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GU: Clin Med IIA > Fluid, Electrolyte, and Acid-Base Disorders > Flashcards

Fluid, Electrolyte, and Acid-Base Disorders Flashcards

1
Q

Much of the care of AKI is what type?

A

supportive

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2
Q

common complications of AKI

A
  1. Abnormal volume status
  2. Hyperphosphatemia
  3. Hyperkalemia
  4. Hyponatremia
  5. Uremia
  6. Severe metabolic acidosis (pH < 7.2)
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3
Q

Drop in osmotic pressure or blood volume causes the body to make several adjustments:

A
  1. Increased:
    - Sympathetic nervous system output
    - RAAS activity
    - ADH levels
    - Thirst
  2. Decreased:
    - Atrial natriuretic peptide (ANP)
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4
Q

Increase in osmotic pressure or blood volume causes the body to make several adjustments:

A
  1. Decreased:
    - Sympathetic nervous system output
    - RAAS activity
    - ADH levels
    - Thirst
  2. Increased:
    - Atrial natriuretic peptide (ANP)
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5
Q

what is the net goal of normal balance of sodium and water

A

Adjust water intake, water and sodium retention by the kidney, and vasoconstriction

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6
Q

loss of body fluids, often accompanied by decreased fluid intake

A

Isotonic Fluid Volume Deficit
AKA - “hypovolemia,” volume depletion

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7
Q

causes of Isotonic Fluid Volume Deficit
aka “hypovolemia”

A

Decreased PO intake
Excessive fluid loss - GI, renal, skin
Third spacing - edema, ascites, effusions

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8
Q

Increased thirst, fatigue, altered mental status
Low BP, high HR, weak/thready pulse, flat neck veins, cap refill >3 sec
Wt loss, dry mucous membranes, low skin turgor, sunken eyes or fontanels
these s/s indicate what

A

Isotonic Fluid Volume Deficit

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9
Q

labs for Isotonic Fluid Volume Deficit

A
  1. High Uosm and Urine SG
  2. increased Hct, may see abnormal renal labs
    - If due to renal fluid wasting - may see very dilute urine!
    - If accompanied by blood loss - Hct may also be low!
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10
Q

AKI pts with a ___and signs of ____ can receive PO or IV fluids

A

clinical hx of fluid loss
hypovolemia and/or oliguria

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11
Q

AKI pts with a clinical hx of fluid loss and signs of hypovolemia and/or oliguria can receive what fluid?

A

IV fluids - LR or 0.9% NS

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12
Q

NS in excess can lead to ?
how to tx?

A

hyperchloremic metabolic acidosis
Bicarb solution if needed (e.g., dextrose in H2O with HCO3-)

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13
Q

CI of LR/0.9% NS

A

Signs of volume overload, HF

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14
Q

what to give for volume depletion due to blood loss

A

PRBCs

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15
Q

what to give for volume depletion due to poor CO

A

inotropes

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16
Q

inability to get rid of water and/or sodium, or excess water/sodium intake

A

Isotonic Fluid Volume Excess
AKA - “hypervolemia”

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17
Q

causes of Isotonic Fluid Volume Excess

A
  1. Excess intake - Overadministration of IV fluids, hypertonic IV fluids, dietary intake
  2. Decreased elimination - Heart failure, renal failure, corticosteroids
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18
Q

Decreased thirst, feeling bloated/swollen
Full, bounding pulse; distended neck veins, may see increased BP
Ascites, pulmonary edema, extremity edema
these s/s are indicative of ?

