Critical Care — MCQs

A patient following head injury was admitted to the intensive care ward with signs of raised intracranial pressure. He was put on a ventilator and started on intravenous fluids and diuretics. Twenty-four hours later his urine output was 3.5 litres, serum sodium was 156 mEq/L, and serum osmolarity was 316 mOsm/kg. What is the most likely diagnosis based on these parameters?

Q46Easy

Which of the following is NOT true in ARDS?

Q47Hard

A 26-year-old man is critically ill with multisystem organ failure and has a history of respiratory distress. Which of the following statements regarding Acute Respiratory Distress Syndrome (ARDS) are TRUE? 1. Lung injury in ARDS can be direct, as in sepsis, or indirect, as in toxic inhalation. 2. An arterial partial pressure of oxygen (PaO2) in mmHg divided by the fraction of inspired oxygen (FiO2) ratio less than 200 mmHg is characteristic of ARDS. 3. Ventilator-induced lung injury is more likely with high tidal volume ventilation in ARDS. 4. Mortality was significantly lower in patients ventilated with high tidal volume compared to those ventilated with conventional tidal volume. 5. High-dose glucocorticoids are useful in the care of ARDS patients.

Q48Medium

Which is the best treatment for type IV respiratory failure?

Q49Medium

Which of the following is NOT seen in ARDS?

Q50Medium

Activated protein C is used therapeutically in which of the following conditions?

Critical Care Indian Medical PG Practice Questions and MCQs

Question 41: Which of the following best represents the acid-base status given a pH of 7.2, HCO3 of 36 mmol/L, and PCO2 of 60 mm of Hg?

A. Respiratory acidosis with metabolic alkalosis
B. Respiratory acidosis (Correct Answer)
C. Respiratory alkalosis with metabolic acidosis
D. Respiratory acidosis with metabolic acidosis

Explanation: ### **Explanation** To solve any acid-base question, follow a systematic three-step approach: 1. **Check the pH:** The pH is **7.20** (Normal: 7.35–7.45). Since it is < 7.35, the primary process is **Acidosis** [1]. 2. **Determine the Primary Cause:** * The **$PCO_2$ is 60 mmHg** (Normal: 35–45 mmHg). An elevated $PCO_2$ (hypercapnia) causes acidosis [1]. * The **$HCO_3^-$ is 36 mmol/L** (Normal: 22–26 mmol/L). An elevated bicarbonate causes alkalosis [3]. * Since the $PCO_2$ matches the acidic pH, the primary disturbance is **Respiratory Acidosis** [1]. 3. **Evaluate Compensation:** The elevated $HCO_3^-$ (36 mmol/L) indicates the kidneys are retaining bicarbonate to compensate for the respiratory acidosis [2]. This is a compensatory mechanism, not a separate primary disorder. **Why other options are incorrect:** * **Option A:** While there is an "alkalotic" $HCO_3^-$ level, it is a compensatory response to the primary respiratory issue, not an independent metabolic alkalosis. * **Option C:** This is the opposite of the findings; the pH is acidic, not alkalotic [1]. * **Option D:** In this scenario, the $HCO_3^-$ would be low (< 22 mmol/L), which would further lower the pH. --- ### **High-Yield Clinical Pearls for NEET-PG** * **The "Direction" Rule:** In simple acid-base disorders, $PCO_2$ and $HCO_3^-$ always move in the **same direction** due to compensation. * **Acute vs. Chronic Compensation:** * **Acute Respiratory Acidosis:** $HCO_3^-$ increases by **1** mmol/L for every 10 mmHg rise in $PCO_2$. * **Chronic Respiratory Acidosis:** $HCO_3^-$ increases by **3.5 to 4** mmol/L for every 10 mmHg rise in $PCO_2$ [2]. * In this case, the $PCO_2$ rose by 20 units (from 40 to 60). The $HCO_3^-$ rose by 12 units (from 24 to 36). This suggests a **Chronic Respiratory Acidosis** (e.g., COPD) [2].

Question 42: Which of the following is NOT a feature of ventilator-associated pneumonia?

