Acid/Base & electrolytes

Question 1

Information Obtained from an ABG

Answer 1

Acid base status
Oxygenation
        Dissolved O2 (pO2)
        Saturation of hemoglobin
CO2 elimination, aka ventilation
Levels of carboxyhemoglobin & methemoglobin

Question 2

Contraindications for an ABG

Answer 2

Bleeding diathesis
AV fistula
Severe peripheral vascular disease, absence of an arterial pulse
Infection over site

Question 3

Indications for ABG

Answer 3

Assess the ventilatory status, oxygenation and acid base status
Assess the response to an intervention

Question 4

Pulse Oximetry

Answer 4

Oximetry is non-invasive & provides immediate and continuous data
Oximetry does not assess ventilation (pCO2) or acid base status
Oximetry unreliable when pO2 < 70-80%
Pulse oximetry cannot interpret methemoglobin or carboxyhemoglobin

Question 5

metabolic acidosis

Answer 5

pH= low
HCO3= low
PaCO2= low

Question 6

metabolic alkalosis

Answer 6

pH= high
HCO3= high
PaCO2= high

Question 7

respiratory alkalosis

Answer 7

pH= high
HCO3= low
PaCO2= low

Question 8

respiratory acidosis

Answer 8

pH= low
HCO3= high
PaCO2= high

Question 9

Phase 1 for Salicylate Toxicity

Answer 9

hyperventilation resulting from direct respiratory center stimulation w/ respiratory alkalosis and compensatory alkaluria. K and NaCO3 excreted in the urine. Lasts as long as 12 hours.

Question 10

Phase 2 for Salicylate Toxicity

Answer 10

paradoxic aciduria in the presence of continued respiratory alkalosis occurs when sufficient potassium has been lost from the kidneys. Begins w/ hours & may last 12-24 hours.

Question 11

Phase 3 for Salicylate Toxicity

Answer 11

dehydration, hypokalemia, and progressive metabolic acidosis. Begins 4-6 hours after ingestion in a young infant or 24 hours or more after ingestion in an adolescent or adult.

Question 12

symptoms for salicylate toxicity

Answer 12

Nausea, vomiting, diaphoresis, and tinnitus are the earliest signs
Hyperthermia in severe toxicity, especially in young children

Question 13

Etiology for respiratory alkalosis

Answer 13

CNS stimulation– pain, anxiety, fever
hypoxia–aspiration, PNA
drugs/hormones– pregnancy, cardiac failure
stimulation of chest receptors– flail chest, hemothorax

Question 14

Etiology for respiratory acidosis

Answer 14

stroke 
infection
asthma
emphysema
bronchitis
muscular dystrophies

Question 15

Severe hyponatremia

Answer 15

Sodium < 120 mEq/L
Symptoms to include mental status changes, seizure, or coma
Infusion of 3% hypertonic saline solution

Question 16

How do you correct hyponatremia

Answer 16

hyperglycemia
Corrected Sodium (Hillier, 1999) = Measured sodium + 0.024 * (Serum glucose - 100)
Sodium correction factor of 2.4mEq/L per 100

Question 17

Etiology of hypokalemia

Answer 17

poor intake
increased sweating
V/D
cushing syndrome
magnesium depletion 
hypothermia
medications

Question 18

Etiology of hyperkalemia

Answer 18

Renal failure
Medications
Type IV renal tubular acidosis
increased potassium input
Hemolysis
Rhabdomyolysis

Question 19

Hypokalemia

Answer 19

Usually associated with diuretic therapy
Symptoms are primarily neuromuscular and cardiac
Assess acid–base status
Replace potassium orally whenever possible; IV potassium may be given with caution in severe cases with appropriate monitoring

Question 20

Hyperkalemia

Answer 20

true emergency
Suspect hyperkalemia in patients with renal failure, diabetes, or those taking potassium supplements
Symptoms are primarily neuromuscular and cardiac
EKG findings may progress rapidly from peaked T waves to ventricular fibrillation
Beware of spurious hyperkalemia
Treatment stabilizes cardiac membranes, shifts potassium into cells, and removes potassium from the body

