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GU > Lecture 3: Fluids/Electrolytes/Acid-Base > Flashcards

Lecture 3: Fluids/Electrolytes/Acid-Base Flashcards

1
Q

What systems does our body activate to compensate for a decreased osmotic pressure/blood volume?

A
  • Increased sympathetic
  • Increased RAAS
  • Increased ADH
  • Increased Thirst
  • Decreased ANP
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2
Q

What typically causes isotonic fluid volume deficit?

A
  • Decreased PO intake
  • Excessive fluid loss (renal primarily)
  • Third spacing
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3
Q

What S/S are typically seen in isotonic fluid volume deficit?

A
  • Increased thirst, fatigue, AMS
  • Low BP, tachycardia, weak/thready pulse, flat neck veins, increased cap refill
  • Wt loss, dry mucous membranes, low skin turgor, sunken eyes/fontanelles.

Look under tongue for mucous membranes.

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4
Q

What labs are associated with isotonic fluid volume depletion?

A
  • High Uosm and Urine SG
  • Increased Hct
  • Altered renal labs

SG = specific gravity

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5
Q

If an AKI patient presents with a hx of fluid loss with signs of hypovolemia, what can we give them? What should we be monitoring?

A
  • NS or LR.
  • PRBCs (if blood loss)
  • Poor CO: inotropes
  • Must monitor for hyperchloremic metabolic acidosis, which needs bicarb to treat. (only seen in excess NS)
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6
Q

What S/S are associated with isotonic fluid volume excess or hypervolemia?

A
  • Decreased thirst, feeling bloated/swollen
  • Full, bounding pulse, distended neck veins, increased BP.
  • Ascites, pulmonary edema, extremity edema.
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7
Q

What are common etiologies associated with isotonic fluid volume excess?

A
  • Excess intake: Overadministration of fluids or PO intake.
  • Decreased elimination: HF, Renal failure, corticosteroids
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8
Q

What labs are associated with isotonic fluid volume excess?

A
  • Low Uosm and Urine SG, decreased Hct
  • Abnormal renal labs
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9
Q

What is the primary treatment for isotonic fluid volume excess?

A
  • Loop diuretics if functional kidneys.
  • Dialysis for prolonged or lack of response to diuretics.
  • Restriction of fluid/sodium intake is a MUST to actually improve outcomes.

Increasing urine output alone is not efficacious.

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10
Q

What are the S/S of hyperphosphatemia?

A

Same as hypocalcemia.

  • Hyperreflexia
  • Carpopedal spasm
  • Chvostek’s and/or Trosseau’s

Phosphate binds calcium.
Stones, abdominal groans and psychiatric moans

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11
Q

What is the treatment for hyperphosphatemia?

A
  • Phosphate binders (Calcium carbonate, sevelamer, lanthanum carbonate)
  • Avoiding processed foods with inorganic phosphate (nuts)
  • Restore renal function
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12
Q

What are the common etiologies associated with hypokalemia?

A
  • Intrinsic potassium wasting
  • Diuretics
  • Poor nutrition
  • Insulin
  • Beta-agonists
  • Alkalosis
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13
Q

What are the common S/S associated with hypokalemia?

A
  • Weakness
  • Cramps, constipation
  • Hypotension, palps, dysrhythmias
  • Flattened T waves leading to prolonged QT and U waves, ultimately causing ST depression.

Mainly affects muscles.

Lower K = lower T

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14
Q

What are the common etiologies associated with hyperkalemia?

A
  • Renal: inadequate excretion or metabolic acidosis.
  • Adrenal insufficiency
  • Cellular breakdown: damage/crush
  • ICF release: cell damage or excessive muscle contraction
  • ACEI/ARB, BBs, IV excess
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15
Q

What are the common S/S associated with hyperkalemia?

A
  • Muscular weakness/cramps
  • Cramps, diarrhea, vomiting
  • Hypotension, palps, dysrhythmias, CARDIAC ARREST
  • Peaked T waves => widened QRS and loss of P-waves => sine waves.
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16
Q

What is the treatment protocol for hyperkalemia?

A
  1. Antagonizing cardiac effects via IV calcium gluconate!
  2. Correction of Serum K+ via IV Insulin + IV dextrose (if BG < 250)
  3. Removal of potassium via Cation exchangers (Kayexelate, Lokelma, Veltassa)

Albuterol can be given in step 2 to assist the effects, but caution in cardiac disease.

Insulin effects only last about 6 hours.

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17
Q

What is the fastest GI cation exchanger?

A

Zirconium cyclosilicate or Lokelma.

1 hour to onset

Requires TID dosing.

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18
Q

What is the concern with using Kayexelate?

A

High constipation and many SEs.
Often needs a laxative as well.

Not preferred.

Suggested to only use in life-threatening AKI hyperkalemia without access to dialysis or other therapy.

Can cause hypomagnesemia and hypocalcemia as well.

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19
Q

Aside from GI cation exchangers, what else can be done to help remove potassium in hyperkalemia?

A
  • Loop/Thiazide diuretics
  • Hemodialysis

Hemodialysis is most effective and reliable.

20
Q

Describe isotonic hyponatremia.

A

Low Na but normal serum Osm.

MCC: Extra molecules in the blood.

21
Q

Describe hypertonic hyponatremia.

A

Low Na in the presence of high serum Osm.

MCC: secondary osmotic molecule active, such as glucose, radiocontrast

22
Q

What is the underlying mechanism behind hypovolemic hyponatremia?

