NSG 533W--Advanced Pathophysiology

Module 2: Fluid, Electrolyte, and Acid-Base: Cases and Answers

RUSH UNIVERSITY COLLEGE OF NURSING

NSG 533W--ADVANCED PATHOPHYSIOLOGY

MODULE 2: CASES AND ANSWERS

1. Estimate the total body water in a: a) 50 kg woman, b) 100 kg man, and c) 6 kg. infant.

a) 25 liters
b) 60 liters
c) 4.2 liters

2. A patient has the following chemistries: sodium 140 mEq/L, glucose 180 mg/dl, and BUN
28 mg/dl. What is the calculated serum osmolality? Is this normal, hypo-osmolar, or
hyperosmolar?

300 mOsm/L; Slightly hyperosmolar (280 – 294 mOsm/L is the normal range)

3. A patient with renal failure has the following chemistries: sodium 130 mEq/L, glucose 100
mg/dl, and BUN 120 mg/dl. What is the calculated serum osmolality? Is this patient
hyperosmolar? Hypertonic? Would you expect this osmolality to be associated with
increased thirst?

308 mOsm/L

Hyperosmolar, but not hypertonic as the increase in osmolarity is due to urea,

which is not an effective osmole.

No

5. A 42-year-old patient presents with a serum sodium of 120 mEq/L. What can you say
about the mechanisms of water regulation in this patient? What is the status of the total
body sodium?

The low serum sodium concentration tells us that water regulation is abnormal.
For clinical purposes, disorders of sodium concentration, both hyponatremia and
hypernatremia, can be viewed as originating from abnormalities in the regulation
of water.

6. A 23-year-old man presents with pedal edema, rales, and a third heart sound (S3). His
sodium concentration is 120 mEq/L. Does he have a problem with sodium regulation,
water regulation, or both? Explain.

Both. The extracellular fluid volume (ECFV) is increased (disorder of total body
sodium regulation) and the serum sodium is abnormal (disorder of water
regulation). He has an expanded ECFV (edema, rales, S3) caused by congestive
heart failure and therefore has an excess of total body sodium. The hyponatremia
tells us that there is an excess of water relative to sodium.

7. Which of the following will increase the calculated serum osmolality when added to the
extracellular fluid?

urea
glucose
sodium
ethanol

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 NSG 533W--Advanced Pathophysiology
Module 2: Fluid, Electrolyte, and Acid-Base: Cases and Answers

methanol
isopropanol
ethylene glycol
mannitol
sorbitol

Urea, glucose, and sodium are included in the formula for calculated osmolality. If
the question were regarding measured osmolality, all of the above would
contribute.

8. A patient presents with polyuria and polydipsia and altered mental status. On physical
exam, the patient is poorly responsive. There is poor skin turgor and a blood pressure
drop from 100/84 to 88/62 on sitting, with a pulse increase from 92 to 128. Laboratory
studies show: glucose 2100 mg/dl, sodium 130 mEq/L, BUN 40 mg/dl. The measured
osmolality is 395 mOsm/L. What is the cause of the hyponatremia in this patient? What is
the corrected serum sodium?

This is again a pseudohyponatremia or dilutional hyponatremia caused by massive

elevation of glucose concentration: hyponatremia with severe hypertonicity.

The corrected serum sodium is 162 mEq/L

Case Study #1

A 35-year-old man presented with progressively severe weakness and easy fatigability of several
months' duration. His blood pressure was 105/55 and his heart rate increased from 90 to 115 on
standing. The laboratory evaluation revealed that he had a mild lymphocytosis and 10%
eosinophilia. His serum sodium level was 125mEq/L, potassium was 5.6 mEq/L, bicarbonate was
14 mEq/L, glucose was 55 mg/dl, and BUN 12.

Discussion Questions:

1. By definition, this patient has hyponatremia. What is the normal serum sodium level?

135-145 mEq/L

2. What is the patients serum osmolarity?

257 mOsm/L.

3. What would be your best guess as to his volume status--hypovolemic, euvolemic, or

hypervolemic? Explain.

