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Respiratory‐Cardiovascular Interactions During Mechanical Ventilation: Physiology and Clinical Implications

John Kreit

10.1002/cphy.c210003

Source: Volume 12, Issue 3, July 2022

Published online: April 2022

Full Article on Wiley Online Library



Abstract

Positive‐pressure inspiration and positive end‐expiratory pressure (PEEP) increase pleural, alveolar, lung transmural, and intra‐abdominal pressure, which decrease right and left ventricular (RV; LV) preload and LV afterload and increase RV afterload. The magnitude and clinical significance of the resulting changes in ventricular function are determined by the delivered tidal volume, the total level of PEEP, the compliance of the lungs and chest wall, intravascular volume, baseline RV and LV function, and intra‐abdominal pressure. In mechanically ventilated patients, the most important, adverse consequences of respiratory‐cardiovascular interactions are a PEEP‐induced reduction in cardiac output, systemic oxygen delivery, and blood pressure; RV dysfunction in patients with ARDS; and acute hemodynamic collapse in patients with pulmonary hypertension. On the other hand, the hemodynamic changes produced by respiratory‐cardiovascular interactions can be beneficial when used to assess volume responsiveness in hypotensive patients and by reducing dyspnea and improving hypoxemia in patients with cardiogenic pulmonary edema. Thus, a thorough understanding of the physiological principles underlying respiratory‐cardiovascular interactions is essential if critical care practitioners are to anticipate, recognize, manage, and utilize their hemodynamic effects. © 2022 American Physiological Society. Compr Physiol 12:3425‐3448, 2022.

Keywords: respiratory‐cardiovascular interactions; respiratory physiology; cardiovascular physiology; mechanical ventilation; positive end‐expiratory pressure; hemodynamics