A

Isotonic Fluid Volume Excess

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19
Q

labs of Isotonic Fluid Volume Excess

A
  1. Low Uosm and Urine SG, decreased HCT, may see abnormal renal labs
    - If due to inability of kidneys to get rid of urine - may see concentrated urine or low UO!
    - If anemic - Hct may not be elevated!
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20
Q

tx for Isotonic Fluid Volume Excess

A
  1. Assess underlying cause
    - IV diuretics - acute management
    — Loop diuretics
    - Dialysis - persistent volume overload /no response to diuretics
    - No improvement in outcomes from increasing urine output alone
  2. Restrict fluid and sodium intake
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21
Q

Impaired renal excretion of phosphate

A

Hyperphosphatemia

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22
Q
  1. fatigue, SOB, N/V
  2. Signs of hypocalcemia - Hyperreflexia, carpopedal spasm, + Trousseau or Chvostek sign
    what are these s/s indicative of?
A

hyperphosphatemia

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23
Q

tx for Hyperphosphatemia

A
  1. Limit phosphate intake
    - Phosphate binders with meals can limit GI absorption
    - Avoid processed foods with inorganic phosphate
    - Restoration of renal function
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24
Q

causes of hypokalemia

A
  1. Renal - intrinsic potassium wasting, or due to diuretic SE
  2. GI - poor intake (nutrition, NPO)
  3. Other causes - insulin, beta-agonists, loop diuretics, alkalosis

Less common in AKI/CKD than hyperkalemia, but possible!

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25
Q
  1. s/s often affect muscles (skeletal, smooth, cardiac)
    - weakness, fatigue, cramps, tenderness
    - abd cramps, constipation
    - hypotension, palpitations, dysrhythmias
    - flattened T waves → prolonged QT → U wave → ST depression
    what are these s/s indicative of?
A

Hypokalemia

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26
Q

tx for hypokalemia

A

Correction of underlying cause
1. acute:
- K replacement - oral or IV; potassium chloride or potassium gluconate
— If IV - 10-20 mEq/hr max
— If ora - 10-40 mEq QD to QID
2. chronic, recurrent:
- Increase potassium-rich foods in diet
- K replacement - oral potassium chloride or potassium gluconate
- Adjustment of meds - insulin, beta-agonists, loop diuretics

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27
Q

contributing factors of hypokalemia

A

Hypomagnesemia
Metabolic acidosis
Medication adjustments

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28
Q

monitoring for hypokalemia

A

renal function, electrolytes, symptoms

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29
Q

Very common complication of both AKI and CKD

A

hyperkalemia

30
Q

causes of hyperkalemia

A
  1. Renal - inadequate excretion, metabolic acidosis
  2. Adrenal insufficiency
  3. Cellular breakdown - traumatic stick, hemolysis, crush injury
  4. Release from ICF - cell damage, excessive/severe muscle contraction
  5. Other causes - ACEI/ARB, beta-blockers, excess intake (usually IV)
31
Q
  1. often affect muscles (skeletal, smooth, cardiac)
    - weakness, cramps (including abdominal)
    - abd cramps, D/V
    - hypotension, palpitations, dysrhythmias, cardiac arrest
    - peaked T waves → loss of P waves → widened QRS → sine wave
    these s/s are indicative of?
A

hyperkalemia

32
Q

tx goals for hyperkalemia

A
  1. Immediate treatment warranted if very high levels, ECG changes, or neuromuscular symptoms
  2. 3 steps to hyperkalemia management:
    - Immediate blocking of cardiac effects
    - Rapid reduction in plasma K+
    - Removal of potassium
33
Q

how to Immediate antagonism of cardiac effects - tx hyperkalemia

A
  1. IV calcium - reduces cardiac excitability
  2. 10 mL of 10% calcium gluconate IV over 2-3 min with cardiac monitoring
    - Takes effect in 1-3 min, lasts 30-60 min
    - Repeat if ECG changes do not improve or recur
    - slower infusion of calcium if must be used
  3. May not need if no cardiac s/s or arrhythmias present!
34
Q

caution with IV calcium

A

Potentiates cardiac toxicity of digoxin; consider

35
Q

how to rapidly reduce plasma K+ by forcing into cells - tx hyperkalemia

A
  1. IV insulin - forces shift to occur
  2. 10 U regular insulin IV + 40 mL of 50% dextrose (D50W)
    - Takes effect in 10-20 minutes, peaks in 30-60 min, lasts 4-6 h
  3. Albuterol and insulin + glucose can have an additive effect on K+
    - 10-20 mg albuterol (nebulized) in 4 mL saline inhaled over 10 min
36
Q

what can happen with 10 U of regular insulin IV followed by 40 mL of 50% dextrose (D50W) when treating hyperkalemia?
how to tx?

