Hello there. Welcome to the Society of Critical Care Medicine hemodynamics masterclass. This talk is going to be about heart-lung interactions and an introduction about why they're clinically relevant. You can see my credentials there. I'm an associate professor in the clinical track at the NYU School of Medicine in New York City. And you can email me questions at the email address you see there, and you can follow me on Twitter if you really want to. I have some conflicts of interest to disclose. I'm a member of the medical advisory board for the company Pulsion Medical Systems, which is now a division of Yetinga. I have received some funding from Chita Medical, and I also have relationships with Flosonics Medical. And we may be discussing some of these devices in the talks. The learning objectives for this talk are listed here, and they're pretty self-explanatory. The clinical importance of heart-lung interactions has been recognized for at least 20 years. And this is about the same time I began my fellowship. And I remember that the first time I went to a big conference, a big congress, was American Thoracic Society in 2002. I attended a postgraduate course on ICU physiology, and that was the first time I had heard about heart-lung interactions and their clinical relevance. And I also remember that I don't think I understood anything about what was being said. And that was because, A, I had a relatively weak background in the relevant physiology at that point, and B, the topic is somewhat difficult, and C, I believe the presenter was Michael Pinsky, who has a real gift for making simple topics, well, not so simple. And I can say that because Michael's a friend of mine. About 20 years ago, the first of many papers that established the field of functional hemodynamic monitoring were being published. And this is one of those early ones, which established the value of pulse pressure variation as a way to identify fluid responsiveness among patients who are receiving mechanical ventilation. In a relatively recent review paper from the American Journal of Critical Care Medicine, rather, the American Journal of Respiratory and Critical Care Medicine, otherwise known as the Blue Journal, reviews some of the history of this part of the field and hints at the physiology that underlies it. And I hope to explore these concepts a little bit more with you during this talk. The fundamental principle underlying functional hemodynamic monitoring and understanding heart-lung interactions in critical care medicine is understanding the Frank-Starling cardiac function curves and identifying which curve describes a patient's cardiac function at a given time and where on that curve the patient falls at that given time. Is the patient in a preload-sensitive, steep portion of the curve? That is, is the patient going to increase stroke volume as cardiac preload increases? Or is the patient on the preload-insensitive, flat portion of the curve, where stroke volume will not increase with more preload? You're going to hear me discuss steep and flat portions of the curve throughout my series of talks. The rest of this talk will introduce you to how these principles help us identify fluid-responsive or fluid-unresponsive patients. That is, what are the fundamental physiological principles that make heart-lung interactions useful in clinical decision-making? My other talks will discuss different techniques of assessing volume responsiveness in clinical medicine and how to use or not to use fluids wisely in critical care. The first principle to remember seems pretty obvious, and it is that the heart sits in the chest. It's obvious and so obvious that sometimes it's easy to ignore or forget. The heart is wrapped in the pericardium, and the lungs that also sit in the chest are wrapped by the pleura. The pleural and pericardial spaces describe spaces that act as, for our purposes, sealed chambers. Changes in pleural pressure are transmitted through the lung parenchyma to the pulmonary blood vessels and also to the pericardium, altering pressures and flows within the pulmonary vasculature and the heart. Since I'm not a very good artist, I've decided to make a very basic scheme of the pleural space, the lungs, the pericardium, and the heart. The orange lines represent the pleura and pericardium. The blue chambers represent the right atrium and right ventricle with the oxygenated blood, and the red chambers represent the left atrium and the left ventricle, full of oxygenated red blood. The lungs are the gray ovals. Please pardon the simplicity of my so-called artwork. I now have split the right and left sides of the heart to show the relevant cardiorespiratory elements in series. I've added the great blood vessels. You can see on the left side of the diagram the superior and inferior vena cavi entering the pleural space and then the right atrium. You can see the pulmonary artery emerging from the right ventricle and passing through the lungs where it becomes the pulmonary vein. On the right side of the picture, the pulmonary veins return oxygenated blood to the left atrium, and the oxygenated blood finally exits the heart through the left ventricle and then the pleural space through the aorta. These pressures in these different spaces change, and with changes in pleural pressure, and these changes alter flow and therefore stroke volume. The respiratory cycle essentially has two effects on the circulation. One effect is due to changes in pleural pressure, and the second effect is due to changes in lung volume. For example, consider inspiration. When the diaphragm and other respiratory muscles contract, the pleural pressure falls from its resting level of about negative 5 centimeters of water. How much the pleural pressure falls depends on the strength of the respiratory effort. With resting breathing, it falls about 5 centimeters of water more. With vigorous breathing, such as during exercise or some disease states, breaths are more forceful, and the pleural pressure falls a great deal more, with important implications on blood flow, stroke volume, and cardiac output. During inspiration, lung volume increases with important effects on the pulmonary blood vessels. Number one, effects of changes in pleural pressure. When the pleural pressure falls during inspiration, central venous pressure, the pressure within the intrapleural central veins and right atrium, fall. The pressure difference between the systemic veins that lie outside the pleural space, called the mean systemic filling pressure, or MSFP, and the central venous pressure increases. With this increased pressure difference, blood flow back to the right atrium increases, resulting in a higher right heart preload. The