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Published ahead of print on July 17, 2003, doi:10.1164/rccm.200301-135OC
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American Journal of Respiratory and Critical Care Medicine Vol 168. pp. 671-676, (2003)
© 2003 American Thoracic Society

Original Article

Cyclic Changes in Arterial Pulse during Respiratory Support Revisited by Doppler Echocardiography

Antoine Vieillard-Baron, Karim Chergui, Roch Augarde, Sebastien Prin, Bernard Page, Alain Beauchet and François Jardin

Medical Intensive Care Unit and the Department of Biostatistics, University Hospital Ambroise Paré, Assistance Publique Hôpitaux de Paris, Boulogne Cedex, Paris, France

Correspondence and requests for reprints should be addressed to: François Jardin, M.D., Hôpital Ambroise Paré, 9 Avenue Charles de Gaulle, 92104, Boulogne Cedex, France. E-mail: francois.jardin{at}apr.ap-hop-paris.fr


   ABSTRACT
TOP
 ABSTRACT
METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
It has long been known that there are cyclic changes in arterial pressure during mechanical ventilation. They are caused by cyclic changes in both the right and left ventricular stroke output, occurring in opposite phases. As a result, arterial pulse pressure is increased during inspiration and decreased during expiration. A cyclic improvement in left ventricular systolic function could thus be expected during mechanical lung inflation. We tested this hypothesis in 31 septic patients who were mechanically ventilated in controlled mode by combining left ventricular measurements by transesophageal echocardiography with invasive arterial pressure recordings and Doppler analysis of pulmonary venous flow and right and left ventricular stroke volume. Lung inflation by tidal ventilation significantly improved left ventricular stroke volume (26 ± 0.4 cm3/m2 [mean ± SEM] vs. 22.3 ± 0.4 cm3/m2 at end deflation). Beat-to-beat analysis of pulmonary venous flow velocity illustrated the boosting effect of lung inflation on pulmonary venous return. The beneficial effect of inspiration thus appeared directly related to a significant increase in left ventricular diastolic volume (60.3 ± 1.5 cm3/m2 vs. 53.3 ± 1.4 cm3/m2 at end-expiration) and to a lesser extent to an improved left ventricular ejection fraction. We concluded that the transient beneficial hemodynamic effect of tidal ventilation on the left ventricular pump is essentially mediated by an improved left ventricular filling.

Key Words: mechanical inflation • left ventricular preload • pulmonary venous flow

It has long been known that there are cyclic changes in arterial pulse pressure during respiratory support. An increase in arterial pressure during the inspiratory phase of mechanical ventilation was first recognized by Werko in 1947 (1) and was later emphasized by Massumi and colleagues and called "reversed pulsus paradoxus" (2). In 1983, we performed an extensive evaluation of this phenomenon, using invasive measurements obtained by right heart catheterization (3); however, an increase in arterial pulse during inflation is obviously related to a decrease during deflation, and cyclic changes in arterial pulse during respiratory support can also be described as a decrease in arterial pulse during the expiratory phase. Recently, attention has been focused on measurement of the amplitude of this expiratory decrease to evaluate volume status in mechanically ventilated patients (4, 5). This evaluation was found to be of a great value in detecting fluid responsiveness, provided the patients had no spontaneous respiratory efforts (4, 5).

This study was designed to re-evaluate our first description obtained in 1983 by invasive measurements (3). Particularly, in this previous study, a beat-to-beat analysis of both ventricular stroke volume was performed by an indirect method, the pulse contour method, whereas a direct method, the Doppler technique, is now available for this measurement. Moreover, the respiratory changes in superior vena cava (SVC) diameter, which may affect systemic venous return, and in pulmonary venous return are now both available by a transesophageal approach using Doppler echocardiography and may thus be included in our physiologic reasoning.


   METHODS
TOP
 ABSTRACT
 METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Patients
Over a 30-month period (January 2000 to June 2002), we studied 31 patients (20 men and 11 women with a mean age of 65 ± 12 years) who required mechanical ventilation and invasive arterial pressure monitoring. Inclusion criteria were as follows: (1) sepsis defined by the criteria of the American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference (6); (2) acute circulatory failure defined by the need for vasoactive support to maintain systolic blood pressure of more than 90 mm Hg; and (3) the need for mechanical ventilation for associated acute lung injury, as defined by the North American/European Consensus Conference (7). All patients were free of previous cardiopulmonary disease. They were all ventilated in the control mode, with a tidal volume of 7–9 ml/kg, a respiratory rate of 15 per minute, an inspiratory:expiratory ratio of 1:2, and an end-inspiratory pause of 0.5 seconds. They were all sedated and perfectly adapted to the respirator.

