fluid and electrolytes Flashcards
Na/K pump: what & how
what: active transporthow: Na out / K in
Na function x3
- skeletal + cardiac muscle contraction- nerve impulse transmission- water balance (where Na goes, H2O follows)
- free H2O replenishment quantity calculation
[0.6 x wt (kg)]x[(measured Na/140) -1]
individuals at risk for electrolyte abnormalities
- elderly- altered renal function- Acute/chronic renal disorders- Acute/chronic endocrine disorders- SIADH, DM- Mentally impaired- unable to access fluids- meds that alter fluid/electrolyte levels- all hospitalized patients
thiazide diuretic site of action
distal convoluted tubule
loop diuretic site of action
thick ascending limb
aldosterone site of action
collecting duct
hypernatremia is…
↓ H2O : Na in ECF = ↑ total body Na / ↓ total body H2O↓ intracellular fluid volume because H2O drawn out of cells
acute water deficit rate of correction
1 mMol/hr
chronic water deficit rate of correction
0.5 mMol/hr
hypervolemic hypernatremia is
change in net body soluted/t…hypertonic saline or Na bicarb infusionskayexalate therapy (sodium polystyrene sulfonate)
hypervolemic hypernatremia tx
diuretics w fluid replacement- free H2O- D5Wtreat the cause
hypovolemic hypernatremia is
↓ body H2O + Nabut losing more H2Od/t…insufficient H2O intake: lt 600-700 ml/day loss of free H2O: excessive sweating, GI loss, osmotic diuresis
hypovolemic hypernatremia tx
NS 0.9%- LOSING Na AND H2Omay need add’l fluids to meet needs: free H2O, D5W
isovolemic hypernatremia is
↑Na, body H2O appropriated/t…inability to concentrate urineappropriate free H2O w/o Na excretion↑ serum osmolality (hyperglycemia, mannitol)
isovolemic hypernatremia tx
diuretics w fluid replacement- free H2O- D5Wtreat the cause
results of hypernatremia x4
↑ Na movement @ depolarization, = ↑ excitability/irritabilityH2O drawn osmotically out of cells = intracellular dehydration↓ intracellular fluid vol CNS: H2O shift brain interstitium → capillaries = cerebral atrophy
hypernatremia: clinical signs
neuro- early: lethargy, weakness, irritability - later: twitching, seizures, coma, deathgeneral- dry/sticky mucosa- ↑ body temp (no fluid buffer for metabolic processes)- thirst
hyponatremia is…
↑ H2O : Na in ECF = ↑ total body H2O ECF more dilute than ICF↓ excitable membrane depolarizationcellular swelling
hyperosmolar hyponatremia is
↑ body concentration w ↓Na- ↑ intravascular oncotic P (hyperglycemia, mannitol)- ICF → extracellular space- ↓ TBW- altered urine Na excretion– low - typical, Na retention appropriate—- d/t → extrarenal loss (GI, skin)– normal/high—- d/t → renal loss (diuretic [thiazide], adrenal insufficiency, Na-losing nephropathy)
hypoosmolar hyponatremia types x3
hypervolemichypovolemicisovolemic
isosmolar hyponatremia is…
LESS COMMON usually d/t lab errorNa conc displaced w/o change in TBW contentmachine mistakes the following for electrolytes that don’t exist:- hyperlipidemia- hyperproteinemia- hyperglycemiafix apparent issues above before addressing Na (may be artifactual)
isosmolar hyponatremia tx
determine urgency of replacement: acute onset, Na
hypernatremia vs hyponatremia: difference between the types
hypernatremia: r/t volumehyponatremia: r/t osmolarity
