Heart rate variability with deep breathing as a clinical test of cardiovagal function

Neuromuscular Center, Neurological Institute, Cleveland Clinic, Cleveland, OH

Research into heart rate variability (HRV) and respiration over the past 150 years has led to the insight that HRV with deep breathing (HRVdb) is a highly sensitive measure of cardiovagal or parasympathetic cardiac function. This sensitivity makes HRVdb an important part of the battery of cardiovascular autonomic function tests used in clinical autonomic laboratories. HRVdb is a reliable and sensitive clinical test for early detection of cardiovagal dysfunction in a wide range of autonomic disorders.

Heart rate variability (HRV) has been a focus of interest in cardiovascular physiology for more than 150 years. This review will briefly survey the history of research linking HRV to respiration and then explore the clinical significance of this linkage, with a focus on HRV with deep breathing.

The first report linking HRV to respiration has been credited to Karl Ludwig, who in 1847 noted that heart rate increased with inspiration and decreased with expiration.1,2 The precise origin of this variability has been studied extensively, but a single unifying mechanism defining the determinants of HRV with respiration has not been established. However, several mechanisms have been identified that may be contributing to HRV. Hering in 1871 noted in dog experiments that inflation of the lungs was associated with tachycardia and that additional higher-pressure insufflation resulted in bradycardia. He concluded that HRV was determined by pulmonary reflexes.2,3 Bainbridge observed in dog experiments in 1915 that the heart rate increased during the diastolic filling of the heart that occurred during inspiration.4 In a subsequent article, published in 1920, Bainbridge attributed HRV to this reflex, which now carries his name.5

There is also evidence that HRV may be caused by central nervous system mechanisms. Canine experiments have revealed that rhythmic variations in the heart rate and ventricular pressure waves may coincide with rib cage movements in innervated, isovolumetric, left ventricular preparations.6 These data are consistent with radiation of respiratory center activ- ity to the cardiovascular autonomic centers in the medulla resulting in HRV. There is also evidence that stretch of the right atrium and sinus node region may produce HRV via cardiac reflexes.7 It is likely that all of these mechanisms are contributing at some level to the HRV that is observed with respiration.

Clinical interest in HRV was sparked by the 1973 report of Wheeler and Watkins, who first drew attention to cardiac vagal innervation as the mediator of HRV and its potential value as a clinical test of cardiovagal function.8 These investigators studied HRV with deep breathing (HRVdb) in normal subjects and dia- betic subjects, some with and some without evidence of autonomic neuropathy. They noted that HRVdb was abolished by atropine, implying that the efferent component of the reflex is vagally mediated (Figure 1). They also noted that HRVdb was reduced or abolished in diabetic subjects with autonomic neuropathy. They concluded that HRVdb was a clinically useful test for autonomic neuropathy in diabetic patients.

The relationship between vagal tone of the heart and HRV was further explored by Katona and Jih, who in 1975 reported on their experiments in a canine model.9 They found a linear relationship between HRV as assessed by variations in heart period and parasympathetic control of the heart, defined as the difference in the average heart rate before and after complete abolishment of vagal innervation (Figure 2). They concluded that the magnitude of the respiratory HRV is a measure of parasympathetic cardiac control. Fouad and colleagues duplicated this experiment in humans and found a similar linear relationship between HRVdb and parasympathetic cardiac control, leading them to conclude that HRVdb is an accurate index of cardiac vagal tone (Figure 3).10

Read the full study: Heart rate variability with deep breathing

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