Acute Respiratory Distress Syndrome (ARDS) is often complicated by Right Ventricular Dysfunction (RVD), and the incidence can be as high as 64%. The mechanism includes pulmonary vascular dysfunction and right heart systolic dysfunction. Pulmonary vascular dysfunction includes acute vascular inflammation, pulmonary vascular edema, thrombosis and pulmonary vascular remodeling. Alveolar collapse and over distension can also lead to increased pulmonary vascular resistance, Preventing the development of acute cor pulmonale in patients with acute respiratory distress. ARDS patients with RVD have a worse prognosis and a significantly increased risk of death, which is an independent risk factor for death in ARDS patients. Therefore, implementing a right heart-protective mechanical ventilation strategy may reduce the incidence of RVD. APRV is an inverse mechanical ventilation mode with transient pressure release under continuous positive airway pressure, which can effectively improve oxygenation and reduce ventilator-associated lung injury. However, its effect on right ventricular function is still controversial. Low tidal volume (LTV) is a mechanical ventilation strategy widely used in ARDS patients. Meta-analysis results showed that compared with LTV, APRV improved oxygenation more significantly, reduced the time of mechanical ventilation, and even had a tendency to improve the mortality of ARDS patients However, randomized controlled studies have shown that compared with LTV, APRV improves oxygenation more significantly and also increases the mean airway pressure. Therefore, some scholars speculate that APRV may increase the intrathoracic pressure, pulmonary circulatory resistance, and the risk of right heart dysfunction but this speculation is not supported by clinical research evidence. In addition, APRV may improve right ventricular function by correcting hypoxia and hypercapnia, promoting lung recruitment and reducing pulmonary circulation resistance. Therefore, it is very important to clarify this effect for whether APRV can be safely used and popularized in clinic.we aim to conduct a single-center randomized controlled study to further compare the effects of APRV and LTV on right ventricular function in patients with ARDS, pulmonary circulatory resistance (PVR) right ventricular-pulmonary artery coupling (RV-PA coupling), and pulmonary vascular resistance (PVR).
Acute Respiratory DistressSyndrome (ARDS) is often complicated by Right Ventricular Dysfunction (RVD), and the incidence can be as high as 64%. The mechanism includes pulmonary vascular dysfunction and right heart systolic dysfunction. Pulmonary vascular dysfunction includes acute vascular inflammation, pulmonary vascular edema, thrombosis and pulmonary vascular remodeling. Alveolar collapse and alveolar overdistension can also lead to increased pulmonary vascular resistance, Preventing the development of acute cor pulmonale in patients with acute respiratory distress. ARDS patients with RVD have a worse prognosis and a significantly increased risk of death, which is an independent risk factor for death in ARDS patients \[2-4\]. Therefore, implementing a right heart-protective mechanical ventilation strategy may reduce the incidence of RVD. Mechanical ventilation is the main treatment for moderate to severe ARDS. Mechanical ventilation promotes lung recruitment and reduces mechanical compression of pulmonary vessels between alveoli and alveolar walls. In addition, mechanical ventilation corrected hypoxemia and hypercapnia, thereby reducing reactive pulmonary vasoconstriction. All of the above can reduce pulmonary circulation resistance and right ventricular afterload, thereby improving right ventricular function in patients with ARDS. However, if hyperventilation occurs, it will increase the mechanical compression of pulmonary vessels on the alveolar wall, increase the intrathoracic pressure, and increase the afterload of the right heart, which will adversely affect the function of the right heart. There are a variety of ventilation strategies for patients with ARDS in clinical practice, but which mechanical ventilation has the protective function of right heart or has little effect on right heart function, so far there is a lack of relevant research reports. Airway pressure release ventilation (APRV) is an inverse mechanical ventilation mode with transient pressure release under continuous positive airway pressure, which can effectively improve oxygenation and reduce ventilator-associated lung injury. However, its effect on