The Valsalva Manoeuvre—Cardiovascular Effects and Performance Technique: a Critical Review Robert Looga ∗
Total Page：16
File Type：pdf, Size：1020Kb
Respiratory Physiology & Neurobiology 147 (2005) 39–49 The Valsalva manoeuvre—cardiovascular effects and performance technique: a critical review Robert Looga ∗ Department of Pathophysiology, Faculty of Medicine, University of Tartu, 19 Ravila, 51014 Tartu, Estonia Received 19 May 2004; received in revised form 6 January 2005; accepted 10 January 2005 Abstract Variations in the technique of the Valsalva manoeuvre (VM) have been shown to greatly influence the pattern of cardiovascular response (CVR) to the test. Intra-strain tachycardia, post-strain bradycardia, Valsalva ratio, and baroreflex sensitivity decrease in proportion to an increase in lung volume and a decrease in strain pressure at VM. In conditions of completely expanded lungs and low strain pressure many subjects reveal an intra-strain bradycardic response to VM instead of the usual tachycardic one. Intra-strain arterial hypotension and post-strain hypertension decrease with decrease in strain pressure. The changes in heart rate and blood pressure during an expiratory VM are greater than the responses observed during completition of an inspiratory VM. The rate of the deep inspiration prior to strain has an impact particularly on phase I of the VM. The magnitude of the CVR correlates with the strain duration, particularly at high levels of strain pressure, and depends on the baseline level of the cardiovascular parameters and their variations. The paper discusses the possible mechanisms of different CVRs to variations in the technique of the VM. Some practical recommendations are suggested. © 2005 Elsevier B.V. All rights reserved. Keywords: Valsalva manoeuvre, methods; Cardio-respiratory control, intrapulmonary pressure; Volume, lung; Strain duration, baseline level, cardiovascular response, its mechanisms 1. Introduction clusion finding a significant tachycardia as a typical re- sponse to the VM. The reason for this apparent discrep- In 1851, Ernst Heinrich Weber reported a consider- ancy has remained unclear. One might assume, how- able deceleration or even a transitory arrest of the heart ever, that some differences in experimental conditions in response to the Valsalva manoeuvre (VM). Some and/or in the technique of the VM were involved. The years later, Donders (1854) reached the opposite con- next 150 years witnessed thousands of studies on car- diovascular effects of the VM in normal and diseased ∗ Tel.: +37 2 7374370; fax: +37 2 7374372. subjects. The studies took into consideration a number E-mail address: [email protected]. of experimental conditions and factors affecting the 1569-9048/$ – see front matter © 2005 Elsevier B.V. All rights reserved. doi:10.1016/j.resp.2005.01.003 40 R. Looga / Respiratory Physiology & Neurobiology 147 (2005) 39–49 cardiovascular response (CVR) to the VM. Thus, it was 2. Fundamental mechanisms of the suggested that the VM tests should be performed in cardiovascular response to the Valsalva the morning at least 2 h after a light breakfast. Subjects manoeuvre were requested to abstain from coffee and cigarettes on the previous evening. The room temperature and the Table 1 presents a schematic overview on the fun- subject’s age were to be taken into account (Wieling, damental mechanisms of the CVR to the Valsalva ma- 1993). noeuvre. According to Hamilton et al. (1936), this re- Suprisingly, much less attention has been paid to the sponse is divided into four basic phases. If a final deep effects of the variations in the performance technique breath precedes the VM, as is usually the case, the con- such as volume and rate of the prestrain breath, ex- comitant CVR is treated as phase 0. tent and rate of the strain pressure increase, changes In all phases, the CVR may be divided further into in lung volume and strain pressure, duration of the an earlier subphase (E) and a subsequent later sub- strain period, depth and rate of the poststrain breath- phase (L). As a rule, the subphase E is related to the ing. All these technical conditions have been shown primary mechanical disturbance of arterial blood pres- to affect the patterns of CVR to the VM (Looga, sure by respiratory changes in intrathoracic pressure, 1970). and the subsequent secondary subphase L, to the re- The purpose of the present paper is to review the flex compensatory response to such disturbance. Input cardiovascular effects and their mechanisms of some from the arterial baroreceptors plays the main role in common but mostly neglected, variations in the perfor- this compensatory response (Sharpey-Schafer, 1965; mance technique of the VM. Eckberg, 1980; De Burgh Daly, 1986). However, some Table 1 Fundamental mechanisms of cardiovascular response to the inspiratory Valsalva manoeuvre E: mechanical impact on arterial blood pressure, and L: its subsequent reflex compensation; HR: heart rate; PVR: peripheral vascular resistance; bold, regular, interrupted, and dotted arrow: mechanical, neuroafferent, neuroefferent and hormonal impact on arterial pressure respectively; bold double arrow: competitive counteracting reflex