In our unit, transesophageal echocardiography is integrated in our routine clinical practice applied to mechanically ventilated patients and does not require informed consent, as confirmed by the Clinical Research Ethics Committee of the French Intensive Care Society. Illustrative examples of this practice have been recently published in a clinical commentary (8).

Arterial Pressure Measurements
Systemic arterial pressure was recorded from the radial artery catheter, simultaneously with airway pressure obtained from a side-port of the tracheal tube. Pulse pressure was measured as systolic arterial pressure minus diastolic arterial pressure. Central venous pressure was measured through a jugular vein catheter previously inserted for fluid administration. Pleural pressure (Pl) was inferred from airway pressure using our previously published regressions (9), permitting calculation of the transmural value of systolic arterial pressure (SAPtm). An end-expiratory pause of 6 to 12 seconds was obtained by disconnecting the patient from the ventilator, permitting measurement of the cyclic increase (dUp) and decrease (dDown) of systolic pressure during tidal ventilation (10). All patients were monitored with a nail-bed oxymeter and had an arterial saturation of more than 90%, which was not modified during a short disconnection of 6 to 12 seconds.

Echo-Doppler Measurements
Echo-Doppler studies were performed with a Toshiba "CoreVision" model SSA-350A equipped with a multiplane 5-MHz transesophageal echocardiographic transducer. Special consideration was paid to four beats: an end-expiratory beat defined as the last beat occurring before mechanical lung inflation (beat 1), a beat occurring during the dynamic phase of lung inflation (beat 2), an end-inspiratory beat defined as the last beat occurring during the end-inspiratory pause (beat 3), and a beat occurring at the start of exhalation (beat 4).

Using an esophageal approach, we obtained a four-chamber view of the cardiac cavities. From this view, left (L), atrial (A), and ventricular (V) areas (A) were measured, the former at end systole (ES) and the latter at ES and end diastole (ED). LVES and LVED long axis were measured as the distance from the apex to the midpoint of the mitral valve ring, and the LVES and LVED volumes and ejection fraction were calculated using the single-plane, area-length formula (11).

A short-axis cross-sectional view of the LV at the midpapillary muscle level was obtained by a transgastric approach, permitting measurements of LVA, LV diameters (Diam), and wall thickness (ThED and ThES at end-diastole and end-systole, respectively), combining M-mode.

Doppler aortic and pulmonary artery velocity–time integrals were recorded at the level of LV and RV outflow tract, together with aortic and pulmonary artery diameters, permitting calculation of both LV and RV stroke index (12, 13).

Doppler pulmonary venous velocity-time integral was measured at the level of the left upper pulmonary vein, and SVC diameter was obtained as previously described (14).

Intraobserver and interobserver variabilities in our laboratory concerning the main values used in this study are indicated in Table 1 .


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  		TABLE 1. Intraobserver and interobserver variability of the main echocardiographic measurements used in the study

 
Special Calculations
The collapsibility index of SVC, which is the inspiratory decrease in SVC diameter, was determined as (maximal diameter on expiration - minimal diameter on inspiration)/maximal diameter on expiration and was expressed as a percentage (14).

LV maximal elastance was calculated as SAPtm/LVESV and was expressed in mm Hg · cm-3, indexed to body surface area (15).

LV mean systolic wall stress was calculated using the formula of Quinones and colleagues (16): LV mean systolic wall stress = 1/2 SAPtm (1/2 LVEDDiam + 1/2 LVESDiam)/(1/2 ThED + 1/2 ThES), expressed in dyne · cm-2 · 103, and indexed to body surface area.

Statistical Analysis
Statistical calculations were performed using the Statgraphics plus package V5 (Manugistics, Rockville, MD). Data are expressed as mean ± SD unless otherwise specified. Changes in hemodynamic values throughout a respiratory cycle, evaluated at the four previously described specific beats, were analyzed by analysis of variance for repeated measurements, followed by a Bonferroni's multiple comparison procedure. A p value of less than 0.05 was considered to be statistically significant.


