Step-Up To Medicine: Fluids, Electrolytes, And Ph Homeostasis

Front 1

What is the 60-40-20 rule?

Back 1

(1) TBW is 60% of body weight (50% for women)
(2) ICF is 40% body weight
(3) ECF is 20% body weight; (interstitial fluid 15%, plasma 5%)

Front 2

Distribution of water in the body.

Back 2

(1) ICF = 2/3 of TBW
(2) ECF = 1/3 of TBW; plasma is 1/3 of ECF; interstitial fluid is 2/3 of ECF

Front 3

List the normal water exchange parameters.

Back 3

(1) Normal intake: 1500 mL in fluids taken PO per day; 500 mL in solids or oxidation rxn products
(2) Normal output: 800-1500 mL per day in urine; output of 250 ml per day in stool; from 600-900mL per day in insensible loss (variable but increases with fever, sweating, hyperventilation, and tracheostomies

Front 4

What is the most important thing to do in the assessment of volume status?

Back 4

(1) monitoring urine output, which should be approximately 1.0 mL/kg/hr in normal individuals; low urine output could be a sign of volume depletion
(2) Daily weights may give a more accurate assessment of volume trends than other physical signs, but turgor, mucous membranes, edema, etc. should be assessed as part of a routine PE

Front 5

Key things to keep in mind regarding volume balance in patients:

Back 5

(1) Generally, pts with sepsis, fever, burns, or open wounds have high insensible losses (and higher metabolic demands)
(2) For each degree of atmospheric temperature over 37C, the body’s water loss increases by about 100 mL/day
(3) Patients with liver failure, nephritic syndrome, or any condition causing hypoalbuminemia tend to third-space fluid out of the vasculature and may be total-body hypervolemic but intravascularly depleted
(4) Patients with CHF may have either mulmonary edema or anasarca, depending on which ventricle is involved
(5) Patients with ESRD are very prone to hypervolemia for obvious reasons

Front 6

When is normal saline (NS) used in fluid replacement therapy? When is it not used?

Back 6

(1) often used to increase intravascular volume if the patient is dehydrated or has lost blood
(2) Typically not the best option in patients with CHF unless the patient needs urgent resuscitation

Front 7

When is D51/2NS used in fluid replacement therapy?

Back 7

(1) Often the standard maintenance fluid (often given with 20 mEq of Kcl/L of fluid)
(2) Has some glucose, which can spare muscle breakdown, and has water for insensible losses

Front 8

When is D5W used?

Back 8

(1) Used to dilute powdered medicines
(2) May sometimes be indicated in correcting hypernatremia
(3) Only 1/12 remains intravascular because it diffuses into the TBW compartment so not effective in maintaining intravascular volume

Front 9

When is lactated Ringer’s solution used in fluid replacement therapy?

Back 9

(1) excellent for replacement of intravascular volume, not a maintenance fluid
(2) most common trauma resuscitation fluid
(3) DO NOT use if hyperkalemia is a concern because it contains potassium.

Front 10

Causes of hypovolemia.

Back 10

(1) GI losses due to vomiting, nasogastric suction, diarrhea, fistula drainage, etc.
(2) Third-spacing due to ascites, effusions, bowel obstruction, crush injuries, burns
(3) Inadequate intake
(4) Polyuria (e.g. DKA)
(5) Sepsis, intra-abdominal and retroperitoneal inflammatory processes
(6) Trauma, open wounds, sequestration of fluid into soft tissue injuries
(7) Insensible losses – evaporatory losses through skin (75%) and the respiratory tract (25%)

Front 11

What is the 100/50/20 rule for calculation of maintenance fluids?

Back 11

(1) 100 mL/kg for first 10 kg, 50 mL/kg for next 10 kg, 20 mL/kg for every 1 kg over 20
(2) Divide total by 24 for hourly rate

Front 12

What is the 4/2/1 rule for calculation of maintenance fluids?

Back 12

(1) 4 mL/kg for first 10 kg, 2 mL/kg for next 10 kg, 1 mL/kg for every 1 kg over 20

Front 13

What are the clinical manifestations of hypovolemia?

Back 13

(1) CNS findings: mental status changes, sleepiness, apathy, coma
(2) CV findings (due to decrease in plasma volume): orthostatic hypotension, tachycardia, decreased pulse pressure, decreased CVP, decreased PCWP
(3) Skin: poor skin turgor, hypothermia, pale extremities, dry tongue and mucous membranes
(4) Oliguria
(5) Ileus, weakeness
(6) Acute renal failure due to prerenal azotemia (FENa <1%)

Front 14

Describe the diagnostic findings in hypovolemia.

Back 14

(1) Monitor the urine output and daily weights. If pt is critcally ill and has cardiac or renal dysfunction, consider placing a Swan-Ganz catheter (to measure CVP and PCWP
(2) Elevated serum sodium, low urine sodium, and a BUN/Cr ratio of >20:1 suggest hypoperfusion of kidneys, which usually (but not always) represents hypovolemia
(3) Increased Hct (3% increase for each liter of deficit)
(4) Concentration of formed elements in blood increases with ECF deficit and decreases with an ECF excess

Front 15

How is the treatment of hypovolemia approached?

