Blood Pressure Response to the Valsalva Maneuver

The Valsalva maneuver is basically a forced expiration against a closed glottis. This maneuver is used in our daily life when we try to bear down or strain One way of producing this maneuver is to ask a patient simply to hold the breath and imitate straining on the toilet. One can produce this also by asking a supine patient to actively push his or her abdominal wall against the palm of the examiner's hand placed on the patient's abdomen so as to offer some pressure without causing pain A more controlled way of doing the maneuver would be to have the patient blow into a hollow tube connected to an aneroid manometer to raise the pressure to about 40 mmHg and sustain it at that level for about 20-30 s.

Arterial Pressure Response in the Normal During the Valsalva Maneuver

Four phases are recognized with continuous arterial pressure recordings. Initially the effort of strain raises the intrathoracic pressures, which is directly transmitted to the aorta, causing an initial rise in the arterial pressure. During this first phase, the lungs contract to the lowest volume, emptying most of the pulmonary venous bed and helping to increase the left ventricular output. With the continued strain, the venous return drops as a result of damping of venous circulation from the abdominal viscera and the

Aortic Pressure Waveforms Dampening

Fig. 1. The blood pressure response during the four phases of Valsalva maneuver in a patient with normal left ventricular function is shown diagrammatically. Phase 0 indicates the resting phase before the Valsalva maneuver. Phase I shows the increased blood pressure resulting from the initial increase in pulmonary venous return and the associated increased stroke volume and the increased intrathoracic pressure directly transmitted to the aorta. Phase II shows the decreased blood pressure because of decreased venous return into the thorax and therefore the heart resulting from the increased intrathoracic pressure preventing the venous return from the periphery. Note the increased heart rate secondary to the increased sympathetic tone. Phase III, immediately after the release of the Valsalva strain, shows a temporary drop in the blood pressure resulting from a sudden decrease in the intrathoracic pressure. Phase IV shows an overshoot of the blood pressure following the sudden return of peripherally pooled blood to the vaso-constricted arterial system (secondary to the increased sympathetic tone). The blood pressure then returns back to normal gradually. When the cuff is inflated to levels of 25 mmHg higher than the patient's resting systolic pressure and maintained at that pressure, the Korotkoff sounds that would be heard at the various phases of Valsalva are also depicted at the top. The size of the dots reflects the expected intensities of the sounds.

periphery. This leads to a significant drop in the stroke output, which is accompanied by a fall in the systolic and diastolic blood pressures as well as the pulse pressure (the second phase). The decreased stroke output stimulates the sympathetic system to cause a reflex increase in the heart rate at this time. Upon release of the strain, there is a sudden drop in the intrathoracic pressures, which again directly affects the aortic pressures and therefore the arterial pressure. This third phase is quite momentary and is only appreciated by continuous recordings of arterial pressure. This is almost immediately followed by a sudden surge of venous return from the splanchnic bed and the periphery augmented by the fall in the intrathoracic pressure. This leads to a significant increase in the right and the left ventricular stroke output. During this fourth phase the increased stroke volume ejected into an arterial system, which has been primed by a significant sympathetic stimulation during the earlier strain phase, causes an overshoot of the arterial pressure over and above the control level. The increased stroke volume effect is reflected in the increase in the pulse pressure as well. The rise in the arterial pressure also causes a reflex slowing of the heart rate through the baroreceptor stimulation (Fig. 1).

Fig. 2. Blood pressure response to the Valsalva maneuver in a patient with significant left ventricular dysfunction and heart failure is shown diagrammatically. Because of the chronically elevated venous pressures and the sympathetic tone, the blood pressure response to the Valsalva maneuver is different from that noted in the normal. During Phases I and II there is an elevation of blood pressure, and during Phase III the overshoot does not occur. The appearance of the above tracing resembles a square wave; therefore, it is called the square-wave response and indicates poor left ventricular function.

Fig. 2. Blood pressure response to the Valsalva maneuver in a patient with significant left ventricular dysfunction and heart failure is shown diagrammatically. Because of the chronically elevated venous pressures and the sympathetic tone, the blood pressure response to the Valsalva maneuver is different from that noted in the normal. During Phases I and II there is an elevation of blood pressure, and during Phase III the overshoot does not occur. The appearance of the above tracing resembles a square wave; therefore, it is called the square-wave response and indicates poor left ventricular function.

Arterial Pressure Response to the Valsalva Maneuver in Patients with Heart Failure

The response of patients with heart failure can be described as a square-wave response as seen on a continuous recording of the arterial pressures (Fig. 2). The initial rise in the intrathoracic pressure during the strain and the immediate fall on release ofstrain (namely the first and the third phases mentioned above) will cause an initial rise and a later similar fall in the arterial pressure due to direct transmission effect of the intrathoracic pressures to the aorta. However, because patients with heart failure already have maximal sympathetic stimulation with vasoconstriction (both arterial and venous) and their ventricles are already operating on the flat portion of the Starling curve, whatever decrease occurs in venous return as a result of the dampening effect of strain does not drop the stroke output very much, and for the same reason following release of strain also there is no overshoot in the arterial pressure. This can also be observed in the lack of significant changes in heart rate during strain and after release of strain In other words, no significant tachycardia or bradycardia will be seen to develop during the Valsalva maneuver (46,47).

Blood Pressure Response to the Valsalva Maneuver in the Assessment of Left Ventricular Function in the Absence of Overt Heart Failure

This consists essentially of detecting the presence or the absence of the overshoot in the blood pressure following the release of a Valsalva strain The presence of the overshoot would indicate a normal left ventricular function with a normal ejection fraction (stroke volume over the end-diastolic left ventricular volume expressed as a percentage, normal being 60%). Patients with left ventricular dysfunction who are not in overt failure also often have an abnormal response. They tend to have a resting increase in sympathetic tone and fail to exhibit the overshoot in blood pressure as well as the reflex bradycardia. This can be done at the bedside with the use of a blood pressure cuff. The method involves applying a sustained additional cuff pressure of 25 mmHg over and above the detected systolic pressure in a patient who is supine and listening for the Korotkoff sounds while the patient is performing a Valsalva strain for 20-30 s. First the systolic blood pressure is determined. Then the cuff is inflated to 25 mmHg above the systolic pressure and is held there while the patient is asked to perform a Valsalva strain. During strain, if the patient has normal left ventricular function, there will be an initial rise because of transmission of the intrathoracic pressure to the aorta, and this can be detected by the appearance of the Korotkoff sounds. The fall in blood pressure, which occurs because of the decreased venous return during the strain phase, will lead to the disappearance of the Korotkoff sounds. During the postrelease phase, the Korotkoff sounds will reappear, indicating the presence ofthe expected overshoot in arterial pressure. In patients with left ventricular dysfunction and high sympathetic tone but not in overt failure, however, the Korotkoff sounds may initially appear during strain, but with continued strain the Korotkoff sounds will become inaudible and will never reappear because of the lack of the overshoot response. Failure to achieve an overshoot of 25 mmHg has been correlated with resting left ventricular dysfunction with decreased ejection fraction of 40 +/- 10% (48).

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