   RESULTS
TOP
 ABSTRACT
 METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
The 31 patients studied had clear evidence of sepsis (bacterial pneumonia, 27 cases; meningitis, 2 cases; sepsis of urinary origin, 2 cases). At the time of the study, all patients were hemodynamically stable with a heart rate at 94 ± 13 beats/minute and systolic arterial pressure of 112 ± 26 mm Hg. All patients required hemodynamic support by dobutamine (5 mcg · kg-1 · min-1, two cases), dopamine (12 mcg · kg-1 · min-1, one case), epinephrine (1–2 mcg · kg-1 · min-1, 11 cases), or norepinephrine (1–3 mcg · kg-1 · min-1,17 cases). Nine patients had acute respiratory distress syndrome, and 22 had acute lung injury. Average PaO2 for the group was 94 ± 17 mm Hg, and the average PaCO2 was 44 ± 8 mm Hg. Average lung and chest wall compliance for the entire group at the time of the study was 38 ± 7 ml/cm H2O.

Respiratory Changes in Airway, Pleural, and Central Venous Pressures
Average end-inflation (plateau) pressure was 22 ± 5 cm H2O, and the average end-deflation pressure was 5 ± 2 cm H2O. Calculated from our previously established regressions (9), the average value of Pl was -1.5 ± 0.1, 2.4 ± 0.1, 2.8 ± 0.1, and -1.5 ± 0.1 mm Hg at beats 1, 2, 3, and 4, mean ± SEM, respectively, resulting in an average maximal change close to 4 mm Hg during tidal ventilation. Central venous pressure (transmural value) was slightly but significantly reduced during the inspiratory phase (12 ± 0.1, 10.7 ± 0.1, 10.9 ± 0.1, and 11.8 ± 0.1 mm Hg at beats 1, 2, 3, and 4, mean ± SEM, respectively).

Respiratory Changes in Arterial Pressure and in Left and Right Stroke Volume
An illustrative example of simultaneous recording of systemic arterial and airway pressure is shown in Figure 1 , and measurements of dUp and dDown are illustrated in Figure 2 , together with SVC diameter measurements (see also film 1). Cyclic changes in systemic arterial pressure and in left and right ventricular stroke volumes are presented in Table 2 . When compared with the preinflation value, tidal inflation produced a significant increase in both systolic and diastolic arterial pressures, but the increase in the former was significantly greater, resulting in a significantly enlarged pulse pressure. Conversely, when compared with the end-inflation value, deflation produced a significant decrease in both systolic and diastolic arterial pressures, but the decrease in the former was significantly greater, resulting in a significantly narrowed pulse pressure. Right and LV stroke volume changes were in opposite phases, with an increased LV stroke index at inflation, associated with a decreased RV stroke index at the same time, whereas the opposite was observed during deflation (Figure 3) (see also films 2 and 3). Among the 31 patients studied, 23 had a dUp (3.8 ± 1.8 mm Hg), isolated in seven cases and associated with dDown in 16 cases. Twenty-four patients had a dDown (8.6 ± 7.2 mm Hg), isolated in eight cases and associated with a dUp 16 cases. Individual values of dDown were correlated with individual values of the collapsibility index of SVC (Figure 4) .



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  		Figure 1. An illustrative example of simultaneous recording of systemic arterial and tracheal pressures. Numbers 1 to 4 refer to the four beats concerned by the study.

 


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  		Figure 2. Illustrative examples of an isolated cyclic decrease (dDown) (upper left panel) and of an isolated cyclic increase (dUp) (lower left panel). On the right panel, superior vena cava (SVC) diameter measurements obtained in the same patients evidenced a marked collapsibility associated with dDown (right upper panel) and no collapsibility associated with dUp. Echographic images shown on the left panel include a two-dimensional view (right part of the image) permitting the M-mode beam to be directed perpendicular to the vessel's short axis, and an M-mode recording (left part of the image), permitting an accurate measurement of superior vena caval diameter. The circles underline the end-inflation diameter and end-deflation diameters.

 

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  		TABLE 2. Cyclic respiratory changes in systolic arterial pressure, diastolic arterial pressure, pulse pressure, left ventricular stroke index, and right ventricular stroke index

 


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  		Figure 3. On the top panel, arterial pressure recording during tidal ventilation, followed by disconnection from the ventilator, illustrates in this patient the presence of a dUp, associated with a dDown. On the bottom panel, Doppler pulmonary artery (PA, left) and aortic (right) flow velocity are in opposite phases (note that the aortic velocity is downward as positive because the flow is away from the probe).

