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John B. Pierce Laboratory and Departments of Pediatrics, Epidemiology and Public Health, and Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut 06519
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
ACKNOWLEDGEMENTS
FOOTNOTES
REFERENCES
ABSTRACT 
Peters, Jochen K., George Lister, Ethan R. Nadel, and Gary
W. Mack. Venous and arterial reflex responses to positive-pressure breathing and lower body negative pressure. J. Appl.
Physiol. 82(6): 1889-1896, 1997.
We examined the
relative importance of arteriolar and venous reflex responses during
reductions in cardiac output provoked by conditions that increase
[positive end-expiratory pressure (PEEP)] or decrease
[lower body negative pressure (LBNP)] peripheral venous filling.
Five healthy subjects were exposed to PEEP (10, 15, 20, and 25 cmH2O) and LBNP (
10,
15, 20, and 25 mmHg) to induce progressive but
comparable reductions in right atrial transmural pressure (control to
minimum): from 5.9 ± 0.4 to 1.8 ± 0.7 and from 6.5 ± 0.6 to
2.0 ± 0.2 mmHg with PEEP and LBNP, respectively. Cardiac output
(impedance cardiography) fell less during PEEP than during LBNP (from
3.64 ± 0.21 to 2.81 ± 0.21 and from 3.39 ± 0.21 to 2.14 ± 0.24 l · min
1 · m2
with PEEP and LBNP, respectively), and mean arterial pressure increased. We observed sustained increases in forearm vascular resistance (i.e., forearm blood flow by venous occlusion
plethysmography) and systemic vascular resistance that were greater
during LBNP: from 19.7 ± 2.91 to 27.97 ± 5.46 and from 20.56 ± 2.48 to 50.25 ± 5.86 mmHg · ml1 · 100 ml
tissue1 · min
(P < 0.05) during PEEP and LBNP,
respectively. Venomotor responses (venous pressure in the
hemodynamically isolated limb) were always transient, significant only
with the greatest reduction in right atrial transmural pressure, and
were similar for LBNP and PEEP. Thus arteriolar rather than venous
responses are predominant in blood volume mobilization from skin and
muscle, and venoconstriction is not intensified with venous engorgement
during PEEP.
central venous pressure; venomotor; vasoconstriction; positive
end-expiratory pressure
INTRODUCTION HEMORRHAGE AND POSITIVE-PRESSURE ventilation diminish
venous return to the right side of the heart with a consequent decrease in cardiac output (CO) (1, 2, 6, 7, 23). Both conditions are associated
with a reduction in the transmural pressures of the heart, which
unloads cardiac mechanoreceptors and triggers compensatory reflexes to
restore cardiac filling. Peripheral venoconstriction or arteriolar
constriction augments circulating blood volume by decreasing overall
vascular capacitance (23, 24, 26).
Although the central reflex stimulus may be comparable during
hemorrhage and positive-pressure breathing, the filling state of the
peripheral blood vessels, specifically the venous capacitance system,
is not. During hemorrhage, venous volume is diminished and pressures
are low; during positive-pressure breathing, venous volume is increased
and peripheral venous pressures are elevated. Therefore,
positive-pressure breathing should counteract fluid reabsorption from
the interstitium, despite the decrease in cardiac preload, whereas
fluid reabsorption will increase circulating blood volume within 5 min
of hemorrhage (9, 23). In addition, elastic recoil forces that
passively reduce venous capacitance when arterial inflow decreases may
become less effective at high venous distending pressures (20), as with
positive-pressure breathing. Moreover, by increasing pleural and
pericardial pressure, positive-pressure breathing may reduce left
ventricular afterload (4, 15, 21), whereas hemorrhage has no direct
effect on these pressures.
Fessler et al. (12) and Nanas and Magder (19) demonstrated in dogs that
the pressure gradient for venous return (mean circulatory filling
pressure On the basis of these observations, we hypothesized that the reflex
responses of the peripheral circulation to changes in right heart
pressure would differ between LBNP (hemorrhage) and PEEP (or any other
form of positive-pressure breathing). Hence, the purpose of this study
was to examine the relative importance of the peripheral arteriolar and
venous reflex responses with these interventions. We were particularly
interested in the effects of PEEP on venomotor regulation in humans
because of the paucity of information, despite its widespread use.