Question 21

Etiology of Hypercalcemia

Answer 21

Hyperparathyroidism
Increased PTH-related protein in NSCLC, RCC, prostate ca., multiple myeloma
Milk-alkali syndrome
Thiazide diuretics
Granulomatous diseases
Vitamin D intoxication

Question 22

Hypocalcemia

Answer 22

Occurs often in critically ill patients, although rarely life-threatening in itself
Usually asymptomatic until severe
Neuromuscular and respiratory symptoms predominate
Often associated with disorders of magnesium and phosphate
Always check serum phosphate before replacing calcium IV
Use caution in giving IV calcium to patients taking digoxin

Question 23

Hypercalcemia

Answer 23

Usually caused by malignancy or hyperparathyroidism
Symptoms are primarily neuromuscular and renal
Volume replacement/expansion is primary therapy
Treatment promotes calcium excretion, inhibits osteoclast activity, and decreases calcium absorption

Question 24

Etiology of hyperphosphatemia

Answer 24

decreased absorption
renal losses
carbohydrate infusion
rapid cellular uptake
medication/ hormone effect

Question 25

Hypophosphatemia

Answer 25

Hypophosphatemia is often asymptomatic unless severe and commonly occurs along with disorders of calcium, magnesium, and potassium
Assess acid–base status
Oral replacement is preferred and should be initiated even in asymptomatic patients
IV replacement may be used cautiously in severely symptomatic patient

Question 26

Hyperphosphatemia

Answer 26

Hyperphosphatemia is often associated with renal disease or hypoparathyroidism
Increased phosphate may be a manifestation of tumor lysis or rhabdomyolysis
Initial treatment consists of volume expansion and using insulin and glucose to shift phosphate into cells

Question 27

Hypophosphatemia Treatment

Answer 27

Phosphate replacement appropriate regardless of symptoms
Oral supplementation is safe & preferred (milk contains 1 mg of phosphate/ml, or oral formulations containing sodium or potassium phosphate)
Severe symptomatic hypophosphatemia, IV infusion of sodium or potassium phosphate at a rate not to exceed 2.5 mg/kg over 6 hours

Question 28

Hyperphosphatemia Treatment

Answer 28

Normal renal function, volume expansion using isotonic saline coupled with acetazolamide (15 mg/kg, 500 mg in an average adult) will excrete phosphate: Ca may also be lowered
IV insulin and glucose to move phosphate into the cells (as with hyperkalemia)
Dialysis if renal failure
Chronic hyperphosphatemia - primary focus is reducing intestinal absorption

Question 29

Etiology of Hypomagnesemia

Answer 29

decreased intake
diarrhea
malabsorption
fistula
alcohol
medications
diuresis

Question 30

Hypomagnesemia

Answer 30

Frequently associated with disorders of calcium, potassium, and phosphate
Common in malnourished patients and those with renal disease
Symptoms are primarily neuromuscular and similar to those seen with hypocalcemia
Oral replacement is preferred except in severe symptomatic cases

Question 31

Hypermagnesemia

Answer 31

Symptoms are rare until magnesium levels are severely elevated
Usually secondary to renal failure or excess magnesium intake
Calcium gluconate can be used to reverse respiratory paralysis until forced diuresis or dialysis lowers serum magnesium levels

Question 32

Hypomagnesemia Treatment

Answer 32

correction of electrolytes
oral replacement for mild symptoms- mag oxide/ gluconate
parenteral therapy for symtpoms 
magsulfate in 20% solution
with renal failure mag should be halved

Question 33

Hypermagnesemia Treatment

Answer 33

Calcium gluconate as temporizing measure in cases of impending respiratory paralysis
Patients with normal renal function should undergo forced diuresis with isotonic saline and furosemide to promote renal excretion
Dialysis is indicated for severe hypermagnesemia and renal insufficiency