Orthostatic changes in pulse, fatigue and muscle weakness could point to

hypotonic hypovolemia

4. What signs, symptoms, or diagnostic findings would you expect if this case represents
true hyponatremia? Explain.

Central nervous system manifestations would be

primary--confusion/disorientation, irritability, decreased level of consciousness,
seizures, signs of increased intracranial pressure

5. If the serum osmolarity were found to be 291 mOsm/L what other tests would be relevant
in assessing the hyponatremia?

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 NSG 533W--Advanced Pathophysiology
Module 2: Fluid, Electrolyte, and Acid-Base: Cases and Answers

Serum lipid levels and serum protein levels would need to be assessed--both can
lead to pseudohyponatremia

6. If this patient's serum glucose was 550 mg/dl instead of 55 mg/dl, what would his actual
serum sodium level be (use 100 mgs/dl as normal glucose level)?

132 mEq/L

Case Study #2

A hysterical young woman was admitted to the Emergency Department after an automobile
accident in which she fractured her arm. She complained of circumoral paresthesia and then
fainted. Arterial blood gas findings included a pH of 7.53, PCO2 of 20 mmHg and HCO3 of 22.

Discussion Questions:

1. The patient is demonstrating signs and symptoms of tetany. What is the probable cause?
What is the normal serum calcium level? Which is most affected--the ionized calcium or
the protein-bound calcium?

Hyperventilation due to the anxiety of the accident results in respiratory alkalosis.

The associated increase in pH leads to decreased ionization of calcium (more
ionized calcium binds to proteins) and hypocalcemia.

8.5-10.5 mg/dL

Ionized calcium

2. Explain the pathophysiologic basis for her fainting episode.

Respiratory alkalosis results in intense cerebrovascular vasoconstriction and

brain hypoxia that can result in unconsciousness.

3. What additional clinical manifestations might you expect in this patient while still
untreated?

a. prolonged QT interval on EKG

b. depressed ST segment on EKG
c. elevated ST segment on EKG
d. shortened QT interval on EKG

a. Indicating prolonged ventricular depolarization and decreased cardiac

contractility.

Case Study #3

A 46-year-old woman with end-stage renal disease (ESRD) was admitted with a secondary
diagnosis of seizure activity and multi-infarct dementia. She required dialysis twice a week. On
admission, laboratory data from a previous venous sample showed:

Na 138 mEq/L
BUN 41 mg/dl
K 5.8 mEq/L
creatinine 8.2 mg/dl
total calcium 7.0 mg/dl
albumin 3.0 g

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 NSG 533W--Advanced Pathophysiology
Module 2: Fluid, Electrolyte, and Acid-Base: Cases and Answers

PO4 7.1 mEq/L

HCO3 13.5 mEq/L

Discussion Questions:

1. Though the patient's total calcium was below normal, she showed no signs of
hypocalcemia. Why?

Bicarbonate level probably reflects metabolic acidosis. In acidosis, more calcium

becomes ionized and it is the ionized fraction that is the active fraction.

2. What is the normal relationship between serum calcium and serum phosphorus?

They have an inverse relationship

3. What is the relationship between alkalosis and hypocalcemia?

Alkalosis results in decreased ionization of calcium and may lead to hypocalcemic

effects

Case Study #4

A 40-year-old woman was admitted to the hospital with complaints of progressive muscle
weakness. She had been taking a thiazide diuretic for several weeks and had recently developed
vomiting and diarrhea. Postural hypotension was noted--110/70 when supine and 90/60 when
standing. Skin turgor was reduced.

Na 147 mEq/L
K 2 mEq/L
HCO3 40 mEq/L
Cl 70 mEq/L

Discussion Questions:

1. What would be your best guess as to her volume status--hypovolemic, euvolemic, or

hypervolemic? Explain.

Hypovolemic--orthostatic changes, hx vomiting and diarrhea, reduced skin turgor,

taking a thiazide diuretic

2. What is the probable basis for the progressive muscle weakness? Explain. What other
signs, symptoms, or diagnostic findings would you expect?

Hypokalemia. Thiazide diuretics are potassium-wasting. In addition, loss of GI

fluids (vomiting) increase potassium loss.

