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Cardiopulmonary interactions are not a new issue. A PubMed search ( using the keywords “heart–lung interactions” yielded more than 100 references published since 1962. But heart–lung interactions are not just of interest in terms of discussions among physiologists. They also have a strong impact on our ability to accurately interpret hemodynamic measurements and blood gas analysis and to manage patients in the intensive care unit (ICU). In many situations, such as acute respiratory distress syndrome (ARDS), severe asthma, chronic obstructive pulmonary disease (COPD), and mechanical ventilation, heart–lung interactions may account for considerable hemodynamic and blood gas changes. For example, Kumar and colleagues first suggested that positive end-expiratory pressure (PEEP)-induced oxygenation improvement could actually be due to a marked decrease in cardiac index rather than to an improvement in lung recruitment.1


Echocardiography is currently the most accurate tool to evaluate cardiac function beat by beat during the respiratory cycle. It does not require highly sophisticated equipment, but only the opportunity to correctly visualize the heart in either spontaneously breathing or mechanically ventilated patients. The study of cardiopulmonary interactions requires two-dimensional, time-motion, and Doppler modes. Visualization of the airway pressure tracing on the screen of the machine is mandatory.2 We have exhaustively illustrated the different mechanisms promoting heart–lung interactions3 and have also developed a Web site devoted to echocardiography in the ICU, a large part of which covers heart–lung interactions.4


The objectives of this chapter are to briefly report the mechanisms that promote heart–lung interactions, to illustrate how they can be easily described using echocardiography, and to discuss their clinical implications in the ICU. At the end, readers will better understand how to use echocardiography and how fundamental heart–lung interactions are to effective patient management in the ICU.


Cardiopulmonary interactions are mainly related to the fact that a circulation, the pulmonary circulation, is interposed between the right heart and the left heart. This circulation contains close to 500 milliliters (mL) of blood. So, whereas the preload reserve for the right heart is the systemic venous circulation,5 the preload reserve for the left heart is actually pulmonary capillaries and veins.6 For a given cardiac function, the more blood there is in the pulmonary circulation, the higher the left ventricular stroke volume.6


Heart–lung interactions can be separated according to their direct and indirect consequences for cardiac function. The main consequences are direct and are promoted by changes in intrathoracic and transpulmonary pressures and have been extensively reported by Scharf and collegues since 1977.7 They are usually described as the respiratory variations in systolic and pulse pressures, reflecting respiratory variations in left ventricular stroke volume. In spontaneously breathing patients, these variations are called the “pulsus paradoxus” and are observed in diseases such as severe asthma, where left ventricular stroke volume, and thereby pulse pressure, decrease during inspiration and increase during expiration.8 In mechanically ventilated patients, they are called “reverse ...

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