PROPHECY General ICU (Adult) V3:
DISTINCTION-LEVEL Simulation Exam -
Progressive Care RN Competency
Assessment
SECTION 1: MULTI-SYSTEM FAILURE & SEPTIC SHOCK (Questions 1-20)
Scenario 1:
A 68-year-old male is 36 hours post-emergent exploratory laparotomy for perforated
diverticulitis with fecal peritonitis. He is intubated on AC/VC, Vt 450, PEEP 10, FiO2 70%,
RR 28. Sedated on propofol 50 mcg/kg/min, fentanyl 100 mcg/hr. Vasopressors:
norepinephrine 0.25 mcg/kg/min, vasopressin 0.03 units/min. Current data: T 38.9°C,
HR 142 (sinus), BP 74/48 (MAP 57), SpO2 89%. A-line waveform shows respiratory
variation >15%. CVP 6 mm Hg. ScvO2 58%. Lactate 6.8 mmol/L (trending up from 4.2).
Urine output 8 mL/hr last 4 hours. The ventilator high-pressure alarm is sounding with
peak pressures 48 cm H2O (was 32). Breath sounds are diminished bilaterally,
especially on the right. The most appropriate FIRST action is:
A) Increase norepinephrine to achieve MAP >65 mm Hg per Surviving Sepsis guidelines
B) Administer a 30 mL/kg crystalloid bolus for fluid responsiveness
C) Obtain an immediate portable chest X-ray and prepare for needle decompression
D) Increase sedation to achieve ventilator synchrony and reduce peak pressures
Correct Answer: C
,Distinction-Level Solution:
Critical Problem: Tension pneumothorax (likely right-sided) complicating septic
shock—true immediate life threat.
Data Synthesis: While this patient has severe septic shock (high lactate, low ScvO2,
oliguria), the acute change is the ventilator alarm with rising peak pressures (48 cm
H2O), diminished breath sounds, and hypoxemia refractory to high FiO2. The respiratory
variation on A-line suggests intrathoracic pressure changes. In a ventilated patient with
septic shock and abdominal surgery, barotrauma causing tension pneumothorax is a
recognized complication. The hemodynamic collapse (BP 74/48 despite high-dose
pressors) may be partially due to tension physiology impairing venous return.
Intervention Justification: Tension pneumothorax is an immediate cause of
cardiovascular collapse and death. The classic triad is absent in ventilated
patients—hypotension and elevated peak pressures are often the first signs. Needle
decompression must precede imaging if clinical suspicion is high, but given the
complexity, immediate CXR to confirm while preparing for decompression is the most
prudent first step. Fluid and pressor escalation (Choices A/B) will fail if venous return is
obstructed by tension physiology.
Distractor Pitfalls:
● A: Pressor escalation addresses the symptom (hypotension) but not the cause.
In tension pneumothorax, venous return is mechanically obstructed;
norepinephrine cannot overcome this.
● B: Fluid bolus is appropriate for sepsis but potentially harmful if tension
pneumothorax is present (further impaired venous return, right heart strain). The
respiratory variation suggests fluid responsiveness, but the primary problem is
mechanical.
● D: Sedation increase is dangerous—this patient is already deeply sedated, and
the problem is mechanical, not patient-ventilator asynchrony.
,Scenario 2 (SATA):
A 72-year-old female with severe ARDS (P/F ratio 98) is on ARDSnet protocol: AC/VC, Vt
320 (6 mL/kg IBW), PEEP 14, FiO2 90%, RR 32, I:E 1:1. She is proned. Current ABG: pH
7.18, PaCO2 68, PaO2 58, HCO3 24, lactate 3.2. Hemodynamics: HR 118, BP 92/60
(MAP 71) on norepinephrine 0.15 mcg/kg/min, CVP 14 mm Hg. The patient develops
sudden tachycardia to 156, BP drops to 68/42, and the EtCO2 waveform changes from a
normal rectangular shape to a gradual upslope with decreased height. Which findings
indicate the patient may have developed right ventricular failure secondary to ARDS?
Select all that apply.
A) CVP of 14 mm Hg with hypotension
B) Acute elevation in PaCO2 from 55 to 68 over 4 hours
C) Change in EtCO2 waveform morphology
D) P/F ratio <100 despite high PEEP
E) Tachycardia disproportionate to blood pressure drop
F) Elevated lactate with normal bicarbonate
Correct Answers: A, B, C
Distinction-Level Solution:
Critical Problem: Acute cor pulmonale (right ventricular failure) due to severe
ARDS—recognized complication of high PEEP, hypercapnia, and pulmonary vascular
remodeling.
