Fluid, Electrolyte, and Acid-Base Disorders

Question 1

Much of the care of AKI is what type?

Answer 1

supportive

Question 2

common complications of AKI

Answer 2

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

Question 3

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

Answer 3

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

Question 4

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

Answer 4

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

Question 5

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

Answer 5

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

Question 6

loss of body fluids, often accompanied by decreased fluid intake

Answer 6

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

Question 7

causes of Isotonic Fluid Volume Deficit
aka “hypovolemia”

Answer 7

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

Question 8

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

Answer 8

Isotonic Fluid Volume Deficit

Question 9

labs for Isotonic Fluid Volume Deficit

Answer 9

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!

Question 10

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

Answer 10

clinical hx of fluid loss
hypovolemia and/or oliguria

Question 11

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

Answer 11

IV fluids - LR or 0.9% NS

Question 12

NS in excess can lead to ?
how to tx?

Answer 12

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

Question 13

CI of LR/0.9% NS

Answer 13

Signs of volume overload, HF

Question 14

what to give for volume depletion due to blood loss

Answer 14

PRBCs

Question 15

what to give for volume depletion due to poor CO

Answer 15

inotropes

Question 16

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

Answer 16

Isotonic Fluid Volume Excess
AKA - “hypervolemia”

Question 17

causes of Isotonic Fluid Volume Excess

Answer 17

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

Question 18

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 ?

Answer 18

Isotonic Fluid Volume Excess

Question 19

labs of Isotonic Fluid Volume Excess

Answer 19

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!

Question 20

tx for Isotonic Fluid Volume Excess

Answer 20

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

Question 21

Impaired renal excretion of phosphate

Answer 21

Hyperphosphatemia

Question 22

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

Answer 22

hyperphosphatemia

Question 23

tx for Hyperphosphatemia

Answer 23

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

Question 24

causes of hypokalemia

Answer 24

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!

Question 25

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?

Answer 25

Hypokalemia

Question 26

tx for hypokalemia

Answer 26

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

Question 27

contributing factors of hypokalemia

Answer 27

Hypomagnesemia Metabolic acidosis Medication adjustments

Question 28

monitoring for hypokalemia

Answer 28

renal function, electrolytes, symptoms

Question 29

Very common complication of both AKI and CKD

Answer 29

hyperkalemia

Question 30

causes of hyperkalemia

Answer 30

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)

Question 31

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?

Answer 31

hyperkalemia

Question 32

tx goals for hyperkalemia

Answer 32

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

Question 33

how to Immediate antagonism of cardiac effects - tx hyperkalemia

Answer 33

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!

Question 34

caution with IV calcium

Answer 34

Potentiates cardiac toxicity of digoxin; consider

Question 35

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

Answer 35

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

Question 36

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

Answer 36

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

Question 37

what patients can be resistant to albuterol effects when tx hyperkalemia

Answer 37

~20% of ESRD patients are resistant to effects

Question 38

caution with albuterol in these pts

Answer 38

pts with cardiac disease

Question 39

how to remove potassium during hyperkalemia tx

Answer 39

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

Question 40

MOA of GI cation exchangers

Answer 40

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

Question 41

onset of GI cation exchangers

Answer 41

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

Question 42

dosing for GI cation exchangers

Answer 42

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

Question 43

SE of GI cation exchangers

Answer 43

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

Question 44

DDI of GI cation exchangers

Answer 44

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

Question 45

avoid using GI cation exchangers for

Answer 45

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

Question 46

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

Answer 46

SPS

Question 47

Most effective and reliable method for removal of potassium

Answer 47

hemodialysis May be used in combination with other methods

Question 48

types of hyponatremia

Answer 48

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

Question 49

general tx for hyponatremia

Answer 49

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

Question 50

inappropriate salt loss what type of hyponatremia? causes?

Answer 50

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

Question 51

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

Answer 51

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

Question 52

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

Answer 52

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

Question 53

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?

Answer 53

hyponatremia

Question 54

tx for hypovolemic hyponatremia

Answer 54

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

Question 55

tx for Severe Hyponatremia

Answer 55

_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

Question 56

tx for nonemergent hyponatremia

Answer 56

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

Question 57

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

Answer 57

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)

Question 58

s/s of hypernatremia

Answer 58

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

Question 59

labs of Hypernatremia

Answer 59

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!

Question 60

tx for hypernatremia? Speed of correction?

Answer 60

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

Question 61

causes of metabolic alkalosis (3)

Answer 61

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

Question 62

causes of increased acid loss for metabolic alkalosis

Answer 62

GI - vomiting, gastric suction Hypokalemia

Question 63

causes of Excess bicarbonate/alkali for metabolic alkalosis

Answer 63

Bicarbonate administration Hypochloremia Administration of alkaline solutions

Question 64

causes of Abnormal renal excretion/absorption of metabolic alkalosis

Answer 64

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

Question 65

s/s of metabolic alkalosis

Answer 65

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

Question 66

tx for metabolic alkalosis

Answer 66

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

Question 67

Metabolic Acidosis - Major Causes (3)

Answer 67

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

Question 68

s/s of metabolic acidosis

Answer 68

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)

Question 69

Metabolic Acidosis - General Tx Guidelines

Answer 69

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

Question 70

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

Answer 70

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

Question 71

Dialysis for metabolic acidosis AKI if:

Answer 71

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

Question 72

Indications for Dialysis in AKI

Answer 72

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