stretching of the right atrium also affects the sinoatrial node, resulting in an increase in heart rate, the so-called Bainbridge reflex. Number two, effects of increased lung volume. In spontaneous breathing, lung volume rises because the pleural pressure becomes lower than the intraalveolar pressure. As lung volume increases, blood vessels, particularly veins, which hold about 70% of the blood volume, tend to be compressed. This occurs within the chest and also within the abdomen. The net effect of the compression of these veins tends to relate to the circulating blood volume. If the blood volume is high, compressing the veins tends to drive blood flow forwards. If the volume is low, compression of the veins tends to slow blood flow. Inside the chest, as lung volume rises, the alveoli tend to compress the adjacent pulmonary vessels, reducing flow to the left atrium. This effect is more pronounced in West Zones 1 and 2 of the lung. As a result, right ventricular output increases, but left ventricular output falls, leading to a lower systolic blood pressure and a smaller pulse pressure with a higher heart rate. This schematic drawing better shows the effect of increased lung volume on pulmonary vessels. In West Zone 1, where the intraalveolar pressure is greater than the pulmonary arteriolar pressure, the pulmonary capillary pressure, and the pulmonary venous pressure, increases in lung volume have the most pronounced effect on decreasing blood flow to the left atrium. In Zone 2, where the alveolar pressure tends to be greater only than the pulmonary venous pressure, the effect is less pronounced. The net effect is an increase in pulmonary vascular resistance. The circulating blood volume plays a role in determining the relative proportion of Zone 1, Zone 2, and Zone 3 lung proportions. In hypovolemia, Zone 1 and Zone 2 physiology tends to predominate, and the effect of lung volume on left heart output is more pronounced. With very large increases in lung volume, the cardiac chambers can also be compressed. This is rarely clinically relevant, except with very severe emphysema and hyperinflation. A similar effect may occur with auto-PEEP and dynamic hyperinflation. This diagram is from a wonderful series of videos Dr. John Emil Kenney has developed over the years, and this series is a real treasure trove if you'd like to dive deep in cardiorespiratory interactions, and they can be found on YouTube. You can draw a distinction between what happens to the resistance within intraalveolar blood vessels and extraalveolar blood vessels. The extraalveolar blood vessels are depicted in red, and the intraalveolar blood vessels are depicted in orange. As lung volume and alveolar volume increase, the intraalveolar blood vessels are compressed, and the extraalveolar blood vessels are stretched open. And this diagram is taken from a series of lectures that was developed for this course by Dr. Javier Monet, and I'm grateful to him for letting me steal it. The global effect of lung volume can be schematically represented by two asymptotic curves, and functional residual capacity represents the lung volume at which net pulmonary vascular resistance is at its lowest point. The effect of increased lung volume is to shift the Frank Starling function curve down and to the right, as you can see by the arrow. During expiration, the opposite effects occur. Pleural pressure rises, lung volume falls, and the intrapulmonary blood vessels are decompressed. The venous return to the right atrium decreases, reducing the effect of the Bainbridge reflex. The net effect is an increase in left ventricular stroke volume and cardiac output. The heart rate falls, and the systolic blood pressure decreases, increasing the pulse pressure. Typically, the difference between the systolic blood pressure between inspiration and expiration is 10 millimeters of mercury or less. When this difference is exaggerated, we call that finding pulsus paradoxus. That finding occurs in tension pneumothorax, pericardial tamponade, status asthmaticus, and other clinical situations. Theoretically, we learned all about pulsus paradoxus in medical school when we learned physiology in physical examination. We rarely use this maneuver clinically, mostly because asking patients with any of these conditions to hold their breath at the end of inspiration and at the end of expiration to allow us to take the blood pressure is rather difficult. But pulsus paradoxus is a great way to remind ourselves of physiologically relevant cardiorespiratory interactions. In conditions when the cardiac output is very preload sensitive, pulsus paradoxus occurs. Many of the methods that we have to look at fluid responsiveness share this core physiology. Let's now think about what happens to cardiorespiratory interactions when positive pressure ventilation is applied. Let's imagine that our schematic patient got intubated. Now, during inspiration, pleural pressure increases and lung volume increases at the same time. This raises the right atrial pressure, lowering the difference between the mean systemic filling pressure and the right atrial pressure. Lower venous return to the right heart is the result. As lung volume increases, intra-pulmonary vessels are compressed, raising pulmonary vascular resistance and lowering right ventricular output as well as flow to left atrium. As the intrathoracic pressure rises, the afterload on the left ventricle decreases, slightly increasing left ventricular output. Overall, cardiac output tends to fall and blood pressure falls with it. This effect is exaggerated with hypovolemic states. The net effects of positive pressure ventilation can be summed up in this flowchart. These principles are important to keep in mind when we set tidal volume or inspiratory pressure and PEEP. These settings will alter pleural pressure and transalveolar pressure, resulting in changes in venous return, pulmonary vascular resistance, and even gas exchange. Overdescending the lungs or applying a high PEEP will convert more of the lung to Zone 1 conditions, which can diminish alveolar capillary perfusion, resulting in an increase in the physiologic dead space. We will discuss more practical applications of these principles, especially how to exploit these principles to understand which part of the Frank-Starling curve an individual patient's heart is functioning on at any given time. And therefore, we'll use these principles to understand preload sensitivity or lack of preload sensitivity in subsequent presentations. Thank you very much for your attention.

heart-lung interactions

functional hemodynamic monitoring

Frank-Starling cardiac function curves

pleural pressure

positive pressure ventilation