The Effect of PEEP on Pulmonary Vascular Resistance Depends on Lung Recruitability in ARDS Patients.

Rationale. A U-shape relationship should exist between lung volume and pulmonary vascular resistance (PVR), with minimal PVR at functional residual capacity. Thus, positive end-expiratory pressure (PEEP) in patients with acute respiratory distress syndrome (ARDS) should increase PVR if it induces significant lung distension compared to recruitment. However, this has never been proven in patients. Objectives. To study the effects of PEEP on PVR according to lung recruitability, evaluated by the recruitment-to-inflation (R/I) ratio. Methods. In patients with ARDS, we measured hemodynamic (pulmonary artery catheter), echocardiographic and ventilatory variables (including esophageal pressure), at both low PEEP and higher PEEP by 10 cmH2O. Preload responsiveness was assessed by the passive leg raising test at high PEEP. Measurements and Main Results. We enrolled 23 patients, including 10 low recruiters (R/I <0.5) and 13 high recruiters (R/I ≥0.5). Raising PEEP from 4 (2-5) to 14 (12-15) cmH2O increased PVR in low recruiters (from 160 (120-297) to 243 (166-380) dyn.s/cm5, p<0.01), while PVR was unchanged in high recruiters (from 224 (185-289) to 235 (168-300) dyn.s/cm5, p=0.55). Right-to-left ventricular end-diastolic areas ratio simultaneously increased in low recruiters (from 0.54 (0.50-0.59) to 0.64 (0.56-0.70), p<0.01), while remaining stable in high recruiters (from 0.70 (0.65-0.79) to 0.68 (0.58-0.80), p=0.48). Raising PEEP decreased cardiac index only in preload responsive patients. Conclusions. PEEP increases PVR only when it induces significant lung distension compared to recruitment according to the recruitment-to-inflation ratio. Tailoring PEEP on this recruitability index should mitigate its hemodynamic effects.

The effects of respiratory rate and tidal volume on pulse pressure variation in healthy lungs-a generalized additive model approach may help overcome limitations.

Pulse pressure variation (PPV) is a well-established method for predicting fluid responsiveness in mechanically ventilated patients. The predictive accuracy is, however, disputed for ventilation with low tidal volume (VT) or low heart-rate-to-respiratory-rate ratio (HR/RR). We investigated the effects of VT and RR on PPV and on PPV's ability to predict fluid responsiveness. We included patients scheduled for open abdominal surgery. Prior to a 250 ml fluid bolus, we ventilated patients with combinations of VT from 4 to 10 ml kg-1 and RR from 10 to 31 min-1. For each of 10 RR-VT combinations, PPV was derived using both a classic approach and a generalized additive model (GAM) approach. The stroke volume (SV) response to fluid was evaluated using uncalibrated pulse contour analysis. An SV increase > 10% defined fluid responsiveness. Fifty of 52 included patients received a fluid bolus. Ten were fluid responders. For all ventilator settings, fluid responsiveness prediction with PPV was inconclusive with point estimates for the area under the receiver operating characteristics curve between 0.62 and 0.82. Both PPV measures were nearly proportional to VT. Higher RR was associated with lower PPV. Classically derived PPV was affected more by RR than GAM-derived PPV. Correcting PPV for VT could improve PPV's predictive utility. Low HR/RR has limited effect on GAM-derived PPV, indicating that the low HR/RR limitation is related to how PPV is calculated. We did not demonstrate any benefit of GAM-derived PPV in predicting fluid responsiveness.Trial registration: ClinicalTrials.gov, reg. March 6, 2020, NCT04298931.

Can carotid artery Doppler variations induced by the end-expiratory occlusion maneuver predict fluid responsiveness in septic shock patients?

