Vasopressors and Inotropes: Push-dose Epinephrine, Norepinephrine, Dopamine, and Dobutamine Practice Questions
25 multiple-choice questions on Vasopressors and inotropes: push-dose epinephrine, norepinephrine, dopamine, and dobutamine 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
After induction, a 40-year-old with normal heart function becomes hypotensive at 78/40 mmHg with a heart rate of 150. Which push-dose pressor best avoids adding tachycardia?
- A. Epinephrine
- B. Phenylephrine
- C. Dopamine
- D. Isoproterenol
Show answer
Answer: B. Phenylephrine
Phenylephrine is a pure alpha-1 agonist, so it raises vascular resistance and pressure without beta-1 stimulation, and the reflex response tends to slow the heart, a reasonable choice for transient vasodilatory hypotension in a tachycardic patient with good cardiac function. Epinephrine and dopamine both have beta-1 effects that would push the rate higher. Isoproterenol is a pure beta agonist that speeds the heart and lowers diastolic pressure. In a patient with poor cardiac function or bradycardia, epinephrine is preferred instead.
On a low-dose epinephrine infusion, a patient develops a faster heart rate, a stronger pulse, a wider pulse pressure, and a lower diastolic pressure. These effects are mainly from:
- A. Beta-1 and beta-2 effects at low doses
- B. Alpha-1 effects that dominate at low doses
- C. Dopamine receptor effects on the kidneys
- D. V1 receptor effects like those of vasopressin
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Answer: A. Beta-1 and beta-2 effects at low doses
At low infusion rates epinephrine acts mostly on beta receptors: beta-1 raises heart rate and contractility (stronger pulse, higher systolic pressure), and beta-2 dilates muscle vessels, lowering diastolic pressure and widening the pulse pressure. Alpha-1 vasoconstriction becomes dominant at higher doses. Epinephrine has no meaningful action on dopamine receptors. V1 receptors are the target of vasopressin, not catecholamines.
Before starting a vasopressor in hypotensive non-cardiogenic shock, the first priority is usually to:
- A. Give a beta-blocker to slow the heart rate first
- B. Place the patient in a high Fowler position
- C. Correct hypovolemia with fluid or blood
- D. Confirm the diagnosis with a 12-lead ECG
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Answer: C. Correct hypovolemia with fluid or blood
Vasopressors squeeze an empty system and can worsen organ ischemia if the patient is still hypovolemic, so volume is restored first unless the pressure is critically low. A 12-lead is useful but should not delay resuscitation.
After a 10-mcg push-dose epinephrine bolus for transient hypotension, you should expect its effect to:
- A. Begin after 15 minutes and last for hours
- B. Last as long as a norepinephrine infusion
- C. Appear after a second dose is given
- D. Begin within a minute and fade in 5 to 10
Show answer
Answer: D. Begin within a minute and fade in 5 to 10
Push-dose epinephrine acts within about a minute and wears off in roughly 5 to 10 minutes, which is why it is a bridge: repeat doses are titrated every 2 to 5 minutes while the cause is treated and an infusion is prepared if hypotension persists. It does not have a delayed onset or a duration of hours. It cannot match a continuous infusion, which maintains a steady level. Each dose works on its own; a second dose is needed only if the first effect fades.
The usual adult dose of push-dose epinephrine at 10 mcg/mL is:
- A. 10 mL (100 mcg) every 3 to 5 minutes as needed
- B. 0.5 to 2 mL (5 to 20 mcg) every 2 to 5 minutes
- C. 0.1 mL (1 mcg) once, then a continuous infusion
- D. 1 mL of 1 mg/mL (1 mg) every 3 to 5 minutes
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Answer: B. 0.5 to 2 mL (5 to 20 mcg) every 2 to 5 minutes
Push-dose epinephrine is given as 5 to 20 mcg boluses every 2 to 5 minutes, titrated to blood pressure. A 1-mg dose is the cardiac arrest dose and in a patient with a pulse can cause severe hypertension, ischemia, and dysrhythmias.
The most dangerous error associated with push-dose vasopressors in EMS is:
- A. Mixing or dosing errors causing a tenfold overdose
- B. Allergic reaction to the sulfite preservative in the vial
- C. Tachyphylaxis that makes later doses fail
- D. Hyperglycemia from repeated epinephrine doses
Show answer
Answer: A. Mixing or dosing errors causing a tenfold overdose
Push-dose pressors are mixed in the field from concentrated vials, so wrong-concentration and wrong-volume errors can deliver massive overdoses. Clear labeling, standard mixing, and a second-person check reduce the risk. Sulfite allergy, tachyphylaxis, and a modest rise in glucose are uncommon or minor next to the harm of a tenfold overdose, which can cause severe hypertension, dysrhythmias, and myocardial ischemia.
