Critical Care Practice Questions

Q: What is the recommended chest compression rate (per minute) during CPR for adults?

100-120 compressions per minute. ***100-120 compressions per minute*** - This rate ensures adequate **blood flow** to vital organs, especially the brain and heart, during CPR [1]. - Delivering compressions within this range is a key component of high-quality CPR to maximize survival outcomes [1]. *60-80 compressions per minute* - This rate is too slow and would result in **insufficient blood flow** to the brain and other critical organs. - Inadequate compression rates can significantly reduce the effectiveness of CPR and patient survival chances. *40-60 compressions per minute* - This rate is critically low and would provide almost no effective **circulation** during cardiac arrest. - Such a slow rate would be highly detrimental and unlikely to sustain life or improve the patient's condition. *20-40 compressions per minute* - This rate is far below the recommended guidelines and would be entirely ineffective in maintaining **perfusion**. - Performing CPR at this rate would likely result in no meaningful benefit to the patient.

Q: In hypovolemic shock, the percentage of fluid depletion is:

15-45%. 15-45% - This range represents the **fluid depletion** levels that can lead to hypovolemic shock, with higher percentages associated with more severe shock categories. - Shock is typically classified into four classes (I-IV), where Class I (minimal shock) involves up to 15% fluid loss, and Class IV (severe shock) can involve over 40% fluid loss. 70% - A **70% fluid depletion** would represent an **extremely severe and likely fatal** fluid loss, far beyond the typical range described for hypovolemic shock. - Such a massive loss would invariably lead to **irreversible organ damage** and death. 10-15% - A **10-15% fluid depletion** generally corresponds to **Class I hypovolemic shock**, which is usually compensated and often does not present with the overt signs of shock unless other factors are contributing. - While it is a form of fluid depletion, it is at the **lower end** and typically not considered the full spectrum of established hypovolemic shock. 43-63% - While a depletion of **over 40%** would certainly cause severe hypovolemic shock (Class IV) [1], defining the overall range as 43-63% is **too narrow** and does not encompass the full spectrum, including the lower classes of shock. - This range represents an **extremely high and critical level** of fluid loss, indicating very severe shock, but not the entire classification of hypovolemic shock.

Q: Following pathogenetic mechanisms operate in septic shock except -

Increased peripheral vascular resistance. Following pathogenetic mechanisms operate in septic shock except - ***Increased peripheral vascular resistance*** - Septic shock is characterized by profound **vasodilation** and a subsequent **decrease in systemic vascular resistance (SVR)**, leading to hypoperfusion. - The body's compensatory mechanisms attempt to increase cardiac output rather than constrict peripheral vessels, making increased PVR an unlikely finding in established septic shock. [1] *Direct toxic endothelial injury* - **Bacterial products** (e.g., endotoxins from Gram-negative bacteria) and inflammatory mediators directly damage the **endothelium**, leading to capillary leak and microvascular dysfunction. - This endothelial damage contributes significantly to the widespread organ damage seen in sepsis. *Veno constriction* - While initial compensatory mechanisms might involve elements of vasoconstriction to maintain blood pressure, the hallmark of septic shock is widespread **vasodilation**, which includes both arterial and venous beds. - Early, fleeting venoconstriction is overshadowed by the profound venodilation and loss of venous tone that ultimately contributes to reduced preload and distributive shock. *Activation of complement* - The innate immune response in sepsis triggers the **complement cascade**, leading to the generation of potent inflammatory mediators. - Complement activation contributes to endothelial damage, leukocyte recruitment, and further amplification of the systemic inflammatory response.

Q: Treatment of choice in severe dehydration is:

Normal saline. ***Normal saline*** - **Normal saline (0.9% sodium chloride)** is an isotonic solution, making it the preferred initial intravenous fluid for rapidly correcting severe dehydration and restoring intravascular volume [1]. - Its **electrolyte composition** closely mimics the body's extracellular fluid, minimizing osmotic shifts and providing effective volume expansion [1]. *Plasma* - **Plasma** is primarily used for expanding blood volume in cases of **hemorrhage** or severe **protein deficiency**, not for simple dehydration. - It carries risks of allergic reactions and disease transmission, making it inappropriate for routine dehydration treatment. *Isolyte P* - **Isolyte P** is a hypotonic solution, typically used for maintenance fluid therapy in children, especially in situations where **sodium restriction** is desirable. - It is not suitable for rapid volume expansion in severe dehydration due to its low sodium content, which could worsen hypotonicity in an already depleted patient. *Ringer lactate* - **Ringer's lactate** is an isotonic crystalloid solution often used for fluid resuscitation, but it contains **lactate**, which is metabolized in the liver to bicarbonate. - While generally safe, in severe shock situations with impaired liver function or lactic acidosis, the metabolism of lactate can be compromised, potentially exacerbating acidosis. **Normal saline** avoids this concern as a first-line agent [2].

Q: Fluid of choice in shock is?

