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Am J Physiol Heart Circ Physiol 287: H798-H804, 2004. First published April 1, 2004; doi:10.1152/ajpheart.01174.2003
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Effects of thoracic blood volume on Valsalva maneuver

Julian M. Stewart,1,2 Marvin A. Medow,1,2 Barbara Bassett,1 and Leslie D. Montgomery3

Departments of 1Pediatrics and 2Physiology, New York Medical College, Valhalla, New York 10595; and 3LDM Associates, San Jose, California 95126

Submitted 15 December 2003 ; accepted in final form 26 February 2004


   ABSTRACT
TOP
 ABSTRACT
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
The Valsalva maneuver (VM) is frequently used to test autonomic function. However, the VM is also affected by changes in blood volume and blood volume redistribution. We hypothesized that even a standardized VM may produce a wide range of thoracic blood volume shifts. Larger blood volume shifts in some normovolemic individuals may be sufficient to induce decreases in blood pressure (BP) that preclude autonomic restoration of BP in phase II of the VM. To test this hypothesis, we studied 17 healthy volunteers aged 15–22 yr. All had similar vasoconstrictor responses when supine and upright and normal blood volume measurements. We assessed changes in thoracic blood volume by impedance plethysmography before and during the VM performed while subjects were supine. In some subjects, large decreases in BP were produced by thoracic hypovolemia. The maximum fractional decrease in BP correlated well (r2 = 0.64; P < 0.001) with thoracic hypovolemia and with systolic BP at the end of phase II of the VM (r2 = 0.67; P < 0.001). The BP overshoot in phase IV of the VM was uncorrelated to phase II changes, which suggests intact autonomic vasoconstriction. We conclude that the BP decrease during the VM is related to a variable decrease in thoracic blood volume that may be sufficient to preclude pressure recovery during phase II even with normal resting peripheral vasoconstriction. The VM depends on vascular as well as autonomic activation, which broadens its utility but complicates its analysis.

vasoconstriction; veins; thoracic; supine; upright; pleural; cardiac

THE VALSALVA MANEUVER IS classically defined as forcible exhalation against a closed glottis, which thereby increases pressure within the thoracic cavity and impedes venous return of blood to the heart (11). Pleural pressure so obtained is highly variable; therefore, for comparative purposes investigators use the "quantitative Valsalva maneuver" wherein the subject exhales with an open glottis against a known expiratory pressure (typically 30–40 mmHg) to generate comparable increases in intrapleural and right atrial pressures (15). This is thought to reduce variation in venous return due to differences in straining between subjects and so provide a standard volume-change stimulus.

The responses of heart rate and blood pressure (BP) to the maneuver comprises one of the most frequently used tests of circulatory autonomic function (23). Typical arterial pressure and heart rate changes are shown in Fig. 1. There is a brief increase in BP, denoted phase I, during which there is a mechanical increase in BP due to propulsion of blood from the thorax. Subsequently, decreased BP and increased baroreflex-mediated heart rate are produced by the decreased venous return and the consequent decreased cardiac output and BP during early phase II. Late phase II is marked by recovery of BP that is produced by a combination of vasoconstriction, sympathetic cardiac stimulation, and tachycardia. Once exhalation is complete, the release of strain results in restoration of the normal negative intrathoracic pressure and leads to the BP drop of phase III, which results in rapid refilling of the thoracic vasculature. Afterward, phase IV hypertension and reflex bradycardia occur, and a characteristic overshoot is produced by restored venous return and cardiac output with continued sympathetic stimulation of the heart and arterial vasoconstriction (26, 36). Baroreceptor-mediated tachycardia in phase II and bradycardia in phase IV are used as indexes of cardiovagal integrity (21). BP recovery in phase II and hypertensive response in phase IV are often used as indexes of baroreceptor-mediated sympathetic integrity (10). However, both early- and late-phase II periods are affected by changes in blood volume (7); therefore, BP changes cannot be regarded as entirely determined by autonomic responses.