A. Fever
B. Tachycardia (Correct Answer)
C. New shadows on chest X-ray
D. Leucocytosis

Explanation: **Explanation:** Ventilator-associated pneumonia (VAP) is defined as pneumonia occurring more than 48 hours after endotracheal intubation [1]. The diagnosis is primarily clinical, based on a combination of systemic signs of infection and new pulmonary findings. **Why Tachycardia is the correct answer:** While tachycardia is a common sign of systemic inflammatory response syndrome (SIRS) and can occur in patients with VAP [2], it is **not** a specific diagnostic criterion for VAP. The standard clinical criteria (such as the Modified Clinical Pulmonary Infection Score - CPIS) focus on temperature, white cell count, secretions, and oxygenation. Tachycardia is too non-specific in a critical care setting, as it can be caused by pain, agitation, arrhythmias, or medications. **Analysis of Incorrect Options:** * **Fever (A):** Temperature >38°C (or <36°C) is a core systemic component of the diagnostic criteria for VAP [2]. * **New shadows on CXR (C):** This is the **most essential** requirement. A diagnosis of VAP cannot be made without a new or progressive radiographic infiltrate, consolidation, or cavitation. * **Leucocytosis (D):** A white blood cell count >11,000/mm³ or <4,000/mm³ is a standard diagnostic feature reflecting the body’s immune response to the pulmonary infection [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Timeframe:** VAP occurs **>48 hours** after intubation [1]. * **Gold Standard Diagnosis:** Quantitative culture of lower respiratory tract secretions (via Bronchoalveolar Lavage - BAL or protected specimen brush). * **Common Pathogens:** *Pseudomonas aeruginosa* (most common Gram-negative), *Staphylococcus aureus* (including MRSA), and *Acinetobacter*. * **Prevention:** The "Ventilator Bundle" includes head-of-bed elevation (30-45°), daily "sedation vacation," peptic ulcer prophylaxis, and DVT prophylaxis.

Question 43: What is true about critical illness myoneuropathy?

A. Neurological recovery is complete.
B. Sequential nerve demyelination followed by inflammatory myopathy during the course of the disease.
C. Cranial nerves are involved more commonly than peripheral nerves.
D. Diaphragmatic atony due to prolonged intubation may cause it. (Correct Answer)

Explanation: **Critical Illness Myoneuropathy (CIMN)** is a common complication in ICU patients, encompassing Critical Illness Polyneuropathy (CIP) and Critical Illness Myopathy (CIM). It is a major cause of difficulty in weaning patients from mechanical ventilation [1]. ### **Explanation of Options** * **Option D (Correct):** Prolonged mechanical ventilation leads to **disuse atrophy** of the diaphragm (diaphragmatic atony). This, combined with the systemic inflammatory response and metabolic derangements of critical illness, results in muscle wasting and weakness, making it a primary driver of CIMN and failed extubation [1]. * **Option A (Incorrect):** While some patients recover, many suffer from **long-term functional deficits**. Neurological recovery is often incomplete, leading to persistent muscle weakness and reduced quality of life post-discharge. * **Option B (Incorrect):** The pathophysiology involves **axonal degeneration** (not demyelination) and **non-inflammatory thick-filament (myosin) loss** (not inflammatory myopathy). It is primarily a metabolic and microvascular insult rather than an immune-mediated inflammatory process like Guillain-Barré Syndrome. * **Option C (Incorrect):** CIMN characteristically **spares the cranial nerves**. It typically presents as symmetric, flaccid limb weakness (proximal > distal) and respiratory muscle involvement. ### **High-Yield Pearls for NEET-PG** * **Risk Factors:** Sepsis, Multi-Organ Failure (MOF), hyperglycemia, and the use of **Corticosteroids** or **Neuromuscular Blocking Agents (NMBAs)**. * **Clinical Presentation:** "Floppy" patient with difficulty weaning from the ventilator despite improvement in the primary illness [1]. Deep Tendon Reflexes (DTRs) are usually decreased or absent. * **Diagnosis:** Electromyography (EMG) shows reduced Compound Muscle Action Potential (CMAP) and sensory nerve action potentials (SNAPs) in CIP, while SNAPs are preserved in pure CIM. * **Management:** Primarily supportive; strict glycemic control and early mobilization are the only proven preventive strategies.

