scholarly journals Effects of Pulmonary Vascular Resistance Index on Oxygen Saturation in Patients with Atrial Septal Defect

2020 ◽  
Vol 31 (1) ◽  
pp. 66
Author(s):  
Supomo Supomo
Keyword(s):  
Oxygen Saturation ◽  
Atrial Septal Defect ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Medical Records ◽  
Septal Defect ◽  
Resistance Index ◽  
Heart Catheterization ◽  
Pulmonary Vascular Resistance Index ◽  
The Right

<p>Atrial septal defect (ASD) is a congenital lesion in atrium septum. The lesion may cause pulmonary hypertension due to the high pressure in the right ventricle. This condition leads to cyanosis in ASD patient, but the pathophysiology of cyanosis in ASD patient is still unknown. This study aimed to identify the pathophysiology of cyanosis in ASD patients using the Pulmonary Vascular Resistance index (PVRi). The design of this study was retrospective cohort study. The data used in this study were the results of right heart catheterization procedure taken from forty ASD patient medical records at Dr. Sardjito general hospital. The exclusions criteria were the history of previous vasodilator administration and incomplete medical records. The median age of the patients was 30 (18-55) years old. The mean of the Qp/Qs ratio was 1.210 (0.57-6.33). Optimum oxygen saturation was found in vessel leaving the heart. The PVRi median is 61.98 (-15.58-676.64). The PVRi has a significant correlation with oxygen saturation, except in the right atrium. There is a significant correlation between PVRi and oxygen saturation in various heart chambers. Pathophysiology of cyanosis in ASD patients is central cyanosis.</p>

Decline in arterial partial pressure of oxygen after exercise: a surrogate marker of pulmonary vascular obstructive disease in patients with atrial septal defect and severe pulmonary hypertension

2011 ◽  
Vol 21 (3) ◽  
pp. 292-298 ◽  
Author(s):  
Srinivas Laksmivenkateshiah ◽  
Anil K. Singhi ◽  
Balu Vaidyanathan ◽  
Edwin Francis ◽  
Sundaram R. Karimassery ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Partial Pressure ◽  
Atrial Septal Defect ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Septal Defect ◽  
Resistance Index ◽  
Partial Pressure Of Oxygen ◽  
Arterial Partial Pressure ◽  
Pulmonary Vascular Resistance Index

AbstractObjectivesTo examine the utility of decline in arterial partial pressure of oxygen after exercise as a marker of pulmonary vascular obstructive disease in patients with atrial septal defect and pulmonary hypertension.MethodsTreadmill exercise was performed in 18 patients with atrial septal defect and pulmonary hypertension. Arterial blood gas samples were obtained before and after peak exercise. A decline in the arterial pressure of oxygen of more than 10 millimetres of mercury after exercise was considered significant based on preliminary tests conducted on the controls. Cardiac catheterisation was performed in all patients and haemodynamic data sets were obtained on room air, oxygen, and a mixture of oxygen and nitric oxide (30–40 parts per million).ResultsThere were 10 patients who had more than a 10 millimetres of mercury drop in arterial partial pressure of oxygen after exercise and who had a basal pulmonary vascular resistance index of more than 7 Wood units per square metre. Out of eight patients who had less than a 10 millimetres of mercury drop in arterial partial pressure of oxygen after exercise, seven had a basal pulmonary vascular resistance index of less than 7 Wood units per square metre, p equals 0.0001. A decline in arterial partial pressure of oxygen of more than 10 millimetres of mercury predicted a basal pulmonary vascular resistance index of more than 7 Wood units per square metre with a specificity of 100% and a sensitivity of 90%.ConclusionsA decline in arterial partial pressure of oxygen following exercise appears to predict a high pulmonary vascular resistance index in patients with atrial septal defect and pulmonary hypertension. This test is a useful non-invasive marker of pulmonary vascular obstructive disease in this subset.

