cause of hypotension in shock/trauma

[IVAN HRONEK]

Neurogenic shock is hypotension with or without bradycardia - depending on the cause - in high spinal cord lesions they will be bradycardic as to the interruption of cardiac sympathetic accelerators. In neurogenic shock due to brain lesion or thoracic spine injury the bradycardia is not necessarily present. The term is "relative bradycardia" i.e. heart rate not appropriate to the degree of hypotension ..which your patient actually could be told to have - a HR of 110/min in a young man with a barely palpable pulse is certainly not a high enough reflex heart rate, you'd expect at least 140 / min or so. 
The problem with teaching about shock is that the bradycardia is the one thing one can easily remember about spinal shock - however, it does not have to be present and then everyone is surprised.
As dr. M. would say, a gentle clinician's touch is required here - this is the time to use it  - the diff.dg is clinical and that is whether or not the patient's skin is cold and clammy or warm and dry - hypovolemic vs. neurogenic shock. 
 
 





Patients with neurogenic shock are hypotensive and usually have warm, dry skin.8 Bradycardia is characteristic but not universal. ...www.accessmedicine.com/content.aspx?aID=588768 - Similar pages
  

Goldman: Cecil Medicine, 23rd ed.
Chapter 422 - TRAUMATIC BRAIN INJURY AND SPINAL CORD INJURY
Neurogenic Shock and Dysautonomia 

After traumatic spinal cord injury, patients are at risk for neurogenic shock and dysautonomia. Lesions of the cervical and thoracic spine disrupt the descending sympathetic pathways to the intermediolateral cell column of the thoracolumbar spinal cord, thereby leading to peripheral vasodilation and hypotension. If the lesion is at T3 or above, sympathetic tone to the heart is compromised. In this setting, hypotension is accompanied by bradycardia, thus producing the neurogenic shock triad of bradycardia, hypotension, and peripheral vasodilation.
Initial therapy for dysautonomia should be fluid administration to restore an adequate circulating volume with a target CVP of 4 to 6 mm Hg. A hematocrit of 30 is optimal for perfusion of the central nervous system, so blood can be used if the patient is anemic. If blood is not required, either colloid (e.g., albumin solutions) or crystalloid (e.g., normal saline) may be used. If there is a suspicion of cardiac or pulmonary disease, a pulmonary artery catheter may be needed briefly to assess fluid status and the relationship between pulmonary pressure and CVP.
Once adequate circulating volume has been achieved, hypotension should be managed with vasopressive agents such as phenylephrine (see earlier), norepinephrine (see earlier) or dopamine (beginning at 1 μg/kg/min by continuous intravenous infusion) ( Chapter 107 ), with the goal of a mean arterial pressure of 85 mm Hg or greater. Symptomatic bradycardia can be treated with atropine (1 mg intravenously).
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Let me further speculate that the cause of arrest in this patient was probably brain herniation after the admin. of fluid  - prior to that when hypotensive prolonged CNS ischemia as to elevated ICP and minimal perfusion pressure and cardiac output. Bilat. pupils fixed & dilated - probably due to the brain injury or prolonged brain hypoperfusion that was generalized in nature - i.e. brain swelling and high ICP. After RL and blood administration patient arrested - RL as it is hypoosmolar goes extravascular and increases ICP leading to herniation. Brainstem herniation can cause cardiac arrest as to compression of the cardiac regulatory center in the brainstem. 
 
In hypotensive pts. who have a concomitant brain injury it is probably advisable to increase perfusion pressure with vasopressors rather than with fluids, especially hypotonic fluids. If you have to, NS is theoretically better than RL, although the difference may not be clinically apparent. 
 
Ivan Hronek MD 
SFMC, Los Angeles
cell: 310 487-3288
http://health.groups.yahoo.com/group/Anesthideas/
Don't fight darkness. Bring the light, and darkness will disappear.
Maharishi Mahesh Yogi



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----- Original Message ----From: Dr.Asif Huda Ansari <asifhansari at yahoo.com>To: trauma-list at trauma.orgSent: Sunday, February 24, 2008 5:25:59 AMSubject: cause of hypotensionSUB: Cause of hypotension in MVA patient.Hellow,i am a Gen.Surg resident and in 2 years of i have seen 2 pts coming to trauma, in shock,25yr male,Unconscious(intubated),BP not recordable,peripheral pulse absent, Pupils B/L dilated and fixed,chest-B/L breath sound +,CVS-audible heart sounds. Abdomen Soft/lax/Bowel sound+aftr resuusitation with 2 Lit RL and 2 U PRBC, BP  came to 110/70,pulse110CXR no pneumo/hemoPelvic xray-no #USG abdomen- no free fluidwe decide to shift the pt to CT with the above vitals-as the pt is shifted to CT table, pt. arrest , CPR done 40mins but pt declared dead.my question here is, what could be cause of shock if we excluded hemorhage, as there was no bleeding in the chest/abdomen/pelvic/no long bone fractures.the only thing was the pupils B/L Dilated and fixed !now is there any cause in the Head which can cause this?i mean after excluding Hemorrhagic cause, if we label  Neurogenic shock, the pt should be Hypertensive and Bradycardic.please give your expert opinions.ThanksDr.Asif.H.Ansari;MBBS, MRCS (Std)King Khalid HospitalSaudi ArabiaIvan Hronek MDChief, Critical Care & Trauma AnesthesiaSFMC Gas, Inc.St. Francis Medical Center3630 E. Imperial HighwayLynwood, CA 90262 Cell: 310 487-3288Pager: 310 636-6020