Specifically, we asked the following questions:
1) What is the hierarchy of
arteriolar vs. venous reflex responses to a reduced cardiac filling
pressure and a reduced CO? 2) Is
this hierarchy shifted toward venomotor responses when the pressure
status of the peripheral venous system is elevated during
positive-pressure breathing?
To address these questions we compared the changes in forearm vascular
resistance (FVR) and forearm venomotor tone as a function of the change
in right atrial transmural pressure induced by PEEP and LBNP.
METHODS Subjects
right atrial pressure) during positive end-expiratory
pressure (PEEP) is maintained through a rise in mean circulatory
filling pressure matching that in right atrial pressure. This led to
the conclusion that the fall in CO during PEEP is caused by an
increased peripheral venous resistance that was, in part, explained by
venoconstriction (11). In humans, positive-pressure breathing increases
muscle sympathetic nerve activity, plasma norepinephrine
concentrations, and muscle and skin vascular resistance (29, 30, 34);
however, human peripheral venomotor responses to positive-pressure
breathing have not been well defined. Lower body negative pressure
(LBNP), which has been used to simulate hemorrhage, also increases
muscle sympathetic nerve activity and vascular resistance in muscle and
skin (14, 28, 32, 33). However, during mild levels of LBNP (<20
mmHg), significant venoconstriction has not been a consistent finding, suggesting the prominent role of arteriolar constriction and passive recoil of the capacitance vessels in blood volume mobilization during
hemorrhage (32, 33).
Measurements
To assess vascular responses we measured changes in forearm venous pressure during complete vascular occlusion and in forearm arterial blood flow (FBF) during venous occlusion while the subjects were exposed to various levels of PEEP and LBNP. In addition, right atrial transmural pressure, stroke volume (SV), heart rate (HR), and arterial blood pressure were measured during each condition. FVR and total vascular resistance were calculated from the relevant variables.Venomotor Tone
We used the occluded limb technique (27) to measure changes in venomotor tone (i.e., change in pressure at constant volume). An 18-gauge catheter was inserted into a large cutaneous vein of the subject's right forearm and connected to a Gould Statham P23 ID pressure transducer. With the subject in the supine position, the right hand was secured in a glove and the arm was suspended at 30-45° from the horizontal plane in an effort to allow free drainage of venous blood. The zero reference level was the tip of the catheter. Pneumatic occlusion cuffs placed around the wrist and the upper arm were rapidly inflated (<1 s) to 270-300 mmHg to isolate the forearm for ~8 min. Within 1-2 min after the occlusion, venous pressures reached a steady state (usually within 1 min). All subsequent pressure changes while the limb's circulation was isolated were interpreted as changes in venomotor tone. A Whitney mercury-in-Silastic strain gauge (35) was placed around the forearm just proximal to the tip of the catheter to verify that no volume changes occurred during the occlusion. In pilot studies using an indwelling arterial cannula, we demonstrated rapid equilibration between venous and arterial pressures in the occluded limb under these conditions (Fig. 1).
FBF and FVR
Venous occlusion plethysmography (35) was used to measure forearm blood flow (FBF). With the arm suspended as described above, the hand was excluded from the circulation by cuff occlusion of the wrist at 270-300 mmHg. At 20-s intervals another occlusion cuff, placed above the elbow, was rapidly inflated to 48 mmHg to stop venous outflow for 8-10 s. The rate of increase in forearm circumference was measured with a Whitney mercury-in-Silastic strain gauge. FBF (ml · 100 ml tissue1 · min1)
was calculated from the linear part of the slope of the volume change.
FVR
(mmHg · ml1 · 100 ml
tissue1 · min)
was calculated as MAP CVP/FBF, where MAP is mean arterial pressure and CVP is central venous pressure.
