# Situation: During the hot season, the emergency department of a coastal district hospital receives three clients from a beach outing. Client 1 is a 24-year-old man who collapsed after a long run on the sand at midday. Client 2 is a 30-year-old woman who was pulled from the sea after being found face down in the water. Client 3 is a 35-year-old man who dove headfirst into shallow water and was pulled out by friends. Client 3 cannot move his arms or legs. His blood pressure is 80/46 mmHg, heart rate 50/min, and his skin is warm and dry. The team identifies neurogenic shock. Spinal cord injuries at which level typically produce this type of shock?

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> url: https://mymerci.kr/pages/nclex_q.php?qn_id=630045  
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> subject: Nursing Practice V — Care of Clients with Maladaptive Patterns of Behavior; Care of Clients with Life-Threatening Conditions, Acute Multi-Organ Problems, High Acuity and Emergency Situations

## 문제

Situation: During the hot season, the emergency department of a coastal district hospital receives three clients from a beach outing. Client 1 is a 24-year-old man who collapsed after a long run on the sand at midday. Client 2 is a 30-year-old woman who was pulled from the sea after being found face down in the water. Client 3 is a 35-year-old man who dove headfirst into shallow water and was pulled out by friends.

Client 3 cannot move his arms or legs. His blood pressure is 80/46 mmHg, heart rate 50/min, and his skin is warm and dry. The team identifies neurogenic shock. Spinal cord injuries at which level typically produce this type of shock?

## 보기

1. At or below the first lumbar level
2. At or above about the sixth thoracic level **✔ 정답**
3. Only at the first to fourth cervical levels
4. At or below the twelfth thoracic level

**정답: 2**

## 해설

Neurogenic shock follows spinal cord injury at or above about the sixth thoracic level, where the injury cuts off enough sympathetic outflow to cause widespread vasodilation and bradycardia. It is not limited to high cervical injuries, and injuries of the lower cord do not usually produce it.

## 심화 해설

Why T6 is the watershed level

Neurogenic shock is a distributive shock caused by loss of sympathetic vasomotor tone after spinal cord injury (SCI). The sympathetic preganglionic neurons that control vascular tone and heart rate exit the spinal cord from T1 through L2, with the most clinically important cardioaccelerator and vasoconstrictor outflow concentrated in the upper thoracic segments. When the cord is injured at or above approximately the sixth thoracic level (T6), the descending sympathetic pathways are sufficiently interrupted to produce widespread vasodilation, venous pooling, and unopposed vagal activity, resulting in the classic triad of hypotension, bradycardia, and warm dry skin seen in Client 3 [1][4].

Key point! The sympathetic chain receives supraspinal input that descends through the cord. An injury below T6 leaves enough sympathetic outflow intact to maintain vascular tone in most of the body, so neurogenic shock is uncommon with lower thoracic or lumbar injuries [3][4].

Anatomical basis of the T6 threshold

Sympathetic fibers to the heart arise from T1–T4, while splanchnic vasomotor control—responsible for a large portion of total peripheral resistance—originates from T5–T9. An injury at T6 or above disrupts both cardiac sympathetic drive and splanchnic vasoconstriction. The result is a functional sympathectomy: blood vessels dilate, systemic vascular resistance falls, and the baroreceptor reflex cannot mount a compensatory tachycardia because vagal tone is unopposed [1][3]. This explains Client 3’s heart rate of 50/min and blood pressure of 80/46 mmHg.

Watch out! Bradycardia is a hallmark that distinguishes neurogenic shock from hypovolemic or septic shock, where tachycardia is the expected compensatory response. The warm, dry skin also contrasts with the cool, clammy skin of hypovolemic shock because vasodilation, not vasoconstriction, dominates [1].

