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| | '''Heart rate turbulence''' ('''HRT''') is a physiological phenomenon characterized by a short-term fluctuation in the [[heart rate]] following a naturally occurring [[premature ventricular contraction]] ('''PVC'''). It reflects the heart’s ability to regulate and return to its baseline rhythm after a disruption in normal electrical activity. |
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| '''Heart rate turbulence (HRT)''' is the return to equilibrium of [[heart rate]] after a [[premature ventricular contraction]] (PVC). It consists of a brief speed-up in heart rate, followed by a slow decrease back to the baseline rate. An important feature of HRT is that PVCs occur naturally in most adults, so measuring the characteristics of a given person's HRT offers a noninvasive way to evaluate his or her cardiac function without applying artificial external stimuli.
| | == Overview == |
| | After a PVC, the heart momentarily speeds up, followed by a gradual slowing down back to the baseline heart rate. This biphasic pattern—first an acceleration, then a deceleration—is what defines heart rate turbulence. Unlike many cardiac diagnostic tests that require external stimuli or stress, HRT can be measured noninvasively during routine [[ambulatory electrocardiographic monitoring]] (such as a [[Holter monitor]]) since PVCs are commonly observed in the general population. |
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| The measured values of HRT parameters have been shown to be a [[statistical significance|statistically significant]] predictor of the probability of dying from cardiac disease after a patient suffers a [[myocardial infarction]].<ref>{{cite journal|vauthors=Barthel P, Schneider R, Bauer A, Ulm K, Schmitt C, Schömig A, Schmidt G |title=Risk Stratification After Acute Myocardial Infarction by Heart Rate Turbulence|journal=Circulation|year=2003|doi=10.1161/01.CIR.0000088783.34082.89|pmid=12939209|url=http://circ.ahajournals.org/content/108/10/1221.long|volume=108|issue=10|pages=1221–6}}</ref> HRT can also be used to predict death in patients with [[congestive heart failure]] from a lethal [[ventricular tachycardia|arrhythmia]].<ref>{{cite journal|last=Cygankiewicz|first=Iwona|title=Heart rate turbulence predicts all-cause mortality and sudden death in congestive heart failure patients|journal=Heart Rhythm|date=25 April 2008|volume=5|issue=8|pages=1095–1102|pmid=18675217|url=http://www.heartrhythmjournal.com/article/S1547-5271(08)00480-3/references|doi=10.1016/j.hrthm.2008.04.017}}</ref>
| | == Physiology == |
| | HRT is thought to be mediated by the [[baroreflex]], a homeostatic mechanism that helps maintain blood pressure stability. A PVC temporarily reduces [[cardiac output]], triggering a reflex response that accelerates the heart rate. This is quickly followed by a baroreceptor-mediated slowing as the heart adjusts to the transient change in hemodynamics. |
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| HRT has nothing to do with [[turbulence]] in [[fluid dynamics]]. | | == Parameters == |
| | HRT is typically quantified using two main parameters: |
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| See also [[Heart rate variability]].
| | * '''Turbulence onset (TO)''': The initial acceleration in heart rate after the PVC. |
| | * '''Turbulence slope (TS)''': The rate at which the heart rate slows down and returns to baseline. |
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| == History ==
| | Lower or absent HRT responses (blunted TO and TS) are associated with impaired autonomic function and reduced vagal tone. |
| The concept of HRT was introduced to the medical community by Georg Schmidt and colleagues from the [[Technical University of Munich]] in 1999 in the British medical journal [[the Lancet]]. While studying PVC characteristics, Schmidt and his colleagues had noticed that heart rate seemed to speed up after a [[Premature ventricular contraction|PVC]]. To get a clearer picture, they listed the time from one heartbeat's [[R-wave]] to the next R-wave (called RR intervals) and synchronized these lists to the time of the PVC beat and averaged the values in the list. A plot of this averaged RR interval list (called a PVC tachogram) not only confirmed their observation that heart rate sped up for a few beats after a PVC, but highlighted another less obvious feature, that heart rate then slows down beyond what it was before the PVC, before returning to the original heart rate.