BACKGROUND: An increase in cardiac index (CI) during an end-expiratory occlusion test (EEOt) predicts fluid responsiveness in ventilated patients. However, if CI monitoring is unavailable or the echocardiographic window is difficult, using the carotid Doppler (CD) could be a feasible alternative to track CI changes. This study investigates whether changes in CD peak velocity (CDPV) and corrected flow time (cFT) during an EEOt were correlated with CI changes and if CDPV and cFT changes predicted fluid responsiveness in patients with septic shock. METHODS: Prospective, single-center study in adults with hemodynamic instability. The CDPV and cFT on carotid artery Doppler and hemodynamic variables from the pulse contour analysis EV1000™ were recorded at baseline, during a 20-s EEOt, and after fluid challenge (500 mL). We defined responders as those who increased CI ≥ 15% after a fluid challenge. RESULTS: We performed 44 measurements in 18 mechanically ventilated patients with septic shock and without arrhythmias. The fluid responsiveness rate was 43.2%. The changes in CDPV were significantly correlated with changes in CI during EEOt (r = 0.51 [0.26-0.71]). A significant, albeit lower correlation, was found for cFT (r = 0.35 [0.1-0.58]). An increase in CI ≥ 5.35% during EEOt predicted fluid responsiveness with 78.9% sensitivity and 91.7% specificity, with an area under the ROC curve (AUROC) of 0.85. An increase in CDPV ≥ 10.5% during an EEOt predicted fluid responsiveness with 96.2% specificity and 53.0% sensitivity with an AUROC of 0.74. Sixty-one percent of CDPV measurements (from - 13.5 to 9.5 cm/s) fell within the gray zone. The cFT changes during EEOt did not accurately predict fluid responsiveness. CONCLUSIONS: In septic shock patients without arrhythmias, an increase in CDPV greater than 10.5% during a 20-s EEOt predicted fluid responsiveness with > 95% specificity. Carotid Doppler combined with EEOt may help optimize preload when invasive hemodynamic monitoring is unavailable. However, the 61% gray zone is a major limitation (retrospectively registered on Clinicaltrials.gov NCT04470856 on July 14, 2020).

First experience with real-time magnetic resonance imaging-based investigation of respiratory influence on cardiac function in pediatric congenital heart disease patients with chronic right ventricular volume overload.

BACKGROUND: Congenital heart disease (CHD) is often associated with chronic right ventricular (RV) volume overload. Real-time magnetic resonance imaging (MRI) enables the analysis of cardiac function during free breathing. OBJECTIVE: To evaluate the influence of respiration in pediatric patients with CHD and chronic RV volume overload. METHODS AND MATERIALS: RV volume overload patients (n=6) and controls (n=6) were recruited for cardiac real-time MRI at 1.5 tesla during free breathing. Breathing curves from regions of interest reflecting the position of the diaphragm served for binning images in four different tidal volume classes, each in inspiration and expiration. Tidal volumes were estimated from these curves by data previously obtained by magnetic resonance-compatible spirometry. Ventricular volumes indexed to body surface area and Frank-Starling relationships referenced to the typical tidal volume indexed to body height (TTVi) were compared. RESULTS: Indexed RV end-diastolic volume (RV-EDVi) and indexed RV stroke volume (RV-SVi) increased during inspiration (RV-EDVi/TTVi: RV load: + 16 ± 4%; controls: + 22 ± 13%; RV-SVi/TTVi: RV load: + 21 ± 6%; controls: + 35 ± 17%; non-significant for comparison). The increase in RV ejection fraction during inspiration was significantly lower in RV load patients (RV load: + 1.1 ± 2.2%; controls: + 6.1 ± 1.5%; P=0.01). The Frank-Starling relationship of the RV provided a significantly reduced slope estimate in RV load patients (inspiration: RV load: 0.75 ± 0.11; controls: 0.92 ± 0.02; P=0.02). CONCLUSION: In pediatric patients with CHD and chronic RV volume overload, cardiac real-time MRI during free breathing in combination with respiratory-based binning indicates an impaired Frank-Starling relationship of the RV.

Heart-lung interactions in COVID-19: prognostic impact and usefulness of bedside echocardiography for monitoring of the right ventricle involvement.