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  		Fig. 1. A representative Valsalva maneuver: arterial blood pressure (BP; A) and heart rate (in beats/min; B). After inspiration, the subject blows against a resistance of ~40 mmHg. This produces an initial brief increase in BP in phase I, a decrease in BP that is later restored in phase II, a brief decrease in BP with inspiration in phase III, and an overshoot in phase IV. Hypotension in phase II is associated with tachycardia, whereas hypertension in phase IV is associated with bradycardia. See text for further details.

 
Implicit in the interpretation of the maneuver is that a given increase in intrapleural pressure produces a well-defined decrease in venous return. Also, provided cardiac function is normal, a given decrease in venous return produces a given decrease in cardiac output and BP. The decreases in venous return and cardiac output thus generate the early phase II decrease in BP, which is the actual stimulus to the baroreflex that results in the heart rate and BP responses.

We hypothesized that even a standardized Valsalva maneuver with controlled expiratory pressure may produce a wide range of thoracic blood volume shifts. These would include large volume shifts that produce decreased BP during phase II that cannot be restored by autonomic compensation. Thus the true vascular stimulus during normovolemia in the Valsalva maneuver (i.e., decreased venous return leads to decreased cardiac output which leads to decreased BP) could be sufficiently decreased so that autonomic compensation fails to restore BP in phase II.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Subjects and Experimental Outline

To test this hypothesis, we studied 17 healthy volunteers (7 male and 10 female) aged 14–22 yr (median, 17 yr). Volunteer subjects were recruited from young people referred for innocent heart murmur. All subjects were evaluated with normal ECGs and echocardiograms and had normal estimated resting cardiac output values. Subjects with a history of syncope or orthostatic intolerance were specifically excluded. Only those found on cardiac exam to be free from heart disease were eligible to participate. There were no trained competitive athletes or bedridden subjects among subjects. Informed consent was obtained, and all protocols were approved by the Committee for the Protection of Human Subjects of New York Medical College.

We assessed changes in estimated thoracic blood volume by impedance plethysmography (IPG) along with changes in heart rate and BP before and during the Valsalva maneuver, which was performed while subjects were supine. The Valsalva response has been shown to be strongly posture dependent (16, 28). We chose to perform the maneuver with subjects in the supine position to separate autonomic stimuli that arise due to orthostasis from stimuli due to the Valsalva maneuver.

Details of Method

Tests began in a temperature-controlled room after subjects were fasted overnight. After a 30-min acclimatization period, tests were performed in the following order with at least 15 min allowed for recovery in between each test: supine blood flow and arterial resistance measurements, Valsalva maneuver, and upright (at 35°) blood flow and arterial resistance measurements. Supine and upright peripheral blood flow and resistance measurements were used to demonstrate that current vasoconstrictor responses are consistent with data obtained from healthy control subjects during previous protocols (32, 33).

Peripheral blood flow, venous pressure, and arterial resistance measurements. We used venous occlusion strain-gauge plethysmography to measure forearm and calf blood flow. Supine measurements were made at the beginning of the experiments. Occlusion cuffs were placed around the upper and lower limbs ~10 cm above a strain gauge attached to a Whitney-type strain-gauge plethysmograph (Hokanson). While the subject was supine, blood flow was estimated using rapid cuff inflation to a pressure below diastolic pressure (e.g., 40 mmHg) to prevent venous egress (12). A smaller secondary cuff was briefly inflated to suprasystolic BP to prevent ankle blood flow. Systolic and diastolic BP values of the arm and leg were determined by oscillometry. Arterial inflow (in units of ml·100 ml tissue–1· min–1) was estimated as the rate of change of the rapid increase in limb cross-sectional area. For normative purposes, we previously collected peripheral blood flow data from 42 control subjects from a number of prior research protocols. For purposes of this study, decreased supine calf blood flow was defined as <1.2 ml·100 ml tissue–1·min–1, which was the smallest calf blood flow value we have measured in control subjects. Increased supine calf blood flow was defined as >3.6 ml·100 ml tissue–1·min–1, which was the largest calf blood flow value we have measured in control subjects. Capacitance vessel pressure [venous pressure (PV)] was also assessed in the steady state. After the strain-gauge dimensions returned to baseline levels following blood flow measurement, we measured PV by gradually increasing the occlusion cuff pressure until an increase in limb volume was just detected; this closely approximates invasive measurements of venous pressure (2). Peripheral resistance was calculated using the formula (mean arterial pressure – PV)/resting flow, where mean arterial pressure (MAP) was calculated as (systolic BP + 2 x diastolic BP)/3.