Right Atrial Transmural Pressure
We estimated transmural pressure from the difference between CVP and esophageal pressure at end expiration. CVP was measured through a 4-Fr central venous catheter inserted under local anesthesia into the left antecubital vein and advanced to the superior vena cava. The length of insertion was determined from anatomic surface measurements, and the pressure tracing was analyzed to exclude positioning of the catheter tip in the right ventricle. Esophageal pressure was measured through a fluid-filled 8-Fr nasogastric feeding tube that was advanced to the lower one-third of the intrathoracic esophagus. Correct position of the esophageal catheter was verified from changes in pressure during respiration. Both pressures were referenced to the midaxillary line and measured with a fluid-filled transducer (Gould Statham P23 ID).SV, CO, and Systemic Vascular Resistance
SV was measured noninvasively by impedance cardiography (Minnesota Impedance Cardiograph model 304 B) from four silver tape electrodes, two around the neck and two around the torso, using the equation of Kubicek et al. (17). Subjects were not asked to hold their breath during measurements; rather the impedance signals were recorded continuously and processed as the ensemble average of cardiac cycles over a 25-s period. HR was recorded on-line from an electrocardiogram, and CO was calculated as follows: HR × SV. Systolic (SBP) and diastolic blood pressure (DBP) were measured noninvasively at 1-min intervals by a Colin STBP 780 monitor. We calculated MAP and pulse pressure (PP) as follows: MAP = (2 · DBP + SBP)/3 and PP = SBP DBP. Systemic vascular resistance was calculated as
systemic vascular resistance index (SVRI, in
mmHg · l1 · min)
as follows: SVRI = (MAP CVP)/CO.
Experimental Protocol
Application of PEEP. Subjects breathed humidified air from a continuous-flow system at 60 l/min containing a large reservoir (~50 liters). The circuit consisted of large-caliber tubing and a low-resistance valve with a mouthpiece from which airway pressure was measured via a side port. A noseclip was used to ensure complete pressure transmission to the airways. PEEP was generated by placing the end of the expiratory tube under water, e.g., 10, 15, 20, and 25 cm. Airway pressure was measured directly at the mouthpiece with a Gould Statham P23 ID pressure transducer. Application of LBNP. During the entire experiment, subjects were lying with the lower one-half of their body enclosed in an airtight box with a flexible seal around their waist to prevent air entry. Negative pressure was generated by graded suctioning of air from the box and was continuously measured with a water manometer. Study sequence. After experimental preparation, subjects were allowed to rest for 30 min. Subsequently, eight experimental epochs were performed in each subject to measure venomotor responses to PEEP and LBNP. Each epoch lasted 8-9 min and was preceded by a baseline recording of nonoccluded venous pressure and forearm circumference. Then complete vascular occlusion was induced, and pressure was permitted to equilibrate (1-2 min). Next, two levels (2 min at each level) of PEEP or LBNP were applied in sequence, and 2 min were allowed for recovery. Before the release of the occlusion, intact venoreactivity was documented by a rise in venous pressure in response to a deep breath. Baseline conditions were regained during 15-min rest periods, during which all catheters were flushed with heparinized saline to maintain patency. Epochs with PEEP and LBNP were alternated. PEEP levels of 10 and 20 or 15 and 25 cmH2O and LBNP levels of10 and 20 or 15 and 25 mmHg were applied
during one epoch. The order of the PEEP or LBNP levels within an epoch
was reversed in a subsequent epoch with the same intervention. On the
basis of pilot experiments, we anticipated that these levels of PEEP
and LBNP would induce comparable reductions in right atrial transmural
pressure. When PEEP was used, baseline recordings were performed with
the subject already breathing from the circuit but without expiratory
load (zero PEEP). LBNP was started and stopped gradually over ~10 s.
After the occlusion experiments, FBF was measured during graded
increases in PEEP (baseline, 10, 15, 20, and 25 cmH2O PEEP, and recovery) and LBNP
(baseline, 10, 15, 20, and 25 mmHg LBNP,
and recovery).
