The tilt-table test is a simple, noninvasive, and informative test first described in 1986 as a diagnostic tool for patients with syncope of unknown origin.[1] It is usually performed in hospital electrophysiology departments with the endpoint of reproducing syncope and subsequent appropriate therapy.
The causes of syncope have been divided into 6 major categories, as listed below.[2] After a careful history and physical examination, tilt-table testing is particularly helpful in confirmation of the etiology of syncope dysfunction of the autonomic nervous system, encompassing primary or secondary dysautonomias, postural orthostatic tachycardia syndrome (POTS), and vasodepressor or vasovagal syncope. Other venues of investigation, such as a 12-lead electrocardiogram, orthostatic blood pressure readings, Holter/event recording, serum glucose and electrolytes, echocardiography, and psychiatric and/or neurology consultation should be considered prior to tilt-table testing to rule out malignant dysrhythmic, metabolic, cardiac mechanical, or psychological/neurological etiologies of syncope.[3]
The 6 major categories of syncopal etiologies[2]
Neurological disorders
Vertebrobasilar transient ischemic attacks
Subclavian steal syndrome
Normal pressure hydrocephalus
Seizure disorders
Metabolic disorders
Hypoxia
Hyperventilation
Hypoglycemia
Mechanical heart disease
Aortic stenosis
Mitral stenosis
Global ischemia
Aortic dissection
Pulmonic dissection
Obstructive cardiomyopathy
Left atrial myxoma
Prosthetic valve dysfunction
Pulmonary embolus
Pulmonary hypertension
Cardiac arrhythmias/brady arrhythmias/tachyarrhythmias
Bradycardia/pauses
Sinus node dysfunction
AV conduction disease
Psychiatric disorders
Panic attacks
Hysteria
Autonomic Nervous System Dysfunction
Primary and secondary dysautonomias
Postural orthostatic tachycardia syndrome (POTS)
Postural orthostatic hypotension
Vasodepressor or vasovagal syncope
Consider tilt-table testing in patients with signs or symptoms suggestive of orthostatic hypotension, vasodepressor or vasovagal syncope, postural orthostatic tachycardia, or when other causes of syncope have been eliminated. In general, consider tilt-table testing for patients with the following issues:
Hypotension (unexplained)
Tachycardia when standing
Pallor when upright
Orthostatic palpitations
Dizziness (unexplained)
Lightheadedness
History of frequent unexplained falls
History of episodes of fainting or loss of consciousness
The ACC expert consensus document for tilt-table testing including indications was first published in 1996.[4] The European Society of Cardiology formed a taskforce to update guidelines for the diagnosis and management of syncope in 2001, which was revised in 2009.[3] It includes indications for tilt-table testing with classes of recommendation and levels of evidence (see Table 1).
Table 1. European Society of Cardiology 2009 Indications for Tilt-Table Testing [3] (Open Table in a new window)
Recommendations |
Class |
level |
Tilt table is indicated in the case of an unexplained single syncopal episode in high-risk settings (eg, occurrence of, or potential risk of physical injury or with occupational implications)or recurrent episodes in the absence of organic heart disease, after cardiac causes of syncope have been excluded |
I |
B |
Tilt testing is indicated when it is of clinical value to demonstrate susceptibility to reflex syncope to the patient |
I |
C |
Tilt testing should be considered to discriminate between reflex and orthostatic hypotensive syncope |
IIa |
C |
Tilt testing may be considered for differentiating syncope with jerking movement from epilepsy |
IIb |
C |
Tilt testing may be indicated for evaluating patients with recurrent unexplained falls |
IIb |
C |
Tilt testing may be indicated for evaluating patients with frequent syncope and psychiatric disease |
IIb |
C |
Tilt testing is not recommended for assessment of treatment |
III |
B |
Isoproterenol tilt testing is contraindicated in patients with ischemic heart disease |
III |
C |
Contraindications to tilt-table testing include the following:[3]
Coma
Feeble patient unable to stand
Lower extremity fractures
Severe anemia
Recent stroke (within seven days)
Recent myocardial infarction
Severe proximal cerebral or coronary arterial disease
Critical mitral or aortic stenosis
Left ventricular outflow tract obstruction
Hypotensive shock
Tachyarrhythmias
Severe metabolic acidosis
Electrolyte imbalance
End-stage renal failure
Severe heart failure
Avoid invasive intra-arterial blood pressure monitoring during tilt-table testing because catheterization may provoke a vasovagal reaction. Use a manual sphygmomanometer or digital plethysmography.[5]
Generally tilt-table testing is safe, but complications may occur related to decreased perfusion of the heart, including the following:
Electrocardiographic changes of transient myocardial ischemia with or without angina.
