8.2 Core Workflows and Decision Points

Sepsis and Septic Shock: The Hour-1 Bundle

Sepsis is life-threatening organ dysfunction caused by a dysregulated host response to infection; septic shock is sepsis with persisting hypotension requiring vasopressors to keep mean arterial pressure (MAP) ≥65 mmHg plus a lactate >2 mmol/L despite adequate fluids. The CEN tests the Surviving Sepsis Campaign Hour-1 bundle, which collapsed the old 3-hour and 6-hour bundles into actions begun within the first hour of recognition.

The lactate is both a severity marker and a resuscitation gauge: a level ≥4 mmol/L marks high mortality, and a repeat value that fails to clear signals ongoing tissue hypoperfusion. Antibiotics should not be delayed—each hour of delay in septic shock raises mortality—but cultures are drawn first when it does not slow antibiotic delivery.

Recognizing sepsis at the bedside

Recognition triggers the bundle, so the CEN expects you to spot the screening criteria. The bedside qSOFA score flags risk with any two of: respiratory rate ≥22, systolic blood pressure ≤100 mmHg, and altered mentation. Older SIRS criteria—temperature >38°C or <36°C, heart rate >90, respiratory rate >20, and abnormal white count—remain a common triage screen. Neither score diagnoses sepsis by itself; sepsis is suspected infection plus organ dysfunction.

The most important early cue on the exam is altered mental status in a febrile or hypotensive patient, which moves the case from "infection" to "possible sepsis" and starts the clock on the Hour-1 actions.

Fluids, Vasopressors, and Source Control

The 30 mL/kg crystalloid bolus (balanced crystalloid or normal saline) is given for sepsis-induced hypotension or lactate ≥4 mmol/L. In the 2021 guidelines this recommendation was downgraded from strong to weak, so dynamic measures of fluid responsiveness (passive leg raise, pulse-pressure variation) increasingly guide additional boluses—but the 30 mL/kg starting point remains the tested default.

When blood pressure does not respond, norepinephrine is the first-line vasopressor, titrated to MAP ≥65 mmHg. Guidelines now support starting norepinephrine through a peripheral line rather than delaying while central access is obtained, because earlier MAP restoration improves outcomes. Vasopressin is added as the second agent to reduce norepinephrine dose, and epinephrine is third-line. Source control—draining an abscess, removing an infected line, debriding necrotic tissue—must happen promptly; antibiotics alone cannot cure an undrained source.

The ED nursing sequence

1. Recognize: fever or hypothermia, tachycardia, hypotension, altered mentation, mottling.
2. Draw lactate and blood cultures; obtain IV access.
3. Hang broad-spectrum antibiotics per protocol.
4. Bolus 30 mL/kg crystalloid; reassess perfusion.
5. Start norepinephrine if MAP stays <65; remeasure lactate.
6. Pursue source control and ICU disposition.

Anaphylaxis: Epinephrine First

Anaphylaxis is a rapid, IgE-mediated hypersensitivity reaction with multisystem involvement—urticaria/angioedema, bronchospasm and stridor, hypotension, and GI symptoms—often within minutes of an allergen. The single most important and most-tested fact: first-line treatment is intramuscular epinephrine, given before antihistamines or steroids.

• Dose: epinephrine 0.3–0.5 mg of the 1:1000 (1 mg/mL) concentration IM, injected into the anterolateral (mid-outer) thigh for fastest absorption.
• Repeat every 5–15 minutes as needed; most deaths follow delayed epinephrine.
• Position the hypotensive patient supine with legs elevated; sudden upright posture can cause empty-ventricle arrest.
• Adjuncts: IV fluids for hypotension, albuterol for bronchospasm, H1 (diphenhydramine) and H2 (famotidine) antihistamines, and corticosteroids—all secondary and intended partly to blunt a biphasic reaction that can recur 1–72 hours later.

A classic distractor pairs an antihistamine or steroid as the “first” drug, or lists the 1:10,000 cardiac-arrest concentration—that dilution is for IV push in arrest, not IM anaphylaxis. Patients who receive epinephrine are observed for the biphasic risk and discharged with an epinephrine auto-injector and allergy referral.

Refractory Cases and Recognition Cues

Most anaphylaxis responds to one or two IM epinephrine doses, but refractory anaphylaxis—persistent hypotension or airway compromise after repeat IM dosing—calls for escalation: an epinephrine infusion, aggressive crystalloid (1–2 L isotonic fluid for distributive shock), and early airway management because laryngeal edema can close the airway in minutes. Patients on beta-blockers may respond poorly to epinephrine; glucagon is the tested adjunct because it bypasses the beta-receptor to support heart rate and contractility.

Recognition is half the question. Anaphylaxis is likely when there is acute onset with skin or mucosal involvement plus either respiratory compromise or hypotension, or when two or more body systems are involved after a known allergen. The CEN frequently disguises it: a patient "feels a lump in the throat" with new hoarseness (early laryngeal edema), or becomes hypotensive and flushed during an antibiotic or contrast infusion. Treat on clinical suspicion—do not wait for hives, since up to 20% of anaphylaxis lacks skin findings.

Sepsis-versus-anaphylaxis distinction

Both produce distributive shock with warm, vasodilated skin and hypotension, but the cues differ. Anaphylaxis is sudden, allergen-linked, and accompanied by urticaria, wheeze, or angioedema, and it responds to epinephrine. Sepsis is slower, infection-driven, accompanied by fever and a rising lactate, and it responds to the Hour-1 bundle. Letting the timeline and the trigger in the stem steer you toward epinephrine versus the sepsis bundle is the core decision this workflow tests.