Data Acquisition and Analysis
Data were recorded continuously with an eight-channel computerized data-acquisition system (MacLab, Macintosh). SV, HR, CO, and blood pressure data are reported as means ± SE during each condition. Venous pressure is reported as the maximum pressure that was observed over a 25-s period after the application of PEEP or LBNP. FBF was measured three to four times during each condition and is reported as the mean ± SE.Hemodynamic responses within and between the various levels of PEEP and LBNP were compared by an analysis of variance for repeated measures, and post hoc comparisons were done by paired t-tests with the appropriate Bonferroni correction. Regression lines of right atrial transmural pressure vs. HR, SV, CO, FVR, and SVRI were determined for each subject using the least-squares means method. The mean slopes for each relationship during PEEP and LBNP were compared by paired t-test. P < 0.05 was considered significant.
RESULTS
Central Hemodynamics
Figure 2 shows representative pressure tracings from one subject for experimental epochs of PEEP and LBNP. As intended, PEEP and LBNP decreased right atrial transmural pressure and subsequently reduced SV and CO while HR increased (Table 1). By design, right atrial transmural pressure was similar at the various levels of PEEP and LBNP. CO, however, was consistently greater during PEEP than during LBNP (P = 0.001). This disparity was mainly related to the greater SV during PEEP, most evidently at the two highest levels (P < 0.01). For further analysis, we plotted SV, HR, and CO as a function of right atrial transmural pressure, and there was no difference in the slopes of the resulting regression lines (Fig. 3).
10 and 20 mmHg lower body negative pressure (LBNP).
Thick vertical bars, breaks in recording between epochs and occlusion,
i.e., initiation of occluded limb technique before application of PEEP or LBNP (not shown for deep breath). Dashed vertical lines, initiation of event. All pressure recordings represent raw, unfiltered tracings; heart rate is derived from raw electrocardiogram tracing using a
ratemeter function. bpm, Beats/min.
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) or LBNP
(
). Values are means ± SE.
Correspondingly, SVRI was always lower during PEEP than during LBNP.
Reduction in right atrial transmural pressure produced proportional
increases in SVRI, and the slope of this linear relationship tended to
be steeper during LBNP than during PEEP
(P = 0.08; Fig. 4).
) or LBNP (). Values are means ± SE.
PEEP caused a progressive rise in MAP, whereas there was no change
during LBNP. This increase in MAP during PEEP compensated for the rise
in CVP, so the pressure gradient for systemic blood flow (MAP CVP) was maintained. There was a small but consistent reduction in
esophageal pressure with LBNP.
FBF and Venomotor Tone
The changes in the forearm circulation are illustrated in Table 2. LBNP induced a graded and sustained increase in arteriolar resistance, whereas the PEEP-induced changes were significant only at the highest level. Accordingly, the slope of the regression line relative to right atrial transmural pressure was steeper with LBNP than with PEEP (P < 0.05; Fig. 4).
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Complete isolation of the limb was obtained during the occlusions, as
indicated by constant forearm volumes after the initial plateau was
reached. Therefore, all changes in venous pressure reflected changes in
venomotor tone. As shown in Fig. 5 and
Table 2, significant venoconstriction occurred only at the highest level of PEEP and LBNP, and there was no difference between the two
conditions for a given reduction in right atrial transmural pressure.
In general, the venomotor responses were transient and never lasted
>1 min. Moreover, during LBNP there was an increase in FVR at levels
(10, 15, and 20 mmHg) where there was no change in
venomotor tone. Although varying in magnitude, a venomotor response to
a deep breath could be demonstrated in all subjects throughout the
experiment.
, change.
DISCUSSION
Our first aim was to examine the hierarchy of reflex changes in arteriolar and venous tone in response to reductions in right atrial transmural pressure provoked by LBNP or PEEP. These manipulations serve as accepted paradigms for hemorrhage or positive-pressure ventilation, respectively. The immediate and sustained increase in FVR, especially during LBNP, demonstrates that, in skin and muscle, arteriolar constriction is the predominant early effect of baroreceptor stimulation. In comparison, venomotor responses were minimal, provoked only at the greatest reduction in right atrial transmural pressure, and, most importantly, were transient.
