Vasopressors and inotropic support US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Vasopressors and inotropic support. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Vasopressors and inotropic support US Medical PG Question 1: A 28-year-old research assistant is brought to the emergency department for severe chemical burns 30 minutes after accidentally spilling hydrochloric acid on himself. The burns cover both hands and forearms. His temperature is 37°C (98.6°F), pulse is 112/min, respirations are 20/min, and blood pressure is 108/82 mm Hg. Initial stabilization and resuscitation is begun, including respiratory support, fluid resuscitation, and cardiovascular stabilization. The burned skin is irrigated with saline water to remove the chemical agent. Which of the following is the most appropriate method to verify adequate fluid infusion in this patient?
- A. The Parkland formula
- B. Blood pressure
- C. Pulmonary capillary wedge pressure
- D. Heart rate
- E. Urinary output (Correct Answer)
Vasopressors and inotropic support Explanation: ***Urinary output***
- Maintaining a specific **urinary output** (e.g., adult with major burns: 0.5-1.0 mL/kg/hr or 30-50 mL/hr) is the most reliable clinical indicator of adequate fluid resuscitation in burn patients.
- This ensures sufficient end-organ perfusion and avoids both under-resuscitation (leading to shock and organ damage) and over-resuscitation (risk of compartment syndrome and pulmonary edema).
*The Parkland formula*
- The **Parkland formula** is used to *calculate* the initial fluid volume needed, but it does not *verify* the adequacy of the infusion once started.
- This formula provides a starting point for fluid administration, which then needs to be adjusted based on the patient's response.
*Blood pressure*
- **Blood pressure** can be misleading in burn patients; it may remain deceptively normal due to compensatory mechanisms even with significant fluid deficits.
- It is a late indicator of hypovolemic shock, and relying solely on it can lead to under-resuscitation.
*Pulmonary capillary wedge pressure*
- **Pulmonary capillary wedge pressure (PCWP)** requires invasive monitoring via a pulmonary artery catheter, which is rarely indicated for routine fluid management in burn patients due to its invasiveness and associated risks.
- Less invasive and equally effective methods, like urinary output, are preferred for monitoring resuscitation.
*Heart rate*
- **Heart rate** is a sensitive but non-specific indicator of fluid status; it can be elevated due to pain, anxiety, or infection, not solely hypovolemia.
- While a decreasing heart rate can indicate improved fluid status, it is not as reliable or direct an indicator of end-organ perfusion as urinary output.
Vasopressors and inotropic support US Medical PG Question 2: A 32-year-old woman comes to the office for a regular follow-up. She was diagnosed with type 2 diabetes mellitus 4 years ago. Her last blood test showed a fasting blood glucose level of 6.6 mmol/L (118.9 mg/dL) and HbA1c of 5.1%. No other significant past medical history. Current medications are metformin and a daily multivitamin. No significant family history. The physician wants to take her blood pressure measurements, but the patient states that she measures it every day in the morning and in the evening and even shows him a blood pressure diary with all the measurements being within normal limits. Which of the following statements is correct?
- A. The physician has to measure the patient’s blood pressure because it is a standard of care for any person with diabetes mellitus who presents for a check-up. (Correct Answer)
- B. Assessment of blood pressure only needs to be done at the initial visit; it is not necessary to measure blood pressure in this patient at any follow-up appointments.
- C. The physician should not measure the blood pressure in this patient and should simply make a note in a record showing the results from the patient’s diary.
- D. The physician should not measure the blood pressure in this patient because she does not have hypertension or risk factors for hypertension.
- E. The physician should not measure the blood pressure in this patient because the local standards of care in the physician's office differ from the national standards of care so measurements of this patient's blood pressure cannot be compared to diabetes care guidelines.
Vasopressors and inotropic support Explanation: **The physician has to measure the patient’s blood pressure because it is a standard of care for any person with diabetes mellitus who presents for a check-up.**
- For individuals with **diabetes mellitus**, regular **blood pressure monitoring** by a healthcare professional is a fundamental component of their routine care, regardless of home measurements.