Why the other levels are incorrect

| Injury level | Effect on sympathetic outflow | Neurogenic shock expected? |
| --- | --- | --- |
| C1–C4 only | Complete loss of all sympathetic and parasympathetic control; often fatal respiratory failure | Yes, but neurogenic shock is not limited to this range |
| T6 or above | Interrupts cardiac (T1–T4) and splanchnic (T5–T9) sympathetic outflow | Yes—this is the defining threshold |
| T12 or below | Most sympathetic outflow remains intact; only lower extremity and pelvic vasomotor control lost | No—hypotension is not typically neurogenic in origin |
| L1 or below | Below the sympathetic preganglionic outflow (T1–L2), minimal vasomotor impact | No—neurogenic shock is not expected |

Clinical application for the emergency department

The initial priority for Client 3 is stabilization using the ABCDE approach, with spinal immobilization maintained throughout. Because neurogenic shock reflects loss of vascular tone rather than volume loss, fluid resuscitation alone is often insufficient. Vasopressor support—typically an alpha-agonist such as norepinephrine or phenylephrine—is used to restore vasomotor tone and maintain a mean arterial pressure (MAP) above 85–90 mmHg to preserve spinal cord perfusion and reduce secondary ischemic injury [4]. Continuous hemodynamic monitoring is essential because the loss of sympathetic compensation makes these clients exquisitely sensitive to position changes and positive pressure ventilation [1].

Key point! The level of injury predicts the hemodynamic pattern. A client with a cervical or high thoracic injury who presents with hypotension and bradycardia should be assumed to have neurogenic shock until proven otherwise, and vasopressor therapy should be initiated early rather than waiting for fluid resuscitation to fail [4].References (research sources)

- [1][Neurogenic shock].Research articleMeister R, Pasquier M, Clerc D, Carron PN (2014)

- [3]Vascular dysfunctions following spinal cord injury.Research articlePopa C, Popa F, Grigorean VT, Onose G, Sandu AM, Popescu M (2010)

- [4]Contemporary hemodynamic management of acute spinal cord injuries with intravenous and enteral vasoactive agents: A narrative review.Research articleIovine JA, Villanueva RD, Werth CM, Hlavacek NL, Rollstin AD, Tawil I (2022) · DOI: 10.1093/ajhp/zxac164

## 임상 시나리오

Neurogenic Shock: The T6 ThresholdRecognizing spinal cord injury levels that cause distributive shock
Neurogenic shock results from loss of sympathetic vasomotor tone after spinal cord injury. The critical watershed is T6—injuries at or above this level interrupt enough sympathetic outflow to cause widespread vasodilation and bradycardia.

Sympathetic preganglionic neurons exit from T1 to L2, but the most clinically important cardioaccelerator and vasoconstrictor fibers are concentrated in the upper thoracic segments. An injury at T6 or above disrupts both cardiac sympathetic drive (T1-T4) and splanchnic vasoconstriction (T5-T9), producing a functional sympathectomy.

The classic triad is hypotension, bradycardia, and warm dry skin—the baroreceptor reflex cannot mount compensatory tachycardia because vagal activity is unopposed.

CautionInjuries below T6 typically spare enough sympathetic outflow to maintain vascular tone, so neurogenic shock is uncommon with lower thoracic or lumbar injuries. Do not assume all spinal cord injuries cause this shock pattern.

## 핵심 개념

- **Neurogenic shock** — Distributive shock from loss of sympathetic vasomotor tone after spinal cord injury, causing hypotension, bradycardia, and warm dry skin.
- **T6 watershed level** — Spinal cord injuries at or above the sixth thoracic level interrupt enough sympathetic outflow to produce neurogenic shock.
- **Sympathetic preganglionic neurons** — Neurons exiting the spinal cord from T1 to L2 that control vascular tone and heart rate.
- **Functional sympathectomy** — Loss of sympathetic vasoconstriction leading to vasodilation, decreased systemic vascular resistance, and unopposed vagal activity.
- **Splanchnic vasomotor control** — Sympathetic control of abdominal visceral blood vessels originating from T5-T9, a major contributor to total peripheral resistance.

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