Question 44: Obstructive shock is due to which of the following mechanisms?

A. Mechanical impediment to blood flow (Correct Answer)
B. Cardiac pump failure
C. Peripheral pooling of blood
D. Hypovolemia

Explanation: Shock is defined as a state of cellular and tissue hypoxia due to reduced oxygen delivery or increased oxygen consumption [3]. **Obstructive shock** occurs when there is a **mechanical impediment to blood flow** into or out of the heart, despite normal myocardial function and adequate intravascular volume [1]. This obstruction leads to a drastic fall in cardiac output. **Why the other options are incorrect:** * **Cardiac pump failure (Option B):** This describes **Cardiogenic shock**, where the primary defect is the heart's inability to contract effectively (e.g., Myocardial Infarction) [3]. * **Peripheral pooling of blood (Option C):** This is the hallmark of **Distributive shock** (e.g., Sepsis, Anaphylaxis), characterized by massive vasodilation and decreased systemic vascular resistance [1]. * **Hypovolemia (Option D):** This defines **Hypovolemic shock**, caused by a loss of intravascular volume (e.g., Hemorrhage or dehydration). **High-Yield Clinical Pearls for NEET-PG:** 1. **Common Causes:** The "Big Three" causes of obstructive shock are **Tension Pneumothorax**, **Cardiac Tamponade**, and **Massive Pulmonary Embolism** [1], [2]. 2. **Hemodynamics:** Characterized by **decreased Cardiac Output (CO)** and **increased Systemic Vascular Resistance (SVR)** as a compensatory mechanism. 3. **Jugular Venous Pressure (JVP):** Unlike hypovolemic shock, JVP is typically **elevated** in obstructive shock (except in rare cases of SVC syndrome). 4. **Pulsus Paradoxus:** A classic finding in Cardiac Tamponade (an inspiratory drop in SBP >10 mmHg) [2]. 5. **Beck’s Triad:** (Hypotension, Muffled heart sounds, Distended neck veins) is specific for Cardiac Tamponade.

Question 45: A patient following head injury was admitted to the intensive care ward with signs of raised intracranial pressure. He was put on a ventilator and started on intravenous fluids and diuretics. Twenty-four hours later his urine output was 3.5 litres, serum sodium was 156 mEq/L, and serum osmolarity was 316 mOsm/kg. What is the most likely diagnosis based on these parameters?

A. High urine output due to diuretics (Correct Answer)
B. Diabetes insipidus
C. Excessive infusion of normal saline
D. Cerebral salt wasting syndrome

Explanation: **Explanation:** The clinical presentation involves a post-head injury patient with polyuria (3.5L), hypernatremia (156 mEq/L), and high serum osmolarity (316 mOsm/kg). **Why Option A is Correct:** The patient was specifically started on **diuretics** (likely Mannitol or Furosemide) to manage raised intracranial pressure (ICP). Mannitol is an osmotic diuretic that works by drawing fluid from the brain parenchyma into the vascular compartment, which is then excreted by the kidneys [1]. This process leads to **solute diuresis**, resulting in high urine output and a relative loss of free water, which explains the elevated serum sodium and osmolarity [1]. **Why Other Options are Incorrect:** * **B. Diabetes Insipidus (DI):** While DI is common after head injury and causes polyuria/hypernatremia, the question explicitly states the patient was *started on diuretics*. In a clinical vignette, if a drug is introduced and the subsequent labs match its side-effect profile, the drug is the most likely culprit [1]. * **C. Excessive infusion of normal saline:** While this can cause hypernatremia, it typically leads to volume overload rather than significant polyuria unless the kidneys are compensating perfectly; however, it doesn't explain the high serum osmolarity as effectively as diuretic-induced dehydration. * **D. Cerebral Salt Wasting (CSW):** This is characterized by **hyponatremia** and volume depletion due to inappropriate sodium excretion. The patient here has hypernatremia, ruling out CSW [1]. **NEET-PG High-Yield Pearls:** * **Mannitol:** The drug of choice for acutely raised ICP. It can cause initial volume expansion followed by dehydration and hypernatremia [1]. * **SIADH vs. CSW:** Both present with hyponatremia in CNS triggers, but SIADH is **euvolemic**, whereas CSW is **hypovolemic** [1]. * **Diabetes Insipidus:** Suspect if urine osmolarity is low (<200 mOsm/kg) despite high serum osmolarity.

