01.

Acid Base and

Electrolytes
Secrets

How do you analyze arterial blood gas values?

1. pH- acidosis or alkalosis (primary), then the body

compensates (secondary).
2. High CO2- respiratory acidosis (pH: < 7.4) or
compensating for metabolic alkalosis (pH: > 7.4).
Low CO2- respiratory alkalosis (pH: > 7.4) or
compensating for metabolic acidosis (pH: < 7.4).
3. High bicarbonate- metabolic alkalosis (pH: > 7.4)
or compensating for respiratory acidosis (pH: < 7.4).
Low bicarbonate- metabolic acidosis (pH: < 7.4) or
compensating for respiratory alkalosis (pH: > 7.4).

Does the body compensate beyond a

normal pH?

Overcorrection does not occur. 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), the pH will not
correct to > 7.4.

Common causes of respiratory

acidosis?

 COPD
Asthma
Drugs (opioids, benzodiazepines,
barbiturates, alcohol, other respiratory
depressants)
Chest wall problems (paralysis, pain)
Sleep apnea.

Common causes of metabolic

acidosis?

 Ethanol
Diabetic ketoacidosis
Uremia
Lactic acidosis (e.g., sepsis, shock,
bowel ischemia)
Methanol/ethylene glycol,
aspirin/salicylate overdose
Diarrhea
Carbonic anhydrase inhibitors

Common causes of respiratory

alkalosis?

 Anxiety/hyperventilation
Aspirin/salicylate overdose.

Common causes of metabolic

alkalosis?

 Diuretics (except carbonic anhydrase

inhibitors)
Vomiting
Volume contraction
Antacid abuse/milk-alkali syndrome
Hyperaldosteronism.

What type of acid-base disturbance

does aspirin overdose cause?

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.

What happens to the blood gas of

patients with chronic lung conditions?

In certain people with chronic lung

conditions (especially 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). Remember
sleep apnea, like other chronic lung
diseases, can cause right-sided heart
failure (cor pulmonale).

Should you give bicarbonate to a

patient with acidosis?

For Step 2, almost never. First try

intravenous fluids and correction of
the underlying disorder. If all other
measures fail and the pH remains <
7.0, bicarbonate may be given.

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?

For Step 2 purposes, the patient is probably

crashing. The 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 beta 2
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.

Signs and symptoms of hyponatremia?

Lethargy
Seizures
Mental status changes
Confusion
Cramps
Anorexia
Coma

How do you determine the cause of

hyponatremia?

The first step in determining the

cause is to look at the volume status:
Hypovolemic- Dehydration,
diuretics, diabetes, Addison's disease/
hypoaldosteronism (low potassium)
Euvolemic- SIADH, psychogenic
polydipsia, oxytocin use
Hypervolemic- Heart failure,
nephrotic syndrome, cirrhosis,
toxemia, renal failure

How is hyponatremia treated?

 Hypovolemic hyponatremia- normal

saline.
Euvolemic and hypervolemic
hyponatremia-water/fluid restriction:
diuretics may be needed for
hypervolemic hyponatremia.

What medication is used to treat

SIADH if water restriction fails?

Demeclocycline- induces nephrogenic

diabetes insipidus.

What happens if hyponatremia is

corrected too quickly?

You 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.

What causes spurious (false) hyponatremia?

 Hyperglycemia (once glucose is >

200 mg/dl, sodium decreases by 1.6
mEq/L for each rise
of 100 mg/dl in glucose)
Hyperproteinemia
Hyperlipidemia
In these instances, the lab value is
low, but the total body sodium is
normal. Do not give the patient extra
salt or saline.

What causes hyponatremia in

postoperative patients?

The most common cause is the

combination of pain and narcotics
(causing SIADH) with
overaggressive administration of
intravenous fluids. A rare cause that
you may see is adrenal insufficiency
(potassium is high and the blood
pressure is low).

What is the classic cause of

hyponatremia in pregnant patients
about to deliver?

Oxytocin, which has an antidiuretic

hormone-like effect.

Signs and symptoms of hypernatremia?

Same as the signs and symptoms of

hyponatremia:
Mental status changes/ confusion
Hyperreflexia
Seizures, and/or coma

What causes hypernatremia?

The most common cause is dehydration (free

water loss) due to 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 intravenous 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.

How is hypernatremia treated?

Treatment involves water replacement,

but the patient often is severely
dehydrated; therefore, normal saline is
used most frequently. Once the patient is
hemodynamically stable, he or she often
is switched to 1/2 normal saline. Five
percent dextrose in water (D5W) should
not be used for hypernatremia.

What are the signs and symptoms of

hypokalemia?

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. Best known and best studied,
however, is the effect of hypokalemia on the
heart. EKG findings include loss of T wave or
T-wave flattening, U waves, premature
ventricular and atrial complexes, and
ventricular and atrial tachyarrhythmias.

What is the effect of pH on serum potassium?

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.

Describe the interaction between

digitalis and potassium.

The heart is particularly sensitive to

hypokalemia in patients taking
digitalis. Potassium levels should be
monitored carefully in all patients
taking digitalis, especially if they are
also taking diuretics (a common
occurrence).

