Flashcards in Fluids- electrolytes Deck (60):
Components of body fluid?
- ICF: 2/3 of total body fluid
ISF, plasma, and lymphatic fluid
Electrolytes in ECF and ICF?
- ECF: Na+ (142 mEq/L), Cl- (103 mEq/L), HCO3-
- ICF: K+ (140 mEq/L), Mg, phosphates
Water movement regulation?
- starling forces: hydrostatic pressures and osmotic pressures:
Capillary hydrostatic pressure: pressure in capillary pushing fluid out
Interstial fluid hydrostatic pressure: pushing fluid in from ISF
- Osmotic force due to plasma concentration (drawing fluid into capillaries)
- Osmotic force due to ISF protein concentration (drawing fluid out)
What is osmolality? What is most important factor?
- concentration of an osmotic soln when measured in osmols of solvent
plasma: 280-295 mOsm/kg
- Na+ is most impt plasma osmolality factor (water follows Na+)
Process of fluid and electrolyte replacement? IV solutions?
- assess ins and outs
- oral replacement preferred when tx dehydration
saline equivalents: crystalloids - normal saline or LR
water equivalents: D5W
if 3% NS - have to do central line (will destroy peripheral veins)
What are the components of LRs?
- 250-273 mOsm/L
- Na+, Cl-, lactate, Ca+, K+
- albumin: 290-31- mOsm/L
- blood products:
packed RBCs, fresh frozen plasma
Saline: 3%, 5%, D5W1/2NS adverse effects?
- ICF depletion
- fluid overload
Albumin adverse effects?
- allergic reactions
- possible infection transmission (hepatitis)
Impt steps in assessing types of fluid loss?
- pt hx
- vital signs and PE
What is hypervolemia?
- too much Na+
- expansion of effective arterial blood volume
- CHF, cirrhosis, aldosterone, renal disease
WHat is hypovolemia?
- too little Na+
- volume contraction
- dehydration: V/D, exercise, not drinking enough water
What is hyponatremia? Hypernatremia? Edema?
- too much water
- not enough Na+
- too little water (dehydration)
- excess Na+
edema: too much Na+ with water retention in the ISF (abdomen, lungs) - alcoholics, cirrhosis, metastatic cancers
Severity of edema?
- 1+ = 2 mm
- 2+ = 4 mm
- 3+ = 6 mm
- 4+ = 8 mm
How to tx mild dehydration?
- oral replacement:
fluids with electrolytes are preferred
- avoid fluids with high sugar concentration
- water and sports drink or in children pediolyte
- stop activities that create ongoing losses
Assessing degree of fluid loss for moderate hypovolemia?
- hx: any GI losses (V/D), excessive exercise, renal losses
- sx: easy fatiguability, thirst, muscle cramps, postural dizziness, abdominal pain, CP, lethargy, confusion, decreased urination
- clinical manifestations: decreased skin turgor, tachycardia, dry mucus membranes
How do electrolyte imbalances present? How do these imbalances occur?
- sxs: precipitate as CV, neuro, and neuromuscular abnormalities
- disruptions occur: via drugs, disease states, diarrhea, vomiting, infection, hormone imbalances, malignancies
- to tx these: need results of lab tests then start IV fluids
Etiologies of hyponatremia?
- hypovolemia: GI losses: vomiting, and diarrhea, dehydratioon
renal losses: (thiazide diuretics), ACEIs, mineralocorticoid deficiency
- normovolemia: SIADH, primary polydipsia/marathon runners, low dietary solute intake, psychogenic polydipsia
- hypervolemia: CHF, cirrhosis, nephrotic syndrome, advanced syndrome (rare)
- others: hypothyroidism, primary adrenal insufficiency, drugs
What lab values do you want to know for hyponatremia? lab value indications?
hyponatremia is less than 135 meq/L
- serum osmolality impt
- urine Na+
- assess severity:
less or equal to 120 meq/L panic value***
- 120-130: depends on sxs and situations
- greater than 130 is generally not tx
Clinical manifestations of chronic hyponatremia?