right ventricular function is still controversial, so its clinical application is not popular, and it is only used as one of the salvage treatments for ARDS patients. Low tidal volume (LTV) is a mechanical ventilation strategy widely used in ARDS patients, but it does not further reduce mortality in patients with moderate to severe ARDS. Meta-analysis results showed that compared with LTV, APRV improved oxygenation more significantly, reduced the time of mechanical ventilation, and even had a tendency to improve the mortality of ARDS patients \[7\]. However, randomized controlled studies have shown that compared with LTV, APRV improves oxygenation more significantly and also increases the mean airway pressure \[8\]. Therefore, some scholars speculate that APRV may increase the intrathoracic pressure, pulmonary circulatory resistance, and the risk of right heart dysfunction , but this speculation is not supported by clinical research evidence. In addition, the results of animal experiments suggest that APRV improves oxygenation, promotes lung recruitment, and improves the heterogeneity of lung lesions in ARDS, without causing lung hyperventilation, suggesting that APRV may not increase pulmonary circulatory resistance. In addition, APRV may improve right ventricular function by correcting hypoxia and hypercapnia, promoting lung recruitment and reducing pulmonary circulation resistance. Therefore, the impact of APRV on right ventricular function is still unclear, and it is very important to clarify this effect for whether APRV can be safely used and popularized in clinic. Therefore, our research group conducted a prospective observational study, "The effect of APRV on right ventricular function evaluated by Transthoracic Echocardiography, \[2022\] Lun Lun Zi (0075)". The study results suggested that APRV improved lung perfusion in ARDS patients while effectively improving oxygenation and promoting lung recruitment. The incidence of RVD was not increased, and there was no hemodynamic deterioration in ARDS patients. APRV is safe and effective for patients with ARDS. However, the results of a single-arm prospective observational study with a small sample size cannot provide strong evidence for clinical practice. In the previous studies, all the right ventricular function was assessed by transthoracic echocardiography. Due to the limitation of the sound window of transthoracic echocardiography, the right ventricular function of some ARDS patients could not be evaluated. Therefore, this study intends to use transesophageal echocardiography or transthoracic echocardiography to fully evaluate the right ventricular function of all enrolled patients as much as possible, and to conduct a single-center randomized controlled study to further compare the effects of APRV and LTV on right ventricular function in patients with ARDS, pulmonary circulatory resistance (PVR), right ventricular-pulmonary artery coupling (RV-PA coupling), and pulmonary vascular resistance (PVR).Whether there are different effects on hemodynamics and mortality. It is hoped that the results of this study will provide more evidence support for the clinical application of APRV and benefit more ARDS patients.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
TREATMENT
Masking
SINGLE
Enrollment
60
ventilator parameters were set according to the study protocol, P high: Tidal volume (VT) was set at 6ml/kg of ideal body weight, and plateau pressure (Pplat) was measured. Initial Phigh was set at Pplat, usually 20-32 cmH2O. The APRV end-expiratory flow rate was set at 75% of the peak expiratory flow rate.
The ARDSnet method was used for LTV mechanical ventilation, and the tidal volume was set according to 4-8ml/kg, so that the Pplat was \<30cmH2O
Union Hospital, Tongji Medical College, Huazhong University of Science and Technology
Wuhan, Hubei, China
Incidence of right heart dysfunction in ARDS patients with APRV or LTV mechanical ventilation for 24h
Incidence of right heart dysfunction in ARDS patients with APRV or LTV mechanical ventilation for 24h.Abnormal findings on any of the following ultrasound measures can be considered as right ventricular dysfunction, including: tricuspid annular plane systolic excursion (TAPSE) \<17 mm, tricuspid annular plane systolic velocity (S') \<9.5 cm/s, right ventricular fractional area change (FAC) \<35%, ratio of right ventricular end-diastolic area to left ventricular end-diastolic area (RVEDA/LVEDA) \>0.6, or right ventricular to left ventricular end-diastolic diameter ratio (RV/LV ratio) \>1.
