Spontaneous baroreflex control of heart rate versus cardiac output: altered coupling in heart failure

Abstract

Sala-Mercado JA, Ichinose M, Hammond RL, Coutsos M, Ichinose T, Pallante M, Iellamo F, O'Leary DS. Spontaneous baroreflex control of heart rate versus cardiac output: altered coupling in heart failure. Am J Physiol Heart Circ Physiol 294: H1304-H1309, 2008. First published January 11, 2008 doi:10.1152/ajpheart.01186.2007.-Dynamic cardiac baroreflex responses are frequently investigated by analyzing the spontaneous reciprocal changes in arterial pressure and heart rate (HR). However, whether the spontaneous baroreflex-induced changes in HR translate into changes in cardiac output (CO) is unknown. In addition, this linkage between changes in HR and changes in CO may be different in subjects with heart failure (HF). We examined these questions using conscious dogs before and after pacing-induced HF. Spontaneous baroreflex sensitivity in the control of HR and CO was evaluated as the slopes of the linear relationships between HR or CO and left ventricular systolic pressure (LVSP) during spontaneous sequences of greater or equal to three consecutive beats when HR or CO changed inversely versus pressure. Furthermore, the translation of baroreflex HR responses into CO responses (HR-CO translation) was examined by computing the overlap between HR and CO sequences. In normal resting conditions, 44.0 Ϯ 4.4% of HR sequences overlapped with CO sequences, suggesting that only around half of the baroreflex HR responses cause CO responses. In HF, HR-LVSP, CO-LVSP, and the HR-CO translation significantly decreased compared with the normal condition (Ϫ2.29 Ϯ 0.5 vs. Ϫ5.78 Ϯ 0.7 beats ⅐ min Ϫ1 ⅐ mmHg Ϫ1 ; Ϫ70.95 Ϯ 11.8 vs. Ϫ229.89 Ϯ 29.6 ml ⅐ min Ϫ1 ⅐ mmHg Ϫ1 ; and 19.66 Ϯ 4.9 vs. 44.0 Ϯ 4.4%, respectively). We conclude that spontaneous baroreflex HR responses do not always cause changes in CO. In addition, HF significantly decreases HR-LVSP, CO-LVSP, and HR-CO translation.arterial baroreflex sensitivity; parasympathetic activity; stroke volume THE ARTERIAL BAROREFLEX is the primary short-term regulator of systemic blood pressure via modulation of parasympathetic and sympathetic nerve activity (26). Changes in arterial blood pressure result in arterial baroreflex-mediated reciprocal changes in heart rate (HR) and total peripheral resistance. Arterial baroreflex sensitivity (cardiac component) has often been assessed via techniques that analyze normally occurring spontaneous changes in blood pressure and the reciprocal changes in HR (3,12,21,32). This technique has been used as an index of cardiac baroreflex function in a number of species, including humans, and in many experimental and pathological conditions (1,3,11,13,18,21,25,32). Sinoaortic baroreflex denervation virtually abolishes baroreflex sensitivity assessed via this method, indicating that the spontaneous reciprocal changes in HR that occur as a result of changes in arterial pressure are indeed mediated by the baroreflex (1, 19). However, changes in HR do not necessarily dictate changes in cardiac output (CO) because stroke volume (SV) may also vary, for example, with ...

Progressive muscle metaboreflex activation gradually decreases spontaneous heart rate baroreflex sensitivity during dynamic exercise

“…Our approach to evaluate the arterial baroreflex control of HR based on spontaneous fluctuations in blood pressure and HR has advantages and disadvantages, which have previously been described in detail (39,40). Briefly, the spontaneous baroreflex technique enables a qualitative and quantitative estimate of the baroreceptor-cardiac response relationships during spontaneous blood pressure fluctuations without the necessity of any mechanical or pharmacological intervention.…”

Neural Regulation of Cardiovascular Response to Exercise: Role of Central Command and Peripheral Afferents

“…Baroreflex control over chronotropicity (as well as inotropicity) is a means to the end of controlling arterial pressure via changes in CO. However, changes in HR do not always result in changes in CO. Studies employing the spontaneous baroreflex technique showed that only about one-half of the baroreflex mediated changes in HR actually cause changes in CO at rest and during exercise this transfer is decreased even lower [85, 86]. At rest, there exists a wide range of HR over which sustained, steady-state changes in HR yield no change in CO due to reciprocal changes in SV [87, 88].…”

Dynamic cardiac output regulation at rest, during exercise, and muscle metaboreflex activation: impact of congestive heart failure

“…Our approach that was employed to evaluate arterial baroreflex control of HR and CO (based on spontaneous fluctuations in blood pressure, HR, and CO) has several advantages and disadvantages, as discussed previously (34,35). Briefly, this approach only examines the baroreflex gain over a relatively modest range of pressure, which, therefore, does not allow the calculation of the entire, sigmoidal baroreflex stimulus-response relationship.…”

“…Previous studies suggest that low-frequency (Lo-F: 0.04 -0.15 Hz) blood pressure fluctuations are buffered by the dynamic baroreflex control of HR (25, 28). However, we and others have observed that changes in HR do not necessarily elicit proportional changes in CO because stroke volume (SV) may also vary with the changes in ventricular filling time (17,34,48). Furthermore, transient increases in CO will lower ventricular filling pressure (and decreases in CO will raise filling pressure), thereby providing a self-limiting response (6,30,40).…”