 


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  		Figure 4. Individual values of dDown are plotted against individual values of SVC collapsibility.

 
Respiratory Changes in LV Preload
Cyclic changes in LA systolic and LV diastolic dimensions are presented in Table 3 . Tidal inflation produces a significant increase in LA size associated with a significant increase in LV diastolic dimensions, measured in both the long and short axes. Cyclic changes in pulmonary venous velocity-time integral are depicted in Figure 5 (see also film 4). In patients exhibiting a dUp (Figure 5, left upper panel), we observed a significant increase in pulmonary venous velocity-time integral during the dynamic phase of lung inflation (beat 2) followed by a significant drop during the expiratory phase (beat 4). In patients with an isolated dDown (Figure 5, right upper panel), pulmonary venous velocity-time integral was not increased by lung inflation, but the significant drop during deflation was also present. Two illustrative examples are also shown in Figure 5 (lower panel).


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  		TABLE 3. Cyclic respiratory changes in left atrial area, left ventricular end-diastolic area in the short axis, left ventricular end-systolic area in the short axis, left ventricular end-diastolic volume, and left ventricular end-systolic volume

 


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  		Figure 5. Average respiratory changes in Doppler pulmonary venous velocity-time integrals (PVVTI) are presented on the upper panel, in patients exhibiting a dUp, isolated or associated with a dDown (16 cases, left panel), and in patients exhibiting an isolated dDown (eight cases, right panel). On the bottom panel, two illustrative examples of Doppler pulmonary venous flow velocity, corresponding to the same subgroups, are presented. *p < .05 versus beat 1.

 
Respiratory Changes in LV Systolic Function
Cyclic changes in LV ejection fraction, in LV maximal elastance, and in LV systolic wall stress are presented in Table 4 . Tidal ventilation was accompanied by a significant increase in LV ejection fraction and in LV fractional area contraction in the short axis. LV maximal elastance was unchanged. LV mean systolic wall stress was significantly increased by lung inflation.


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  		TABLE 4. Cyclic respiratory changes in left ventricular area contraction short axis, in left ventricular ejection fraction, in left ventricular maximal elastance, and in left ventricular mean systolic wall stress

 

   DISCUSSION
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
We observed in this study that tidal ventilation was accompanied by a transient improvement in LV efficiency, leading to a significant increase in arterial pressure and in LV stroke volume measured by the Doppler technique. This finding was in accord with our previous study (3) and also in part with a recent report by Denault and colleagues (17). Because this inspiratory improvement in LV stroke volume occurred together with a significant improvement in ejection fraction, it could be attributed in the first analysis to the positive effect of a small increase in Pl on the LV afterload, as conceptualized by McGregor (18) and subsequently studied experimentally during mechanical ventilation by Pinsky and colleagues (19). However, when calculating LV systolic wall stress, an index of left ventricular afterload (20), which integrates the transmural value of systolic arterial pressure, LV dimensions, and LV thickness, we observed a significant increase in this parameter during tidal ventilation. Thus, the transient improvement in LV efficiency observed in this study during inspiration was not explainable by the McGregor concept because LV afterload was actually increased and not decreased during Pl rise by inflation, as expected in a setting where both ventricular size and arterial pressure increased. However, the McGregor hypothesis has been reported to explain cyclic changes in arterial pulse observed during major swings in Pl in spontaneously breathing patients, and McGregor never addressed mechanical ventilation and afterload. Moreover, it is difficult to imagine that the small increase in Pl estimated during lung inflation in our patient would have any measurable effect on LV ejection pressure.

