Heart-Lungs Interactions: Basics and Clinical Implications PDF

Jozwiak and Teboul Annals of Intensive Care (2024) 14:122 Annals of Intensive Care https://doi.org/10.1186/s13613-024-01356-5 REVIEW...

Jozwiak and Teboul https://doi.org/10.1186/s13613-024-01356-5 REVIEW Heart–Lungs interactions: the basics and clinical implications Mathieu Jozwiak1,2* and Jean‑Louis Teboul3 Abstract Heart–lungs interactions are related to the result from the respiratory-induced changes in ties and to the changes in alveolar pressure, patients, consequences of heart–lungs interactions and afterload, a decrease in left ventricular lated patients, consequences of heart–lungs tricular preload, an increase in right ventricular ventricular afterload. Physiologically and during hemodynamic consequences. Nevertheless, in some tive pulmonary disease, acute left heart failure lead to significant hemodynamic consequences. ing a marked inspiratory negativity of intrathoracic and an increase in intra-abdominal pressure. of fluid responsiveness in mechanically ventilated tions was the respiratory variation of pulse using heart–lungs interactions have been developed, volume or the respiratory variations of the inferior limitations, the most frequent being low tidal diac arrhythmia. Nevertheless, when their main in the decision-making process regarding fluid Keywords Cardiac loading conditions, Intrathoracic *Correspondence: Mathieu Jozwiak [email protected] normal breathing, heart–lungs interactions do not lead to significant hemodynamic consequences. This is not 06200 Nice, France Université Côte d’Azur, the case during acute exacerbation of asthma or chronic obstructive pulmonary disease, acute left heart failure Paris-Saclay, 94270 Le and during weaning from mechanical ventilation. In the first part of this review, heart–lungs interactions in Author(s) 2024. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this visit http://creativecommons.org/licenses/by/4.0/. (2024) 14:122 Page 2 of 13 Heart–lungs interactions in spontaneously breathing patients A simple way to describe heart–lungs interactions is to consider the interactions between two pumps: the smaller (circulatory pump) being contained within the larger (respiratory pump). While the respiratory pump acts as a suction pump, developing a negative pressure to allow air entry into the airways and blood into cardiac cavities, the circulatory pump acts as a pressure pump, developing a positive pressure to eject blood towards the arterial tree. As the circulatory pump is contained within spontaneously breathing patients and in mechanically ventilated patients. In physiological increase in right ventricular (RV) preload and decrease in left ventricular (LV) preload are the two loading conditions. In patients with healthy lungs and heart (mechanical ventilation), decrease insufflation are the two predominant global effects of ventilation on cardiac loading conditions Page 3 of 13 negativity of the intrathoracic pressure is transmitted to the right atrium, thus increasing the pressure gradient between the extrathoracic venous territory and the right atrium. Simultaneously, the increase in intra-abdominal pressure due to the descent of the diaphragm, contrib- utes to the increase in this gradient since it increases the mean systemic pressure and drives venous blood into the thorax. Inspiratory increase in right ventricular afterload From a serial component viewpoint, the pulmonary cir- culation may be divided in extra-alveolar vessels and intra-alveolar vessels. Lung volume expansion dur- ing inspiration compresses lumens of intra-alveolar ves- sels resulting in an exponential increase in intra-alveolar vessels resistance. By contrast, increase in lung volume induces an exponential decrease in extra-alveolar vessels. resistance. Indeed, as lung volume increases the radial interstitial forces increase, resulting in widening of extra- alveolar vessels diameters. Thus, the resulting total pul- monary vascular resistance describes a U shape with a nadir corresponding to a lung volume equal to the func- tional residual capacity (FRC) (Fig. 2) [4–6]. From a parallel component viewpoint, the pulmonary circulation is distributed along a gravitational gradient of the vascular-alveolar pressure difference (Fig. 3). Accordingly, by decreasing intrathoracic pressure more than alveolar pressure, spontaneous inspiration may resistance and lung volume. The dotted blue line represents the pulmonary vascular resistance line represents the pulmonary vascular resistance of the intra-alveolar vessels Page 4 of 13 illustrating the distribution of the pulmonary circulation along a gravitational gradient Palv alveolar pressure, PPV pulmonary venous pressure, PPA pulmonary artery pressure non-extensive envelope with high elastance, resulting in a constant sum of the volumes of the right and left ven- tricles. Finally, the small inspiratory increase in transpul- monary pressure could result in a shift of blood from the pulmonary venous circulation to the left atrium. Never- theless, this mechanism is probably of minor importance since studies in normal subjects showed a decrease in left ventricular preload during inspiration [7, 9, 10]. It is likely that the parallel and more importantly the serial ventricular interdependence phenomena are responsi- ble for the decrease in left ventricular preload during inspiration, which eventually results in a decrease in left