Ringer lactate. ***Ringer lactate*** - **Ringer's lactate** is an **isotonic crystalloid solution** that closely mimics the electrolyte composition of plasma, making it an excellent choice for initial fluid resuscitation in shock. - It replenishes intravascular volume directly and also buffers acidosis due to its lactate content, which is metabolized to bicarbonate. *Dextran* - **Dextran** is a **colloid** solution that is potent in expanding plasma volume but carries risks such as **anaphylaxis** and interference with **coagulation**, making it less suitable as the first-line fluid. - Its use is limited due to potential adverse effects on bleeding and kidney function, especially in hemorrhagic shock. *Albumin* - **Albumin** is a **colloid** that effectively increases intravascular volume by drawing fluid from the interstitial space, but costs more and has not consistently shown superior outcomes over crystalloids in severe shock. - While it can be useful in specific situations (e.g., severe sepsis with hypoalbuminemia), it's not generally recommended as the initial fluid of choice due to its high cost and lack of proven survival benefit over crystalloids. *Hydroxyethyl starch* - **Hydroxyethyl starch (HES)** is a **colloid** that was once widely used but has been associated with increased risk of **acute kidney injury** and **mortality** in critically ill patients, thus its use is largely restricted. - Due to these significant safety concerns, especially regarding renal impairment, HES is generally not recommended as the fluid of choice for shock resuscitation.

Q: Treatment of choice for anaphylactic shock is:

Adrenaline 0.5 mL of 1:1000 solution by intramuscular route. ***Adrenaline 0.5 mL of 1:1000 solution by intramuscular route*** - **Intramuscular adrenaline** (epinephrine) is the **first-line treatment** for anaphylaxis due to its rapid absorption and systemic effects [1]. - The recommended dose for adults is **0.3-0.5 mg (0.3-0.5 mL of 1:1000 solution)**, administered into the **anterolateral thigh**. *Adrenaline 1 mL of 1:10000 by intravenous route* - **Intravenous adrenaline** is generally reserved for patients in **cardiac arrest** or those who do not respond to IM injections, and should be administered cautiously due to the risk of arrhythmias and hypertension. - The concentration of **1:10,000 (0.1 mg/mL)** is typically given intravenously in much smaller, titrated doses (e.g., 0.1 mg, repeated as needed) compared to the initial IM dose. *Atropine 3 mg intravenously* - **Atropine** is an **anticholinergic agent** used primarily to treat **bradycardia** and certain poisonings, but it has no role in the management of anaphylactic shock. - It does not counteract the vasodilation, bronchoconstriction, or increased vascular permeability characteristic of anaphylaxis. *Adenosine 12 mg intravenously* - **Adenosine** is an **antiarrhythmic drug** used to treat **supraventricular tachycardia** by transiently blocking the AV node. - It would be ineffective in anaphylactic shock and could potentially worsen the patient's condition by causing further vasodilation or hypotension.

Q: How is modified shock index represented as?

HR/MAP. HR/MAP - The **modified shock index (MSI)** is calculated as the **heart rate (HR)** divided by the **mean arterial pressure (MAP)**. - This index is considered a more refined predictor of adverse outcomes than the traditional shock index, especially in identifying **hypoperfusion**. *MAP/HR* - This formula represents the inverse of the modified shock index and is **not** the correct representation. - An inverse relationship would interpret changes in **hemodynamic stability** differently and inaccurately for shock assessment. *HR/SBP* - This formula represents the **traditional shock index (SI)**, where **SBP** is **systolic blood pressure**. - While useful for initial assessment, the traditional shock index can be less sensitive in detecting subtle changes in **hemodynamics** compared to the modified shock index. *HR/DBP* - This formula uses **diastolic blood pressure (DBP)** in the denominator and is **not** a standard calculation for either the traditional or modified shock index. - Relying solely on DBP can be misleading as changes in **perfusion status** [1].

Q: Best predictor of mortality in pulmonary embolism?

Right ventricular strain. ***Right ventricular strain*** - **Right ventricular (RV) strain** is the *best predictor of mortality* in pulmonary embolism (PE) because it indicates the severity of the hemodynamic compromise caused by the increased afterload on the right heart due to the clot [1]. - RV dysfunction, visualized on **echocardiogram** or **CT angiography**, signifies an increased risk of cardiogenic shock and death [2]. *Arterial hypoxemia* - While **hypoxemia** is common in PE and reflects impaired gas exchange, it is not the *most immediate or direct predictor of mortality* compared to RV strain [1]. - The degree of hypoxemia can vary and may not always correlate directly with the *hemodynamic impact* of the PE on the heart. *Chest pain severity* - **Chest pain** is a frequent symptom of PE (often pleuritic), but its *severity does not directly correlate with the embolic burden or the risk of death*. - Many patients with large, life-threatening PEs may have *mild or atypical chest pain*. *D-dimer level* - An elevated **D-dimer** is a useful diagnostic marker to *rule out PE* when negative, but its *predictive value for mortality after a confirmed diagnosis is limited*. - A *high D-dimer* indicates fibrinolysis but does not specifically quantify the mechanical obstruction or its *hemodynamic consequences* on the heart.

