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7520 Final > Electrolytes > Flashcards

Electrolytes Flashcards

1
Q

what does RAAS do?

A

decreased renal perfusion to kidneys:
Angiotensin II –>
1. vasoconstricts (increase vol and afterload)
2. releases Aldosterone : water (increase vol and preload)
3. triggers the production of Vasopressin (ADH) (water: volume)

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2
Q

Aldosterone

A

acts on kidneys to reabsorb water and Na to increase volume

Volume only!

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3
Q

ADH

A

vasopressin secreted from the post-pit.

  • primary controller of the ECF volume. By osmolality (tonicity)
  • feedback from osmoreceptors
  • water ONLY
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4
Q

ANP

where does it come from and what does it do

A

from cells in the heart.

from stretch receptors from increasing volume

ANP blocks aldosterone and ADH produciton

= excretes H2O and Na

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5
Q

whats the cardinal rule re Na **

A

where Na goes, H2O follows

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6
Q

what is Hct

A

the ratio of vol of blood expressed as a percent

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7
Q

what happens to solutes from blood sample if the PT had 2L fluid bolus

A

the concentration would go down from earlier labs

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8
Q

where is Na ICF or ECF

what are a few functions

A

ECF

  • ECF osmolality/tonicity
  • fluid balance
  • cellular depolarization
  • contributes to acid/base balance
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9
Q

what is Na influenced by? hormones

A

aldosterone and ANP

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10
Q

clinical manifestation of hyponatremia?

A
  • too dilute
  • confusion, irritable, seizure
  • headache, muscle weakness
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11
Q

how do you treat hyponatremia

A

fluid restriction, possible admin hypertonic sol 3% Nacl

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12
Q

Hypernatremia

clinical manifestations

A
  • dehydrated/water def

- confused, twitch, seizures, coma, thirst, flushed

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13
Q

how to treat hypernatremia

A

Slowly replace H2O with D5W

  • limit Na intake
  • free water to enteral feeds
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14
Q

where is K+ located

function?

A

ICF

  • essential for nerve impulses conduction and muscle contraction
  • acid/base balance
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15
Q

how is K+ influenced by acid/base balance

A

-when the serum pH is low, there are more H+ ions. These H+ go into the ICF, which pushes the K+ out =

Hyperkalemia

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16
Q

Hypokalemia causes:

clinical manifestations

A

cause: inadequate intake, GI loss, diurese, shift in cells (acid/base or from glucose/insulin)
- flattened T, dysrhythmias, skeletal muscle weakness

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17
Q

how does insulin and glucose influence K+ and what else does it influence?

what would you do in an emergency?

A
  • insulin shifts glucose into cells and K+ and PO4 follows, reducing serum K+ and phos

hyperkalemia emerg: give D50 IV followed by insulin to shift K + into cells

  • can help of delay lethal arrhythmias while waiting for other interventions (dialysis)
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18
Q

hypokalemia treatment

A
  • replace loss, treat acid/base imbalance, food, reconsider meds (diuretics)
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19
Q

Hyperkalemia cause:

Manifestation

A

high intake, renal dysfunction, acidosis, cell injury

Manifestation: ECG changes, peaked T, bradycardia and blocks , skeletal muscle weakness, cramps, nausea

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20
Q

hyperkalemia treatment

A
  • resolve acid/base, remove with diuretics, kayexalate, dialysis
21
Q

phosphate PO4 ****

where is it?

Functions?

A

80% bones, 20% ICF

  • cell mem structure
  • formation of ATP and 2,3 DPG **
  • cofactor in enzyme reactions
22
Q

PO4 regulation *****

A
  • absorbed in GI tract
  • competes with Ca for absorbtion
  • PO4 and Ca++ have inverse relationship ***
  • influenced by acid/base
    when insulin moves glucose into cells, PO4 and K+ go with
23
Q

hypophosphatemia*** causes

manifestations

A
  • intake, shift into cells (alkalosis/insulin), poor absorption, diarrhea, renal loss
    man: loss ATP = muscle weak, irritable, confusion, poor contractility

Low 2,3 DPG (stabilizes deoxygenated form of Hgb) - left shift curve, decreased O2 delivery

24
Q

hypoPO4

treatment

A
  • replace loss

- correct alkalosis, treat diarrhea, diuretic?

25
Q

hyperPO4

causes:

Manifestations:

A
  • massive cellular lysis
  • renal dysfunction
  • parathyroid dysfunction
  • similar to hypocalcemia (inverse relation)
  • increased cell membrane excitability, anxiety, irritable twitching
  • decreased cardiac contractility and prolonged QT
26
Q

how do you treat hyperPO4

A

correct hypocalcemia , limit intake, ensure adequate renal function

27
Q

Mg - location ***

functions

A

ICF

function: supports the Na/K pump
- facilitates cardiac function **
- important for neuromuscular activity: conduction of nerve impulses, helps Ca move into muscle, promotes vasodilation
- cofactor in intracellular enz actions (ATP)
- protein and DNA synthesis

28
Q

Mg regulation

A
  • we eat it and get rid through vomit, urine and feces
29
Q

hypoMg *****

causes

clinical manifestations

A

cause: inadequate intake or poor absorption
- GI loss: vomit, diarrhea, loss- diuretics

Manifest: neuromuscular overstim, muscle cramps, twitching, hyperrefexia

In severe: resp muscle weakness/paralysis, altered mental status, coma, dysrhythmias, N/V ***?

