Fluid, Electrolyte, and Acid-Base Disorders Flashcards
what are common complications of AKI
- abnormal volume status
- hyperphosphatemia
- hyperkalemia
- hyponatremia
- uremia
- severe metabolic acidosis (pH<7.2)
what adjustments are made in the body when there is a drop in osmotic pressure or blood volume
- increased SNS output
- increased RAAS activity
- increased ADH levels
- Increased thirst
- decreased atrial natriuretic peptide (ANP)
what are the adjustments made by the body with increase in osmotic pressure or blood volume
- decreased SNS output
- decreased RAAS activity
- decreased ADH levels
- decreased thirst
- increased atrial natriuretic peptide (ANP)
what is the body’s net goal of controlling osmotic pressure and blood volume
adjust water intake, water and sodium retention by the kidney, and vasoconstriction
what is isotonic fluid volume deficit
AKA hypovolemia - volume depletion.
what is the etiology of isotonic fluid volume deficit
loss of body fluids, often accompanied by decreased fluid intake.
* decreased PO intake
* Excessive fluid loss - GI, renal, skin
* Third Spacing - edema, ascites, effusions
what are signs and symptoms of isotonic fluid volume deficit
- General - increased thirst, fatigue, altered mental status
- CV - low BP, high HR, weak/thready pulse, flat neck veins, cap refill >3 sec
- Low ECF - Wt loss, dry mucous membranes, low skin turgor, sunken eyes or fontales
what labs are seen in isotonic fluid volume deficit
- High Uosm and Urine SG
- increased Hct (if blood loss or anemia may be low)
- abnormal renal labs
- if d/t renal fluid wasting may see very dilute urine
How do you manage volume depletion (isotonic fluid loss)
- fluid loss/hypovolemia/oliguria - PO fluids or IV fluids (LR or .9% NS)
- blood loss - PRBCs
- Poor Cardiac output - inotropes
what is the cause of hyperchloremic metabolic acidosis. How do you treat this?
excess NS given for treatment of volume depletion
treat with bicarb solution (dextrose in H2O with HCO3)
how do you monitor the target physiologic endpoint of treatment for volume depletion
patient status
mean arterial pressure
urine output
what is isotonic fluid volume excess
hypervolemia
what is the etiology of isotonic fluid volume excess
Excess intake of water/sodium - overadmin of IV fluids, hypertonic IV fluids, dietary changes
Decreased elimination - HF, Renal failure, corticosteroids
( this is the one where jensen said people come in after holidays cuz they ate too much sodium and now theyre retaining all the water!!)
what are signs and symptoms of isotonic fluid volume excess
- general - decreased thirst, feeling bloated/swollen
- CV - full, bounding pulse; distended neck veins, may see increased BP
- High ECF - ascites, pulmonary edema, extremity edema
what are the labs present with isotonic fluid volume excess
- low Uosm and urine SG
- decreased Hct
- abnormal renal labs
- if d/t inability to get rid of urine may see concentrated rine or low UO
what is the management for isotonic fluid volume excess
- assess underlying cause
- IV diuretics (loops preferred - furosemide)
- dialysis ( if no response to diuretics or persistent volume overload)
- restrict fluid and sodium intake
What is the cause of hyperphosphatemia
impaired renal excretion of phosphate
what are the signs and symptoms of hyperphosphatemia
fatigue
SOB
N/V
signs of hypocalcemia
what are signs of hypocalcemia
hyperreflexia
carpopedal spasm
+trousseau’s or Chvostek signs
what is the treatment for hyperphosphatemia
limit phosphate intake by:
- phosphate binders w meals
- avoid processed foods containing inorganic phosphate
- restoration of renal function
what is the etiology of hypokalemia
Less common in AKI/CKD than hyperkalemia, but possible!
- renal - intrinsic potassium wasting, or d/t diuretic SE
- GI - poor intake (nutrition/NPO)
- other - insulin, beta-agonists, loops, alkalosis
What are the signs and symptoms of hypokalemia
often effects smooth, skeletal and cardiac muscle!
MSK - weak, fatigue, cramps, tenderness
GI - abdominal cramps, constipation
Cardiac - hypotension, palps, dysrhythmias
ECG - flattened T waves -> prolonged QT -> U wave -> ST depression
what is the general management of hypokalemia?
