Acid base and electrolytes

Question 1

True or false: The body does not compensate beyond a normal pH.

Answer 1

True. For example, a patient with metabolic acidosis will eliminate CO2 to help restore a normal pH.
However, if respiratory alkalosis is a compensatory mechanism (and not a rare, separate primary
disturbance), then the pH will not correct to greater than 7.4. Overcorrection does not occur

Question 2

List the common causes of acidosis

Answer 2

Respiratory acidosis: Chronic obstructive pulmonary disease, asthma, drugs (e.g., opioids, benzodiazepines,
barbiturates, alcohol, other respiratory depressants), chest wall problems (paralysis, pain),
and sleep apnea.
Metabolic acidosis: Ethanol, diabetic ketoacidosis, uremia, lactic acidosis (e.g., sepsis, shock,
bowel ischemia), methanol/ethylene glycol, aspirin/salicylate overdose, diarrhea, and carbonic
anhydrase inhibitors.

Question 3

List the common causes of alkalosis.

Answer 3

Respiratory alkalosis: Anxiety/hyperventilation and aspirin/salicylate overdose.
Metabolic alkalosis: Diuretics (except carbonic anhydrase inhibitors), vomiting, volume contraction,
antacid abuse/milk-alkali syndrome, and hyperaldosteronism

Question 4

How does hypokalemia cause alkalosis?

Answer 4

Decreased levels of hypokalemia causes an increase in bicarbonate reabsorbtion.

Question 5

What type of acid-base disturbance does aspirin overdose cause?

Answer 5

Respiratory alkalosis and metabolic acidosis (two different primary disturbances). Look for coexisting
tinnitus, hypoglycemia, vomiting, and a history of “swallowing several pills.” Alkalinization of the
urine with bicarbonate speeds excretion

Question 6

What is the use of an anion gap?

Answer 6

Assist the diagnosis of metabolic acidosis.

Question 7

What happens to the blood gas of patients with chronic lung conditions?

Answer 7

In certain people with chronic lung conditions (especially those with sleep apnea), pH may be alkaline
during the day because they breathe better when awake. In addition, just after an episode of bronchitis
or other respiratory disorder, the metabolic alkalosis that usually compensates for respiratory acidosis
is no longer a compensatory mechanism and becomes the primary disturbance (elevated pH and
bicarbonate). As a side note, remember that sleep apnea, like other chronic lung diseases, can cause
right-sided heart failure (cor pulmonale).

Question 8

Should you give bicarbonate to a patient with acidosis?

Answer 8

For purposes of the Step 2 boards, almost never. First try intravenous (IV) fluids and correction of the
underlying disorder. If all other measures fail and the pH remains less than 7.0, bicarbonate may be given

Question 9

The blood gas of a patient with asthma has changed from alkalotic to normal,
and the patient seems to be sleeping. Is the patient ready to go home?

Answer 9

For Step 2 purposes, this scenario means that the patient is probably crashing. Remember that pH is
initially high in patients with asthma because they are eliminating CO2. If the patient becomes tired
and does not breathe appropriately, CO2 will begin to rise and pH will begin to normalize. Eventually
the patient becomes acidotic and requires emergency intubation if appropriate measures are not
taken. If this scenario is mentioned on boards, the appropriate response is to prepare for possible
elective intubation and to continue aggressive medical treatment with beta2 agonists, steroids, and
oxygen. Fatigue secondary to work of breathing is an indication for intubation. Asthmatic patients are
supposed to be slightly alkalotic during an asthma attack. If they are not, you should wonder why

Question 10

List the signs and symptoms of hyponatremia.

Answer 10

Lethargy
n Seizures
n Mental status changes or confusion
n Cramps
n Anorexia
n Coma

Question 11

How do you determine the cause of hyponatremia?

Answer 11

Assess the fluid volume status. If hypovolemic, euvolemiac, hyprevolemic.

Question 12

If hyponatremic and hypovolemic what would be the possible causes?

Answer 12

Dehydration, diuretics,
diabetes, Addison disease/
hypoaldosteronism (high
potassium)

Question 13

If hyponatremic and euvolemic what would be the possible causes?

Answer 13

SIADH, psychogenic
polydipsia, oxytocin
use

Question 14

If hyponatremic and hypervolaemic what would be the possible causes?

Answer 14

Heart failure, nephrotic
syndrome, cirrhosis,
toxemia, renal failure

Question 15

How is hyponatremia treated?

Answer 15

For hypovolemic hyponatremia, the treatment is normal saline. Euvolemic and hypervolemic
hyponatremia are treated with water/fluid restriction; diuretics may be needed for hypervolemic
hyponatremia

Question 16

What medication is used to treat the syndrome of inappropriate antidiuretic
hormone secretion (SIADH) if water restriction fails?