- altered urine excretion of Na in hyponatremia x2
low - typical, Na retention appropriate- low Na d/t → extrarenal loss (GI, skin)normal/high- low Na d/t → renal loss (diuretic [thiazide], adrenal insufficiency, Na-losing nephropathy)
hypervolemic hypoosmolar hyponatremia
- see often d/t fluid dilution- ↑ hydrostatic P → peripheral edema, ascites, pulm edema- r/t ADH release from intravascular dehydration (CHF, cirrhosis, nephrotic syndrome, ARF or CRF)
hypovolemic hypoosmolar hyponatremia
- presentation: dehydrated- intrinsic free H2O repletion exceeds Na repletion– d/t renal: over-diuresis, adrenal insufficiency, cerebral Na-wasting syndrome– d/t extrarenal: n/v, skin loss (ex: burn)
isovolemic hypoosmolar hyponatremia
total body fluid normal w high ingestion lyte-deplete fluids- more common if excretion impaired- psychogenic polydipsia- beer potomania (beer-drinkers hyponatremia)- SIADH
hyponatremia tx
- free H2O restriction (when appropriate; look @ volume status)- vasopressin V2 receptor antagonists (collecting ducts)- medical tx: aquaphoresis, slow continuous ultrafiltration (SCUF)- Na replacement: foods, IVF- hypertonic saline (3% NS) EXTREME CAUTION! can cause dramatic shift – monitor rate, serial BMP q4-6 hours
hyponatremia results
H2O osmotically drawn into cells: intracellular overhydration, cell lysis,;↑ ICF volume
hypernatremia vs hyponatremia results
hyper: cell atrophy (water out)hypo: cell lysis (water in)
hypovolemic hypoosmolar hyponatremia causes x2
renal: overdiuresis, adrenal insufficiency, cerebral salt wasting syndromeextrarenal: n/v, skin loss
K function x6
H2O balancenerve impulse transmissiontissue synthesismuscle contractioncarb metabolismacid-base balance
hyperkalemia is…
↑ extracellular K+↓ difference between ICF / ECF concentrationsfux up electrical neutrality- ↑ excitability- easy spontaneous stim / difficult appropriate stimulation
hyperkalemia causes
- 2 much repletion- ↑ intake- renal dz (+ K replacement)- hypoaldosteronism- ACE inhibitors, ARBs- spironolactone (aldosterone antagonist)- RBC hemolysis- tumor lysis syndrome- acidosis (excess extracellular H+)– body wants H+ → cell ∴ K+ → extracellular
relationship between hyperkalemia and acidosis
acidosis = excess extracellular H = H → cell∴ K → ECF (balance)
hyperkalemia clinical signs
NEUROneuralgias, paresthesias, weakness/paralysis, muscle twitchingGIn, d, intermittent colic↑ non specific / will kill you ↓CARDIAC- ↓ RMP- ↓ relative refractory period- peaked T waves- prolonged QRS,- ↓ P wave- sine wave, v fib, asystoleearly: excitable / late: 2 much K = slower conduction (Na open slow)!! often asymptomatic until cardiac arrest !!
lyte imbalance often asymptomatic until cardiac arrest
hyperkalemia
hyperkalemia tx
FIND THE CAUSE ASAPsymptomatic = intervene faster!!- restrict intake / potentiating rx- promote → cell– IV Insulin w 50% Dextrose (D50) – albuterol- remove from body– dialysis (HD or PD)– PD only if already on - don’t initiate– emergent dialysis if K ↑↑↑– kayexalate (Na for K in gut)- stabilize membrane action potential- Ca (Chloride/Gluconate/Carbonate)– CaCl = 3x available Ca vs gluconate + CENTRAL LINE – CaCarb = PO- Na bicarb (shifts acid-base bal so K back in)
hyperkalemia tx: promote K+ → cell x2