Pulmonary hemodynamics and tissue damage after one lung infusion of Pseudomonas aeruginosa in sheep

1992 ◽  
Vol 72 (4) ◽  
pp. 1386-1392 ◽  
Author(s):  
H. M. Loick ◽  
D. J. Dehring ◽  
R. Tokyay ◽  
H. A. Linares ◽  
M. J. Evans ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Tissue Damage ◽  
Left Lung ◽  
Resistance Index ◽  
Pulmonary Hemodynamics ◽  
Pulmonary Vascular Resistance Index ◽  
Bacterial Toxicity ◽  
Bacterial Infusion

The relative roles of hematogenous mediators and direct bacterial toxicity due to phagocytosis by pulmonary intravascular macrophages were determined by selective bacterial infusion into the left pulmonary artery and comparison of right and left lungs at 24 h. Chronically instrumented sheep received 15-min pulmonary arterial infusions of live Pseudomonas aeruginosa (0.35–2.9 x 10(9), n = 6) or saline (n = 5). The saline group demonstrated stable cardiopulmonary function over time. Left lung blood flow, measured by Doppler flow probe, decreased 15 min into the bacterial infusion, with a concomitant sevenfold increase in left lung pulmonary vascular resistance index. The right lung pulmonary vascular resistance index doubled at 1 h, in association with increased plasma thromboxane B2 levels. An increase in cardiac index and decrease in systemic vascular resistance occurred at 12 h. The wet-to-dry weight ratio of the Pseudomonas-infused left lung was increased compared with that of the sham-infused lung. The tissue count of neutrophils in the lungs was doubled in both sides, but neutrophils on the left were more degranulated. The left lung tissue damage was caused by direct bacterial toxicity, including activation of phagocytic cells. Hematogenous mediators induced pulmonary and systemic hemodynamic changes and right lung neutrophil sequestration, but they did not damage the noninfused lung.

Abstract 13374: Larger Atria and Increased Atrial Filling Pressures in Corrected Atrial Septal Defect Patients

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Zarmiga Karunanithi ◽  
Mads Andersen ◽  
Søren Mellemkjær ◽  
Mathias Alstrup ◽  
Farhad Waziri ◽  
...  
Keyword(s):  
Atrial Septal Defect ◽  
Septal Defect ◽  
Holter Monitoring ◽  
Cardiopulmonary Exercise Test ◽  
Right Heart Catheterization ◽  
Morbidity And Mortality ◽  
Volume Index ◽  
Heart Catheterization ◽  
Pulmonary Arterial ◽  
The Right

Introduction: After atrial septal defect (ASD) correction, pulmonary arterial pressures drop and the right-sided chambers start to remodel. Full normalization may not occur, which can explain the increased morbidity and mortality observed later in life. We described cardiac physiology in adults with a corrected ASD in order to understand the long-term morbidity and mortality. Hypothesis: ASD patients have enlarged right atria and increased pulmonary arterial pressures despite correction. Methods: Participants (percutaneously (n=19) and surgically (n=19) corrected ASD patients and 11 controls of similar age) underwent echocardiography, International Physical Activity Questionnaire, right heart catheterization, cardiopulmonary exercise test, and Holter-monitoring 15-20 years after ASD correction as part of a larger study. Echocardiographic measurements and invasive pressures obtained at rest are reported. Results: Right and left atrial end-systolic volumes, volume index, and filling pressures are higher in corrected ASD patients (particularly the surgically corrected) when compared with controls. Conclusion: ASD patients (particularly surgically corrected) have higher atrial volumes compared with healthy matched controls 15-20 years after correction, while still within the normal range. During systole, the peak atrial pressures are increased in ASD corrected patients, which correlate well with the atrial volumes seen on echocardiography. These findings show that cardiac remodeling has occurred post-correction, but full normalization is not reached. The differences in atrial size and filling pressure in corrected ASD compared to that in controls may be a marker of ASDs leading to myocardial disease and explain why ASD patients experience increased morbidity and mortality later in life.