Due to the SARS-CoV-2 infection-related severe pulmonary tissue damages associated with a relative specific widespread thrombotic microangiopathy, the pathophysiologic role of heart-lung interactions becomes crucial for the development and progression of right ventricular (RV) dysfunction. The high resistance in the pulmonary circulation, as a result of small vessel thrombosis and hypoxemia, is the major cause of right heart failure associated with a particularly high mortality in severe COVID-19. Timely identification of patients at high risk for RV failure, optimization of mechanical ventilation to limit its adverse effects on RV preload and afterload, avoidance of medication-related increase in the pulmonary vascular resistance, and the use of extracorporeal membrane oxygenation in refractory respiratory failure with hemodynamic instability, before RV failure develops, can improve patient survival. Since it was confirmed that the right-sided heart is particularly involved in the clinical deterioration of patients with COVID-19 and pressure overload-induced RV dysfunction plays a key role for patient outcome, transthoracic echocardiography (TTE) received increasing attention. Limited TTE focused on the right heart appears highly useful in hospitalized COVID-19 patients and particularly beneficial for monitoring of critically ill patients. In addition to detection of right-sided heart dilation and RV dysfunction, it enables assessment of RV-pulmonary arterial coupling and evaluation of RV adaptability to pressure loading which facilitate useful prognostic statements to be made. The increased use of bedside TTE focused on the right heart could facilitate more personalized management and treatment of hospitalized patients and can contribute towards reducing the high mortality associated with SARS-CoV-2 infection.

Cardiorespiratory coupling is associated with exercise capacity in patients with chronic obstructive pulmonary disease.

BACKGROUND: The interaction between the pulmonary function and cardiovascular mechanics is a crucial issue, particularly when treating patients with chronic obstructive pulmonary disease (COPD). Synchrogram index is a new parameter that can quantify this interaction and has the potential to apply in COPD patients. Our objective in this study was to characterize cardiorespiratory interactions in terms of cardiorespiratory coupling (CRC) using the synchrogram index of the heart rate and respiratory flow signals in patients with chronic obstructive pulmonary disease. METHODS: This is a cross-sectional and preliminary data from a prospective study, which examines 55 COPD patients. K-means clustering analysis was applied to cluster COPD patients based on the synchrogram index. Linear regression and multivariable regression analysis were used to determine the correlation between the synchrogram index and the exercise capacity assessed by a six-minute walking test (6MWT). RESULTS: The 55 COPD patients were separated into a synchronized group (median 0.89 (0.64-0.97), n = 43) and a desynchronized group (median 0.23 (0.02-0.51), n = 12) based on K-means clustering analysis. Synchrogram index was correlated significantly with six minutes walking distance (r = 0.42, p = 0.001) and distance saturation product (r = 0.41, p = 0.001) assessed by 6MWT, and still was an independent variable by multivariable regression analysis. CONCLUSION: This is the first result studying the heart-lung interaction in terms of cardiorespiratory coupling in COPD patients by the synchrogram index, and COPD patients are clustered into synchronized and desynchronized groups. Cardiorespiratory coupling is associated with exercise capacity in patients with COPD.

Arterial Pulse Pressure Variation with Mechanical Ventilation.

Fluid administration leads to a significant increase in cardiac output in only half of ICU patients. This has led to the concept of assessing fluid responsiveness before infusing fluid. Pulse pressure variation (PPV), which quantifies the changes in arterial pulse pressure during mechanical ventilation, is one of the dynamic variables that can predict fluid responsiveness. The underlying hypothesis is that large respiratory changes in left ventricular stroke volume, and thus pulse pressure, occur in cases of biventricular preload responsiveness. Several studies showed that PPV accurately predicts fluid responsiveness when patients are under controlled mechanical ventilation. Nevertheless, in many conditions encountered in the ICU, the interpretation of PPV is unreliable (spontaneous breathing, cardiac arrhythmias) or doubtful (low Vt). To overcome some of these limitations, researchers have proposed using simple tests such as the Vt challenge to evaluate the dynamic response of PPV. The applicability of PPV is higher in the operating room setting, where fluid strategies made on the basis of PPV improve postoperative outcomes. In medical critically ill patients, although no randomized controlled trial has compared PPV-based fluid management with standard care, the Surviving Sepsis Campaign guidelines recommend using fluid responsiveness indices, including PPV, whenever applicable. In conclusion, PPV is useful for managing fluid therapy under specific conditions where it is reliable. The kinetics of PPV during diagnostic or therapeutic tests is also helpful for fluid management.

Evaluation of fluid responsiveness during COVID-19 pandemic: what are the remaining choices?