Data Synthesis: Severe ARDS causes pulmonary hypertension through hypoxic
vasoconstriction, vascular remodeling, and microthrombi. High PEEP (14 cm H2O) and
, hypercapnia (PaCO2 68) increase pulmonary vascular resistance (PVR), straining the
RV. The acute hemodynamic collapse with characteristic EtCO2 waveform change
(upslope = prolonged expiratory time, decreased height = reduced cardiac output)
signals RV failure with inadequate pulmonary blood flow.
Intervention Justification:
● A (CVP 14 with hypotension): Elevated CVP with systemic hypotension indicates
RV failure (cannot forward flow) or tamponade physiology. In ARDS, this
suggests RV dilation impairing LV filling.
● B (Rising PaCO2): Hypercapnic acidosis causes pulmonary vasoconstriction,
increasing PVR and RV afterload. Acute rises worsen RV strain.
● C (EtCO2 waveform): The upsloping waveform indicates prolonged expiratory
time (air trapping, auto-PEEP) and decreased cardiac output—classic for RV
failure with reduced pulmonary perfusion.
Distractor Pitfalls:
● D: Low P/F ratio indicates severe ARDS but does not specifically indicate RV
failure; many ARDS patients have low P/F without RV dysfunction.
● E: Tachycardia is nonspecific and expected in shock; the disproportion is not
specific to RV failure.
● F: Elevated lactate with normal bicarbonate indicates lactic acidosis from poor
perfusion, common to all shock states, not specific to RV failure.
Scenario 3:
A 54-year-old male with necrotizing pancreatitis and infected pancreatic necrosis is on
CRRT (CVVHDF) for AKI. Current settings: BFR 200 mL/min, dialysate 25 mL/kg/hr,
replacement fluid pre-filter 20 mL/kg/hr, net ultrafiltration 100 mL/hr. He is on
norepinephrine 0.3 mcg/kg/min, vasopressin 0.04 units/min, epinephrine 0.05
mcg/kg/min. Temp 38.6°C, HR 134, BP 82/56 (MAP 65), CVP 8 mm Hg. The CRRT
circuit pressures show: Access pressure -180 mm Hg (was -120), Return pressure +85
mm Hg (was +45), Transmembrane pressure (TMP) 350 mm Hg (was 180). The effluent
is becoming pink-tinged. The most appropriate immediate action is:
DISTINCTION-LEVEL Simulation Exam -
Progressive Care RN Competency
Assessment
SECTION 1: MULTI-SYSTEM FAILURE & SEPTIC SHOCK (Questions 1-20)
Scenario 1:
A 68-year-old male is 36 hours post-emergent exploratory laparotomy for perforated
diverticulitis with fecal peritonitis. He is intubated on AC/VC, Vt 450, PEEP 10, FiO2 70%,
RR 28. Sedated on propofol 50 mcg/kg/min, fentanyl 100 mcg/hr. Vasopressors:
norepinephrine 0.25 mcg/kg/min, vasopressin 0.03 units/min. Current data: T 38.9°C,
HR 142 (sinus), BP 74/48 (MAP 57), SpO2 89%. A-line waveform shows respiratory
variation >15%. CVP 6 mm Hg. ScvO2 58%. Lactate 6.8 mmol/L (trending up from 4.2).
Urine output 8 mL/hr last 4 hours. The ventilator high-pressure alarm is sounding with
peak pressures 48 cm H2O (was 32). Breath sounds are diminished bilaterally,
especially on the right. The most appropriate FIRST action is:
A) Increase norepinephrine to achieve MAP >65 mm Hg per Surviving Sepsis guidelines
B) Administer a 30 mL/kg crystalloid bolus for fluid responsiveness
C) Obtain an immediate portable chest X-ray and prepare for needle decompression
D) Increase sedation to achieve ventilator synchrony and reduce peak pressures
Correct Answer: C
,Distinction-Level Solution:
Critical Problem: Tension pneumothorax (likely right-sided) complicating septic
shock—true immediate life threat.
Data Synthesis: While this patient has severe septic shock (high lactate, low ScvO2,
oliguria), the acute change is the ventilator alarm with rising peak pressures (48 cm
H2O), diminished breath sounds, and hypoxemia refractory to high FiO2. The respiratory
variation on A-line suggests intrathoracic pressure changes. In a ventilated patient with
septic shock and abdominal surgery, barotrauma causing tension pneumothorax is a
recognized complication. The hemodynamic collapse (BP 74/48 despite high-dose
pressors) may be partially due to tension physiology impairing venous return.