Arteriolar constriction acts to preserve MAP and tissue perfusion pressure and to redistribute blood flow in favor of vital organs. Although this has no direct effect on cardiac preload, Browse and Hardwick (3), Rothe (22), Rothe and Gaddis (24), and Rowell (25) showed that the decrease in blood flow through the peripheral tissues reduces the pressure gradient across the venous resistances and results in elastic recoil of these capacitance vessels, shifting blood volume centrally. Our observation that the progressive reduction in right atrial transmural pressure triggered sustained changes in FVR before venoconstriction provides further evidence for the importance of passive, flow-dependent mechanisms in the control of venous capacitance. In contrast to arteriolar responses, all active changes in venomotor tone were transient, which is in accordance with earlier reports from the literature examining the circulatory adaptations to orthostatic stress (14, 27, 28) but contrary to what has been inferred in more recent studies using LBNP or PEEP (12, 32, 33). Recognizing the inherent difficulties in assessing venomotor responses in an intact subject, we believe that our observations were legitimate and not an artifact for the following reasons: 1) in pilot studies we demonstrated that venous and arterial pressures equilibrate in the occluded limb, 2) the veins were still responsive to a deep inspiration at the end of each epoch, and 3) we saw no change in forearm circumference under inflow and outflow occlusion, so we assume that no blood was lost from the forearm segment studied. Thus, under the conditions of these experiments, arteriolar responses were much more important than venomotor reflexes for restoring circulatory homeostasis.
Although it has been argued that cutaneous veins do not respond to baroreflexes and that muscle veins are only sparsely innervated (25), intense constriction of forearm veins is known to occur in response to mental strain, emotional stimuli, and deep breaths (3). In pilot studies, we have also seen dramatic increases of >30 mmHg in venous pressure in the occluded limb when MAP falls and when syncope was imminent during LBNP. Therefore, baroreceptor-mediated venoconstriction in muscle and skin veins may play some role in the rapid restoration of cardiac preload. However, sustained increases in venomotor tone may be detrimental for at least two reasons: 1) an increase in the resistance to venous flow may hinder passive mobilization of blood from various tissues (19), and 2) an increase in the upstream pressure would facilitate fluid extravasation from the vasculature and thus limit the effective blood volume expansion in the restoration of cardiac preload (16).
Our second aim was to examine whether the arteriolar and venous reflex responses during PEEP were different from those provoked during LBNP because of the fundamental differences in the state of the peripheral veins between these conditions, despite their similar effect on cardiac filling pressures. For comparable reductions in preload, our study demonstrates a better protection of CO during PEEP than during LBNP. This disparity was predominantly related to the changes in SV, which was higher at any given right atrial transmural pressure (Fig. 3). In response, we observed greater changes in FVR during LBNP than during PEEP and a similar trend in systemic vascular resistance. There were, however, no differences in the venomotor responses.
The higher CO during PEEP was probably related to a reduced afterload subsequent to the increased intrathoracic pressure (4, 15, 21). Alternatively, the impedance measurements of cardiac SV could have been influenced by an altered baseline impedance (Z) or dz/dt subsequent to a change in lung volume or position of the diaphragm. Impedance cardiography has been compared with dye dilution during graded exercise (8) and with the CO2-rebreathing technique at different lung volumes ranging from total lung capacity to residual volume and during a 50% increase in functional residual capacity induced by addition of an expiratory resistance (10). However, in these studies the strong correlation between changes in CO measured by the different techniques was not affected by lung volume. Lung volume changes induced by PEEP or LBNP are less than that considered by Edmunds et al. (10) and therefore unlikely to contribute to a significant artifact in the measurement of SV by impedance cardiography. A further concern was the use of an esophageal catheter to estimate pleural pressure, because this technique may underestimate pleural and juxtacardial pressures during positive-pressure breathing (18). However, such an error would yield a falsely high right atrial transmural pressure and could not explain the higher CO with PEEP. Thus the difference in afterload is the likely cause, and this is supported by the lower vascular resistances during PEEP.
