The Valsalva maneuver: mechanisms and clinical implications.

The previous discussion has focused on the mechanisms, both respiratory and circulatory, that occur during the Valsalva maneuver. The increase in intrathoracic pressure that occurs during the Valsalva maneuver incites a sequence of rapid changes in preload and afterload stress. During the strain, venous return to the heart is decreased and peripheral venous pressures become increased. Within the next few beats, systolic and pulse pressures begin to fall while mean arterial pressure remains near (or is elevated above) control levels owing to the transmission of airway pressure. Thus it would appear that the benefits to cardiac contractility derived from a decrease in systolic and pulse pressure are counterbalanced by an increase in mean arterial pressure. Increases in total peripheral resistance that begin after about 7 seconds of strain produce further increases in afterload. Recruitment of autonomically mediated increases in heart rate and cardiac contractility assists the heart to maintain its cardiac output in the presence of diminished venous return. With the increased venous return that accompanies termination of Valsalva strain, there is an increase in diastolic filling and stroke volume output by means of the Frank-Starling mechanism. Heart rate and total peripheral resistance continue to be increased during the immediate poststrain period, and the ejection of an increased stroke volume into a constricted arterial system produces a rapid and marked increase in arterial pressure--the phase IV overshoot with its subsequent slowing of heart rate.