1mmHg)
PaCO2 *partial pressure of CO2 | *reflects adequacy of alveolar ventilation, regulated by lungs, alterations indicate resp disturbance | *normal values 35-45 mmHg (less is alkalotic, more is acidotic)
respiratory alkalosis managment (4) correct cause, rebreathe CO2 as needed, alter ventilation rate, sedatives (for anxiety)
respiratory alkalosis assessment (7) VS, ABGs, RR/depth, LOC/anxiety, neuro checks, injury potential, I&O
respiratory alkalosis CV signs tachycardia, palpitations, increased myocardial irritability
respiratory alkalosis respiratory signs rapid shallow breathing (trying to retain CO2, oxygenate), chest tightness
respiratory alkalosos CNS signs (10) paresthesia, dizzyness, confusion, tetany, convulsion, numb/tingling, light headed, anxiety/panic, Loss of consciousness, hyperactive reflexes
respiratory alkalosis causes (4) hyperventilation, sepsis/infection, over ventilation, hepatic cirrhosis
respiratory alkalosis: labs low CO2, pH high >7.45, bicarb normal if no compensation or decreased if compensation, hypokalemia, hypocalcemia
respiratory acidosis management (7) correct cause, CPT, TCDB if able, suction as needed, semi-Fowlers, fluids to thin secretions, low-flow O2 as needed
respiratory acidosis assessment (8) VS, ABGs, RR/depth, apical pulse, LOC, EKG, skin color/nail beds/mucous membranes, I&O
respiratory acidosis cardiac signs hypotension, peripheral vasodilation weak thready pulse, tachycardia, warm flushed skin
respiratory acidosis respiratory signs dyspnea, slow shallow respirations, hypoxia and hypoventilation, cyanosis
respiratory acidosis CNS signs (6) HA, seizures, altered LOC, papilledema, twitching/tremors, drowsy --> coma
respiratory acidosis causes (4) respiratory depression/arrest, inadequate chest expansion, airway obstruction, interference with alveolar capillary exchange
respiratory acidosis: labs pH low <7.35, PaCO2 high >42, HCO3- normal (or elevated with compensation), hyperkalemia
metabolic alkalosis mgmnt (3) correct cause, restore normal fluid balance, adequate chloride (enhance renal absorption of sodium and excretion of bicarb)
metabolic alkalosis assessment (6) VS, ABGs, RR/depth, LOC, I&O, ECG
metabolic alkalosis GI signs (3) n/v, anorexia, paralitic ileus (hypokalemia)
metabolic alkalosis CNS signs (10) dizzy, nervous, tremors, hyperreflexia, paresthesias, irritability, confusion/apathy/stupor, cramps, tetany, seizures
met alkalosis respiratory signs (2) hypoventilation, respiratory failure
met alkalosis CV signs (5) tachycardia, HTN, PVC, atrial tachycardia, dysthrythmias (from FVE)
met alkalosis causes (4) vomiting, NG suctioning, eating bicarb-based antacids, diuretics
met alkalosis: labs increased pH, increased BE, increased bicarb, decreased anion gap (low K and Na)
met acidosis mgmnt (6) correct cause, treat ketoacidosis (fluids, insulin), give alkaline fluids, hydrate, mechanical ventilation if needed, possible dialysis
insulin used to treat metabolic acidosis (ketoacidosis), forces potassium back into cells
alkaline fluids for met acidosis if severe, sodium bicarb if pH<7.20, salts of organic acid (lactate, citrate), tromethamine THAM
met acidosis assessment (7) VS, ABGs, RR/depth, apical and peripheral pulses, ECG (bc of dramatic K changes), LOC, I&O
metabolic acidosis CV signs (4) dramatic affects: hypotension, dysrhythmias, peripheral vasodilation, warm flushed skin (from dilation, leaking of capillaries)
metabolic acidosis resp signs Kussmaul/deep/rapid respirations, trying to blow off CO2
metabolic acidosis CNS signs (6) think of septic patient: drowsy, HA (from cerebral edema), lethargy, coma, confusion/restless, weakness
metabolic acidosis GI signs (3) n/v, diarrhea, abdominal pain
causes of metabolic acidosis chronic diarrhea, malnutrition, starvation, renal failure, DKA, trauma, shock, sepsis, fever, salicylate toxicity
metabolic acidosis: labs low bicarb, decreased BE, increased anion gap, hyperkalemia (from breakdown of cells from acidosis), high metabolic acids (lactic acids, ketoacids)
causes of metabolic acidosis chronic diarrhea, malnutrition, starvation, renal failure, DKA, trauma, shock, sepsis, fever, salicylate toxicity
metabolic acidosis: labs low bicarb, decreased BE, increased anion gap, hyperkalemia (from breakdown of cells from acidosis), high metabolic acids (lactic acids, ketoacids)
alkaline fluids for met acidosis if severe, sodium bicarb if pH<7.20, salts of organic acid (lactate, citrate), tromethamine THAM
met acidosis assessment (7) VS, ABGs, RR/depth, apical and peripheral pulses, ECG (bc of dramatic K changes), LOC, I&O
metabolic acidosis CV signs (4) dramatic affects: hypotension, dysrhythmias, peripheral vasodilation, warm flushed skin (from dilation, leaking of capillaries)
metabolic acidosis resp signs Kussmaul/deep/rapid respirations, trying to blow off CO2
metabolic acidosis CNS signs (6) think of septic patient: drowsy, HA (from cerebral edema), lethargy, coma, confusion/restless, weakness
metabolic acidosis GI signs (3) n/v, diarrhea, abdominal pain
causes of metabolic acidosis chronic diarrhea, malnutrition, starvation, renal failure, DKA, trauma, shock, sepsis, fever, salicylate toxicity
metabolic acidosis: labs low bicarb, decreased BE, increased anion gap, hyperkalemia (from breakdown of cells from acidosis), high metabolic acids (lactic acids, ketoacids)
Created by: 1382359715
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