A

Inappropriate salt loss.

Extrarenal: V/D, Burns, Dehydration
Renal: ACEi, diuretics, intrinsic salt wasting, etc.

Unable to reabsorb salt properly.

Greater loss of salt than volume.

23
Q

What is the underlying mechanism behind hypervolemic hyponatremia?

A

Retention of Na, but even higher retention of volume.

Renal: intrinsic renal fluid retention, nephrotic syndrome
Other: HF, liver disease

Impaired ability to get rid of fluid.

Na is generally not that low, but the increased volume status makes it seem so.

24
Q

What are the underlying etiologies behind euvolemic hyponatremia?

A
  • SIADH
  • Hypothyroidism
  • Psychogenic polydipsia
  • Beer potomania

Need Urine Na and Uosm to determine ADH activity.

MC type of hypotonic hyponatremia.

25
Q

What are the S/S of hyponatremia?

A

Neurologic symptoms d/t cerebral edema.

  • N/V, HA, confusion, lethargy
  • Seizure, brainstem herniation, coma, death

Weakness and cramps are only in very acute cases generally.

26
Q

What is the general treatment protocol for hypovolemic hyponatremia?

A

Give isotonic NS for mild-mod.

Give Hypertonic saline for severe.

27
Q

What is the main danger of infusing too much sodium? How do we prevent it?

A

Osmotic demyelination syndrome (ODS).
Prevented with loop diuretic and/or DDAVP to prevent volume overload.

28
Q

For OP treatment of hyponatremia, what are the mainstays of treatment?

A
  • Fluid restriction
  • Vasopressin receptor antagonists (Conivaptan or tolvaptan)
  • Salt tablets/NS/IV hypertonic saline

Conivaptan: combined V1, V2, IV.
Tolvaptan: V1, oral.

29
Q

What is the main concern with vasopressin receptor antagonists?

A

Hepatotoxicity.
Max recommended duration of use is 30 days.

No fluid restriction needed with vasopressin receptor antagonists.

Monitor with LFTs and BMP.

30
Q

What does hypernatremia with normal Urine osmolality suggest for etiology?

A

Excessive water loss via renal or non-renal.

31
Q

What does hypernatremia with low Urine osmolality suggest for etiology?

A

DI (neurogenic or nephrogenic)

32
Q

What does hypervolemic hypernatremia suggest for etiology?

A

Excess Na intake via IV, salt tablets, or bicarb with water loss.

33
Q

What are the S/S of hypernatremia?

A
  • Neuro: Increased thirst, HA, agitation, delirium, seizures, coma, death
  • CV: Low BP, high HR, weak/thready pulse, dry mucous membranes, low skin turgor.

Suggestive of hypovolemia as well.

34
Q

What are the mainstays of treatment for hypernatremia?

A
  • Free water fluids such as 1/2 NS or D5W.

Restoring renal function is the goal.

35
Q

What are the 3 major causes of metabolic alkalosis? (elevated pH)

A
  • Increased H+ loss
  • Excess bicarb/alkali: Bicarb, hypochloremia, alkaline solutions.
  • Abnormal renal excretion/absorption: Diuretics.

Hypovolemia + hypochloremia + hypokalemia + reduced GFR => metabolic alkalosis

36
Q

What are the S/S of metabolic alkalosis?

A

Depends on underlying cause, but alkalosis in general causes neuronal excitability.
Will be functionally similar to HYPOcalcemia.

Being basic is excitatory

37
Q

What are the 3 major causes of metabolic acidosis?

A
  • Increased acid generation: Lactic acidosis, ketoacidosis, ingestion (same as alkalosis)
  • Loss of bicarb: Severe diarrhea, urine exposure to GI mucosa, proximal renal tubular acidosis.
  • Decreased renal acid excretion: Decreased GFR, distal renal tubular acidosis

General underlying mechanism is decreased GFR.

Proximal tubule: Reabsorption of bicarb.

Distal tubule: Acid excretion.

38
Q

What are the S/S of metabolic acidosis?

A

Decreased neuronal excitability, such as confusion, weakness, increased thirst.

39
Q

How is severe metabolic acidosis treated? (< 7.2)

A

IV bicarb to raise to 7.2 first.

40
Q

How is mild-mod metabolic acidosis treated? (> 7.2)

A

Typically, the body can begin converting ketoacids and lactate to bicarb and restore themselves if the underlying cause is fixed.

Need pH above 7.2 for body to function well enough.

41
Q

What lifestyle change can help with chronic metabolic acidosis?

A

Avoiding animal proteins.

42
Q

With a pt in metabolic acidosis secondary to AKI, what is the recommended treatment?

A

Dialysis and bicarb.

43
Q

In what situations is bicarb recommended in metabolic acidosis due to AKI?

A
  • Non-anion gap acidosis due to diarrhea.
  • Waiting for dialysis
  • Readily reversible AKI cause (volume depletion or obstruction)
  • Rhabdo w/o any other indications of dialysis or hypervolemia.
44
Q

When is dialysis recommended for metabolic acidosis due to AKI?

A

Anything with a pH < 7.1, even if cause is reversible.

45
Q

When is dialysis indicated for AKI?

A
  • Life-threatening electrolyte disturbances (esp hyperkalemia)
  • Volume overload refractory to diuresis
  • Metabolic acidosis < 7.1 (esp if can’t receive bicarb)
  • Uremic complications
  • Prolonged AKI

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