distributive shock Flashcards

(45 cards)

1
Q

What is distributive shock (definition)?

A

Relative hypovolemia due to intravascular volume redistribution from loss of vascular toneor increased capillary permeability.

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2
Q

What types of distributive shock exist?

A

Neurogenic, Anaphylactic, Septic.

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3
Q

What common feature unites distributive shock types?

A

Intravascular volume maldistribution (not always actual loss of total body fluid).

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4
Q

What causes neurogenic shock?

A

Hemodynamic consequence of spinal cord injury or spinal anesthesia causing loss of sympathetic outflow.

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5
Q

When can neurogenic shock occur and for how long?

A

Can occur within 30 minutes of spinal cord injury and may last up to 6 weeks.

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6
Q

Which spinal levels are usually involved in neurogenic shock?

A

Cervical or high thoracic injuries.

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7
Q

What is the pathophysiology of neurogenic shock?

A

Loss of SNS tone → massive vasodilation → pooling of blood → hypotensionand often bradycardia.

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8
Q

What is unique about heart rate in neurogenic shock?

A

Bradycardia is typical — it’s the only shock type commonly with bradycardia due to lost sympathetic tone.

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9
Q

What are clinical manifestations of neurogenic shock?

A

Hypotension, bradycardia, difficulty with temperature regulation, bowel/bladder dysfunction, skin perfusion changes (cool or warm, dry skin), deficits tied to level of injury.

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10
Q

How is neurogenic shock treated?

A

Treat cause (spinal stability and precautions), then manage hypotension/bradycardia: vasopressors(phenylephrine) to maintain BP, atropine for bradycardia.

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11
Q

How should fluids be given in neurogenic shock?

A

Cautiously — hypotension isn’t due to true volume loss; avoid fluid overload.

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12
Q

What else must be monitored in neurogenic shock?

A

Temperature regulation and hypotonic dysfunction.

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13
Q

What is anaphylactic shock?

A

An acute, life-threatening hypersensitivity reaction to a sensitizing antigen (drug, food, insect venom, vaccine) causing massive vasodilation and increased capillary permeability.

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14
Q

What routes of exposure can cause anaphylaxis?

A

Injection (IM), inhalation, ingestion, topical — IM (e.g., bee sting, vaccine) often produces severe responses.

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15
Q

How quickly does anaphylaxis require action?

A

Immediate action is needed to prevent progression to anaphylactic shock.

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16
Q

What are the pathophysiologic changes in anaphylaxis?

A

Release of vasoactive mediators → massive vasodilation and capillary leak → fluid shifts out of vascular space.

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17
Q

What are hallmark respiratory manifestations of anaphylaxis?

A

Laryngeal edema, severe bronchospasm, respiratory distress, wheeze, stridor, and possible airway compromise.

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18
Q

What are other common clinical manifestations for anaphylactic shock?

A

Dizziness, chest pain, incontinence, swelling of lips/tongue, flushing, pruritus, urticaria (hives), angioedema, anxiety/confusion, sense of impending doom.

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19
Q

What is first-line medication for anaphylactic shock?

A

Epinephrine (IM or SQ outside of a code).

20
Q

Why avoid IV epinephrine except in code situations?

A

IV epi in non-arrest can cause severe cardiac complications.

21
Q

What adjunctive meds help in anaphylaxis?

A

Diphenhydramine, H2 blockers (e.g., famotidine) to block histamine; corticosteroids to reduce inflammation.

22
Q

What airway measures are used for anaphylaxis?

A

Maintain airway: nebulized bronchodilators, aerosolized epinephrine, ET intubation if needed.

23
Q

What is the fluid strategy for anaphylaxis?

A

Aggressive crystalloids to counter vasodilation and capillary leak.

24
Q

What key history item helps prevent anaphylaxis?

A

Prior allergic history — identify triggers to avoid.

25
What defines septic shock?
A subset of sepsis with profound circulatory, cellular, and metabolic abnormalities leading to persistent hypotension and increased mortality.
26
What precedes septic shock?
Infection → sepsis → septic shock.
27
What pathogens can cause septic shock?
Gram-negative & Gram-positive bacteria, and sometimes parasites, fungi, or viruses.
28
How often is a causative agent not identified in sepsis?
Approximately 30% of cases have no identified causative organism.
29
What are common clinical manifestations of septic shock?
Persistent hypotension despite fluids, tachycardia, dysregulated temperature (high or low), decreased ejection fraction, GI issues (paralytic ileus, GI bleed), altered LOC, ↓ urine output.
30
What severe peripheral complications can occur in septic shock?
Ischemic necrosis of extremities (fingers, toes, nose) due to poor perfusion.
31
What laboratory abnormalities occur in septic shock?
Elevated lactate, elevated blood glucose, decreased platelets, positive blood cultures (if identified), abnormal WBC (high/low), elevated procalcitonin, increased urine specific gravity.
32
What is initial fluid resuscitation in septic shock?
30 mL/kg isotonic crystalloid (initial bolus).
33
What is the target MAP when resuscitating septic shock?
MAP ≥ 65 mmHg.
34
What if hypotension persists after fluids in septic shock?
Start vasopressors — norepinephrine is first-line.
35
What other vasoactive agents are used for septic shock?
Epinephrine, dobutamine (to increase O₂ delivery), and add others if needed.
36
When should broad-spectrum antibiotics be started?
Within the first hour of recognizing sepsis/septic shock — obtain cultures before antibiotics if feasible.
37
What glucose control target is recommended in septic shock?
Maintain glucose < 180 mg/dL.
38
What prophylactic measures are indicated in septic shock?
Stress ulcer prophylaxis (PPI such as pantoprazole) and VTE prophylaxis(heparin or enoxaparin).
39
What is the main treatment principle for septic shock?
Treat underlying infection, restore intravascular volume, maintain perfusion (vasopressors), and support organ systems.
40
Which shock types usually get aggressive fluid resuscitation?
Hypovolemic, septic shock, and anaphylactic require aggressive fluids.
41
Which shock types should fluids be given cautiously or avoided aggressively?
Cardiogenic and neurogenic shock — avoid overloading as the problem isn’t primarily low volume.
42
Which shock is associated with bradycardia?
Neurogenic shock (unique among shock types).
43
Which shock type commonly uses norepinephrineas first-line vasopressor?
Septic shock (if hypotension persists after fluids) and often used in cardiogenic cases post-MI.
44
What bedside marker signals poor tissue perfusion across shock types?
Elevated lactate (indicator of anaerobic metabolism).
45
What is the nursing priority across all shock types?
Early recognition, maintain airway/oxygenation, support circulation (IV access, fluids/vasopressors as appropriate), monitor urine output and mental status, and treat the underlying cause.