Answer 16

Demeclocycline, which induces nephrogenic diabetes insipidus

Question 17

What happens if hyponatremia is corrected too quickly?

Answer 17

Overly quick correction may cause brainstem damage (central pontine myelinolysis). Hypertonic
saline is used only when a patient has seizures from severe hyponatremia—and even then, only
briefly and cautiously. Normal saline is a better choice 99% of the time for board purposes. In chronic
severe symptomatic hyponatremia, the rate of correction should not exceed 0.5 to 1 mEq/L/hr.

Question 18

What causes spurious (false) hyponatremia?

Answer 18

Hyperglycemia (Once glucose is greater than 200 mg/dL, sodium decreases by 1.6 mEq/L for
each rise of 100 mg/dL in glucose. Make sure you know how to make this correction.)
n Hyperproteinemia
n Hyperlipidemia
In these instances, the laboratory value is low, but the total body sodium is normal. Do not give the
patient extra salt or saline.

Question 19

What causes hyponatremia in postoperative patients?

Answer 19

The most common cause is the combination of pain and narcotics (causing SIADH) with overaggressive
administration of IV fluids. A rare cause that you may see on the USMLE is adrenal insufficiency; in this
instance, potassium is high and the blood pressure is low.

Question 20

What is the classic cause of hyponatremia in pregnant patients about to
deliver?

Answer 20

Oxytocin, which has an antidiuretic hormone–like effect

Question 21

What are the signs and symptoms of hypernatremia?

Answer 21

Basically the same as the signs and symptoms of hyponatremia:
n Mental status changes or confusion
n Seizures
n Hyperreflexia
n Coma

Question 22

What causes hypernatremia?

Answer 22

The most common cause is dehydration (free water loss) caused by inadequate fluid intake relative
to bodily needs. Watch for diuretics, diabetes insipidus, diarrhea, and renal disease, as well as
iatrogenic causes (administration of too much hypertonic IV fluid). Sickle cell disease, which may lead
to renal damage and isosthenuria (inability to concentrate urine), is a rare cause of hypernatremia, as
are hypokalemia and hypercalcemia, which also impair the kidney’s concentrating ability.

Question 23

How is hypernatremia treated?

Answer 23

Treatment involves water replacement, but the patient is often severely dehydrated; therefore normal
saline is used most frequently. Once the patient is hemodynamically stable, he or she is often switched
to ½ normal saline. Five percent dextrose in water (D5W) should not be used for hypernatremia.

Question 24

What are the signs and symptoms of hypokalemia?

Answer 24

Hypokalemia causes muscular weakness, which can lead to paralysis and ventilatory failure. When
smooth muscles also are affected, patients may develop ileus and/or hypotension. However, the
best known and most tested effect of hypokalemia is on the heart. Electrocardiogram (ECG) findings
include loss of the T wave or T-wave flattening, the presence of U waves, premature ventricular and
atrial complexes, and ventricular and atrial tachyarrhythmias

Question 25

What is the effect of pH on serum potassium?

Answer 25

Changes in pH cause changes in serum potassium as a result of cellular shift. Alkalosis causes
hypokalemia, whereas acidosis causes hyperkalemia. For this reason, bicarbonate is given to
severely hyperkalemic patients. If the pH is deranged, normalization most likely will correct the
potassium derangement automatically without the need to give or restrict potassium

Question 26

Describe the interaction between digoxin and potassium.

Answer 26

The heart is particularly sensitive to hypokalemia in patients taking digoxin. Potassium levels should
be monitored carefully in all patients taking digoxin, especially if they are also taking diuretics
(a common occurrence).

Question 27

How should potassium be replaced?

Answer 27

Like all electrolyte abnormalities, hypokalemia should be corrected slowly. Oral replacement is
preferred, but if the potassium must be given intravenously for severe derangement, do not give more
than 20 mEq/hr. Put the patient on an ECG monitor when giving IV potassium because potentially
fatal arrhythmias may develop

Question 28

When hypokalemia persists even after administration of significant amounts
of potassium, what should you do?

Answer 28

Check the magnesium level. When magnesium is low, the body cannot retain potassium effectively.
Correction of a low magnesium level allows the potassium level to return to normal.

Question 29

What are the signs and symptoms of hyperkalemia?

Answer 29

Weakness and paralysis may occur, but the cardiac effects are the most tested. ECG changes (in
order of increasing potassium value) include tall peaked T waves, widening of QRS, prolongation of
the PR interval, loss of P waves, and a sine wave pattern (Figure 1-1). Arrhythmias include asystole
and ventricular fibrillation.

