Abstract
The process of weaning from mechanical ventilation imposes an additional workload on the cardiovascular system, which may result in impaired myocardial function, increase in left ventricular filling pressure and respiratory distress. These mechanisms may ultimately result in weaning failure and need for prolonged respiratory support, which in turn increases the length of stay in the intensive care unit and the risk of complications. Among surgical patients, those undergoing heart surgery are particularly susceptible to cardiac dysfunction induced by weaning because of inadequate cardiovascular reserve. Early identification of patients at risk has potential therapeutic implications. The aim of this study was to depict the pathophysiological changes in hemodynamics assessed by echocardiography during the steps of weaning and to identify possible predictors of weaning failure. We enrolled 34 consecutive patients undergoing isolated coronary artery bypass grafting in our institution; data were collected by intraoperative transesophageal echocardiography before sternotomy (T0), and by transthoracic echocardiography at the beginning of weaning (T1) and at the time of extubation (T2). Weaning failure was defined as deferral of planned extubation or respiratory failure needing reintubation or non-invasive mechanical ventilation within 48 hours. Left ventricular outflow tract velocity–time index (LVOT-VTI) and ventricular-arterial coupling (VAC) measured at the beginning of the weaning process showed a significant correlation with outcome, with LVOT-VTI emerging as the best predictor of weaning failure. Significant increase in E/e’ suggested a cardiogenic etiology of respiratory distress in patients who failed the weaning trial. Overall, our study showed that serial assessment of hemodynamic parameters by means of echocardiography is feasible in cardiac surgical patients and can provide insight into pathophysiological changes during weaning. Although these preliminary data need to be confirmed in a larger population sample, LVOT-VTI emerged as a promising predictor of subsequent weaning failure.
Introduction
Cardiopulmonary interaction during weaning
The transition from mechanical ventilation to spontaneous breathing implies a shift from a positive intrathoracic pressure to a negative pleural pressure generated by the respiratory muscles: these changes impose an additional load on the cardiovascular system by affecting ventricular preload and afterload and increasing oxygen consumption. Negative intrathoracic pressure increases the systemic venous return to the right ventricle (RV) and RV preload: this, in turn, determines an increase in RV ejection, central blood volume and left ventricular (LV) preload. The negative intrathoracic pressure also increases the LV transmural pressure, resulting in an increase in LV afterload; the latter also rises in response to the increased adrenergic tone and work of breathing1-3. Furthermore, the occurrence of hypoxia and hypercapnia causes a rise in pulmonary vascular resistance, with consequent RV dilation and impairment of LV filling because of ventricular interdependence. The combination of these mechanisms can have detrimental consequences in patients with pre-existing cardiovascular disease by increasing left ventricular end-diastolic pressure (LVEDP) and eventually inducing pulmonary edema4 (Figure 1). Moreover, weaning from MV entails an increase in oxygen consumption from both the myocardium and the respiratory muscles5, potentially inducing myocardial ischemia6, 7. For these reasons, withdrawal of mechanical ventilation acts as a cardiac stress test and can unmask cardiac dysfunction in predisposed subjects8. Acute LV dysfunction during weaning was first described by Lemaire et al. in 19889, while the definition of “weaning induced cardiac dysfunction” was introduced in 200210
; the detection of weaning induced cardiac dysfunction grew in the following years and it is now recognized as one of the main causes of weaning failure.
Role of diastolic dysfunction and echocardiography
Recent findings highlight the role of LV diastolic dysfunction with preserved contractility as a mediator of weaning failure11-14. Traditionally, weaning-induced cardiac failure was suspected following a significant increase in pulmonary capillary wedge pressure (PCWP) detected by a pulmonary artery catheter, but nowadays less invasive diagnostic methods are preferred. Estimation of LV filling pressure (LVFP) with echocardiography has been extensively performed in the last 20 years and involves the assessment of a variety of indices of diastolic function15, 16.
Doppler echocardiography and tissue Doppler imaging (TDI) are increasingly employed in the intensive care unit (ICU) as a tool to detect weaning induced cardiac dysfunction17, 18, allowing
noninvasive assessment of myocardial contractility and relaxation, cardiac output and LVFP. A number of studies found higher LVFP, estimated by E/e’, in difficult to wean patients17, 19, 20. In some studies, transthoracic echocardiography provided early detection of LV diastolic dysfunction and predicted subsequent failure of the spontaneous breathing trials13, 14. Other sonographic techniques, such as lung and diaphragmatic ultrasound, can be combined with echocardiography for a systematic assessment of the mechanisms underlying weaning failure3, 21-24.
Weaning the cardiac surgical patient
Even if surgical patients show a lower incidence of weaning failure compared to patients exposed to long-standing ventilation, prolonged MV is a relatively common postoperative complication in cardiac surgical patients and is associated with increased length of stay in the ICU, higher resource utilization and poor outcome25-29. Pre-existing coronary artery disease has long been recognized as a risk factor for difficult weaning30, 31; additionally, patients referred for coronary artery bypass grafting (CABG) display a high incidence of comorbidities linked to prolonged ventilation, such as reduced LV ejection fraction (LVEF), diabetes mellitus, and chronic kidney disease (CKD)32. Timely extubation following intervention is associated with improved patient comfort, cardiac function, better cardiac function and reduced respiratory complications33.
A growing interest for the prognostic role of diastolic dysfunction in surgical patients appears in the recent literature. A meta-analysis by Fayad et al. indicated perioperative diastolic dysfunction as an independent risk factor for adverse cardiovascular outcomes after non-cardiac surgery34; Zhou et al. found an association between pre-existing grade III diastolic dysfunction and the occurrence of major adverse cardiac events (MACE) after surgery35. Salem et al. reported a predictive role of LVEDP measured by right heart catheterization for mortality in patients undergoing cardiac surgery36. However, the relationship between baseline diastolic dysfunction and difficult weaning has not been specifically investigated in patients undergoing cardiac surgery. Moreover, the pathophysiology of weaning failure in this patient population is largely unknown.
