Abstract
The Valsalva manoeuvre is performed by forced expiration against a closed glottis. It is attributed to Antonio Valsalva (1666–1723), who described it as a test of Eustachian tube patency and as a method of expelling pus from the middle ear.
What is the Valsalva manoeuvre? What was it originally used for?
The Valsalva manoeuvre is performed by forced expiration against a closed glottis. It is attributed to Antonio Valsalva (1666–1723), who described it as a test of Eustachian tube patency and as a method of expelling pus from the middle ear.
How might a patient perform a Valsalva manoeuvre?
The Valsalva manoeuvre involves increasing intrathoracic pressure to ~40 cmH2O and holding it for 10 s. The methods of achieving this depend on whether the patient is awake or anaesthetised:
Awake. The patient attempts to forcibly exhale whilst keeping their mouth and nose closed. This can be difficult to explain to a patient – the same effect can be gained by asking a patient to try to blow the plunger out of a syringe.
Anaesthetised. The adjustable pressure-limiting valve of the anaesthetic circuit is closed and the airway pressure is increased to 40 cmH2O and held for 10 s. This is really only possible for intubated patients; laryngeal mask airways are prone to leak above pressures of 20 cmH2O.
What are the cardiovascular changes that occur during the Valsalva manoeuvre?
A sudden generation of a high intrathoracic pressure, such as that occurring during the Valsalva manoeuvre, results in dramatic changes to mean arterial pressure (MAP), cardiac output and heart rate (HR). The Valsalva manoeuvre is divided into four phases (Figure 41.1):
Phase 1. At the start of the Valsalva manoeuvre, the increase in intrathoracic pressure compresses the pulmonary vessels, squeezing blood into the left side of the heart. This transiently increases the stroke volume (SV), resulting in a transient increase in MAP. The baroreceptor reflex responds to the rise in MAP by transiently reducing HR.
Phase 2. Next, the high intrathoracic pressure prevents venous return to the heart. SV is reduced, which leads to a steady fall in MAP. Again, the baroreceptor reflex is triggered: HR increases, which returns MAP to near normal.
Phase 3. After 10 s, the high intrathoracic pressure is released. Venous return fills the empty intrathoracic vessels. SV decreases, resulting in a further fall in MAP and a further reflex rise in HR.
Phase 4. As left ventricular preload is restored, the MAP increases. However, because the HR is still high, there is an overshoot in MAP. The baroreceptor reflex rapidly corrects this, causing a reflex bradycardia through vagal stimulation. Both MAP and HR then return to normal.