Non-protocolized fluid administration in critically ill patients, especially those with acute respiratory distress syndrome (ARDS), is associated with poor outcomes. Therefore, fluid administration in patients with Coronavirus disease (COVID-19) should be properly guided. Choice of an index to guide fluid management during a pandemic with mass patient admissions carries an additional challenge due to the relatively limited resources. An ideal test for assessment of fluid responsiveness during this pandemic should be accurate in ARDS patients, economic, easy to interpret by junior staff, valid in patients in the prone position and performed with minimal contact with the patient to avoid spread of infection. Patients with COVID-19 ARDS are divided into two phenotypes (L phenotype and H phenotype) according to their lung compliance. Selection of the proper index for fluid responsiveness varies according to the patient phenotype. Heart-lung interaction methods can be used only in patients with L phenotype ARDS. Real-time measures, such a pulse pressure variation, are more appropriate for use during this pandemic compared to ultrasound-derived measures, because contamination of the ultrasound machine can spread infection. Preload challenge tests are suitable for use in all COVID-19 patients. Passive leg raising test is relatively better than mini-fluid challenge test, because it can be repeated without overloading the patient with fluids. Trendelenburg maneuver is a suitable alternative to the passive leg raising test in patients with prone position. If a cardiac output monitor was not available, the response to the passive leg raising test could be traced by measurement of the pulse pressure or the perfusion index. Preload modifying maneuvers, such as tidal volume challenge, can also be used in COVID-19 patients, especially if the patient was in the gray zone of other dynamic tests. However, the preload modifying maneuvers were not extensively evaluated outside the operating room. Selection of the proper test would vary according to the level of healthcare in the country and the load of admissions which might be overwhelming. Evaluation of the volume status should be comprehensive; therefore, the presence of signs of volume overload such as lower limb edema, lung edema, and severe hypoxemia should be considered beside the usual indices for fluid responsiveness.

Hemodynamic effects of incremental lung hyperinflation.

Dynamic hyperinflation (DH) is common in chronic obstructive pulmonary disease and is associated with dyspnea and exercise intolerance. DH also has adverse cardiac effects, although the magnitude of DH and the mechanisms responsible for the hemodynamic impairment remain unclear. We hypothesized that incrementally increasing DH would systematically reduce left ventricular (LV) end-diastolic volume (LVEDV) and LV stroke volume (LVSV) because of direct ventricular interaction. Twenty-three healthy subjects (22 ± 2 yr) were exposed to varying degrees of expiratory loading to induce DH such that inspiratory capacity was decreased by 25%, 50%, 75%, and 100% (100% DH = inspiratory capacity of resting tidal volume plus inspiratory reserve volume ≈ 0.5 l). LV volumes, LV geometry, inferior vena cava collapsibility, and LV end-systolic wall stress were assessed by triplane echocardiography. 25% DH reduced LVEDV (-6 ± 5%) and LVSV (-9 ± 8%). 50% DH elicited a similar response in LVEDV (-6 ± 7%) and LVSV (-11 ± 10%) and was associated with significant septal flattening [31 ± 32% increase in the radius of septal curvature at end diastole (RSC-ED)]. 75% DH caused a larger reduction in LVEDV and LVSV (-9 ± 7% and -16 ± 10%, respectively) and RSC-ED (49 ± 70%). 100% DH caused the largest reduction in LVEDV and LVSV (-13 ± 9% and -18 ± 9%) and an increase in RSC-ED (56 ± 63%). Inferior vena cava collapsibility and LV afterload (LV end-systolic wall stress) were unchanged at all levels of DH. Modest DH (-0.6 ± 0.2 l inspiratory reserve volume) reduced LVSV because of reduced LVEDV, likely because of increased pulmonary vascular resistance. At higher levels of DH, direct ventricular interaction may be the primary cause of attenuated LVSV, as indicated by septal flattening because of a greater relative increase in right ventricular pressure and/or mediastinal constraint. NEW & NOTEWORTHY By systematically reducing inspiratory capacity during spontaneous breathing, we demonstrate that dynamic hyperinflation (DH) progressively reduces left ventricular (LV) end diastolic volume and LV stroke volume. Evidence of significant septal flattening suggests that direct ventricular interaction may be primarily responsible for the reduced LV stroke volume during DH. Hemodynamic impairment appears to occur at relatively lower levels of DH and may have important clinical implications for patients with chronic obstructive pulmonary disease.

Cardiopulmonary physiology: why the heart and lungs are inextricably linked.