Therapeutic options
Positive fluid balance and extracellular lung water have been related to weaning failure. Given the fundamental role of fluid overload, fluid removal by diuretic administration appears as a reasonable approach. Cardiac preload status can be assessed by passive leg raising (PLR) to guide fluid removal until restoration of preload dependence37. B-type natriuretic peptide (BNP) and N-terminal (NT) proBNP have been used as biomarkers of cardiovascular dysfunction and fluid overload: due
to its shorter half-life of about 20 minutes, BNP appears an interesting dynamic marker in the context of weaning38. A strategy of BNP-guided fluid management has also proved beneficial39. Nitroglycerine, as a preload- and afterload-reducing drug and coronary vasodilator, has been investigated in difficult to wean patients with hypertension showing a favorable hemodynamic effect40.
Phosphodiesterase-3 inhibitors such as enoximone show systemic and pulmonary vasodilating properties: two studies investigated the effect of enoximone in cardiac surgical patients, demonstrating a possible role in preventing weaning induced cardiac dysfunction41, 42.
Levosimendan appears as a particularly promising drug since its positive inotropic effect is independent of myocardial oxygen demand. Furthermore, in vitro43 and in vivo evidence showed levosimendan exerted a positive lusitropic effect by reducing LVFP and pulmonary vascular resistance. Levosimendan also appears to enhance diaphragmatic contractility44. A pilot study is currently investigating the role of levosimendan in weaning patients with LV dysfunction45.
Methods
In this prospective observational study, we enrolled 34 consecutive patients (mean age 73 ± 8,8 years, 88% males) undergoing isolated CABG in our institution over a period of 20 weeks (from 1st of June to 15th of October 2019). Exclusion criteria were out-of-hospital cardiac arrest as clinical presentation, coexistence of significant valvular disease, and contraindication to TEE.
Demographic characteristics and clinical data relevant for risk stratification were collected from the medical history (Table 1).
Intraoperative TEE was performed in all patients; echocardiographic and Doppler findings, listed in Table 2, were recorded during general anesthesia and invasive mechanical ventilation (IMV) before sternotomy (T0), in order to assess cardiac function under standardized loading conditions. Evaluation of diastolic function was conducted with a stepwise approach as indicated by current guidelines46, and included mitral inflow velocities (Figure 2a), TDI (Figure 2b) and pulmonary venous flow (Figure 2c). Ventricular-arterial coupling (VAC) was calculated as the ratio between arterial elastance (Ea) and ventricular elastance (Ees), where non-invasive measurement of Ees was obtained according to Chen’s method47
using a specifically designed calculator (iElastance© - Apple iOSApp) and Ea was calculated as systolic blood pressure (SBP) × 0.9/stroke volume (SV). Measurements used for Ees calculation were SBP, diastolic blood pressure (DBP), SV, LVEF, total ejection time (TET) and pre-ejection time (PET) (Figure 2d).
Relevant procedural data such as cardiopulmonary bypass (CPB) time, number of vessels treated and postoperative drugs are detailed in Table 3.
Weaning was performed according to the ICU protocol by switching the ventilation mode from synchronized intermittent mandatory ventilation (SIMV) to assisted spontaneous breathing (ASB) with progressive de-escalation of pressure support. The attending intensivist evaluated readiness for extubation considering clinical data (body temperature, absence of active bleeding, neurological status, respiratory rate and tidal volume) and arterial blood gas analysis. A TTE was performed at the beginning of weaning (T1) and at the time of extubation (T2).
Weaning failure was defined as a composite endpoint including deferral of planned extubation, re-intubation within the next 48 hours or respiratory failure needing non-invasive mechanical ventilation (NIMV). Serum high sensitivity cardiac troponin (HSTn) and BNP levels were measured after completion of weaning to detect cardiac ischemia and pulmonary congestion.
Duration of weaning attempts, total duration of postoperative IMV and ICU length of stay were recorded (Table 4).
Statistical analysis was performed using NCSS Software, LLC. Normality test was performed using the Shapiro-Wilk W test. Continuous variables are presented as mean ± SD in case of normal distribution, otherwise as median and interquartile range. Categorical variables are reported as absolute number and percentage. Differences between groups were performed using a two-sample t-test for variables with normal distribution and the Mann-Whitney U t-test in case of non-normal distribution, while the chi-square test was employed for categorical variables. Changes of variables between T0, T1 and T2 were evaluated using one-way ANOVA. Logistic regression was applied to verify correlation between continuous variables and outcome. All results were considered significant when P < 0,05.
Results
Comparison of measures between the preoperative setting (T0) and the start of weaning process (T1), described in Table 5, showed a significant change in hemodynamic parameters such as HR (56,68 vs 80,19, P < 0,0001), SBP (112,79 vs 124,16, P 0,041) and DBP (57,03 vs 63,32, P 0,027). While LVEF and S velocity did not change significantly, there was a significant variation of LVOT-VTI (18,04 vs 15,79, P 0,017), Ea (1,83 vs 2,21, P 0,032) and VAC (1,14 vs 1,47, P 0,022), demonstrating changes in LV performance and its relationship with systemic afterload. Variation of E/A ratio (1,08
vs 0,81, P 0,002) and IVRT (138,15 vs 103,65, P < 0,0001) showed a change in diastolic function. The significant reduction in TAPSE (16,28 vs 11,87, P < 0,0001) can be attributed to post-CBP RV dysfunction. There was no significant difference between echocardiographic parameters measured at T1 and T2.
Among 34 patients, 7 (20,6%) met the criteria for weaning failure: in 2 cases (5,9%) failure was due to inadequate neurological status, whereas in 5 cases (14,7%) was caused by respiratory distress. Among the latter group, 4 patients needed delayed extubation, while one was initially extubated but developed respiratory failure that required treatment with NIMV. One patient underwent tracheostomy due to slow neurological recovery and need for prolonged IMV.