- This practice ensures accuracy, identifies **white coat hypertension**, and allows for early detection and management of **cardiovascular risks** inherent to diabetes.
*Assessment of blood pressure only needs to be done at the initial visit; it is not necessary to measure blood pressure in this patient at any follow-up appointments.*
- This statement is incorrect as **regular blood pressure monitoring** is essential for all follow-up visits in diabetic patients due to their elevated risk of developing **hypertension** and associated complications.
- Even if initial measurements are normal, blood pressure can change over time, necessitating continuous assessment to maintain optimal **cardiovascular health**.
*The physician should not measure the blood pressure in this patient and should simply make a note in a record showing the results from the patient’s diary.*
- Relying solely on **patient-recorded blood pressure** measurements, while valuable, does not replace the need for an **in-office measurement** by a healthcare provider.
- This is crucial for verifying the accuracy of home devices, assessing for **masked hypertension**, and ensuring compliance with **clinical guidelines**.
*The physician should not measure the blood pressure in this patient because she does not have hypertension or risk factors for hypertension.*
- This is incorrect; the patient's diagnosis of **Type 2 Diabetes Mellitus** itself is a significant **risk factor for hypertension** and cardiovascular disease.
- All individuals with diabetes require ongoing **blood pressure monitoring**, irrespective of their current blood pressure status or other obvious risk factors.
*The physician should not measure the blood pressure in this patient because the local standards of care in the physician's office differ from the national standards of care so measurements of this patient's blood pressure cannot be compared to diabetes care guidelines.*
- This statement is generally incorrect and illogical; **national guidelines** for diabetes care, including blood pressure monitoring, are established to ensure consistent and high-quality care across different settings.
- Healthcare providers are expected to adhere to these **national standards of care** or explain any deviations, making the measurement of blood pressure a critical part of a diabetic patient's visit.
Vasopressors and inotropic support US Medical PG Question 3: An 83-year-old male presents with dyspnea, orthopnea, and a chest radiograph demonstrating pulmonary edema. A diagnosis of congestive heart failure is considered. The following clinical measurements are obtained: 100 bpm heart rate, 0.2 mL O2/mL systemic blood arterial oxygen content, 0.1 mL O2/mL pulmonary arterial oxygen content, and 400 mL O2/min oxygen consumption. Using the above information, which of the following values represents this patient's cardiac stroke volume?
- A. 30 mL/beat
- B. 70 mL/beat
- C. 40 mL/beat (Correct Answer)
- D. 60 mL/beat
- E. 50 mL/beat
Vasopressors and inotropic support Explanation: ***40 mL/beat***
- First, calculate cardiac output (CO) using the **Fick principle**: CO = Oxygen Consumption / (Arterial O2 content - Venous O2 content). Here, CO = 400 mL O2/min / (0.2 mL O2/mL - 0.1 mL O2/mL) = 400 mL O2/min / 0.1 mL O2/mL = **4000 mL/min**.
- Next, calculate stroke volume (SV) using the formula: SV = CO / Heart Rate. Given a heart rate of 100 bpm, SV = 4000 mL/min / 100 beats/min = **40 mL/beat**.
*30 mL/beat*
- This answer would result if there was an error in calculating either the **cardiac output** or if the **arteriovenous oxygen difference** was overestimated.
- A stroke volume of 30 mL/beat with a heart rate of 100 bpm would yield a cardiac output of 3 L/min, which is sub-physiologic for an oxygen consumption of 400 mL/min given the provided oxygen content values.
*70 mL/beat*
- This stroke volume is higher than calculated and would imply either a significantly **lower heart rate** or a much **higher cardiac output** than derived from the Fick principle with the given values.
- A stroke volume of 70 mL/beat at a heart rate of 100 bpm would mean a cardiac output of 7 L/min, which is inconsistent with the provided oxygen consumption and arteriovenous oxygen difference.
*60 mL/beat*
- This value is higher than the correct calculation, suggesting an error in the initial calculation of **cardiac output** or the **avO2 difference**.
