Autonomic nerve disorder
- 0Jan 29, '12 by thelema13sorry, this is a repost from ed, thought it might get answered here.
so, i was called in to work extra an as 'ed hold nurse' the other day, got an admitted pt for hyponatremia with hx of nasopharyngeal ca, no sx just radiation. he does have hx of autonomic nerve disorder post radiation and for the past 3 years he has wildly varying bp's. i mean when i got him, 190/130, 200/150, steadily climbing 220/160, 245/190. he states this is normal, i am starting to freak out, although he is completely asymptomatic. i am paging the admitting doctor to get orders before this guy strokes out on me. doc phones up, orders 0.1mg clonidine po, i ask for clarification, she says "he has autonomic nerve disorder, it's okay." so no other orders, i run and get the clonidine and give it to the pt. pt initially refuses, says he is super-sensitive to bp meds, he takes it, at this point he is on q5 min bp. so his bp starts dropping 10 mins after admin, 170/90, 120/65, 78/59, and eventually 64/39. btw, those bp's are 5 mins apart. i throw him in trendelenburg, open his maintenance fluids up as i page the admitting doc again. the whole time, pt talking and watching tv, does not complain of any s/s. doc tells me "it's okay, only phone me again if his systolic is in the 40's. dc his fluids."
i say what?
so the entire time, his hr never moves from 70-75. no complaints whatsoever. admitting doc comes in, assesses pt and says everything is hunky-dory. she leaves, he wants to go to the bathroom, i give him a urinal. at this point i go to get my cow so i can eyeball him. upon returning, he is out of bed and in the bathroom (did i mention our ed is like the marriott? private rooms with bathrooms, flat screens, i'm surprised they didn't put in marble counter tops. and we didn't get our yearly raise, but that's another story). i run in and grab him before he syncopes on me, he is surprised that i am so surprised. gets back in bed, bp 190/70. so now i am scratching my head, the whole time he is asymptomatic, but that varying bp is scary.
as he is resting, i am charting what has transpired, made sure to include "no further orders given," and the admitting doc walks back in to admit another pt. i beg of her to explain. she goes on to tell me his vagus nerve was damaged, so he has been dealing with this for the past 3 years. i ask why his hr isn't affected, or even trying to compensate, she can't give an answer. after looking at all my resources at home, using google, i can't find much.
now i turn to the an gurus. has anyone encountered something like this before? could one of you guys explain it, cause the admitting doc sure as heck could not. thanks!
- 2Jan 29, '12 by Esme12, BSN, RN Senior ModeratorAutonomic nerve disorders (dysautonomia) refer to disorders of autonomic nervous system (ANS) function. Dysautonomia is a general term used to describe a breakdown or abnormal function of the ANS. The autonomic nervous system controls much of your involuntary functions. Symptoms are wide-ranging and can include problems with the regulation of heart rate, blood pressure, body temperature, perspiration, and bowel and bladder functions. Other symptoms include fatigue, lightheadedness, feeling faint or passing out (syncope), weakness, and cognitive impairment.
The autonomic nervous system works below the level of consciousness to maintain the body's equilibrium. It regulates blood pressure, pulse and breathing rates among many other variables. It assures the normal function of all of our internal organs. The autonomic nervous system also responds instantaneously to any type of stress. (stress should be understood as any physical or emotional stimuli that threatens the balance of our body). There are close connections between the autonomic nervous system and the endocrine system that regulates hormone secretion.
When you flip a light switch on in your house, you know what the end-result will be. The light switch connects a circuit that produces light when the electrons reach the filament. Your computer is similar. While you type a report or surf the Internet, the computer performs an abundance of unseen tasks in the background: checking for printer signals, moving data to the hard drive, and organizing its memory. It is easy to take these tasks for granted, because they operate behind the scenes; they donít seem relevant to the task at hand.
The human body functions much the same way. Every process in the body is controlled by signals sent from the brain, through the nerves, to each individual organ or muscle. Like the example of our computer, there is an abundance of tasks the body performs that can be easily taken for granted. These background tasks are referred to as the ďautonomic nervous systemĒ. Heart rate, sleep, digestion, and vascular pressure are all normal bodily functions that donít receive a second thought. But, what if the body didnít perform these functions correctly?
There are a few illnesses that cause autonomic nervous system dysfunction. As if by design, the areas of the brain controlling the autonomic nervous system were made the most secure. Even in degenerative neurological diseases such as Alzheimerís or Parkinsonís, autonomic functions like heart rate and digestion remain untouched until the late stages of the illness.
Autonomic Nervous System Dysfunction (ANS) and Chronic Fatigue Syndrome (CFS)
Symptoms of dysautonomia are numerous and vary widely from person to person. Since dysautonomia is a full-body condition, a large number of symptoms may be present that can greatly alter a person's quality of life. Each patient with dysautonomia is differentósome are affected only mildly, while others are left completely bed-ridden and disabled.
