Pathophysiology of Poor Perfusion: Oxygen Delivery, Cellular Metabolism, and Lactate Practice Questions

25 multiple-choice questions on Pathophysiology of poor perfusion: oxygen delivery, cellular metabolism, and lactate for paramedic and EMT students, from Chapter 41 (Management and Resuscitation of the Critical Patient). Read each question, pick your answer, then tap Show answer to check it and read the explanation.

25 practice questions

1. A 70-year-old in cardiogenic shock has an SpO2 of 97%, a normal hemoglobin, and a very low cardiac output. The tissue hypoxia he has is best described as:

   1. A. Hypoxemic hypoxia from a low PaO2
   2. B. Anemic hypoxia from too little hemoglobin
   3. C. Stagnant hypoxia from low blood flow
   4. D. Histotoxic hypoxia from blocked cell use
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   Answer: C. Stagnant hypoxia from low blood flow

   Tissue hypoxia has four broad mechanisms. With a normal saturation and hemoglobin, the blood leaving the lungs carries plenty of oxygen, but a failing pump moves too little of it, so the problem is stagnant (circulatory) hypoxia, the basic mechanism of shock. Hypoxemic hypoxia means low arterial oxygen from a lung or ventilation problem, which an SpO2 of 97% argues against. Anemic hypoxia means too little hemoglobin to carry oxygen, but his hemoglobin is normal. Histotoxic hypoxia means cells cannot use delivered oxygen, as in cyanide poisoning.

2. A 58-year-old in septic shock has a temperature of 40 °C (104 °F), is shivering hard, and is agitated. Controlling the fever, shivering, and agitation helps her mainly by:

   1. A. Raising the oxygen content of her blood
   2. B. Increasing the preload to her right heart
   3. C. Making hemoglobin hold oxygen more tightly
   4. D. Lowering her tissues' demand for oxygen
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   Answer: D. Lowering her tissues' demand for oxygen

   Shock is a mismatch between oxygen delivery and demand. Fever raises metabolic rate by roughly 10% per degree Celsius, and vigorous shivering and agitation can multiply muscle oxygen use, so reducing them lowers consumption and eases the imbalance while delivery is being restored. These measures do not change arterial oxygen content, which depends on hemoglobin and saturation. They do not raise preload; that requires volume. Cooling does shift the curve slightly toward tighter binding, but that would hinder, not help, oxygen release to the tissues.

3. Why does prolonged hypoperfusion of the gut in shock contribute to organ failure days later, even after the blood pressure is restored?

   1. A. Damaged gut lining lets bacteria into the blood
   2. B. The gut stops absorbing the fluid given by IV
   3. C. Bowel ischemia causes immediate severe bleeding
   4. D. The liver stores the excess lactate permanently
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   Answer: A. Damaged gut lining lets bacteria into the blood

   Blood is diverted away from the gut early in shock, and the intestinal lining is very sensitive to ischemia. When it is damaged, bacteria and their toxins can cross into the portal and systemic circulation and add to the inflammatory response that drives multiple organ dysfunction syndrome after resuscitation. This is one reason early, complete restoration of perfusion matters. The gut is not the route for IV fluid, so its absorption is irrelevant. Ischemic bowel can bleed, but massive immediate hemorrhage is not the usual consequence. The liver clears lactate; it does not store it.

4. A 45-year-old with no history of diabetes has a glucose of 228 mg/dL early in hemorrhagic shock. The most likely cause is:

   1. A. Undiagnosed type 1 diabetes in ketoacidosis
   2. B. Dextrose absorbed from the normal saline infusion
   3. C. Stress hormones releasing glucose from the liver
   4. D. Adrenal failure caused by the acute blood loss
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   Answer: C. Stress hormones releasing glucose from the liver

   Early in shock, epinephrine, norepinephrine, cortisol, and glucagon break down glycogen and drive gluconeogenesis, while catecholamines suppress insulin release, so the glucose rises (stress hyperglycemia). It is common, needs no treatment in the field, and signals the severity of the stress response. New type 1 diabetes in ketoacidosis would come with days of thirst, urination, and ketotic breathing, not an acute bleed. Normal saline contains no dextrose. Adrenal failure lowers glucose rather than raising it, and blood loss does not cause it.