- To get 60 mL/beat, the cardiac output would need to be 6000 mL/min, which would mean an avO2 difference of 0.067 mL O2/mL, not 0.1 mL O2/mL.
*50 mL/beat*
- This stroke volume would result from an incorrect calculation of the **cardiac output**, potentially from a slight miscalculation of the **arteriovenous oxygen difference**.
- A stroke volume of 50 mL/beat at 100 bpm would mean a cardiac output of 5 L/min, requiring an avO2 difference of 0.08 mL O2/mL, which is not consistent with the given values.
Vasopressors and inotropic support US Medical PG Question 4: An 82-year-old male with congestive heart failure experiences rapid decompensation of his condition, manifesting as worsening dyspnea, edema, and increased fatigue. Labs reveal an increase in his serum creatinine from baseline. As part of the management of this acute change, the patient is given IV dobutamine to alleviate his symptoms. Which of the following effects occur as a result of this therapy?
- A. Decreased cardiac contractility
- B. Decreased heart rate
- C. Increased myocardial oxygen consumption (Correct Answer)
- D. Increased systemic vascular resistance due to systemic vasoconstriction
- E. Slowed atrioventricular conduction velocities
Vasopressors and inotropic support Explanation: ***Increased myocardial oxygen consumption***
- Dobutamine is a **beta-1 adrenergic agonist** that increases **myocardial contractility** and **heart rate**.
- This enhanced cardiac workload directly leads to an **increased demand for oxygen** by the heart muscle.
*Decreased cardiac contractility*
- Dobutamine is primarily used in heart failure to **increase cardiac contractility** (positive inotropic effect), thus improving cardiac output.
- Decreased contractility would worsen the patient's condition, which is contrary to the therapeutic goal of dobutamine.
*Decreased heart rate*
- Dobutamine, through its beta-1 agonism, typically causes an **increase in heart rate**, not a decrease.
- A decreased heart rate would further compromise cardiac output in a decompensated heart failure patient.
*Increased systemic vascular resistance due to systemic vasoconstriction*
- Dobutamine has a relatively weak effect on alpha-1 adrenergic receptors, and its primary action is to cause **vasodilation**, which tends to **decrease systemic vascular resistance**.
- While other inotropes like norepinephrine can cause vasoconstriction, dobutamine's effect on SVR is generally minimal or mildly vasodilatory, which helps to reduce afterload.
*Slowed atrioventricular conduction velocities*
- Beta-1 agonists like dobutamine generally tend to **increase atrioventricular (AV) conduction velocity** and can even precipitate arrhythmias.
- Slowed AV conduction is characteristic of drugs like beta-blockers or calcium channel blockers, which would be contraindicated in this setting.
Vasopressors and inotropic support US Medical PG Question 5: A 75-year-old male arrives by ambulance to the emergency room severely confused. His vitals are T 40 C, HR 120 bpm, BP 80/55 mmHg, RR 25. His wife explains that he injured himself about a week ago while cooking, and several days later his finger became infected, oozing with pus. He ignored her warning to see a doctor and even refused after he developed fever, chills, and severe fatigue yesterday. After being seen by the emergency physician, he was given antibiotics and IV fluids. Following initial resuscitation with IV fluids, he remains hypotensive. The ED physicians place a central venous catheter and begin infusing norepinephrine. Which of the following receptors are activated by norepinephrine?
- A. Alpha 1, Alpha 2, Beta 1, Beta 2
- B. Alpha 1, Alpha 2, Beta 1 (Correct Answer)
- C. Alpha 2
- D. Alpha 1, Beta 1, Dopamine 1
- E. Alpha 1, Beta 1
Vasopressors and inotropic support Explanation: ***Alpha 1, Alpha 2, Beta 1***
- **Norepinephrine** primarily activates **alpha-1** (peripheral vasoconstriction), **alpha-2** (presynaptic inhibition and some vasoconstriction), and **beta-1** (increased heart rate and contractility) adrenergic receptors.
