ANS Tests Part 2: The Valsalva Maneuver

In this video Dr. Goldstein presents the Valsalva autonomic function test and describes normal vs. abnormal results.

Once you’ve conducted an intelligent autonomic history, then you can choose from a variety of laboratory tests to confirm or refute your idea about what the pathophysiological mechanisms are in a particular patient.  The most important autonomic function test after the history is the beat-to-beat blood pressure and heart rate response to the Valsalva maneuver.  It’s where you blow against the resistance for several seconds and then you relax.  Forget what happens to the heart rate, I don’t really care, but the blood pressure is important.

The blood pressure changes in four phases.  At first you sort of hunker down, you’re blowing against the resistance, you’re increasing pressure in the chest, so the blood comes out the chest and goes down the arms, the blood pressure goes up, that’s a mechanical thing.  It doesn’t have anything to do with reflexes.  Then as you continue to blow against the resistance there’s less blood coming to the heart so the heart pumps out less blood.  The brain picks up on that immediately – where’s my blood?  This causes the reflex to occur, you saw that baroreflex arc, and the sympathetic noradrenergic system gets turned on.  Norepinephrine, which is the chemical messenger of the sympathetic nerves and cardiovascular regulation, gets released.  It binds to the receptors, remembers those alpha receptors on smooth muscle walls, and the blood vessels tightened.  Because the blood vessels tighten, the blood pressure starts to creep up, even though the person still has the low stroke volume, the amount of blood that the heart is pumping is decreased.  I use the analogy of a garden hose.  Think about the pressure in a garden hose.  If you turn down the faucet, the pressure in the hose is going to go down.  But you can bring up the pressure by tightening the nozzle.  And that’s what the brain is trying to do, tighten the vascular nozzle by way of the sympathetic noradrenergic system.  Then you relax, when you relax, that’s phase 3.  In phase 3, the blood pressure goes down.  It’s like a mirror image of what happened in phase 1, it’s just a mechanical thing, it doesn’t have anything to do with reflexes.  And finally, in phase 4, you’re just lying there.  There’s no reason why the blood can’t come up with the heart and it does, and the heart pumps blood, but it pumps the blood into this reflexively constricted vasculature.  It’s like you turned the faucet back up to where it was but you forgot to loosen the nozzle.  Because of that the pressure overshoots and that’s what happens in phase 4.

If you have a problem with this reflex, whether it’s because the brain doesn’t know that the blood pressures changed because there’s a baroreceptor problem.  The brain doesn’t care because there’s a brain disease.  The sympathetic nervous system isn’t there because there’s a degenerative loss of the nerves.  Norepinephrine isn’t being released.  The receptors are blocked.  It doesn’t matter, you get the same abnormal pattern that looks like this.  Here in phase 2, the blood pressure just goes down, down, down.   Well that’s because the person can’t tighten the vascular nozzle.  And in phase 4, the blood pressure slowly comes up to baseline, but it doesn’t overshoot.  For the same reason, the person couldn’t tighten the vascular nozzle.  So, that’s the finding that we’re looking for in somebody who has orthostatic hypotension.  We want to find out if it’s neurogenic.  If it’s from a failure of the sympathetic noradrenergic system somewhere.  And this is what the Valsalva blood pressure will look like.  Although it’s a very sensitive measure for picking up sympathetic neurocirculatory failure, it’s of no value in terms of differential diagnosis.  In Parkinson’s with orthostatic hypotension, in pure autonomic failure, and in Multiple System Atrophy, you see the same abnormal blood pressure response.  So, it’s sensitive, but it’s not specific at all.

Wolfgang Singer, MD

Associate Professor of Neurology
Mayo Clinic Rochester, MN

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