5. A patient's stroke volume falls from 70 to 40 mL while her heart rate rises from 80 to 120/min. Her cardiac output has:

   1. A. Fallen from 5.6 to 4.8 L/min
   2. B. Risen from 5.6 to 6.4 L/min
   3. C. Stayed at 5.6 L/min
   4. D. Fallen from 5.6 to 2.4 L/min
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   Answer: A. Fallen from 5.6 to 4.8 L/min

   Cardiac output is heart rate × stroke volume: 80 × 70 mL = 5.6 L/min before and 120 × 40 mL = 4.8 L/min after. Tachycardia partly offsets a falling stroke volume, but it cannot fully restore output, which is why tachycardia alone does not mean perfusion is adequate.

6. A trauma patient's point-of-care blood gas shows a base deficit of 10 mmol/L, although his BP is 112/70 mmHg. This finding most likely means:

   1. A. A breathing problem that is retaining CO2
   2. B. Hypoperfusion causing a metabolic acidosis
   3. C. A lab error, since his blood pressure is normal
   4. D. Mild dehydration that oral fluid will correct
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   Answer: B. Hypoperfusion causing a metabolic acidosis

   Base deficit measures how much base is missing from the blood because of metabolic acid, mostly lactate from poor perfusion. A deficit above about 6 mmol/L signals moderate to severe shock and predicts transfusion need and death, even when the blood pressure is still normal. Respiratory acidosis from CO2 retention does not create a base deficit.

7. A 74-year-old in cardiogenic shock with crackles receives a 1-L fluid bolus and becomes more hypoxic, with no rise in blood pressure. This is best explained by:

   1. A. Excess sympathetic tone from the cold IV fluid
   2. B. A normal Frank-Starling response to more preload
   3. C. Fluid shifting into the cells instead of the vascular space
   4. D. A failing ventricle on the flat part of the Starling curve
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   Answer: D. A failing ventricle on the flat part of the Starling curve

   A failing ventricle cannot convert extra stretch into more stroke volume, so added preload only raises filling pressures and pushes fluid into the lungs. A normal heart would respond to the same volume with a stronger contraction.

8. When oxygen delivery falls, the first way the tissues maintain oxygen consumption is by:

   1. A. Switching immediately to anaerobic metabolism
   2. B. Lowering the metabolic rate of every organ at once
   3. C. Releasing oxygen stored inside the skeletal muscle cells
   4. D. Extracting a larger fraction of the oxygen delivered
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   Answer: D. Extracting a larger fraction of the oxygen delivered

   Tissues normally extract about 25% of delivered oxygen and can raise extraction substantially when delivery falls. Only when extraction is maxed out does consumption become supply-dependent and anaerobic metabolism begin.

9. Ten minutes after bleeding is controlled and a unit of blood given, a patient's lactate is still 6 mmol/L, but his mentation, pulse, and skin have improved. The best interpretation is:

   1. A. Resuscitation has failed and must be escalated
   2. B. Lactate lags, so trend it over the next hours
   3. C. His improving signs are falsely reassuring
   4. D. The lactate meter is malfunctioning
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   Answer: B. Lactate lags, so trend it over the next hours

   Lactate falls over hours, not minutes, as the liver and kidneys clear what accumulated during hypoperfusion, so it is measured as a trend (for example, every 2 hours) alongside clinical signs. Better mentation, a slower and stronger pulse, and warmer skin are real evidence that perfusion is improving. An unchanged early value does not mean resuscitation has failed; a lactate that keeps rising or fails to fall over hours would. Dismissing clear clinical improvement because of one early number ignores the best bedside evidence. Nothing suggests a meter fault.

10. A serum lactate above which level is generally considered elevated and a marker of possible hypoperfusion?

    1. A. 0.5 mmol/L
    2. B. 1 mmol/L
    3. C. 2 mmol/L
    4. D. 10 mmol/L
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    Answer: C. 2 mmol/L

    A lactate above 2 mmol/L is abnormal, and 4 mmol/L or more marks high-risk hypoperfusion and septic shock criteria. Waiting for a value like 10 mmol/L would miss most patients who benefit from early resuscitation.

11. A septic patient's lactate falls from 5.2 to 2.8 mmol/L after resuscitation. This trend most likely indicates:

    1. A. Improving tissue perfusion
    2. B. Worsening liver failure
    3. C. A laboratory error
    4. D. Ongoing occult bleeding into the gut
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    Answer: A. Improving tissue perfusion

    Lactate clearance after fluids and vasopressors suggests that oxygen delivery is better matching demand, and it is associated with improved survival. A worsening liver would reduce lactate clearance, causing levels to rise, not fall.