Figure 1. Figure 1. Illustration showing the transmural pressure of the lungs (PL‐TM), chest wall (PCW‐TM), and respiratory system (PRS‐TM). PAW, airway pressure; PALV, alveolar pressure; PPL, pleural pressure; PATM, atmospheric pressure. From Kreit J. Mechanical Ventilation. Oxford University Press, 2018. Reproduced with permission of the licensor through PLSclear.
Figure 2. Figure 2. Static expiratory volume‐transmural pressure curves of the lungs (PL‐TM), chest wall (PCW‐TM), and respiratory system (PRS‐TM). PCW‐TM equals pleural pressure, PRS‐TM equals alveolar pressure, and PL‐TM equals alveolar pressure minus pleural pressure. V, volume; PTM, transmural pressure; TLC, total lung capacity; EV, equilibrium volume; RV, residual volume; +, positive transmural pressure; −, negative transmural pressure. From Kreit J. Mechanical Ventilation. Oxford University Press, 2018. Modified with permission of the licensor through PLSclear.
Figure 3. Figure 3. Dynamic pressure‐time curves showing the change in alveolar (PALV), pleural (PPL), lung transmural (PL‐TM), and intra‐abdominal (PAB) pressure during a spontaneous breath. Based on, with permission, Mead J and Whittenberger JL, 1953 86; Mead J, 1961 85; Otis AB, et al., 1950 98; Rodarte JR and Rehder K, 2011 119.
Figure 4. Figure 4. Dynamic pressure‐time curves during a passive, mechanical breath with constant inspiratory flow and positive end‐expiratory pressure (PEEP) of 0 cmH2O (A) and 10 cmH2O (B). PEEP causes a proportional rise in airway (PAW), alveolar (PALV), pleural (PPL), lung transmural (PL‐TM), and intra‐abdominal (PAB) pressure throughout the respiratory cycle. When inspiratory flow stops and expiration is delayed by an end‐inspiratory pause, PAW falls to PALV. Based on, with permission, Van den Berg PCM, et al., 2002 142.
Figure 5. Figure 5. Schematic illustration of the left ventricular (LV) pressure‐volume loop. The pressure and volume changes during isovolumic contraction, ejection, isovolumic relaxation, and ventricular filling are shown. The base of the loop is the LV diastolic pressure‐volume relationship.
Figure 6. Figure 6. The relationship between diastolic pressure and volume when ventricular compliance is normal, decreased, and increased. As compliance falls, end‐diastolic volume decreases at a given end‐diastolic pressure, and a higher end‐diastolic pressure is required for a given end‐diastolic volume. Note that compliance rapidly falls when end‐diastolic volume exceeds the normal working range of the ventricle (dashed black lines), and there is little or no increase in ventricular volume as pressure rises. This creates the plateau on the ventricular function curve.
Figure 7. Figure 7. Idealized depiction of a ventricular function or Starling curve. Within the optimal working range of the ventricle, stroke volume increases rapidly with end‐diastolic volume with little increase in end‐diastolic pressure. At high end‐diastolic volumes, however, ventricular compliance rapidly falls, and end‐diastolic pressure increases with little or no change in end‐diastolic volume and stroke volume.
Figure 8. Figure 8. Venous return curves. Mean systemic filling pressure is the point at which each curve intersects the X‐axis. The effect of volume loading, hypovolemia, and decreased resistance to venous return (RVR) is shown. RA, right atrial; RVR, resistance to venous return; +, positive pressure; −, negative pressure. Based on, with permission, Guyton AC, et al., 1959 47; Guyton AC, et al., 1956 49; Guyton AC, et al., 1957 50; Guyton AC, 1955 47.
Figure 9. Figure 9. Superimposition of venous return and ventricular function (Starling) curves. Venous return curves over a wide range of intravascular volume and mean systemic filling pressures are shown. Each intersection of a venous return curve with the ventricular function curve (filled circles) defines the right atrial intramural pressure, venous return, and cardiac output at that level of mean systemic filling pressure and ventricular function. RA, right atrial; +, positive pressure; −, negative pressure.
Figure 10. Figure 10. A schematic illustration of the change in the baseline left ventricular (LV) pressure‐volume loop (black) with an increase in preload, afterload, and contractility. The slope of a line connecting the end‐systolic pressure and volume of loops obtained with different preload and afterload is proportional to ventricular contractility. The LV diastolic pressure‐volume relationship and the point at which diastolic compliance rapidly falls (dashed black line) are also shown. Figure modified, with permission, from Tanai E and Frantz S, 2016 136.
Figure 11. Figure 11. A series of Starling curves showing the effect of changes in ventricular preload, afterload, and contractility. Increases and decreases in preload move ventricular function to the right (A → C) and left (A → B), respectively along the same curve. Increased contractility or decreased afterload move ventricular function upward and to the left (A → E), thereby increasing stroke volume at a lower preload. Increased afterload or decreased contractility move the curve down and to the right, and stroke volume falls at a higher preload (A → D). From Kreit J. Mechanical Ventilation. Oxford University Press, 2018. Reproduced with permission of the licensor through PLSclear.
Figure 12. Figure 12. The “compartments” of the cardiovascular system. The extra‐thoracic compartment contains the blood vessels in the head, neck, arms, and extra‐pleural chest wall. The extra‐abdominal compartment consists of the lower body and the extra‐peritoneal abdominal wall. PATM, atmospheric pressure; PPL, pleural pressure; PALV, alveolar pressure; PAB, intra‐abdominal pressure; ALV, alveolar vessels; Ex‐ALV, extra‐alveolar vessels; R, right atrium and ventricle; L, left atrium and ventricle. From Kreit J. Mechanical Ventilation. Oxford University Press, 2018. Reproduced with permission of the licensor through PLSclear.
