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FORUMS > EMERGENCY CARE ESSENTIALS FORUM [ REFRESH ]
Thread Title: Neurogenic Shock
Created On Mon Dec 19, 2005 2:37 PM


larsbland
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Mon Dec 19, 2005 2:37 PM

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Can someone explain the physiology of neurogenic shock and also its prehospital manifestations ... I am a huge advocate of c-spine, and I really want to learn more about spinal/TBI injuries ... Any TBI/ICP protocols? How about fluid resus in the above situations? Any calls you want to share?
Lars B
Madison, WI

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grambograham
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Mon Dec 19, 2005 6:15 PM

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Neurogenic shock (vasogenic shock) occurs when the sympathetic nervous system's control of the vascular system is interrupted. Normally the arteries and veins are not allowed to fully dilate and are always partially constricted by their smooth muscles located in the walls of the vessles. When the sympathetic system fails, the veins and arteries dilate. This drops the peripheral resistance and causes a drop in BP. You may see this in spinal injuries, people who become frightened, or suffer from some cardiovascular diseases.

S/S
Dilated pupils
Dull appearance of eyes
Shallow, rapid breathing
Pale or cyanotic appearance
Patient may be nauseous or vomitting
Patient may feel thirsty
Pulse weak and rapid
BP low

Hope that helps.

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Doczilla
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Mon Dec 19, 2005 8:07 PM

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Great summary grambo.

To clarify, I would add that the syndrome comes when there is interruption of stimulus to the sympathetic chain ganglia. This is a chain of nerves that runs down either side of the spinal cord from T1 down to the lumbar spine. These ganglia send nerves to the vessels, and interruption of this pathway leads to vasodilation just as grambo described. With severing of the spinal cord, the stimulus to the ganglia is lost. Neurogenic shock is a phenomenon of vasodilation, so vasoconstrictors are the drugs of choice for treatment. Rather than dopamine, this would get treated with neosynepherine or norepinepherine, which have greater effect on alpha receptors to cause vasoconstriction as opposed to beta receptors which cause increased cardiac output.


'zilla

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larsbland
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Mon Dec 19, 2005 9:14 PM

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Holy %$^& - now I remember why I post here! Doczilla - could you further explain why no Dopamine? And am I correct to assume that an injury to the spinal cord ABOVE T1 wouldnt be cause for neurogenic shock?
Lars B.

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AZCEP
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Mon Dec 19, 2005 9:48 PM

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Any spinal cord injury above T-4 has the potential of developing neurogenic shock symptoms. This is a patient that will be flushed, bradycardic, and typically eupneic(normal respiratory rate and depth) Dopamine can be used but the dosing must be more aggressive to get it into the alpha response range. Levophed and phenylephrine are potent alpha agents at much lower doses than dopamine, so you will get the response you want quicker, with fewer of the bad side effects that go with higher doses.

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grambograham
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Tue Dec 20, 2005 12:46 AM

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From my understanding, dopamine is an beta receptor stimulant. It causes greater cardiac output as Doczilla pointed out. Vasoconstrictors using an alpha will have more effect on the peripheral system and cause vasoconstriction. This will increase the peripheral resistance and force the blood pressure up closer to normal.

As Azcep said, any injury above T1 can cause these effects. If there is a severence anywhere above T4 neurogenic shock may occur. Just remember that a severence of or above C5 can result in respiratory difficulty to the point of apnea.

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 If you can keep your head while all else around you are losing theirs'............................... You probably haven't checked with your answering service!

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Doczilla
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Tue Dec 20, 2005 1:49 PM

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If dopamine is the only pressor you have, then it's okay. AZCEP rightly pointed out that you will have to be more aggressive with dopamine to get the alpha response. Dopamine usually goes like this:
2-5 mcg/kg/min: activated dopamine receptors, most notably in the kidneys, dilating the renal arteries. We used to give small doses of dopamine to improve renal function in sick folks, but this has fallen out of favor.
5-10 mcg/kg/min: activates beta receptors, causing increased HR, increased contractility. It will also cause a small amount of vasodilation.
10-20 mcg/kg/min: activates alpha receptors, causing vasoconstriction.

The concern is that there may be more beta activation with dopamine, leading to increased myocardial oxygen demand (and possibly ischemia) and arrhythmia. Norepi has some beta activity, but less, so the thought is that you are getting more to the root of the problem. This is why norepi is the DOC for neurogenic shock as well as septic shock, since they are primarily problems of vasodilation. Anaphylactic shock is too, but there is bronchoconstriction as well, which is why we like epi for this.

Really it's not that big a concern if the only pressor you've got is dopamine (give it).

Spinal cord injury above T1 will cause neurogenic shock, but will, as grambo said, cause some serious respiratory problems if you get up into the territory of the phrenic nerve (controls diaphragm) which is C3, C4, C5. Spinal injury above this point will paralyze the diaphragm, and the patient will be unable to breathe spontaneously.

Spinal cord injury below C5 and above T8 will also cause respiratory difficulty, as the patient will be unable to move the intercostal muscles to expand the chest. He will thus be forced to "belly breathe" (since the diaphragm is the only part of the system that's working), which may make him SOB.

While we're on the subject of spinal injuries, I wanted to drop a little bit of trivia. Assuming the patient survives the initial spinal cord injury and is discharged, what is he likely to die from?


'zilla

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grambograham
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Wed Dec 21, 2005 12:26 AM

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Pneumonia would be my guess doczilla.... due to not mobilizing, or using incentive spirometers.

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