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| If Schmidt et al. had stopped there, it would have been an interesting observation to be found in the footnotes of an [[electrocardiography]] textbook. Instead, they reasoned that just as loss of variability in heart rate indicated patients more likely to be at high risk of dying after a heart attack, this phenomenon might also be an indicator of a healthy control of heart rate in such patients. They proceeded to test this hypothesis using 24-hour electrocardiogram ([[Holter monitor]]) recordings from one hundred survivors of [[heart attack]]s with frequent PVCs. Greater turbulence seemed correlated with better prognosis. They then used this data to determine the optimal discriminating threshold between normal and abnormal HRT values, and came up with the values TS=2.5, TO=0%. Now came the test. Would HRT and these threshold values also work in the real world? These thresholds were applied to Holter records from a total of 1191 patients who had experienced a heart attack. There were 162 deaths (13.6%) during the follow-up period of about 2 years. Patients with abnormal HRT were approximately 3 times more likely to die than those with normal HRT, beating out some other commonly used predictors. Thus the field of HRT was born.
| | == Clinical Significance == |
| | HRT has emerged as a valuable noninvasive marker in risk stratification for patients with various cardiovascular conditions: |
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| == Mechanism of HRT ==
| | * After a [[myocardial infarction]] (heart attack), abnormal HRT has been shown to be a significant predictor of [[cardiac mortality]]. |
| HRT is widely considered{{By whom|date=March 2013}} to be a [[baroreflex]] phenomenon. That is, a PVC interrupts the normal [[cardiac cycle]], so the [[ventricle (heart)|ventricle]]s of the [[heart]] haven't had time to fill up to their normal level, before contracting and pumping their contents out. This results in a pulse ([[blood pressure]]) weaker than expected and triggers normal homeostatic mechanisms that try to compensate by constricting arteries and increasing heart rate (the turbulence onset part of HRT). This is accomplished by the brain reflexively withdrawing the [[Parasympathetic nervous system|parasympathetic]] nerve signals and increasing the [[Sympathetic nervous system|sympathetic]] nerve signals it sends to the heart. The compensatory constriction of the arteries and increased heart rate frequently cause blood pressure to overshoot normal values (overcompensates), and activate the baroreflex in reverse. This time, the brain reinstates parasympathetic nerve signals and decreases sympathetic nerve signals, which cause the heart rate to slow (the turbulence slope part of HRT).
| | * In patients with [[congestive heart failure]], abnormal HRT may indicate a higher risk of [[sudden cardiac death]] due to malignant [[ventricular arrhythmias]]. |
| | * HRT, when used in conjunction with other [[cardiac risk markers]] such as [[left ventricular ejection fraction]] and [[heart rate variability]], enhances the predictive power of identifying high-risk individuals. |
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| The exact quantitative contribution of the parasympathetic and sympathetic nervous flow to the heart to HRT is unknown. The simplistic view assumes that HRT is solely dependent upon parasympathetic activity because [[atropine]], a parasympathetic activity blocker abolishes HRT while a [[beta-blocker]] (sympathetic blocker) has no effect on HRT. The contribution of the [[compensatory pause]], the pause between the PVC and the next normal beat, to HRT is also unknown. Whether the single beat blood pressure increase after a compensatory pause occurs in both normal and compromised hearts as well is at present uncertain. To date, no physiological parameter has been linked in a quantitative manner to turbulence slope{{Citation needed|date=March 2013}}, whereas turbulence onset was shown by researchers in Calgary, Canada to be linearly dependent upon duration of subnormal blood pressure in a well designed experiment.<ref>Raj SR, Sheldon RS, Koshman M, Roach DE. "Role of hypotension in heart rate turbulence physiology." Heart Rhythm 2005 Aug;2(8):820-7. {{PMID|16051116}}</ref>
| | == Advantages == |
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| | * Noninvasive and cost-effective |
| Finally, the reason the size of HRT after a PVC predicts cardiac death is suggested by its mechanism. Parasympathetic nervous activity to the heart is believed to be protective and sympathetic nervous activity, deleterious, to the heart. Especially after a heart attack, sympathetic nervous activity tends to be increased. A healthy HRT indicates the presence of a healthy amount of parasympathetic activity, countering sympathetic activity. To take a wider view, however, it may be that a healthy HRT is also an indication of a healthy brain, and is the reason small HRT also predicts a likelihood of death from non- cardiac causes as well as from cardiac causes.