Patients were allocated into groups based on the occurrence of failure of the first weaning trial (FAILURE vs SUCCESS) and on the evidence of respiratory distress as a cause of weaning failure (RESPIRATORY vs OTHER).
As expected, both weaning duration (206,5 vs 54,26 minutes, P 0,00175) and postoperative length of stay (2 vs 4 days, P 0,01) in the ICU were significantly longer in case of weaning failure, whereas the difference in IMV duration did not reach statistical significance (5,98 vs 4,5, P 0,176). Weaning duration (180 vs 47 minutes, P 0,009) was also significantly longer in patients with respiratory failure compared to other patients, while there was no significant difference in total IMV duration (4,82 vs 4,5 hours, P 0,51) and ICU length of stay (2 vs 3 days, P 0,22) (Table 6).
Comparison of demographic, clinical and procedural characteristics between groups is reported in Table 7. There was a statistically significant association between CKD and weaning failure of any origin.
Evaluation of baseline echocardiographic parameters at T0 showed a significant difference in VAC (1,40 vs 1,08, P 0,04; Figure 3) and a borderline significant difference in TAPSE (14,43 vs 16,76, P 0,06; Figure 4) between patients with or without weaning failure; however, no parameter related to outcome when only respiratory failure was considered (Table 8). No significant difference in terms of weaning outcome emerged when patients were stratified into groups according to diastolic dysfunction grade.
Measures obtained at the beginning of the weaning process (T1) are presented in Table 9. Patients with subsequent weaning failure showed a significantly lower LVOT VTI (12,45 vs 16,63, P 0,003; Figure 5) and a significant difference in VAC (2,08 vs 1,31, P 0,006; Figure 6). Similar results emerged when only failure of respiratory origin was considered (11,60 vs 16,43, P 0,003 for LVOT-VTI; 2,44 vs 1,32, P 0,0003 for VAC; see Figures 7 and 8).
Logistic regression showed LVOT-VTI measured at T1 was able to predict weaning failure of any origin (P 0,01734, R2 0,30996) and respiratory weaning failure (P 0,03817, R2 0,31957). After modeling ROC curves, a cutoff value of 15 cm provided the best accuracy for weaning failure of any origin, with a sensitivity of 100% and specificity of 71%; positive predictive value (PPV) and negative predictive value (NPV) were 46% and 100%, respectively. The Area Under Curve (AUC) was 0,8669 (Figure 9). For respiratory weaning failure, the best discriminatory performance was obtained with a cutoff value of 11,7 cm, which showed a 75% sensitivity and a 100% specificity with a 100% PPV and a 96% NPV; the corresponding AUC was 0,8978 (Figure 10).
VAC calculated at T1 showed a borderline significant correlation with outcome in logistic regression model when weaning failure of any origin was considered (P 0,0507, R2 0,21184) and a significant correlation with respiratory weaning failure (P 0,04482, R2 0,31779). However, we could not find an optimal threshold value due to ROC curve crossing the intercept line (Figures 11 and 12).
Echocardiographic measures assessed at the time of extubation (T2) are reported in Table 10. Patients with weaning failure of respiratory origin showed a significantly higher E/e’ ratio (13,44 vs 9,96, P 0,02; Figure 13), indicating an increase in LVFP. E/A ratio was significantly lower in patients with weaning failure, irrespective of the mechanism (1,27 vs 0,81, P 0,014 for weaning failure; 1,33 vs 0,81, P 0,02 for respiratory weaning failure. See Figures 14 and 15).
Laboratory findings
Measurements of serum HSTn and BNP before and after weaning did not show any significant difference between groups (Table 11). This finding could be due to the high prevalence of acute coronary syndromes (ACS) among patients, which probably conditioned the temporal trend of these markers acting as a confounding factor.
Discussion
Difficult weaning occurred in a significant proportion (20,6%) of CABG patients and was mainly due to respiratory manifestations (14,7%); comparison of this finding with other studies is hampered by heterogeneous definition of weaning failure or prolonged mechanical ventilation48-51. Delayed extubation conditioned a significant increase in the ICU length of stay, but the main contribution to prolonged ICU hospitalization came from inadequate neurological recovery, so the increase in length of stay was not significant when only patients with respiratory failure were considered. Even if weaning duration in known to be a main contributor to total IMV time52, we found only a numerical difference in IMV duration between groups: the absence of statistical significance could be due to the small population sample, but also to other variables influencing readiness for weaning, such as time required for normalization of body temperature or bleeding. The main finding of this analysis was the association between lower LVOT-VTI and delayed extubation. LVOT-VTI provides a measure of LV systolic function, which, unlike LVEF, does not rely on geometric assumption and can be assessed even in patients with poor acoustic window and insufficient visualization of the endocardium. While S velocity could overcome the technical difficulties of LVEF, it only describes the longitudinal component of LV contractility and thus provides an incomplete description of systolic function. In our population, reduced LVOT-VTI could identify an underlying impairment of systolic performance that resulted in increased filling pressure upon removal of ventilator support. LVOT-VTI demonstrated excellent accuracy in predicting weaning failure; however, these data need to be confirmed in larger populations.
The finding of higher E/A and E/e’ ratio at the time of extubation in patients with respiratory distress suggested a cardiac etiology was implied: a number of studies showed that, when systematically looked for, cardiovascular dysfunction represented a major cause of respiratory distress during weaning3, 13, 31, 53. Several studies reported increased E/e’ at the beginning of weaning process as a predictor of weaning failure12, 19, 20: in our population, however, the increase in LVFP was apparent after (T2) but not at the start (T1) of the weaning trial. This inconsistency could be due to the different weaning protocol, as the majority of studies used SBTs with a T-piece instead of transition to pressure-support ventilation: the former modality has been found to elicit a higher burden on respiratory and cardiocirculatory system54 and could therefore result in earlier manifestations of cardiovascular dysfunction.
The association between preexisting CKD and delayed extubation is consistent with the literature 55-58
. Nevertheless, while other variables such as gender, age and CBP duration were reported to be significant risk factors, our study did not replicate these findings.