Because the heart and lungs are confined within the thoracic cavity, understanding their interactions is integral for studying each system. Such interactions include changes in external constraint to the heart, blood volume redistribution (venous return), direct ventricular interaction (DVI), and left ventricular (LV) afterload. During mechanical ventilation, these interactions can be amplified and result in reduced cardiac output. For example, increased intrathoracic pressure associated with mechanical ventilation can increase external constraint and limit ventricular diastolic filling and, therefore, output. Similarly, high intrathoracic pressures can alter blood volume distribution and limit diastolic filling of both ventricles while concomitantly increasing pulmonary vascular resistance, leading to increased DVI, which may further limit LV filling. While LV afterload is generally considered to decrease with increased intrathoracic pressure, the question arises if the reduced LV afterload is primarily a consequence of a reduced LV preload. A thorough understanding of the interaction between the heart and lungs can be complicated but is essential for clinicians and health science students alike. In this teaching review, we have attempted to highlight the present understanding of certain salient aspects of cardiopulmonary physiology and pathophysiology, as well as provide a resource for multidisciplined health science educators and students.

Dynamic Variables Fail to Predict Fluid Responsiveness in an Animal Model With Pericardial Effusion.

OBJECTIVES: The reliability of dynamic and volumetric variables of fluid responsiveness in the presence of pericardial effusion is still elusive. The aim of the present study was to investigate their predictive power in a porcine model with hemodynamic relevant pericardial effusion. DESIGN: A single-center animal investigation. PARTICIPANTS: Twelve German domestic pigs. INTERVENTIONS: Pigs were studied before and during pericardial effusion. Instrumentation included a pulmonary artery catheter and a transpulmonary thermodilution catheter in the femoral artery. Hemodynamic variables like cardiac output (COPAC) and stroke volume (SVPAC) derived from pulmonary artery catheter, global end-diastolic volume (GEDV), stroke volume variation (SVV), and pulse-pressure variation (PPV) were obtained. MEASUREMENTS AND MAIN RESULTS: At baseline, SVV, PPV, GEDV, COPAC, and SVPAC reliably predicted fluid responsiveness (area under the curve 0.81 [p = 0.02], 0.82 [p = 0.02], 0.74 [p = 0.07], 0.74 [p = 0.07], 0.82 [p = 0.02]). After establishment of pericardial effusion the predictive power of dynamic variables was impaired and only COPAC and SVPAC and GEDV allowed significant prediction of fluid responsiveness (area under the curve 0.77 [p = 0.04], 0.76 [p = 0.05], 0.83 [p = 0.01]) with clinically relevant changes in threshold values. CONCLUSIONS: In this porcine model, hemodynamic relevant pericardial effusion abolished the ability of dynamic variables to predict fluid responsiveness. COPAC, SVPAC, and GEDV enabled prediction, but their threshold values were significantly changed.

Can we predict poor hemodynamic tolerance of intermittent hemodialysis with echocardiography in intensive care patients?

OBJECTIVES: Tolerance of intermittent hemodialysis is potentially poor for patients hospitalized in the intensive care unit, particularly those in shock. The aim of this study was to determine whether an evaluation of the hemodynamic state by echocardiography before an intermittent hemodialysis session could predict tolerance during the session. METHODS: Before an intermittent hemodialysis session, transesophageal echocardiography was performed on sedated patients, and transthoracic echocardiography was performed on nonsedated patients. Poor tolerance during intermittent hemodialysis was defined by the following criteria: greater than 20% decrease in mean arterial pressure, need for fluid loading (≥500 mL), a 15% increase in catecholamine if the dose was stable before the session or doubling the speed of catecholamine infusion if necessary, arrhythmia, and the necessity to stop the session before its prescribed end. RESULTS: A total of 54 patients were included: 20 (37%) were intubated under controlled mechanical ventilation (group 1) and underwent transesophageal echocardiography; 14 (26%) were intubated under pressure support ventilation (group 2) and underwent transthoracic echocardiography; and 20 (37%) had no ventilation support (group 3). Twenty-four patients (46%) had poor tolerance criteria. A comparison of groups showed no significant difference in tolerance. Similarly, there was no difference with and without ultrafiltration. Increased respiratory variation of the vena cava was not predictive of poor tolerance in groups 1 and 2. In group 3, there was greater variation in patients with poor tolerance. In patients receiving mechanical ventilation, greater respiratory variability of the maximum velocity measured in the pulmonary artery was predictive of poor tolerance. CONCLUSIONS: The hemodynamic profile of patients receiving mechanical ventilation was unable to predict tolerance of an intermittent hemodialysis session. In patients without mechanical ventilation, hypovolemia before the session appeared to be predictive of poor tolerance.

