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Advanced Health Assessment Unit 2 > Electrolytes > Flashcards

Electrolytes Flashcards

1
Q

What is the principle extracellular cation, essential for the generation of action potentials in neuro and cardiac tissue?

A

Sodium

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2
Q

The most common electrolyte disturbance in hospitalized patients; typically an excess of TBW (not decreased Na)

A

Hyponatremia

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3
Q

S/Sx are dependent on the rate and severity of decrease.
Arterial HTN, increased CVP, pulm edema, decreased cardiac function, arrhythmias, malaise, headache, lethargy, seizure/coma

A

Hyponatremia

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4
Q

Why do rapid decreases in plasma Na cause an increase in brain swelling?

A

Blood-Brain barrier is not really permeable to sodium, but is freely permeable to water

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5
Q

Plasma Na > ____ is safe for general anesthesia

A

130

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6
Q

TURP surgeries use hypotonic irrigation fluids during the resection. What are the anesthesia plans for a patient undergoing a TURP?

A

1) Use neuraxial block with an awake patient to monitor neuro status
2) Use isotonic solutions to replace fluid/blood loss

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7
Q

How to calculate the Na deficit?

A

0.6 x wt in kg x (desired Na - actual Na) → amt mEq to give
-½ deficit replaced in first 8 hours, remainder over 24-72 hours if S&S resolved → 0.9% NS with loop diuretic

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8
Q

Raise serum Na slowly to about 120-125 meq/L to avoid ____?

A

CNS complications (Pontine demyelination)

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9
Q

Absolute or relative TBW deficit related to Na; Plasma Na > 145 causes water loss from cells/crenation; loss of ability to concentrate urine & decreased thirst in geriatric patients

A

Hypernatremia

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10
Q

Tremors, weakness, irritability, confusion, seizures/coma, hypovolemia, renal insufficiency, diabetes insipidus

A

Hypernatremia

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11
Q

Due to water loss exceeding Na loss: diarrhea, vomiting, osmotic diuresis, inadequate intake, fever, burns, exposed surgical areas, prolonged positive pressure ventilation w/o humidity
-Hypotension, dec CVP, dec UOP, dec skin turgor, inc HR
-Tx: replace with 0.45 or 0.9 NS and then remaining free water deficit with D5W

A

Hypovolemia with Hypernatremia

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12
Q

Due to Na overload: dialysis with hypertonic solutions, treatment with hypertonic saline, Na bicarb administration
-Inc weight, inc BP, edema, CHF, rales
-Tx: dialysis, diuretics, replace water deficit with D5W

A

Hypervolemia with hypernatremia

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13
Q

The principle intracellular cation; essential for maintaining resting membrane potentials and in generating action potentials in neuro & cardiac tissue

A

Potassium

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14
Q

Causes:
-redistribution from ECV to ICV due to inc activity of Na/K pump (alkalemia, insulin, beta2 agonists, hypercalcemia, hypomagnesemia)
-total body K deficit (vomiting, diarrhea, NG suction, diuresis, hyperaldosteronism, surgical trauma, excess cortisol)
-decreased intake

A

Hypokalemia

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15
Q

Why does hypomagnesemia precipitate hypokalemia?

A

Hypomagnesemia impairs retention of K+ in the kidneys, resulting in increased excretion in the urine.

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16
Q

Weakness, augmentation of NMB, decreased cardiac contractility, ECG changes due to hyperpolarization of the cardiac cell (flattened T/U, increased PR/QT, ST depression, arrhythmias)

A

Hypokalemia S/Sx

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17
Q

Anesthesia Considerations:
avoid glucose fluids (bc carbs increase insulin), avoid hyperventilation, rapid correction of acidosis may lead to fatal hypokalemia, consider replacing Mg

A

Hypokalemia

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18
Q

No need to correct chronic hypoK unless digitalis therapy, IV replacement → < 10meq/hr. Slow PO correction is safest

A

Hypokalemia treatment

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19
Q

Causes:
-Decreased excretion
-ICF to ECF shift
-inability to excrete K (caution w/ penicillin, NSAID, ACEI, CSA in renal failure patients)
-hypoaldosteronism (potassium sparing diuretics act as aldosterone antagonists & interferes with renal elimination of potassium)
-acidosis (0.1 pH decrease increases K conc by 0.5 meq/L)
-upregulation of receptors following burns, stroke, paraplegia, prolonged bed rest (be careful giving succinylcholine because all the receptors open at once!)

A

Hyperkalemia

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20
Q

Muscle weakness (esp legs/resp system), paresthesia, cardiac conduction changes (prolonged PR, loss of P, wide QRS, peaked T, eventually asystole)
Most detrimental effects are on the cardiac conduction system!!