Figure 13. Figure 13. Schematic representation of the right atrium (RA) and superior vena cava (SVC) within the thoracic compartment and the inferior vena cava (IVC) within the abdominal compartment. The figure shows the change in pressure within the RA (PRA‐IM), SVC (PSVC‐IM), abdomen (PAB), and IVC (PIVC‐IM) when pleural pressure (PPL) is increased by a positive‐pressure breath or positive end‐expiratory pressure. For the sake of clarity, a rapid, continuous process has been separated into three steps (A, B, and C). The total change in PPL, PRA‐IM, PAB, and transmural RA (PRA‐TM), SVC (PSVC‐TM), and IVC (PIVC‐TM) pressure is shown in the box. The width of the arrows indicates the magnitude of flow. The size of the RA, SVC, and IVC reflect transmural pressure and volume. Purple arrows represent flow from the extra‐thoracic, abdominal, and extra‐abdominal compartments. Light blue arrows represent flow from the splanchnic venous reservoir. Based on, with permission, Jellinek H, et al., 2000 64; Lansdorp B, et al., 2014 72; Pinsky M, 1984 111; Pinsky MR, 1984 112; Takata M, Beloucif S, Shimada M, Robotham JL. Superior and inferior vena caval flows during respiration: pathogenesis of Kussmaul's sign. Am J Physiol 262: H763‐H770, 1992; Takata M and Robotham JL, 1990 134; Takata M, et al., 1992 135; Van den Berg PCM, et al., 2002 142; Vieillard‐Baron, A, et al., 2001 151; 137. Vieillard‐Baron A, et al., 2004 147.
Figure 14. Figure 14. The zones of the lung. PALV, alveolar pressure; PC‐I, capillary inflow pressure; PC‐O, capillary outflow pressure. From Kreit J. Mechanical Ventilation. Oxford University Press, 2018. Reproduced with permission of the licensor through PLSclear.
Figure 15. Figure 15. (A) Schematic representation of the changes in right atrial intramural pressure (PRA‐IM) and right and left ventricular (RV, LV) preload, afterload, and stroke volume during a passive, positive‐pressure breath. Insp., inspiration; Exp., expiration. (B) Schematic representation of changes in systemic blood pressure during a passive, positive‐pressure breath. The maximal (SBPMAX) and minimal (SBPMIN) systolic blood pressure, the maximal increase (Δup) and decrease (Δdown) in systolic blood pressure from end expiration, and the maximal (PPMAX) and minimal (PPMIN) pulse pressure are shown (see later section: 29). From Kreit J. Mechanical Ventilation. Oxford University Press, 2018. Reproduced with permission of the licensor through PLSclear.
Figure 16. Figure 16. The change in alveolar, extra‐alveolar, and total pulmonary vascular resistance (PVR) as lung transmural pressure (PL‐TM) increases from residual volume (RV) to total lung capacity (TLC). Total PVR is lowest near the equilibrium volume of the respiratory system (EV), which is normally functional residual capacity. Based on, with permission, Fishman AP, 2011 41; Lumb AB, 2010 75; Purmutt S and Wise RA, 2011 115.
Figure 17. Figure 17. Illustration showing the left ventricle (circle) and the aorta (narrow rectangle). The ventricle and proximal aorta are within the thorax (black square) and exposed to pleural pressure (PPL). The intramural left ventricular end‐diastolic pressure (PIM) and the diastolic blood pressure (DBP) are shown. (A) In this example, when PPL is 0 mmHg, the LV must increase its intramural pressure (ΔPIM) by 72 mmHg during isovolumic contraction to open the aortic valve, and, at the onset of the ejection phase, ventricular transmural pressure (PTM) is 80 mmHg. (B) When PPL increases to 10 mmHg, PIM rises by the same amount during isovolumic contraction. Since DBP does not change, the ventricle must generate only 62 mmHg, PTM decreases to 70 mmHg, and LV afterload falls. (C) Reducing DBP by 10 mmHg has the same effect on ΔPIM, PTM, and LV afterload as increasing PPL by 10 mmHg.
Figure 18. Figure 18. (A) Normal, static, expiratory volume‐transmural pressure curves of the lungs, chest wall, and respiratory system showing the increase in pleural pressure (ΔPPL‐1) and lung transmural pressure (ΔPL‐TM‐1) during tidal inflation. When tidal volume (VT) is constant, a decrease (arrows) in chest wall (B) or lung (C) compliance (i.e., a decrease in slope) reduces the equilibrium volume (EV) of the respiratory system and causes a larger tidal increase in pleural pressure (ΔPPL‐2 > ΔPPL‐1) and lung transmural pressure (ΔPL‐TM‐2 > ΔPL‐TM‐1), respectively. PTM, transmural pressure; PALV, alveolar pressure; PL‐TM, lung transmural pressure; PPL, pleural pressure; V, volume; VT, tidal volume; TLC, total lung capacity; RV, residual volume; +, positive transmural pressure; −, negative transmural pressure. From Kreit J. Mechanical Ventilation. Oxford University Press, 2018. Reproduced with permission of the licensor through PLSclear.
Figure 19. Figure 19. Static, expiratory volume‐transmural pressure curves of the lungs, chest wall, and respiratory system showing normal lung and chest wall compliance (A), decreased chest wall compliance (B), increased lung compliance (C), and decreased lung compliance (D). In each figure, the new equilibrium volume (EV‐2) produced by PEEP of 10 cmH2O (arrow) and the resulting volume increase (ΔV) above the original equilibrium volume (EV) are shown. Also shown is the partitioning of the increase in alveolar pressure (ΔPALV = 10 cmH2O) between the increase in pleural (ΔPPL) and lung transmural (ΔPL‐TM) pressure. Note that PEEP = ΔPALV and ΔPALV = ΔPPL + ΔPL‐TM. V, volume; PTM, transmural pressure; TLC, total lung capacity; RV, residual volume; +, positive transmural pressure; −, negative transmural pressure.Based on, with permission, Chapin JC, et al., 1979 20; Jardin F, et al., 1985 61; O'Quinn RJ, et al., 1985 96.