Glossopharyngeal insufflation and breath-hold diving: the more, the worse?

OBJECTIVE: The glossopharyngeal insufflation maneuver (lung packing) is largely performed by competitive breath-hold divers to improve their performance, despite observational evidence of fainting and loss of consciousness in the first seconds of apnea. METHODS: We describe here the time course of hemodynamic changes, induced by breath-holding with and without lung packing, in 2 world-class apnea competitors. RESULTS: When compared with apnea performed after a deep breath (100% vital capacity), lung packing leads to a decrease in cardiac output, blood pressure, and cerebral blood flow during the first seconds after the beginning of apnea. The major hemodynamic disorders were observed in diver 1, who exhibited the greater increase in pulmonary volume after lung packing (+22% for diver 1 vs +10% for diver 2). After the initial drop in both cardiac output and blood pressure, the time course of hemodynamic alterations became quite similar between the two apneas. CONCLUSIONS: Some recommendations, such as limiting the number of maneuvers and performing lung packing in the supine position, should be expressed to avoid injuries secondary to the use of glossopharyngeal insufflation.

Comparison of an automated respiratory systolic variation test with dynamic preload indicators to predict fluid responsiveness after major surgery.

BACKGROUND: Predicting the response of cardiac output to volume administration remains an ongoing clinical challenge. The objective of our study was to compare the ability to predict volume responsiveness of various functional measures of cardiac preload. These included pulse pressure variation (PPV), stroke volume variation (SVV), and the recently launched automated respiratory systolic variation test (RSVT) in patients after major surgery. METHODS: In this prospective study, 24 mechanically ventilated patients after major surgery were enrolled. Three consecutive volume loading steps consisting of 300 ml 6% hydroxyethylstarch 130/0.4 were performed and cardiac index (CI) was assessed by transpulmonary thermodilution. Volume responsiveness was considered as positive if CI increased by >10%. RESULTS: In total 72 volume loading steps were analysed, of which 41 showed a positive volume response. Receiver operating characteristic (ROC) curve analysis revealed an area under the curve (AUC) of 0.70 for PPV, 0.72 for SVV and 0.77 for RSVT. Areas under the curves of all variables did not differ significantly from each other (P>0.05). Suggested cut-off values were 9.9% for SVV, 10.1% for PPV, and 19.7° for RSVT as calculated by the Youden Index. CONCLUSION: In predicting fluid responsiveness the new automated RSVT appears to be as accurate as established dynamic indicators of preload PPV and SVV in patients after major surgery. The automated RSVT is clinically easy to use and may be useful in guiding fluid therapy in ventilated patients.

Understanding cardiopulmonary interactions through esophageal pressure monitoring.

Esophageal pressure is the closest estimate of pleural pressure. Changes in esophageal pressure reflect changes in intrathoracic pressure and affect transpulmonary pressure, both of which have multiple effects on right and left ventricular performance. During passive breathing, increasing esophageal pressure is associated with lower venous return and higher right ventricular afterload and lower left ventricular afterload and oxygen consumption. In spontaneously breathing patients, negative pleural pressure swings increase venous return, while right heart afterload increases as in passive conditions; for the left ventricle, end-diastolic pressure is increased potentially favoring lung edema. Esophageal pressure monitoring represents a simple bedside method to estimate changes in pleural pressure and can advance our understanding of the cardiovascular performance of critically ill patients undergoing passive or assisted ventilation and guide physiologically personalized treatments.

Cardio-respiratory interactions in acute asthma.

Asthma encompasses of respiratory symptoms that occur intermittently and with varying intensity accompanied by reversible expiratory airflow limitation. In acute exacerbations, it can be life-threatening due to its impact on ventilatory mechanics. Moreover, asthma has significant effects on the cardiovascular system, primarily through heart-lung interaction-based mechanisms. Dynamic hyperinflation and increased work of breathing caused by a sharp drop in pleural pressure, can affect cardiac function and cardiac output through different mechanisms. These mechanisms include an abrupt increase in venous return, elevated right ventricular afterload and interdependence between the left and right ventricle. Additionally, Pulsus paradoxus, which reflects the maximum consequences of this heart lung interaction when intrathoracic pressure swings are exaggerated, may serve as a convenient bedside tool to assess the severity of acute asthma acute exacerbation and its response to therapy.