12. Which condition can raise lactate without any shock state being present?

    1. A. A simple vasovagal faint
    2. B. A generalized seizure
    3. C. Mild seasonal allergies
    4. D. A stable sinus rhythm
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    Answer: B. A generalized seizure

    Intense muscle activity during a seizure, as well as drugs such as metformin, can raise lactate without systemic hypoperfusion. A transient faint resolves in seconds and does not produce a significant lactate rise.

13. The metabolic acidosis of shock causes the respiratory rate to increase because:

    1. A. Lactate directly stimulates the stretch receptors
    2. B. Acidosis lowers the oxygen content of the alveoli
    3. C. The body exhales CO2 to buffer the acid load
    4. D. The diaphragm needs more ATP when the pH falls
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    Answer: C. The body exhales CO2 to buffer the acid load

    Chemoreceptors sense the falling pH, and increased ventilation removes CO2 to shift the bicarbonate buffer and limit the drop in pH. Lactate does not act on pulmonary stretch receptors.

14. A 68-year-old man with sepsis has a BP of 118/70 mmHg and a lactate of 4.6 mmol/L. The best interpretation is that he:

    1. A. Has occult hypoperfusion needing resuscitation
    2. B. Is stable because his blood pressure is normal
    3. C. Has a lab error, since lactate rises only with hypotension
    4. D. Needs only oral fluids and outpatient follow-up
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    Answer: A. Has occult hypoperfusion needing resuscitation

    A lactate of 4 mmol/L or more signals tissue hypoperfusion even with a normal blood pressure (cryptic shock), carries high mortality, and calls for 30 mL/kg of crystalloid and close monitoring. Lactate rises before hypotension appears, so a normal pressure does not make the value an error.

15. Severe acidosis worsens shock mainly by:

    1. A. Making the blood vessels constrict more effectively
    2. B. Increasing the oxygen affinity of hemoglobin in the tissues
    3. C. Raising the blood pressure by retaining more sodium
    4. D. Depressing contractility and the response to pressors
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    Answer: D. Depressing contractility and the response to pressors

    A pH below about 7.2 depresses contractility and blunts the effect of endogenous and administered vasopressors. Acidosis actually shifts the oxyhemoglobin curve right, releasing more oxygen, so increased affinity is incorrect.

16. The 'cellular' phase of shock, when cell membranes break down and lysosomal enzymes are released, leads to:

    1. A. A return to compensated shock
    2. B. Multiple organ dysfunction syndrome
    3. C. Rebound vasoconstriction and hypertension
    4. D. Reduced capillary permeability
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    Answer: B. Multiple organ dysfunction syndrome

    Cell injury releases enzymes and inflammatory mediators that damage remote organs, producing multiple organ dysfunction syndrome even after the original insult is treated. Cell breakdown marks progression toward irreversible shock, not a return to the compensated stage, and the mediators released cause vasodilation and hypotension rather than rebound vasoconstriction. Capillary permeability increases, not decreases, causing edema and further volume loss.

17. In the microcirculation, the systemic inflammatory response of shock causes:

    1. A. Tighter endothelial junctions that preserve plasma volume
    2. B. A shift of interstitial fluid back into the capillaries
    3. C. Capillary leak and fluid loss into the interstitial space
    4. D. Increased red cell flexibility that improves flow
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    Answer: C. Capillary leak and fluid loss into the interstitial space

    Inflammatory mediators disrupt the endothelium, so plasma leaks out of the capillaries, worsening hypovolemia and causing tissue edema. This is why some patients need large fluid volumes yet still become edematous.

18. Which organ is usually the first to show reduced perfusion as the body diverts blood in shock?

    1. A. The brain
    2. B. The heart
    3. C. The lungs
    4. D. The skin
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    Answer: D. The skin

    The sympathetic response shunts blood away from the skin, gut, and kidneys first, which is why pale, cool skin is an early sign. Flow to the brain and heart is preserved as long as possible.

19. A patient in shock has an SpO2 of 98% and ETCO2 of 19 mmHg with a normal respiratory rate. The low ETCO2 most likely reflects:

    1. A. Reduced pulmonary blood flow from low cardiac output
    2. B. Excellent ventilation with high oxygen levels in tissue
    3. C. A malfunction because SpO2 and ETCO2 should match
    4. D. Hypoventilation that is causing CO2 retention
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    Answer: A. Reduced pulmonary blood flow from low cardiac output

    ETCO2 depends on CO2 production, delivery to the lungs, and ventilation; with normal ventilation, a low value signals poor pulmonary blood flow. Hypoventilation raises ETCO2, so it cannot explain a low reading.

