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Zorluk: Çok zorPhysiological Adaptation

A rapid response team is called for a client admitted with community-acquired pneumonia who began receiving an initial infusion of intravenous ampicillin-sulbactam 1515 minutes ago. The client presents with acute respiratory distress, audible stridor, and diffuse urticaria. Vital signs are: blood pressure 68/3868/38 mm Hg, heart rate 5252 bpm, respiratory rate 3232 breaths/min, and SpO2 86%86\% on room air. The client's medication history includes daily lisinopril, metoprolol succinate, timolol ophthalmic drops, and atorvastatin. The nurse immediately stops the antibiotic infusion and administers 0.50.5 mg of intramuscular epinephrine. Five minutes later, the client's blood pressure is 70/4070/40 mm Hg, heart rate is 5454 bpm, and severe wheezing persists. Which of the following is the most appropriate priority intervention?

  1. A
    Administer a second dose of intramuscular epinephrine
  2. Administer intravenous glucagonCevap
  3. C
    Administer intravenous methylprednisolone and diphenhydramine
  4. D
    Initiate an intravenous continuous infusion of norepinephrine

Cevap

The most appropriate priority intervention is to administer intravenous glucagon.
The client is experiencing anaphylaxis but is refractory to standard epinephrine therapy due to systemic beta-adrenergic blockade from their home medications (metoprolol and timolol). Glucagon is the evidence-based antidote in this scenario because it directly activates adenylate cyclase to increase intracellular cAMP, functioning completely independently of beta receptors. This effectively reverses both the life-threatening bronchospasm and hypotension.

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1
Analyze the client's clinical presentation and vital signs.
The client is experiencing severe anaphylactic shock (stridor, urticaria, profound hypotension) but presents with paradoxical bradycardia (HR 52-54 bpm).
Identifying the mismatch between the expected compensatory tachycardia of shock and the actual bradycardic state is critical for diagnosing the underlying pathophysiology.
2
Correlate the clinical findings with the client's medication history.
The bradycardia and unresponsiveness to the first dose of epinephrine are caused by systemic beta-adrenergic blockade from the concurrent use of metoprolol and timolol.
Beta-blockers prevent epinephrine from binding to beta-1 and beta-2 receptors, blunting its inotropic, chronotropic, and bronchodilatory effects.
3
Determine the priority pharmacological intervention for refractory anaphylaxis.
Intravenous glucagon is selected as the antidote.
Glucagon directly activates adenylate cyclase independent of the beta-receptor, increasing intracellular cAMP to produce necessary bronchodilation and cardiovascular support.

Anahtar Kavram

Management of Refractory Anaphylaxis in Beta-Blocked Clients
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Konular

Physiological Adaptation

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