Intervention Justification: Tension pneumothorax is an immediate cause of
cardiovascular collapse and death. The classic triad is absent in ventilated
patients—hypotension and elevated peak pressures are often the first signs. Needle
decompression must precede imaging if clinical suspicion is high, but given the
complexity, immediate CXR to confirm while preparing for decompression is the most
prudent first step. Fluid and pressor escalation (Choices A/B) will fail if venous return is
obstructed by tension physiology.
Distractor Pitfalls:
● A: Pressor escalation addresses the symptom (hypotension) but not the cause.
In tension pneumothorax, venous return is mechanically obstructed;
norepinephrine cannot overcome this.
● B: Fluid bolus is appropriate for sepsis but potentially harmful if tension
pneumothorax is present (further impaired venous return, right heart strain). The
respiratory variation suggests fluid responsiveness, but the primary problem is
mechanical.
● D: Sedation increase is dangerous—this patient is already deeply sedated, and
the problem is mechanical, not patient-ventilator asynchrony.
,Scenario 2 (SATA):
A 72-year-old female with severe ARDS (P/F ratio 98) is on ARDSnet protocol: AC/VC, Vt
320 (6 mL/kg IBW), PEEP 14, FiO2 90%, RR 32, I:E 1:1. She is proned. Current ABG: pH
7.18, PaCO2 68, PaO2 58, HCO3 24, lactate 3.2. Hemodynamics: HR 118, BP 92/60
(MAP 71) on norepinephrine 0.15 mcg/kg/min, CVP 14 mm Hg. The patient develops
sudden tachycardia to 156, BP drops to 68/42, and the EtCO2 waveform changes from a
normal rectangular shape to a gradual upslope with decreased height. Which findings
indicate the patient may have developed right ventricular failure secondary to ARDS?
Select all that apply.
A) CVP of 14 mm Hg with hypotension
B) Acute elevation in PaCO2 from 55 to 68 over 4 hours
C) Change in EtCO2 waveform morphology
D) P/F ratio <100 despite high PEEP
E) Tachycardia disproportionate to blood pressure drop
F) Elevated lactate with normal bicarbonate
Correct Answers: A, B, C
Distinction-Level Solution:
Critical Problem: Acute cor pulmonale (right ventricular failure) due to severe
ARDS—recognized complication of high PEEP, hypercapnia, and pulmonary vascular
remodeling.
Data Synthesis: Severe ARDS causes pulmonary hypertension through hypoxic
vasoconstriction, vascular remodeling, and microthrombi. High PEEP (14 cm H2O) and
, hypercapnia (PaCO2 68) increase pulmonary vascular resistance (PVR), straining the
RV. The acute hemodynamic collapse with characteristic EtCO2 waveform change
(upslope = prolonged expiratory time, decreased height = reduced cardiac output)
signals RV failure with inadequate pulmonary blood flow.
Intervention Justification:
● A (CVP 14 with hypotension): Elevated CVP with systemic hypotension indicates
RV failure (cannot forward flow) or tamponade physiology. In ARDS, this
suggests RV dilation impairing LV filling.
● B (Rising PaCO2): Hypercapnic acidosis causes pulmonary vasoconstriction,
increasing PVR and RV afterload. Acute rises worsen RV strain.
● C (EtCO2 waveform): The upsloping waveform indicates prolonged expiratory
time (air trapping, auto-PEEP) and decreased cardiac output—classic for RV
failure with reduced pulmonary perfusion.
Distractor Pitfalls:
● D: Low P/F ratio indicates severe ARDS but does not specifically indicate RV
failure; many ARDS patients have low P/F without RV dysfunction.
● E: Tachycardia is nonspecific and expected in shock; the disproportion is not
specific to RV failure.
● F: Elevated lactate with normal bicarbonate indicates lactic acidosis from poor
perfusion, common to all shock states, not specific to RV failure.
Scenario 3:
A 54-year-old male with necrotizing pancreatitis and infected pancreatic necrosis is on
CRRT (CVVHDF) for AKI. Current settings: BFR 200 mL/min, dialysate 25 mL/kg/hr,
replacement fluid pre-filter 20 mL/kg/hr, net ultrafiltration 100 mL/hr. He is on
norepinephrine 0.3 mcg/kg/min, vasopressin 0.04 units/min, epinephrine 0.05
mcg/kg/min. Temp 38.6°C, HR 134, BP 82/56 (MAP 65), CVP 8 mm Hg. The CRRT
circuit pressures show: Access pressure -180 mm Hg (was -120), Return pressure +85
mm Hg (was +45), Transmembrane pressure (TMP) 350 mm Hg (was 180). The effluent
is becoming pink-tinged. The most appropriate immediate action is:
