Haemodynamic Changes During a Mechanical Breath

Created on Mon, 06/15/2015 - 18:44
Last updated on Tue, 06/16/2015 - 16:37

The effects of positive pressure inspiration and expiration on the preload and afterload.

This is another one of those topics which is amenable to a big complicated diagram.

The substrate for this summary comes from an excellent article on this topic by Frédéric Michard and Jean-Louis Teboul, who explain these issues in a skillful and concise manner. Additonally, the diagrams were informed by this article, which contains tracings of inspiratory hold manoeuvres performed on real patients.

So; the diagram. First the right side of the circulation.

Effects of a positive pressure breath on the central veins and right cardiac chambers

Hemodynamic response to a mechnical breath in the right heart

This part of the system experiences increased load. Positive pressure ventilation impairs both the return of blood to the heart, and the ejection of blood through the pulmonary circulation.

Effects of positive pressure on the central veins and right atrium

The positive pressure in the chest decreases venous return by decreasing the effective central venous pressure, and thereby decreases right ventricular preload. That may sound odd. In fact in the CVP measurement chapter the completely opposite is stated. How can both be true?


The CVP measurement certainly increases with increased PEEP. However, one must remember that our transducer tip is positioned in the SVC, and thus measures both the pressure inside the vein, and the pressure from the thoracic cavity which is transmitted to the transducer. The combination of these pressures is greater than the CVP alone; hence the measured CVP will appear to be higher.

What influence does this have on the flow of venous blood? It has been thought for decades that the increase in thoracic pressure decreases the gradient for venous flow. If the extrathoracic venous pressure is 10mmHg, and the intrathoracic pressure is 2mmHg, obviously venous blood will gush into the chest. However if the intrathoracic pressure rises to 8mmHg, the gradient is less steep, and the gush becomes a trickle.

For a long time this was viewed as a satisfying explanation. Indeed, this is the explanation offered in Tobin's Principles and Practice of Mechanical Ventilation (see Chapter 36 of the 2nd edition). However, more recently various brave explorers of the intrathoracic depths have revealed that the situation is far more complex. The pressure gradient between the extrathoracic and intrathoracic venous circulations may actually remain the same in some patients; however, the increased transmural pressure on the right ventricle impedes its filling, effectively reducing its preload. Furthermore there may be situations when the SVC (or IVC) collapse under the effects of intrathoracic pressure, preventing further blood flow.

In summary, it would be more accurate to say that positive pressure ventilation increases measured CVP, but decreases the influence of central venous pressure on right ventricular preload.

Effects of positive pressure on the right ventricle

Not only is preload to the right ventricle decreased; the afterload is increased by whatever positive pressure is transmitted to the pulmonary arteries. This, of course, depends on what condition these arteries are, as well as on the integrity of the pulmonary valve - but lets not get carried away.

The bottom line is, the effect of positive pressure inspiration on the right ventricle decreases right ventricular stroke volume.

Effects of positive pressure on the pulmonary circulation and the left cardiac chambers

Hemodynamic response to a mechnical breath in the pulmonary circulation and the left heart

The initial increase in positive pressure squeezes blood out of the pulmonary veins, like from a sponge. The sudden gush of blood into the left ventricle is the increased preload. And, as the aorta is under positive pressure, the left ventricular afterload is decreased, which probably does little for the LV stroke volume, but certainly decreases LV workload.

However, this effect is short-lived. Soon after the initial gush, the effects of decreased right ventricular stroke volume manifest. There is decreased flow through the pulmonary circulation due to decreased RV preload and increased RV afterload. The resulting decrease in LV preload depresses LF function. The decreased LV stroke volume translates into a decreased pulse pressure, and generally a decreased blood pressure.

This flow-on effect of decreased RV preload is seen very quickly -within 2 heartbeats, according to some early dog experiments.

Knowing the influence of positive pressure on cardiovascular physiology, one can usefully exploit these predictable mechanisms to make conclusions about the volume status of one's patient, and whether or not that patient might benefit from more volume.

Specifically, the expiratory hold manoeuvre can be used to assess the fluid responsiveness of a shocked patient.



There are numerous excellent articles on this topic.

Morgan, Beverly C., et al. "Hemodynamic effects of intermittent positive pressure respiration." Anesthesiology 27.5 (1966): 584-590.

Michard, Frédéric, and Jean-Louis Teboul. "Using heart-lung interactions to assess fluid responsiveness during mechanical ventilation." Critical Care 4.5 (2000): 282.

Morgan, Beverly C., et al. "Hemodynamic effects of intermittent positive pressure respiration." Anesthesiology 27.5 (1966): 584-590.

Maas, Jacinta J., et al. "Assessment of venous return curve and mean systemic filling pressure in postoperative cardiac surgery patients*." Critical care medicine 37.3 (2009): 912-918.

Cao, F., et al. "[Effect of positive end-expiratory pressure on central venous pressure and common iliac venous pressure in mechanically ventilated patients]." Zhongguo wei zhong bing ji jiu yi xue= Chinese critical care medicine= Zhongguo weizhongbing jijiuyixue 20.6 (2008): 341-344.

Jardin, François, and Antoine Vieillard-Baron. "Right ventricular function and positive pressure ventilation in clinical practice: from hemodynamic subsets to respirator settings." Applied Physiology in Intensive Care Medicine. Springer Berlin Heidelberg, 2009. 251-259.

Magder, Sheldon. "Central venous pressure: A useful but not so simple measurement." Critical care medicine 34.8 (2006): 2224-2227.