© 2004 American Thoracic Society
Respiratory Variations in Arterial PressureTo the Editor:I read with amused interest Dr. Magder's recent Clinical Commentary (1). To explain respiratory variations in arterial pressure, in particular, in mechanically ventilated patients, Dr. Magder uses a simple description of the central circulation that was proposed by Guyton in the 1950s: the heart is a pump with two chambers, the right atrium, which receives the venous return, and the left ventricle, which is responsible for cardiac flow and whose ejection volume determines arterial pressure, all else being equal. This description, which has the merit of simplicity, allows the beautiful illustration that embellishes the cover of the January 15, 2004 issue of AJRCCM, where phenomena involving the right atrium and venous return are colored blue, and red is used for phenomena concerning the left ventricle and arterial pressure. We need to retrace the path of evolution a long way to find a species to which this description applies perfectly: fish. But in humans, is there nothing between the right atrium and the left ventricle? Or is the pulmonary circulation, which starts with the right ventricle and ends with the left atrium, a simple rigid tube, completely insensitive to changes in airway pressure? In an irresistible flash of humor, Dr. Magder invites us to practice a volume expansion among readers of the "Blue Journal." After such a stressful experience, we should scarcely be surprised if most of them suffer a rise in cardiac flow! An unnecessary stress what's more, because these good readers have asked nothing of anyone and have not the slightest need of an increased cardiac flow. In fact though, I don't think that they run the risk of worrying hemodynamic instability, not even on reading Dr. Magder's Clinical Commentary!
Paris, France FOOTNOTES Conflict of Interest Statement: F.J. does not have a financial relationship with a commercial entity that has an interest in the subject of this letter. REFERENCES
From the Author: I appreciated Dr. Jardin's amused interest in my recent Clinical Commentary (1). His observations have been very important for understanding heart–lung interactions, and I reviewed his work in detail when I prepared my article. His criticism is cryptic, but I will attempt to elucidate it. Dr. Jardin emphasizes that the pulmonary circulation sits between the right and left hearts, and that lung inflation can significantly alter right ventricular output. This important concept is often neglected and can lead to faulty reasoning. For example, it has been argued that the rise in cardiac output in sepsis is due to a decrease in systemic vascular resistance and decreased left ventricular afterload. However, pulmonary vascular resistance usually rises in sepsis, which increases right ventricle afterload and makes the effect on the left heart irrelevant (2). On the basis of elegant echocardiographic observation that showed an increase in right heart size in association with a simultaneous decrease in tricuspid inflow during lung inflation, Dr. Jardin has argued that lung inflation during normal tidal breaths has a greater effect on right heart output than the associated rise in pleural pressure, whereas I argue that the change in pleural pressure is more important. There are two problems with his argument. First, Denault and colleagues (3) found that respiratory variations in arterial pressure with lung inflation are not present when the chest is open, and pleural pressure does not change. Second, although a change in load on the right ventricle could explain an inspiratory fall in right ventricular stroke volume, it does not explain why volume status affects the response. Why might echocardiographic observations be misleading? First, there is a question of magnitude. The size of the effect of lung inflation on the right heart is dependent on the magnitude of the change in transpulmonary pressure. With current standard tidal volumes, the effect should be small, yet the change in pleural pressure is still large relative to the gradient for venous return. Second, the volume status is critical. The right heart can adapt to increases in afterload through the Frank-Starling mechanism when the heart is on the responsive part of the cardiac function curve, but not when it is on the plateau of the function curve, in which case lung inflation could decrease right heart output. A third factor is the resolution of echocardiography. Three frequencies interact in this analysis: respiratory rate, heart rate, and sampling rate of the device or operator, all of which make precise timing of events very limited. Perhaps this explains some fishy conclusions!
McGill University Health Centre Montreal, Quebec, Canada FOOTNOTES Conflict of Interest Statement: S.M. does not have a financial relationship with a commercial entity that has an interest in the subject of this letter. REFERENCES
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