- cerebral adaption:
going to have fatigue, nausea, dizziness, confusion, lethargy, muscle cramps, gait disturbances and forgetfulness
Clinical manifestations of acute hyponatremia?
- acute hyponatremic encephalopathy: cerebral over hydration related to degree of hyponatremia
fatigue an malaise are usually the first sxs
- HA, lethargy, coma, seizures and eventually respiratory arrest
- acute hyponatremic encephalopathy may cause permanent neuro damage or death
- can be hyponatremic classified by ECF status: hypovolemic: GI losses, renal losses (thiazides), normovolemic: SIADH, low Na+ intake, hypervolemic: CHF, cirrhosis
How does osmotic demyelination happen?
- try to correct hyponatremia and then you overcorrect making ECF hypernatremic so H2O leaves brain too quickly and it shrinks
How can acute hypotonic hyponatremia occur? WHat are the sxs?
- can result in sxs of neuronal cell expansion and cerebral edema
- Nausea/HA, seizure, coma and death
Hyponatremia etiologies with inability to suppress ADH problem?
- true volume depletion (GI or renal losses - thiazide diuretics), decreased tissue perfusion (reduced CO or systemic vasodilation in cirrhosis for instance)
syndrome of inappropriate ADH secretion (SIADH)
Causes of hyponatremia with appropriate suppression of ADH secretion?
- primary polydipsia
- low dietary solute intake
- advanced renal failure
Causes of hypovolemic hyponatremia?
- GI or renal losses
- if serum Na+ hasn't dropped critically low quickly
- usually just volume replacement orally or IV if more severe
Tx for hypovolemic hyponatremia?
- NS/isotonic saline
- depending on pt status may do slow bolus
- then maintenance depending on ongoing losses
Causes of hypervolemic hyponatremia?
- CHF, cirrhosis, renal failure
Tx of hypervolemic hyponatremia?
- restrict fluids: 1000-1200 ml/day
- restrict sodium: 1000-1200 mg/day
- utilize loop diuretics to remove excess fluid, K+ replacement
What is SIADH? Causes? Tx?
- too much ADH. Either Eu/hypervolemic hypotonic hyponatremic presentation
drug induced: carbamazepine, SSRIs, haloperidol, and thorazine
disease induced: malignancies, CNS disorders, post-surgery, pulmonary infections
Tx: tx underlying cause, fluid restriction is mainstay!!!!! May use oral salt tablets, loop diuretics
What is the therapy for severe hyponatremia?
- this puts pt at risk for brain herniation
- tx: 3% hypertonic saline:
goal to increase Na+ by 4-6 meq/L in 24 hr period, measure serum Na+ q hr, and measure urine output
What risk is there if you correct severe hyponatremia too rapidly? What are the high risk populations?
- develop osmotic demyelination
High risk pops:
- women and children postop period
- pts with hyperacute hyponatremia - psychosis, marathons, ectasy, and those with intracranial pathology
Unreplaced water loss:
- impairment in thirst or access to water
- insensible and sweat losses
- GI losses
- central or nephrogenic diabetes insipidus
- hypothalamic lesions impairing thirst or osmoreceptor fxn:
- primary hypodipsia
- reset osmostat in mineralorticoid excess
water loss into cells:
severe exercise or seizures
intake or administration of hypertonic sodium solns
Acute hypernatremia manifestations?
- rapid decrease in brain volume can rupture cerebral veins leading to focal intracerebral or subarachnoid hemorrhage
- demyelinating brain lesions as seen with overly rapid correction of chronci hyponatremia
Chronic manifestations of hypernatremia?
- brain adapts (within a day) by pulling water from the CSF and increasing the uptake of solute by the cells which also increases the amt of water into the cells
- assessment is difficult because most affected adults already have neuro disease diminishing the thirst response
Etiology of hypernatremia (greater than 145 meq/L?