impacts on arterial pressure. R. Looga / Respiratory Physiology & Neurobiology 147 (2005) 39–49 41 other reflex influences, such as a depressor reflex from autonomic activity (Looga, 2001).Thus, in phase II one the slowly adapting pulmonary stretch receptors and a can observe antagonistic influences from two sets of pressor reflex from lung blood vessel mechanorecep- receptors. tors (Looga, 1997) may essentially modify the barore- The cessation of the VM strain evokes a sudden fall ceptor CVR to the VM. in the intrathoracic pressure with a simultaneous me- The fall in arterial pressure in phase 0E seems to chanical fall in arterial blood pressure (Eckberg, 1980; be the direct mechanical effect of decreasing intratho- De Burgh Daly, 1986), phase IIIE. The inhibited venous racic pressure during deep inspiration. The following return is released again and blood flow rushes into lung rise in the heart rate (HR) and peripheral vascular re- vessels, the volume of which increases abruptly due sistance (PVR) present a reflex-compensatory response to the first post-strain deep inspiration. A reflex com- by the arterial baroreceptors and mechanoreceptors of pensatory response follows from arterial baroreceptors the lung vessels to the decrease in blood pressure and and from the mechanoreceptors of the pulmonary blood an increase in venous return. As a result, blood pressure vessels, whereby the existing tachycardia and periph- rises (phase 0L). eral vasoconstriction from phase IIL are augmented still The phase 0L effect links up to the rise of blood further (phase IIIL). pressure in phase IE. The latter is induced by pro- Next, there is an increase in diastolic filling and pelling a quantity of blood into peripheral arteries stroke volume of the heart. As the total peripheral re- from heart and intrathoracic blood vessels under the sistance remains elevated, the ejection of the increased direct mechanical action of the increased intrathoracic stroke volume into the constricted arterial system pro- pressure (Eckberg, 1980; De Burgh Daly, 1986). In the duces a sharp increase in arterial blood pressure, “over- following compensatory phase, IL, the blood pressure shoot” (Sarnoff et al., 1948), phase IVE. The follow- and the heart rate start to fall under the stimulation ing reflex compensatory mechanism originates from of arterial baroreceptors and pulmonary stretch arterial baroreceptors, phase IVL. However, its impact receptors. presents itself mainly in the form of the bradycardia. Phase IL links up to the mechanical decrease of Although the blood pressure falls significantly from the blood pressure in phase IIE. The latter is induced the level of the overshoot, it still remains elevated for a by a considerable decrease in the stroke volume of considerable time. During this period the sympathetic the left ventricle resulting from obstruction of the nerve activity is low (Smith et al., 1996), and the post- venous return by increased intrathoracic pressure (Fox strain hypertensive state is explained by continuing ac- et al., 1966; Smith et al., 1987). Usually phase IIE tion of the adrenal medulla hormones (Sandroni et al., is evident due to its relatively long duration. Me- 2000). chanical hypotension in phase IIE evokes a powerful Due to deep breathing and continuation of the in- compensatory reflex from the arterial baroreceptors: creased venous return in phase IV (Fox et al., 1966; the HR and PVR start to rise, restoring gradually Smith et al., 1987) one might assume a pressor action the baseline level of blood pressure. Under increased from the mechanoreceptors of the lung blood vessels, sympathetic nerve activity (Smith et al., 1996) the which could counteract the baroreceptor effects. On adrenal medulla is activated and large quantities of the other hand, the latter might be supported by the va- epinephrine and norepinephrine are released into the sodilator reflex from the thoracic aorta resulting from circulating blood (Sandroni et al., 2000). However, the increased pulse pressure in phase IV (Gruhzit et al., in the case of a deep inspiration prior to VM, the 1954). Furthermore, the CVR mechanisms in phase IV pulmonary stretch receptors are stimulated as well, may be further modified by changes in blood gases dur- and a significant depressor impact may restrict or ing the VM (Smith and Hatch, 1959; Meyer et al., 1966; suppress the pressor effect from the baroreceptors. Mateika et al., 2002). Then a bradycardic response appears in place of In summary, the mechanisms of CVR to the VM are tachycardia although the peripheral vasoconstriction related to the neurohormonal response of the heart and still continues. Such situations have been observed by blood vessels to the mechanical alterations in arterial weak stimulation of baroreceptors (due to low strain pressure by changes in intrathoracic pressure before, pressure) with the concomitant vagotonic state of during, and after the strain. 42 R. Looga / Respiratory Physiology & Neurobiology 147 (2005) 39–49 There are a number of procedural technical factors that may considerably modify the pattern and magni- tude of CVR to the VM, provided the autonomic effec- tor function is normal.