Mechanical Ventilation: Negative to Positive and Back Again.

Critical care and mechanical ventilation have a relatively brief history in medicine. Premises existed through the seventeenth to nineteenth centuries but modern mechanical ventilation started in the twentieth century. Noninvasive ventilation techniques had started both in the intensive care unit and for home ventilation at the end of the 1980s and the 1990s. The need for mechanical ventilation is increasingly influenced worldwide by the spread of respiratory viruses, and the last coronavirus disease 2019 pandemic has seen a massive successful use of noninvasive ventilation.

Ventilation Induces Changes in Pulse Wave Transit Time in the Pulmonary Artery.

Pulse wave transit time (PWTT) shortens as pulmonary artery pressure (PAP) increases and was therefore suggested as a surrogate parameter for PAP. The aim of this analysis was to reveal patterns and potential mechanisms of ventilation-induced periodic changes in PWTT under resting conditions. To measure both PWTT and PAP in five healthy pigs, two pulmonary artery Mikro-Tip™ catheters were inserted into the pulmonary vasculature: one with the tip placed in the pulmonary artery trunk, and a second one placed in a distal segment of the pulmonary artery. Animals received pressure-controlled mechanical ventilation. Ventilation-dependent changes were seen in both variables, PWTT and mean PAP; however, changes in PWTT were not synchronous with changes in PAP. Thus, plotting the value of PWTT for each heartbeat over the respective PAP revealed a characteristic hysteresis. At the beginning of inspiration, PAP rose while PWTT remained constant. During further inspiration, PWTT started to decrease rapidly as mPAP was about to reach its plateau. The same time course was observed during expiration: while mPAP approached its minimum, PWTT increased rapidly. During apnea this hysteresis disappeared. Thus, non-synchronous ventilation-induced changes in PWTT and PAP were found with inspiration causing a significant shortening of PWTT. Therefore, it is suggested that the respiratory cycle should be considered when using PWTT as a surrogate for PAP.

Dynamic changes of pulse pressure but not of pulse pressure variation during passive leg raising predict preload responsiveness in critically ill patients with spontaneous breathing activity.

PURPOSE: To evaluate whether the changes in arterial pulse pressure (PP) and/or pulse pressure variation (PPV) during passive leg raising (PLR) can be used to evaluate preload responsiveness in patients with spontaneous breathing activity. MATERIALS AND METHODS: Patients ventilated with pressure support mode or totally spontaneously breathing were prospectively included. The values of PP and PPV were recorded before and at the end of PLR. The changes in cardiac index (CI) or the velocity-time integral (VTI) of the left ventricular outflow tract during PLR were tracked by the pulse contour analysis or transthoracic echocardiography. Patients exhibiting an increase in CI ≥ 10% or VTI ≥ 12% during PLR were defined as preload responders. RESULTS: Among 33 patients included, 28 (80%) received norepinephrine and 14 were preload responders. The increase in PP > 2 mmHg in absolute value (4% in percentage) during PLR (PLRPP) predicted preload responsiveness with an area under the receiver operating characteristic (AUROC) of 0.76 ± 0.09 (p = 0.003 vs. AUROC of 0.5). The changes in PPV during PLR, however, failed to predict preload responsiveness (p = 0.82 vs. AUROC of 0.5). CONCLUSION: In patients with full spontaneous breathing activity, PLR-induced changes in PP had a fair ability to assess preload responsiveness even when norepinephrine was administered. REGISTRATION NUMBER: ClinicalTrials.gov (NCT04369027).

Disruption of cardio-pulmonary coupling in myopathies: Pathophysiological and mechanistic characterization with special emphasis on nemaline myopathy.

The heart and lung are in continuous reciprocal interaction that creates a functional and anatomical reserve referred to as cardiopulmonary coupling (CPC). Disruption of CPC can occur due to various cardiac or pulmonary pathologies but also can occur in patients with myopathies. Nemaline myopathy (NM) is a skeletal muscle heterogeneous disorder due to contractile proteins' gene mutations that impact lung and cardiac mechanics and thus is expected to adversely affect CPC in a complex manner. We present a case of NM and we review the literature on cardiac and pulmonary effects of myopathy-related disruption of CPC.