IV insulin w D50- dex 4 hypoglycemia, preventionalbuterol- can power Na/K pumps
hyperkalemia: stabilize membrane action potential x3
Ca (Chloride/Gluconate/Carbonate)- ↑ threshold potential; re-establishes gap btw resting + threshold. TEMPORARY FIX!– CaCl = 3x available Ca vs gluconate + CENTRAL LINE –CaCarb = PONa bicarb (shifts acid-base bal so K back in)
hypokalemia is
- ↓ extracellular K+- ↑ difference btw ICF + ECF concentrations– ↓ excitability of cellsK+ ↓ ICF + ECF
hypokalemia causes
- ↓ intake, malnutrition- hyperaldosteronism- rx induced: diuretics hyperinsulinism, hyperalimentation- v, gastric suction- alkalosis- contraction alkalosis
hypokalemia s/s
MUSCULARskeletal weakness ↓DTRsNEUROirritability, confusion, lethargyGI smooth muscle weakness↓peristalsis/paralytic ileusCARDIACmore neg RMP↑ relative refractory periodEKG change d/t K hanging out- non‐specific ST changes- T wave flattening / inversion- U wave- sinus brady- arrhythmias (esp vent)- PVC = myocard irritated bc can’t be stim’d
hypokalemia tx
ABOVE ALL: FIND CAUSE- PO supplements- diet- change diuretic– spironolactone – eplerenone (Inspra)– amiloride (Midamor)IV repletion (only if symptomatic)maybe Mg repletion
alkalosis and hypokalemia relationship
↓ H in ECF = H in ICF → ECF to buffer excess bicarbK → ICF (maintain electroneutrality) = serum K ↓- contraction alkalosi
insufficient H2O intake #
less than 600 - 700 mL/day
contraction alkalosis + hypokalemia
loss K d/t loss body fluid not containing bicarb- aka -↑ blood pH d/t fluid lossseen w: diuretic tx- CHF- renal failure- ↑↑ loop diuretics = pee K out = Na + H → cell = BICARB LEFT BEHIND– even w K replacement, H + Na still shift = alkalotic- iatrogenic- GI losses
when is IV K appropriate for hypokalemia
symptomatic only!
Mg #s
1.5 - 2.6
Mg critical for
skeletal muscle contraction, carb metabolism, ATP formation, vitamin activation, cellular growth
hyper vs hypo mag
hyper: ↓ membrane excitabilityhypo: ↑ membrane excitability
hypermag causes
↑ intake- antacids- laxatives- excessive Mg2+ replacement↓ renal function
hypomag causes
↓ intake -OR- ↑ loss- malnutrition/starvation- EtOH ingestion- upper GI loss, d/steatorrhea, malabs conditions– ex: bariatric surgery, celiac, ulcerative colitis- rx interactions: diuretics, aminoglycosides, amphotericin B
rx interactions leading to hypomag
etics, aminoglycosides, amphotericin B
hypermag s/s
EKG similar to hyperK, better toleratedovert s/s at gt 4.0CV- brady- periph vasodilation- hypotension- prolonged PRI- widened QRS- ↓ diastolic BPCNS- ↓ nerve impulse transmission- drowsy/lethargicNEURO- ↓ DTRs- progressively weaker skel musc contractions
hypomag s/s
VERY VERY IRRITABLENEURO- hyperactive DTRs- paresthesias - muscle spasms @ rest CNS- psych depression- psychosis- confusionGI - paralytic ileus- n/v- anorexia/constipation
hypermag tx
mimic hyperkalemia tx- insulin/D50/IVF- d/c supplementation- loopsdialysisprevention (cautious repletion) body tends to tolerate / manage mag well on its own
body tends to tolerate/manage which lyte imbalance well on its own?
magnesium
hypomag tx
FIND CAUSE (iatrogenic?)d/c pharm contribspharm repletionMg Gluconate or ChlorideMg Sulfate IVMg Oxide (NOT Hydroxide ← laxative!!)