A

Hypoglycemia is common!
10% dextrose at 50-75 mL/h, glucose monitoring
Not necessary to give if glucose 250+ mg/dL

37
Q

what patients can be resistant to albuterol effects when tx hyperkalemia

A

~20% of ESRD patients are resistant to effects

38
Q

caution with albuterol in these pts

A

pts with cardiac disease

39
Q

how to remove potassium during hyperkalemia tx

A
  1. GI cation exchangers - Sodium polystyrene sulfonate (SPS, Kayexelate), zirconium cyclosilicate (Lokelma), patiromer (Veltassa)
  2. Loop or Thiazide Diuretics
  3. Hemodialysis
40
Q

MOA of GI cation exchangers

A

Exchanges Na+ for K+ in GI tract, ￪ fecal K+ excretion

41
Q

onset of GI cation exchangers

A

Zirconium cyclosilicate - 1 hour
Patiromer - 7 hours
SPS - 2-24 hours

42
Q

dosing for GI cation exchangers

A
  1. varies with medication, usually 1-3 times per day
    - Usually QD for patiromer, TID for zirconium cyclosilicate and SPS
    - SPS may be dosed with a laxative (lactulose or PEG)
    - May require repeated/ongoing doses
43
Q

SE of GI cation exchangers

A
  1. GI - intestinal necrosis, GI upset, constipation, fecal impaction
  2. Endocrine - ↑ Na; ↓ Mg, K, Ca
44
Q

DDI of GI cation exchangers

A

sorbitol (increased risk of intestinal necrosis)
digitalis
antacids or laxatives with Al or Mg
lithium
LT4
metformin

45
Q

avoid using GI cation exchangers for

A

hx of bowel obstruction
post-op patients
slow intestinal transit
hx of ischemic bowel disease
hx of renal transplant

46
Q

what medication is ONLY used in a patient with potentially life-threatening hyperkalemia, no ready dialysis, and cannot use other therapies

A

SPS

47
Q

Most effective and reliable method for removal of potassium

A

hemodialysis
May be used in combination with other methods

48
Q

types of hyponatremia

A
  1. Isotonic hyponatremia - low Na, normal Sosm
    - Extra molecules in the blood - protein, lipids
  2. Hypertonic hyponatremia - low Na, high Sosm
    - Another osmotically active molecule is present
    - Glucose, radiocontrast, mannitol
  3. Hypovolemic - Na loss
    - Extrarenal - GI loss (V/D), burns, dehydration
    - Renal - ACEi, diuretics, mineralocorticoid deficiency, intrinsic renal salt wasting
  4. Hypervolemic - Na retained, but H2O > Na retention
    - Renal - intrinsic renal fluid retention, nephrotic syndrome
    - Other organs - HF, liver disease
  5. Euvolemic - SIADH, hypothyroidism, psychogenic polydipsia, beer potomania, others
    - UNa+ & Uosm - ADH activity
49
Q

general tx for hyponatremia

A

gradually correcting underlying cause and monitoring for changes in osmolality/tonicity

50
Q

inappropriate salt loss
what type of hyponatremia?
causes?