| | * Can be measured from long-term ECG recordings |
| | * Reflects both [[autonomic nervous system]] and baroreflex activity |
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| ==References== | | == Limitations == |
| <references />
| | * Requires a sufficient number of PVCs for accurate analysis |
| | | * Affected by beta-blockers and other autonomic-modulating drugs |
| == Further reading ==
| | * Not applicable in individuals with [[atrial fibrillation]] or frequent arrhythmias that mask normal sinus responses |
| * The [http://www.h-r-t.org HRT website] offers further information. | |
| * Georg Schmidt, "Heart-rate turbulence after ventricular premature beats as a predictor of mortality after acute myocardial infarction. ''Lancet'' 1999; Vol. 353; No. 9162; 1390-96" | |
| * Mari Watanabe, "Heart Rate Turbulence: a Review", [http://www.ipej.org/0301/watanabe.htm Indian Pacing Electrophysiol. ''J''. 2003;3(1):10] | |
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| | == See Also == |
| | * [[Heart rate variability]] |
| | * [[Baroreflex]] |
| | * [[Sudden cardiac death]] |
| | * [[Myocardial infarction]] |
| | * [[Ventricular arrhythmia]] |
| | * [[Holter monitor]] |
| | {{nt}} |
| | [[Category:Cardiology]] |
| | [[Category:Electrophysiology]] |
| | [[Category:Cardiac arrhythmia]] |
| | [[Category:Heart rate]] |
| | [[Category:Medical tests]] |
| [[Category:Cardiology]] | | [[Category:Cardiology]] |
| [[Category:Cardiac electrophysiology]] | | [[Category:Cardiac electrophysiology]] |
Heart rate turbulence (HRT) is a physiological phenomenon characterized by a short-term fluctuation in the heart rate following a naturally occurring premature ventricular contraction (PVC). It reflects the heart’s ability to regulate and return to its baseline rhythm after a disruption in normal electrical activity.
Overview[edit]
After a PVC, the heart momentarily speeds up, followed by a gradual slowing down back to the baseline heart rate. This biphasic pattern—first an acceleration, then a deceleration—is what defines heart rate turbulence. Unlike many cardiac diagnostic tests that require external stimuli or stress, HRT can be measured noninvasively during routine ambulatory electrocardiographic monitoring (such as a Holter monitor) since PVCs are commonly observed in the general population.
Physiology[edit]
HRT is thought to be mediated by the baroreflex, a homeostatic mechanism that helps maintain blood pressure stability. A PVC temporarily reduces cardiac output, triggering a reflex response that accelerates the heart rate. This is quickly followed by a baroreceptor-mediated slowing as the heart adjusts to the transient change in hemodynamics.
Parameters[edit]
HRT is typically quantified using two main parameters:
- Turbulence onset (TO): The initial acceleration in heart rate after the PVC.
- Turbulence slope (TS): The rate at which the heart rate slows down and returns to baseline.
Lower or absent HRT responses (blunted TO and TS) are associated with impaired autonomic function and reduced vagal tone.
Clinical Significance[edit]
HRT has emerged as a valuable noninvasive marker in risk stratification for patients with various cardiovascular conditions:
Advantages[edit]
- Noninvasive and cost-effective
- Can be measured from long-term ECG recordings
- Reflects both autonomic nervous system and baroreflex activity
Limitations[edit]
- Requires a sufficient number of PVCs for accurate analysis
- Affected by beta-blockers and other autonomic-modulating drugs
- Not applicable in individuals with atrial fibrillation or frequent arrhythmias that mask normal sinus responses
See Also[edit]