Heart rate and BP monitoring. ECG strips were monitored continuously. Upper-extremity BP values were continuously monitored with an arterial tonometer (Colin Instruments; San Antonio, TX) that was placed on the right radial artery and recalibrated automatically every 5 min against oscillometric BP values. Leg BP was measured intermittently by oscillometry on the calf contralateral to the strain gauge. ECG and pressure data were interfaced to a personal computer through an analog-to-digital converter (DataQ; Akron, OH). All data were multiplexed with strain-gauge and impedance information and were effectively synchronized.

Dye-dilution measurement of blood volume, cardiac output, and total peripheral resistance. Indocyanine green dye-dilution technique (1) employing a noninvasive spectrophotometric finger photosensor (DDG, Nihon-Kohden) was used to estimate blood volume, cardiac output, and total peripheral resistance. This technique has been verified during clinical studies (13, 14). First-pass kinetics were used to obtain cardiac output by Stewart's classic area-under-the-curve method (31). Cardiac index was obtained by dividing the cardiac output by the subject's body surface area (BSA), which was computed from the formula of Dubois and Dubois (4) as BSA (in m2) = [weight0.425 (in kg)] x [height0.725 (in cm)] x 0.00718. The dye-decay curve is a monoexponential equation that represents clearance by the liver. Once the hematocrit (Hct) was measured, we extrapolated the dye-decay curve to the time of dye injection (time 0) to yield the estimated blood volume. Total peripheral resistance was estimated by dividing the mean arterial BP (measured in the right arm while the subject was supine) by the cardiac index.

IPG to measure changes in thoracic blood volume. IPG has been used to quantify relative regional body fluid volumes (22, 27), but it cannot accurately quantify absolute total blood volumes (hence the green-dye measurements). Relationships between impedance and changes in fluid-compartment volumes and transient blood flows have been quantitated during orthostasis (3, 5). A tetrapolar high-resolution impedance monitor digital impedance plethysmograph (UFI; Morro Bay, CA) was used to measure volume shifts in the thoracic segment. Disposable ECG electrodes were attached to the foot of each subject's left leg, on the same side of the body at the lower ribcage near the xyphoid process, at the left shoulder, and on the left arm at the back of the hand. The IPG introduces a high-frequency (50 kHz), low-amperage (0.1 mA root mean square) constant current signal between the foot and hand electrodes. Electrical resistance values were measured using the shoulder and rib electrodes as sampling electrodes. Anatomic features were selected as the most appropriate locations for comparing changes within and across subjects. This combination of electrodes gives highly repeatable regional volume shifts and has been tested in a wide range of experiments by our group (19, 20, 35). The distance between the sampling electrodes (L) was measured.

We estimated the change in blood volume during the Valsalva maneuver from the formula (8) {Delta}volume = {rho} x (L/R0)2 x {Delta}R, where {rho} is the electrical conductivity of blood, which we estimated as 53.2 x exp(Hct x 0.022); Hct is the packed cell volume, which we measured as described by Geddes and Sadler (9); R0 is the baseline resistance; and {Delta}R is the time-dependent change in resistance during the maneuver. Volume change was calculated from the maximum decrease in {Delta}R during the maneuver using the value of R0 that immediately preceded initiation of exhalation as the starting point for calculation (as shown in Fig. 2). An initial transient {Delta}R value was relatively constant until release (Fig. 3). However, sometimes there was a systematic change as shown in Fig. 2. The average value of R0 was used, and {rho} was regarded as constant during the course of the maneuver. IPG measurements allow us to track acute blood volume changes in the thoracic compartment during the Valsalva maneuver.



