Case Scenario Answer key

ABG case scenario 1

1.
Oxygenation (PaO2)
The PaO2 is low, so we know the patient is in respiratory failure, however, we don’t yet know what type.
pH
You should then note that the pH reveals an acidosis and assess the CO2 to see if it is contributing to the acidosis (↑CO2).
PaCO2
In this case, the PaCO2 is raised significantly and this is likely to be the cause of the acidosis.
In the context of low PaO2, a raised PaCO2 suggests the patient has type 2 respiratory failure.
HCO3–
The HCO3– is normal, so the metabolic system is not contributing to the acidosis and also isn’t compensating for the respiratory
acidosis, suggesting that this is an acute derangement.
Base excess (BE)
The base excess is within normal limits as there has been no significant change in the amount of HCO3–.
If this respiratory acidosis was chronic we would expect that the kidneys would have generated more HCO3– to compensate,
which would have resulted in an increased BE.
Interpretation
Respiratory acidosis

2. The respiratory acidosis has been caused by type 2 respiratory failure (a failure of ventilation) leading to increased levels of
CO2 (hypercapnia).

3.
Confusion
Reduced consciousness level
Asterixis
Bounding pulse

4.
Type 2 respiratory failure occurs as a result of ventilatory failure. The potential causes of this include those listed below.

Potential causes of type 2 respiratory failure

Increased airways resistance – COPD/asthma
Reduced breathing effort – drug effects (e.g. opiates)/brain stem lesion/extreme obesity
A decrease in the area of the lung available for gas exchange – chronic bronchitis
Neuromuscular problems – Guillain-Barré syndrome/motor neuron disease
Deformity – ankylosing spondylitis/flail chest

5. Impaired Gas Exchange

ABG case scenario 2

1.
Oxygenation (PaO2)
A PaO2 of 13 kPa is normal, ruling out hypoxia as a cause for the patient’s confusion.
pH
A pH of 7.3 is abnormally low and therefore the patient is acidotic.
The next step is to figure out whether the respiratory system is contributing to the acidosis (e.g. ↑ CO2).
PaCO2
The CO2 is actually low and therefore the respiratory system doesn’t appear to be contributing to the acidosis.
The next step is to look at the HCO3– and see if it is contributing to the acidosis.
HCO3-
HCO3– is low, which is in keeping with an acidosis, so the metabolic system is the cause of this patient’s acidosis.
Base Excess
Base excess is low, in keeping with a metabolic acidosis.
Compensation
There is evidence of respiratory compensation for this metabolic acidosis (e.g. ↓CO2).
Interpretation
Metabolic acidosis with respiratory compensation

2.
Capillary blood glucose:
32 mmol/L
Urinalysis:
Glucose +++
Ketones +++

3.
Diabetic ketoacidosis (DKA)

4.
Diabetic ketoacidosis arises because of a lack of insulin in the body.
The lack of insulin and a corresponding elevation of glucagon leads to increased release of glucose by the liver, but an inability
for cells to utilise the glucose.
High serum glucose levels result in increased urinary excretion of glucose, taking water and solutes along with it in a process
known as osmotic diuresis (this leads to polyuria, dehydration and polydipsia).
The absence of insulin also leads to the release of free fatty acids from adipose tissue (lipolysis) as the body needs to generate
energy from a source other than glucose.
These fatty acids are converted into ketone bodies to be used as an energy source.
The ketone bodies cause the blood to become more acidic (metabolic acidosis).
The body attempts to compensate for the metabolic acidosis by hyperventilating to blow off CO2 and thereby increase pH.
This hyperventilation, in its extreme form, may be observed as Kussmaul respiration.

5.
The only definitive way to diagnose metabolic acidosis is by simultaneous measurement of serum electrolytes and arterial blood
gases (ABGs), which shows pH and PaCO2 to be low; calculated HCO3- also is low.

