<i>Value of Intraoral Pressure as a Measure of Intrapleural Pressure</i>

Elisberg, Edward I.; Goldberg, Harry; Snider, Gordon L.

doi:10.1152/jappl.1951.4.3.171

Cited by 21 publications

(11 citation statements)

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“…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).…”

Section: Pressure Decrease During Early Valsalva Maneuver Is Independmentioning

confidence: 64%

Effects of thoracic blood volume on Valsalva maneuver

Stewart¹,

Medow²,

Bassett³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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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 (r(2) = 0.64; P < 0.001) with thoracic hypovolemia and with systolic BP at the end of phase II of the VM (r(2) = 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.

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Section: Pressure Decrease During Early Valsalva Maneuver Is Independmentioning

confidence: 64%

Effects of thoracic blood volume on Valsalva maneuver

Stewart¹,

Medow²,

Bassett³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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“…After 'total' blockade, all subjects showed an expiratory pressure-related rise in central and peripheral vein pressures, a lowering of cardiac output, entirely through reduction in stroke volume, and a proportional fall in blood pressure, with no change in resistance. The peripheral venous pressure rise was probably due to translocation of blood volume from the thorax and abdomen to limb veins (Hamilton et ul., 1936;Rushmer, 1947;Elisberg, Goldberg & Snider, 1951;Sharpey-Schafer, 1965). In all groups the main reflex effects consisted of a rise in total peripheral resistance and a rise in heart rate during the latter part of the manoeuvre.…”

Section: Discussionmentioning

confidence: 99%

Valsalva constrictor and heart rate reflexes in subjects with essential hypertension and with normal blood pressure

Pi¹,

Tonkin²,

Uther³

1979

Clin Exp Pharmacol Physiol

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1.The haemodynamic and heart rate responses to graded expiratory pressures were studied during Valsalva manoeuvres of standard 30 s duration in two groups of normotensives in the upper (n = 10) and lower (n = 9) halves of the 'normal' blood pressure range, and in a group of essential hypertensive subjects with minimal complications (n = 10). Haemodynamic variables were arterial, atrial and peripheral vein pressures, cardiac output and total peripheral resistance.2. Reflex and mechanical effects of the manoeuvre were assessed in each subject from changes in the relationship between the expiratory pressure and circulatory responses before autonomic blockade, after cardiac effector block and after 'total' blockade.3. The relationships between expiratory pressure and central and peripheral vein pressures were not changed by autonomic blockade, indicating that they depended on mechanical factors. In hypertensives the rise in venous pressures per unit expiratory pressure was significantly smaller than in normotensive subjects.4. The expiratory pressure-related rise in total peripheral resistance was reflex and was similar in magnitude in all groups before autonomic blockade. However, after cardiac effector blockade the rise was greatest in the hypertensive subjects. The sensitivity of the constrictor response was related t o the subjects' resting total peripheral resistance index when measurements from all subjects were included. 5.The reflex heart rate responses of the hypertensives showed: (i) accentuation of the bradycardia at the start of forced expiration; (ii) an increased threshold for eliciting tachycardia during the latter part of the manoeuvre; and (iii) attenuation of the 'overshoot' bradycardia following release of expiratory pressure.6. The differences between the responses of hypertensives and normotensives were relatively small and probably depended at least partly on differences in venous filling, structural differences of resistance vessels and different afferent inputs through arterial and cardiopulmonary baroreceptors.

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“…In addition, the decrease in thoracic filling, which varies from group to group, depends on blood volume, on the time-dependent changes of venous resistance and venous pressure in regional circulations, and on right atrial pressure. Intrapleural pressure is very similar to intraoral pressure (4). Right atrial pressure appears to change in direct proportion with increasing intrapleural pressure.…”

Section: Discussionmentioning

confidence: 70%

Splanchnic hyperemia and hypervolemia during Valsalva maneuver in postural tachycardia syndrome

Stewart¹,

Medow²,

Montgomery³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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Prior work demonstrated dependence of the change in blood pressure during the Valsalva maneuver (VM) on the extent of thoracic hypovolemia and splanchnic hypervolemia. Thoracic hypovolemia and splanchnic hypervolemia characterize certain patients with postural tachycardia syndrome (POTS) during orthostatic stress. These patients also experience abnormal phase II hypotension and phase IV hypertension during VM. We hypothesize that reduced splanchnic arterial resistance explains aberrant VM results in these patients. We studied 17 POTS patients aged 15-23 yr with normal resting peripheral blood flow by strain gauge plethysmography and 10 comparably aged healthy volunteers. All had normal blood volumes by dye dilution. We assessed changes in estimated thoracic, splanchnic, pelvic-thigh, and lower leg blood volume and blood flow by impedance plethysmography throughout VM performed in the supine position. Baseline splanchnic blood flow was increased and calculated arterial resistance was decreased in POTS compared with control subjects. Splanchnic resistance decreased and flow increased in POTS subjects, whereas splanchnic resistance increased and flow decreased in control subjects during stage II of VM. This was associated with increased splanchnic blood volume, decreased thoracic blood volume, increased heart rate, and decreased blood pressure in POTS. Pelvic and leg resistances were increased above control and remained so during stage IV of VM, accounting for the increased blood pressure overshoot in POTS. Thus splanchnic hyperemia and hypervolemia are related to excessive phase II blood pressure reduction in POTS despite intense peripheral vasoconstriction. Factors other than autonomic dysfunction may play a role in POTS.vasoconstriction; splanchnic arterial resistance; mesenteric artery; autonomic dysfunction; orthostatic intolerance IN PREVIOUS WORK WE DEMONSTRATED (31) the dependence of decrease in blood pressure on degree of thoracic hypovolemia during phase II of the Valsalva maneuver in healthy volunteers. We later showed that splanchnic hypervolemia during the Valsalva maneuver determines the magnitude of decrease in thoracic blood volume during early phase II of the maneuver (31). This, in turn, governs pressure recovery during late phase II (31).Prior work has shown that postural tachycardia syndrome (POTS), characterized by excessive tachycardia when upright in association with symptoms of orthostatic intolerance, is linked to thoracic hypovolemia (31). In POTS, thoracic hypovolemia may be produced by absolute hypovolemia, as observed in a variant of POTS with low peripheral blood flow (15), or may be produced by an excessive redistribution of blood volume away from the thoracic compartment, as observed in other variants (33). One such subset of POTS patients with redistributive thoracic hypovolemia, we designated "normal-flow POTS." This variant is characterized by normovolemia, normal cardiac output, and normal peripheral blood flow while resting supine. During orthostasis, however, there is thoracic ...

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Value of Intraoral Pressure as a Measure of Intrapleural Pressure

Cited by 21 publications

References 0 publications

Effects of thoracic blood volume on Valsalva maneuver

Effects of thoracic blood volume on Valsalva maneuver

Valsalva constrictor and heart rate reflexes in subjects with essential hypertension and with normal blood pressure

Splanchnic hyperemia and hypervolemia during Valsalva maneuver in postural tachycardia syndrome

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