The clinical picture associated with pathology of the autonomic nervous systemThe autonomic nervous system contains three main components -
Tests for autonomic dysfunction.
Blood pressure, as it is a gauge pressure, increases at the beginning of the manoeuvre. The baroreceptors cause a transient decrease in heart rate during this period. The raised intrathoracic pressure impedes venous return which causes a decrease in cardiac output, and the blood pressure then gradually decreases to below baseline, despite the baroreceptors causing a progressive tachycardia and peripheral vasoconstriction. On release of glottic closure, the blood pressure will drop because it is a gauge pressure, further rising the heart rate. The compensatory reflexes combined with a now unimpeded venous return to the heart will cause the blood pressure to steadily rise, most often to above baseline until all the compensatory mechanisms and the heart rate have returned to normal These dramatic variations in heart rate are absent in autonomic dysfunction
Heart rate response to standing. In order to compensate for the decrease in blood pressure from the lying to standing position there is a reflex tachycardia which is maximal after ~ 15 beats. Blood pressure is restored to above baseline which causes a reflex brady cardia which is maximal after ~ 30 beats. Sympathetic
On standing the decreased blood pressure is usually compensated for by a reflex tachycardia and vasoconstriction, neither of these mechanism work well in autonomic dysfunction leading to a marked difference in systolic blood pressure between lying and sitting / standing. The normal is <10mmHg, pathological is when the difference is >30mmHg.
Sustained handgrip as measured by a dynamometer causes a reflex increase in heart rate and cardiac output without changing systemic vascular resistance, diastolic blood pressure thus normally increases.
Pre-operative History to elicit the cause of the neuropathy and the degree of symptomatology present. Co-morbid disease should be activly sought.
The examination is directed at finding evidence of cardiac decompensation and
concommitant peripheral neuropathy.
A thorough airway evaluation is necessary.
Bed side examination for autonomic dysfunction generally involves finding postural hypotension and noting the heart rate response to a Valsalva manoeuvre.
Investigations area aimed at determining the degree of renal dysfuntion, checking the degree of myocardial ischaemi and cervical spine X rays for ligament laxity.
Intra-operative Anaesthesia technique
Good pre-oxygenation followed by a rapid sequence intubation with a cuffed oral tracheal tube.
If a difficult larygoscopic view is anticipated then endotracheal intubation must be secured while the patient is awake
Centroneuraxial naesthesia is complicated by difficult blood pressure maintenance.
The presence of peripheral neuropathy must be well documented prior to any regional procedure
Inhalational anaesthesia with air, oxygen and a volatile agent titrated to effect Opioid supplementation must be done judiciously to avoid precipitate drops in blood pressure and post operative respiratory depression
Complete reversal of any non-depolarising muscle relaxant to ensure excellent airway control. Extubate the patient only when fully awake and in the recovery position with good suction available.
Positioning and padding
Slow controlled positioning is necessary to avoid sudden blood pressure changes.
These patients are at an increased risk of iatrogenic nerve injuries so excellent attention must be paid to padding vulnerable areas
Supplemental oxygen (40%) and close respiratory monitoring for at least 24 hrs.
Close haemodynamic monitoring, with correction of hypotension for at least 24 hours
Good post operative analgesia - patient controlled analgesia or regional anaesthesia or nurse controlled, with anti-emetic prophylaxis
|Date of First Publication: 2000||Date of Last Update: 2006/10/24||Web page author: Click here|