Back 15

(1) Correct the volume deficit
(2) Use bolus to achieve euvolemia. Begin with isotonic solution (lactated Ringer’s or NS); DO NOT combine bolus fluids with dextrose, can lead to hyperglycemia, or potassium , which can cause hyperkalemia
(3) Frequent monitoring of HR, BP, urine output, and weight is essential
(4) Maintain urine output at 0.5 to 1.0 mL/kg/hr
(5) In the setting of blood loss, replace blood loss with crystalloid at a 3:1 ratio

Front 16

Maintenance fluid

Back 16

(1) D51/2NS solution with 20 mEq KCl/L is the most common adult maintenance fluid (dextrose added to prevent muscle breakdown)

Front 17

What are the common causes of hypervolemia?

Back 17

(1) Iatrogenic: parenteral overhydration
(2) Fluid-retaining states: CHF, nephrotic syndrome, cirrhosis, ESRD

Front 18

What are the primary clinical findings in hypervolemia?

Back 18

(1) Weight gain
(2) Peripheral edema (pedal or sacral), ascites, pulmonary edema (most cases of edema result from renal sodium retention)
(3) Jugular venous distention
(4) Elevated CVP and PCWP
(5) Pulmonary rales
(6) Low Hct and albumin concentrations

Front 19

How is the treatment of hypervolemia approached?

Back 19

(1) Fluid restriction
(2) Judicious use of diuretics
(3) Monitor urine output and daily weights, consider placement of Swan-Ganz catheter depending on the pt’s condition

Front 20

List the general features of hypnatremia.

Back 20

(1) Refers to too much water in relation to sodium in the plasma
(2) Defined as a serum Na+ concentration <135 mmol/L
(3) Sx usually begin when the Na+ level falls to >120 mEq/L. An important exception is increased ICP. As ECF osmolality decreases, water shifts into brain cells, further increasing ICP. Therefore, it is critical to keep serum sodium normal or slightly high in such pts.

Front 21

What are the three primary classifications of hyponatremia?

Back 21

(1) Hypotonic hyponatremia
(2) Isotonic hyponatremia
(3) Hypertonic hyponatremia

Front 22

What are the three main types of hyotonic hyponatremia?

Back 22

(1) Hypovolemic hypotonic hyponatremia
(2) Euvolemic hypotonic hyponatremia
(3) Hypervolemic hypotonic hyponatremia

Front 23

What are the main causes of hypovolemic hypotonic hyponatremia?

Back 23

(1) Low urine sodium (<10mEq/L), which implies increased sodium retention by the kidneys to compensate for extrarenal losses of sodium-containing fluids (e.g. diarrhea, vomiting, nasogastric suctioning, diaphoresis, third-spacing, burns, pancreatits)
(2) High urine sodium (>20 mEq/L), suggesting that renal salt loss is likely (e.g. diuretic excess, decreased aldosterone (ACE inhibition), ATN

Front 24

What are the main causes of euvolemic hypotonic hyonatremia?

Back 24

(1) SIADH
(2) Psychogenic polydispsia
(3) Postoperative hyponatremia
(4) Hypothyroidism
(5) Administration of a relative excess of free water—if a patient is given D5W (or other hypotonic solution) to replace fluids, or if water alone is consumed after intensive exertion (with profuse sweating)

Front 25

What are the main causes of hypervolemic hypotonic hyponatremia?

Back 25

(1) This is due to water-retaining states. The relative excess of water in relation to sodium results in hyponatremia.
(2) CHF, Nephrotic syndrome, liver disease

Front 26

What are the main casues of isotonic hypnatremia?

Back 26

(1) Increase in plasma solids, which lowers the plasma sodium concentration; the total amount of sodium in plasma is normal (referred to as pseudohyponatremia)
(2) This can be caused by any condition that leads to elevated protein or lipid levels

Front 27

What are the main causes of hypertonic hyponatremia?

Back 27

(1) Caused by the presence of osmotic substances that cause an osmotic shift of water out of cells. These substances cannot cross the cell membrane and therefore create osmotic gradients
(2) Glucose—hyperglycemia increases osmotic pressure and water shifts from cells into ECF; leading to a dilutional hyponatremia. For every 100 mg/dL increase in blood glucose level above normal, the serum sodium level decreases about 3 mEq/L. Note that the actual sodium concentration in ECF remains unchanged
(3) Mannitol, sorbitol, glycerol, maltose
(4) Radiocontrast agents

Front 28

What are the clinical features of hyponatremia?

Back 28

(1) Neurologic symptoms predominate, caused by “water intoxication”—osmotic water shifts, which leads to increased ICF volume, specifically brain cell swelling or cerebral edema; headache,
(2) HA, delirium, irritability
(3) Muscle twitching, weakness
(4) Hyperactive DTRs
(5) Increased ICP, seizures, coma
(6) GI: nausea, vomiting, ileus, watery diarrhea
(7) CV: hypertension due to increased ICP
(8) Increased salivation and lacrimation
(9) Oliguria progressing to anuria—MAY NOT BE REVERSIBLE IF TX IS DELAYED
(10) Note that when hyponatremia develops gradually, the clinical features do not appear until the degree of hyponatremia is more severe, due to compensatory responses

Front 29

Diagnosis of hyponatremia.