ventricular stroke volume (if the left ventricle is preload- dependent) [9, 10] and thus in arterial pulse pressure during inspiration. result in Inspiratory increase in left ventricular afterload The left ventricular afterload can be thought as the effort required by the left ventricle to eject blood up to the level of pressure of the extrathoracic vessels (atmospheric pressure for the vessels of the neck and upper limbs, intra-abdominal pressure for the abdominal aorta). At inspiration, the negative intrathoracic pressure places the left ventricle at a lower level and makes its ejecting effort greater, thus increasing the left ventricular afterload [11, 12]. The hemodynamic consequences of an increase in left ventricular afterload are negligible in patients with normal left ventricular function due to the physiological Page 5 of 13 resistance by an amount depending on tidal volume in an exponential way. The second mechanism is related to the more pronounced increase in alveolar pressure than intrathoracic pressure during insufflation, which may potentially result in a transfer of West’s zone 3 to West’s zone 2. This mechanism may occur when the alveolar pressure becomes higher than the pulmonary venous pressure during insufflation. The main conditions of this occurrence are the presence of a low pulmonary venous pressure (e.g. in case of low central blood volume) and a marked insufflation-related increase in transpulmonary pressure (alveolar pressure minus intrathoracic pressure) due to high tidal volume ventilation or to reduced lung compliance, which reduces the airway pressure trans- mission [14, 15]. So, the lower the lung compliance (or the lower the compliance of the respiratory system), the lower the transmission of the airway pressure and the higher the transpulmonary pressure. For all these rea- sons, mechanical insufflation should increase pulmonary vascular resistance and right ventricular afterload. However, in patients with normal compliance of the res- piratory system, this effect should be limited if low tidal volume ventilation is used, what is usually the case in critically ill patients who receive mechanical ventilation. Increase in left ventricular preload during insufflation First, the increase in transpulmonary pressure during insufflation may induce a shift of blood from the pulmo- nary venous circulation to the left atrium, thus increas- ing the filling of the left ventricle at the same time. Second, due to the serial ventricular interdependence, the decrease in systemic venous return combined with the impeded right ventricular ejection during insuffla- tion result in a decrease in the left ventricular filling and preload during the following expiration because of the long pulmonary transit time. In accordance with these mechanisms, an increase in echocardiographic indexes of left ventricular preload during insufflation was demon- strated. It is noteworthy that if the right ventricular ejection is markedly impeded during insufflation, right ventricular overload might occur and result in a leftward septal shift. This septal shift during insufflation could reduce the distensibility of the left ventricle and impedes its filling through the parallel ventricular interdepend- ence [8, 18]. Nevertheless, even if the right ventricular stroke volume decreases during insufflation [17, 19] due to the combined effects of decrease in right ventricu- lar preload and increase in right ventricular afterload, unchanged and not enlarged right ventricular end-dias- tolic volume during insufflation was reported [17, 19] making the occurrence of a pronounced leftward septal shift during insufflation unlikely. Page 6 of 13 implications. Heart–lungs interactions in these different clinical settings will be briefly summarized below. the Acute exacerbation of chronic obstructive pulmonary disease Dynamic hyperinflation is one of the characteristics of acute exacerbation of characteristics of chronic obstructive pulmonary disease (COPD). Such a phe- nomenon is favored by (i) increased airway resistance related to bronchoconstriction, mucosal oedema and excessive sputum, (ii) decrease elastic recoil pres- sure, (iii) tachypnea, which reduces the time devoted to expiration, and (iv) mainly expiratory airflow limi- tation. This results in an end-expiratory lung volume higher than the relaxation lung volume and therefore in a positive static end-expiratory elastic recoil pres- sure called intrinsic positive end-expiratory pressure (PEEP). This leads to accentuated inspiratory negativity of intrathoracic pressure and increased work of breath- ing. These events should increase cardiac output to meet increased oxygen demand. Increased sympa- thetic activity leading to tachycardia participates in this response. The marked negativity of the intrathoracic pressure also contributes to increasing systemic venous return and cardiac output since it decreases the right atrial pressure. At the same time the increase in intra- abdominal pressure increases the mean systemic pres- sure so that the venous return pressure gradient should increase. However, in case of a very marked inspiratory negativity of intrathoracic pressure, the intra-abdomi- nal pressure may become so positive in relation to the right atrial pressure that it leads to collapse of the infe- rior vena cava in its subdiaphragmatic segment, which interrupts the inspiratory increase in systemic venous return (Fig. 