Question 30

What causes hyperkalemia?

Answer 30

Renal failure (acute or chronic)
n Severe tissue destruction (because potassium has a high intracellular concentration)
n Hypoaldosteronism (watch for hyporeninemic hypoaldosteronism in diabetes)
n Medications (stop potassium-sparing diuretics, beta blockers, nonsteroidal antiinflammatory drugs
(NSAIDs), angiotensin-converting enzyme (ACE) inhibitors, and angiotensin receptor blockers)
n Adrenal insufficiency (also associated with low sodium and low blood pressure

Question 31

What should you suspect if an asymptomatic patient has hyperkalemia?

Answer 31

With hyperkalemia, the first consideration (especially if the patient is asymptomatic and the ECG is
normal) is whether the laboratory specimen is hemolyzed. Hemolysis causes a false hyperkalemia
result because of high intracellular potassium concentrations. Repeat the test.

Question 32

The specimen was not hemolyzed. What is the first treatment?

Answer 32

Obtain an ECG first to look for cardiotoxicity. In general, the best therapy for hyperkalemia is
decreased potassium intake and administration of oral sodium polystyrene resin (Kayexalate). But if
the potassium level is greater than 6.5 or cardiac toxicity is apparent (more than peaked T waves),
immediate IV therapy is needed. First give calcium gluconate (which is cardioprotective, although
it does not change potassium levels); then give sodium bicarbonate (alkalosis causes potassium to
shift inside cells) and glucose with insulin (insulin also forces potassium inside cells and glucose
prevents hypoglycemia). Beta2 agonists also drive potassium into cells and can be given if the other
choices are not listed on the test. If the patient has renal failure (high creatinine) or initial treatment is
ineffective, prepare to institute emergent dialysis.

Question 33

What are the signs and symptoms of hypocalcemia?

Answer 33

Hypocalcemia produces neurologic findings, the most tested of which is tetany. Tapping on the facial
nerve at the angle of the jaw elicits contraction of the facial muscles (Chvostek sign), and inflation of
a tourniquet or blood pressure cuff elicits hand muscle (carpopedal) spasms (Trousseau sign). Other
signs and symptoms are depression, encephalopathy, dementia, laryngospasm, and convulsions/
seizures. The classic ECG finding is QT-interval prolongation.

Question 34

What should you do if the calcium level is low?

Answer 34

First, remember that hypoproteinemia (i.e., low albumin) of any etiology can cause hypocalcemia
because the protein-bound fraction of calcium is decreased. In this instance, however, the patient is
asymptomatic because the ionized (unbound, physiologically active) fraction of calcium is unchanged.
Thus you should first check the albumin level and/or the ionized or free calcium level to make sure
“true” hypocalcemia is present. For every 1 g/dL decrease in albumin below 4 g/dL, correct the
calcium by adding 0.8 mg/dL to the given calcium value.

Question 35

What causes hypocalcemia?

Answer 35

DiGeorge syndrome (tetany 24–48 hr after birth, absent thymic shadow on x-ray)
n Renal failure (remember the kidney’s role in vitamin D metabolism)
n Hypoparathyroidism (watch for a postthyroidectomy patient; all four parathyroids may have
been accidentally removed)
n Vitamin D deficiency
n Pseudohypoparathyroidism (short fingers, short stature, mental retardation, and normal levels of
parathyroid hormone with end-organ unresponsiveness to parathyroid hormone)
n Acute pancreatitis
n Renal tubular acidosis

Question 36

Describe the relationship between low calcium and low magnesium.

Answer 36

It is difficult to correct hypocalcemia until hypomagnesemia (of any cause) is also corrected.

Question 37

How does pH affect calcium levels?

Answer 37

Alkalosis can cause symptoms similar to hypocalcemia through effects on the ionized fraction of
calcium (alkalosis causes calcium to shift intracellularly). Clinically, this scenario is most common
with hyperventilation/anxiety syndromes, in which the patient eliminates too much CO2, becomes
alkalotic, and develops perioral and extremity tingling. Treat by correcting the pH. Reduce anxiety if
hyperventilation is the cause.

Question 38

Describe the relationship between calcium and phosphorus.

Answer 38

Phosphorus and calcium levels usually go in opposite directions (when one goes up, the other
goes down), and derangements in one can cause problems with the other. This relationship
becomes clinically important in patients with chronic renal failure, in whom you must not only
try to raise calcium levels (with vitamin D and calcium supplements) but also restrict/reduce
phosphorus.
35.