A

Hypovolemic hyponatremia
- Extrarenal - GI loss (V/D), burns, dehydration
- Renal - ACEi, diuretics, mineralocorticoid deficiency, intrinsic renal salt wasting

51
Q

sodium is retained, but H2O retention is disproportionately larger than Na retention
what type of hyponatremia

A

Hypervolemic hyponatremia
- Renal - intrinsic renal fluid retention, nephrotic syndrome
- Other organs - heart failure, liver disease

52
Q

SIADH, hypothyroidism, psychogenic polydipsia, beer potomania, others
what type of hyponatremia

A

Euvolemic hyponatremia
UNa+ and Uosm can help us have an idea of ADH activity!

53
Q
  1. primarily neurologic d/t cerebral edema
    - Early - N/V, HA, confusion, lethargy
    - Late - seizure, brainstem herniation, coma, death
    - Others - May see muscle cramps or weakness, third spacing of fluid
    - If chronic (>48 h), less likely to have severe s/s
    these s/s are indicative of what?
A

hyponatremia

54
Q

tx for hypovolemic hyponatremia

A

if not severe, IV rehydration with isotonic 0.9% NS - raises serum Na by 1 mEq per L

55
Q

tx for Severe Hyponatremia

A

hypertonic saline + loops + dDAVP

  1. achieve 4-6 mEq/L increase in sodium ASAP
    - Hypertonic saline (3% saline in 100 mL IV bolus) - raises Na by 2-3 mEq/L
    — May repeat 1-2x at 10 min intervals if serum Na or s/s do not improve
    — Measure Na frequently (~every 2 hrs) to monitor replacement
    — co-administer loop diuretic - avoid volume overload and/or desmopressin (dDAVP) to avoid osmotic demyelination syndrome
56
Q

tx for nonemergent hyponatremia

A
  1. NS, slower infusion of hypertonic saline, and/or oral salt tabs
  2. Fluid restriction
  3. Vasopressin receptor antagonists - start or change dose while in the hospital
    - conivaptan (Vaprisol) - IV, tolvaptan (Samsca) - oral
    - Fluid restriction CI while on a vasopressin receptor antagonist
    - Maximum recommended use of 30 days due to SE of hepatotoxicity
    - Monitoring - LFTs, renal function, electrolytes
  4. Restoration of renal function
57
Q

loss of body water or inability to retain water appropriately, and/or excessive sodium intake
what is this condition?
types? (3, Uosm)

A
  1. Hypernatremia
    - Normal Uosm - excessive water loss through renal (includes excessive diuresis) or non-renal (GI, skin, fever) sources
    - Low Uosm - diabetes insipidus (neurogenic or nephrogenic)
    - hypervolemia - excess Na intake (IV, NaHCO3, salt tablets)
58
Q

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

59
Q

labs of Hypernatremia

A

Increased Hct, abnormal Uosm and Urine SG, may see abnormal renal labs
- If due to renal fluid wasting - may see very dilute urine!
- If accompanied by blood loss - Hct may also be low!

60
Q

tx for hypernatremia?
Speed of correction?

A
  1. Correction of underlying cause
  2. Fluid replacement - may use “free water” fluids (½ NS or D5W)
  3. Speed of sodium correction depends on duration of abnormal labs
    - If acute (<48 hrs) - try to correct within 24 hours to avoid CNS damage
    - If chronic (>48 hrs) - correct more gradually at 6-12 mEq/L per 24 hrs
  4. Restoration of renal function
61
Q

causes of metabolic alkalosis (3)

A

Increased acid (H+) loss
Excess bicarbonate/alkali
Abnormal renal excretion/absorption

62
Q

causes of increased acid loss for metabolic alkalosis

A

GI - vomiting, gastric suction
Hypokalemia

63
Q

causes of Excess bicarbonate/alkali
for metabolic alkalosis

A

Bicarbonate administration
Hypochloremia
Administration of alkaline solutions

64
Q

causes of Abnormal renal excretion/absorption of metabolic alkalosis

A

Diuretics→volume depletion
The combination of hypovolemia, hypochloremia, hypokalemia, and reduced GFR create the perfect setting for metabolic alkalosis