Back 29

(1) Plasma osmolality will be low in a patient with true hyponatremia
(2) Urine osmolality—low if kidneys are responding appropriately by diluting the urine (e.g. primary polydipsia); elevated if there are increased levels of ADH (e.g. SIADH, CHF, hypothyroidism)
(3) Urine sodium concentration—should be low in the setting of hyponatremia; if >20 mmol/L, consistent with salt-wasting nephropathy or hypoaldosteronism, diuretics may also produce this; if >40mmol/L, consistent with (but not diagnostic of) SIADH

Front 30

Describe the treatment approach of a patient with hyponatremia.

Back 30

(1) Isotonic and hypertonic hyponatremia—diagnose and treat the underlying disorder
(2) In mild hypotonic hyponatremia (Na+ = 120-130 mmol/L) withhold free water and allow the pt to reequilibrate spontaneously
(3) In moderate hypotonic hyonatremia (Na+ = 110-120 mmol/L) loop diuretics (given with saline to prevent renal concentration of urine due to high ADH)
(4) In severe hypotonic hyponatremia (Na+ <110) give hypertonic saline to increase serum sodium by 1 to 2 mEq/L per hour until symptoms improve

Front 31

Define hypernatremia.

Back 31

(1) Plasma sodium concentration >145 mmol/L
(2) Refers to excess sodium in relation to water, which can result from water loss or sodium infusion

Front 32

Describe the steps in the clinical assessment of ECF volume.

Back 32

(1) Hypervolemic hypernatremia (sodium stores are depleted, but more water loss than sodium loss); can be from renal loss (e.g. diuretics, osmotic diuresis, renal failure) or extrarenal loss (e.g. diarrhea, diaphoresis, respiratory losses)
(2) Isovolemic hypernatremia (sodium stores are normal, water is lost); common causes include diabetes insipidus and insensible respiratory loss (tachypnea)
(3) Hypervolemic hypernatremia (sodium excess); occurs infrequently; MCCs include iatrogenic (NaHCO3, TPN), exogenous glucocorticoids, Cushing’s syndrome, saltwater drowning, primary hyperaldosteronism

Front 33

What is a common concern during the correction of hypernatremia?

Back 33

(1) Excessively rapid correction of hypernatremia can cause central pontine myelinolysis and/or cerebral edema
(2) Rate of correction should not exceed 12 mEq/L per day and should be less than 8 mEq/L in the first 24h

Front 34

What are the primary clinical features of hypernatremia? What is the underlying mechanism that leads to these features?

Back 34

(1) Neurologic symptoms are most predominant; altered mental status, restlessness, weakness, focal neurologic deficits; can progress to confusion, seizures, and coma
(2) Dry mucous membranes, decreased salivation (in hypovolemic hypernatremia)
(3) Clinical features are secondary to osmotic effects on the brain (i.e. water shifts out of brain cells); Sx are more prominent and severe when sodium levels increase rapidly

Front 35

Describe the diagnostic steps when working a patient up for hypernatremia.

Back 35

(1) Assess urine volume; should be low if kidneys are responding appropriately
(2) Urine osmolality should be >800 mOsm/kg
(3) Desmopressin should be given to differentiate nephrogenic from central diabetes insipidus, if this entity is suspected

Front 36

Describe the treatment of hypernatremia.

Back 36

(1) Hypovolemic hypernatremia: give isotonic NaCl to restore hemodynamics. Correction of hypernatremia can wait until the patient is hemodynamically stable then replace the free water deficit
(2) Isovolemic hypernatremia: patients with DI require vasopressin; prescribe oral fluids, or if the patient cannot drink, give D5W
(3) Hypervolemic hypernatremia: Give diuretics (furosemide) and D5W to remove the excess sodium. Dialyze patients with renal failure.

Front 37

What are the common causes of hypocalcemia?

Back 37

(1) Hypoparathyroidism (MCC); usually due to surgery on the thyroid gland with damage to nearby parathyroids
(2) Acute pancreatitis; deposition of calcium in soft tissue lowers serum Ca2+ levels
(3) Renal insufficiency; mainly due to decreased production of 1,25-dihydroxy vitamin D
(4) Hyperphosphatemia; phosphate precipitates with Ca2+, resulting in calcium phosphate deposition
(5) Pseudohypoparathyroidism; autosomal recessive disease causing congenital end-organ resistance to PTH (leading to high serum PTH levels); also characterized by short metacarpal bones and mental retardation
(6) Hypomagnesemia leads to decreased PTH secretion
(7) Vitamin D deficiency
(8) Malabsorption; as in short bowel syndrome
(9) Blood transfusion (with citrated blood) as citrate chelates Ca2+
(10) Osteoblastic metastases
(11) Hypoalbuminemia; ionized fraction is normal (this entity is clinical irrelevant); hospitalized patients frequently have low serum albumin concentrations. Therefore if you see a low calcium level, look at the albumin level (it is usually low as well). A low serum ionized calcium level is much less common.

Front 38

List the clinical features of hypocalcemia.

Back 38

(1) Asymptomatic
(2) Rickets and osteomalacia
(3) Increased neuromuscular irritability—numbness, tingling (circumoral, fingers, toes); tetany (hyperactive DTRs); grand mal seizures
(4) Basal ganglia calcifications
(5) Cardiac manifestations include arrhythmias, prolonged QT interval on ECG – hypocalcemia should ALWAYS be in the DDx for a prolonged QT interval

Front 39

What is Chovstek’s sign? What is Trousseau’s sign?