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  		Fig. 2. An increase in impedance (A) and a decrease in blood volume (B) precede the decrease in BP (related to blood volume transit times; C). BP then decreases steadily through early phase II. Impedance decreases and calculated thoracic volume from the impedance measurement increases throughout the latter portions of phase II, which suggests venoconstriction. BP never regains resting levels, however, despite autonomically mediated tachycardia and intact orthostatic vasoconstriction in this subject. Phase IV hypertension and bradycardia are evident.

 


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  		Fig. 3. Fractional thoracic volume (A) and fractional BP (B) values during the Valsalva maneuver. Minimum phase II BP is mildly, moderately, and markedly decreased in association with mildly, moderately, and markedly decreased thoracic blood volume, respectively. BP recovery in late phase II is complete for the mild subject, nearly complete for the moderate subject (a normal volunteer), and incomplete for the marked subject.

 
Quantitative Valsalva maneuver. The quantitative Valsalva maneuver was performed while the subject was supine: he or she exhaled with an open glottis into a mouthpiece connected to the mercury column of a sphygmomanometer with an air leak. A pressure of 35–40 mmHg was maintained for 15 s. Pressure was released and care was taken to prevent deep breathing. Two attempts were made with 10 min of intervening quiet breathing to secure an adequate Valsalva maneuver with sustained intraoral pressure. The first adequate exhalation was used for data acquisition. All subjects were able to produce the maneuver, although in one case the pressure was unsustained (see below). BP, ECG, heart rate, and thoracic impedance values were recorded continuously throughout the maneuver. The BP response was quantified during straining and during the pressure overshoot. We used the maximum decline in BP to indicate the end of early stage II. Typically this occurred ~7 s into exhalation. We used the point of subsequent maximum systolic BP preceding release to indicate late stage II. Early BP changes are independent of the sympathetic nervous system, which requires at least some seconds to exert any effect (29, 34).

Size measurement. The inlet circumference (Cin) of the thorax was measured with a tape measure by encircling the chest under the axillae. The thoracic outlet circumference (Cout) was similarly measured by encircling the waist at the level of the xyphoid process. The thoracic inlet and outlet cross-sectional areas were, respectively, {pi} x (Cin/2{pi})2 and {pi} x (Cout/2{pi})2. We estimated thoracic volume as the average of the inlet and outlet cross-sectional areas multiplied by L, or L x 0.5 x [{pi} x (Cin/2{pi})2 + {pi} x (Cout/2{pi})2] = L x [(Cin)2 + (Cout)2]/8{pi}.

Orthostatic challenge. We used a low-angle tilt test to produce well-defined changes in peripheral resistance in response to orthostasis. An electrically driven tilt table (Cardiosystems 600; Dallas, TX) with a footboard was used. After supine measurements were complete, the subjects were tilted to 35° for 15 min to obtain steady-state measurements. Earlier work indicated that a 35° upright tilt produces an adequate orthostatic response (33). PV and limb blood flow values were remeasured at steady state, and forearm and calf arterial resistances were calculated.

Statistics

Tabular data concerning supine and upright blood flow, PV, heart rate, BP, and peripheral resistance values were compared by one-way ANOVA before and after the maneuvers. When significant interactions were demonstrated, the ratio of F values was converted to a t-distribution using Scheffé's test, and probabilities were thereafter determined. Correlations were obtained using the Spearman rank-order correlation statistic. All tabular results are reported as means ± SE.


   RESULTS
TOP
 ABSTRACT
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
All subjects were able to perform the supine quantitative Valsalva maneuver while maintaining the expiratory pressure at 35–40 mmHg for at least 15 s. Results are shown in Table 1 and Figs. 2– 5.


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  		Table 1. Size and hemodynamic data

 


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  		Fig. 5. Relationship between the fraction changes (decreases) in BP and intrathoracic blood volume calculated from impedance plethysmography. A linear fit to these data is constrained to pass through the origin, because a zero volume change produces no pressure decrement.

 
Hemodynamics and size measurements. Table 1 shows the sizes and peripheral hemodynamic measurements for all subjects. Total blood volume, thoracic volume, cardiac index, total peripheral resistance, and BSA values were similar for all subjects and did not relate to the magnitude of volume changes during the Valsalva maneuver. Blood volume was also uncorrelated with changes in BP during the Valsalva maneuver. Although there is copious evidence that the Valsalva response relates strongly to blood volume (7, 16, 28), all of our subjects had similar normal blood volumes. Resting heart rate, mean arterial pressure, and venous pressure measurements were also similar and, except for heart rate, changed similarly with upright tilt of the subject to 35°. The leg MAP and PV values increased to a similar extent with tilt in all subjects. Peripheral arterial resistance increased in all subjects, which indicates postural vasoconstriction.

Impedance, thoracic blood volume, and pressure changes during Valsalva maneuver. Young subjects often have wide ranges of BP and thoracic blood volume measurements. Thus for example, for a subject whose resting systolic BP is 95 mmHg (within normal range for age 14 yr), a decrease in BP of 20 mmHg is relatively more important than for another subject whose BP is 120 mmHg. Hence, for purposes of comparison, we chose to examine changes in BP as fractional changes in pressure, and similarly, changes in thoracic blood volume as fractional changes in blood volume. Figure 2 shows changes in impedance, blood volume, and BP for a representative subject. A decrease in thoracic blood volume that exceeds 25% is associated with a large change in BP. Resting and orthostatic BP, venous pressure, and arterial blood flow and resistance measurements were completely normal.

In Fig. 3, several subjects are compared with varying degrees of change in calculated thoracic blood volume and associated BP. Two of the three subjects shown did not have complete recovery of BP during late phase II, because thoracic blood volume and thus cardiac filling were insufficient and precluded recovery. Peripheral arterial resistance values while subjects were supine and during orthostatic testing were similar to results for healthy volunteers in prior experiments (32, 33). As shown in Fig. 4, early phase II systolic BP was poorly correlated with arm and leg arterial resistances while subjects were supine and upright. In all subjects, the expected phase II tachycardia and phase IV bradycardia and pressure overshoot were present, which is consistent with intact autonomic functioning. Changes in phase II BP values paralleled changes in thoracic blood volume in these subjects. The phase II fractional change in BP for volunteer subjects was 0.20 ± 0.03. The fractional change in thoracic blood volume for volunteer subjects was 0.15 ± 0.02.



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  		Fig. 4. Relationship between the minimum fractional systolic BP (SBP) during early phase II of the Valsalva maneuver and peripheral arterial resistance measurements in arms and legs while subjects are supine (A) and upright (B). BP is expressed as the fraction of baseline systolic BP preceding the maneuver. Resistance values are poorly correlated to early phase II pressure measurements. For supine subjects, r2 = 0.008 and 0.06 for arm and leg measurements, respectively. For upright subjects, r2 = 0.0008 and 0.001 for arm and leg measurements, respectively.

 
To demonstrate the relationship between BP and intrathoracic filling during early phase II of the Valsalva maneuver, we plotted the fractional BP as a function of fractional intrathoracic volume measured by impedance methods. This appears in Fig. 5. We used a linear fit: fractional BP change = a0 x fractional volume change, constrained to pass through the origin. The best fit (r2 = 0.64; P < 0.0001) is shown superimposed on the data. The graph suggests that there is a good relationship between phase II volume and BP changes during the Valsalva maneuver, which is similar from subject to subject once it is normalized.