Pulmonary vascular resistance index and mortality after paediatric heart transplant

2014 ◽  
Vol 25 (6) ◽  
pp. 1141-1147 ◽  
Author(s):  
Bryan G. Maxwell ◽  
Ahmad Y. Sheikh ◽  
Chinwe C. Ajuba-Iwuji ◽  
Eugenie S. Heitmiller ◽  
Luca A. Vricella
Keyword(s):  
Confidence Interval ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Heart Transplant ◽  
Odds Ratio ◽  
Resistance Index ◽  
Continuous Variable ◽  
Receiver Operating Curve ◽  
Pulmonary Vascular Resistance Index ◽  
The Relationship

AbstractBackground: Although some prior studies have provided evidence to question the historical belief that pulmonary vascular resistance index ⩾6 Wood Units×m2 should be a contraindication to heart transplantation in children, no national analyses specific to the modern area have addressed this question. Methods: Data were analysed for paediatric heart transplant recipients from 1 January, 2002 to 1 September, 2012 (n=699). The relationship between pulmonary vascular resistance and all-cause 30-day mortality was evaluated using univariate and multivariate analyses. Results: The 30-day mortality included 10 patients (1.43%), which is lower than in the previous analyses. Receiver operating curve analysis of pulmonary vascular resistance index as a predictor of mortality yielded a cut-off value of 3.37 Wood Units×m2, but the area under the curve and specificity of this threshold was weaker than in previous analyses. Whereas pulmonary vascular resistance index treated as a dichotomised variable was a significant predictor of mortality in univariate (odds ratio 4.92, 95% confidence interval 1.04–23.33, p=0.045) and multivariate (odds ratio 5.26, 95% confidence interval 1.07–25.80, p=0.041) analyses, pulmonary vascular resistance index treated as a continuous variable was not a significant predictor of mortality in univariate (p=0.12) or multivariate (p=0.11) analyses. Conclusions: The relationship between pulmonary vascular resistance and post-heart transplant mortality in children is less convincing in this analysis of a comprehensive, contemporary database than in previous series. This suggests the possibility that modern improvements in the management of post-transplant right ventricular dysfunction have mitigated the contribution of pulmonary hypertension to early mortality.

scholarly journals Pulmonary Vascular Resistance as Assessed by Bicycle Stress Echocardiography in Patients With Atrial Septal Defect Type Secundum

2011 ◽  
Vol 4 (3) ◽  
pp. 237-245 ◽  
Author(s):  
Alexander Van De Bruaene ◽  
Andre La Gerche ◽  
David L. Prior ◽  
Jens-Uwe Voigt ◽  
Marion Delcroix ◽  
...  
Keyword(s):  
Atrial Septal Defect ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Stress Echocardiography ◽  
Septal Defect ◽  
Defect Type

scholarly journals Chronic Inhibition of Toll‐Like Receptor 9 Ameliorates Pulmonary Hypertension in Rats

2021 ◽  
Vol 10 (7) ◽  
Author(s):  
Tomohito Ishikawa ◽  
Kohtaro Abe ◽  
Mariko Takana‐Ishikawa ◽  
Keimei Yoshida ◽  
Takanori Watanabe ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Interleukin 6 ◽  
Vascular Remodeling ◽  
Mrna Level ◽  
Systolic Pressure ◽  
Resistance Index ◽  
Pulmonary Vascular Resistance Index ◽  
Macrophage Accumulation