- These are the **primary receptors** responsible for norepinephrine's clinical effects: vasoconstriction (alpha-1, alpha-2) and positive inotropic/chronotropic effects (beta-1).
- This receptor profile makes norepinephrine an ideal **vasopressor** in septic shock, as seen in this patient.
*Alpha 1, Alpha 2, Beta 1, Beta 2*
- While **norepinephrine** does activate alpha-1, alpha-2, and beta-1 receptors, it has **negligible affinity for beta-2 receptors**.
- **Epinephrine** (not norepinephrine) is the catecholamine with significant **beta-2 activity**, causing bronchodilation and vasodilation in skeletal muscle.
- Including beta-2 is a common mistake when confusing norepinephrine with epinephrine.
*Alpha 2*
- This option is far too incomplete as **norepinephrine** has significant action on **alpha-1** and **beta-1** receptors, which are crucial for its vasoconstrictive and inotropic effects.
- Activating only alpha-2 receptors would primarily lead to presynaptic inhibition and limited vasoconstriction, not the broad cardiovascular support required in septic shock.
*Alpha 1, Beta 1, Dopamine 1*
- While **norepinephrine** does activate **alpha-1** and **beta-1** receptors, it does **not** activate **dopamine 1 (D1) receptors**.
- Only **dopamine** itself or specific **dopamine agonists** stimulate D1 receptors, leading to renal and mesenteric vasodilation.
- This option incorrectly attributes dopaminergic activity to norepinephrine.
*Alpha 1, Beta 1*
- This option correctly identifies two of the main receptors activated by **norepinephrine**: alpha-1 (vasoconstriction) and beta-1 (positive inotropy and chronotropy).
- However, it **omits alpha-2 receptors**, which norepinephrine also activates, contributing to both presynaptic feedback inhibition and additional vasoconstriction.
- While not completely wrong, this is an incomplete answer.
Vasopressors and inotropic support US Medical PG Question 6: A 60-year-old woman is brought to the emergency department by paramedics after being found unresponsive. It is not possible to obtain a history. Her blood pressure is 75/30 mmHg and pulse is 108/min. Her extremities are cool and mottled. She is admitted to the intensive care unit (ICU) for further supportive care, where she is started on a norepinephrine intravenous drip. After several hours on this infusion, which of the following changes in vitals would be expected?
- A. Blood pressure decreases; pulse decreases
- B. Blood pressure increases; pulse increases
- C. Blood pressure decreases; pulse increases
- D. Blood pressure increases; pulse remains unchanged
- E. Blood pressure increases; pulse decreases (Correct Answer)
Vasopressors and inotropic support Explanation: ***Blood pressure increases; pulse decreases***
- **Norepinephrine** is a potent **vasoconstrictor** that increases systemic vascular resistance, leading to an **increase in blood pressure**.
- The increased blood pressure activates **baroreceptors**, triggering a **reflex bradycardia** (decreased heart rate or pulse) to maintain cardiovascular homeostasis.
*Blood pressure decreases; pulse decreases*
- **Norepinephrine** is expected to *increase* blood pressure, not decrease it.
- A decrease in both blood pressure and pulse in this context would suggest worsening shock or an adverse reaction, not a therapeutic effect.
*Blood pressure increases; pulse increases*
- While norepinephrine increases blood pressure, the direct stimulation of beta-1 receptors on the heart causing an increased heart rate is often *overridden* by the **baroreceptor reflex** that reduces heart rate due to the sharp rise in blood pressure.
- An increase in both parameters is less typical with norepinephrine as the predominant effect on heart rate is usually reflex bradycardia.
*Blood pressure decreases; pulse increases*
- **Norepinephrine** is a powerful pressor agent and would not cause a *decrease* in blood pressure, especially in a hypotensive patient.
- This combination of vital signs would indicate worsening **hypotension** and **tachycardia**, often seen in uncontrolled shock.
*Blood pressure increases; pulse remains unchanged*
- While **blood pressure increases** as expected with norepinephrine, it is very unlikely for the **pulse to remain unchanged** due to the robust **baroreceptor reflex** responding to the significant rise in blood pressure.
