Emergency management algorithm for shock

General principles of anti-shock therapy

Management of any shock state is based on restoring normal circulating blood volume (CBV) and microcirculation. The basic treatment regimen includes three main areas:

1. Administration of vasoconstrictors: vasopressors (epinephrine, norepinephrine, ephedrine) are used for rapid blood pressure stabilization.
2. Normalization of CBV: carried out using intravenous infusions of colloidal solutions (gelatin, medium-molecular-weight dextran 30,000–40,000).
3. Antigen inactivation: a specific measure when the shock has an allergic origin. For example, in penicillin antibiotic reactions, the enzyme penicillinase (beta-lactamase) is used.

In the event of severe or refractory reactions, an anesthesiologist-intensivist must be involved. General management always starts with epinephrine, followed by fluid loading and administration of glucocorticoids (dexamethasone or prednisolone).

Step-by-step algorithm in anaphylactic shock

Anaphylaxis requires emergency intervention. The use of diuretics, antibiotics, or bronchodilators at the initial stage is not a life-saving measure. Action must be taken according to the following algorithm:

• Step 1. Recognition. Diagnosis is established based on a burdened allergic history and life-threatening symptoms (stridor, respiratory distress, clinical picture of shock). Important: cutaneous manifestations, such as urticaria, may be absent.
• Step 2. Primary assessment and basic measures. Evaluation is performed using the ABC system (airway, breathing, circulation). Contact with the allergen is immediately interrupted (e.g., drug injection is stopped). If possible, oxygen is administered immediately (O₂).
• Step 3. First-line pharmacotherapy. Standardly, a 0.1% solution of epinephrine is administered intramuscularly at a dose of 0.01 mg/kg (maximum 0.5 mg per single dose). In severe shock, slow intravenous administration is permitted. If the patient has pronounced bronchospasm, inhalations of topical glucocorticoids (budesonide) and bronchodilators (salbutamol) are added.
• Step 4. Dynamic monitoring. The effect is assessed precisely after 5 minutes. If there is no improvement, epinephrine injections are repeated every 5–10 minutes until stabilization. In refractory hypotension, fluid infusion is initiated (20 mL/kg).

Adjuvant therapy and allergic laryngeal edema

Additional drug support is symptomatic in nature. To relieve immediate-type hypersensitivity reactions, systemic antihistamines (H1-receptor blockers) are prescribed, which eliminate itching and rash associated with mast cell degranulation. Glucocorticoids (GCs) are administered intramuscularly or intravenously to prevent late complications.

In allergic laryngeal edema, the markers of which are often urticarial rash, lip and eyelid edema, mandatory hospitalization is indicated. Treatment is also based on the administration of epinephrine, systemic GCs, and antihistamines. If blood pressure changes upon administration of any trigger drug, the infusion must be stopped immediately until complete state stabilization.

Specifics of care in cardiogenic and septic shock

Emergencies can be triggered not only by allergies, but also by cardiac or infectious pathologies.

• Acute left ventricular failure: If the condition is accompanied by high blood pressure (systolic BP ≥ 110 mm Hg) and pulmonary congestion, the first-line drug is nitroglycerin (intravenous drip) to reduce pre- and afterload. Concurrently, furosemide is administered as a bolus (40 to 80 mg in full-blown pulmonary edema).
• Cardiogenic shock: If left ventricular failure presents with marked hypotension (systolic BP < 90 mm Hg) and hypoperfusion, vasodilators and diuretics are strictly contraindicated. Inotropic support and vasopressors come to the forefront.
• Septic shock (SS): Frequently accompanies hemorrhagic fever with renal syndrome (HFRS). In endemic regions (the Volga Federal District accounts for more than 86% of cases in Russia), HFRS runs a severe course and requires rapid identification of not only SS, but also acute renal failure (uremia), hemorrhages, and the risk of renal capsule rupture.

Transformation of hypersensitivity reactions

Shock states are often associated with immune responses to medications. Broad-spectrum antibiotics can provoke both immediate-type hypersensitivity (anaphylaxis, urticaria) and delayed-type hypersensitivity (contact dermatitis). Furthermore, they can suppress T-lymphocyte and macrophage activity, promoting opportunistic mycoses. In clinical practice, different types of reactions can transition into one another: for example, in rheumatic fever, early exudative changes are replaced by the formation of specific granulomas, while atopic asthma may involve type III and IV mechanisms.

Class and exam questions

What else to study on this topic

• Precise regimens and dosages of inotropic drugs in cardiogenic shock (dobutamine, levosimendan).
• Non-invasive ventilation protocols in severe respiratory failure.
• Strict indications for hemodialysis in acute renal failure associated with HFRS.
• Pathogenesis of autoimmune cytopenias and details of type II hypersensitivity.
• Mechanisms of transition from immediate-type to delayed-type reactions in systemic vasculitis.

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