Skeletal muscle weakness leading to respiratory failure; arrhythmias; postural

hypotension

3. What changes would you expect to see on this patient's EKG?

a. widened QRS
b. sine wave
c. flattened T wave
d. absent P wave

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 NSG 533W--Advanced Pathophysiology
Module 2: Fluid, Electrolyte, and Acid-Base: Cases and Answers

Answer: C

A flattened T wave is a sign of hypokalemia. A widened QRS, sine wave (very wide
QRS that looks like a pulse wave form), tall peaked T waves, and wide flat p wave
are indicative of Hyperkalemia

Case Study #5

Your patient, who was diagnosed with type 1 diabetes mellitus when he was 12 years old, is now
a third-year medical student. His diabetes remained in control throughout middle school and high
school, college and first 2 years of medical school. When the patient started his surgery clerkship,
his regular schedule of meals and insulin injections was completely disrupted. One morning, after
a very late night in trauma surgery, he completely forgot to take his insulin. Before rounds at 5
AM, he drank orange juice and ate 2 doughnuts. At 7 AM he drank more orange juice because he
was very thirsty. He mentioned to the student next to him that he felt "strange" and that his heart
was racing. At 9 AM he excused himself from surgery because he thought he was going to faint.
That morning, he was found unconscious in the on-call room. He was transferred immediately to
the Emergency Department.

Height 5 feet, 3 inches

Weight 100 lb. (115 lb. at checkup 2 months earlier)
Blood pressure 90/55 lying; 75/45 standing
HR 130, regular
RR 32, deep and rapid

Glucose 560
BUN 22
Na 132
K 5.8
Cl 96
HCO3 8
Ketones 2+
PO2 112
PCO2 20
pH 7.22

Discussion Questions:

1. What is the acid-base disorder present? What was its etiology?

Primary (simple) elevated anion gap metabolic acidosis

Diabetic ketoacidosis

2. Why was his breathing so rapid and deep? What is this type of breathing called?

Physiological response to decreasing increasing metabolic acid load and

bicarbonate is hyperventilation (reduces carbonic acid load and increases pH)

Kussmaul Respirations

3. What was the anion gap? What is its significance?

28 --indicates accumulation of unmeasured anions (ketoacids)

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 NSG 533W--Advanced Pathophysiology
Module 2: Fluid, Electrolyte, and Acid-Base: Cases and Answers

4. What factors contributed to the high potassium level?

Decreased renal excretion related to poor renal perfusion

Muscle protein breakdown related to lack of insulin with release of potassium
Redistribution of potassium to extracellular space in exchange for hydrogen ions

5. Is the serum sodium associated with low, normal, or high osmolarity? What is the
corrected serum sodium?

Osmolality is 303--slightly hyperosmolar

Na = 139

6. Given his Osmolality is 302, how would you describe his fluid status?

Hypertonic, Hypovolemic

Case Study #6

Your patient's wedding to the man of her dreams was perfect in every respect. However, while on
their honeymoon to Mexico, she developed severe traveler's diarrhea. Despite attempts to control
the diarrhea with OTC medications, she continued to have 8-10 watery stools daily. She became
progressively weaker and on the third day, she was taken to the local Emergency Department.
On physical exam, her eyes were sunken, her mucous membranes were dry, and her jugular
veins were flat when lying supine. She was pale and her skin was cool and clammy. Her BP was
90/60 lying and 60/40 upright. HR was 120 supine. RR were deep and rapid at 24.

pH 7.25
PCO2 32
HCO3 16
Na 148
K 2.3
Cl 112
Glucose 98
BUN 24

Discussion Questions:

1. What is the acid-base disorder present? What is its etiology?

Primary (simple) elevated anion gap metabolic acidosis

Hypovolemiaischemialactic acidosis

2. Why was her breathing so rapid and deep?

Physiological response to increasing metabolic acid load and decreasing

bicarbonate is hyperventilation (reduces carbonic acid load and increases pH)

Kussmaul respirations

3. What was the anion gap? What is its significance?

20 --elevated. Lactic acidosis is associated with an elevated anion gap

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 NSG 533W--Advanced Pathophysiology
Module 2: Fluid, Electrolyte, and Acid-Base: Cases and Answers

4. What factors contributed to the low potassium level?

Severe diarrhea (and this level will drop even more with treatment as she has the
same factors present as in case #1 that would tend to increase her potassium)

Case Study #7

Your patient is a 20-year-old philosophy major at a state university. When the "24-hour" stomach
flu went around campus during final exams, she vomited for 3 days. During that time, she was
unable to keep anything down, and she sucked on ice chips to relieve her thirst. By the time she
was seen in the student health center, the vomiting had stopped, but she could barely hold her
head up. BP 100/60, decreased skin turgor, and dry mucous membranes.

pH 7.53
HCO3 37
PCO2 45
Na 137
K 2.8
Cl 82

Discussion Questions:

1. What is the acid-base disorder present? What was its etiology?

Metabolic alkalosis (contraction alkalosis)

Vomiting with continued water (ice) intake. HCl loss from vomiting results in
bicarbonate retention. This problem is maintained by the hypovolemia.