Question 46: Which of the following is NOT true in ARDS?

A. Decreased pulmonary compliance
B. Increased pulmonary artery pressure
C. Increased left atrial pressure (Correct Answer)
D. Severe hypoxemia

Explanation: ### Explanation The core definition of **Acute Respiratory Distress Syndrome (ARDS)** relies on the presence of **non-cardiogenic pulmonary edema**. [1] **1. Why "Increased left atrial pressure" is the correct answer:** According to the **Berlin Criteria**, ARDS is characterized by respiratory failure that is *not* fully explained by heart failure or fluid overload. [1] An increased left atrial pressure (measured via Pulmonary Capillary Wedge Pressure/PCWP >18 mmHg) suggests **cardiogenic pulmonary edema** (e.g., congestive heart failure). In ARDS, the edema is caused by increased alveolar-capillary permeability ("leaky capillaries"), not hydrostatic pressure; therefore, left atrial pressure remains normal. **2. Analysis of incorrect options:** * **Decreased pulmonary compliance:** In ARDS, the lungs become "stiff" due to the loss of surfactant, alveolar collapse (atelectasis), and inflammatory exudate. [1] This significantly reduces compliance, making ventilation difficult. * **Increased pulmonary artery pressure:** Hypoxic pulmonary vasoconstriction and inflammatory damage to the pulmonary vasculature often lead to **Pulmonary Hypertension**, which can progress to right heart strain. * **Severe hypoxemia:** This is a hallmark of ARDS. It is typically refractory to supplemental oxygen due to significant **intrapulmonary shunting** (blood perfusing non-ventilated, fluid-filled alveoli). [1] **3. High-Yield Clinical Pearls for NEET-PG:** * **Berlin Criteria (Timing):** Onset within 1 week of a known clinical insult. [1] * **Radiology:** Bilateral opacities on CXR/CT not fully explained by effusions or collapse. [1] * **Oxygenation (P/F Ratio):** * Mild: 200–300 mmHg * Moderate: 100–200 mmHg * Severe: <100 mmHg * **Management Strategy:** "Lung Protective Ventilation" using **Low Tidal Volume (6 mL/kg)** to prevent volutrauma and high PEEP to maintain alveolar recruitment. * **Histopathology:** The characteristic finding is **Hyaline Membranes** lining the alveoli.

Question 47: A 26-year-old man is critically ill with multisystem organ failure and has a history of respiratory distress. Which of the following statements regarding Acute Respiratory Distress Syndrome (ARDS) are TRUE? 1. Lung injury in ARDS can be direct, as in sepsis, or indirect, as in toxic inhalation. 2. An arterial partial pressure of oxygen (PaO2) in mmHg divided by the fraction of inspired oxygen (FiO2) ratio less than 200 mmHg is characteristic of ARDS. 3. Ventilator-induced lung injury is more likely with high tidal volume ventilation in ARDS. 4. Mortality was significantly lower in patients ventilated with high tidal volume compared to those ventilated with conventional tidal volume. 5. High-dose glucocorticoids are useful in the care of ARDS patients.

A. Statements 1, 2, and 5 are True, and 3 and 4 are False.
B. All statements are True.
C. All statements are False. (Correct Answer)
D. Statements 3 and 4 are True, and 1, 2, and 5 are False.