To demonstrate that the decrease in systolic BP during phase II is related to systolic BP in late phase II, we plotted fractional systolic BP values during late phase II normalized to baseline BP measurements against fractional BP values during early phase II. As shown in Fig. 6, the best fit to all subject data is a straight line (r2 = 0.67; P < 0.0001). An exaggerated decrease in BP during early phase II is related to a reduction in late phase II BP.



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  		Fig. 6. Relationship between the maximum fractional systolic BP at end of Valsalva maneuver phase II (i.e., recovery) and the minimum systolic BP during early phase II. BP values are expressed as the fraction of baseline systolic BP preceding the maneuver. Least-squares linear fit to all data is shown. Lower early phase II BP correlates with lower late phase II BP values.

 
We examined phase IV overshoot BP values. As shown in Fig. 7, there is no significant correlation between minimum phase II systolic BP and phase IV overshoot values (r2 = 0.06; P = not significant). However, an overshoot is noted even when there is failure of pressure recovery (see Fig. 3).



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  		Fig. 7. Relationship between the minimum fractional systolic BP during early phase II and the maximum systolic BP during phase IV. BP values are expressed as the fraction of baseline systolic BP preceding the maneuver. Least-squares linear fit to all data is shown. There is no significant correlation.

 

   DISCUSSION
TOP
 ABSTRACT
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
Our results demonstrate a quantitative relationship between early and late BP changes and decreases in thoracic blood volume during phase II of the Valsalva maneuver. That decreased venous return produces decreased thoracic blood volume is not new. The new observation comprises the wide variation in venous return from subject to subject, which is sufficient to produce large decreases in BP that cannot be compensated for by sympathetic vasoconstriction. We demonstrated an uncompensated decrease in phase II BP that is independent of baseline vasoconstrictive ability and unrelated to decreased blood volume but that can produce late phase II findings, which suggests sympathetic impairment when none is present. Results suggest a variable redistribution of blood volume in individual subjects during the maneuver. The vascular as well as autonomic dependence of the Valsalva maneuver broadens its utility but complicates its analysis.

Pressure Decrease During Early Valsalva Maneuver is Independent of Sympathetic Activation

Sympathetic activation takes time. On the basis of data from Tyden (34), Rowell (25) estimated that a lag of 5–15 s occurs before vasoconstriction or venoconstriction takes place. During the early Valsalva maneuver, blood volume redistribution may therefore occur dependent on basal resistance and compliance properties. This coincides with early phase II. Cardiac activation may occur more rapidly, but exerts only a modest effect on pressure recovery, which instead depends on compensation for inadequate venous return. Indeed, Smith et al. (29) have carefully demonstrated a similar, although somewhat shorter, delay in the onset of muscle sympathetic nerve activity after Valsalva straining. Baseline sympathetic tone could play a role, but there is no evidence among our subjects of any difference in baseline peripheral vascular resistance or phase IV variation. We propose along with others (24) that during expiratory strain, there is a rapid decrease in venous return that was detected here as an increase in thoracic impedance.

The decrease in BP during phase II depends on the decrease in thoracic filling, which varies from subject to subject (see Figs. 3–5). Thoracic filling depends on blood volume, the time-dependent changes of venous resistance and venous pressure in regional circulations, and right atrial pressure. Intrapleural pressure is very similar to intraoral pressure (6). Right atrial pressure appears to change in a deterministic way with increasing intrapleural pressure, although the increase in atrial pressure is only ~70% of the increase in intrapleural pressure (15). Therefore, in subjects with similar total blood volume, thoracic filling depends on venous properties and provides insight into venous mechanisms. The data suggest that large intersubject variations in venous resistance, peripheral venous pressure, or both determine intersubject variation in venous return during early phase II. Given that resting arterial constriction and venoconstriction (inferred from peripheral venous capacity) are similar in all subjects, the data may indicate that individual differences relate to differences in venous mechanical properties. Prior work has supported the ability to generate well-defined venous return curves from graded use of the quantitative Valsalva maneuver (18), whereas other investigators have shown that such graded expiratory pressures produce graded changes in splanchnic venous pooling (17). In this regard, Fig. 4 resembles a ventricular function curve, albeit one obtained from a number of subjects, that reflects the ability to generate BP as a function of thoracic blood volume.