Ca2+ #s
9 - 10.5 mg/dL – BOUND4.5 - 5.6 (free/ionized)
hypercalcemia is…
- ↑ serum Ca- dysfxnal control mechanism- excitable tissues less sensitive to stim: heart, skeletal, & smooth muscles, nerves– takes less stimuli to contract ∴ cells not as responsive- ↓ clotting time (faster clot)- kidney stones (d/t attempt to excrete)
hypocalcemia is…
- ↓ serum concentrations- ↑ Na across membranes- ↑ membrane excitability- depolarizations easier & inappropriate
hypercalcemia causes
- ↑ intake (milk‐alkali syndrome)- vit D toxicity (↑D3 = ↑ gut abs)- immobility- hyperparathyroidism- malignancies (tumor lysis syndrome)- rx: thiazides, glucocorticoids
what is required for gut absorption of Ca
Vit D3
rx causes of hypercalcemia
thiazidesglucocorticoids
hypocalcemia causes
- ↓ intake/malnutrition- vit D deficiency- hypoparathyroid- hyperphosphatemia- EtOH abuse- citrate (anticoag in RBC transfusions)- pancreatitis- bicarb infusion- sepsis
hypercalcemia s/s
neuro: AMS/lethargy/coma, muscle weakness, ↓ DTRsGI: constipation, paralytic ileus, anorexia, n/vheme: ↑ clotting (DVTs)behavioral: mild change to psychosisrenal: polyuria, polydipsiaCV: tachycardia → bradycardia“tachy-brady syndrome”, htn (↑ vascular tone)
tachy brady syndrome assoc with which lyte abnormality
hypercalcemia
hypocalcemia s/s
neuro: paresthesias peripherally (pins & needles), facial twitching/tingling, trousseau’s sign, chvostek’s signCV: brady, hypo, prolonged ST & QTGI: ↑ peristalsis, abd spasms, diarrheaMS: muscle spasm @ rest, osteoporosis, hyperactive DTRs
trousseau’s sign
BP cuff inflation = twitchy twitchyassoc with hypoca
chvostek’s sign
poke cheeky = twitchy twitchyassoc with hypoca
hyperca tx
d/c: LR, Ca2+ & vit D supplements (MVI/antacids), thiazide diuretics0.9% sodium chloride & loop sglucocorticoids (cause & tx; bone demineralization or suspends Ca in blood to excrete)prostaglandin synthesis inhibitors (NSAIDS)bisphosphates ⊣ bone resorption (Pamidronate, Etidronate) Ca binders (Plicamycin, Penicillamine)PO4 salts (last resort - Ca/PO4 balance)- K‐phos- Neutra‐phosHD
this lyte imbalance needs adjustment for hypoalbuminemia
hypocalcemia
hypocalcemia tx
nutritional support: dairy, green leafy vegetables, nuts, fishreplacement- PO: Caltrate/Oscale, Ca carbonate- IV: Ca Gluconate (central not req but could necrose), Ca Chloride - CENTRAL LINE!
Ca replacement requiring central line
CALCIUM CHLORIDE
PTH actions: effect, bone, gut, kidney
effect: ↑ Ca ↓ PO4bone: ↑ osteoclastsgut: indirect via vit Dkidney: Ca in PO4 out
Vit D3: effect, bone, gut, kidney
effect: ↑ Ca ↑PO4bone: nonegut: ↑ Ca ↑PO4kidney: none
serum bicarb + kidneys relationship
HCO3 takes time to change! high level = chronic acidosis causing bicarb to be retained in response
BMP CO2 tells us what
it’s equivalent to HCO3 ABG BUT it is CO2 in serum NOT in gas (that’s ABG)
THIS LYTE TAKES TIME TO CHANGE!!!!
HCO3 via kidneys
elevated bicarb causes
metabolic alkalosisprimary ingestion (ex: tums for heart burn)iatrogenic: over‐replacementcontraction alkalosis (volume depletion)metabolic response to respiratory acidosis- poss norm for chronic COPDer- sometimes tolerated given PMH DON’T JUST TX OUT OF RANGE #
contraction alkalosis and volume relationship
volume CONTRACTION (depletion) hence the name!
elevated bicarb tx
FIND CAUSEadjust pharmmaximize renal perfusion (consider supplementation if kidneys screwy)
low bicarb causes
non‐gap (hyperchloremic): 8-16 = normal range ← d/t lossrenal tubular acidosisdiarrhea (bicarbonate loss)urinary diversionsgap 16+ (low bicarb or retaining H)MUDPILESMethanolUremiaDiabetic ketoacidosisPropylene glycol (in IV ativan, fireball)IsoniazidLactic acidosisEthylene glycol (antifreeze, radiator moonshine)Salicylates
** MUDPILES
gap acidosis (16+)M ethanolU remiaD KAP ropylene glycol I soniazidL actic acidosisE thylene glycol S alicylates
elevated BUN causes
aka azotemiaAKICKDpre‐renal state (CHF, shock, hypovolemia)hypercatabolic state/steroidsupper GI bleedhigh protein feedingaggressive diuretic tx
elevated BUN aka
azotemia
low BUN… wtf?!