20. Mixed venous or central venous oxygen saturation falls in hypovolemic shock because:

    1. A. Less oxygen is bound to hemoglobin in the arterial blood
    2. B. Shunting sends venous blood past the tissue beds
    3. C. Tissues extract more oxygen from slowly flowing blood
    4. D. Tissues consume less oxygen as flow falls
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    Answer: C. Tissues extract more oxygen from slowly flowing blood

    With low flow, each unit of blood spends longer in the tissues and gives up more oxygen, so the returning venous blood is less saturated. Arterial saturation is usually normal in hemorrhage, and tissue oxygen consumption is maintained, not reduced, early in shock. Shunting of blood past the tissue beds is a septic mechanism that tends to raise venous saturation, which is why in septic shock impaired extraction can leave venous saturation normal or high.

21. Why is a normal or even high central venous oxygen saturation possible in septic shock despite tissue hypoxia?

    1. A. Septic patients have a higher hemoglobin level
    2. B. Fever increases the amount of oxygen dissolved in plasma
    3. C. The heart rate is too slow to deliver oxygen
    4. D. Cells cannot use oxygen, and blood bypasses them
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    Answer: D. Cells cannot use oxygen, and blood bypasses them

    In sepsis, mitochondrial dysfunction and microcirculatory shunting prevent tissues from extracting oxygen, so venous blood returns well saturated. A high value therefore does not prove adequate perfusion.

22. A 70-year-old woman with sepsis has a capillary blood glucose of 52 mg/dL. The best explanation for hypoglycemia in shock is:

    1. A. Depleted glycogen and impaired hepatic glucose output
    2. B. Excess insulin secretion that is triggered by catecholamines
    3. C. Glucose loss through the lungs during tachypnea
    4. D. Increased glucose uptake by the brain alone
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    Answer: A. Depleted glycogen and impaired hepatic glucose output

    Prolonged shock and sepsis deplete liver glycogen, impair gluconeogenesis, and increase glucose use by inflamed tissues, so glucose can fall; hypoglycemia in sepsis is a marker of severe illness and should be treated. Catecholamines suppress, rather than stimulate, insulin secretion. The lungs do not lose glucose, and the brain's glucose use does not rise enough on its own to explain this value.

23. A 64-year-old in prolonged septic shock has a pH of 7.08 and develops peaked T waves on the monitor. Which electrolyte disturbance is most expected?

    1. A. Hypokalemia
    2. B. Hyperkalemia
    3. C. Hypernatremia
    4. D. Hypercalcemia
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    Answer: B. Hyperkalemia

    Failing sodium-potassium pumps and acidosis drive potassium out of cells, raising serum potassium and risking dysrhythmias. Hypokalemia would be expected with alkalosis, not acidosis.

24. A 62-year-old with COPD and a baseline SpO2 of 89% develops septic shock. Which change would most improve his oxygen delivery if he is hypotensive with low cardiac output?

    1. A. Raising his SpO2 from 92% to 100% with more oxygen
    2. B. Restoring cardiac output with fluid and vasopressors
    3. C. Increasing his PaO2 to 300 mmHg on high-flow oxygen
    4. D. Slowing his breathing with a sedative to save energy
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    Answer: B. Restoring cardiac output with fluid and vasopressors

    Once hemoglobin is reasonably saturated, raising PaO2 adds little oxygen content, because dissolved oxygen is minimal; restoring flow improves delivery far more. Sedating a patient who is compensating for acidosis can precipitate collapse.

25. Reperfusion after prolonged shock can worsen injury because:

    1. A. Returning blood carries too much glucose into the injured tissues
    2. B. Returning blood is strongly alkaline and lowers the ionized calcium level
    3. C. The sudden rise in blood pressure ruptures the reperfused capillaries
    4. D. Restored flow carries acid, potassium, and free radicals to the heart
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    Answer: D. Restored flow carries acid, potassium, and free radicals to the heart

    When perfusion returns, metabolites accumulated in ischemic tissue, including acid, potassium, and oxygen free radicals, enter the central circulation and can cause dysrhythmias and further organ injury. This is the basis of reperfusion injury after crush or prolonged shock. The washout is acidic rather than alkaline, and the harm comes from these metabolites and the resulting dysrhythmias, not from blood pressure rupturing the reperfused capillaries.