Figure 1. Illustration showing the transmural pressure of the lungs (PL‐TM), chest wall (PCW‐TM), and respiratory system (PRS‐TM). PAW, airway pressure; PALV, alveolar pressure; PPL, pleural pressure; PATM, atmospheric pressure. From Kreit J. Mechanical Ventilation. Oxford University Press, 2018. Reproduced with permission of the licensor through PLSclear.


Figure 2. Static expiratory volume‐transmural pressure curves of the lungs (PL‐TM), chest wall (PCW‐TM), and respiratory system (PRS‐TM). PCW‐TM equals pleural pressure, PRS‐TM equals alveolar pressure, and PL‐TM equals alveolar pressure minus pleural pressure. V, volume; PTM, transmural pressure; TLC, total lung capacity; EV, equilibrium volume; RV, residual volume; +, positive transmural pressure; −, negative transmural pressure. From Kreit J. Mechanical Ventilation. Oxford University Press, 2018. Modified with permission of the licensor through PLSclear.


Figure 3. Dynamic pressure‐time curves showing the change in alveolar (PALV), pleural (PPL), lung transmural (PL‐TM), and intra‐abdominal (PAB) pressure during a spontaneous breath. Based on, with permission, Mead J and Whittenberger JL, 1953 86; Mead J, 1961 85; Otis AB, et al., 1950 98; Rodarte JR and Rehder K, 2011 119.


Figure 4. Dynamic pressure‐time curves during a passive, mechanical breath with constant inspiratory flow and positive end‐expiratory pressure (PEEP) of 0 cmH2O (A) and 10 cmH2O (B). PEEP causes a proportional rise in airway (PAW), alveolar (PALV), pleural (PPL), lung transmural (PL‐TM), and intra‐abdominal (PAB) pressure throughout the respiratory cycle. When inspiratory flow stops and expiration is delayed by an end‐inspiratory pause, PAW falls to PALV. Based on, with permission, Van den Berg PCM, et al., 2002 142.


Figure 5. Schematic illustration of the left ventricular (LV) pressure‐volume loop. The pressure and volume changes during isovolumic contraction, ejection, isovolumic relaxation, and ventricular filling are shown. The base of the loop is the LV diastolic pressure‐volume relationship.


Figure 6. The relationship between diastolic pressure and volume when ventricular compliance is normal, decreased, and increased. As compliance falls, end‐diastolic volume decreases at a given end‐diastolic pressure, and a higher end‐diastolic pressure is required for a given end‐diastolic volume. Note that compliance rapidly falls when end‐diastolic volume exceeds the normal working range of the ventricle (dashed black lines), and there is little or no increase in ventricular volume as pressure rises. This creates the plateau on the ventricular function curve.


Figure 7. Idealized depiction of a ventricular function or Starling curve. Within the optimal working range of the ventricle, stroke volume increases rapidly with end‐diastolic volume with little increase in end‐diastolic pressure. At high end‐diastolic volumes, however, ventricular compliance rapidly falls, and end‐diastolic pressure increases with little or no change in end‐diastolic volume and stroke volume.


Figure 8. Venous return curves. Mean systemic filling pressure is the point at which each curve intersects the X‐axis. The effect of volume loading, hypovolemia, and decreased resistance to venous return (RVR) is shown. RA, right atrial; RVR, resistance to venous return; +, positive pressure; −, negative pressure. Based on, with permission, Guyton AC, et al., 1959 47; Guyton AC, et al., 1956 49; Guyton AC, et al., 1957 50; Guyton AC, 1955 47.


