QLexNursing

Anaphylaxis

1. The rapid onset of flushing, diffuse erythema, hives (urticaria), nausea, hypotension, and tachycardia minutes after the infusion is classic for anaphylaxis, a life‑threatening systemic hypersensitivity reaction.
2. In anaphylaxis, mast‑cell mediator release (e.g., histamine) triggers peripheral vasodilation and capillary leak, producing the observed hypotension and warm, flushed skin.
3. The development of hives distinguishes this from simple rate‑related flushing and indicates a generalized immunologic reaction requiring emergency treatment.
4. Untreated, anaphylaxis can progress to airway edema/bronchospasm, shock, and multisystem compromise.
5. Immediate priorities are stop the offending agent, activate emergency response, ensure airway/breathing/circulation, and administer epinephrine with high‑flow oxygen and IV fluids as indicated.

Dysrhythmias

1. During anaphylaxis, profound vasodilation and relative hypovolemia can precipitate myocardial hypoperfusion, predisposing to cardiac dysrhythmias.
2. Concurrent tachycardia (compensatory) and hypotension increase myocardial oxygen demand while decreasing supply, further raising arrhythmia risk.
3. Emergency therapies (e.g., epinephrine, beta‑agonists) are lifesaving but can also provoke dysrhythmias, especially in older adults or those with cardiac history.
4. Continuous cardiac monitoring, prompt correction of hypoxia and hypotension, and judicious use of vasoactive agents are essential to minimize this risk.
5. Early recognition and stabilization of hemodynamics reduce progression to malignant rhythms.

Cardiac arrest

1. Severe anaphylaxis can deteriorate to distributive shock with refractory hypotension, culminating in cardiac arrest if not rapidly reversed.
2. Airway edema and bronchospasm may cause hypoxemia, another direct pathway to pulseless arrest.
3. Escalating dysrhythmias in the setting of hypoxia and shock can degenerate into ventricular fibrillation or asystole.
4. Given the patient’s age and cardiac history, the threshold for rapid escalation (airway equipment at bedside, ACLS readiness, large‑bore IV access, aggressive crystalloid boluses) should be low.
5. Early epinephrine, oxygenation/ventilation, and volume resuscitation are the proven measures that prevent progression to arrest.