Back 39

(1) Chovstek’s sign—Tapping a facial nerve leads to a contraction of facial muscles
(2) Trousseau’s sign—inflate BP cuff to a pressure higher than the patient’s systolic BP for 3 minutes, which occludes blood flow in forearm; this elicits carpal spasms

Front 40

How would you work up a patient with low serum calcium?

Back 40

(1) Obtain BUN, Cr, magnesium, albumin, and ionized calcium
(2) If clinically warranted, order serum lipase, amylase, and LFTs
(3) Serum phosphate is high in renal insufficiency and in hypoparathyroidism, low in primary vitamin D deficiency
(4) PTH is a) low in hypoparathyroidism, b) elevated in vitamin D deficiency, and c) very high in pseudohypoparathyroidism

Front 41

Describe the treatment of a hypocalcemic patient.

Back 41

(1) If symptomatic, provide emergency treatment with IV calcium gluconate. Make sure that magnesium is replaced.
(2) For long-term management, use oral calcium supplements and vitamin D.
(3) For PTH deficiency, replacement therapy with vitamin D plus a high oral calcium intake; also thiazide diuretics can be used to lower urinary calcium to prevent urolithiasis

Front 42

What are the four main etiologic categories of hypercalcemia?

Back 42

(1) Endocrinopathies
(2) Malignacies
(3) Pharmacologic
(4) Other

Front 43

What are the main endocrinopathies that lead to hypercalcemia?

Back 43

(1) Hyperparathyroidism (increased Ca2+, low phosphate)
(2) Renal failure (usually produces hypocalcemia, but occasionally secondary hyperparathyroidism elevates PTH levels high enough to cause hypercalcemia)
(3) Paget’s disease of bone (due to osteoclastic bone resorption)
(4) Hyperparathyroidism, acromegaly, Addison’s disease

Front 44

What types of malignancies can cause hypercalcemia?

Back 44

(1) Metastatic cancers—bony mets result in bone destruction due to osteoclastic activity. Most tumors that metastasize to bone cause both osteolytic and osteoblatic activity.
(2) Multiple myeloma—hypercalcemia is secondary to lysis of bone by tumor cells and release of osteoclast-activating factor by myeloma cells
(3) Tumors that release PTHrP (squamous cell carcinoma of the lung, breast CA, RCC)

Front 45

List the pharmacologic causes of hypercalcemia.

Back 45

(1) Vitamin D intoxication
(2) Milk-alkali syndrome—hypercalcemia, alkalosis, and renal impairment due to excessive intake of calcium and certain absorbable antacids
(3) Thiazide diuretics inhibit renal secretion
(4) Lithium increases PTH levels in some patients

Front 46

List the most common clinical features of hypercalcemia.

Back 46

(1) “Stones”—nephrolithiasis, nephrocalcinosis
(2) “Bones”—bone aches and pains; osteitis fibrosa cystica or “brown tumors” predispose to pathologic fractures
(3) “Groans”—muscle pain and weakness, pancreatitis, PUD, gout, constipation
(4) “Psychiatric overtones”—depression, fatigue, anorexia, sleep disturbances, anxiety, lethargy
(5) Other findings may include polydipsia, polyuria, hypertension, weight loss, shortened QT interval on ECG
(6) Patients may be asymptomatic

Front 47

Describe the workup of a patient with with hypercalcemia.

Back 47

(1) Obtain BUN, Cr, magnesium, albumin, and ionized calcium
(2) Radioimmunoassay of PTH, which is elevated in primary hyperparathyroisism, low in occult malignancy
(3) Radioimmunoassay of PTHrP: elevated in malignancy
(4) Bone scan or bone survey to identify lytic lesions
(5) Urinary cAMP: markedly elevated in primary hyperparathyroidism

Front 48

Describe the steps in treating a patient with hypercalcemia.

Back 48

(1) Increase urinary excretion: IV fluids are first step in management, diuretics further inhibit calcium reabsorption
(2) Inhibit bone resorption in patients with osteoclastic disease with bisphosphonates and/or calcitonin
(3) Give glucocorticoids if vitamin D-related mechanisms (intoxication, granulomatous disorders) and multiple myeloma are the cause of the hypercalcemia. However, glucocorticoids are ineffective in most other forms of hypercalcemia
(4) Use dialysis in patients with renal insufficiency
(5) Phosphate is effective but increases the risk of metastatic calcifications

Front 49

Hypokalemia can broadly be categorized into three categories. List them.

Back 49

(1) GI-related potassium loss
(2) Renal calcium loss
(3) Transcellular shift and other causes

Front 50

List the main causes of GI-related potassium loss.

Back 50

(1) Vomiting and nasogastric drainage; note that volume depletion and metabolic alkalosis also result
(2) Diarrhea
(3) Laxatives and enemas
(4) Intestinal fistulae
(5) Decreased potassium absorption in intestinal disorders

Front 51

List the main causes of renal potassium loss.

