# A nurse is caring for a patient who is experiencing anaphylaxis after receiving a penicillin injection. The patient's blood pressure is 70/40 mmHg, heart rate is 130 bpm, and oxygen saturation is 85%. What is the nurse's priority action?

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## 문제

A nurse is caring for a patient who is experiencing anaphylaxis after receiving a penicillin injection. The patient's blood pressure is 70/40 mmHg, heart rate is 130 bpm, and oxygen saturation is 85%. What is the nurse's priority action?

## 보기

1. Administer high-flow oxygen via non-rebreather mask
2. Administer epinephrine 0.3-0.5 mg intramuscularly **✔ 정답**
3. Establish large-bore IV access for fluid resuscitation
4. Position the patient in Trendelenburg position

**정답: 2**

## 해설

Epinephrine is the first-line treatment for anaphylaxis and must be given immediately to counteract severe allergic reactions and prevent cardiovascular collapse. Other interventions like oxygen, IV access, and positioning are supportive but secondary to epinephrine administration.

## 심화 해설

Understanding the Priority: Anaphylaxis with Hemodynamic Compromise

The scenario describes a patient in decompensated, life-threatening anaphylactic shock following a penicillin injection. The vital signs—blood pressure 70/40 mmHg, heart rate 130 bpm, and oxygen saturation 85%—indicate profound vasodilation, increased vascular permeability, and bronchoconstriction, leading to circulatory collapse and hypoxemia. In this critical situation, the nurse must identify the intervention that directly targets the underlying pathophysiology to prevent rapid deterioration and death.

Why Epinephrine is the Priority Action

Administering epinephrine 0.3-0.5 mg intramuscularly into the anterolateral thigh is the definitive first-line treatment and the nurse's immediate priority. The rationale is rooted in its unique pharmacological profile, which directly counteracts the mediators of anaphylaxis. Epinephrine is a potent sympathomimetic agent with alpha- and beta-adrenergic agonist properties. Its alpha-1 effects cause vasoconstriction, which increases systemic vascular resistance, reduces mucosal edema, and elevates blood pressure. Its beta-1 effects increase cardiac inotropy and chronotropy, supporting cardiac output. Crucially, its beta-2 effects cause bronchodilation and suppress further release of inflammatory mediators like histamine and tryptase from mast cells and basophils [2].

Delaying epinephrine administration is the most common and preventable cause of fatal anaphylaxis outcomes. The literature emphasizes that epinephrine is the first-line therapy essential to prevent progression to airway compromise, circulatory collapse, and death [1]. While other interventions are supportive and important, none reverse the core multi-system pathology as rapidly and comprehensively as epinephrine. For instance, fluid resuscitation helps compensate for intravascular volume loss but does not reverse vasodilation or bronchoconstriction. Oxygen therapy addresses hypoxemia but not the underlying airway edema and shock. Therefore, the immediate administration of epinephrine is the non-negotiable step that must occur first.

Analysis of Incorrect Options

- Option 1: Administer high-flow oxygen via non-rebreather mask. Applying oxygen is a critical supportive measure for an oxygen saturation of 85%. However, it is not the priority action. Hypoxemia in anaphylaxis is primarily caused by bronchoconstriction and upper airway edema, which are most effectively relieved by epinephrine. Oxygen therapy alone cannot overcome these mechanical and inflammatory obstructions. It is a simultaneous, but secondary, intervention that can be delegated or performed immediately after the life-saving medication is given.

- Option 3: Establish large-bore IV access for fluid resuscitation. Aggressive fluid resuscitation with isotonic crystalloids is a cornerstone of managing anaphylactic shock because massive vasodilation and increased capillary permeability can shift up to 35% of intravascular volume into the interstitial space within minutes. However, obtaining IV access and starting a fluid bolus does not address the underlying vasodilation and bronchoconstriction. The priority is to administer epinephrine intramuscularly, which can be done instantly without waiting for vascular access. The IM route into the vastus lateralis muscle provides rapid systemic absorption, often faster and more reliably than attempting emergent IV access in a profoundly hypotensive patient.

- Option 4: Position the patient in Trendelenburg position. The Trendelenburg position (head down, feet elevated) was historically used for hypotension, but current evidence does not support its routine use in anaphylaxis. It can shift abdominal organs against the diaphragm, further compromising ventilation in a patient already struggling with bronchoconstriction and airway edema. The recommended position is supine with legs elevated, if tolerated, to promote venous return without respiratory compromise. This positioning is a supportive comfort and circulatory measure, not a life-saving priority over definitive pharmacological therapy.

Clinical Integration and Safety Note

The case report by Liang et al. serves as a critical reminder that while epinephrine is life-saving, it is a potent sympathomimetic that can provoke severe cardiovascular responses, such as hypertensive emergency, in susceptible patients [1]. This does not diminish its role as first-line therapy but highlights the need for careful dosing and monitoring. The recommended dose of 0.3-0.5 mg IM for adults is based on balancing maximal therapeutic effect with minimal cardiovascular risk. The nurse must administer the correct dose and be prepared to monitor for both therapeutic response and potential adverse effects, such as severe hypertension or tachycardia, especially in patients with pre-existing cardiovascular conditions. The existence of biphasic or multiphasic anaphylaxis, where symptoms can recur hours after a full clinical response, further underscores the critical importance of early and effective initial management with epinephrine to stabilize the patient and the need for a prolonged observation period .References (research sources)

- [1]Hypertensive Emergency and Brainstem Hemorrhage Temporally Associated With Intramuscular Epinephrine: A Case Report.Case reportLiang KR, Kundan R, Puno T, Tahir N. (2026) · DOI: 10.7759/cureus.109136

- [2]Acute Allergic Reactions and Severe Anaphylaxis: Underlying Causes, Management Strategies, and Future Directions.Research articleEllorin A, Agrawal DK. (2026)

## 임상 시나리오

Epinephrine Administration for Anaphylactic ShockImmediate Priority Action
Administer epinephrine 0.3-0.5 mg intramuscularly into the anterolateral thigh as the first and most critical action. This is the only intervention that directly counteracts the underlying pathophysiology of vasodilation, bronchoconstriction, and increased vascular permeability.

Epinephrine's alpha-1 effects cause vasoconstriction, elevating blood pressure and reducing edema. Its beta-2 effects cause bronchodilation and suppress further release of inflammatory mediators from mast cells.

CautionDelay in epinephrine administration is the most common factor in fatal anaphylaxis. Do not prioritize secondary measures like oxygen or IV fluids over this definitive treatment. Monitor for the potential need for a repeat dose every 5-15 minutes if symptoms persist.

## 핵심 개념

- **Anaphylaxis** — A severe, life-threatening systemic hypersensitivity reaction characterized by rapid onset of airway, breathing, or circulatory problems.
- **Epinephrine** — A sympathomimetic agent with alpha- and beta-adrenergic effects, acting as the first-line treatment for anaphylaxis by causing vasoconstriction and bronchodilation.
- **Intramuscular (IM) Injection** — A technique of injecting medication directly into a muscle; the anterolateral thigh is the preferred site for epinephrine in anaphylaxis due to rapid absorption.
- **Vasodilation** — The widening of blood vessels, which decreases systemic vascular resistance and leads to hypotension, a key feature of distributive shock in anaphylaxis.

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