4) [22, 23]. This phenomenon may occur mostly when patients are hypovolemic. In addi- tion, due to the marked negativity of the intrathoracic pressure compared to the alveolar pressure, the right ventricular afterload should increase more during acute exacerbation than during quiet breathing conditions in patients with COPD. Moreover, worsening of hypox- emia during acute exacerbation of COPD may aggra- vate the pulmonary hypertension and hence induce a more marked increase in the right ventricular after- load through the hypoxic pulmonary vasoconstriction mechanism. The role of hypercapnia on pulmonary vas- cular resistance is less clear as it was reported to have a pulmonary vasodilatory or a pulmonary vasoconstrict- ing effect depending on some experimental conditions may. However, it is likely that during hypoxemia, hyper- capnia should further increase pulmonary vasocon- striction. In patients with prior right ventricular dysfunction, as it is sometimes the case in COPD, an (2024) 14:122 Page 7 of 13 illustrating the effects of intra-abdominal pressure on systemic venous return. IAP of inferior vena cava at the level of the diaphragm, PC critical closing transmural pressure situation could be risky if the episode of acute respiratory failure is only related to acute exacerbation of COPD. Acute left heart failure In spontaneously breathing patients with acute heart failure, the same initiating phenomena than those described above for patients with acute exacerbation of chronic obstructive pulmonary disease may partici- pate to the hemodynamic consequences of heart–lungs interactions. In this clinical setting, the accentuated inspiratory negativity of intrathoracic pressure is related to reduced lung compliance and increased air- way resistance. The reduced lung compliance is a consequence of interstitial and/or alveolar oedema. The increase in airway resistance may be related to several mechanisms [27, 28]: (i) a bronchial wall thick- ening because of bronchial oedema formation and/ or increased vascular volume, (ii) a reflex broncho- constriction of vagal origin, stimulated by increased pulmonary vascular pressures and/or interstitial or peribronchial oedema and/or (iii) a bronchial hyper- reactivity. The marked decrease in intrathoracic pres- sure during inspiration along with the increase in intra-abdominal pressure should markedly increase the left ventricular afterload with potential decrease Page 8 of 13 benefits in terms of clinical and/or oxygenation improve- ment [30, 37–40]. Cardiac dysfunction induced by weaning from mechanical ventilation Echocardiographic studies have shown that left ventricu- lar diastolic dysfunction and increased left ventricular filling pressure are common during weaning failure [41, 42]. In a high percentage of cases of weaning failure, a cardiogenic pulmonary oedema may occur. The risk factors for weaning-induced pulmonary oedema (WIPO) are COPD, cardiopathy (dilated and/or hypertrophic and/or hypokinetic cardiopathy and/or significant valvu- lar disease) and obesity. The WIPO is mainly induced by the shift from a posi- tive to a negative pressure ventilation after disconnect- ing the ventilator [44–46]. The inspiratory negativity of intrathoracic pressure may be accentuated by the resist- ance of the chest tube. This results in the heart–lungs interactions described above in spontaneously breathing patients, leading to unfavorable loading cardiac condi- tions (increase in right ventricular preload and afterload and increase in left ventricular afterload) and eventually to WIPO. In patients with chronic right ventricular dysfunction, right ventricular enlargement during wean- ing can play a role in the development of WIPO through a biventricular interdependence mechanism. In patients with chronic left ventricular dysfunction, increase in left ventricular afterload due to accentuated negativ- ity of intrathoracic pressure, increased intra-abdominal pressure and sympathetic-related arterial hypertension should also play an important role in the occurrence of WIPO. In any case, a positive fluid balance also contrib- utes to WIPO. Some studies also suggested a potential role of myo- cardial ischemia in the development of WIPO. Myocar- dial ischemia would be related to the increase in cardiac work (secondary to the increased work of breathing), the increase in left ventricular afterload and to the decrease in coronary perfusion [49, 50]. Nevertheless, recent find- ings suggest that myocardial ischemia plays no major role in the pathophysiology of WIPO [43, 48, 51]. Finally, it is well-established that left ventricular dias- tolic dysfunction is also involved in the pathophysiol- ogy of WIPO [41, 42, 48], while the potential role of left ventricular systolic dysfunction remains unclear and is the subject of ongoing study (SystoWean study, NCT05226247).Since WIPO can be secondary to dif- ferent mechanisms, it is important not only to diagnose it (for example using changes in hemoconcentration parameters during a weaning trial) but to identify what are the main underlying mechanism(s) in order to apply the most appropriate treatment. Page 9 of 13 ARDS include both closed alveoli units, which could be re-opened, and normal alveoli units, which could be overdistended. Thus, the impact of PEEP on pulmonary vascular resistance would depend on the recruitment/ overdistension ratio for a given patient and at a given time of the