Back 51

(1) Diuretics
(2) Renal tubular or parenchymal disease
(3) Primary and secondary hyperaldosteronism
(4) Excessive glucocorticoids
(5) Magnesium deficiency
(6) Bartter’s syndrome—chronic volume depletion secondary to an autosomal-recessive defect in salt reabsorption in the TAL leads to hyperplasia of JGA which leads to increased renin levels and secondary aldosterone elevations

Front 52

List the other causes of hypokalemia (besides renal and GI causes).

Back 52

(1) Insufficient dietary intake
(2) Insulin administration
(3) Certain antibiotics
(4) Profuse sweating
(5) Epinephrine (β2-agonists)—hypokalemia occurs in 50%-60% of trauma patients, perhaps due to increased epinephrine levels

Front 53

What are the main clinical features of hypokalemia?

Back 53

(1) Arrhythmias—hypokalemia prolongs normal cardiac conduction
(2) Muscular weakness, fatigue, paralysis, muscle cramps
(3) Decreased DTRs
(4) Paralytic ileus
(5) Polyuria, polydipsia
(6) Nausea and vomiting
(7) Exacerbates digitalis toxicity

Front 54

What are the primary ECG findings in the setting of hypokalemia?

Back 54

(1) Flattened T wave
(2) If severe, T wave inverts
(3) U wave appears

Front 55

Describe the management of a patient with hypokalemia.

Back 55

(1) Identify and treat the underlying cause
(2) Discontinue any medications that can aggravate hypokalemia
(3) Oral KCl is the preferred method of replacement and is appropriate in most instances. Always retest the K+ levels after administration. Using 10 mEq of KCl increases K+ levels by 0.1 mEq/L; comes in slow-acting and fast-acting forms
(4) IV KCl can be given if the hypokalemia is severe (<2.5) or if the patient has arrhythmias secondary to the hypokalemia; give slowly to avoid hyperkalemia; monitor K+ concentration and cardiac rhythm when giving IV K+

Front 56

List 3 pearls related to IV potassium infusion.

Back 56

(1) Maximum infusion rate of 10 mEq/hr in peripheral IV line
(2) Maximum infusion rate of 20 mEq/hr in central line
(3) May add 1% lidocaine to bag to decrease pain

Front 57

Why might HTN be useful in diagnosing the cause of hypokalemia?

Back 57

(1) if the patient has HTN, excessive aldosterone activity is likely. If the patient is normotensive, either GI or renal loss of K+ is likely.

Front 58

What electrolyte must be monitored in patients taking digoxin? Why?

Back 58

(1) Potassium
(2) It is common for patients on digoxin to also be taking diuretics for CHF, which can cause hypokalemia.
(3) Hypokalemia predisposes the patient to digoxin toxicity

Front 59

Causes of hyperkalemia can broadly be divided into three categories. What are these three categories?

Back 59

(1) Increased total body potassium
(2) Redistribution—translocation of potassium from intracellular to extracellular space
(3) Pseudohyperkalemia (spurious)

Front 60

What are the primary causes of increased total body potassium?

Back 60

(1) Renal failure—either acute or chronic
(2) Addison’s disease
(3) Potassium-sparing diuretics (spironolactone)
(4) Hyporeninemic hypoaldosteronism
(5) ACE inhibitors
(6) Iatrogenic overdose—be especially cautious when administering potassium to patients with renal failure
(7) Blood transfusion

Front 61

What are the main causes of “redistribution-related” hyperkalemia?

Back 61

(1) Acidosis (not organic) leads to potassium shift
(2) Tissue/cell breakdown releases potassium (e.g. rhabdomyolysis, hemolysis, burns)
(3) GI bleeding
(4) Insulin deficiency
(5) Rapid administration of a beta-blocker

Front 62

How does insulin deficiency contribute to hyperkalemia?

Back 62

(1) Insulin stimulates the Na+/K+ ATPase, thereby causing potassium to shift into cells
(2) Insulin deficiency and hypertonicity (high glucose) promote K+ efflux from ICF to ECF

Front 63

What is pseudohyperkalemia and what are the main causes?

Back 63

(1) Refers to an artificially elevated plasma K+ concentration due to K+ movement out of cells immediately before or after venipuncture
(2) Contributing factors include prolonged use of a tourniquet with or without repeated fist clenching. This can cause acidosis and subsequent K+ loss from cells.

Front 64

What ECG changes are common in hyperkalemia?

Back 64

(1) Peaked T waves (by 10mm)
(2) A prolonged PR interval
(3) Widening of QRS and merging of QRS with T wave
(4) Ventricular fibrillation and cardiac arrest (with increasing K+ concentration)

Front 65

What are the common clinical findings in hyperkalemia?

Back 65

(1) Arrhythmias—crucial; check ECG immediately in hyperkalemic patient
(2) Muscle weakness and (rarely) flaccid paralysis
(3) Decreased DTRs
(4) Respiratory failure
(5) Nausea/vomiting, intestinal colic, diarrhea

Front 66

Describe the steps in management of a hyperkalemic patient.

