Critical Thinking Case- ADULT RESPIRATORY DISTRESS SYNDROME
John Smith , a 30-year-old male, was brought into the Emergency Department following a near drowning. He was diving with friends when the found him floating face down in the river. He was not breathing when he was pulled from the river and his friends administered CPR. John was awake when the EMS unit arrived.
Upon arrival to the Emergency Department, John was extremely fatigued but was oriented X3. His blood pressure was 122/80, heart rate 120/minute, and respiration 28/minutes. His breath sounds were diminished bilaterally with crackles and expiratory wheeze audible throughout all lung fields. He was receiving 50% 02 via venturi mask and his ABGs were as follows:
pH 7.48
PaCO2 30
PaO2 60
SaO2 91%
HCO3 24
All other laboratory data were normal. John was admitted to the ICU with a diagnosis of near drowning. He was stable for 24 hours, at which time he manifested dyspnea, tachypnea, tachycardia, and progressive hypoxemia. Despite increasing the FIO2 via venturi mask, Brian’s ABGs continued to deteriorate. Twenty- six hours after admission, his ABGs on a nonrebreathing mask were:
pH 7.50
PaCO2 26
PaO2 48
SaO2 76%
HCO3 23
He was intubated and placed on a volume-controlled ventilator at the following settings:
Mode Assist Control
Rate 12
FIO2 0.60
Tidal Volume 800
PEEP +5
His initial static compliance was 30ml/cm H2O, and his post-intubation chest x-ray revealed appropriate endotracheal tube placement and bilateral, diffuse, patchy infiltrates. A pulmonary artery catheter was placed with the following data obtained:
PAP 24/10
PCWP 9
CVP 6
CO 7.5
1. What is the definition of ARDS? What are the associated clinical indicators?
2. What conditions did this patient experience that are common risk factors
associated with ARDS?
3. Describe the major pathophysiological alterations in ARDS. What is the common
V:Q mismatch associated with ARDS? What is the cause of hypoxemia in ARDS
and how is it treated? What is the clinical significance of static compliance? How is
decreased static compliance demonstrated in the patient’s case?
4. Early indications of ARDS include hyperventilation and respiratory alkalosis. What is the interpretation of this patient’s acid-base balance? What is the cause of this imbalance?
5. What effects could PEEP have on the patient’s pulmonary and cardiovascular status?
6. What is the primary nursing diagnosis for this patient upon admission to ICU? (Diagnosis must include the “related to” and “as evidenced by”).
7. Identify the top three nursing interventions for this patient. How do these interventions improve pulmonary status?
8. What is the prognosis in patients with ARDS? What increases morbidity?
Critical Thinking Case : part 2 DM
Mrs. S is a 28-year-old patient, with a 12-year history of type I diabetes mellitus. Her husband states that she has had a “bad cold” for several days. Yesterday she stayed in bed and slept all day. She was “too ill” to check her blood sugar, and since she was not really eating, she did not take her insulin. This morning, she was not able to stand up and vomited twice. A Gram stain of Mrs. S’s blood contains gram-positive cocci in clusters. Her admission vital signs are: BP = 90/60; HR = 118 bpm (sinus tachycardia); RR = 32/min; T = 102.3° F; O2 sat via pulse oximetry = 96%. Her serum glucose is 398 mg/dl, and she is positive for serum ketones. She is admitted with a diagnosis of DKA.
Her baseline ABGs on 2 L of oxygen are: pH = 7.25; PCO2 = 28; HCO3 = 14; PaO2 = 92; O2 sat = 96%. Her respirations are deep, rapid, and labored. She has bronchial breath sounds in the right axillary area. There is bilateral chest expansion and no evidence of cyanosis.
A regular insulin bolus is given and a regular insulin drip is initiated. Mrs. S’s IV fluids are infusing at 800 ml/hr. Her vital signs after 2 hours in the unit are: BP = 120/70; HR = 78 bpm (normal sinus rhythm); RR = 22/min; O2 sat = 100%. Her serum glucose is 250 mg/dl and serum potassium is 4.0 mEq/L. She is more alert and is feeling hungry.
1. What is insulin’s function in the body? What is the most significant basic defect in the development of DKA?
2. What is the cause of Ms. S experiencing DKA? Describe the pathophysiologic rationale for your answer.
3. List the classic signs and symptoms of DKA. Which signs and symptoms did Ms. S experience? What are the pathophysiologic causes of these signs and symptoms?
4. What is an anion gap? Why is the anion gap important to follow in the treatment of DKA?
5. What acid base disturbance is Ms. S experiencing? What compensatory mechanisms are in effect at this time?
6. What is the primary nursing diagnosis for Ms. S.? What are the goals for treatment (both independent and collaborative)? What interventions are imperative to initiate immediately? What interventions are important within the next 12-24 hours?
7. What are potential lab abnormalities for a patient in DKA?
8. What nursing considerations are important in planning Ms. S’s discharge?
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