Explanation: This question tests the fundamental understanding of the **Berlin Definition** and management protocols for ARDS [1]. The correct answer is **C** because every statement provided contains a factual error based on current clinical guidelines. ### **Analysis of Statements** 1. **Statement 1 is False:** The mechanisms are swapped. **Sepsis** is the most common cause of **indirect** lung injury (mediated by systemic cytokines), while **toxic inhalation** or pneumonia causes **direct** lung injury. 2. **Statement 2 is False:** According to the Berlin Criteria, ARDS is defined by a $PaO_2/FiO_2$ ratio of **$\leq$ 300 mmHg** (with PEEP $\geq$ 5 $cmH_2O$) [1]. While a ratio < 200 is "Moderate ARDS," it is not the threshold for the diagnosis itself. 3. **Statement 3 is False:** This is a trick of terminology. High tidal volume causes **Volutrauma**, but the statement implies it is "more likely" in ARDS compared to other conditions [2]. However, the standard of care is **Low Tidal Volume Ventilation (LTVV)** (6 mL/kg PBW) to *prevent* injury. 4. **Statement 4 is False:** The landmark **ARMA trial** proved that **low tidal volume** (6 mL/kg) significantly **decreases mortality** compared to conventional/high tidal volume (12 mL/kg). 5. **Statement 5 is False:** Routine **high-dose** glucocorticoids are not recommended and may increase mortality in early ARDS. While low-to-moderate doses may be used in specific subsets (e.g., COVID-19 or late fibroproliferative phase), "high-dose" therapy is generally contraindicated. ### **NEET-PG High-Yield Pearls** * **Berlin Criteria:** Acute onset (<1 week), bilateral opacities on imaging (not fully explained by effusions/collapse), and respiratory failure not fully explained by heart failure/fluid overload [1]. * **Severity:** Mild ($PaO_2/FiO_2$ 201–300), Moderate (101–200), Severe ($\leq$ 100) [1]. * **Management:** Use **Low Tidal Volume** (6 mL/kg) and **Prone Positioning** (if $PaO_2/FiO_2$ < 150) to improve survival.

Question 48: Which is the best treatment for type IV respiratory failure?

A. Non-invasive ventilation with tight-fitting face mask
B. Intubation with mechanical ventilation (Correct Answer)
C. Continuous positive pressure ventilation
D. High-frequency jet ventilation

Explanation: Respiratory failure is classified into four types based on the underlying pathophysiology [1]. **Type IV respiratory failure** is defined as respiratory failure associated with **shock** (hypoperfusion). In this state, there is a profound imbalance between oxygen delivery and demand, often due to cardiogenic, septic, or hypovolemic shock. **Why Option B is Correct:** In Type IV failure, the primary goal is to decrease the work of breathing (WOB) and redistribute blood flow from the overworked respiratory muscles to vital organs. **Intubation and mechanical ventilation** is the treatment of choice because it provides total control over the airway, eliminates the metabolic cost of breathing, and allows for aggressive hemodynamic stabilization. **Why Other Options are Incorrect:** * **Option A & C (NIV/CPAP):** While non-invasive ventilation is excellent for Type II (hypercapnic) failure (e.g., COPD/Pulmonary Edema), it is often insufficient in Type IV [2]. Patients in shock are frequently hemodynamically unstable, have altered sensorium, or cannot tolerate the high pressure required, making NIV risky due to the potential for sudden collapse or aspiration. * **Option D (HFJV):** High-frequency jet ventilation is a specialized modality used primarily in neonatal care or specific airway surgeries; it is not a standard first-line treatment for shock-related respiratory failure. **NEET-PG High-Yield Pearls:** * **Type I:** Hypoxemic ($PaO_2 < 60$ mmHg) – e.g., Pneumonia, ARDS [1]. * **Type II:** Hypercapnic ($PaCO_2 > 50$ mmHg) – e.g., COPD, Neuromuscular disorders [1]. * **Type III:** Perioperative (Atelectasis). * **Type IV:** Shock (Hypoperfusion). * **Key Concept:** In Type IV, the lungs may be "normal," but the patient requires ventilation to reduce the oxygen consumption ($VO_2$) of the diaphragm.

Question 49: Which of the following is NOT seen in ARDS?