Time frame: at the time of 24 hours after inclusion
Incidence of right heart dysfunction in ARDS patients with APRV or LTV mechanical ventilation for 48h
Incidence of right heart dysfunction in ARDS patients with APRV or LTV mechanical ventilation for 24h.Abnormal findings on any of the following ultrasound measures can be considered as right ventricular dysfunction, including: right ventricular end-diastolic diameter/left ventricular end-diastolic diameter(RVEDD/LVEDD)\>1.0, right ventricular fractional area change(FAC)\<35%,tricuspid annular plane systolic excursion(TAPSE)\<17mm,Systolic S'velocity of tricuspid annulus \<9.5 cm/s by TDI
Time frame: at the time of 48 hours after inclusion
Incidence of right heart dysfunction in ARDS patients with APRV or LTV mechanical ventilation for 72h
Incidence of right heart dysfunction in ARDS patients with APRV or LTV mechanical ventilation for 24h.Abnormal findings on any of the following ultrasound measures can be considered as right ventricular dysfunction, including: right ventricular end-diastolic diameter/left ventricular end-diastolic diameter(RVEDD/LVEDD)\>1.0, right ventricular fractional area change(FAC)\<35%,tricuspid annular plane systolic excursion(TAPSE)\<17mm,Systolic S'velocity of tricuspid annulus \<9.5 cm/s by TDI
Time frame: at the time of 72 hours after inclusion
Values of tricuspid annular plane systolic excursion at 24th hour
Tricuspid annular plane systolic excursion(TAPSE) was measured by echocardiography in the apical four-chamber view, using M mode measurements, with the sampling line aligned to the tricuspid annulus.
Time frame: at the time of 24 hours after inclusion
Values of tricuspid annular plane systolic excursion at 48th hour
Tricuspid annular plane systolic excursion(TAPSE) was measured by echocardiography in the apical four-chamber view, using M mode measurements, with the sampling line aligned to the tricuspid annulus.
Time frame: at the time of 48 hours after inclusion
Values of tricuspid annular plane systolic excursion at 72th hour
Tricuspid annular plane systolic excursion(TAPSE) was measured by echocardiography in the apical four-chamber view, using M mode measurements, with the sampling line aligned to the tricuspid annulus.
Time frame: at the time of 72 hours after inclusion
Values of right ventricular end-diastolic diameter/left ventricular end-diastolic diameter(RVEDD/LVEDD) at 24th hour
The maximum transverse diameter of the right/left ventricular inflow tract near the basal 1/3 was measured in the apical four-chamber view
Time frame: at the time of 24 hours after inclusion
Values of right ventricular end-diastolic diameter/left ventricular end-diastolic diameter(RVEDD/LVEDD) at 48th hour
The maximum transverse diameter of the right/left ventricular inflow tract near the basal 1/3 was measured in the apical four-chamber view
Time frame: at the time of 48 hours after inclusion
Values of right ventricular end-diastolic diameter/left ventricular end-diastolic diameter(RVEDD/LVEDD) at 72th hour
The maximum transverse diameter of the right/left ventricular inflow tract near the basal 1/3 was measured in the apical four-chamber view
Time frame: at the time of 72 hours after inclusion
Values of right ventricular fractional area change(RVFAC) at 24th hour
RVFAC = (end-diastolic area - end-systolic area)/end-diastolic area ×100%.The right ventricle is shown in the apical four-chamber cardiac view.
Time frame: at the time of 24 hours after inclusion
Values of right ventricular fractional area change(RVFAC) at 48th hour
RVFAC = (end-diastolic area - end-systolic area)/end-diastolic area ×100%.The right ventricle is shown in the apical four-chamber cardiac view.
Time frame: at the time of 48 hours after inclusion
Values of right ventricular fractional area change(RVFAC) at 72th hour
RVFAC = (end-diastolic area - end-systolic area)/end-diastolic area ×100%.The right ventricle is shown in the apical four-chamber cardiac view.
Time frame: at the time of 72 hours after inclusion
Values of Systolic S'velocity of tricuspid annulus by at 24th, 48th and 72th hour
Tissue Doppler sampling volume is placed in the middle of the right ventricular tricuspid annulus or basal segment of the right ventricular free wall to measure systolic velocity S'.
Time frame: at the time of 24 hours (h), 48h and 72h after inclusion
Values of hemodynamic measures at 24th, 48th and 72th hour
hemodynamic measures including: heart rate, mean arterial pressure,central venous pressure,Dose of vasoactive agents accumulated over 24 hours,cumulative fluid balance over 24 hours.