Vasospasm with isoproterenol administration.[6]
Occasionally, cardiac arrhythmias result in termination of the test, such as advanced atrioventricular block (second or third degree), severe bradycardia or pauses, atrial fibrillation, or tachyarrhythmias.
Complications may also occur related to decreased perfusion of the brain, including the following :
Seizures from prolonged hypotension (this is a transient phenomenon and not indicative of a seizure disorder)
Rarely, transient ischemic attacks or strokes occur.
Transient mental confusion can occur.
Patients may also experience nonspecific symptoms such as nausea or anxiety.
Discuss the test findings with both the patient and a companion to increase proper understanding of the results.
To avoid dehydration on the day of the study in patients who have been NPO after midnight, or receiving diuretic therapy, infuse 250 mL of 0.9% saline prior to tilt testing. Administer IV saline cautiously in patients with heart failure or renal failure.
Hold all medications the night before the procedure and in the morning to increase the sensitivity of the study. However, if diuretic or antihypertensive medications are a suspected etiology of syncopal episodes, allow the patient to take medications as usual the morning of the procedure.
Equipment/personnel should be as follows:[7]
Tilt table
Blood pressure monitor
Heart rate monitor
ECG rhythm monitor
Oxygen saturation monitor
Crash cart with defibrillator available
Infusion pumps
Quiet, air conditioned room
Soft background music (optional)
Direct physician supervision and nurse or trained technician assistance
Anesthesia is not to be used for this procedure. The patient must remain alert and awake to detect the moment of unconsciousness.
See the Technique section.
Discharge patient to home if blood pressure and heart rate are back to baseline and patient is not symptomatic.
Advise patient not to drive for 2 hours after the procedure.
The tilt-table test involves placing a patient on a flat table with a foot support, then tilting the table upward for a period of time to observe changes in blood pressure and heart rate. The patient is initially positioned supine and horizontal on the table, then tilted by degrees to a completely vertical, upright position. During the study, blood pressure, heart rate, oxygen saturation, and cardiac rhythms are recorded and monitored for the end point of fainting, which indicates a positive tilt-test result.[7] The patient is also observed for signs and symptoms that would necessitate early termination of the study.
The following steps describe positioning and technique in tilt-table testing:[8]
Dress patient in hospital gown without restrictive binding around abdomen or legs.
Insert an intravenous catheter and start a maintenance IV fluid drip with 0.9% NaCl.
Place patient supine on tilt table and secure patient with protective straps to avoid falls.
Apply blood pressure, heart rate, oxygen saturation, and rhythm monitors and record baseline measurements.
Have the patient rest supine for 10 minutes.
Provide a room that is quiet, dim, and a comfortable temperature.
Raise tilt table up to 80°.
Record blood pressure, heart rate, and oxygen saturations every minute.
Tilt table upright for 20-45 minutes depending on protocol.
Record rhythm changes on ECG strip.
Decide if pharmacologic provocation with nitroglycerine after 5 minutes of tilt or isoproterenol after 20 minutes of tilt is needed to provoke a response.
Record any symptoms or signs observed.
Terminate tilt if systolic blood pressure falls below 70 mmHg, even if symptoms are not present.
Terminate tilt if patient faints, and return patient to supine position.
Place patient in reverse Trendelenburg position if blood pressure does not normalize.
Administer a 250-mL bolus of 0.9% NaCl for hypotension.
Record blood pressure and heart rate until back to baseline.
Disconnect patient and allow patient to sit in chair for 5 minutes.
If provocative pharmaceuticals such as isoproterenol or nitroglycerine are used, differentiate the expected pharmacological effects of the drug from an abnormal response.
If avoidance of pharmacologic testing is desired, such as in a patient with ischemic heart disease, proceed with an upright tilt for 45 minutes. If a fainting response does not occur, the test is negative.
