Step Up - Fluids and Electrolytes Flashcards
Describe the distribution of fluid in the body in terms of ICF, ECF, plasma, and interstitial fluid.
1) ICF - 2/3 of TBW
2) ECF - 1/3 of TBW
a) Plasma 1/3 of ECF
b) Interstitial fluid 2/3 of ECF
What is the best way of assessing volume status? What is expected? What else can be used to assess volume status?
1) Urine output 0.5-1.0ml/kg/hr in adults
2) Clinical picture is important
a) burns, fever, open wounds lead to greater insensible losses
b) Patients with liver failure, nephrotic syndrome, CHF, hypoalbuminemia third-space and are intravascularly deplete despite normal TBW
c) ESRD leads to hypervolemia
What are the causes of hypovolemia (5)?
GI loss (vomiting, diarrhea, NG suction) third-spacing (ascites, effusions) Low intake Polyuria (DKA) Sepsis and inflamatory processes Trauma, open-wounds, burns Insensible losses - diaphoresis, tachypnea
What are the clinical features of hypovolemia (5)?
1) CNS deficits - mental status change, sleepiness, apathy, coma
2) CV findings - orthostatic hypotension, tachycardia, low pulse pressure, decreased CVP
3) Skin change - poor turgor, cold, pale
4) Oliguria
5) Ileus, weakness
6) AKI - azotemia
What is the rule for calculating maintenance fluids? What is typically used for maintenance fluid?
1) 4//2/1 - 4ml/kg first 10kg, 2ml/kg second 10kg, 1ml/kg for weight over 20kg (gives 110ml/hr for 70kg person).
2) D51/2NS with 20mEq/L KCL
What are the causes of hypervolemia (2)? What are the clinical features (5)? How is it treated (2)?
1) Causes: iatrogenic, fluid-retaining states (CHF, nephrotic syndrome, cirrhosis, ESRD)
2) Clinically: wt gain, peripheral edema/ascites/pulm edema, JVP elevated, High CVP, pulmonary rales, low hematocrit
3) Tx: fluid restrict, diuretics
What does hyper/hyponatremia represent? What does hyper/hypovolemia represent?
1) Too much or too little WATER
2) Too much or too little NA
Where does furosemide work in the kidney and what does it impair? Where do thiazides work in the kidney, what does it impair?
1) Furosemide - works on ascending loop, blocks Na/Cl/K transporter
2) Thiazides - works on early distal tubule, blocks Na/Cl transporter.
`How is serum osmolality calculated?
Sosmo = 2Na + Urea + Glc (all in mmol/L)
What is the first step in the work-up of hyponatremia? Briefly describe each category.
Check serum osmolality and classify hyponatremia as follows:
1) Osmo > 295: hypertonic hyponatremia (osmotic substances present - hyperglycemia, mannitol, glycerol)
2) Osmo 280-295: isotonic hyponatremia (pseudohyponatremia, increased plasma solids such as proteins or TGs)
3) Osmo less than 280: hypotonic hyponatremia - this is true hyponatremia
How is hypotonic hyponatremia further subclassified (3)? What are the causes of each?
1) Hypovolemic:
a) Low urine sodium: extrarenal losses (diarrhea, vomiting, diaphoresis, third-spacing, burns)
b) High urine sodium: renal losses (ATN, diuretics, low aldosterone (ACEi)).
2) Euvolemic: SIADH, psychogenic polydipsia, hypothyroidism, oxytocin use, excess free water administration, drugs (haldol)
3) Hypervolemic: water retaining states with more water than sodium retained. Cause: CHF, nephrotic syndrome, liver disease
What are the clinical features of hyponatremia (5)?
1) Neuro findings - cerebral edema, headache, delirium, irritability, muscle twitching, weakness, hyperactive DTR
2) Increased ICP - seizures, coma
3) GI - N/V, ileus, watery diarrhea
4) CV - hypertension 2nd to high ICP
5) Increased sallvation and lacrimation
6) Oliguria
Will the urine osmolality be high or low in true hyponatremia?
Depends on cause:
1) If kidneys are responding properly, then osmolality is low (dilute urine). Ex. primary polydipsia
2) Osmolality high if high ADH. Ex. CHF, SIADH
How is true hyponatremia treated (hypotonic hyponatremia)?
1) Mild (Na 120-130): water restrict
2) Moderate (Na 110-120): loop diuretics and saline (to prevent ADH activation)
3) Severe (under 110): hypertonic saline to correct
- Do not correct by more than 8mmol/L in 24hrs.
What is the first step in working-up hypernatremia? How is hypernatremia classified? What are the causes of each type?
1) Assess clinical ECF volume
2) types:
a) Hypovolemic hypernatremia
- low Na and low water (more so)
- Renal loss: diuretics, osmotic diuresis (glucose), renal failure
- Extrarenal loss: diarrhea, diaphoresis, respiratory
b) Euvolemic hypernatremia
- normal Na, low water
- DI, insensible respiratory (tachypnea)
c) Hypervolemic hypernatrmia
- Gain of water and gain of Na (more so)
- Iatrogenic (TPN, NaHCO3), exogenous glucocorticoids, cushing’s syndrome
- rare.
