Management of Hypotensive Bradycardia in Neurogenic Shock
In neurogenic shock with hypotensive bradycardia, norepinephrine is the first-line vasopressor, with atropine for acute bradycardia management and fluid resuscitation as initial therapy. 1
Pathophysiology and Recognition
Neurogenic shock results from disruption of sympathetic outflow, typically following spinal cord injury, causing:
- Hypotension due to loss of vasomotor tone
- Bradycardia due to unopposed vagal tone
- Warm, dry skin (unlike hypovolemic shock)
Initial Management Algorithm
Fluid Resuscitation
Acute Bradycardia Management
- Administer atropine 0.5-1 mg IV for heart rates <50 bpm 3
- May repeat every 3-5 minutes (maximum total dose: 3 mg)
- Mechanism: Blocks vagal tone to increase heart rate
Vasopressor Therapy
Adjunctive Therapies
Pharmacological Adjuncts
Physical Measures
Monitoring Parameters
- Continuous cardiac monitoring
- Arterial line for beat-to-beat blood pressure monitoring
- Urine output (target >0.5 mL/kg/hr)
- Serial lactate measurements to assess tissue perfusion
- Skin perfusion and mental status
Special Considerations
Avoid medications that worsen hypotension:
- β-blockers
- Calcium channel blockers
- ACE inhibitors/ARBs
- Diuretics
Duration of therapy:
Pitfalls to avoid:
- Don't mistake neurogenic shock for hypovolemic shock (check skin temperature and moisture)
- Excessive fluid administration can worsen spinal cord edema
- Failure to recognize concurrent traumatic injuries causing hemorrhage
- Delaying vasopressor therapy while giving excessive fluids
Weaning strategy:
Neurogenic shock management requires a balance between maintaining adequate perfusion pressure to the injured spinal cord while avoiding excessive fluid administration that may worsen cord edema. Early recognition and prompt treatment with the appropriate vasopressors are essential for preventing secondary injury.