- The reflex arc aims to normalize blood pressure by modulating heart rate, typically causing a decrease.
Vasopressors and inotropic support US Medical PG Question 7: A 35-year-old woman volunteers for a study on respiratory physiology. Pressure probes A and B are placed as follows:
Probe A: between the parietal and visceral pleura
Probe B: within the cavity of an alveolus
The probes provide a pressure reading relative to atmospheric pressure. To obtain a baseline reading, she is asked to sit comfortably and breathe normally. Which of the following sets of values will most likely be seen at the end of inspiration?
- A. Probe A: -6 mm Hg; Probe B: 0 mm Hg (Correct Answer)
- B. Probe A: 0 mm Hg; Probe B: -1 mm Hg
- C. Probe A: -4 mm Hg; Probe B: 0 mm Hg
- D. Probe A: -4 mm Hg; Probe B: -1 mm Hg
- E. Probe A: -6 mm Hg; Probe B: -1 mm Hg
Vasopressors and inotropic support Explanation: ***Probe A: -6 mm Hg; Probe B: 0 mm Hg***
- At the **end of inspiration**, the **intrapleural pressure (Probe A)** is at its most negative, typically around -6 to -8 cm H2O (equivalent to -4 to -6 mmHg), reflecting the maximum expansion of the thoracic cavity.
- At the **end of inspiration**, just before exhalation begins, there is **no airflow**, so the **intrapulmonary pressure (Probe B)** equalizes with atmospheric pressure, resulting in a 0 mm Hg reading.
*Probe A: 0 mm Hg; Probe B: -1 mm Hg*
- An **intrapleural pressure of 0 mm Hg** would indicate a **pneumothorax** since it should always be negative to prevent lung collapse.
- An **intrapulmonary pressure of -1 mm Hg** would indicate that **inspiration is still ongoing**, as air would be flowing into the lungs.
*Probe A: -4 mm Hg; Probe B: 0 mm Hg*
- While an **intrapulmonary pressure of 0 mm Hg** is correct at the end of inspiration, an **intrapleural pressure of -4 mm Hg** is typical for the **end of expiration (Functional Residual Capacity)** during quiet breathing, not the end of inspiration.
- The **intrapleural pressure becomes more negative** during inspiration due to increased thoracic volume, so -4 mm Hg would be insufficient.
*Probe A: -4 mm Hg; Probe B: -1 mm Hg*
- An **intrapleural pressure of -4 mm Hg** is the normal pressure at the **end of expiration**, not the end of inspiration, where it becomes more negative.
- An **intrapulmonary pressure of -1 mm Hg** indicates that **inspiration is still in progress**, not at its end, as air would still be flowing into the lungs.
*Probe A: -6 mm Hg; Probe B: -1 mm Hg*
- While an **intrapleural pressure of -6 mm Hg** is consistent with the end of inspiration, an **intrapulmonary pressure of -1 mm Hg** means that **airflow is still occurring into the lungs**.
- At the **very end of inspiration**, just before the start of exhalation, airflow momentarily ceases, and intrapulmonary pressure becomes zero relative to the atmosphere.
Vasopressors and inotropic support US Medical PG Question 8: A 38-year-old previously healthy woman develops septic shock from necrotizing fasciitis of the lower extremity. Despite three debridements, broad-spectrum antibiotics (vancomycin, meropenem, clindamycin), IVIG, and aggressive critical care support, she develops refractory shock requiring norepinephrine 1.2 mcg/kg/min, vasopressin 0.04 units/min, and epinephrine 0.1 mcg/kg/min. Lactate is 15 mmol/L. Surgical team recommends hemipelvectomy as last option for source control. Family is devastated. ICU team notes SOFA score of 18. Synthesize an approach to management and decision-making.