2. Why was her serum Cl so low?

Loss of HCl via vomiting

3. What factors contributed to the low potassium level?

Vomiting is associated with loss of potassium ions. In addition, because of

metabolic alkalosis, kidney begins retaining hydrogen ions in exchange for
excreting potassium ions and cells give up hydrogen ions and take in potassium
ions.

4. Which of the following best describes the patient's current situation?

a. The disorder is saline-sensitive and can be corrected with 0.9% NSS.

b. The disorder is saline-resistant and cannot be corrected with 0.9% NSS.
c. The disorder is saline-sensitive and can be corrected with 0.9% NSS after
potassium and chloride are normalized.
d. The disorder is saline-resistant and can be corrected with 0.9% NSS after
potassium and chloride are normalized.

c. Think about what would happen to the K if you only gave this patient 0.9%
NSS? You would dilute (decrease) the K even more. Remember you must also
correct the Cl and K levels with the fluid replacement.

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 NSG 533W--Advanced Pathophysiology
Module 2: Fluid, Electrolyte, and Acid-Base: Cases and Answers

Case Study #8

Your patient is a 73-year-old seamstress who had COPD secondary to a long history of cigarette
smoking. Six months before her death, she had a routine office visit.

PO2 48
PCO2 69
HCO3 34
pH 7.32

Against her physician's warnings, she refused to stop smoking. Six months later, she was taken
to the Emergency Department by her sister.

PO2 35
PCO2 69
HCO3 20
pH 7.09

Discussion Questions:

1. What is the acid-base disorder present 6 months ago? What was its etiology?

Chronic primary (simple) respiratory acidosis due to COPD

2. Why was her HCO3 level increased?

Physiological response to increased carbonic acid load--kidney begins to generate

and retain more bicarbonate to increase pH

3. At the terminal admission, why has the pH gotten lower? What mechanism could explain
a lower than normal HCO3 at the second admission when it was above normal on the first
visit?

First visit reflects chronic stable acid-base picture associated with COPD. Kidneys
were able to retain enough bicarbonate to return pH almost to normal. On second
admission, she had had an acute episode probably associated with renal failure
and inability of kidneys to "compensate." Bicarbonate level dropped and pH
dropped.

Case Study #9

Your patient is a 55-year-old interior designer who is terrified of flying ever since she had a "bad"
experience on a commuter flight. Nevertheless, she and her husband planned a trip to Paris to
celebrate their 30th wedding anniversary. As the time for the trip approached, the patient had what
she called recurrent "anxiety attacks." One evening, a few days before the scheduled flight, she
started hyperventilating uncontrollably. She became lightheaded and her hands and feet were
numb and tingling. She thought she was having a stroke. Her husband rushed her to the
Emergency Department.

pH 7.56
PCO2 23
HCO3 20

The ED staff had her breath into and out of a paper bag.

pH 7.41

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 NSG 533W--Advanced Pathophysiology
Module 2: Fluid, Electrolyte, and Acid-Base: Cases and Answers

PCO2 41
HCO3 25

Discussion Questions:

1. What is the acid-base present in the original data? What was its etiology?

Primary (simple) respiratory alkalosis c/o hyperventilation

2. Why was her HCO3 level decreased?

Physiological response to decreased carbonic acid load – the kidney excretes

bicarb in the urine to lower the pH

3. What was she light-headed?

Alkalosis causes cerebral vasoconstriction and cerebral hypoxia

4. Why did she experience numbness and tingling?

Alkalosis is associated with decreased ionization of calcium, resulting in

manifestations of hypocalcemia.

5. How did breathing in and out of a paper bag correct the acid-base imbalance?

Forced her to rebreath air with increased CO2 content to elevate PCO2 and
decrease pH.