Q: A patient presents with severe vomiting and confusion. ABG shows pH 7.55, HCO3 30 mEq/L, and pCO2 48 mmHg. What is the diagnosis?

Metabolic alkalosis. ### ***Metabolic alkalosis*** - The **pH of 7.55** indicates **alkalemia (alkalosis)**, as it is significantly above the normal range of 7.35-7.45 [2]. - The **elevated HCO3 (30 mEq/L)** is the primary driver of the alkalemia, pointing to a **metabolic origin**. The pCO2 of 48 mmHg indicates a compensatory respiratory acidosis [1]. ### *Metabolic acidosis* - This would be characterized by a **low pH** (acidemia) and a **low HCO3** [3]. - The patient's pH is high, and HCO3 is also high, directly contradicting metabolic acidosis. ### *Respiratory acidosis* - This would present with a **low pH** due to **elevated pCO2** [2]. - While the pCO2 is elevated, the pH is high, and the primary disturbance is the high HCO3, not the pCO2. ### *Mixed acidosis* - This indicates the presence of **both metabolic and respiratory acidosis**, resulting in a very low pH, which is not seen here. - The patient's pH is elevated, indicating an alkalosis, not an acidosis [3].

Q: Which electrolyte abnormality is expected in tumor lysis syndrome?

Hyperkalemia. ***Hyperkalemia*** - **Tumor lysis syndrome (TLS)** leads to the rapid breakdown of malignant cells, releasing their intracellular contents, including a large amount of **potassium**, into the bloodstream. [1] - This excessive release of intracellular potassium overwhelms renal excretion mechanisms, resulting in **hyperkalemia**, which can cause life-threatening cardiac arrhythmias. [1] *Hypocalcemia* - **Hypocalcemia** does occur in TLS but is not due to direct release from lysed cells. It results from the precipitation of **calcium** with the massive release of **phosphate** from the lysed cells. - The elevated phosphate levels bind to free calcium in the serum, forming **calcium phosphate crystals** that deposit in tissues, thereby lowering serum calcium levels. *Hyponatremia* - **Hyponatremia** is not a characteristic feature of tumor lysis syndrome. Sodium is primarily an extracellular ion, and its levels are not directly impacted by massive cell lysis in the same way as potassium or phosphate. - While fluid shifts or renal dysfunction in severe TLS could indirectly affect sodium, it's not a primary or expected electrolyte derangement of the syndrome itself. *Hypernatremia* - **Hypernatremia (elevated sodium)** is not expected in tumor lysis syndrome. The primary electrolyte disturbances involve intracellular components like potassium, phosphate, and uric acid, and secondary effects on calcium. - Hypernatremia would typically be associated with dehydration or impaired water balance, not the massive release of intracellular contents seen in TLS.

Question 1

What is the recommended chest compression rate (per minute) during CPR for adults?

Accepted Answer

100-120 compressions per minute

Answer

60-80 compressions per minute

Answer

40-60 compressions per minute

Answer

20-40 compressions per minute

Question 2

In hypovolemic shock, the percentage of fluid depletion is:

Accepted Answer

15-45%

Answer

70%

Answer

10-15%

Answer

43-63%

Question 3

Following pathogenetic mechanisms operate in septic shock except -

Accepted Answer

Increased peripheral vascular resistance

Answer

Direct toxic endothelial injury

Answer

Veno constriction

Answer

Activation of complement

Question 4

Treatment of choice in severe dehydration is:

Accepted Answer

Normal saline

Answer

Plasma

Answer

Isolyte P

Answer

Ringer lactate

Question 5

Fluid of choice in shock is?

Accepted Answer

Ringer lactate

Answer

Dextran

Answer

Albumin

Answer

Hydroxyethyl starch

Question 6

Treatment of choice for anaphylactic shock is:

Accepted Answer

Adrenaline 0.5 mL of 1:1000 solution by intramuscular route

Answer

Adrenaline 1 mL of 1:10000 by intravenous route

Answer

Atropine 3 mg intravenously

Answer

Adenosine 12 mg intravenously

Question 7

How is modified shock index represented as?

Accepted Answer

HR/MAP

Answer

MAP/HR

Answer

HR/SBP

Answer

HR/DBP

Question 8

Best predictor of mortality in pulmonary embolism?

Accepted Answer

Right ventricular strain

Answer

Arterial hypoxemia

Answer

Chest pain severity

Answer

D-dimer level

Question 9

A patient presents with severe vomiting and confusion. ABG shows pH 7.55, HCO3 30 mEq/L, and pCO2 48 mmHg. What is the diagnosis?

Accepted Answer

Metabolic alkalosis

Answer

Metabolic acidosis

Answer

Respiratory acidosis

Answer

Mixed acidosis

Question 10

Which electrolyte abnormality is expected in tumor lysis syndrome?

Accepted Answer

Hyperkalemia

Answer

Hypocalcemia

Answer

Hyponatremia

Answer

Hypernatremia

Critical Care — MCQs

Critical Care — MCQs

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