Lecture 3: Fluids/Electrolytes/Acid-Base Flashcards
What systems does our body activate to compensate for a decreased osmotic pressure/blood volume?
- Increased sympathetic
- Increased RAAS
- Increased ADH
- Increased Thirst
- Decreased ANP
What typically causes isotonic fluid volume deficit?
- Decreased PO intake
- Excessive fluid loss (renal primarily)
- Third spacing
What S/S are typically seen in isotonic fluid volume deficit?
- 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.
What labs are associated with isotonic fluid volume depletion?
- High Uosm and Urine SG
- Increased Hct
- Altered renal labs
SG = specific gravity
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?
- 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)
What S/S are associated with isotonic fluid volume excess or hypervolemia?
- Decreased thirst, feeling bloated/swollen
- Full, bounding pulse, distended neck veins, increased BP.
- Ascites, pulmonary edema, extremity edema.
What are common etiologies associated with isotonic fluid volume excess?
- Excess intake: Overadministration of fluids or PO intake.
- Decreased elimination: HF, Renal failure, corticosteroids
What labs are associated with isotonic fluid volume excess?
- Low Uosm and Urine SG, decreased Hct
- Abnormal renal labs
What is the primary treatment for isotonic fluid volume excess?
- 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.
What are the S/S of hyperphosphatemia?
Same as hypocalcemia.
- Hyperreflexia
- Carpopedal spasm
- Chvostek’s and/or Trosseau’s
Phosphate binds calcium.
Stones, abdominal groans and psychiatric moans
What is the treatment for hyperphosphatemia?
- Phosphate binders (Calcium carbonate, sevelamer, lanthanum carbonate)
- Avoiding processed foods with inorganic phosphate (nuts)
- Restore renal function
What are the common etiologies associated with hypokalemia?
- Intrinsic potassium wasting
- Diuretics
- Poor nutrition
- Insulin
- Beta-agonists
- Alkalosis
What are the common S/S associated with hypokalemia?
- 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
What are the common etiologies associated with hyperkalemia?
- 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
What are the common S/S associated with hyperkalemia?
- Muscular weakness/cramps
- Cramps, diarrhea, vomiting
- Hypotension, palps, dysrhythmias, CARDIAC ARREST
- Peaked T waves => widened QRS and loss of P-waves => sine waves.
What is the treatment protocol for hyperkalemia?
- Antagonizing cardiac effects via IV calcium gluconate!
- Correction of Serum K+ via IV Insulin + IV dextrose (if BG < 250)
- 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.
What is the fastest GI cation exchanger?
Zirconium cyclosilicate or Lokelma.
1 hour to onset
Requires TID dosing.
What is the concern with using Kayexelate?
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.
Aside from GI cation exchangers, what else can be done to help remove potassium in hyperkalemia?
- Loop/Thiazide diuretics
- Hemodialysis
Hemodialysis is most effective and reliable.
Describe isotonic hyponatremia.
Low Na but normal serum Osm.
MCC: Extra molecules in the blood.
Describe hypertonic hyponatremia.
Low Na in the presence of high serum Osm.
MCC: secondary osmotic molecule active, such as glucose, radiocontrast
What is the underlying mechanism behind hypovolemic hyponatremia?
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.
What is the underlying mechanism behind hypervolemic hyponatremia?
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.
What are the underlying etiologies behind euvolemic hyponatremia?
- SIADH
- Hypothyroidism
- Psychogenic polydipsia
- Beer potomania
Need Urine Na and Uosm to determine ADH activity.
MC type of hypotonic hyponatremia.
What are the S/S of hyponatremia?
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.
What is the general treatment protocol for hypovolemic hyponatremia?
Give isotonic NS for mild-mod.
Give Hypertonic saline for severe.
What is the main danger of infusing too much sodium? How do we prevent it?
Osmotic demyelination syndrome (ODS).
Prevented with loop diuretic and/or DDAVP to prevent volume overload.
For OP treatment of hyponatremia, what are the mainstays of treatment?
- Fluid restriction
- Vasopressin receptor antagonists (Conivaptan or tolvaptan)
- Salt tablets/NS/IV hypertonic saline
Conivaptan: combined V1, V2, IV.
Tolvaptan: V1, oral.
What is the main concern with vasopressin receptor antagonists?
Hepatotoxicity.
Max recommended duration of use is 30 days.
No fluid restriction needed with vasopressin receptor antagonists.
Monitor with LFTs and BMP.
What does hypernatremia with normal Urine osmolality suggest for etiology?
Excessive water loss via renal or non-renal.
What does hypernatremia with low Urine osmolality suggest for etiology?
DI (neurogenic or nephrogenic)
What does hypervolemic hypernatremia suggest for etiology?
Excess Na intake via IV, salt tablets, or bicarb with water loss.
What are the S/S of hypernatremia?
- 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.
What are the mainstays of treatment for hypernatremia?
- Free water fluids such as 1/2 NS or D5W.
Restoring renal function is the goal.
What are the 3 major causes of metabolic alkalosis? (elevated pH)
- Increased H+ loss
- Excess bicarb/alkali: Bicarb, hypochloremia, alkaline solutions.
- Abnormal renal excretion/absorption: Diuretics.
Hypovolemia + hypochloremia + hypokalemia + reduced GFR => metabolic alkalosis
What are the S/S of metabolic alkalosis?
Depends on underlying cause, but alkalosis in general causes neuronal excitability.
Will be functionally similar to HYPOcalcemia.
Being basic is excitatory
What are the 3 major causes of metabolic acidosis?
- 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.
What are the S/S of metabolic acidosis?
Decreased neuronal excitability, such as confusion, weakness, increased thirst.
How is severe metabolic acidosis treated? (< 7.2)
IV bicarb to raise to 7.2 first.
How is mild-mod metabolic acidosis treated? (> 7.2)
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.
What lifestyle change can help with chronic metabolic acidosis?
Avoiding animal proteins.
With a pt in metabolic acidosis secondary to AKI, what is the recommended treatment?
Dialysis and bicarb.
In what situations is bicarb recommended in metabolic acidosis due to AKI?
- 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.
When is dialysis recommended for metabolic acidosis due to AKI?
Anything with a pH < 7.1, even if cause is reversible.
When is dialysis indicated for AKI?
- 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