disease, as it was illustrated in a recent clinical study. This maybe explains why different responses of the right ventricular afterload to PEEP were reported in ARDS patients [55–59]. It is noteworthy that if PEEP improves gas exchange, it should decrease hypoxic vaso- constriction and thus decrease the pulmonary vascular resistance. In addition, PEEP could exert effects on the systemic venous return determinants. By increasing the intratho- racic pressure, the right atrial pressure, which is the downstream pressure to systemic venous return should increase, although the reduced airway pressure transmis- sion during ARDS should attenuate this effect [14, 15]. On the other hand, the mean systemic pressure (i.e. the upstream pressure to systemic venous return) should also. increase and therefore limit the effects of the increase in intrathoracic pressure on venous return due to combined effects of the PEEP-induced increased intra-abdominal pressure and to other adaptive mechanisms including sympathetic-mediated mechanisms. In particu- lar, the activation of the renin–angiotensin–aldosterone system during positive pressure ventilation may increase the mean systemic pressure by inducing a venoconstric- tion of the splanchnic vasculature which in turn results in a shift of blood into the systemic circulation. Never- theless, both the PEEP-induced increased intra-abdomi- nal pressure and the other adaptive mechanisms may also increase venous resistance in some extent [61, 63]. If dur- ing ARDS, it seems thus unlikely that PEEP would mark- edly reduce cardiac output through a primary impact on systemic venous return, such a mechanism cannot be excluded in patients who receive heavy sedation able to blunt the adaptive responses to PEEP. Previous clinical data have suggested that the decrease in right ventricular preload secondary to decreased sys- temic venous return may play an important role in the PEEP-induced decrease in cardiac output [55–57, 64, 65]. Others have suggested a predominant role of the increased right ventricular afterload [59, 66]. Many of the following factors could explain such divergent results: the capacity of PEEP to induce lung recruitment vs. overd- istension, its capacity of improving arterial oxygenation, the amount of tidal volume, the degree of airway pressure transmission, the level of sedation, the degree of right ventricular preload-dependence and afterload-depend- ence, and the degree of left ventricular preload-depend- ence and afterload-dependence. Finally, the volume status also plays a key role. In case of decreased central blood Page 10 of 13 several limitations exist in critically ill patients, the most frequent ones being low tidal volume ventilation, persis- tent spontaneous breathing activity, and cardiac arrhyth- mia [82–84]. It is noteworthy that in patients with ARDS, particularly when they are ventilated with high PEEP level, a high PPV might be related to right ventricu- lar failure and to be a sign of right ventricular afterload dependence rather than fluid responsiveness. In this case of possible false positive PPV, it is suggested to assess the changes in PPV during a passive leg raising. If no change in PPV is observed, a high PPV indicates right ventricular afterload dependence, while a decrease in PPV suggests fluid responsiveness [82, 85]. Several other heart–lungs interaction tests have been developed to predict fluid responsiveness. Some of them such as pulse contour-based stroke volume varia- tion and respiratory variation of the inferior or superior vena cava diameters assessed by ultrasound imaging are not superior to PPV [86, 87] and share the same limita- tions as PPV [83, 84]. In patients ventilated with a tidal volume < 8 mL/kg, the tidal volume challenge can reliably predict fluid responsiveness by assessing the response of PPV to a brief increase in tidal volume (by 2 mL/kg) with ARDS. Recently, it was shown that the response of PPV to. Therefore, is it currently recommended to assess passive leg raising can also predict fluid responsiveness in cases of low tidal volume ventilation [89–91], even in the case of persistent spontaneous breathing activity. This test and the tidal volume challenge have the advan- tage to require only an arterial catheter. Very recently, it has been shown the increase in cardiac output or the pulse pressure induced by a PEEP decrease may also reli- ably predict fluid responsiveness in patients with ARDS receiving low tidal volume ventilation. Conclusion Heart–lungs interactions describe the interactions between the respiratory and the circulatory pump in the confined space of the thorax and result from the respiratory-induced changes in intrathoracic pressure, which are transmitted to the cardiac cavities and to the changes in alveolar pressure, which may impact the lung microvessels. Physiologically, heart–lungs interactions do not lead to significant hemodynamic consequences. In patients with acute respiratory failure, heart–lungs interactions may have significant hemodynamic conse- quences that can worsen the clinical conditions. The use of PEEP in patients mechanically ventilated for ARDS may result in hemodynamic compromise, especially when PEEP exerts excessive lung overdistension. The most recent application of heart–lungs interactions is the prediction of fluid responsiveness in mechanically venti- lated patients. 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