30
Q

Treat HypoMg

A

increase intake and replace losses

31
Q

HyperMg

Causes

Manifest

A

cause: high intake and renal dysfunction

Manifest: neuromuscular depression; decreased muscle activity, hypoactive reflexes, general weakness

  • flushing and mild hypotension
32
Q

treating hyperMg

A

minimize intake, ensure adequate fluid vol to support urine output, dialysis

33
Q

Calcium

found?

functions?

A

99% bones, 1% in ECF

Ionized- active free floating
Bound- albumin and competes with H+ for sites

Fnctn: cell permeability, membrane stability

  • skeletal and heart muscle contraction
  • blood coagulation
34
Q

Ca regulation **

A
  • diet
  • excrete urine
  • parathyroid horm mobilizes Ca from bones, promote GI absorption, decrease renal excretion
  • Ca influences pH and albumin levels ***
    (more H in the plasma than bound to alb = acidotic, more Ca in plasma than bound to alb = alkalosis)
  • calcitonin decreases absorption and increases renal excretion
  • uptake Ca influenced by PO4 and Vit D levels

** Ca and PO4 have an inverse relationship**

35
Q

hypocalcemia **
causes

manifestations

A

cause:
- inadequate intake, GI malabsorption (when PO4 is elevated in gut, fight for uptake), blood transfusion (citrate binds with Ca)
- thyroid cancer, increased renal losses

manifest: increased cell membrane excitability, reduced stability
- anxiety, confusion, irritable, twitch, cramp
- muscle spasms: laryngeal, abd, bronchial
- prolonged QT, decreased cardiac contractility
- impaired coagulation process

36
Q

hypoCa treatment *****

A
  • correct albumin levels and acid/base imbalance

- replace losses (IV CaCl, Cagluc)

37
Q

HyperCalcemia
causes

Manifestations

A

cause: cancer (esp with bone mets), renal dysfunction (excreted by kidneys)

manifest: decreased cell membrane excitability
- fatigue, confusion, depression
- muscle weakness, hyporefexia
- dysrhythmias, short QT, short ST

38
Q

hyperCa treatment

A
  • correct PO4 levels (inverse), ensure adequate vol to support urine output
  • correct acid/base balance
  • diuretic/dialysis
39
Q

Chloride
where?

function

regulation

A

in the ECF

  • along with Na helps regulate serum osmolality
  • helps maintain acid/base balance

reg: ingested, reabsorbed/excrete by kidneys to maintain acid/base balance
- has inverse relation with HCO3

40
Q

Hypochloremia
causes

manifestations

A

cause: Na deficit, excess HCO3
- GI losses (vomit-hydrochloric acid, diarrhea)
- increased renal losses (diuetics)

man: signs of alkalosis (confusion, twitching, nausea, lightheaded, numbness), incld low Na or low K
- overexcitability, crams, twitch, seizure, coma
- dysrhythmias

41
Q

hypoCl treating

A
  • correct underlying cause, usually acid/base imbalance (alkalosis), ensure adequate hydration
42
Q

hyperchloremia
cause

manifest

A

cause: Na excess, HCO3 deficit, acidosis

man: signs of metabolic acidosis (tachypnea, lethargy, weakness)
- dysrhythmias, decreased CO
- deceased LOC, coma
- role in acid/base balance will also affect Na and K levels

43
Q

hyperCl treatment

A

correct cause, usually acid/base imbalance (acidosis)

44
Q

explain pH and K+ relation **

A

too many H+ = acidosis in ECF and moves into ICF and pushes K out causing = hyperkalemia

consider if it is a deficit or if K+ has just shifted before you treat

45
Q

explain glucose/insulin affect on pH****

A

insulin drives glucose into cells (ICF) taking with it K+ and PO4 making the ECF alkalotic

46
Q

explain influencing factors albumin, pH, and Ca*******

A

serum exists in 2 forms
ionized- active free in serum
bound- Ca fights H for binding to albumin. if there is more Ca bound to albumin than H+, then there is more H+ in serum = acidotic

47
Q

explain chloride and pH relation

A

chloride depletion is one of the most common causes of metabolic alkalosis in critical illness

  • from diuretic use
  • Na and Cl are inhibited and excreted
  • hydrochloric acid is depleted in gastric secretions (vomit/NG)

Metabolic acidosis- from hyperchloremia when HCO3 is lost from body from severe diarrhea or lack of retention from kidneys

OR large/rapid infusion NaCl

48
Q

metabolic acidosis can rise from?

maybe*****

A
  • lactic acidosis (inadequate cell O2)
  • renal dysfunction (alter HCO3 regulation)
  • loss HCO3 from diarrhea, or fistula
49
Q

metabolic acidosis wide-ranging effects**

A
  • often in septic PTs, the HCO3 gets eaten up
  • decreased cardiac contractility –> reduced CO
  • vasodilation–> hypotension
  • pulm vasoconstriction –> impaired gas exchange
  • reduces effectiveness of vasoactive drugs (epi, levo), esp when pH falls below 7.2 (think about parameters re; permissive hypercapnia
  • cardiac dysrhythmias
  • LOC changes
  • shift Oxy/Hgb curve to the right
  • increase inflam response
  • impairs immune response
  • decreased response to insulin/increased insulin resistance
  • decreased ATP production
  • vasopressin doesnt cause vasoconstrict to pulm vasculature

7520 Final (5 decks)

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