Intraoperative TEE provides an opportunity for a thorough evaluation of cardiac structure and hemodynamics in patients undergoing cardiac surgery and allows evaluation of descriptors of diastole, such as flow pattern in the pulmonary veins, less feasible to assess by the transthoracic approach. Yet, this technique proved inadequate in identifying predictors of extubation outcome: this could be due to the small population sample but also to intrinsic limitations of measurements performed in this setting, such as poorer Doppler alignment compared to TTE. Notably, current algorithms for evaluation of diastolic function have been validated only for TTE.
A significant ventricular-arterial uncoupling, both at baseline evaluation and at the beginning of weaning, related with subsequent weaning failure. Uncoupling reflects a reduction in LV efficiency, which can result in energetic failure; higher VAC could identify a subset of patients at risk for weaning induced cardiac dysfunction and prolonged ventilation. Importantly, VAC was the only echocardiography-derived parameter that related to weaning failure when evaluated in the preoperative setting, thus could represent the earlier indicator of subsequent outcome. At the time of transition to spontaneous breathing, uncoupling could reflect the unfavorable balance between the LV performance and the increased afterload.
Taken together, these data suggest that disconnection from mechanical ventilation could unmask latent LV impairment, best identified by altered VAC and low LVOT-VTI, resulting in increased LVFP and clinical signs of respiratory distress; this in turn could lead to deferred extubation and need for prolonged ventilator support. Insight in the mechanism of weaning failure could also prompt the institution of appropriate measures, such as fluid removal or inotropic support.
What’s new
A variety of predictive models for prolonged MV after cardiac surgery have been proposed, but few included echocardiographic parameters other than left ventricular ejection fraction (LVEF). To our knowledge, this is the first study that serially assessed echocardiographic parameters during the steps of weaning after heart surgery. Whereas raised E/e’ in difficult-to-wean patients has been reported in other studies, its association with weaning failure has not been previously investigated in cardiac surgical patients. Furthermore, LVOT-VTI and VAC could discriminate patients with subsequent weaning failure, while LVEF did not display any significant association with outcome.
Conclusions
Our study showed that serial assessment of hemodynamic parameters by means of echocardiography is feasible in cardiac surgical patients and can provide insight into pathophysiological changes during weaning. LVOT-VTI emerged as a predictor of subsequent weaning failure when measured at the beginning of weaning process. Patients with respiratory weaning failure showed echocardiographic signs of increased LVFP, indicating a cardiogenic mechanism is implied. A timely identification of patients at risk of weaning failure could lead to institution of therapeutic measures and modification of the weaning strategy. Furthermore, understanding of the mechanism underlying weaning failure can guide the choice of therapeutic approach.
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Figure 1: pathophysiological changes induced by weaning from mechanical ventilation. ITP=intrathoracic pressure; LV=left ventricle; LVEDP=left ventricular end-diastolic pressure; PaCO2=carbon dioxide arterial pressure; PaO2=oxygen arterial pressure; WOB=work of breathing. From Routsi et al. Ann. Intensive Care (2019) 9:6
Figure 3 Figure 4
Figure 2a: transmitral diastolic flow Doppler recording. Figure 2b: tissue Doppler imaging at the lateral mitral annulus.
Figure 2c: pulmonary vein flow pattern. Figure 2d: left ventricular outflow tract velocity-time integral, pre-ejection time and total ejection time.
Figure 5 Figure 6
Figure 9 Figure 10
Table 1: Patient demographic and clinical characteristics Age (years) 73,41 ± 8,82 Male 30 (88%) BMI (kg/m2) 25,37 ± 3,24 BSA (m2) 1,84 ± 0,16 Hypertension 29 (85%) DM 14 (41%) CKD 7 (20%) History of AF 3 (9%) Previous MI 15 (44%) Previous PCI 12 (35%) Preoperative EF (%) 52,32 ± 8,97 Furosemide 10 (29%) Beta-blockers 20 (59%) ACE-inhibitors/ARBs 26 (77%) MRAs 1 (3%) HR (bpm) 56,68 ± 10,16 SBP (mmHg) 112,79 ± 22,91 DBP (mmHg) 57,03 ± 10,51
Table 1: ACE=angiotensin converting enzyme, AF=atrial fibrillation, ARBs=angiotensin receptor blockers, BMI=body mass index, BSA=body surface area, CKD=chronic kidney disease, DBP=diastolic blood pressure, DM=diabetes mellitus, EF=ejection fraction, HR=heart rate, MI=myocardial infarction, MRAs=mineralcorticoid receptor antagonists, PCI=percutaneous coronary intervention, SBP=systolic blood pressure.
Table 2: echocardiographic parameters at T0 EDV (ml) 93,14 ± 27,79 ESV (ml) 44,65 ± 21,84 LVIDd (mm) 46,70 ± 6,42 IVStd (mm) 10,96 ± 2,00 PWtd (mm) 9,04 ± 1,17 LVOT (mm) 20,56 ± 2,12 LVOT VTI (cm) 18,04 ± 4,02 E (cm/s) 57,49 ± 10,14 A (cm/s) 57,77 ± 14,91 DT (ms) 252,56 ± 72,35 IVRT (ms) 138,15 ± 27,40 Adur (ms) 171,24 ± 29,51 e'lat (cm/s) 6,98 ± 1,66 e'set (cm/s) 5,89 ± 1,30 S (cm/s) 8,67 ± 2,03 S polm (cm/s) 47,18 ± 21,40 D polm (cm/s) 35,83 ± 11,88 Arev (cm/s) 19,32 ± 6,45 Arev(dur) (ms) 112,41 ± 27,60 TAPSE (mm) 16,28 ± 2,94 TR gradient (mmHg) 18,78 ± 7,62 s' (cm/s) 9,45 ± 2,46 PET (ms) 83,03 ± 22,39 TET (ms) 387,88 ± 76,27
Table 2: DT=deceletarion time, EDV=end-diastolic diameter, ESV=end-systolic diameter, IVRT=isovolumic relaxation time, IVStd=interventricular septum diastolic thickness, LVIDd=left ventricular diastolic internal diameter, LVOT=left ventricular outflow tract, LVOT-VTI=left ventricular outflow tract velocity-time integral, PET=pre-ejection time, PWtd=posterior wall diastolic thickness, TAPSE=tricuspid annulus systolic excursion TET=total ejection time, TR=tricuspid regurgitation.