A. Pulmonary edema
B. Hypercapnia (Correct Answer)
C. Hypoxemia
D. Stiff lung

Explanation: **Explanation:** Acute Respiratory Distress Syndrome (ARDS) is characterized by diffuse alveolar damage leading to severe gas exchange failure [1]. The hallmark of ARDS is **refractory hypoxemia** (Option C) caused by right-to-left intrapulmonary shunting [2]. **Why Hypercapnia (Option B) is the correct answer:** In the early to mid-stages of ARDS, patients typically present with **hypocapnia** (low $PaCO_2$) and respiratory alkalosis [3]. This occurs because the profound hypoxemia and irritation of juxtacapillary (J) receptors trigger a compensatory increase in respiratory rate (tachypnea). While $CO_2$ diffusion is rarely impaired early on [4], hypercapnia only develops in the terminal stages of the disease due to respiratory muscle fatigue or as a result of "protective lung ventilation" strategies (permissive hypercapnia). Therefore, it is not a primary feature of ARDS [2]. **Analysis of other options:** * **Pulmonary edema (Option A):** ARDS is defined by non-cardiogenic pulmonary edema [1]. Increased capillary permeability leads to protein-rich fluid leaking into the alveoli. * **Stiff lung (Option B):** The accumulation of fluid and loss of surfactant significantly reduce **lung compliance** [1]. This makes the lungs "stiff," requiring higher pressures to ventilate. **High-Yield NEET-PG Pearls:** 1. **Berlin Criteria:** Onset within 1 week, bilateral opacities on imaging, non-cardiogenic origin (PCWP < 18 mmHg), and $PaO_2/FiO_2$ ratio < 300 [1]. 2. **Management:** Low tidal volume ventilation (6 mL/kg) is the gold standard to prevent Volutrauma. 3. **Prone Positioning:** Indicated if $PaO_2/FiO_2$ < 150 to improve V/Q matching.

Question 50: Activated protein C is used therapeutically in which of the following conditions?

A. Abnormal PT/PTT
B. Myocardial Infarction
C. Fungal infection
D. Sepsis (Correct Answer)

Explanation: **Explanation:** **Activated Protein C (Drotrecogin alfa)** is a recombinant form of human activated protein C that was historically used in the management of **severe sepsis and septic shock**. **Why Sepsis is the Correct Answer:** Sepsis involves a complex systemic inflammatory response that triggers widespread microvascular thrombosis, inflammation, and impaired fibrinolysis [2]. Activated Protein C acts as a potent **anticoagulant** (by inactivating Factors Va and VIIIa) and possesses **anti-inflammatory and profibrinolytic properties**. By limiting thrombin generation and reducing the inflammatory cascade, it was intended to prevent multi-organ dysfunction syndrome (MODS) in critically ill patients with a high risk of death [4]. **Why Other Options are Incorrect:** * **Abnormal PT/PTT:** These are markers of coagulopathy. Activated Protein C actually *increases* the risk of bleeding; it is not a treatment for coagulation factor deficiencies [3]. * **Myocardial Infarction:** The primary treatment involves antiplatelets, anticoagulants (like Heparin), or thrombolytics (like Alteplase). Activated Protein C has no role in coronary plaque rupture management. Recombinant t-PA is used for coronary artery patency [1]. * **Fungal Infection:** This requires antifungal therapy (e.g., Amphotericin B or Azoles). While sepsis can be fungal, the drug targets the host's inflammatory response, not the pathogen itself. **High-Yield Clinical Pearls for NEET-PG:** * **The PROWESS Trial:** This study initially led to the FDA approval of Drotrecogin alfa for severe sepsis. * **Current Status:** It is important to note that the drug was **withdrawn from the market globally** (following the PROWESS-SHOCK trial) because it failed to show a survival benefit and significantly increased the risk of serious bleeding. * **Mechanism:** It specifically inhibits **Factors Va and VIIIa**. * **Endogenous Protein C:** It is a vitamin K-dependent protein synthesized in the liver. Deficiency is associated with Purpura Fulminans and Warfarin-induced skin necrosis.

Practice by Chapter

Shock Syndromes and Management

Practice Questions

Acute Respiratory Distress Syndrome

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Mechanical Ventilation Principles

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Hemodynamic Monitoring

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Nutrition in Critical Illness

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Sedation and Analgesia in ICU

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Multi-organ Dysfunction Syndrome

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Acid-Base and Electrolyte Disturbances

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Toxicologic Emergencies

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Neurological Emergencies in ICU

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Renal Replacement Therapy

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End-of-Life Care in ICU

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