The primary symptoms that present in patients with dysautonomia are:
- Excessive fatigue
- Excessive thirst (polydipsia)
- Lightheadedness, dizziness or vertigo
- Feelings of anxiety or panic, a sense of impending doom (not mentally induced)
- Rapid heart rate or slow heart rate
- Orthostatic hypotension, sometimes resulting in syncope (fainting)
There is another condition but is associated with spinal cord injurues.
Autonomic dysreflexia (AD) is a syndrome of massive imbalanced reflex sympathetic discharge occurring in patients with spinal cord injury (SCI) above the splanchnic sympathetic outflow (T5-T6).
This condition is associated with a medical emergency, so recognizing and treating the earliest signs and symptoms efficiently can avoid dangerous sequelae of elevated blood pressure. SCI patients, caregivers, and medical professionals must be knowledgeable about this syndrome and its management. Medscape: Medscape Access
It is characterised by severe paroxysmal hypertension (episodic high blood pressure) associated with throbbing headaches, profuse sweating, nasal stuffiness, flushing of the skin above the level of the lesion, bradycardia, apprehension and anxiety, which is sometimes accompanied by cognitive impairment. The sympathetic discharge that occurs is usually in association with spinal cord injury (SCI) or disease (e.g. multiple sclerosis). AD is believed to be triggered by afferent stimuli (nerve signals that send messages back to the spinal cord and brain) which originate below the level of the spinal cord lesion. It is believed that these afferent stimuli trigger and maintain an increase in blood pressure via a sympathetically mediated vasoconstriction in muscle, skin and splanchnic (gut) vascular beds. Automatic Dysreflexia (Hyperreflexia)
I hope this helps....
- 1Jan 29, '12 by Esme12, BSN, RN Senior ModeratorTreatment.....
Is to decrease the symptoms of POTS. Doctors admit that treatment can be a challenge and that no single therapy is uniformly successful. Medications that are useful in some patients may have no effect in others (Jacob & Biaggioni, 1999). Occasionally medications can worsen symptoms. Medications used to treat POTS include the following:Anti-arrhythmic drugs, such as disopyramide (norpace), have been used to treat POTS patients. However, studies have shown that some anti-arrhythmic drugs may increase the risk of death, and they are usually used only to treat life-threatening arrhythmias.
Benzodiazepines, such as Clonazepam (klonopin) or alprazolam (xanax), are not used as a first-line of treatment and can worsen tachycardia and hypotension. However, they may be helpful in select patients. Klonapin has been shown to be effective in the treatment of some patients with neurally mediated syncope (Kadri, Hee, Rovang, Mohiuddin, Ryan, Ashraf, Huebert & Hilleman, 1999). These drugs are central nervous system depressants. They are thought to enhance the effect of gaba, an inhibitory neurotransmitter. Benzodiazepines should be used with caution, as they are highly addictive. Some physicians do not advocate their use.
Beta Blockers are especially useful in those with elevated norepinephrine levels, beta-receptor supersensitivity and a hyperadrenergic state. Beta blockers can exacerbate hypotension and are not well tolerated by some dysautonomics. Beta blockers need to be used with caution, as they are known to reduce plasma renin activity. Research shows that hypovolemic orthostatic intolerant patients commonly have inappropriately low levels of plasma renin activity. Reduced plasma renin activity may be an important pathophysiologic component of the syndrome of orthostatic intolerance. Hence, some POTS patients may have low plasma renin activity that is contributing to their disorder. Beta blockers may further lower plasma renin activity in these patients. Therefore, the use of beta blockers in some hypovolemic patients may be counterproductive. Beta blockers should be used with caution, if at all, in those with mast-cell activation disorders. Beta blockers may trigger mast-cell activation.
Cerefolin is a vitamin supplement that may help patients combat fatigue and feel more alert.
Clonidine (Catepres) is a centrally acting alpha-agonist agent. Clonidine inhibits sympathetic outflow. It can stabilize heart rate and blood pressure in patients with post-ganglionic sympathetic involvement. Clonidine will actually display a vasoconstrictive effect in these patients. Clonidine is started at 0.1 mg a day and titrated upward. It is available in a long-acting patch form.
Last edit by Esme12 on Jan 29, '12
- 0Jan 30, '12 by Esme12, BSN, RN Senior ModeratorI am, on here......Seriously, I was and I have only worked critical care/emergency medicine. I am sidelinde right now. I have an auto immune disorder, imflammatory myopathy myositis, that has me on the sidelines the last couploe of years . So, I haunt the pages here to keep me from going crazy and to keep up "The Craft"