Background Recent accumulating evidence suggests that toll‐like receptor 9 (TLR9) is involved in the pathogenesis of cardiovascular diseases. However, its role in pulmonary hypertension remains uncertain. We hypothesized that TLR9 is involved in the development of pulmonary hypertension. Methods and Results A rat model of monocrotaline‐induced pulmonary hypertension was used to investigate the effects of TLR9 on hemodynamic parameters, vascular remodeling, and survival. Monocrotaline‐exposed rats significantly showed increases in plasma levels of mitochondrial DNA markers, which are recognized by TLR9, TLR9 activation in the lung, and interleukin‐6 mRNA level in the lung on day 14 after monocrotaline injection. Meanwhile, monocrotaline‐exposed rats showed elevated right ventricular systolic pressure, total pulmonary vascular resistance index and vascular remodeling, together with macrophage accumulation on day 21. In the preventive protocol, administration (days −3 to 21 after monocrotaline injection) of selective (E6446) or nonselective TLR9 inhibitor (chloroquine) significantly ameliorated the elevations of right ventricular systolic pressure and total pulmonary vascular resistance index as well as vascular remodeling and macrophage accumulation on day 21. These inhibitors also significantly reduced NF‐κB activation and interleukin‐6 mRNA levels to a similar extent. In the short‐term reversal protocol, E646 treatment (days 14–17 after monocrotaline injection) almost normalized NF‐κB activation and interleukin‐6 mRNA level, and reduced macrophage accumulation. In the prolonged reversal protocol, E6446 treatment (days 14–24 after monocrotaline injection) reversed total pulmonary vascular resistance index and vascular remodeling, and improved survival in monocrotaline‐exposed rats. Conclusions TLR9 is involved in the development of pulmonary hypertension concomitant via activation of the NF‐κB‒IL‐6 pathway. Inhibition of TLR9 may be a novel therapeutic strategy for pulmonary hypertension.

scholarly journals Pulmonary hemodaynamic in obesity

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
N Zhou ◽  
M Klass ◽  
S Corentin ◽  
F Kevin ◽  
Y Motoji ◽  
...  
Keyword(s):  
Right Ventricular ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Resistance Index ◽  
Exercise Stress ◽  
Pulmonary Hemodynamics ◽  
Pulmonary Hemodynamic ◽  
Pulmonary Vascular Resistance Index ◽  
Healthy Control ◽  
Obese Subjects

Abstract Background Higher prevalence of pulmonary hypertension exist in obesity subjects. Little known about pulmonary hemodynamics during exercise in obesity population. Purpose To assess and compare the response of pulmonary vascular resistance during exercise in obese subjects vs healthy controls. Methods Seventeen obesity subjects (gender: 25%men, age: 44±11 years, height: 1.7±0.1 m, weight: 111±17 kilogram, BMI: 38±4 kg/m2) were compared to twenty gender-, age-, height- and race-matched healthy control subjects (age: 46±12 years, height: 1.7±0.1 m, weight: 64±11 kilogram, BMI: 22±2 kg/m2). All subjects underwent an incremental exercise stress echocardiography with measurements of pulmonary artery pressure (PAP), cardiac output (CO), cardiac index (CI) and tricuspid annular plane systolic excursion (TAPSE) at rest and at increasing exercise intensities. Total pulmonary vascular resistance index (PVRi) was calculated as mean PAP/CI and right ventricular-arterial coupling as TAPSE/systolic PAP. Results The results are described in the table 1. Pulmonary hemodynamic was not different at rest between two groups, but lower at maximal exercise in obesity subjects. In obesity subjects, identical exercise level was associated with a higher mean PAP and PVRi, and a lower TAPSE/systolic PAP ratio. Conclusion While pulmonary hemodynamic seems preserved at rest in obesity patients, pulmonary vascular resistance is increased and right ventricular coupling is decreased, particularly at exercise. Funding Acknowledgement Type of funding source: None

scholarly journals VALIDATING THE USE OF PULMONARY ARTERY ACCELERATION TIME IN ESTIMATING PULMONARY PRESSURE IN NEONATES

2018 ◽  
Vol 23 (suppl_1) ◽  
pp. e25-e26
Author(s):  
Soume Bhattacharya ◽  
Patrick McNamara ◽  
Amish Jain ◽  
Philip Ye ◽  
Karl McNamara
Keyword(s):  
Pulmonary Artery ◽  
Right Ventricular ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Resistance Index ◽  
Acceleration Time ◽  
Pulmonary Pressure ◽  
Doppler Waveform ◽  
Pulmonary Vascular Resistance Index ◽  
Ventricular Ejection Time

