Tilt-table test
- a tilt table test may be used to investigate a patient with a history of episodes of unexplained syncope
- tilt table testing not warranted in certain circumstances (1)
- a single syncopal episode, without injury and not in a high risk setting with evident neurocardiogenic features
- syncope where a specific cause has already been established and where demonstrating a neurocardiogenic component would not alter treatment plans
- tilt table testing not warranted in certain circumstances (1)
- tilt-table testing is a provocative test used to determine a patient’s susceptibility to vasovagal syncope (2)
- an orthostatic stimulus causes blood to pool in the lower extremities - in susceptible individuals, vasovagal syncope often ensues within approximately 20 minutes
- triggering mechanism in vasovagal syncope is believed to be caused by a relatively central hypovolemia - this occurs because of blood pooling in the lower extremities
- afferent end of this reflex may be mediated by left ventricular or right atrial mechanoreceptors that are activated during vigorous contraction around underfilled chambers in a situation similar to severe hemorrhage
- information from these mechanoreceptors travels along vagal afferent C fibers to the brain stem
- this pathway mediates the efferent response consisting of withdrawal of sympathetic vasomotor tone and a vagally mediated bradycardia.
- information from these mechanoreceptors travels along vagal afferent C fibers to the brain stem
- an orthostatic stimulus causes blood to pool in the lower extremities - in susceptible individuals, vasovagal syncope often ensues within approximately 20 minutes
- observations suggest the provoked response during tilt-table testing is essentially equivalent to the response during a spontaneous vasovagal syncopal episode
- patients often describe the symptoms produced by tilt-table testing as identical to those experienced during spontaneous episodes of syncope
- there are numerous variations in the methods used for tilt-table testing
- tilt-table tests are often done in 2 stages: a prolonged period of head-up tilt in the drug-free state, followed by a shorter period of head-up tilt after administration of a provocative pharmaceutical agent e.g. sublingual glyceryl trinitrate
- a typical protocol comprises:
- 30 min of lying flat on the tilt-table, during which time baseline values of pulse-rate and blood pressure are measured
- 40 min of lying at 60 degrees to the ground, during which time:
- the pulse-rate and blood pressure are monitored
- any symptoms are recorded
- a typical protocol comprises:
- the sensitivity of the drug-free head-up tilt table test, i.e., weighed against a classical clinical presentation of vasovagal syncope, for establishing a diagnosis of vasovagal syncope has been reported to range between 30 and 85% (3)
- tilt-table tests are often done in 2 stages: a prolonged period of head-up tilt in the drug-free state, followed by a shorter period of head-up tilt after administration of a provocative pharmaceutical agent e.g. sublingual glyceryl trinitrate
- interpretation of results of tilt table test:
- patients with vasovagal syncope have an abrupt decrease in blood pressure accompanied by some decrease in heart rate
- patients with a dysautonomic response to head-up tilt demonstrate a gradual and progressive decrease in blood pressure, usually with only a small or insignificant change in heart rate
- patients with postural orthostatic tachycardia syndrome demonstrate an early and sustained increase in heart rate, often associated with a progressive decrease in blood pressure, although it can be associated with frank hypotension and syncope
Reference:
- Grubb BP, Kosinski D. Tilt table testing: concepts and limitations. Pacing Clin Electrophysiol. 1997 Mar;20(3 Pt 2):781-7.
- Sutton R, Bloomfield DM. Indications, methodology, and classification of results of tilt-table testing. Am J Cardiol. 1999 Oct 21;84(8A):10Q-19Q.
- American college of cardiology expert consensus document. Tilt table testing for assessing syncope. J Am Coll Cardiol 1996;28: 263–275.
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