Table 3: procedural characteristics Emergency 25 (74%) OPCAB 6 (18%) N. of vessels 2 ± 1 CPB duration (minutes) 60,35 ± 34,19 Norepinephrine 20 (59%) Esmolol 1 (3%) Furosemide 24 (71%) Levosimendan 6 (18%) Enoximone 6 (18%)
Table 3: CPB=cardio-pulmonary bypass, OPCAB=off-pump coronary artery bypass.
Table 4
Weaning duration (minutes) 50 (34; 97)
IMV duration (hours) 4,5 (3,4; 9,7)
Postoperative ICU stay (days) 2 (2; 4)
Table 5: serial assessment of hemodynamic and echocardiographic variables T0 T1 T2 P (T0;T1) P (T1;T2) HR (bpm) 56,68 ± 11,16 80,19 ± 17,11 80,58 ± 16,75 < 0,0001* 0,93 SBP (mmHg) 112,79 ± 22,91 124,16 ± 20,71 130,19 ± 21,04 0,041* 0,26 DBP (mmHg) 57,03 ± 10,51 63,32 ± 11,84 63,10 ± 11,16 0,027* 0,94 EF (%) 53,70 ± 9,86 51,09 ± 7,38 51,66 ± 9,31 0,24 0,79 LVOT VTI (cm) 18,04 ± 4,02 15,79 ± 3,23 16,31 ± 4,11 0,017* 0,58 DT (ms) 252,56 ± 72,35 237,65 ± 84,55 207,27 ± 58,54 0,45 0,11 IVRT (ms) 138,15 ± 27,40 103,65 ± 26,04 101,1 ± 14,08 < 0,0001* 0,64 E/A 1,08 ± 0,41 0,81 ± 0,25 0,90 ± 0,37 0,002* 0,25 E/e’avg 9,36 ± 3,35 9,96 ± 3,07 10,42 ± 3,64 0,46 0,59 S (cm/s) 8,67 ± 2,03 8,31 ± 2,74 8,72 ± 1,76 0,54 0,49 TAPSE (mm) 16,28 ± 2,94 11,87 ± 3,24 13,26 ± 3,71 < 0,0001* 0,13 s' (cm/s) 9,45 ± 2,46 8,27 ± 2,83 9,09 ± 3,02 0,08 0,29 PAPs (mmHg) 27,57 ± 7,35 28,11 ± 6,70 0,78 Ees 1,76 ± 0,68 1,65 ± 0,56 1,59 ± 0,48 0,47 0,71 Ea 1,83 ± 0,71 2,21 ± 0,64 2,38 ± 0,73 0,032* 0,34 VAC 1,14 ± 0,46 1,47 ± 0,64 1,61 ± 0,73 0,022* 0,42
Table 5: DBP=diastolic blood pressure, DT=deceletarion time, Ea=arterial elastance, Ees=ventricular elastance, EDV=end-diastolic diameter, EF=ejection fraction, ESV=end-systolic diameter, HR=heart rate, IVRT=isovolumic relaxation time, LVOT-VTI=left ventricular outflow tract velocity-time integral, PAPs=pulmonary artery systolic pressure, SBP=systolic blood pressure, TAPSE=tricuspid annulus systolic excursion, TR=tricuspid regurgitation, VAC=ventricular-arterial coupling.
Table 6
FAILURE SUCCESS P RESPIRATORY OTHER P
Weaning (min) 206,5 (50; 1065) 54,26 (32; 65) 0,00175* 180 47 (36; 65) 0,009*
IMV (hrs) 5,98 (4; 24,33) 4,5 (3,33; 7,47) 0,176 4,82 4,5 (3,53; 8) 0,51
ICU stay (days) 4 (2; 31) 2 (2; 3) 0,01* 3 2 (2; 3) 0,22
Table 7: comparison of baseline characteristics between groups
FAILURE SUCCESS P RESPIRATORY OTHER P
Clinical characteristics Age (years) 74,29 ± 10,05 73,19 ± 8,67 0,77 71,4 ± 10,57 73,79 ± 8,65 0,59 Male 6 (85,71%) 24 (88,89%) 0,82 4 (80%) 26 (89,66%) 0,54 BMI (kg/m2) 24,52 ± 2,14 25,60 ± 3,46 0,44 24,79 ± 2,40 25,48 ± 3,39 0,67 BSA (m2) 1,79 ± 0,11 1,85 ± 0,16 0,36 1,78 ± 0,13 1,85 ± 0,16 0,35 Hypertension 7 (100%) 22 (81,48%) 0,23 5 (100%) 24 (82,76%) 0,32 DM 3 (42,86%) 11 (40,74%) 0,92 2 (40%) 12 (41,38%) 0,95 CKD 4 (57,14%) 3 (11,11%) 0,007* 2 (40%) 5 (17,24%) 0,25 History of AF 1 (14,29%) 2 (7,41%) 0,57 1 (20%) 2 (6,90%) 0,34 Previous MI 5 (71,43%) 10 (37,04%) 0,10 4 (80%) 11 (37,93%) 0,08 Previous PCI 4 (57,14%) 8 (29,63%) 0,18 3 (60%) 9 (31,04%) 0,21 Preop EF (%) 52,29 ± 9,66 52,33 ± 8,97 0,99 54 ± 11,18 52,04 ± 8,74 0,66 Preoperative drugs Furosemide 4 (57,14%) 6 (22,22%) 0,07 2 (40%) 8 (27,59%) 0,57 Beta-blockers 6 (85,71%) 14 (51,85%) 0,09 4 (80%) 16 (55,17%) 0,30 ACE-i/ARBs 5 (71,43%) 21 (77,78%) 0,72 3 (60%) 23 (79,31%) 0,35 MRAs 1 (14,29%) 0 (0%) 0,07 1 (20%) 0 (0%) 0,15 Procedural data HR (bpm) 60,86 ± 10,67 55,59 ± 9,94 0,23 60,8 ± 12,36 55,97 ± 9,81 0,33 SBP (mmHg) 127,14 ± 26,94 109,07 ± 20,71 0,06 127,6 ± 30,42 110,24 ± 20,98 0,12 DBP (mmHg) 59,43 ± 10,15 56,41 ± 10,70 0,51 59,4 ± 10,24 56,62 ± 10,54 0,59 Emergency 6 (85,71%) 19 (70,37%) 0,41 4 (80%) 21 (72,41%) 0,72 OPCAB 0 (0%) 6 (22,22%) 0,17 0 (0%) 6 (20,69%) 0,26 N, of vessels 2,43 ± 0,54 2,48 ± 0,85 0,88 2,4 ± 0,55 2,48 ± 0,83 0,83 CPB (min) 64 ± 19,95 59,41 ± 37,25 0,757 58,8 ± 11,84 60,62 ± 36,64 0,91