Abstract BACKGROUND Estimation of right ventricular peak systolic pressure (RVSP) or pulmonary pressure using echocardiography is crucial in neonates with acute or chronic pulmonary hypertension. Conventionally in echocardiography, the maximal velocity of the Tricuspid Regurgitant jet (TR Vmax) is used to estimate the RVSP. However, TR jet can often be absent or unmeasurable in neonates, resulting in a need to search for alternative echocardiographic measures of pulmonary pressure in neonates. Pulmonary Artery Doppler Waveform Parameter known as Pulmonary Artery Acceleration Time (PAAT) has been investigated in adults and older children and found to be reliable in estimating pulmonary pressure. To date, no such validation study exists for neonates.Hence we designed this study to explore the role of Pulmonary Artery Acceleration Time in estimating pulmonary pressures in neonates. OBJECTIVES To identify the pulmonary artery doppler waveform parameter that most closely reflects pulmonary pressure and analyse the impact of baseline variables and measurement techniques on this relationship. DESIGN/METHODS This was a retrospective cohort analysis conducted at two tertiary neonatal intensive care units. All neonates who underwent Targeted Neonatal Echocardiographic(TnECHO) assessments over May 2014-May 2017 were assessed for eligibility. Neonates whose echocardiography revealed a complete, measurableTR jet were included. Baseline characteristics such as gestational age, chronological age at echo, weight, blood pressure, ventilation and diagnosis were collected. Echocardiographic parameters such as TR Vmax, Pulmonary artery doppler waveform parameters such as Right Ventricular Ejection Time (RVET) and Pulmonary Artery Acceleration Time (PAAT) were measured by a single expert operator. Pulmonary Vascular Resistance Index (PVRI) was calculated as a ratio between RVET and PAAT. Correlation between pulmonary artery waveforms and RVSP estimated from the TR jet was examined using Pearson or Spearman analysis as appropriate. Univariate and multivariate regression analysis was used to further explore the influence of relevant factors on this relationship. Ethical approval was obtained from the institutional ethic board. RESULTS 678 neonates with 1767 echocardiographic studies were screened for eligibility of which 201 scans were included. Mean gestational age of this cohort was 30.5+/-5.7 weeks with mean birthweight of 1635 +/-1115 grams. Pulmonary Vascular Resistance Index (ratio of RVET to PAAT) also known as indexed PAAT, measured by Pulsed Wave Doppler at the level of the main pulmonary artery was found to have the strongest correlation with RVSP estimated from TRVmax. [r=0.45,P<0.05]. Using regression analysis, we could generate an equation to estimate systolic pulmonary artery pressures(ESPAP) directly from PVRI. [ESPAP= 25.53 + 3.97xPVRI, p<0.0001]. At the multivariate level, factors such as the Systolic Blood Pressure at time of echocardiogram and the presence or absence of PDA were found to have a statistically significance influence on this relationship. Pulmonary Vascular Resistance Index could be measured on all eligible scans. Inter-observer and intra-observer reliability assessment completed on a random subset of 30 showed excellent reliability for PVRI. [ICC =0.88, P<0.000] CONCLUSION This important validation study shows that PAAT indexed to right ventricular ejection time(PVRI) has statistically significant correlation with pulmonary pressures as measured by TR jet in neonates. However the strength of correlation in neonates is moderate at best. The measurement is feasible with good interobserver agreement and potentially can play an important role in serial monitoring of pulmonary pressures in neonates without any demonstrable TR jet on echocardiography.

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