A

Hyperkalemia S/Sx

21
Q

Anesthesia Considerations:
-Patient history (renal issues? Meds that retain K+?)
-consider canceling elective surgery if K > 5.5, always treat >6
-Avoid hypoventilation
-avoid succhinycholcine use
-remove K from IV fluids
-Meds: emergency drugs ready, muscle relaxant responses unclear.
-Consider using smaller doses of NMB and frequent neuromuscular monitoring with nerve stimulator

A

Hyperkalemia

22
Q

Tx:
-1 amp CaCl -> Stabilize myocardium to prevent vfib
-Shift K into cell: Administer 10 units Insulin and 25g D50 - monitor glucose or
administer a beta agonist (Albuterol)
-Enhance K+ elimination -> Loop diuretic
-Hemodialysis

A

Hyperkalemia

23
Q

Intracellular ion, NMDA receptor antagonist, essential for many enzyme rxns (DNA/Protein synthesis, energy metabolism, glucose utilization, FFA synthesis/breakdown), controls K reabsorption in renal tubules, stabilizes cell membranes, influences release of neurotransmitters (endogenous Ca antagonist- inhibits entry of Ca into presynaptic nerve terminals)

A

Magnesium

24
Q

Why do you frequently see hypokalemia with hypomagnesemia?

A

The Na/K pump is Mg dependent

25
Q

Causes:
inadequate intake, protracted vomiting/diarrhea, renal insufficiency

A

Hypomagnesemia

26
Q

S/Sx: skeletal muscle spasm/weakness, CNS irritability, seizures, hyperreflexia, confusion, ataxia, cardiac irritability

A

Hypomagnesemia

27
Q

Tx: bolus with MgSO4 1 gram over 15-20 min; rate of infusion no greater than 1 meq/min

A

Hypomagnesemia

28
Q

Look for other associated disturbances (hypoK, hypoNa, HypoCa), frequently occurs in alcoholic patients

A

Hypomagnesemia

29
Q

Causes: acute/chronic renal failure, toxemia from Mg therapy, over administration of Mg-containing compounds (antacids, cathartics)

A

Hypermagnesemia

30
Q

S/Sx: skeletal muscle weakness (watch for resp arrest!), vasodilation with myocardial depression & hypotension (complete heart block, cardiac arrest), hyporeflexia (diminished DTRs), sedation/somnolent

A

Hypermagnesemia

31
Q

Tx: stop Mg intake, increase excretion (loop diuretic), antagonize CV or NM toxicity with CaCl or Cagluc

A

Hypermagnesemia

32
Q

This potentiates the action of non-depolarizing NMB (lasts a lot longer)
-Intubate OB patients if respiratory or reflexes are compromised

A

Hypermagnesemia

33
Q

50% of serum Ca is ____, only type physiologically active. The rest of Ca is protein bound (Albumin)

A

Ionized

34
Q

Regulated by calcitonin and parathyroid hormone, essential for all motor movement (skeletal muscle/myocardial), neuromuscular releases, secondary messenger systems (cAMP), and cardiac pacemaker activity (plateau phase)

A

Calcium

35
Q

Causes:
malabsorption, increased excretion from chronic renal insufficiency, hypoparathyroidism, chelation from citrate in blood transfusions (typically transient and negligible unless renal/hepatic failure or hypothermia), shift into cell with alkalemia (H ion conc decreased)

A

Hypocalcemia

36
Q

CNS (paresthesias, confusion, seizures), CV (decreased myocardial contractility, hypotension, cardiac failure, arrhythmias, prolonged QTc), NM (twitching, cramping, Trousseau’s sign, Chvostek’s sign, convulsions, laryngospasm)
-May antagonize CCBs (monitor for hypertension)

A

Hypocalcemia

37
Q

Supplementation with CaCl (3-5mL of 10% solution)
-Treat hypoMg and/or HyperPhos
-Don’t treat hypoKalemia without correcting hypocalcemia due to risk of tetany
-Avoid Alkalosis (drives Ca into cells)
-Monitor levels and VS during tx

A

Hypocalcemia

38
Q

90% of cases are due to decreased renal excretion from hyperparathyroidism or bone malignancies.
Other: immobility, increased intake (antacids or vitamin D)

A

Hypercalcemia

39
Q

Muscle weakness, CNS depression, nephrolithiasis (kidney stones), increased digoxin sensitivity, HTN, prolonged PR/wide QRS

A

Hypercalcemia

40
Q

Hydration with NS + lasix to inhibit renal reabsorption/promote Ca excretion, dialysis, chelators (phosphate & EDTA-pull toxins from blood. Be cautious- can overshoot and get significant hypoCa), Bisphosphonates (inhibit bone breakdown - relatively slow onset but long duration of action), calcitonin (faster onset but short duration - in conjunction w bisphosphonates)
-Invasive monitoring
-Lower doses of Non-depolarizing NMB if skeletal weakness present (ensure patient is VERY STRONG before extubating)
-Acidemia increases ionized Ca

A

Hypercalcemia

41
Q

Examines buffers (total bicarbonate) in relation to other measured electrolytes.
= Na - (HCO3 + Cl)

A

Anion Gap

42
Q

8-12

A

Normal Anion Gap

43
Q

Indicates a metabolic acidosis from unmeasured organic ions (lactic acidosis or ketoacidosis)

A

Elevated Anion Gap

44
Q

Indicates a hyperchloremic acidosis (from renal or GI bicarb loss; renal tubular acidosis or diarrhea)

A

Normal AG in patient with metabolic acidosis

45
Q

Augments NMB

A

Hypokalemia

46
Q

Avoid Succ, response to NDMR is unclear. Possible decreased requirements intra-op

A

Hyperkalemia

47
Q

Potentiates action of NDNMBs

A

Hypermagnesemia

48
Q

Use lower doses of NDNMB if skeletal muscle weakness is present

A

Hypercalcemia

Advanced Health Assessment Unit 2 (6 decks)

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