Physiology of the Valsalva manoeuvre

This chapter answers Section G6(ii) of the 2017 CICM Primary Syllabus, which expects the exam candidate to "Explain the physiological consequences of ...the Valsalva manoeuvre". It had only appeared once in the CICM First Part written exam, in Question 3 from the first paper of 2013. The poor representation of this item in the past papers should not discourage even the most cynical trainee from reading about it, as it has a rich and storied history of appearing in vivas. Or rather, in the ANZCA exam vivas; and CICM has a rich and storied history of lifting whole swaths of material from ANZCA syllabus documents and exam content. Ergo, our trainees should be prepared for this question as their inevitable future. Not to worry; it's quite straightforward.

The Valsalva manoeuvre is, fortunately, a favourite topic of reviewers, and there is no shortage of material to act as references; so much so that the trainee short on time is at risk of wasting it by having to filter through this abundance of material. One is advised to pick a resource and stick to it, as they all contain exactly the same information The best and most detailed one is probably Pstras et al (2015), but it is paywalled by Wiley. They already have enough money, so instead of buying Pstras, the next best (and free) article has to be Junqueira (2008), as it also contains all the graphs you might be called upon to reproduce, moreover being written in an easy engaging style. The asynchronous learner is redirected there for an example of what good technical writing is supposed to look like. Locally, cackhanded explanations of the cardiovascular responses to positive pressure ventilation may fill in some of the blanks which might not be totally clear from reading this chapter (eg. what happens to the LV transmural pressure). Apart from that unreliable non-peer-reviewed resource, the cream of the FOAM universe includes superb summaries by CVphysiology.com, LITFL, Part One and CICMwrecks. 

The "standard" Valsalva manoeuvre

Antonio Valsalva originally developed this manoeuvre in the 18th century, for the purposes of expelling purulent material from an infected middle ear. His work was preceded by 17th and 16th century works by mainly surgical specialists (Leonard of Bertapaglia and Ambroise Paré), who described the technique first, and it was followed by Edward Weber who described its cardiovascular effects; and so it is unclear how it could still be called the Valsalva manoeuvre. For the purposes of rapidly explaining it to somebody, the manoeuvre can be defined as:

"Forced expiration against a closed glottis"

However, that would probably not satisfy the examiners, as not all of our patients have control over their glottis. Pstras et al (2015) prefer to describe it as 

"A forced expiratory effort against a closed airway"

That's more ICUish, but still does not describe exactly how forced, how much effort, and for how long. To add that level of complexity,  others have been even more prescriptive, demanding that a certain airway pressure be maintained, and for a certain duration. According to Kumar et al (2018) and Junqueira (2008):

"The Valsalva maneuver (VM) involves expiratory effort against a closed mouth and/or glottis in the sitting or supine position with the increased intraoral and intrathoracic pressure raised to 40 mmHg for 15-20 sec"

This is also the description of the Valsalva manoeuvre used by the 2015 ACC/AHA/HRS guideline for the management of SVT, which they recommended on the basis of a couple of studies comparing the efficacy of different vagal manoeuvres. The argument for the ongoing use of this definition is therefore purely functional: the Valsalva should look like this because that's the kind of Valsalva that gets results.  To take things even further, Looga (2005) outlined a whole range of variation, including an inspiratory Valsalva manoeuvre and an "intermediate" one in which a smaller intrathoracic volume is used. 

The four phases of the Valsalva manoeuvre

"Graphs required were those of the changes in intrathoracic pressure, the pulse pressure response and the heart rate response", the college remarked in their comments on Question 3 from the first paper of 2013. This is a good guide as to how one might discuss this topic, as one's encounters with the Manoeuvre are typically framed by the borders of a monitoring screen. A good arterial pressure trace was stolen from Wenner et al (2006) to facilitate the imagemaking process, and to add some much-needed authenticity to what is otherwise a fairly sterile hypothetical diagram.  Additionally, in case this picture is not worth a thousand words, some of what follows includes letters which were arranged into incomplete sentences, potentially with a beneficial educational effect. 