- A. Transfer to ECMO center for consideration of VA-ECMO as bridge to hemipelvectomy
- B. Multidisciplinary meeting with surgery, ICU, palliative care, and family to discuss realistic outcomes, quality of life, and patient values before decision (Correct Answer)
- C. Continue medical management for 24 hours and proceed with hemipelvectomy only if shock improves
- D. Decline surgery based on futility given SOFA score >15 and initiate comfort care
- E. Proceed with hemipelvectomy immediately as only chance for survival with informed consent from family
Vasopressors and inotropic support Explanation: ***Multidisciplinary meeting with surgery, ICU, palliative care, and family to discuss realistic outcomes, quality of life, and patient values before decision***
- In high-acuity cases with refractory shock and high **SOFA scores (>15)**, shared decision-making is essential to align surgical intervention with the patient’s **goals of care**.
- This approach ensures that the **prognosis**, which carries a high risk of mortality and morbidity from **hemipelvectomy**, is transparently communicated by the entire medical team.
*Transfer to ECMO center for consideration of VA-ECMO as bridge to hemipelvectomy*
- **VA-ECMO** is generally not indicated in septic shock with refractory vasoplegia and severe multi-organ failure as it doesn't solve the **source control** issue.
- The logistics and physiological stress of a transfer in the setting of **1.2 mcg/kg/min norepinephrine** would be highly unstable and likely fatal.
*Continue medical management for 24 hours and proceed with hemipelvectomy only if shock improves*
- Delaying source control in **necrotizing fasciitis** while shock is worsening usually leads to death, as medical management alone cannot overcome the focus of infection.
- Waiting for improvement in the setting of a **lactate of 15 mmol/L** and triple vasopressors is unrealistic without definitive surgical intervention.
*Decline surgery based on futility given SOFA score >15 and initiate comfort care*
- While the **SOFA score** indicates a very high mortality risk, unilateral physician declaration of **medical futility** is ethically complex and can damage family trust.
- Comfort care should remain a possibility, but first requires a thorough **interdisciplinary discussion** to ensure legal and ethical standards are met.
*Proceed with hemipelvectomy immediately as only chance for survival with informed consent from family*
- Performing such a **mutilating surgery** without a detailed discussion of the expected **quality of life** and long-term functional loss is poor surgical practice.
- Immediate surgery without addressing the massive **operative mortality** risk ignores the patient's potential preference for a dignified death over a futile procedure.
Vasopressors and inotropic support US Medical PG Question 9: A 52-year-old woman with septic shock from intra-abdominal infection undergoes emergency exploratory laparotomy for perforated diverticulitis with fecal peritonitis. Surgery reveals extensive contamination requiring damage control approach. Postoperatively, she requires norepinephrine 0.8 mcg/kg/min plus vasopressin 0.04 units/min, has lactate of 8.5 mmol/L, temperature 35.2°C, INR 2.8, pH 7.18, and base deficit -12. Planned return to OR is in 48 hours. Evaluate the priority interventions to optimize outcome.
- A. Immediate return to OR for definitive repair and anastomosis
- B. Start therapeutic hypothermia and delay reoperation until hemodynamically stable off vasopressors
- C. Initiate high-dose vasopressors to maintain MAP >75 mmHg and early enteral nutrition
- D. Administer massive transfusion protocol and emergency re-exploration within 6 hours
- E. Aggressive rewarming, correction of coagulopathy, ongoing resuscitation, and source control at planned reoperation (Correct Answer)
Vasopressors and inotropic support Explanation: ***Aggressive rewarming, correction of coagulopathy, ongoing resuscitation, and source control at planned reoperation***
- This patient presents with the **lethal triad** (coagulopathy, acidosis, and hypothermia) in the setting of **septic shock**, necessitating physiologic stabilization before definitive surgery.
- The gold standard for **damage control** is to stabilize the patient in the ICU by correcting **base deficit**, improving **lactate clearance**, and restoring normal temperature and coagulation parameters.
*Immediate return to OR for definitive repair and anastomosis*
- Attempting **definitive repair** or anastomosis in an unstable patient with fecal peritonitis and high-dose **vasopressor requirements** carries a prohibited risk of dehiscence and death.