Time frame: at the time of 24 hours (h), 48h and 72h after inclusion
Values of respiratory mechanics parameters at 24th, 48th and 72th hour
Respiratory mechanics parameters including Peak pressure, Plateau pressure,Driving pressure,Respiratory system compliance and Airway resistance are measured by using routine procedures
Time frame: at the time of 24 hours (h), 48h and 72h after inclusion
28-day mortality
28-day mortality after study entry
Time frame: Day 28 after study entry
in hospital mortality
in hospital mortality after study entry
Time frame: Maximum 90-day in-hospital mortality
28 days of ventilator free days
28 days of ventilator free days after study entry
Time frame: Day 28 after study entry
Values of arterial partial pressure of oxygen/fraction of inspired oxygen at 24th, 48th and 72th hour
arterial partial pressure of oxygen/fraction of inspired oxygen are measured at 24th, 48th and 72th hour after inclusion
Time frame: at the time of 24 hours (h), 48h and 72h after inclusion
Values of arterial partial pressure of carbon dioxide at 24th, 48th and 72th hour
arterial partial pressure of carbon dioxide are measured at 24th, 48th and 72th hour after inclusion
Time frame: at the time of 24 hours (h), 48h and 72h after inclusion
ventilation ratio at 24th, 48th and 72th hour
VR=\[minute ventilation ×PaCO2\]/\[predicted body weight ×100×37.5\]
Time frame: at the time of 24 hours (h), 48h and 72h after inclusion
Incidence prone position ventilation during hospitalization
Incidence of prone position ventilation during hospitalization after study entry
Time frame: Day 28 after study entry
ventilator settings at 24th, 48th and 72th hour
ventilator settings including minute ventilation, Fraction of inspired oxygen, tidal volume, positive end-expiratory pressure, respiratory rate, mean airway pressure
Time frame: at the time of 24 hours (h), 48h and 72h after inclusion
Velocity-time integral of left ventricular outflow tract at 24th, 48th and 72th hour
Velocity-time integral(Vti) of left ventricular outflow tract are measured at the apical five-chamber heart view. The sampling volume was placed in the left ventricular outflow tract, below the aortic valve, in pulsed Doppler mode with a window width of 2-4mm. The velocity time integral (VTI) image of aortic blood flow can be obtained by placing the sampling volume below the aortic valve orifice , adjusting the probe so that the direction of blood flow is as parallel as possible to the sampling line, and selecting the pulsed Doppler mode (PW)
Time frame: at the time of 24 hours (h), 48h and 72h after inclusion
Stroke volume at 24th, 48th and 72th hour
Stroke volume(SV)=15.VTI×π(D/2)\*(D/2), D=Left ventricular outflow tract diameter(LVOT diameter)
Time frame: at the time of 24 hours (h), 48h and 72h after inclusion
cardiac output at 24th, 48th and 72th hour
cardiac output(CO)=SV\*HR
Time frame: at the time of 24 hours (h), 48h and 72h after inclusion
Velocity-time integral of right ventricular outflow tract at 24th, 48th and 72th hour
Velocity-time integral(Vti) of right ventricular outflow tract are measured at the view of the right ventricular outflow tract. The sampling volume was placed in the right ventricular outflow tract, below the aortic valve, in pulsed Doppler mode with a window width of 2-4mm. The velocity time integral (VTI) image of aortic blood flow can be obtained by placing the sampling volume below the aortic valve orifice , adjusting the probe so that the direction of blood flow is as parallel as possible to the sampling line, and selecting the pulsed Doppler mode (PW)
Time frame: at the time of 24 hours (h), 48h and 72h after inclusion
Tricuspid annular diameter
Tricuspid annular diameters are measured at the apical four-chamber heart view
Time frame: at the time of 24 hours (h), 48h and 72h after inclusion
The velocity of tricuspid regurgitation
The velocity of tricuspid regurgitation are measured at the apical four-chamber heart view.The CW Doppler sampling line was placed at the tricuspid valve orifice.
Time frame: at the time of 24 hours (h), 48h and 72h after inclusion
Length of hospital stay
hospital stay after hospital entry
Time frame: Maximum 90-day hospital stay
Length of ICU stay
hospital stay after ICU entry
Time frame: Maximum 90-day ICU stay
Incidence of tracheotomy
Incidence of tracheotomy during hospitalization after study entry
Time frame: Day 28 after study entry
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