If a reduced afterload may be excluded, another explanation for the transient increase in LV stroke volume should be examined. This improvement might result from improved preload, improved contractility, or both. Improved preload was actually present in this study, where tidal ventilation was accompanied by a significant increase in LV end-diastolic volume. This finding was concordant with a previous study of our group, illustrating LV enlargement during tidal ventilation and suggesting that a sudden increase in alveolar pressure during tidal delivery might boost blood from the pulmonary capillary bed and thus transiently increase pulmonary venous return (3). This phenomenon was experimentally demonstrated by Versprille and was designated by these authors as an "ebb tide," in contrast to a "flow tide" occurring during the deflation phase (21). Left atrial enlargement observed during inflation in this study was in accord with a transient increase in pulmonary venous return. Moreover, in patients in whom a dUp was present, we observed that the dynamic phase of lung inflation significantly increased Doppler pulmonary venous flow velocity, whereas this velocity was reduced during deflation in all patients. However, the profile of pulmonary blood flow velocity, as reflecting a change in pulmonary venous blood flow, should be interpreted with caution. In selected cases, we observed that lung inflation was accompanied by an enlargement of pulmonary venous diameter. Thus, the lack of significant increase in pulmonary blood flow velocity observed in patients with an isolated dDown, associated with a similar average pattern of pulmonary blood flow velocity in both subgroups, strongly suggested that pulmonary blood flow was also increased by lung inflation in patients with an isolated dDown. However, the discharging volume through the pulmonary veins is probably less important when the pulmonary vascular bed is depleted, resulting in an isolated dDown. Experimental work by Brower and colleagues has demonstrated the quantitative influence on the respective distribution of pulmonary capillary zone conditions in changes in pulmonary venous return: Whereas a clear increase in pulmonary venous return by lung inflation was observed in a zone 3 condition, it was not observed when a predominant zone 2 condition was present (22).

Whereas this study was essentially devoted to elucidate the increase in arterial pressure produced by lung inflation, described by others as a dUp (10), we obviously observed that the expiratory phase was characterized by a drop in arterial pressure, described by others as a dDown (10). This drop was produced by a decrease of LV stroke volume during deflation. The left ventricle is filled by the blood present in the pulmonary capillary bed, and this filling reserve is suddenly emptied by inflation because the sudden increase in transpulmonary pressure boosts blood from the capillary bed. Additionally, the sudden rise in transpulmonary pressure increases right ventricular outflow impedance (23), precluding any immediate refilling of the pulmonary capillary bed. As recently emphasized, the drop in arterial pressure (4) and in arterial pulse pressure during deflation (5) is more marked in hypovolemic patients, and an expiratory drop in arterial pulse pressure of greater than 13% was a powerful index of volume status in a mechanically ventilated patient (5). In the same manner, recent experimental and clinical studies have emphasized the marked changes in peak aortic velocity produced by hypovolemia (24, 25). More recently, we observed that a marked collapsibility of the superior vena cava during Pl increase may also indicate an insufficient volume status during mechanical ventilation, delaying refilling of the pulmonary capillary bed by right ventricular output (14). Concordant with this previous report, a strong correlation was evidenced in this study between individual values of dDown and SVC collapsibility.

Finally, we also observed a transient increase in LV ejection fraction during tidal ventilation. This increase suggested an improved LV systolic function, despite increased afterload, that is, an improved contractility. However, ejection fraction is a load-dependent parameter (26), not totally accurate in characterizing LV contractility, and improvement observed during lung inflation in this study might be a positive effect of increased preload. By assuming that the transmural value of systolic arterial pressure reflects transmural LV end-systolic pressure, as proposed by Buda and colleagues (27), we also calculated LV end-systolic elastance to characterize contractility, as proposed by Slutsky and colleagues (15). This calculation demonstrated that in our patients LV contractility was unaffected by lung inflation. One may also hypothesize that a mechanical effect produced by a phasic lung volume increase, which may exert a somewhat higher external pressure on the left ventricle than reflected by Pl (28), might be able to assist LV systole (29).

In conclusion, the main finding of this study was the demonstration that lung inflation produced a transient improvement in LV filling, resulting from a transient increase in pulmonary venous blood flow. To our knowledge, this phenomenon, previously observed in experimental studies (21, 22), was never clearly demonstrated in humans. This suggests that the respiratory pump might also act as an additional circulatory pump, which cyclically improves LV filling by helping to mobilize blood from the pulmonary capillary bed.


   FOOTNOTES
 
This article has an online supplement, which is accessible from this issue's table of contents online at www.atsjournals.org

Conflict of Interest Statement: A.V-B. has no declared conflict of interest; K.C. has no declared conflict of interest; R.A. has no declared conflict of interest; S.P. has no declared conflict of interest; B.P. has no declared conflict of interest; A.B. has no declared conflict of interest; F.J. has no declared conflict of interest.

Received in original form January 30, 2003; accepted in final form July 8, 2003


   REFERENCES
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

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Proc. Am. Thorac. Soc. Am. J. Respir. Cell Mol. Biol.
Copyright © 2003 American Thoracic Society