nicko18

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is anyone here able to give a brief rundown on why the heart rate slows in cases of spinal shock? I had a case where there was an incomplete lesion around the T6 level, which is obviosly going to affect sympathetic innervation to the viscera. But i thought heart rate was primarily controlled by the vagus, and withdrawal of parasympathetic input was responsible for the baro reflex.

Why is there no reflex tachycardia in spinal shock following a drop in BP?
 

dynx

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nicko18 said:
is anyone here able to give a brief rundown on why the heart rate slows in cases of spinal shock? I had a case where there was an incomplete lesion around the T6 level, which is obviosly going to affect sympathetic innervation to the viscera. But i thought heart rate was primarily controlled by the vagus, and withdrawal of parasympathetic input was responsible for the baro reflex.

Why is there no reflex tachycardia in spinal shock following a drop in BP?
I think usually this is in cases above T6, but I don't remember to clearly. the idea is disruption of the sympathetic flow from T1 to L2 so to use a car analogy you remove the "gas" from the heart completely. At the same time there is no way to physiologically remove all vagal output, even completely unstimulated nerves have a degree of random firing, and with the complex input to the vagus I would suspect it's much higher than most other nerves, so you can only take your foot off the brake so much, the net change is negative.
Remove just the sympathetics and leave the bare minimum physiologically possible amount of parasympathetics and its going to be lower than that, even if it doesnt hit <60 its bradycardia relative to the BP
 

omarsaleh66

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Hope this helps:



If the spinal cord injury is high in the patient and the sympathetics of the patient are damaged, then the parasympathetic system is unopposed. This leads to increased vascular space caused by the parasympathetic dominated cholinergic stimulation that results in symptoms such as hypothermia, hypotension and bradycardia. The pathophysiology behind this is due to the decreased venous constriction due to lack of alpha adrenergic stimulation and this leads to vasodilation and pooling of the blood. The lack of vasoconstriction can cause the patient to present with hypotension. Moreover, the patient suffers from hypothermia in cases where there is no vasoconstriction response to cold. The bradycardia comes results from the slowed heart rate due to the predominance of the muscarinic action on the heart and no beta 1 receptor stimulation. These symptoms can lead to complications such as circulatory instability and hypotension.
Lack of adequate perfusion to the spinal cord secondary to hypotension can cause more insult to an already injured area. Adequate cardiac output can be maintained by keeping the arterial blood pressure at 70 mm Hg or greater to prevent additional injury to the spinal cord.A The ischemia in the spinal cord can be prevented by irrigating cold perfusate to the spinal cord and producing regional hypothermia. The high plasma glucose in spinal cord during ischemia may cause adverse effects, the spinal cord metabolizes the glucose with anaerobic pathway and increase tissue acid levels. The adverse effect of glucose is still a debated topic, therefore it is advised to avoid glucose-containing IV solutions. In addition to the prefusate to protect the spinal cord, a high dose methyprednisone in acute spinal cord injuries can improve neurological function if given withing 8 hr of onset of injury.
When correcting hypotension, one can use IV atropine to block the bradycardia. Administering fluids will offset the pooling of the blood that is caused by the vasodilation. Further, the cardiac output can be monitored with a pulmonary artery catheter, and while transesophageal echocardiography can monitor the changes in chamber size of the heart when adding fluid. If there is no improvement in the circulation, then add beta agonists such as dopamine or dobutamine. Alpha agonists like such as phenylephrine may help with increasing vascular resistance by vasoconstriction but may be harmful due to increasing afterload and impede cardiac output. If the left ventricular systolic function is weak then, alpha agonists are contraindicated.
 
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nicko18

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omarsaleh66 said:
Hope this helps:

The bradycardia comes results from the slowed heart rate due to the predominance of the muscarinic action on the heart and no beta 1 receptor stimulation.
:thumbup: thanks Omar and dynx, it certainly does. I was confused when somebody told me that in transplanted hearts, it demonstrated just what little effect sympathetic stimulation from noradrenaline had on the heart, so i thought, that since there was such little input from sympathetic inputs as it was, the baro reflex wouldnt be affected too much. Obviously it plays a bigger role than what i assumed