Figure 9. Superimposition of venous return and ventricular function (Starling) curves. Venous return curves over a wide range of intravascular volume and mean systemic filling pressures are shown. Each intersection of a venous return curve with the ventricular function curve (filled circles) defines the right atrial intramural pressure, venous return, and cardiac output at that level of mean systemic filling pressure and ventricular function. RA, right atrial; +, positive pressure; −, negative pressure.


Figure 10. A schematic illustration of the change in the baseline left ventricular (LV) pressure‐volume loop (black) with an increase in preload, afterload, and contractility. The slope of a line connecting the end‐systolic pressure and volume of loops obtained with different preload and afterload is proportional to ventricular contractility. The LV diastolic pressure‐volume relationship and the point at which diastolic compliance rapidly falls (dashed black line) are also shown. Figure modified, with permission, from Tanai E and Frantz S, 2016 136.


Figure 11. A series of Starling curves showing the effect of changes in ventricular preload, afterload, and contractility. Increases and decreases in preload move ventricular function to the right (A → C) and left (A → B), respectively along the same curve. Increased contractility or decreased afterload move ventricular function upward and to the left (A → E), thereby increasing stroke volume at a lower preload. Increased afterload or decreased contractility move the curve down and to the right, and stroke volume falls at a higher preload (A → D). From Kreit J. Mechanical Ventilation. Oxford University Press, 2018. Reproduced with permission of the licensor through PLSclear.


Figure 12. The “compartments” of the cardiovascular system. The extra‐thoracic compartment contains the blood vessels in the head, neck, arms, and extra‐pleural chest wall. The extra‐abdominal compartment consists of the lower body and the extra‐peritoneal abdominal wall. PATM, atmospheric pressure; PPL, pleural pressure; PALV, alveolar pressure; PAB, intra‐abdominal pressure; ALV, alveolar vessels; Ex‐ALV, extra‐alveolar vessels; R, right atrium and ventricle; L, left atrium and ventricle. From Kreit J. Mechanical Ventilation. Oxford University Press, 2018. Reproduced with permission of the licensor through PLSclear.


Figure 13. Schematic representation of the right atrium (RA) and superior vena cava (SVC) within the thoracic compartment and the inferior vena cava (IVC) within the abdominal compartment. The figure shows the change in pressure within the RA (PRA‐IM), SVC (PSVC‐IM), abdomen (PAB), and IVC (PIVC‐IM) when pleural pressure (PPL) is increased by a positive‐pressure breath or positive end‐expiratory pressure. For the sake of clarity, a rapid, continuous process has been separated into three steps (A, B, and C). The total change in PPL, PRA‐IM, PAB, and transmural RA (PRA‐TM), SVC (PSVC‐TM), and IVC (PIVC‐TM) pressure is shown in the box. The width of the arrows indicates the magnitude of flow. The size of the RA, SVC, and IVC reflect transmural pressure and volume. Purple arrows represent flow from the extra‐thoracic, abdominal, and extra‐abdominal compartments. Light blue arrows represent flow from the splanchnic venous reservoir. Based on, with permission, Jellinek H, et al., 2000 64; Lansdorp B, et al., 2014 72; Pinsky M, 1984 111; Pinsky MR, 1984 112; Takata M, Beloucif S, Shimada M, Robotham JL. Superior and inferior vena caval flows during respiration: pathogenesis of Kussmaul's sign. Am J Physiol 262: H763‐H770, 1992; Takata M and Robotham JL, 1990 134; Takata M, et al., 1992 135; Van den Berg PCM, et al., 2002 142; Vieillard‐Baron, A, et al., 2001 151; 137. Vieillard‐Baron A, et al., 2004 147.


Figure 14. The zones of the lung. PALV, alveolar pressure; PC‐I, capillary inflow pressure; PC‐O, capillary outflow pressure. From Kreit J. Mechanical Ventilation. Oxford University Press, 2018. Reproduced with permission of the licensor through PLSclear.