Greater difficulties arise if one tries to explain the hierarchy in the signal processing by the baroreceptors that resulted in greater resistance changes during LBNP than during PEEP relative to the reduction in right atrial transmural pressure. Even the lowest level of LBNP induced a significant increase in FVR with no change in HR or blood pressure. This response was presumably mediated by cardiopulmonary mechanoreceptors, which include myelinated vagal afferents, C-fiber vagal afferents, and pulmonary stretch receptors. The tonic vasomotor inhibition of the vagal afferents on central neurons controlling sympathetic outflow to the peripheral circulation is thought to be mediated primarily by unmyelinated afferents (31). The increased HR during the higher levels of LBNP indicates unloading of the arterial baroreceptors by the falling pulse pressure, although MAP was preserved (Table 2). With PEEP, a comparable rise in FVR may have been attenuated by the observed increase in MAP, which should augment arterial baroreceptor input and induce vasodilation and cardiodeceleration. Moreover, this signal may have prevented greater changes in venomotor tone. Although the HR responses were not different between the two conditions, we suggest that PEEP results in conflicting signals to cardiopulmonary and arterial baroreceptors and that the arterial baroreflexes prevail.
Our study could not identify a greater role for venomotor responses in skin and muscle during PEEP than during LBNP. Therefore, other mechanisms must be responsible for the increase in mean circulatory filling pressure during PEEP, which has been shown to match the rise in CVP (12, 19). These include blood flow redistribution, splanchnic venoconstriction, and mechanical translocation of blood volume out of the chest. In dogs the rise in mean circulatory filling pressure was attenuated by 17 and 49% after carotid sinus and vagal denervation or total spinal anesthesia, respectively, demonstrating the contribution of baroreflexes (12). However, a specific analysis of the venomotor changes has not been possible with that approach.
A limitation of our study is that our measurements were restricted to the large forearm veins, and therefore we could not assess changes in the splanchnic circulation. Although skin and muscle veins constitute two of the largest capacitance beds, the splanchnic (venous) circulation may be the most responsive to baroreceptor regulation (16, 25). Therefore, our data may have underestimated the importance of active venoconstriction in the whole body response to changes in cardiac preload. We used the occluded limb technique, because it permits the most accurate measurement of changes in venous tone. The changes in forearm vascular capacitance, however, cannot be quantified. It is therefore difficult to judge the biological significance of small changes in venous pressure.
PEEP was applied as continuous positive airway pressure to ensure increased airway pressures throughout the respiratory cycle. While the net work of breathing is lowered, inspiratory work is exchanged for expiratory work with increasing levels of PEEP (13). No blood gas analyses were performed during PEEP, but, on the basis of the rate and depth of breathing, the higher levels of PEEP may have induced hyperventilation in some subjects. Therefore, we cannot exclude that respiratory alkalosis or an increased activation of pulmonary stretch receptors has contributed to the transient venomotor responses (3, 27). In addition, it is possible that an altered breathing pattern (e.g., increased tidal volumes) during PEEP may facilitate venous return during inspiration. Moreover, some subjects reported a sense of anxiety while breathing under high levels of PEEP. In these circumstances, some of our observations, such as the changes in HR, blood pressure, or breathing, may have been influenced by emotional stimuli and may therefore not be fully attributable to the activation of baroreflexes. On the other hand, this may help explain why there was no difference in the HR responses between the two conditions, whereas theoretically one might have expected a lower HR during PEEP than during LBNP.
In conclusion, our study demonstrates that, in the skin and muscle of the human forearm, arteriolar responses to right heart transmural pressure changes predominate in the compensation for a reduced CO, supporting the concept that arteriolar tone is an important factor regulating venous capacitance (5, 16, 24). Compared with the reduction in right atrial transmural pressure during LBNP, active venoconstriction is not intensified when CVP increases during positive-pressure breathing with PEEP.
ACKNOWLEDGEMENTS
We thank Tamara Morocco, Cheryl Kokoszka, and John Stofan for technical assistance and the subjects for their time and cooperation.
FOOTNOTES
Address for reprint requests: G. W. Mack, John B. Pierce Laboratory, 290 Congress Ave., New Haven, CT 06519.
Received 11 October 1996; accepted in final form 12 February 1997.
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