A 64-year-old intubated patient's BP falls to 70/40 mmHg after induction. He has received 1 L of fluid. While you prepare an infusion, the best bridge is:
- A. Atropine, 1 mg IV repeated every 3 minutes
- B. Epinephrine 1 mg IV from the arrest box
- C. Push-dose epinephrine, 10 to 20 mcg IV
- D. Vasopressin, 40 units IV push
Show answer
Answer: C. Push-dose epinephrine, 10 to 20 mcg IV
Push-dose epinephrine quickly supports pressure during transient post-intubation hypotension while fluids and an infusion are set up. Atropine treats symptomatic bradycardia and does not address vasodilation or low output. A 1-mg epinephrine push is a cardiac arrest dose, 50 to 100 times the push-dose amount, and would cause severe hypertension and dysrhythmias in a patient with a pulse; 40 units of vasopressin is likewise a former arrest dose, not a bridging dose.
A septic patient on norepinephrine has a MAP of 88 mmHg with warm hands and good mentation. The ordered target is 65 mmHg. You should:
- A. Increase it to keep the MAP above 85 mmHg
- B. Stop it abruptly now that she is better
- C. Leave it, since a high MAP is harmless
- D. Wean the infusion down toward the target
Show answer
Answer: D. Wean the infusion down toward the target
Vasopressors are titrated to the lowest dose that meets the target, because excess vasoconstriction raises the risk of dysrhythmias and of gut, kidney, and digit ischemia; a MAP well above 65 with good perfusion means the dose can come down in small steps. Raising it further adds risk with no benefit for most patients. Stopping abruptly can drop the pressure sharply because the drug acts for only minutes. A higher MAP is not harmless when it is bought with more drug.
A septic patient on norepinephrine at 0.3 mcg/kg/min still has a MAP of 58 mmHg. The Surviving Sepsis Campaign suggests adding:
- A. Dopamine
- B. Phenylephrine
- C. Vasopressin
- D. Dobutamine
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Answer: C. Vasopressin
For adults with septic shock on norepinephrine with inadequate MAP, the 2021 Surviving Sepsis guideline suggests adding vasopressin (usually once norepinephrine is in the 0.25 to 0.5 mcg/kg/min range) rather than escalating norepinephrine alone; epinephrine is the next option. Dopamine causes more dysrhythmias than norepinephrine and is no longer favored. Phenylephrine adds pure alpha effect and can lower cardiac output. Dobutamine is an inotrope for low output and can drop the pressure further.
Compared with norepinephrine, dopamine used for shock is associated with:
- A. Better kidney protection
- B. Lower doses for the same effect
- C. Less extravasation injury
- D. More tachydysrhythmias
Show answer
Answer: D. More tachydysrhythmias
The SOAP II trial found more dysrhythmias with dopamine and higher mortality in the cardiogenic subgroup. The belief that low-dose dopamine protects the kidneys has been disproved.
A patient on high-dose norepinephrine with a good MAP develops cold, dusky fingertips on both hands. This is most likely:
- A. Ischemia from intense vasoconstriction
- B. Extravasation at the IV insertion site
- C. A sign that the dose is too low
- D. Hypothermia from the cold IV fluids
Show answer
Answer: A. Ischemia from intense vasoconstriction
Symmetric dusky, cold fingertips on a high vasopressor dose reflect drug-induced vasoconstriction of the digits, a known complication; it calls for the lowest effective dose, addressing volume, and reporting the finding. Extravasation causes blanching and swelling around one IV site, not both hands. A dose that is too low would show as a low MAP. Cold fluids cool the core gradually and do not cause isolated dusky fingertips with a good pressure.
A septic patient's BP is 58/30 mmHg (MAP 39) and fluids have just been started. The best approach to the vasopressor is to:
- A. Wait until the full 30 mL/kg has been given
- B. Start it now while the fluids continue
- C. Hold it until a second liter fails
- D. Avoid it because of the risk of ischemia
Show answer
Answer: B. Start it now while the fluids continue
Fluid normally comes first, but a MAP this low threatens the brain and heart within minutes, so a vasopressor (norepinephrine) is started at once while fluids run, rather than waiting for the full volume; it can be weaned once volume is restored. Waiting for 30 mL/kg or a second liter leaves dangerous hypotension untreated for too long. The risk of ischemia from a short course of a pressor is far smaller than the risk of persistent profound hypotension.
