Tilt table test

From Wikipedia, the free encyclopedia

 This article does not cite any references or sources. (November 2007)
Please help improve this article by adding citations to reliable sources. Unverifiable material may be challenged and removed.

A tilt table test is a medical procedure often used to diagnose dysautonomia or syncope. Patients with symptoms of dizziness or lightheadedness, with or without a loss of consciousness (fainting), suspected to be associated with a drop in blood pressure are good candidates for this test.

Contents

[edit] Preparations

Before actually taking the test, the patient may be instructed to fast for a period before the test will take place, and to stop taking any medications. On the day of the tilt table test, a patient may be monitored using an electrocardiogram (ECG) while lying down. Some facilities insert an intravenous line in case the patient needs to be given medication quickly; however, this may influence the results of the test and may only be indicated in particular circumstances. More recently, most investigators monitor cerebral perfusion using mean flow velocity recording with transcranial Doppler ultrasound in supine horizontal position, during and after head-up tilt. A 2MHz ultrasound transducer is placed on the temporal bone above the zygomatic arch, using a head gear to hold the probe in place.

[edit] Procedure

A tilt table test can be done in different ways and be modified for individual circumstances. In some cases, the patient will be strapped to a tilt table lying flat and then tilted or suspended completely or almost completely upright (as if standing). Most of the time, a patient is suspended at an angle of sixty to eighty degrees. Sometimes, the patient will be given a drug, such as Glyceryl trinitrate or isoproterenol, to create further susceptibility to the test. In all cases, the patient is instructed not to move. Symptoms, blood pressure, pulse, electrocardiogram, and sometimes blood oxygen saturation are recorded. The test ends when the patient faints or has other significant symptoms, at which time he or she is given medical attention, or after a set period of time (usually from 20 to 45 minutes, depending on the facility or individualized protocol).

[edit] Diagnostic symptoms

A tilt table test is considered positive if the patient experiences symptoms associated with a drop in blood pressure or cardiac arrhythmia. A normal person's blood pressure will not drop dramatically while standing, because the body will compensate for this posture with a slight increase in heart rate and constriction of the blood vessels in the legs.

If this process does not function normally in the patient, the test could provoke minor symptoms to a very severe cardiac episode, depending on the person. A common side effect during tilt table testing is a feeling of heaviness and warmth in the lower extremities. This is due to blood pooling in the legs and, to onlookers, the patient's lower extremities may appear blotchy, pink, or red. Dizziness or lightheadedness may also occur. Tilt table testing could provoke fainting or syncope as this is the purpose of the test and it may not be appropriate, or indeed possible to stop the test before this occurs as the drop in blood pressure or pulse rate associated with a faint can come on in seconds, This is why the patient's blood pressure and ECG should be continuously monitored during the test. In extreme, rare cases, tilt table testing could provoke seizures, or even prolonged asystole. If at any time in tilt table testing, a patient loses consciousness, he or she will be returned to a supine or head down position and will be given immediate medical attention, which could include being given fluids or perhaps atropine or adrenaline.

[edit] Cerebral perfusion in syncope

In 1991, Njemanze, first observed cerebral mean blood flow velocity (MFV) reduction during tilt-table testing, as premonitory signs (lightheadedness and dizziness) developed in patients. There was a significant reduction in MFV during actual syncope.[1] Subsequently, Grubb and colleagues made similar observations.[2] Furthermore, it was observed that as MFV fell to about -25% of the initial baseline MFV, premonitory symptoms developed, and at -50% of baseline MFV, syncope ensued in most patients.[3] In 1993, Njemanze, first observed that, in some group of patients he termed type 1, syncope occurred while patients had normal blood pressure levels, with a -53% drop in MFV, and a 58% increase in heart rate. In another other group, he termed type 2, syncope occurred with -33% drop in blood pressure, and a -58% reduction in MFV, but no change in heart rate.[4] It was suggested that, while in type 1, syncope was precipitated by paradoxical cerebral vasoconstriction, in type 2, syncope resulted from hypotension. Similar observations were made in syncopal patients who had had heart transplantation[5] and heart-lung transplantation[6]. This may imply that, cardiopulmonary reflexes may not be implicated in type 1 syncope, rather the mechanism was mediated by neurotransmitters involved in the regulation of cerebral vasoconstriction (adrenergic system) and vasodilation (nitroxidergic or nitrergic system). The latter derive from the pterygopalatine ganglion and innervate the arteries of the circle of Willis[7];[8];[9] Moreover, cerebral hypoperfusion preceded hypotension in single case observations[10];[11]. However, others, contend that, cerebral hypoperfusion without hypotension during head-up tilt, could arise from hyperventilation [12].

[edit] References

  1. ^ Njemanze, P.C. (1991). Transcranial Doppler evaluation of syncope: an application in aerospace physiology. Aviation, Space and Environmental Medicine, 62, 569-572.
  2. ^ Grubb, B.P., Gerard, G., Roush, K., Temesy-Armos, P., Montford, P., Elliott, L., Hahn, H., Brewster P. (1991). Cerebral vasoconstriction during head-upright tilt-induced vasovagal syncope. A paradoxic and unexpected response.Circulation, 84, 1157-1164.
  3. ^ Njemanze, P.C. (1992). Critical limits of pressure-flow relation in the human brain. Stroke, 23, 1743-1747.
  4. ^ Njemanze, P.C. (1993). Cerebral circulation dysfunction and hemodynamic abnormalities in syncope during upright tilt test. Canadian Journal of Cardiology, 1993, 9, 238-242.
  5. ^ Njemanze, P.C. (1993). Isoproterenol induced cerebral hypoperfusion in a heart transplant recipient. Pacing and Clinical Electrophysiology, 16, 491-495.
  6. ^ Njemanze, P.C. (1992). Cerebrovascular dysautoregulation syndrome in heart-lung transplant recipient, Journal of Cardiovascular Technology, 10, 227-232
  7. ^ Kamiya, A., Iwase, S., Michikami, D., Fu, Q., Mano, T., Kitaichi, K., Takagi, K. (2002). Increased vasomotor sympathetic nerve activity and decreased plasma nitric oxide release after head-down bed rest in humans: disappearance of correlation between vasoconstrictor and vasodilator. Neuroscience Letters, 281, 21-24.
  8. ^ Lee, T.J. (2002). Sympathetic modulation of nitrergic neurogenic vasodilation in cerebral arteries. Japanese Journal of Pharmacology, 88, 26-31.
  9. ^ Okamura, T., Ayajiki, K., Fujioka, H., Shinozaki, K., Toda, N. (2002). Neurogenic cerebral vasodilation mediated by nitric oxide. Japanese Journal of Pharmacology, 88, 32-38.
  10. ^ Njemanze, P. C. (1994). Cerebrovascular dysautoregulation syndrome complex--brain hypoperfusion precedes hypotension and cardiac asystole, Japanese Circulation Journal, 58, 293-297
  11. ^ Njemanze, P.C., Antol, P.J., Lundgren, C.E. (1993). Perfusion of the visual cortex during pressure breathing at different high-G stress profiles, Aviation, Space, and Environmental Medicine, 64 (5), 396-400
  12. ^ Novak, V., Spies, J.M., Novak, P., McPhee, B.R., Rummans, T.A., Low, P.A. (1998). Hypocapnia and cerebral hypoperfusion in orthostatic intolerance. Stroke, 29, 1876-1881.

[edit] External links