Back 66

(1) The three main steps in treatment are to first, stabilize cellular membranes; second, reduce serum K+ by inducing shift from ECF to ICF; and third, remove excess K+ from body
(2) If hyperkalemia is severe or ECG changes are present, give IV calcium; stabilizes the resting membrane potential of myocardial membranes; NOTE: use caution when administering calcium to patients on digoxin
(3) Administer glucose and insulin; glucose stimulates insulin release from beta-cells, but exogenous insulin is more rapid. Both are given together to prevent hypoglycemia
(4) Sodium bicarbonate can also be given, as it increases pH level, which shifts K+ into cells; this is reserved as emergency measure in sevee hyperkalemia
(5) Kayexalate is given, which absorbs K+ in colon, preventing absorption; hemodialysis is the most rapid and effective way of lowering plasma K+, but is reserved for intractable hyperkalemia and for those with renal failure
(6) Diuretics (furosemide)

Front 67

List the main causes of hypomagnesemia.

Back 67

(1) GI—Malabsorption, steatorrheic states (MCC), prolonged fasting, fistulas, TPN w/o Mg2+ supplementation
(2) Alcoholism (common)
(3) Renal causes—SIADH, diuretics, Bartter’s syndrome, drugs such as gentamicin, aphotericin B, cisplatin, renal transplantation
(4) Other: postparathyroidectomy, DKA, throtoxicosis, lactation, burns, pancreatitis

Front 68

What are the clinical features common to hypomagnesemia?

Back 68

(1) Marked neuromuscular and CNS hyperirritability (muscle twitching, weakness, tremors, hyperreflexia, seizures, mental status change
(2) Effect on calcium levels—coexisting hypocalcemia is COMMON because of decreased release of PTH and bone resistance to PTH when Mg2+ is low
(3) Coexisting hypokalemia in up to 50% of cases—in muscle and myocardium, when either intracellular Mg2+ or K+ decreases, a corresponding decrease in the other cation takes place
(4) ECG changes—prolonged QT interval, T wave flattening, and ultimately torsade de pointes

Front 69

What is the appropriate treatment for hypomagnesemia?

Back 69

(1) Oral Mg2+ for mild cases
(2) Parenteral Mg2+ for severe cases

Front 70

List the common causes of hypermagnesemia.

Back 70

(1) Renal failure (MCC)
(2) Early-stage burns, massive trauma or surgical stress, severe ECF volume deficit, severe acidosis
(3) Excessive intake of magnesium-containing laxatives or antacids combined with renal insufficiency
(4) Adrenal insufficiency
(5) Rhabdomyolysis
(6) Iatrogenic—in the obstetric setting in women with preeclampsia or eclampsia

Front 71

What are the clinical features of hypermagnesemia?

Back 71

(1) Nausea, weakness
(2) Facial paresthesias
(3) Progressive loss of DTRs
(4) ECG changes resemble those seen with hyperkalemia (increased PR interval, widened QRS, elevated T waves)
(5) Somnolence leading to coma and muscular paralysis occur late
(6) Death is usually caused by respiratory failure or cardiac arrest

Front 72

Describe the treatment approach to hypermagnesemia.

Back 72

(1) Withhold exogenously administered magnesium
(2) Prescribe IV calcium gluconate for emergent symptoms (i.e. for cardioprotection)
(3) Administer saline and furosemide
(4) Order dialysis in renal failure patients

Front 73

What are the commonest causes of hypophosphatemia?

Back 73

(1) Decreased intestinal absorption due to alcohol abuse, vitamin D deficiency, malabsorption of phosphate, excessive use of phosphate-binding antacids, PTN, starvation
(2) Increased renal excretion—Excess PTH states (vitamin D deficiency, hyperparathyroidism)
(3) Increased renal excretion—hyperglycemia, oncogenic osteomalacia, ATN, RTA, etc.
(4) Other causes include respiratory alkalosis, steroids, severe hyperthermia, DKA, hungry bone syndrome (deposition of bone material after parathyroidectomy

Front 74

List the clinical features of hypophosphatemia.

Back 74

(1) Neurologic findings: encephalopathy, confusion, seizures, numbness, paresthesias
(2) Musculoskeletal: muscle weakness, myalgias, bone pain, rickets/osteomalacia
(3) Hematologic: hemolysis, RBC dysfunction, WBC dysfunction, platelet dysfunction
(4) Cardiac: cardiomyopathy and myocardial depression secondary to low ATP levels, may lead to cardiac arrest
(5) Rhabdomyolysis
(6) Anorexia
(7) Difficulty in ventilator weaning

Front 75

What is the appropriate treatment for hypophosphatemia?

Back 75

(1) if mild (>1mg/dL), oral supplementation; Neutra-Phos capsules, K-Phos tablets, milk
(2) If severe/symptomatic or if patient is NPO: parenteral supplementation

Front 76

What are the commonest causes of hyperphosphatemia?

Back 76

(1) Decreased renal excretion of phosphate due to renal insufficiency (MCC)
(2) Bisphosphonates
(3) Hypoparathyroidism
(4) Vitamin D intoxication
(5) Tumor calcinosis
(6) Increased phosphate administration
(7) Rhabdomyolysis, cell lysis, or acidosis

Front 77

What are the clinical features of hyperphosphatemia?

Back 77

(1) Metastatic calcification and soft-tissue calcifications: a calcium-phosphorus product; NOTE that (serum calcium x serum phosphate) >70 indicates that calcification is likely to occur
(2) Associated hypocalcemia and its manifest findings

Front 78

Treatment of hyperphosphatemia.