- Surgery should be limited to **staged re-intervention** only after the metabolic and physiologic insults have been partially reversed.
*Start therapeutic hypothermia and delay reoperation until hemodynamically stable off vasopressors*
- **Hypothermia** is a component of the lethal triad that worsens **coagulopathy** by inhibiting the clotting cascade; metabolic rewarming is required, not cooling.
- While stability is the goal, waiting to be completely off vasopressors might dangerously delay **source control** if the infection is driving the shock.
*Initiate high-dose vasopressors to maintain MAP >75 mmHg and early enteral nutrition*
- Focus should be on **volume resuscitation** and reversing tissue hypoxia (lactate) rather than solely escalating vasopressors, which can cause **mesenteric ischemia**.
- **Early enteral nutrition** is contraindicated in the immediate postoperative phase of an open abdomen with significant **hemodynamic instability** and high pressor requirements.
*Administer massive transfusion protocol and emergency re-exploration within 6 hours*
- **Massive transfusion protocol** is typically reserved for active, uncontrolled hemorrhage, whereas this patient primarily requires reversal of **septic shock** and metabolic derangements.
- **Re-exploration within 6 hours** is too early for a damage control patient who has not yet been adequately rewarmed or had their **acidosis** corrected.
Vasopressors and inotropic support US Medical PG Question 10: A 70-year-old man with recently diagnosed small cell lung cancer presents with septic shock from pneumonia. After initial resuscitation, he requires norepinephrine 0.6 mcg/kg/min and has a lactate of 7.8 mmol/L. His SOFA score is 14. The family requests 'everything be done,' but the patient had previously told his oncologist he would not want prolonged intensive care if his cancer prognosis was poor. Staging shows extensive-stage disease. The ICU team debates goals of care. What represents the most ethically appropriate approach to decision-making?
- A. Continue maximum therapy per family wishes as they are legal decision-makers
- B. Obtain ethics consultation to overrule family wishes based on futility
- C. Arrange urgent palliative care consultation and family meeting to discuss patient's previously expressed wishes and realistic prognosis (Correct Answer)
- D. Continue current therapy for 72 hours then reassess based on clinical trajectory
- E. Transition to comfort care based on poor oncologic prognosis and high SOFA score
Vasopressors and inotropic support Explanation: ***Arrange urgent palliative care consultation and family meeting to discuss patient's previously expressed wishes and realistic prognosis***
- The most ethically sound approach is to use **substituted judgment**, which prioritizes the patient's **previously expressed wishes** about avoiding prolonged intensive care.
- A **multidisciplinary family meeting** helps reconcile medical reality with patient values, ensuring informed **shared decision-making** rather than a unilateral or discordant approach.
*Continue maximum therapy per family wishes as they are legal decision-makers*
- While families are **surrogate decision-makers**, their role is to advocate for what the **patient would want**, not their own personal desires.
- Blindly following "everything be done" ignores the patient's prior statement to his oncologist and risks providing **non-beneficial treatment**.
*Obtain ethics consultation to overrule family wishes based on futility*
- The term **medical futility** is often controversial; ethics consultations are designed to **mediate conflicts** rather than simply provide a mechanism to overrule families.
- Unilateral decisions should only follow exhaustive attempts at **communication and mediation**, which have not yet occurred in this case.
*Continue current therapy for 72 hours then reassess based on clinical trajectory*
- A "time-limited trial" is a valid tool but fails to address the immediate ethical conflict regarding the **patient's autonomous refusal** of prolonged care.
- This approach may unnecessarily prolong the dying process and ignore the **prognostic alignment** required between the oncology and ICU teams.
*Transition to comfort care based on poor oncologic prognosis and high SOFA score*
- Clinicians should not unilaterally transition to **comfort care** without discussing the patient's prognosis and values with the family/surrogates first.
- While the **high SOFA score** and extensive cancer indicate a poor prognosis, the process must respect the legal and ethical requirements of **informed consent and withdrawal of care**.
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