Figure 15. (A) Schematic representation of the changes in right atrial intramural pressure (PRA‐IM) and right and left ventricular (RV, LV) preload, afterload, and stroke volume during a passive, positive‐pressure breath. Insp., inspiration; Exp., expiration. (B) Schematic representation of changes in systemic blood pressure during a passive, positive‐pressure breath. The maximal (SBPMAX) and minimal (SBPMIN) systolic blood pressure, the maximal increase (Δup) and decrease (Δdown) in systolic blood pressure from end expiration, and the maximal (PPMAX) and minimal (PPMIN) pulse pressure are shown (see later section: 29). From Kreit J. Mechanical Ventilation. Oxford University Press, 2018. Reproduced with permission of the licensor through PLSclear.


Figure 16. The change in alveolar, extra‐alveolar, and total pulmonary vascular resistance (PVR) as lung transmural pressure (PL‐TM) increases from residual volume (RV) to total lung capacity (TLC). Total PVR is lowest near the equilibrium volume of the respiratory system (EV), which is normally functional residual capacity. Based on, with permission, Fishman AP, 2011 41; Lumb AB, 2010 75; Purmutt S and Wise RA, 2011 115.


Figure 17. Illustration showing the left ventricle (circle) and the aorta (narrow rectangle). The ventricle and proximal aorta are within the thorax (black square) and exposed to pleural pressure (PPL). The intramural left ventricular end‐diastolic pressure (PIM) and the diastolic blood pressure (DBP) are shown. (A) In this example, when PPL is 0 mmHg, the LV must increase its intramural pressure (ΔPIM) by 72 mmHg during isovolumic contraction to open the aortic valve, and, at the onset of the ejection phase, ventricular transmural pressure (PTM) is 80 mmHg. (B) When PPL increases to 10 mmHg, PIM rises by the same amount during isovolumic contraction. Since DBP does not change, the ventricle must generate only 62 mmHg, PTM decreases to 70 mmHg, and LV afterload falls. (C) Reducing DBP by 10 mmHg has the same effect on ΔPIM, PTM, and LV afterload as increasing PPL by 10 mmHg.


Figure 18. (A) Normal, static, expiratory volume‐transmural pressure curves of the lungs, chest wall, and respiratory system showing the increase in pleural pressure (ΔPPL‐1) and lung transmural pressure (ΔPL‐TM‐1) during tidal inflation. When tidal volume (VT) is constant, a decrease (arrows) in chest wall (B) or lung (C) compliance (i.e., a decrease in slope) reduces the equilibrium volume (EV) of the respiratory system and causes a larger tidal increase in pleural pressure (ΔPPL‐2 > ΔPPL‐1) and lung transmural pressure (ΔPL‐TM‐2 > ΔPL‐TM‐1), respectively. PTM, transmural pressure; PALV, alveolar pressure; PL‐TM, lung transmural pressure; PPL, pleural pressure; V, volume; VT, tidal volume; TLC, total lung capacity; RV, residual volume; +, positive transmural pressure; −, negative transmural pressure. From Kreit J. Mechanical Ventilation. Oxford University Press, 2018. Reproduced with permission of the licensor through PLSclear.


Figure 19. Static, expiratory volume‐transmural pressure curves of the lungs, chest wall, and respiratory system showing normal lung and chest wall compliance (A), decreased chest wall compliance (B), increased lung compliance (C), and decreased lung compliance (D). In each figure, the new equilibrium volume (EV‐2) produced by PEEP of 10 cmH2O (arrow) and the resulting volume increase (ΔV) above the original equilibrium volume (EV) are shown. Also shown is the partitioning of the increase in alveolar pressure (ΔPALV = 10 cmH2O) between the increase in pleural (ΔPPL) and lung transmural (ΔPL‐TM) pressure. Note that PEEP = ΔPALV and ΔPALV = ΔPPL + ΔPL‐TM. V, volume; PTM, transmural pressure; TLC, total lung capacity; RV, residual volume; +, positive transmural pressure; −, negative transmural pressure.Based on, with permission, Chapin JC, et al., 1979 20; Jardin F, et al., 1985 61; O'Quinn RJ, et al., 1985 96.
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Article Title: Respiratory‐Cardiovascular Interactions During Mechanical Ventilation: Physiology and Clinical Implications
 

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John Kreit. Respiratory‐Cardiovascular Interactions During Mechanical Ventilation: Physiology and Clinical Implications. Compr Physiol 2022, 12: 3425-3448. doi: 10.1002/cphy.c210003