A positive tilt-table test result may be described as mixed, cardio inhibitory, or vasodepressor (see Overview).[9]
One particular problem with tilt-table testing is the plethora of protocols with differing sensitivity, which can make reproduction of results unreliable. The reliability and accuracy of tilt-table studies is improved when combined with hemodynamic and volume measurements.[10] These procedures include nuclear hemodynamic studies, which can be performed in conjunction with an outpatient tilt-table test. They can be repeated at follow-up visits to assess response to treatment. Autonomic reflex testing, which includes the combination of vascular reactivity measures with the tilt-table test, can also be performed to improve the sensitivity of tilt-table testing.[10] However, a criterion standard for positivity remains to be. Adherence to positivity criteria is essential (see Table 2). If hemodynamic changes occur without syncope, the test is a false positive.[7]
Table 1. Classification of Positive Responses to Tilt Testing [9] (Open Table in a new window)
Type 1 - Mixed |
Heart rate falls at the time of syncope, but the ventricular rate does not fall to less than 40 beats/min-1 or falls to less 40 beats/min-1 for less than 10 s with or without asystole of less than 3 s. Blood pressure falls before the heart rate falls. |
Type 2 - Cardioinhibitory |
A) Cardioinhibition without asystole: heart rate falls to a ventricular rate less than 40 beats/min-1 for more than 10 s, but asystole of more than 3 s does not occur before the heart rate falls. B) Cardioinhibition with asystole: Asystole occurs for more than 3 s. Blood pressure falls with or occur before the heart rate fall. |
Type 3 - Vasodepressor |
Heart rate does not fall more than 10% from its peak at the time of syncope. |
|
Exception 1. Chronotropic incompetence: No heart rate rise during the tilt testing (ie, less than 10% from the pre-tilt rate). |
|
Exception 2. Excessive heart rate rise: An excessive heart rate both at the onset of the position and throughout its duration before syncope (ie, greater than 130 beats/min-1). |
Deficiency of mechanisms that increase α- and β- adrenergic tone as a result of baroreceptor stimulation to compensate for a decrease of venous blood return to the heart
Abbreviation for head-up tilt test
Reduction in systolic blood pressure 25 mmHg from baseline supine values, sustained for at least 1 minute, with no associated increase in heart rate, and accompanied by symptoms of presyncope
Acute hypotension with or without bradycardia
Greater than 20-30 mmHg drop in systolic blood pressure plus a greater than 10 mmHg drop in diastolic blood pressure: Orthostatic hypotension is a common cause of a temporary loss of consciousness or feelings of lightheadedness, which results from changing body position from a supine or sitting position to a more vertical or upright position. Normally, blood tends to pool in the lower extremities due to gravity whenever a person stands up, potentially reducing the amount of blood available to return to the heart or brain.
The sympathetic nervous system regulates blood vessel tone by modulating nerve traffic to lower extremity blood vessels. The arterial and venous circulations compensate for pooling by constricting; thus redirecting blood flow from the leg veins back toward the heart. However, poor sympathetic tone to the lower extremity blood vessels can cause the mechanisms of arterial and venous constriction to fail, resulting in a disproportionate pooling of blood in the legs, instead of returning blood to the circulation, resulting in less oxygen supplied to the brain and heart. As a result, a person feels lightheaded and may even faint.
The occurrence of orthostatic symptoms in association with either a 30 beats/ minute increase in heart rate from baseline within 10 minutes of being tilted upright, sustained for 1 minute or more, or a heart rate of higher than 120 beats/ minute in the same period
The presence of premonitory symptoms and signs of imminent syncope such as severe weakness, lightheadedness, nausea, or diaphoresis
Pan-cerebral hypoperfusion accompanied by a lack of postural tone and unconsciousness without focal neurological deficit
Abrupt drop in blood pressure with symptoms
Abrupt drop in blood pressure and heart rate with symptoms: The hallmark of vasovagal syncope is the occurrence of one to several symptoms either before, during, and immediately after a brief loss of consciousness. Symptoms are varied, and may include nausea, flushing, headache, vertigo, palpitations, and asthenia.[11]
See the list below:
Brignole M. An Update on the Treatment of Vasovagal Syncope. HJC.(2004);45,132-135.Accessed Dec 6, 2010. http://www.hellenicjcardiol.com/archive/full_text/2004/3/2004_3_132.pdf
National Dysautonomia Research Foundation
The goals of pharmacotherapy are to reduce morbidity and prevent complications.
Vasodilators decrease preload and/or afterload.
This agent causes relaxation of vascular smooth muscle by stimulating intracellular cyclic GMP; the result is a decrease in blood pressure. Dosage forms include SL, TD, and IV preparations. The distinction between short-acting preparations for treatment of acute attacks and long-acting preparations for prevention of recurrent episodes is important.
Administration of 300-400 µg of sublingual nitroglycerine) in order to increase average heart rate by approximately 20-25% over baseline to trigger abnormal responses in susceptible patients after a tilt stabilization phase of 5 minutes.[4]
When given systemically, isoproterenol stimulates beta receptors in the heart, which produces positive inotropic and chronotropic effects. This results in increased cardiac output.
Isoproterenol has sympathomimetic effects; specifically, beta1- and beta2-adrenergic receptor agonist activity.
Intravenous medication used in incremental doses (usually 3 µg/min) in order to increase average heart rate by approximately 20-25% over baseline to trigger abnormal responses in susceptible patients after a tilt stabilization phase of 20 minutes.[4]
Isotonic sodium chloride (normal saline [NS]) is a standard crystalloid intravenous (IV) fluid used for initial volume resuscitation. It expands the intravascular and interstitial fluid spaces. Typically, about 30% of administered isotonic fluid stays intravascular; therefore, large quantities may be required to maintain adequate circulating volume.
NS restores interstitial and intravascular volume. Administer a 250-mL bolus of 0.9% NaCl for hypotension.