We use Valsalva’s maneuver at various places –
- to elicit certain cardiac murmurs (such as the one of HOCM)
- to slow down the heart rate for a diagnostic window in supraventricular tachycardia
- to quantify damage to the autonomic nervous system (as in small fibre neuropathy)
- to provoke a right-left-shunt in PFO testing
If you are not careful, you can even invoke Valsalva’s accidentally when you really want to determine cerebrovascular reserve.
In yesterday’s session we derived the four phases of the Valsalva reaction from the rudiments of what we should remember about cardiovascular physiology, in particular the baroreflex (carotid sinus), Bainbridge reflex and the role that the sympathetic and parasympathetic nervous system play as mediators of tachycardia/hypertension.
We then went on to examine the role of various practical parameters in the Valsalva maneuver, such as the depth of the initial inhalation, the length of straining (phase II) and the straining pressure, using transcranial doppler and an ecg to monitor the heart rate and blood pressure changes. In my experiences, TCD is still the best way to measure changes in blood pressure continuously if you don’t have an arterial line and cannot afford a Finapres device. But you have to make sure that you do not extend the straining phase too much (otherwise CO2 increases and you get an increase in flow), so I only use 10 seconds instead of the usual 15 seconds that are recommended (this publication seems to show that this is still ok).
We also discussed the inherent difficulties in defining normal values for autonomous nervous system examinations because of the wide variation in base vagal tone, reactivity, hydration and more.
- A note on the historic Valsalva and what he did
- A detailled exposition of the physiology behind the maneuver and how to use it as the problem base for teaching cardiovascular physiology