65
Q

s/s of metabolic alkalosis

A
  1. usually related to underlying cause(s)
    - Neuro - increased neuronal excitability - dizziness, panic, light-headedness, seizures
    —Increased protein-binding to calcium → functional hypocalcemia - Muscle tetany, numbness/tingling, Chvostek and Trosseau signs
    - CV - dysrhythmias
    - GI - may have hx of abdominal pain, N/V, GI suctioning
66
Q

tx for metabolic alkalosis

A

Antiemetics, decreasing or discontinuing GI suctioning
Reducing bicarbonate administration
Supplementing with fluids and electrolytes as needed
Tx of adrenal disease (Cushing’s or hyperaldosteronism) if present
Restoration of renal function

67
Q

Metabolic Acidosis - Major Causes (3)

A
  1. Increased acid generation
    - Lactic acidosis - impaired tissue oxygenation
    - Ketoacidosis - uncontrolled DM, excess alcohol intake, fasting
    - Ingestion - methanol, ethylene glycol, aspirin poisoning, chronic APAP, tolulene
  2. Loss of bicarbonate
    - Severe diarrhea
    - Urine exposure to GI mucosa
    - Proximal renal tubular acidosis
  3. Decreased renal acid excretion
    - Decreased GFR
    - Distal renal tubular acidosis
68
Q

s/s of metabolic acidosis

A
  1. usually related to underlying cause(s)
    - Neuro - decreased neuronal excitability - confusion, weakness, drowsiness
    — Decreased protein-binding to calcium → functional hypercalcemia - Muscle weakness, increased thirst, nephrolithiasis (if chronic)
    - CV - vasodilation (flushing), dysrhythmias
    - GI - abd pain, N/V/D/C
    - Pulm - increased depth and rate of respiration
    - Bone - decreased density (if chronic)
69
Q

Metabolic Acidosis - General Tx Guidelines

A
  1. Primary goal of tx - correction of underlying cause
  2. Acute metabolic acidosis (general tx)
    - If severe (pH <7.2) and symptomatic
    — IV HCO3- to get pH >7.2
    - Less severe (pH 7.2 +) - HCO3- often not needed
  3. Chronic metabolic acidosis
    - Usually due to GI loss, CKD, renal tubular acidosis
    - HCO3- replacement often indicated
    - Decreasing animal content (especially animal proteins) in diet
  4. Low GFR hinders the kidney’s ability to excrete acid and regenerate HCO3-
  5. Other factors often contribute
    - Sepsis, trauma, organ failure → may see increased
    lactic acids and ketoacids
    - Other causes → diarrhea, direct loss of bicarbonate
  6. Tx in context of AKI - dialysis or bicarbonate
70
Q

Bicarbonate administration if severe acidosis and what other factors? (4)

A
  1. Non-anion gap acidosis due to diarrhea
  2. Waiting for dialysis treatment
  3. Readily reversible AKI cause
  4. Rhabdomyolysis w/o other dialysis indications or hypervolemia
71
Q

Dialysis for metabolic acidosis AKI if:

A
  1. Severe oligouric or anuric AKI, volume overload, and severe metabolic acidosis (pH <7.1)
    - Regardless of underlying cause
    - HCO3- can cause large sodium load → may contribute to volume overload
  2. AKI and organic acidosis (lactic or keto) and pH < 7.1
    - Esp if oliguric/anuric
    - Due to risk for developing volume overload
72
Q

Indications for Dialysis in AKI

A
  1. Azotemia
  2. Uremia
  3. Severe or life-threatening electrolyte disturbances
    - Hyperkalemia >6.5 or rapidly rising, refractory to therapy
  4. Volume overload unresponsive to diuresis
  5. Metabolic acidosis (pH < 7.1)
    - esp pts who cannot receive bicarbonate
  6. Uremic complications (encephalopathy, pericarditis, seizures)

Dialysis may also be indicated for patients with prolonged AKI even without meeting all of these criteria

GU: Clin Med IIA (13 decks)

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