How should potassium be replaced?

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 EKG
monitor when giving IV potassium
because
potentially fatal arrhythmias may
develop.

When hypokalemia persists even

after administration of significant
amounts of potassium, what should
you do?

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.

What are the signs and symptoms of

hyperkalemia?

Weakness and paralysis may occur, but the

cardiac effects are the best studied. EKG
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 EKG.
Arrhythmias include asystole and ventricular
fibrillation. Tall, peaked T waves are
commonly prominent in V2-V5.

What causes hyperkalemia?

 Renal failure (acute or chronic)

Severe tissue destruction (because
potassium has a high intracellular
concentration)
Hypoaldosteronism (watch for hyporeninemic
hypoaldosteronism in diabetes)
Medications (stop potassium-sparing
diuretics, beta blockers, nonsteroidal
antiinflammatory drugs, and angiotensinconverting enzyme inhibitors)
Adrenal insufficiency (also associated with
low sodium and low blood pressure)

What should you suspect if an

asymptomatic patient has
hyperkalemia?

With hyperkalemia, the first

consideration (especially if the
patient is asymptomatic and the EKG
is normal) is whether the lab
specimen is hemolyzed. Hemolysis
causes a false hyperkalemia due to
high intracellular potassium
concentrations. Repeat the test.

The specimen was not hemolyzed.

What is the first treatment?

Get an EKG first to look for cardiotoxicity. In general,

the best therapy for hyperkalemia is decreased
potassium intake and administration of oral sodium
polystyrene resin. But if the potassium level is > 6.5
and/or cardiac toxicity is apparent (more than peaked T
waves), immediate intravenous 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). Beta 2 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 dialysis emergently.

What are the signs and symptoms of

hypocalcemia?

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 EKG finding is QT-interval prolongation.

What should you do if the calcium level is low?

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.
Those of you who are mathematically inclined may
want to know that for every 1 -gm/dl decrease in
albumin below 4 gm/dl, you should correct the
calcium by adding 0.8 mg/dl to the given calcium
value.

What causes hypocalcemia?

 DiGeorge's syndrome (tetany 24-48 hours after birth,

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

Describe the relationship between

low calcium and low magnesium.

It is difficult to correct hypocalcemia

until hypomagnesemia (of any cause)
also is corrected.

How does pH affect calcium levels?

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.

Describe the relationship between

calcium and phosphorus.

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 phosphorus.

What are the signs and symptoms of

hypercalcemia?

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 (may be due to peptic ulcer
disease and/or pancreatitis, both of which have an
increased incidence with hypercalcemia), anorexia,
constipation, ileus, nausea, vomiting)
Psychiatric overtones (depression, psychosis,
delirium/confusion)
The EKG classically shows QT-interval shortening.

What causes hypercalcemia?

Hypercalcemia in outpatients most commonly is due

to hyperparathyroidism. In inpatients, the most
common cause is malignancy. 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 ionized (unbound) fraction is
unchanged.

Why is asymptomatic hypercalcemia

usually treated?

Prolonged hypercalcemia can cause

nephrocalcinosis and renal failure due
to calcium salt deposits in the kidney
and may result in bone disease
secondary to loss of calcium.

How is hypercalcemia treated?

First, give intravenous fluids. Then, 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; intravenous
administration can be dangerous), calcitonin,
diphosphonates (e.g., etidronate, which often
is used in Paget's disease), plicamycin, or
prednisone (especially for malignancy-induced
hypercalcemia). Correction of the underlying
cause of hypercalcemia is the ultimate goal.
The above measures are all temporary until
definitive treatment can be given. For
hyperparathyroidism, surgery is the treatment
of choice.

In what clinical scenario is

hypomagnesemia usually seen?

Alcoholism. Magnesium is wasted

through the kidneys.

What are the signs and symptoms of

hypomagnesemia?

Signs and symptoms are similar to

those of hypocalcemia (prolonged QT
interval on EKG
and possibly tetany).

In what clinical scenario is

hypermagnesemia seen?

Hypermagnesemla is classically iatrogenic in

pregnant patients who 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.

How is hypermagnesemia treated?

First, stop any magnesium infusion!

Remember the ABCs, and intubate the
patient if necessary. If the patient is
stable, start intravenous fluids.
Furosemide can be given next, if
needed to cause a magnesium
diuresis. The last resort is dialysis.

In what clinical scenarios is

hypophosphatemia seen? What are
the signs and symptoms?

Primarily in patients with uncontrolled

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

What is the intravenous fluid of

choice in trauma patients?

Ringer's lactate. The second choice is

normal saline.

What is the intravenous fluid of

choice in nontrauma, hypovolemic
patients?

Normal saline or Ringer's lactate

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

What is the maintenance fluid of

choice for patients who are not
eating?

One-half normal saline with 5%

dextrose in adults and one-fourth or
one-third normal saline with 5%
dextrose in children (because of renal
differences).

Should anything be added to the

intravenous fluid for patients who are
not eating?

Usually potassium chloride, 10 or 20

mEq, is added to a liter of
intravenous fluid each day
to prevent hypokalemia (assuming
that the baseline potassium level is
normal).