correction of underlying cause
what is the management of acute severe hypokalemia
potassium replacement:
* oral or IV K chloride or K gluconate
* IV - 10-20mEq/hr max
* oral - 10-40 QD - QID
how do you treat chronic recurrent hypokalemia
- increase potassium rich foods in diet
- K replacement (K chloride or K gluconate)
- adjust meds (isulin, beta agonists, loops)
what are the possible contributing factors of hypokalemia
hypomagnesemia
metabolic alkalosis
medications
what should be monitored with hypokalemia
renal function
electrolytes
general symptoms
What are the possible etiologies of hyperkalemia
VERY common complication of AKI and CKD
causes include:
* Renal - inadequate excretion, metabolic acidosis
* Adrenal insufficiency
* Cellular breakdown - traumatic stick, hemolysis, crush injury
* Release from ICF - cell damage, excessive/severe muscle contraction
* Other causes - ACEI/ARB, beta-blockers, excess intake (usually IV)
What are the signs and symptoms of hyperkalemia
Often affects muscles
- MSK - weakness, cramps (including abdominal)
- GI - abdominal cramps, diarrhea, vomiting
- Cardiac - hypotension, palpitations, dysrhythmias, cardiac arrest
- ECG - peaked T waves → loss of P waves → widened QRS → sine wave
when should hyperkalemia be treated
immediate treatment if very high levels, ECG changes or neuromuscular symptoms
what are the three steps to managing hyperkalemia
- immediate clocking of cardiac effects
- rapid reduction in plasma K+
- removal of potassium
How do you antagonize cardiac effects in hyperkalemia
- IV calcium - reduced cardiac excitability
- 10mL of 10% calcium gluconate IV over 2-3 minutes w monitoring
- repeat if ECG changes do not improve or recur in 1-3 minutes
- may not be needed if there are no cardiac s/s or arrhythmias present
Note: Caution - potentiates cardiac toxicity of digoxin; consider
slower infusion of calcium if it must be used
(im not sure what this means)
how do you rapidly reduce plasma K+ in hyperkalemia
- IV insulin - 10 units regular insulin followed by 40 mL of 50% dextrose
- albuterol and insulin + glucose (caution in CHF pts, ESRD patients do not respond to this)
cannot use albuterol by itself, must combine with insulin
how do you remove potassium in hyperkalemic patients
GI cation exchangers
Loop diuretics
thiazide diuretics
Hemodialysis
what are the GI cation exchangers
- sodium polystyrene sulfonate (aka SPS or Kayexelate)
- zirconium cyclosilicate (lokelma)
- patiromer (veltassa)
what is the MOA of GI cation exchangers
exchanges Na+ for K+ in GI tract which increases fecal excretion of K+
what is the onset of action for the GI cation exchangers
- SPS - 2-24 hours
- Zirconium cyclosilicate - 1 hour
- Patiromer - 7 hours
what are the SE of GI cation exchangers
- GI - intestinal necrosis, GI upset, constipation, fecal impaction
- Endocrine - ↑ Na; ↓ Mg, K, Ca
What are major DD interactions of GI cation exchangers
- sorbitol (increased risk intestinal necrosis)
- digitalis
- antacids or laxatives w Al or Mg
- Lithium
- LT4
- metformin
what are contraindications/cautions for GI cation Exchangers
avoid with:
* hx of bowel obstruction
* post op pts
* slow intestinal transit
* hx ischemic bowel disease
* hx renal transplant
when are loop or thiazide diuretics used for removal of potassium
in volume replete or hypervolemic pts with enough renal function for diuretic response
be sure to monitor for other electrolyte imbalances!
What is the most effective/reliable method of potassium removal
hemodialysis!
may be used in combo with other meds
What are the types of hyponatremia
isotonic hyponatremia
hypertonic hyponatremia
what is isotonic hyponatreamia
low Na with normal serum osmolality.
(caused by extra molecules in the blood like proteins and lipids)
PAY ATTENTION CUZ I DONT GET THIS
what is hypertonic hyponatremia
low Na with high serum osmolality
other molecules are present such as glucose, radiocontrast, mannitol
PAY ATTENTION CUZ WHAT
What is hypovolemic hyponatremia
inappropriate salt loss in the presence of decreased blood volume (from google)
what are the etiologies of hypovolemic hyponatremia
- GI loss (N/V)
- burns
- dehydration
- ACEi
- diuretics
- mineralocorticoid deficiency
- intrinsic renal salt wasting
what is hypervolemic hyponatremia
sodium is retained but water retention is disproportionately larger than Na retention
(too much water, normal amount of sodium = hypervolemic hyponatremia)
what are the etiologies of hypervolemic hyponatremia
- intrinsic renal fluid retention
- nephrotic syndrome
- heart failure
- liver disease
what is euvolemic hyponatremia
having normal H2O retention and blood volume but having too little Na
(google)
what are the etiologies of euvolemic hyponatremia
- SIADH
- Hypothyroidism
- psychogenic polydipsia
- beer potomania
what is evaluated to assess ADH activity
UNa+ and Uosm
what are the signs and symptoms of hyponatremia
primarily neurologic s/s 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 hyponatremia (>48 h), less likely to have severe s/s
How do you manage non severe hypovolemic hyponatremia
IV rehydration with isotonic 0.9% NS
how do you manage severe hyponatremia
- achieve 4-6mEq/L increase in sodium ASAP
- repeat 1-2x at 10 min intervals if serum Na or s/s do not improve
- monitor tx by measuring Na every 2 hours
- may co admin a loop to avoid volume overload and/or desmopressin to avoid osmotic demyelination syndrome
how do you treat nonemergent hyponatremia
hypertonic saline
salt tablets
fluid restriction
vasopressin receptor antagonists
what are the vasopressin receptor antagonists
conivaptan (vaprisol) IV
tolvaptan (samsca) Oral
what is CI for vasopressin receptor antagonists
Fluid restriction CI while on a vasopressin receptor antagonist
what is the major concerning SE of vasopressin receptor antagonists
Hepatotoxicity. max recommended use of 30 days d/t this.