Question 39

What are the signs and symptoms of hypercalcemia?

Answer 39

Hypercalcemia is often asymptomatic and discovered by routine lab tests. When symptoms are
present, recall the following rhyme:
Bones (bone changes such as osteopenia and pathologic fractures).
Stones (kidney stones and polyuria).
Groans (abdominal pain, anorexia, constipation, ileus, nausea, and vomiting).
Psychiatric overtones (depression, psychosis, and delirium/confusion).
Abdominal pain may also be caused by peptic ulcer disease and/or pancreatitis, both of which
have an increased incidence with hypercalcemia. The ECG classically shows QT-interval shortening
when hypercalcemia is present.

Question 40

What causes hypercalcemia?

Answer 40

Hypercalcemia in outpatients is most commonly caused by hyperparathyroidism. In inpatients, the
most common cause is malignancy. Check the parathyroid hormone level to differentiate hyperparathyroidism
from other causes.
Other causes include vitamin A or D intoxication, sarcoidosis, thiazide diuretics, familial hypocalciuric
hypercalcemia (look for low urinary calcium, which is rare with hypercalcemia), and immobilization.
Hyperproteinemia (e.g., high albumin) of any etiology can cause hypercalcemia because of an increase
in the protein-bound fraction of calcium, but the patient is asymptomatic because the ionized (unbound)
fraction is unchanged.

Question 41

Why is asymptomatic hypercalcemia usually treated?

Answer 41

Prolonged hypercalcemia can cause nephrocalcinosis, urolithiasis, and renal failure because of
calcium salt deposits in the kidney and may result in bone disease secondary to loss of calcium

Question 42

How is hypercalcemia treated?

Answer 42

First, give IV fluids. Once the patient is well hydrated, give furosemide (i.e., a loop diuretic) to
cause calcium diuresis. Thiazides are contraindicated because they increase serum calcium
levels. Other treatments include phosphorus administration (use oral phosphorus; IV administration
can be dangerous), calcitonin, bisphosphonates (e.g., etidronate, which is often used in Paget
disease), plicamycin, or prednisone (especially for malignancy-induced hypercalcemia). Correction
of the underlying cause of hypercalcemia is the ultimate goal. The previous measures are all
temporary until definitive treatment can be given. For hyperparathyroidism, surgery is the treatment
of choice.

Question 43

In what clinical scenario is hypomagnesemia usually seen?

Answer 43

Alcoholism. Magnesium is wasted through the kidneys

Question 44

What are the signs and symptoms of hypomagnesemia?

Answer 44

Signs and symptoms are similar to those of hypocalcemia (prolonged QT interval on ECG and possibly
tetany).

Question 45

In what clinical scenario is hypermagnesemia seen?

Answer 45

Hypermagnesemia is classically iatrogenic in patients who are pregnant and are treated for preeclampsia
with magnesium sulfate. It also commonly occurs in patients with renal failure. Patients who receive
magnesium sulfate should be monitored carefully because the physical findings of hypermagnesemia
are progressive. The initial sign is a decrease in deep tendon reflexes, then hypotension and respiratory
failure occur sequentially.

Question 46

How is hypermagnesemia treated?

Answer 46

First, stop any magnesium infusion. Remember the ABCs (airway, breathing, circulation), and
intubate the patient if necessary. If the patient is stable, start IV fluids. Furosemide can be given next,
if needed, to cause a magnesium diuresis. The last resort is dialysis.

Question 47

In what clinical scenarios is hypophosphatemia seen? What are the signs and
symptoms?

Answer 47

Primarily in patients with uncontrolled diabetes (especially diabetic ketoacidosis) and alcoholic
patients. Signs and symptoms of hypophosphatemia include neuromuscular disturbances (encephalopathy,
weakness), rhabdomyolysis (especially in alcoholic patients), anemia, and white blood cell
and platelet dysfunction

Question 48

What is the IV fluid of choice in hypovolemic patients?

Answer 48

Normal saline or lactated Ringer solution (regardless of other electrolyte problems). First fill the tank;
then correct the imbalances that the kidney cannot sort out on its own.

Question 49

What is the maintenance fluid of choice for patients who are not eating?

Answer 49

One half normal saline with 5% dextrose in adults. Typically one fourth normal saline with 5%
dextrose in children weighing less than 10 kg; one third or one half normal saline with 5% dextrose
in children weighing more than 10 kg.

Question 50

Should anything be added to the IV fluid for patients who are not eating?

Answer 50

Usually potassium chloride, 10 or 20 mEq, is added to a liter of IV fluid each day to prevent
hypokalemia (assuming that the baseline potassium level is normal).