Elsevier

Heart Rhythm

Volume 2, Issue 8, August 2005, Pages 807-813
Heart Rhythm

Original-clinical
Effect of cough on heart rate and blood pressure in patients with “cough syncope”

https://doi.org/10.1016/j.hrthm.2005.04.022Get rights and content

Background

“Cough syncope” is uncommon, and its mechanism remains controversial.

Objectives

This study evaluated susceptibility to cough-triggered neural reflex hypotension-bradycardia among cough syncope patients. We hypothesized that individuals with cough syncope would manifest not only more profound cough-triggered hypotension than do other fainters but also an inappropriate chronotropic response accompanying cough-induced hypotension, thereby supporting the notion that a neural reflex hypotension-bradycardia contributes to the condition.

Methods/Results

Three patient groups were studied. Group 1 patients (n = 9) had “cough syncope.” The remaining patients had recurrent faints of other causes: group 2 (n = 13) had a positive head-up tilt test, and group 3 (n = 18) had a negative tilt test. With cough, group 1 patients exhibited a greater drop in systolic pressure (−51 ± 19.3 mmHg) than did either group 2 (−23 ± 11.1 mmHg, P < .04) or group 3 patients (−28 ± 12.4 mmHg, P < .05). Recovery time to normalization of systolic pressure was greater in group 1 (25 ± 9.1 seconds) than in group 2 or 3 (8 ± 2.7 seconds and 9 ± 6.1 seconds, respectively, both P < .01 vs group 1). The expected positive chronotropic response accompanying cough-induced hypotension was diminished in group 1 patients (0.16 ± 0.21 bpm/mmHg) compared with that in either group 2 (0.74 ± 0.60 bpm/mmHg, P < .05 vs group 1) or group 3 (0.33 ± 0.15 bpm/mmHg, P = .06 vs group 1).

Conclusion

Cough syncope patients not only exhibit more pronounced hypotension in response to cough than other fainters, but they also manifest an inappropriate cough-triggered blood pressure-heart rate relationship. These findings argue in favor of the importance of a neurally mediated reflex contribution to symptomatic hypotension in cough syncope.

Introduction

Vigorous cough often triggers symptomatic hypotension in the form of transient “lightheadedness,” but complete loss of consciousness (so-called ‘cough syncope’) is uncommon.1 Given the infrequent occurrence of cough syncope, few studies have addressed its pathophysiology, and each has been able to evaluate only small numbers of patients.2, 3, 4, 5, 6, 7 Consequently, although cough syncope is widely recognized by clinicians, the basis for susceptibility to cough-triggered faints remains incompletely understood.

Various mechanisms have been proposed as the basis for cough syncope. For instance, it has been suggested that prolonged spasms of coughing impair venous return to the heart, resulting in decreased cardiac output and reduced systemic pressure.2 Alternatively, it has been argued that sustained coughing increases cerebrospinal fluid pressure and thereby initiates loss of consciousness by an ill-defined cerebral ischemia mechanism.3, 4 However, cough-induced hypotension, and even ‘cough syncope,’ may occur without prolonged periods of coughing. Thus, it has been presumed that, at least in some affected individuals, an abrupt transient increase of intraarterial pressure may trigger hypotension via a baroreceptor-initiated neural vasodilator-bradycardia reflex comparable to that believed responsible for other forms of neurally mediated reflex syncope.

In this study, we sought to determine whether individuals prone to cough syncope differ from fainters of other etiologies in terms of their hemodynamic response to a brief cough “intervention.” Specifically, we hypothesized that cough syncope patients would manifest not only a more pronounced cough-induced hypotension but that their chronotropic response to cough-triggered hypotension would be inappropriate. To this end, we measured the impact of a brief cough-induced arterial pressure impulse on heart rate and blood pressure in fainters of various etiologies.

Section snippets

Methods

All patients included in this study had been referred to the Cardiac Arrhythmia Center at the University of Minnesota, Minneapolis, Minnesota, or the Cardiac Arrhythmia Service at Central Minnesota Heart Center, St. Cloud, Minnesota, for evaluation of recurrent syncope. Three patient groups were identified. Group 1 patients consisted of individuals with a history compatible with “cough syncope.” These individuals presented with a history of two or more syncope episodes closely associated with

Clinical features

The study population comprised 40 individuals referred for diagnostic evaluation and treatment of syncope (Table 1). Group 1 consisted of 9 individuals (2 women and 7 men; age 64 ± 7.1 years) with a medical history compatible with cough syncope. In three cases, single or brief periods of coughing caused symptoms; in four cases, the history suggested longer coughing spasms were responsible; and in two instances the history was unclear. Head-up tilt testing was positive (i.e., induced syncope) in

Discussion

Cough syncope is an infrequent but well-recognized condition that has remained incompletely understood despite a number of important studies examining its pathophysiology.2, 3, 4, 5, 6, 7 In this context, this study provides four principal findings regarding blood pressure and heart rate responses associated with susceptibility to cough syncope. First, despite exposure to only a brief cough-induced pressure pulse (>220 mmHg) while in the supine position, individuals susceptible to ‘cough

Conclusion

Cough-induced syncope is a recognized clinical entity but one in which the pathophysiology remains controversial.1, 14 Findings reported here indicate that cough syncope patients exhibit more pronounced hypotension and a slower recovery process in response to cough than do fainters of other etiologies. This response occurs with even very brief cough stress with the patients in the supine position, tending to diminish the probability of a cerebral ischemia mechanism. In addition, our

Acknowledgments

We acknowledge the Electrophysiology Laboratory staff at Fairview-University Medical Center, Minneapolis, Minnesota, and at the Central Minnesota Heart Center, St. Cloud, Minnesota, for assistance with this project, and Barry L.S. Detloff for assistance with the illustrations.

References (15)

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    As early as 1953, a baroreflex mechanism was implicated in the etiology of cough syncope [8]. Over a half century later, Benditt and colleagues [71] shed further light on this issue by comparing the effects of a brief, volitional cough effort (requiring the induction of a transient increase in systolic blood pressure to > 220 mm Hg) in subjects with a history of cough syncope and individuals with syncope of other etiologies. The investigators reported a number of significant observations.

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This work was supported in part by grants from the Midwest Arrhythmia Research Foundation, Edina, Minnesota, to Drs. Samniah and Ermis.

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