- loss of water
- addition of hypertonic soln
- sodium overload
Tx of hypernatremia?
- replace free water with D5W, add normal saline soln if hypovolemic - use a seond IV
- if replacing ongoing electrolyte losses (use 0.45% NS possibly with added K+)
- fast onset, less than 24 hrs, decrease by 1 meq/L/hr correction
- insidious is greater than 24 hrs, decrease in serum Na+ by no more than 10 mEq/24 hrs
- monitor serum Na+/K+ closely
What is central DI? what is the tx?
- not enough ADH production (tumors, or lesions on the brain)
- tx: desmopression: 10 mcg/day, ADH like activity
- titrate to 10 mcg/bid intranasally, and restrict fluid intake
What is nephrogenic DI? Tx?
- kidney resistant to ADH
- tx: thiazide diuretic to decrease ECF and Na+, Na+ restriction (2000 mg/day)
How do you tx hypernatremia?
- for hypernatremia from unreplaced water loss:
need to est water deficit
- need to replace ongoing losses, any ongoing GI losses and urine losses
- obligatory losses: sweat and stool
- determin safe rate plasma Na+ can be normalized:
usually less than 0.5 mEq/L/hr or about 10 mEq/day, usually use 0.45% NS with K+
- monitor lytes closely (q 4 hrs)
- overly rapid correction: can lead to cerebral edema
What percentage of Ca2+ is bound to albumin? Where is calcium normally found?
- each 1 g/dL drop of albumin below 4.5g/dL, decreases serum calcium by 0.8 mg/Dl
- when you look at Ca2+ levels make sure you are looking at albumin levels too if Ca levels are off
- it is an extracellular electrolyte, and it is in an unbound/free fraction active form
- normal serum range (free): 8.5-10.5 mg/dL
Etiologies of hypercalcemia?
- greater than 10.5
- cancer and primary hyperparathyroidism (primary causes
- drugs: thiazide diuretics, calcium supplements, lithium
Sxs of hypercalcemia? What can occur if left untx?
N/V, anorexia, constipation
- if left untx:
metastatic calcification, nephroliathisis, renal failure
Outcome and tx of hypercalcemic crisis?
- outcome: oliguric renal failure, coma, v-arrhythmias, death
- tx: saline and loop diuretics: 2-3 mg/dL, drop in 24-48 hrs
bisphophonates: for malignant etiologies: zoledronic acid: 4 mg IV over 15 min
- osteoclast inhibitors: calcitonin
Etiologies of hypocalcemia? sxs?
- hypoparathyroidism, vit D deficiency, loop diuretics, and high or normal phosphates
- correct level for hypoalbuminemia
- hypomagnesemia assoc with refractory severe hypocalcemia
- sxs: tetany, paresthesias around mouth - hallmark sxs
- EKG: QT prolongation, decreased myocardial contractility
How do you tx acute sx HypoCa++?
- IV admin of calcium salts
- 100-300 mg elemental calcium IV over 5-10 min (less than 60 mg/min)
- continuous infusion: 0.5-2 mg/kg/hr for 2-4 hrs
- maintenance infusion 0.3-0.5 mg/kg/hr
- gluconate over chloride for peripheral admin because of less irritation
- Magnesium if hypomagnesaemia present
How do you tx chronic hypocalcemia?
- oral calcium supp (give Vit C with Ca, and Vit D if not responding)
- 1-3 grams elemental calcium/day: watch for -
constipation, GI upset, carbonate less expensive than gluconate/citrate , but citrate better absorption
- if not responding - add vit D: 1000 IU/day
Normal serum level of phosphorus? Hyperphosphatemia? Tx?
- 2-4.5 mg/dL
-hyperphosphatemia: decreased excretion due to low GFR (renal disease), chemo and rhabdomyolysis
- sxs due to Ca-phosphate interaction
- hypocalcemia results with chronic hyperphostphatemia
- tx: GI binders - IV Ca++ salts
Tx of hyperphosphatemia?