causes…younger agemalnourishedhemodilutionhepatic failure tx: given cause, is intervention really necessary?
elevated BUN s/s
NEUROMUSCULAR- AMS- coma- encephalopathy- fatigue/weakness- myalgias- neuropathy- seizuresGIanorexia, nauseaGUamenorrhea, sexual dysfxnMISCaltered taste/smellsleep disturbancesuremic frost (N excreted via skin)
uremic frost
N excreted via skin r/t elevated BUN
elevated BUN tx
ID THE DAMN CAUSE- pathologic?- GI bleed, over diuresis, hyperalimentation?- pharmacologic?
what is creatinine
catabolic byproduct of creatine phosphatereleased from muscle @ constant ratefiltered through kidneys (waste product) @ constant rateGFR marker
what does a rise in creatinine indicate?
kidneys are excreting out less - GFR MARKER!DOES NOT MEAN MORE MADE
elevated creat causes
impaired renal fxn: AKI, CKD
low creat causes
muscle wasting ∴ mass loss- liver disease- malnutritionpregnancy
elevated creat s/s
low‐grade feverfatigue/lethargy/malaiseanorexia, weight changedehydrationheadachedyspneamental status changes (encephalopathy)
elevated creat tx
↓ production not possibleDETERMINE CAUSEdialysis: look at patient’s clinical picture to decide when
how to tell if renal fxnal level appropriate?
- is creatinine appropriate?2. compare to BUNgreater than 20 = prerenal failureless than 10:1 = intrarenal failure10 - 20:1 =- normal - if ↑ creat + proportional BUN, post-renal failure
phosphate #s
3 to 4.5 mg/dL
dietary phosphate
red meat, fish, poultry, eggs, milk, whole grains, nuts, legumes ; cola beverages ; prepackaged fast foods; preservatives
hyperphosphatemia is
greater than 4.5 mg/dLTYPICALLY WELL TOLERATEDeffects d/t hypocalcemia
hyperphosphatemia s/s
hypocalcemia!neuro: paresthesias peripherally (pins & needles), facial twitching/tingling, trousseau’s sign, chvostek’s signCV: brady, hypo, prolonged ST & QTGI: ↑ peristalsis, abd spasms, diarrheaMS: muscle spasm @ rest, osteoporosis, hyperactive DTRs
hyperphosphatemia tx
dietary restrictions: soft drinks super badoral phosphate binders- Phoslo (Calcium Acetate)- Renagel (Sevelamer)- Alucaps (Aluminum Hydroxide‐ base for antacids)MUST BE GIVEN WITH FOOD– these don’t pull phosphate out of blood!IVF in severe cases
hypophosphatemia causes
- malnutrition/starvation- Mg & Al-based antacids- excessive phosphate binder - hyperparathyroidism- hyperalimentation (PO/PT/IV)- renal failure- EtOH abuse (lytes depleted)
hypophosphatemia s/s
hypercalcemia!
phosphate and calcium
BALANCE ∴ INVERSE RELATIONSHIP!hypocalcemia = hyperphosphatemiahypercalcemia = hypophosphatemia
hypophosphatemia tx
dietary repletionpharmacologic repletion- PO/PT: K‐Phos/Neutra‐Phos- IV: Na Phosphate/K Phosphate– pay attention to Na and K levels!CAUTION with IV repletion- do not exceed 7 mmol/hr- K+ /Na+ supplementation
** hypophosphatemia: caution with IV repletion **
- do not exceed 7 mmol/hr- K+ /Na+ supplementation
best fluid for volume restoration
NORMAL SALINE!
