- Tilt table test
A tilt table test is a
medical procedureoften used to diagnose dysautonomiaor 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 pressureare good candidates for this test.
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 medicationquickly; 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 Dopplerultrasound 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.
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).
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 vesselsin 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
bloodpooling 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 atropineor adrenaline.
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. [Njemanze, P.C. (1991). Transcranial Doppler evaluation of syncope: an application in aerospace physiology. Aviation, Space and Environmental Medicine, 62, 569-572.] Subsequently, Grubb and colleagues made similar observations. [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.] 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. [Njemanze, P.C. (1992). Critical limits of pressure-flow relation in the human brain. Stroke, 23, 1743-1747.] 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. [Njemanze, P.C. (1993). Cerebral circulation dysfunction and hemodynamic abnormalities in syncope during upright tilt test. Canadian Journal of Cardiology, 1993, 9, 238-242.] 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 [Njemanze, P.C. (1993). Isoproterenol induced cerebral hypoperfusion in a heart transplant recipient. Pacing and Clinical Electrophysiology, 16, 491-495.] and heart-lung transplantation [Njemanze, P.C. (1992). Cerebrovascular dysautoregulation syndrome in heart-lung transplant recipient, Journal of Cardiovascular Technology, 10, 227-232] . 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 [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.] ; [Lee, T.J. (2002). Sympathetic modulation of nitrergic neurogenic vasodilation in cerebral arteries. Japanese Journal of Pharmacology, 88, 26-31.] ; [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.] Moreover, cerebral hypoperfusion preceded hypotension in single case observations [Njemanze, P. C. (1994). Cerebrovascular dysautoregulation syndrome complex--brain hypoperfusion precedes hypotension and cardiac asystole, Japanese Circulation Journal, 58, 293-297] ; [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] . However, others, contend that, cerebral hypoperfusion without hypotension during head-up tilt, could arise from hyperventilation [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.] .
* [http://www.escardio.org/guidelines-surveys/esc-guidelines/Pages/syncope.aspx 2004 European Society of Cardiology Guidelines on Management (Diagnosis and Treatment) of Syncope.]
* [http://www.med.umich.edu/1libr/chheart/noninv13.htm University of Michigan: Tilt Table Testing]
* [http://hora.cpmc.columbia.edu/dept/syncope/tiltfaq.html Tilt Table Test: Frequently Asked Questions]
* [http://www.postgradmed.com/issues/1998/01_98/grubb.htm Head-Upright Tilt Table Testing]
* [http://heartdisease.about.com/cs/syncope/a/tilttabltesting.htm Tilt Table Testing]
* [http://heartcenter.seattlechildrens.org/what_to_expect/tilt_table_test.asp Tilt Table Test information] from Children's Hospital Heart Center, Seattle.
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