Postoperative drugs Norepinephrine 4 (57,14%) 16 (59,26%) 0,92 2 (40%) 18 (62,07%) 0,35 Esmolol 1 (14,29%) 0 (0%) 0,21 1 (20%) 0 (0%) 0,15 Furosemide 6 (85,71%) 18 (66,67%) 0,32 4 (80%) 20 (68,97%) 0,62 Levosimendan 2 (28,57%) 4 (14,82%) 0,40 1 (20%) 5 (17,24%) 0,88 Enoximone 2 (28,57%) 4 (14,82%) 0,40 1 (20%) 5 (17,24%) 0,88
Table 7: ACE=angiotensin converting enzyme, AF=atrial fibrillation, ARBs=angiotensin receptor blockers, BMI=body mass index, BSA=body surface area, CKD=chronic kidney disease, CPB=cardio-pulmonary bypass, DBP=diastolic blood pressure, DM=diabetes mellitus, DT=deceletarion time, EDV=end-diastolic diameter, EF=ejection fraction, ESV=end-systolic diameter, HR=heart rate, IVRT=isovolumic relaxation time, IVStd=interventricular septum diastolic thickness, LVIDd=left ventricular diastolic internal diameter, LVOT=left ventricular outflow tract, LVOT-VTI=left ventricular outflow tract velocity-time integral, MI=myocardial infarction, MRAs=mineralcorticoid receptor antagonists, OPCAB=off-pump coronary artery bypass, PCI=percutaneous coronary intervention, PET=pre-ejection time, PWtd=posterior wall diastolic thickness, SBP=systolic blood pressure, TAPSE=tricuspid annulus systolic excursion TET=total ejection time, TR=tricuspid regurgitation.
Table 8: comparison of echocardiographic measures at T0 between groups
T0 FAILURE SUCCESS P RESPIRATORY OTHER P
EDV (ml) 100,34 ± 30,27 91,27 ± 27,41 0,45 102,08 ± 36,89 91,6 ± 26,44 0,45 ESV (ml) 50,74 ± 25,56 43,07 ± 21,03 0,42 49,84 ± 31,24 43,76 ± 20,42 0,57 EF (%) 51,47 ± 9,76 54,27 ± 9,99 0,51 54,14 ± 10,54 53,62 ± 9,94 0,91 LVIDd (mm) 49 ± 6,53 45,98 ± 6,37 0,27 4,78 ± 0,71 4,64 ± 0,64 0,65 IVStd (mm) 10,29 ± 1,89 11,13 ± 1,03 0,33 10,8 ± 1,92 10,98 ± 2,05 0,85 PWtd (mm) 8,8 ± 1,27 9,1 ± 1,16 0,55 0,89 ± 0,11 0,91 ± 0,12 0,81 LVMI (g/m2) 94,71 ± 30,45 89,26 ± 28 0,65 95,89 ± 32,13 89,43 ± 27,90 0,64 RWT 0,36 ± 0,06 0,40 ± 0,06 0,15 0,38 0 ± 0,06 0,40 ± 0,06 0,56 LVOT (mm) 21,28 ± 2,43 20,37 ± 2,04 0,31 21,4 ± 2,61 20,41 ± 2,05 0,35 LVOT VTI (cm) 17,41 ± 2,79 18,21 ± 4,31 0,65 17,89 ± 3,20 18,08 ± 4,19 0,91 E (cm/s) 52,33 ± 9,80 58,82 ± 9,96 0,13 52,28 ± 11,34 58,39 ± 9,8 0,21 A (cm/s) 55,9 ± 12,35 58,25 ± 15,68 0,72 55,44 ± 14,94 58,17 ± 15,14 0,71 DT (ms) 253,57 ± 45,89 252,30 ± 78,47 0,97 267,6 ± 40,84 249,97 ± 76,70 0,62 IVRT (ms) 136,29 ± 31,90 138,63 ± 26,78 0,84 130,2 ± 11,80 139,52 ± 29,19 0,49
E/A 1,00 ± 0,43 1,10 ± 0,41 0,57 1,03 ± 0,52 1,09 ± 0,40 0,78 Adur (ms) 186,29 ± 42,90 167,33 ± 24,57 0,13 191,8 ± 50,22 167,69 ± 24,03 0,09 e'lat (cm/s) 6,65 ± 1,44 7,07 ± 1,72 0,56 7,09 ± 1,48 6,97 ± 1,71 0,88 e'set (cm/s) 5,45 ± 0,75 6,00 ± 1,40 0,36 5,52 ± 0,89 5,96 ± 1,36 0,49 e'avg (cm/s) 6,07 ± 1,00 6,53 ± 1,31 0,39 6,31 ± 1,09 6,46 ± 1,29 0,81 E/e’avg 8,79 ± 1,98 9,50 ± 3,64 0,62 8,48 ± 2,32 9,1 ± 3,1 0,54 S (cm/s) 9,07 ± 2,15 8,57 ± 2,03 0,57 8,76 ± 2,40 8,66 ± 2,01 0,92 S polm (cm/s) 55,19 ± 31,67 45,1 ± 18,11 0,27 46,02 ± 25,06 47,38 ± 21,20 0,90 D polm (cm/s) 42,06 ± 19,26 34,21 ± 8,96 0,12 37,9 ± 16,73 35,47 ± 11,19 0,68 S/D polm 1,26 ± 0,18 1,32 ± 0,43 0,74 1,18 ± 0,14 1,33 ± 0,41 0,42 Arev (cm/s) 18,46 ± 5,23 19,55 ± 6,81 0,70 18,76 ± 3,18 19,42 ± 6,90 0,83 Arev(dur) (ms) 103,29 ± 23,82 114,78 ± 28,42 0,33 108,6 ± 21,52 113,07 ± 28,79 0,74 TAPSE (mm) 14,43 ± 3,59 16,76 ± 2,62 0,06 14,7 ± 2,28 16,56 ± 2,99 0,20 TRg (mmHg) 17,83 ± 3,19 19 ± 8,35 0,74 17,25 ± 2,22 19 ± 8,11 0,68 s' (cm/s) 8,76 ± 0,85 9,63 ± 2,72 0,41 8,79 ± 1,03 9,57 ± 2,63 0,51 Ees 1,59 ± 0,83 1,81 ± 0,65 0,47 1,57 ± 0,88 1,80 ± 0,66 0,51 Ea 1,95 ± 0,66 1,80 ± 0,73 0,63 1,90 ± 0,70 1,82 ± 0,72 0,83 VAC 1,40 ± 0,50 1,08 ± 0,43 0,04* 1,41 ± 0,59 1,10 ± 0,43 0,09
Table 8: DT=deceletarion time, Ea=arterial elastance, EDV=end-diastolic diameter, Ees=ventricular elastance, EF=ejection fraction, ESV=end-systolic diameter, IVRT=isovolumic relaxation time, IVStd=interventricular septum diastolic thickness, LVIDd=left ventricular diastolic internal diameter, LVMI=left ventricular mass index, LVOT=left ventricular outflow tract, LVOT-VTI=left ventricular outflow tract velocity-time integral, PET=pre-ejection time, PWtd=posterior wall diastolic thickness, RWT=relative wall thickness, TAPSE=tricuspid annulus systolic excursion TET=total ejection time, TRg=tricuspid regurgitation gradient.
Table 9: comparison of echocardiographic measures at T1 between groups
T1 FAILURE SUCCESS P RESPIRATORY OTHER P
HR (bpm) 90,71 ± 22,71 77,13 ± 14,28 0,06 92 ± 27,62 77,92 ±14,00 0,09 SBP (mmHg) 121,29 ± 19,76 125 ± 21,31 0,68 119,6 ± 23,63 125,04 ± 20,50 0,60 DBP (mmHg) 57,14 ± 12,97 65,13 ± 11,14 0,12 60,6 ± 12,80 63,85 ± 11,85 0,58 EDV (ml) 108,17 ± 22,68 97,23 ± 22,57 0,30 106,5 ± 29,08 98,33 ± 21,99 0,51 ESV (ml) 53,33 ± 16,53 48,16 ± 17,00 0,51 54 ± 20,51 48,45 ± 16,46 0,55 EF (%) 51,15 ± 6,99 51,07 ± 7,62 0,98 51,25 ± 50,06 51,25 ± 7,56 0,77 LVOT VTI (cm) 12,45 ± 2,43 16,63 ± 2,86 0,003* 11,60 ± 2,84 16,43 ± 2,55 0,003* E (cm/s) 58,25 ± 13,30 61,12 ± 13,84 0,63 62,68 ± 13,21 60,05± 13,83 0,70 A (cm/s) 75,94 ± 15,46 78,52 ± 16,60 0,72 80,16 ± 14,99 77,51 ± 16,59 0,74 DT (ms) 234,57 ± 134,22 238,54 ± 67,98 0,91 176,6 ± 52,26 249,39 ± 85,16 0,08 IVRT (ms) 96,29 ± 23,85 105,79 ± 26,74 0,41 91 ± 26,65 106,08 ± 25,73 0,24 E/A 0,78 ± 0,16 0,81 ± 0,27 0,75 0,79 ± 0,16 0,81 ± 0,26 0,88 e'lat (cm/s) 6,92 ± 2,09 7,50 ± 2,47 0,60 7,60 ± 2,25 7,35 ± 2,44 0,85 e'set (cm/s) 6,21 ± 1,97 5,35 ± 1,57 0,26 6,40 ± 2,09 5,39 ± 1,56 0,26 e'avg (cm/s) 6,56 ± 1,64 6,42 ± 1,84 0,67 7,00 ± 1,65 6,37 ± 1,81 0,52 E/e’avg 9,22 ± 3,09 10,14 ± 3,10 0,52 9,54 ± 3,80 10,02 ± 3,03 0,78 S (cm/s) 7,18 ± 0,95 8,59 ± 2,97 0,26 7,08 ± 1,20 8,50 ± 2,87 0,34 TAPSE (mm) 11,17 ± 3,92 12,05 ± 3,11 0,56 11 ± 4,16 12 ± 3,15 0,57 TRg (mmHg) 18,5 ± 6,47 21,18 ± 7,70 0,44 16,5 ± 2,38 21,29 ± 7,78 0,23 s' (cm/s) 7,97 ± 3,73 8,35 ± 2,65 0,77 7,94 ± 4,74 8,32 ± 2,55 0,81 PAPs (mmHg) 26 ± 5,87 28 ± 7,77 0,56 22,75 ± 2,63 28,38 ± 7,60 0,16 Ees 1,56 ± 0,82 1,67 ± 0,50 0,68 1,35 ± 0,79 1,70 ± 0,52 0,26 Ea 2,51 ± 0,53 2,13 ± 0,65 0,20 2,59 ± 0,64 2,15 ± 0,63 0,19 VAC 2,08 ± 1,14 1,31 ± 0,30 0,006* 2,44 ± 1,21 1,32 ± 0,33 0,0003*
Table 9: DBP=diastolic blood pressure, DT=deceletarion time, Ea=arterial elastance, Ees=ventricular elastance, EDV=end-diastolic diameter, EF=ejection fraction, ESV=end-systolic diameter, HR=heart rate, IVRT=isovolumic relaxation time, LVOT-VTI=left ventricular outflow tract velocity-time integral, PAPs=pulmonary artery systolic
pressure, SBP=systolic blood pressure, TAPSE=tricuspid annulus systolic excursion, TRg=tricuspid regurgitation gradient, VAC=ventricular-arterial coupling.
