Unit 1: Neurogenic Shock Flashcards
Neurogenic Shock
- distributive shock
- a disruption in sympathetic nervous system stimulation
- vasodilation and hypovolemia; hypoperfusion
- loss of vasomotor tone
- vessel walls relaxing and dilating
- bradycardia
- hypotension
Sympathetic Nervous System Disruption
a disruption in SNS stimulation = a inability of vascular smooth muscle to constrict = decreased blood return to the heart and decreased cardiac output
-bradycardia, hypoperfusion
Causes of Neurogenic Shock
- spinal cord injury (above T6 level)
- stroke in the brain stem
- high doses of barbiturates and anesthesia techniques (both general and regional)
Clinical Manifestations of Neurogenic Shcok
- decreased vascular tone; vulnerable to hypoperfusion
- warm and dry skin d/t vasodilation
- hypovolemia b/c the size of the systemic vasculature has expanded w/o current increase in volume to fill that expanded space
- bradycardia
- hypotension
- changes in LOC
- metabolic acidosis
Medical Management of Neurogenic Shock
- Correcting primary etiology
- Correcting the Cardiovascular effects (hypotension, bradycardia)
- Fluid resuscitation (boluses of crystalloids to increase stretch of the myocardial fibers in the atria = an increase in strength of ventricular contractions and increased cardiac output)
- Vasoactive infusions (e.g. norepinephrine (Levophed), epinephrine (adrenaline), phenylephrine (Neo-Synephrine)
- Atropine to block vagal (parasympathetic) stimulation
- Transcutaneous or transvenous pacing capabilities to treat sustained symptomatic bradycardia
Vasoactive Tx for Loss of Vascular Tone
- phenylephrine
- norepinephrine
- epinephrine
- dopamine
Fluid resuscitation
to restore vascular volume and improved systemic perfusion
How to treat Episodic Bradycardia
- parasympatholytic medications (Atropine)
- transcutaneous and then transvenous pacing ay be used to treat repeated episodes of bradycardia
Serum Lactate (lactic acid) Levels and ABGs
to monitor acidosis and judge effectiveness of resuscitation strategies
Ongoing Tx of decreased vascular tone
-oral sympathomimetics, causing constriction of the peripheral vasculature
Complications of Neurogenic Shock
- Continued systemic hypoperfusion leading to multisystem organ failure
- Hypoperfusion occurs as a result of massive systemic vasodilation causing a reduction in cardiac output and blood pressure
- Bradycardia can occur, further compromising blood flow to vital tissues and organs b/c of disruption of sympathetic outflow; contributes to decreased cardiac output and BP
Nursing Management: Assessment and Analysis
w/ neurogenic shock, require cardiovascular monitoring in order to detect bradycardia, dysrhythmias, and hypotension that result from a disruption in sympathetic innervations
> Rapid Medical Interventions:
- atropine
- transcutaneous or transvenous pacing
- fluid resuscitation
- vasoactive medications
- ongoing assessments: monitoring cardiac output, intravascular volume, and other hemodynamic parameters
- mechanical ventilation depending on underlying cause
- management of complications: DVT, PE, and skin breakdown
Rapid Medical Interventions
- Atropine
- Transcutaneous or Transvenous Pacing
- Fluid resuscitation
- Vasoactive medications
- Ongoing Assessments: monitoring cardiac output, intravascular volume, and other hemodynamic parameters
- Mechanical ventilation depending on underlying cause
- Management of complications: DVT, PE, Skin breakdown
Nursing Diagnoses
- Impaired tissue perfusion r/t hypotension, bradycardia, and peripheral vasodilation
- Risk for fluid volume deficit d/t hypovolemia that occurs w/ loss of vasomotor tone and maldistribution of volume in vascular space
- Anticipatory grieving r/t sudden loss of function and accompanying critical illness
Nursing Assessments for Neurogenic Shock
- Vital signs q 1-2 hours for vasoactive infusions
- Hemodynamic Parameters q 2 to 4 hours or after tx of bolus or fluid
- Intake + Output q 1-2 hours
- Physical Assessment at q 4 hours