Anecdotally, large and dramatic venous function variations have occasionally been reported during the Valsalva maneuver up to and including complete collapse of large collecting veins with rapid onset of syncope despite ongoing tachycardia (30).

Pressure Recovery During Phase II of Valsalva Maneuver May Not Occur Despite Adequacy of Sympathetic Nervous System

Peripheral venous properties may so severely limit thoracic venous return during early phase II that no degree of sympathetic vasoconstriction or sympathetic cardiac activation can restore BP. Similar uncompensated phase II hypotension can be contrived by limiting blood volume. Thus Fritsch-Yelle et al. (7) could increase or decrease end-phase II BP values by infusing saline or furosemide. Similar effects are seen with a change in posture particularly if combined with relative hypovolemia (16, 28). However, our subjects were normovolemic and supine.

Limitations

We did not measure vasoconstriction during the Valsalva maneuver. This was not feasible using occlusion plethysmography, but may be addressed in the future by using peripheral impedance flow methods that are presently under consideration. We have used resting and orthostatic peripheral vasoconstriction as surrogates of sympathetic vasoconstrictive adequacy. Clearly, selective regional sympathetic abnormalities can also exist and could alter our conclusions.

Alternatively, a direct measure of sympathetic activity such as muscle sympathetic nerve activity could have enhanced our ability to state that volume changes per se, in the presence of intact sympathetic vasoconstriction, accounted for our findings. However, such instrumentation is often regarded as problematic in subjects of the age range used in our studies and was therefore not pursued. Nevertheless, in the absence of direct measures of sympathetic vasoconstrictor tone such as muscle sympathetic nerve activity, one cannot with certainty assert that vasoconstrictor responses and therefore autonomic vasomotor function were normal during the Valsalva maneuver or even during non-Valsalva intervals.

Posture. We chose to examine subjects in the supine position because we wanted to separate contributions from orthostasis from contributions due only to the Valsalva maneuver. The Valsalva maneuver response has been shown to relate strongly to posture (16, 28).

Effects of lung volume. Thoracic blood volume is affected by lung volume. The amounts of initial inspiration and leakage flow during the Valsalva maneuver can affect impedance measurements. Also, inspiratory volume can vary among subjects. Thus it would be best to include measurements of tidal volume for subjects, but this could not be accomplished using the present experimental design. However, intrapleural pressure, which is a critical external stimulus for blood and impedance changes, was controlled across subjects.

Age limitations may exist to the ability to generalize. Young adults and adolescents may not be perfectly represented by findings for mature adults. However, cardiovascular structure and function are essentially mature by puberty, and therefore, results can be regarded as at least qualitatively similar to those for older age groups. Moreover, younger subjects generally have the advantage of an absence of confounding illness such as heart disease, renal disease, hypertension, and diabetes. Also, the threshold for abnormal tachycardia in adolescents may be higher.


   ACKNOWLEDGMENTS
 
This work was supported by Grant 1RO1 HL-66007 from the National Heart, Lung, and Blood Institute.


   FOOTNOTES
 

Address for reprint requests and other correspondence: J. M. Stewart, Center for Pediatric Hypotension and Division of Pediatric Cardiology, Suite 618, Munger Pavilion, New York Medical College, Valhalla, NY 10595 (E-mail: stewart{at}nymc.edu).

The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.


   REFERENCES
TOP
 ABSTRACT
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

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