- emergency tx seldom necessary: this can be done with dialysis
- usually occurs in renal failure:
diet restriction, phosphate binding gel: selvelamer (decreases mortality), calcium supplements, avoid aluminum containing antacids - this can cause bone disease
What is hypophosphatemia? sxs? Tx?
- less than 2.0
- sxs are rare until under 1 mg/dL
- long term: proximal muscle weakness and osteomalacia
- severe or sx hypophosphatemia:
IV phosphorus - give slowly, NaPO4, K+PO4
- oral phosphate replacement for mild to moderate:
- neutra-phos K: 250 mg phosphate, GI upset
Causes of hypomagnasemia?
- reduced intake: dieting, unbalanced diet, depleted foods
- impaired absorption (malabsorption) - GI diseases -IBD - crohns, ulcerative colitis
- increased excretion: alcoholism, laxative abuse, tx with diuretics or digitalis
Clinical manifestations of hypomagnesemia? drugs that can cause this?
- occurs in nearly 12% of hospitalized pts
- manifestations: neuromuscular, muscle cramps, tetany, seizures, coma
abnormalities of Ca metabolism - hypocalcemia, CV: widened QRS, a fib, ventricular arrhythmias
- drugs that can cause this: diuretics, aminoglycosides, cisplatin, cyclosporine, and alcohol
When and what should you tx hypomagensemia with?
hypomag: is less than 1.4 mEq/L
- tx if less than 1 mEq/mL or sx
- Tx with:
IV MgSO4 if sx/severe:
bolus - can cause flushing, sweating
- a large amt is secreted in the urine so a continuous infusion is need after the bolus to raise the magesium level
- oral replacement if mild-mod:
sustained release preps preferred
otherwise usual dosing 800-1600 mg a day in divided dosing, often causes diarrhea
- Mg 3-5 meq/L: N/V
- Mg 4-7 meq/L: sedation, decreased reflexes, weakness
- Mg 5-10 meq/L: hypotension, bradycardia, quadriplegia
- Mg 10-15 meq/L: no reflexes, respiratory paralysis, cardiac arrest
Tx of hypermagensemia?
- greater than 2 mEq/L
- IV calcium (100-200 mg elemental Ca++) to antagonize neuromuscular and CV effects of magnesium
- tx: renal failure: hemodialysis
if normal renal function: forced diuresis with fluid and loop diuretics
Hypokalemia? Etiologies? Sxs?
- less than 3.5 mEq/L
- etiologies: B-2 agonists, loop diuretics, ACEIs, thiazides, High dose PCNs, amphotericin B, insulin
medical: metabolic acidosis, vomiting, diarrhea
- sxs: low energy, muscle weakness, restlessness, cardiac sxs: EKG changes: U wave, cardiac arrhythmias
- danger in persons on digoxin
- loop or thiazide deficit:
40-100 mEq K supp (BID or TID)
oral therapy is preferred: KCL (given in mEq not mg)
- without food to avoid GI upset
- severe or sx:
IV K in saline bag: dextrose stimulates insulin to further shift K into cells so don't give dextrose!!!
- 10-20 mEq KCL in 100 mL 0.9% saline over one hour
- more than 10 meq/hr monitor EKG
- limit 40-60 mEq/L peripheral line: phlebitis
Etiologies of hyperkalemia?
- greater than 5.5 mEq/L
- increased K+ intake
- decreasd excretion
- aldosterone resistance
- shift to ECF (in DKA)
Clinical manifestations of hyperkalemia?
- ascending muscle weakness
- usually doesn't affect respiratory muscles
- cardiac effects: EKG changes: initially peaked T waves and shortened QT interval, which progresses to prolonged QRS and QT interval and P waves may disappear, can can then lead to dysrhythmias