What are the clinical features of hypernatremia? How is each type treated?
1) Neurological findings - altered mental status, restless, weak, confusion, seizure, coma. Mucous membranes dry
2) Treatment
a) Hypovolemic - give isotonic NaCl to restore volume, replace free water deficit later
b) Euvolemic - Vasopressin for DI. Oral fluids
c) Hypervolemic - diuretics (furosemide) and D5W to replace water deficit
What are the causes of hypocalcemia (5)? What are the clinical features (5)? How is it treated?
1) Causes: hypoparathyroidism, acute pancreatitis, renal insufficiency (low vit D), hyperphosphatemia, pseudohypoparathyroidism, hypomagnesemia, vit D def, malabsorption
2) Clinical: can be asymptomatic, rickets/osteomalacia, neuromuscular irritability (brisk DTR, Chvostek sign, Trousseau sign), basal ganglia calcifications, Cardiac (prolonged QT and arrhythmias)
3) Tx: treat underlying cause
Comment on the serum Phos and PTH in the following causes of hypocalcemia: hypoparathyroidism, vitamin D deficiency, pseudohypoparathyroidism
1) Hypoparathyroidism: high phos, low PTH
2) Vitamin D def: low phos, high PTH
3) Psuedohypoparathyroidism: - , very high PTH
What are the causes of hypercalcemia (5)? What are the clinical features (5)?
1) Causes:
a) Endo - hyperparathyroidism, Paget’s, acromegaly
b) Malignancies - metastatic, multiple myeloma, tumors that secrete PTH-like hormone
c) Pharma - vit D intoxication, milk, thiazide diuretics
2) Clinical
a) Stones
b) Bones - bone pain
c) Groans - muscle pain, pancreatitis, gout
d) Psych overtones - depression, fatigue, anorexia
e) Other - HTN, wt loss, shortened QT
How is hypercalcemia treated (4)?
1) IV fluids and loop diuretics
2) Inhibit bone resorption in malignancy - bisphosphonates
3) Glucocorticoids if vit D-related mechanism
4) Hemodialysis if renal failure.
Provide a differential diagnosis for hypokalemia.
1) Redistributive - insulin excess, metabolic alkalosis, epinephrine
2) Renal loss - RTA, DKA, ureterosigmoidostomy
3) Extra-renal losses - low intake, laxative abuse, perspiration, diarrhea, fistula
4) Spurious - lab error
What are the clinical features of hypokalemia (5)? How is it treated (3)?
1) Clinical: arrhythmias, muscle weakness, low DTR, paralytic ileus, flat T waves with U-waves
2) Tx:
a) Oral or IV K - 10mEq corrects by 0.1
b) IV infusion rate no more than 10mEq/hr
c) Correct Mg deficit if present
What are the causes of hyperkalemia (5)?
1) Redistribution - acidosis, insulin deficiency, B-blockers
2) Renal failure
3) Renal impairment
a) Low aldosterone - ACEi, Addison’s disease
b) N or high aldosterone - potassium sparing diuretics, tubular disorders
4) Spurious - lab error, hemolysis
What are the clinical features of hyperkalemia (5)? How is it treated (4)?
1) Clinical: arrhythmias - peak T waves, widened QRD, PR prolongation, loss of P waves, VFib. Muscle weakness, low DTR, resp failure
2) Tx (severe): IV calcium, glucose and insulin or bicarb to shift K into cells, remove K with Kayexalate, dialysis, or diuretics
Provide a differential for AG metabolic acidosis (4).
1) Ketoacidosis - Dm, prolonged starvation, prolonged alcohol abuse
2) Lactic acidosis - low perfussion, shock states
3) Renal failure - low NH4 excretion
4) Intoxication - salicylate, methanol, ethylene glycol
Provide a differential for non-AG metabolic acidosis (2)/
1) Renal loss of bicard - prox or distal tubule acidosis
2) GI loss of HCO3
What is the anticipated PaCO2 response to a metabolic acidosis (Winter’s formula)?
expect that PaCO2 = 1.5*HCO3 + 8 +or-2
- if response appropriate, then met acidosis
- if response to little, then met acidosis and resp acidossis
- if response to high, then met acidosis, and resp alk
Describe the 2 categories of metabolic alkalosis and what causes each.
1) Saline-sensitive met alk
a) Ucl less than 10
b) Cause: ECF contraction (diuretics) or H loss with vomiting
c) Tx: Saline
2) Saline-resistant met alk
a) Ucl > 10, hypervolemic
b) Cause: adrenal disorders (primary hyperaldosteronism)
c) Tx underlying cause
What is the renal adaptation to a respiratory acidosis in terms of adjustment to HCO3 for every 10mmHG increase in PCO2
Anticipate HCO3 increase of 4mmol/L (in chronic setting)