what should you monitor when administering a vasopressin receptor antagonist
LFTs
Renal function
electrolytes
what is the etiology of hypernatremia
loss of body water of inability to retain water appropriately, and/or excessive sodium intake
what is the etiology of hypernatremia with normal urine osmolality
excessive water loss through renal or non renal sources
what is the etiology of hypernatremia with low urine osmolality
diabetes insipidus (neurogenic or nephrogenic)
what are the signs and symptoms 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
what are the labs associated with hypernatremia
- increased Hct (decreased if accompanied with blood loss)
- abnormal Uosm and Urine SG
- abnormal renal labs
- if d/t renal fluid wasting - dilute urine
what is the treatment for hypernatremia that has been present for less than 48 hours
correction with fluid replacement within 24 hours to avoid CNS damage
what is the treatment for hypernatremia that has been present for more than 48 hours
correction with fluid replacement gradually at 6-12 mEq/L per 24 hours
what are the three etiologic categories of metabolic alkalosis
increased acid loss
excess bicarbonate/alkali
abnormal renal excretion/absorption
what are etiologies of increased acid loss
- GI - vomiting, gastric suction
- Hypokalemia
what are etiologies of excess bicarbonate/alkali
- Bicarbonate administration
- Hypochloremia
- Administration of alkaline solutions
what are the etiologies of abnormal renal excretion leading to metabolic alkalosis
- Diuretics→volume depletion
- The combination of hypovolemia, hypochloremia, hypokalemia, and reduced GFR create the perfect setting for metabolic alkalosis
what are signs and symptoms of metabolic alkalosis
- neuro - Increased neuronal excitability leading to dizziness, panic, lightheadedness, seizures.
- CV - dysrhythmias
- GI - may have hx of abdominal pain, N/V, GI suctioning
how do you treat metabolic alkalosis
- usually directed at underlying cause
- antiemetics and dc GI suctioning
- decrease bicarb admin
- fluid/electrolyte supplements
- tx of adrenal dz if present
what are the major etiologic categories of metabolic acidosis
increased acid generation
loss of bicarbonate
deceased renal acid excretion
what are the etiologies of inceased acid generation
lactic acidosis
ketoacidosis
ingestion (methanol, ethylene glycol, aspirin poisoning, chronic APAP, tolulene)
What are the etiologies of loss of bicarbonate
severe diarrhea
urine exposure to GI mucosa
Proximal renal tubular acidosis
what are the etiologies of decreased renal acid excretion
Decreased GFR
distal renal tubular acidosis
what are the signs and symptoms of metabolic acidosis
Neuro - decreased neuronal excitability - confusion, weakness, drowsiness
CV - vasodilation (flushing), dysrhythmias
GI - Abdominal pain, NVD, constipation
pulm - increased depth and rate of respiration
bone - decreased density with chronic
what during metabolic acidosis can lead to functional hypercalcemia? what are the s/s of this?
decreased protein binding to calcium d/t decreased neuronal excitability.
s/s include muscle weakness, increased thirst, nephrolithiasis (if chronic)
what is considered severe metabolic acidosis
pH<7.2
how do you treat severe metabolic acidosis
remember severe is pH<7.2
treat underlying problem
+
treat w IV HCO3 to get pH to >7.2
how do you treat non-severe metabolic acidosis
correct underlying problem which will allow body to return to normal pH
how do you treat chronic metabolic acidosis
HCO3 replacement.
decreased animal content (esp proteins) in diet
what is chronic metabolic acidosis usually due to
GI loss
CKD
Renal tubular acidosis
how does AKI create metabolic acidosis
a lower GFR hinders the kidneys ability to excrete HCO3 and reabsorb H+
how do you treat metabolic acidosis in the context of AKI
dialysis
HCO3
when would you use bicarbonate as treatment for metabolic acidosis in AKI
if acidosis is severe (pH<7.2) AND:
* non-anion gap acidosis d/t diarrhea
* waiting for dialysis
* readily reversible AKI cause
* rhabdomyolysis w/o other dialysis indications or hypervolemia
when is dialysis indicated for treating metabolic acidosis in AKI
- severe oliguric or anuric AKI with volume overload and severe metabolic acidosis
- AKI and organic acidosis and pH <7.1 especially if oliguric/anuric
what are other indications for dialysis use in AKI
- azotemia
- uremia (the worse the symptoms, the greater the indication for dialysis)
- severe or life threatening electrolyte disturbances
- Volume overload
- Metabolic Acidosis (<7.1)
- uremia
- pateints with prolonged AKI even without meeting the above criteria