Why can dobutamine worsen ischemia in a patient in cardiogenic shock from an acute MI?
- A. It raises heart rate and oxygen demand
- B. It constricts the coronary arteries
- C. It lowers the blood hemoglobin level
- D. It slows conduction through the AV node
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Answer: A. It raises heart rate and oxygen demand
Dobutamine's beta-1 effect increases contractility and heart rate, and both raise myocardial oxygen demand, which can extend ischemia in a heart whose supply is already limited; it can also provoke dysrhythmias. It does not constrict the coronaries. It has no effect on hemoglobin. It speeds rather than slows AV conduction.
A patient on a dobutamine infusion becomes more hypotensive. The most likely reason is:
- A. Alpha-1 constriction that reduces the cardiac output
- B. Beta-2 vasodilation that lowers vascular resistance
- C. Dopaminergic dilation of the mesenteric arteries
- D. Direct suppression of the SA node by the drug
Show answer
Answer: B. Beta-2 vasodilation that lowers vascular resistance
Dobutamine's beta-2 activity dilates peripheral vessels, which can drop the pressure, especially in a patient who is volume-depleted. Its beta-1 effect raises, not suppresses, the heart rate.
A septic patient started on an epinephrine infusion has a rising lactate even though her skin is warmer and her mentation is better. A likely reason is that:
- A. Her perfusion is getting steadily worse
- B. The lactate meter reads high on pressors
- C. Epinephrine blocks lactate removal by the lungs
- D. Epinephrine itself raises lactate production
Show answer
Answer: D. Epinephrine itself raises lactate production
Epinephrine's beta-2 effect speeds glycolysis in muscle and other tissues, raising lactate even when perfusion is adequate, so a rising lactate on epinephrine must be read alongside clinical signs, which here are improving. Worsening perfusion would show as cooler skin and falling mentation. Pressors do not make the meter read falsely high. The lungs do not clear lactate; the liver and kidneys do.
Norepinephrine must run through a peripheral IV during a long transfer. The safest site is:
- A. A small vein on the back of the hand
- B. A vein over the wrist joint
- C. A large antecubital or upper-arm vein
- D. The same IV line used for the blood unit
Show answer
Answer: C. A large antecubital or upper-arm vein
Peripheral vasopressors are acceptably safe for hours when they run through a well-functioning catheter (20 gauge or larger) in a large proximal vein, such as the antecubital fossa or upper arm, with the site checked often; extravasation there is less likely and is noticed early. Small hand veins and veins over a joint are more likely to infiltrate and kink. A pressor needs its own line so that boluses of other products do not flush drug into the patient.
The antidote infiltrated into the tissue after extravasation of norepinephrine or dopamine is:
- A. Naloxone
- B. Atropine
- C. Phentolamine
- D. Hyaluronidase
Show answer
Answer: C. Phentolamine
Phentolamine, an alpha-blocker, reverses the local vasoconstriction and limits necrosis when infiltrated into the area. Atropine blocks muscarinic receptors and has no effect on alpha-mediated vasoconstriction.
Vasopressin is useful as an adjunct in septic shock because it:
- A. Acts on V1 receptors that work in acidosis
- B. Strongly stimulates beta-1 receptors in the heart
- C. Increases the heart rate through the SA node
- D. Works by blocking histamine at the capillaries
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Answer: A. Acts on V1 receptors that work in acidosis
Vasopressin constricts vessels through V1 receptors rather than adrenergic receptors, so it can still work when acidosis blunts the response to catecholamines; septic patients also have a relative vasopressin deficiency. It has no beta-1 effect and does not raise heart rate through the SA node. It does not block histamine.
A 70-year-old has HR 48 and BP 74/40 mmHg, and your partner suggests phenylephrine. Phenylephrine is a poor choice for this patient because it:
- A. Raises the heart rate to dangerous levels
- B. Causes reflex slowing of the heart rate
- C. Mainly increases cardiac contractility
- D. Blocks the AV node like a beta-blocker
Show answer
Answer: B. Causes reflex slowing of the heart rate
Phenylephrine is a pure alpha-1 agonist, and the rise in pressure triggers a baroreceptor reflex that further slows the heart. It has no beta-1 effect, so it does not increase contractility or block the AV node directly; the slowing is reflex. An agent with beta-1 activity, such as norepinephrine or epinephrine, is better in bradycardic shock.