Table 10: comparison of echocardiographic measures at T1 between groups
T2 FAILURE SUCCESS P RESPIRATORY OTHER P
HR (bpm) 87,67 ± 25,33 78,88 ± 14,19 0,26 91,4 ± 26,41 78,5 ± 14,04 0,12 SBP (mmHg) 117,83 ± 21,24 113,16 ± 20,30 0,11 119,4 ± 23,36 132,27 ± 20,40 0,22 DBP (mmHg) 54 ± 12,74 65,28 ± 9,81 0,02* 56,2 ± 12,91 64,42 ± 10,56 0,13 EDV (ml) 115,2 ± 20,86 101,56 ± 23,74 0,24 102,08 ± 36,89 114,7 ± 24,06 0,33 ESV (ml) 59,6 ± 21,97 49,45 ± 19,25 0,30 57,75 ± 24,92 50,13 ± 19,17 0,48 EF (%) 49,05 ± 11,18 52,19 ± 9,06 0,50 50,63 ± 12,25 51,82 ± 9,07 0,82 LVOT VTI (cm) 15,4 ± 5,13 16,5 ± 3,98 0,53 15,98 ± 5,74 16,37 ± 3,96 0,96 DT (ms) 168,2 ± 34,01 215,08 ± 59,72 0,10 167 ± 39,15 213,46 ± 59,10 0,14 IVRT (ms) 104,2 ± 20,25 100,48 ± 1,99 0,60 108,26 ± 20,92 100 ± 12,97 0,28 E/A 1,27 ± 0,35 0,81 ± 0,36 0,014* 1,33 ± 0,37 0,81 ± 0,35 0,02* e'lat (cm/s) 6,88 ± 1,56 7,25 ± 2,18 0,72 6,43 ± 1,37 7,31 ± 2,16 0,44 e'set (cm/s) 5,78 ± 1,53 6,11 ± 1,53 0,66 5,13 ± 0,53 6,75 ± 1,74 0,28 e'avg (cm/s) 6,33 ± 1,36 6,68 ± 1,74 0,68 5,78 ± 0,67 6,46 ± 1,29 0,81 E/e’avg 12,20 ± 2,90 10,07 ± 3,72 0,24 13,44 ± 0,93 9,96 ± 3,68 0,02* S (cm/s) 8,48 ± 1,38 8,77 ± 1,84 0,74 7,94 ± 0,81 8,84 ± 1,84 0,33 TAPSE (mm) 11,8 ± 5,07 13,56 ± 3,43 0,34 10 ± 3,56 14,77 ± 5,53 0,06 TRg (mmHg) 19,2 ± 3,03 21,09 ± 6,80 0,55 19 ± 3,46 21,04 ± 6,66 0,56 s' (cm/s) 9,34 ± 4,71 9,04 ± 2,70 0,84 8,77 ± 5,24 9,14 ± 2,70 0,83 VCI (mm) 15 ± 2,74 16,58 ± 3,97 0,41 15,75 ± 2,5 16,40 ± 4,00 0,71 RAP (mmHg) 6 ± 2,24 7,44 ± 4,48 0,49 6,25 ± 2,5 7,35 ± 4,43 0,81 PAPs (mmHg) 25,2 ± 4,60 28,74 ± 7,00 0,29 25,25 ± 5,32 28,58 ± 6,88 0,37 Ees 1,28 ± 0,61 1,66 ± 0,44 0,10 1,35 ± 0,68 1,64 ± 0,45 0,28 Ea 2,14 ± 0,55 2,43 ± 0,76 0,43 2,22 ± 0,61 2,41 ± 0,75 0,63
VAC 1,91 ± 0,81 1,56 ± 0,71 0,33 1,92 ± 0,93 1,57 ± 0,70 0,37
Table 10: DBP=diastolic blood pressure, DT=deceletarion time, Ea=arterial elastance, Ees=ventricular elastance, EDV=end-diastolic diameter, EF=ejection fraction, ESV=end-systolic diameter, HR=heart rate, IVRT=isovolumic relaxation time, LVOT-VTI=left ventricular outflow tract velocity-time integral, PAPs=pulmonary artery systolic pressure, SBP=systolic blood pressure, TAPSE=tricuspid annulus systolic excursion, TRg=tricuspid regurgitation gradient, VAC=ventricular-arterial coupling.
Table 11: comparison of laboratory markers between groups
FAILURE SUCCESS P RESPIRATORY OTHER P
HSTn (ng/L) 564,67 ± 200,84 553,52 ± 563,56 0,96 550,4 ± 221,11 556,46 ± 553,25 0,98
ΔHSTn (ng/L) 310,83 ± 215,28 135,60 ± 364,52 0,27 291,2 ± 234,61 145,36 ± 361,42 0,39
BNP (pg/dL) 700,83 ± 523,18 817,31 ± 833,04 0,74 567 ± 455,87 837,78 ± 823,76 0,48
ΔBNP (pg/dL) 517,5 ± 452,94 458,31 ± 477,31 0,62 452 ± 386,45 500,12 ± 493,25 0,84