Without further ado:

Phase 1 of the Valsalva manoeuvre: Onset of strain

• The patient strains voluntarily. The intrathoracic pressure increases to 40 mmHg, which is 54 cm H₂O (in case you decide to mislabel your graphs).
• The increase in intrathoracic and intraabdominal pressure puts pressure on intrathoracic structures, most notably:
  • Both the venae cava
  • The pulmonary circulation
  • The aorta
  • The left ventricle
• Increased aortic pressure decreases afterload and displaces a volume of blood into the peripheral circulation, which increases both systolic and diastolic pressure
• Decreased LV transmural pressure also decreases afterload, which increases cardiac output and contributes to the increase in blood pressure.
• Increased pressure on the pulmonary veins increases venous return to the left atrium, which increases LV preload and therefore also increases LV contractility. 

• The increase in blood pressure is sensed by baroreceptors, which slow the heart rate immediately, producing an early bradycardia.
• Meanwhile, in the right side of the circulation, the right ventricle is experiencing an increase in afterload and a decrease in preload, which markedly impairs the right ventricular cardiac output; but because this is still only a few heartbeats into the Valsalva, there is still enough venous blood in the pulmonary veins to keep the LV filled, and so this right-sided emptiness goes unnoticed for now.

Phase 2 of the Valsalva manoeuvre: continued strain

• During this period, the sustained increase in intrathoracic pressure continues to have all of the abovementioned effects on LV afterload, but now also the effects of decreased venous return come into play.
• The decreased venous return due to vena cava pressure results in a decrease in LV stroke volume. Venous blood pooling in extrathoracic veins leads to an increase in extrathoracic venous pressure, so much so that the engorgement of the 
• As the result, cardiac output may be decreased by as much as 50%
• Because of this (well, mainly because of the decreased stroke volume), the systolic blood pressure decreases significantly.

• After some heartbeats, the decreased blood pressure is sensed by the baroreflex.
• This produces a reflexive increase in heart rate
• As vagal baroreflex effects are more rapid than sympathetic effects, the heart rate increases first.
• However, later in Phase 2, sympathetic effects begin to manifest (finally, after enough cAMP was synthesised) and peripheral vasoconstriction occurs. Thus, there is some return to a pre-Valsalva blood pressure. However, the stroke volume remains small (there is now tachycardia, and there is still a problem with venous return). As a consequence of this, the pulse pressure is narrowed:

Phase 3 of the Valsalva manoeuvre: release

• Intrathoracic pressure returns to normal abruptly as the subject releases held breath with a heave of relief. 
• The pressure on the aorta and the LV is released, increasing LV transmural pressure and therefore removing the afterload buff applied during Phases 1 and 2.
• At the same time, the release of pressure in the venous side of the circulation releases the pent-up blood stored in extrathoracic veins, increasing right ventricular preload - so much that the increase in RV filling can affect LV diastolic filling by the phenomenon of interventricular interdependence. 
• All this while, LV preload remains diminished, as the tachycardia persists, and the increased RV preload has not yet translated into an increase in pulmonary blood flow.
• On top of all this, the subject may take a deep breath at this stage (as they were holding their breath for 20 seconds), which decreases intrathoracic pressure, exaggerating the abovementioned responses.
• In summary, everything that happens during the release phase leads to an abrupt drop in blood pressure.
• The heart rate, which would normally be elevated by the baroreceptor reflex, usually has no time to compensate (this phase only tends to last a couple of heartbeats), but most textbooks depict a slight increase in heart rate in Phase 3.

Phase 4 of the Valsalva manoeuvre: recovery

• As a small amount of time passes, the right ventricular output again becomes synchronous with the left, and the LV receives an adequate amount of preload, which means the left ventricular output returns to normal.
• At this stage, the heart rate and peripheral vascular resistance are still high due to the effects of the baroreceptor reflex during Phases 2 and 3.
• As the result, there is a slight overshoot of blood pressure during Phase 4.
• With this increase in blood pressure, the baroreceptor reflex soon restores the heart rate to normal, or perhaps slightly lower than where we started.

Now, it goes without saying that quoting the exact values for any of these changing haemodynamic variables is completely pointless. To inappropriately verb the eponym, one may say that every organism who Valsalvas, Valsalvas differently. As an example, Pstras et al (2015) report that it is possible to completely block your IVC in the course of this manoeuvre, and produce a brief sinus arrest. In short, though the graphs above are presented with reassuring number labels on the y-axis, those numbers can be viewed as purely decorative, and should not be used to generate a sense of perspective, or reproduced in the exam setting.