Hypovolemic Shock Case scenario 1

A 72 year old woman arrives to the ED after a motor vehicle accident. She is alert, but exhibits some confusion as she frequently
asks for her daughter (who is not present). The patient does repeatedly state she is a Jehovah’s Witness. Patient reports feeling
nauseous and has 5 out of 10 abdominal pain. Grimacing is noted upon palpitation of upper abdominal quadrants. Bowel
sounds present x4. BP 76/44, HR 127 with a rhythm of sinus tachycardia, body temperature 36.0 C, RR 25, SpO2 89% on room
air.
1.What type of shock is this patient experiencing? Support your answer by discussing the signs and symptoms this patient is
exhibiting.
2.Explain the pathophysiology of this type of shock. Make sure it relates to this patient and include the stage(s) of shock this
patient is experiencing.
3.Choose three appropriate nursing interventions for this patient. Why did you choose these interventions?
4.Choose one appropriate pharmacological intervention? Explain how this medication works to help the patient.
5.Describe what physiological changes have to happen for this patient to become stable.

Septic Shock Case scenario 2

1. The combination of fever, tachypnea, and tachycardia suggests systemic inflammatory response syndrome (SIRS), which is
usually defined as the presence of two or more of the following: (1) fever (> 38ºC) or hypothermia (< 36ºC); (2) tachypnea (R >
24/min); tachycardia (P > 90/min); and (4) leukocytosis (> 12,000/(l), leukopenia (< 4,000/(l), or >10% bands. SIRS can have an
infectious or noninfectious etiology. In this case, there are obvious signs of microbial infection (pus oozing from a recent skin
wound, fever), so a diagnosis of sepsis (i.e., SIRS with a proven or suspected microbial etiology) is justified. The patient has
obvious hypotension in addition to the standard SIRS/sepsis symptoms, so he appears to have progressed to severe sepsis
(defined as sepsis plus hypotension or one or more signs of organ dysfunction (metabolic acidosis, acute encephalopathy,
oliguria, hypoxemia, or disseminated intravascular coagulation).
2. This is a dangerous situation because the man could rapidly progress to septic shock (defined as sepsis with hypotension and
organ dysfunction), which is often fatal. This patient's history and symptoms (e.g., pus formation) indicate that he almost
certainly has a bacterial infection that is community acquired (i.e., not nosocomial in origin), so antibiotic therapy should be
initiated as soon as possible. You do not know the identity of the causative agent at this time, so the safest course of action is to
order an antibiotic regimen that can provide broad coverage of both Gram-positive and Gram-negative bacteria. (Because this is
not a nosocomial infection, the causative agent is not overly likely to be highly resistant to antibiotics, but you can't be certain of
this unless you run sensitivity tests.)
3. Much of the differential can be eliminated based on the patient's recent history and obvious evidence of microbial infection.
If fever, tachypnea, tachycardia, and (possibly) hypertension were the only symptoms (as might occur if the patient had an
internal infection that they were not yet aware of), the differential could include: cardiogenic shock, acute pancreatitis, systemic
vasculitis, pulmonary embolism, toxic ingestion, exposure-induced hypothermia, fulminant liver failure, and collagen-vascular
diseases.
4. Blood cultures should be ordered in hopes of identifying the causative agent. However, microbial invasion of the
bloodstream (bacteremia) is not required for development of sepsis because local or systemic spread of microbial signal
molecules or toxins can also provoke this response. Blood cultures yield bacteria or fungi in 20-40% of cases of severe sepsis
(i.e., this case) and in 40-70% of cases of septic shock. If the lab manages to isolate and identify the causative agent, you will also
want its sensitivity pattern. (It might be necessary or advisable to change the antibiotic treatment based on these lab findings.)
You could also order a CBC with differential, to look for a left shift.
5. Staphylococcus aureus is the most likely causative agent. The positive catalase test eliminates Streptococcus and
Enterococcus species, and the positive coagulase test essentially eliminates other Staphylococcus species. The production
of yellowish-white pus also points to S. aureus.