A norepinephrine infusion is stopped, and your partner is about to flush the same IV line rapidly with saline. The main danger is:
- A. Precipitation of the drug in the line
- B. Clotting of the catheter from the flush
- C. A drop in pressure from the cold saline
- D. A bolus of the drug left in the tubing
Show answer
Answer: D. A bolus of the drug left in the tubing
The tubing and catheter still hold vasopressor, so a rapid flush pushes it in as a bolus, causing a sudden spike in pressure and possible dysrhythmia; aspirate or change the line, or flush slowly per protocol. Norepinephrine does not precipitate with saline. A flush helps keep a catheter open rather than clotting it. A small volume of room-temperature saline does not lower blood pressure.
Right after you move a patient on a norepinephrine infusion to your stretcher, her MAP falls from 70 to 48 mmHg. The first thing to check is:
- A. Whether the pressor dose needs doubling
- B. That the infusion is still running in
- C. Whether she has had a vasovagal faint
- D. Whether the BP cuff is too small for her
Show answer
Answer: B. That the infusion is still running in
A patient who depends on a short-acting pressor drops within minutes if the line kinks, disconnects, infiltrates, or the pump stops, and moves are when this happens, so trace the line from bag to vein first. Doubling the dose before confirming that the drug is reaching her risks a dangerous surge once the line is fixed, and a vasovagal reaction is far less likely than an interrupted pressor at the moment of a move. A cuff that is too small reads falsely high, not low.
During a transfer, a patient in septic shock still needs rising doses of norepinephrine after adequate fluid. The sending physician orders IV hydrocortisone. Its main purpose is to:
- A. Help the body respond to vasopressors
- B. Treat the underlying infection directly
- C. Slow the heart rate to improve filling
- D. Prevent an allergic reaction to the infusion
Show answer
Answer: A. Help the body respond to vasopressors
Sepsis can cause a relative shortfall of cortisol, and Surviving Sepsis Campaign guidance suggests IV hydrocortisone for adults who need ongoing vasopressor support. It helps restore vascular tone and responsiveness to vasopressors, often allowing the dose to be reduced. It does not kill bacteria; antibiotics and source control do.
A 5-year-old in fluid-refractory septic shock has only an IO line. The vasoactive infusion should be:
- A. Held until a central line is placed
- B. Given as push doses every 5 minutes instead
- C. Replaced by more 20 mL/kg boluses
- D. Started through the IO without delay
Show answer
Answer: D. Started through the IO without delay
The pediatric Surviving Sepsis guideline suggests starting epinephrine or norepinephrine through peripheral or intraosseous access rather than delaying it until central access is placed. Waiting for a central line delays treatment of shock. Push doses are a bridge, not a substitute for an infusion. Continuing boluses after fluid-refractory shock risks overload without fixing the vasodilation or low output.
During a vasopressor infusion, blood pressure should be rechecked at least every:
- A. 15 to 20 minutes en route
- B. 30 minutes after each change
- C. 2 to 5 minutes until stable
- D. Hour, unless symptoms appear
Show answer
Answer: C. 2 to 5 minutes until stable
Pressor effects begin within a minute or two and change quickly with each rate adjustment, so frequent measurements are needed to titrate safely. A 15-minute interval is appropriate for stable patients, not those on infusions.
A 6-year-old in septic shock remains hypotensive after 40 mL/kg of fluid with cool extremities. Pediatric sepsis guidelines suggest which vasoactive agent?
- A. Epinephrine or norepinephrine
- B. Dopamine as the single first agent
- C. Dobutamine or milrinone
- D. Vasopressin or labetalol
Show answer
Answer: A. Epinephrine or norepinephrine
The 2020 pediatric Surviving Sepsis guidelines suggest epinephrine or norepinephrine rather than dopamine for fluid-refractory septic shock in children. Dopamine was the traditional first choice but was associated with worse outcomes.
More Management and Resuscitation of the Critical Patient practice questions
- Recognizing the critical patient: sick vs not sick, early warning signs, and compensation (25)
- Pathophysiology of poor perfusion: oxygen delivery, cellular metabolism, and lactate (25)
- Types of shock: hypovolemic, distributive, cardiogenic, and obstructive (25)
- Fluid resuscitation and blood products in the critical patient (25)
- Vasopressors and inotropes: push-dose epinephrine, norepinephrine, dopamine, and dobutamine
- Critical airway decisions and the physiologically difficult airway (25)
- Multisystem trauma and team-based resuscitation: priorities, leadership, and communication (25)
- Ongoing monitoring, reassessment, and transport of the critical patient (25)
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