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Flashcards in fluid and electrolytes Deck (110)
1

Na/K pump: what & how

what: active transporthow: Na out / K in

2

Na function x3

- skeletal + cardiac muscle contraction- nerve impulse transmission- water balance (where Na goes, H2O follows)

3

* free H2O replenishment quantity calculation

[0.6 x wt (kg)]x[(measured Na/140) -1]

4

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

5

thiazide diuretic site of action

distal convoluted tubule

6

loop diuretic site of action

thick ascending limb

7

aldosterone site of action

collecting duct

8

hypernatremia is...

↓ H2O : Na in ECF = ↑ total body Na / ↓ total body H2O↓ intracellular fluid volume because H2O drawn out of cells

9

acute water deficit rate of correction

1 mMol/hr

10

chronic water deficit rate of correction

0.5 mMol/hr

11

hypervolemic hypernatremia is

change in net body soluted/t...hypertonic saline or Na bicarb infusionskayexalate therapy (sodium polystyrene sulfonate)

12

hypervolemic hypernatremia tx

diuretics w fluid replacement- free H2O- D5Wtreat the cause

13

hypovolemic hypernatremia is

↓ body H2O + Nabut losing more *H2O*d/t...insufficient H2O intake: lt 600-700 ml/day loss of free H2O: excessive sweating, GI loss, osmotic diuresis

14

hypovolemic hypernatremia tx

NS 0.9%- LOSING Na AND H2Omay need add’l fluids to meet needs: free H2O, D5W

15

isovolemic hypernatremia is

↑Na, body H2O appropriated/t...inability to concentrate urineappropriate free H2O w/o Na excretion↑ serum osmolality (hyperglycemia, mannitol)

16

isovolemic hypernatremia tx

diuretics w fluid replacement- free H2O- D5Wtreat the cause

17

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

18

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

19

hyponatremia is...

↑ H2O : Na in ECF = ↑ total body H2O ECF more dilute than ICF↓ excitable membrane depolarizationcellular swelling

20

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)

21

hypoosmolar hyponatremia types x3

hypervolemichypovolemicisovolemic

22

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)

23

isosmolar hyponatremia tx

determine urgency of replacement: acute onset, Na

24

hypernatremia vs hyponatremia: difference between the types

hypernatremia: r/t volumehyponatremia: r/t osmolarity

25

* 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)

26

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)

27

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)

28

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

29

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

30

hyponatremia results

H2O osmotically drawn into cells: intracellular overhydration, cell lysis,;↑ ICF volume

31

hypernatremia vs hyponatremia results

hyper: cell atrophy (water out)hypo: cell lysis (water in)

32

hypovolemic hypoosmolar hyponatremia causes x2

renal: overdiuresis, adrenal insufficiency, cerebral salt wasting syndromeextrarenal: n/v, skin loss

33

K function x6

H2O balancenerve impulse transmissiontissue synthesismuscle contractioncarb metabolismacid-base balance

34

hyperkalemia is...

↑ extracellular K+↓ difference between ICF / ECF concentrationsfux up electrical neutrality- ↑ excitability- easy spontaneous stim / difficult appropriate stimulation

35

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

36

relationship between hyperkalemia and acidosis

acidosis = excess extracellular H = H → cell∴ K → ECF (balance)

37

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 !!

38

lyte imbalance often asymptomatic until cardiac arrest

hyperkalemia

39

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)

40

hyperkalemia tx: promote K+ → cell x2

IV insulin w D50- dex 4 hypoglycemia, preventionalbuterol- can power Na/K pumps

41

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)

42

hypokalemia is

- ↓ extracellular K+- ↑ difference btw ICF + ECF concentrations-- ↓ excitability of cellsK+ ↓ ICF + ECF

43

hypokalemia causes

- ↓ intake, malnutrition- hyperaldosteronism- rx induced: diuretics hyperinsulinism, hyperalimentation- v, gastric suction- alkalosis- contraction alkalosis

44

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

45

hypokalemia tx

ABOVE ALL: FIND CAUSE- PO supplements- diet- change diuretic-- spironolactone -- eplerenone (Inspra)-- amiloride (Midamor)IV repletion (only if symptomatic)maybe Mg repletion

46

alkalosis and hypokalemia relationship

↓ H in ECF = H in ICF → ECF to buffer excess bicarbK → ICF (maintain electroneutrality) = serum K ↓- contraction alkalosi

47

insufficient H2O intake #

less than 600 - 700 mL/day

48

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

49

when is IV K appropriate for hypokalemia

symptomatic only!

50

Mg #s

1.5 - 2.6

51

Mg critical for

skeletal muscle contraction, carb metabolism, ATP formation, vitamin activation, cellular growth

52

hyper vs hypo mag

hyper: ↓ membrane excitabilityhypo: ↑ membrane excitability

53

hypermag causes

↑ intake- antacids- laxatives- excessive Mg2+ replacement↓ renal function

54

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

55

rx interactions leading to hypomag

etics, aminoglycosides, amphotericin B

56

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

57

hypomag s/s

VERY VERY IRRITABLENEURO- hyperactive DTRs- paresthesias - muscle spasms @ rest CNS- psych depression- psychosis- confusionGI - paralytic ileus- n/v- anorexia/constipation

58

hypermag tx

mimic hyperkalemia tx- insulin/D50/IVF- d/c supplementation- loopsdialysisprevention (cautious repletion) body tends to tolerate / manage mag well on its own

59

body tends to tolerate/manage which lyte imbalance well on its own?

magnesium

60

hypomag tx

FIND CAUSE (iatrogenic?)d/c pharm contribspharm repletionMg Gluconate or ChlorideMg Sulfate IVMg Oxide (NOT Hydroxide ← laxative!!)