Back 78

(1) Phosphate binding antacids containing aluminum hydroxide or carbonate (these bind phosphate in the bowel and prevent absorption)
(2) Hemodialysis (in the setting of renal failure)

Front 79

Describe the general characteristics of metabolic acidosis.

Back 79

(1) Characterized by decreased blood pH and a decreased plasma bicarbonate.
(2) The goal is to identify the underlying condition that is causing the metabolic acidosis.

Front 80

What is the equation to calculate anion gap and what does it represent?

Back 80

AG(mEq/L) = [Na+] - ([Cl-] + [HCO3-])

Normal values are 8-15 mEq/L, but can vary a bit.

Reflects ions present in serum but unmeasured (i.e. proteins, phosphate, organic acids, etc.)

Front 81

What are the primary physiologic effects of acidosis?

Back 81

(1) Right shift in oxygen-hemoglobin dissociation curve diminishes the affinity of hemoglobin for oxygen
(2) Depresses the CNS
(3) Decreases pulmonary blood flow
(4) Arrhythmias
(5) Impairs myocardial function
(6) Hyperkalemia

Front 82

What are the primary physiologic effects of alkalosis?

Back 82

(1) Decrease in cerebral blood flow
(2) Left shift in oxygen-hemoglobin dissociation curve increases affinity of hemoglobin for oxygen
(3) Arrhythmias
(4) Tetany, seizures

Front 83

List causes of INCREASED anion gap acidosis.

Back 83

(1) Ketoacidosis - DM, prolonged starvation, prolonged EtOH abuse
(2) Lactic acidosis can occur in many different contexts - Low tissue perfusion, shock states (cardiogenic, septic, hypovolemic); excessive energy expenditure (e.g. seizures)
(3) Renal failure - decreased NH4+ excretion, thus decreasing net acid - Decreased excretion of organic anions, sulfate, phosphate also increases AG
(4) Intoxication - Salicylate, methanol, ethylene glycol

Front 84

List causes of NORMAL anion gap acidosis.

Back 84

(1) Loss of bicarbonate - Diarrhea, CA inhibitors, Proximal RTA, pancreatic ileostomy; pancreatic, biliary, or intestinal fistula
(2) Exogenous administration - NH4Cl or HCl
(3) Decreased renal acid excretion - Distal RTA; renal failure
(4) Misc. - Hyperkalemia; recovery from DKA

Front 85

What are the primary clinical features associated with metabolic acidosis?

Back 85

(1) Hyperventilation (Kussmaul's respirations); cardinal feature seen in severe metabolic acidosis (usually pH <7.20); less prominent when the acidosis is chronic
(2) Decreased cardiac output and decreased tissue perfusion (occurs with severe metabolic acidosis, pH<7.20); acidosis diminishes tissue responsiveness to catecholamines, which can exacerbate the poor tissue perfusion

Front 86

Describe the key components of the diagnostic process in a patient suspected of having a metabolic acidosis?

Back 86

(1) History is very important
(2) Calculate the AG
(3) Winter's formula can be used to predict the expected respiratory compensation to metabolic acidosis.

Front 87

How is Winter's formula interpreted?

Back 87

(1) If the PaCO2 does not fall within an acceptable range, then the patient has another primary acid-base disorder.
(2) If the PaCO2 falls within the predicted range, pt has a simple metabolic acidosis with an appropriate secondary hypocapnia
(3) If the actual PaCO2 is higher than the calculated PaCO2, the pt has metabolic acidosis with respiratory acidosis...SERIOUS FINDING BECAUSE FAILURE OF COMPENSATION CAN BE A SIGN OF IMPENDING RESPIRATORY FAILURE
(4) If the actual PaCO2 is lower than the calculated PaCO2, then the patient has metabolic acidosis with respiratory alkalosis.

Front 88

Describe the standard treatment for metabolic acidosis.

Back 88

(1) Treatment obviously varies depending on the cause
(2) Sodium bicarbonate is sometimes needed (esp. for normal AG acidosis). Correct severe acidosis to 7.20 and realize that it takes 24 hours for the added bicarb to reach the brain, during which time, hyperventilation continues (i.e. the PaCO2 remains low while HCO3- is increasing
(3) Mechanical ventilation may be required if the patient is fatigued from prolonged hyperventilation, esp. in DKA

Front 89

What are the normal ranges of pH, PaCO2 and HCO3-?

Back 89

pH: 7.35-7.45
PaCO2: 36-44
HCO3-: 22-26

Front 90

Describe the general characteristics of metabolic alkalosis.

Back 90

(1) Characterized by an increased blood pH and plasma HCO3-
(2) Uncomplicated metabolic alkalosis is typically transient, due to the kidney's efficiency at secreting excess bicarb
(3) Consider 2 events: event that initiates the alkalosis and the mechanism that maintains the alkalosis

Front 91

Metabolic alkalosis can broadly be divided into two categories. What are these two categories?

Back 91

(1) Saline-sensitive and
(2) Saline-resistant metabolic alkalosis

Front 92

What is saline-sensitive metabolic alkalosis? What are common causes?

Back 92

(1) Urine Cl- <10mEq/L
(2) characterized by ECF contraction and hypokalemia

CAUSES
(1) Vomiting or nasogastic suction (patient looses HCl, and gastric HCO3- is produced)
(2) Diuretics decrease ECF volume while total body HCO3- remains the same; leads to increased plasma HCO3- due to ECF contraction
(3) Villous adenoma of colon, diarrhea with high Cl- content

Front 93

What is saline-resistant metabolic alkalosis? What are the common causes?

Back 93

(1) Urine Cl- >20mEq/L
(2) characterized by ECF expansion and hypertension (due to increased mineralocorticoids)

CAUSES
(1) Most are secondary to adrenal disorders; Increased mineralocorticoids leads to increased tubular reabsorption of Na+ and HCO3- by kidney, and excessive loss of Cl-
(2) Other causes include CUshing's syndrome, severe K+ deficiency, Bartter's syndrome, diuretic abuse

Front 94

What are the clinical features associated with alkalosis?

Back 94

There are no characteristic signs or symptoms.

Patient's medical history is most helpful.

Front 95

List the diagnostic steps involved in diagnosing metabolic alkalosis.

Back 95

(1) Elevated HCO3- level, elevated blood pH
(2) Hypokalemia is common, due to renal loss of K+
(3) PaCO2 is elevated as a compensatory mechanism (rarely exceeds 50-55)
(4) Urine chloride is very important in distinguishing between saline-sensitive and saline-resistant types.

Front 96

What is the treatment for metabolic alkalosis?

Back 96

(1) Treat the underlying disorder
(2) Normal saline plus potassium will restore the ECF volume if the patient is volume contracted
(3) Address the underlying cause (or prescribe spironolactone) if the patient is volume expanded

Front 97

What are the general characteristics of respiratory acidosis?

Back 97

(1) Reduced blood pH and PaCO2 >40mmHg
(2) Renal compensation begins within 12-24h and progresses over about 5 days
(3) Acute respiratory acidosis: An immediate compensatory elevation in HCO3- of 1mmol/L for every 10mm Hg increase in PaCO2
(4) Chronic respiratory acidosis: Renal compensation, HCO3- increases by 4mmol/L for every 10 mm Hg increase in PaCO2; generally seen in patients with underlying lung dz

Front 98

List common causes of respiratory acidosis.

Back 98

All are associated with alveolar HYPOventilation.
(1) Primary pulmonary dz (COPD, airway obstruction)
(2) Neuromuscular dz (myasthenia gravis)
(3) CNS malfunction (brainstem injury)
(4) Drug-induced hypoventilation (morphine anesthetics, sedatives, narcotic OD)
(5) Respiratory muscle fatigue

Front 99

What are the primary clinical features of respiratory acidosis?

Back 99

(1) Somnolence, confusion, and myoclonus with asterixis
(2) Headaches, confusion, and papilledema are signs of acute CO2 retention

Front 100

Describe the treatment approach in a patient with respiratory acidosis.

Back 100

(1) Verify patency of the airway
(2) If PaO2 is low (<60), begin supplemental O2 (be cautious in "CO2 retainers"
(3) Correct reversible causes
(4) Initiate any measure to improve alveolar ventilation (pulmonary toilet, correct reversible pulmonary dz, remove obstruction, administer bronchodilators, etc)
(5) Intubation and mechanical ventilation may be necessary to relieve the acidemia and hypoxia (situations requiring intubation: severe acidosis, PaCO2 >60 or inability to increase PO2 w/o supplemental O2, if patient is obtunded or shows deterioration in mental status, impending respiratory failure)

Front 101

Why does increased PaCO2 cause headaches, confusion, papilledema?

Back 101

Increased PaCO2 leads to increased cerebral blood flow, which, in turn, increases CSF pressure, resulting in generalized CNS depression

Front 102

What are the general characteristics of respiratory alkalosis?

Back 102

(1) Increased blood pH and decreased PaCO2
(2) Acutely, for each 10 mm Hg decrease in PaCO2, plasma HCO3- decreases by 2 mEq/L and blood pH increases by 0.08 mEq/L.
(3) Chronically, for each 10 mm Hg decrease in PaCO2, plasma HCO3- decreases by 5-6 mEq//L and blood pH decreases by 0.02mEq/L

Front 103

List the most common causes of respiratory alkalosis.

Back 103

All causes associated with alveolar HYPERventilation
(1) Anxiety
(2) PE, pneumonia, asthma
(3) Hypoxia
(4) Mechanical ventilation
(5) Pregnancy - increased serum progesterone levels cause hyperventilation
(6) Sepsis
(7) Liver disease (cirrhosis)
(8) Medication (e.g salicylate toxicity
(9) Hyperventilation syndrome

Front 104

What are the main clinical features of respiratory alkalosis?

Back 104

(1) Sx are mostly related to decreased cerebral blood flow (vasoconstriction): lightheadedness, dizziness, anxiety, paresthesias, and perioral numbness
(2) Tetany (indistinguishable from hypocalcemia)
(3) Arrhythmias (if severe)

Front 105

What is the treatment for respiratory alkalosis?

Back 105

(1) Correct the underlying cause
(2) Sometimes this does not need to be treated (e.g. in case of pregnancy)
(3) An inhaled mixture containing CO2 or breathing into a paper bag may be helpful.