61

Ca2+ #s

9 - 10.5 mg/dL -- BOUND4.5 - 5.6 (free/ionized)

62

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)

63

hypocalcemia is...

- ↓ serum concentrations- ↑ Na across membranes- ↑ membrane excitability- depolarizations easier & inappropriate

64

hypercalcemia causes

- ↑ intake (milk‐alkali syndrome)- vit D toxicity (↑D3 = ↑ gut abs)- immobility- hyperparathyroidism- malignancies (tumor lysis syndrome)- rx: thiazides, glucocorticoids

65

what is required for gut absorption of Ca

Vit D3

66

rx causes of hypercalcemia

thiazidesglucocorticoids

67

hypocalcemia causes

- ↓ intake/malnutrition- vit D deficiency- hypoparathyroid- hyperphosphatemia- EtOH abuse- citrate (anticoag in RBC transfusions)- pancreatitis- bicarb infusion- sepsis

68

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)

69

tachy brady syndrome assoc with which lyte abnormality

hypercalcemia

70

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

71

trousseau's sign

BP cuff inflation = twitchy twitchyassoc with hypoca

72

chvostek's sign

poke cheeky = twitchy twitchyassoc with hypoca

73

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

74

this lyte imbalance needs adjustment for hypoalbuminemia

hypocalcemia

75

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!

76

Ca replacement requiring central line

CALCIUM CHLORIDE

77

PTH actions: effect, bone, gut, kidney

effect: ↑ Ca ↓ PO4bone: ↑ osteoclastsgut: indirect via vit Dkidney: Ca in PO4 out

78

Vit D3: effect, bone, gut, kidney

effect: ↑ Ca ↑PO4bone: nonegut: ↑ Ca ↑PO4kidney: none

79

serum bicarb + kidneys relationship

HCO3 takes time to change! high level = chronic acidosis causing bicarb to be retained in response

80

BMP CO2 tells us what

it's equivalent to HCO3 ABG BUT it is CO2 in serum NOT in gas (that's ABG)

81

THIS LYTE TAKES TIME TO CHANGE!!!!

HCO3 via kidneys

82

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 #

83

contraction alkalosis and volume relationship

volume CONTRACTION (depletion) hence the name!

84

elevated bicarb tx

FIND CAUSEadjust pharmmaximize renal perfusion (consider supplementation if kidneys screwy)

85

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

86

** MUDPILES

gap acidosis (16+)M ethanolU remiaD KAP ropylene glycol I soniazidL actic acidosisE thylene glycol S alicylates

87

elevated BUN causes

aka azotemiaAKICKDpre‐renal state (CHF, shock, hypovolemia)hypercatabolic state/steroidsupper GI bleedhigh protein feedingaggressive diuretic tx

88

elevated BUN aka

azotemia

89

low BUN... wtf?!

causes...younger agemalnourishedhemodilutionhepatic failure tx: given cause, is intervention really necessary?

90

elevated BUN s/s

NEUROMUSCULAR- AMS- coma- encephalopathy- fatigue/weakness- myalgias- neuropathy- seizuresGIanorexia, nauseaGUamenorrhea, sexual dysfxnMISCaltered taste/smellsleep disturbancesuremic frost (N excreted via skin)

91

uremic frost

N excreted via skin r/t elevated BUN

92

elevated BUN tx

ID THE DAMN CAUSE- pathologic?- GI bleed, over diuresis, hyperalimentation?- pharmacologic?

93

what is creatinine

catabolic byproduct of creatine phosphatereleased from muscle @ constant ratefiltered through kidneys (waste product) @ constant rateGFR marker

94

what does a rise in creatinine indicate?

kidneys are excreting out less - GFR MARKER!DOES NOT MEAN MORE MADE

95

elevated creat causes

impaired renal fxn: AKI, CKD

96

low creat causes

muscle wasting ∴ mass loss- liver disease- malnutritionpregnancy

97

elevated creat s/s

low‐grade feverfatigue/lethargy/malaiseanorexia, weight changedehydrationheadachedyspneamental status changes (encephalopathy)

98

elevated creat tx

↓ production not possibleDETERMINE CAUSEdialysis: look at patient’s clinical picture to decide when

99

how to tell if renal fxnal level appropriate?

1. 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

100

phosphate #s

3 to 4.5 mg/dL

101

dietary phosphate

red meat, fish, poultry, eggs, milk, whole grains, nuts, legumes ; cola beverages ; prepackaged fast foods; preservatives

102

hyperphosphatemia is

greater than 4.5 mg/dLTYPICALLY WELL TOLERATEDeffects d/t hypocalcemia

103

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

104

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

105

hypophosphatemia causes

- malnutrition/starvation- Mg & Al-based antacids- excessive phosphate binder - hyperparathyroidism- hyperalimentation (PO/PT/IV)- renal failure- EtOH abuse (lytes depleted)

106

hypophosphatemia s/s

hypercalcemia!

107

phosphate and calcium

BALANCE ∴ INVERSE RELATIONSHIP!hypocalcemia = hyperphosphatemiahypercalcemia = hypophosphatemia

108

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

109

** hypophosphatemia: caution with IV repletion **

- do not exceed 7 mmol/hr- K+ /Na+ supplementation

110

best fluid for volume restoration

NORMAL SALINE!