The unique pathophysiologic contributions of obstructive sleep apnea (OSA) toward pulmonary hypertension and right ventricular (RV) dysfunction still represent an understudied area. We aimed to ...investigate the impacts of various respiratory parameters on pulmonary hemodynamics and RV performance in OSA.
Data of consecutive patients with OSA who completed right heart catheterization for evaluation of pulmonary hemodynamics were retrospectively reviewed and analyzed. Univariable and multivariable regression analyses were used to determine the significant respiratory parameter associated with right heart catheterization metrics.
Of 205 patients with OSA (43.4% male), 134 (65.4%) had pulmonary hypertension. Among various sleep parameters, the time percentage spent with SpO
below 90% (T90) was the sole and the strongest independent factor associated with mean pulmonary artery pressure (mPAP) (β = 0.467,
< .001), pulmonary vascular resistance (PVR) (β = 0.433,
< .001), and RV stroke work index (RVSWI) (β = 0.338,
< .001). For every 5-unit increase in T90, there was approximately 36% greater risk of mPAP ≥ 25 mmHg (odds ratio OR 1.36, 95% confidence interval CI 1.16-1.59,
< .001), and 45% greater risk of PVR > 3 Woods units (OR 1.45, 95% CI 1.21-1.74,
< .001), respectively. T90 per 5-unit increment was also related to a nearly 1.2-fold higher risk of RVSWI ≥ 12 g/m
/beat (OR 1.19, 95% CI 1.11-1.28,
< .001). These associations remained significant even after multivariable adjustment for confounding factors (all
< .05).
Increased mPAP, PVR, and RVSWI were associated with prolonged T90 in patients with OSA. Assessment of OSA with insights into hypoxemic duration may aid in early recognition of impaired pulmonary hemodynamics and RV dysfunction.
Huang Z, Duan A, Hu M, et al. Implication of prolonged nocturnal hypoxemia and obstructive sleep apnea for pulmonary hemodynamics in patients being evaluated for pulmonary hypertension: a retrospective study.
. 2023;19(2):213-223.
Objectives:Right heart catheterization (RHC) is a gold standard method for diagnosis, also monitors the level of the disease, the prognosis, and the response to the therapy in patients with pulmonary ...arterial hypertension (PAH). Cardiac power output (CPO) is the product of flow and pressure. Aim of this study was to evaluate right ventricular cardiac power output (RVCPO) in PAH patients as a prognostic factor. Materials and methods: Demographic characteristics, functional class, RHC findings, echocardiographic data, PAH-specific medical treatment usage of 105 treatment-naïve, newly diagnosed Group 1 PAH patients between September 2009 and June 2019 were reviewed. RVCPO (Watt) was calculated as a product of cardiac output (CO) and mean pulmonary artery pressure (mPAP), divided by a constant of 451. Results: RVCPO was lower in high-risk patients (0,25 ± 0,02 W for high risk, 0,42 ± 0,15 W for low risk, and 0,44 ± 0,10 W for intermediate-risk; p=0.04) in comparison with low and intermediate-risk patients. RVCPO showed very high correlation with mPAP while a low positive correlation with CO, and PVR. 0,44 W for RVCPO was found the most accurate predictor value for mortality in low and intermediate-risk patients by ROC analysis. Conclusion: RVCPO could be a promising hemodynamic parameter that represents cardiac pumping ability with PAH patients. RVCPO tends to increase with low and intermediate risk while decrease with high-risk and associated with mortality above 0,44 W with low and intermediate-risk patients. We suggest that RVCPO could be a beneficial hemodynamic tool to discriminate the patients at-risk among the low and intermediate-risk groups.
Among patients with heart failure with preserved ejection fraction (HFpEF), a distinct hemodynamic phenotype has been recently described, ie, latent pulmonary vascular disease (HFpEF-latentPVD), ...defined by exercise pulmonary vascular resistance (PVR) >1.74 WU.
This study aims to explore the pathophysiological significance of HFpEF-latentPVD.
The authors analyzed a cohort of patients who had undergone supine exercise right heart catheterization with cardiac output (CO) measured by direct Fick method, between 2016 and 2021. HFpEF-latentPVD patients were compared with HFpEF control patients.
Out of 86 HFpEF patients, 21% qualified as having HFpEF-latentPVD, 78% of whom had PVR >2 WU at rest. Patients with HFpEF-latentPVD were older, with a higher pretest probability of HFpEF, and more frequently experienced atrial fibrillation and at least moderate tricuspid regurgitation (P < 0.05). PVR trajectories differed between HFpEF-latentPVD patients and HFpEF control patients (Pinteraction = 0.008), slightly increasing in the former and reducing in the latter. HFpEF-latentPVD patients displayed more frequent hemodynamically significant tricuspid regurgitation during exercise (P = 0.002) and had more impaired CO and stroke volume reserve (P < 0.05). Exercise PVR was correlated with mixed venous O2 tension (R2 = 0.33) and stroke volume (R2 = 0.31) in HFpEF-latentPVD patients. The HFpEF-latentPVD patients had had higher dead space ventilation during exercise and higher PaCO2 (P < 0.05), which correlated with resting PVR (R2 = 0.21). Event-free survival was reduced in HFpEF-latentPVD patients (P < 0.05).
The results suggest that when CO is measured by direct Fick, few HFpEF patients have isolated latent PVD (ie, normal PVR at rest, becoming abnormal during exercise). HFpEF-latentPVD patients present with CO limitation to exercise, associated with dynamic tricuspid regurgitation, altered ventilatory control, and pulmonary vascular hyperreactivity, portending a poor prognosis.
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There is a lack of knowledge regarding the contribution of central and peripheral factors to the increases in VO2max following sprint‐interval training (SIT). This study investigated the importance ...of maximal cardiac output (Qmax) in relation to VO2max improvements following SIT and the relative importance of the hypervolemic response on Qmax and VO2max. We also investigated whether systemic O2 extraction increased with SIT as has been previously suggested. Healthy men and women (n = 9) performed 6 weeks of SIT. State‐of‐the‐art measurements: right heart catheterization, carbon monoxide rebreathing and respiratory gas exchange analysis were used to assess Qmax, arterial O2 content (caO2), mixed venous O2 content (cvO2), blood volume (BV) and VO2max before and after the intervention. In order to assess the relative contribution of the hypervolemic response to the increases in VO2max, BV was re‐established to pre‐training levels by phlebotomy. Following the intervention, VO2max, BV and Qmax increased by 11% (P < 0.001), 5.4% (P = 0.013) and 8.8% (P = 0.004), respectively. cvO2 decreased by 12.4% (P = 0.011) and systemic O2 extraction increased by 4.0% (P = 0.009) during the same period, both variables were unaffected by phlebotomy (P = 0.589 and P = 0.548, respectively). After phlebotomy, VO2max and Qmax reverted back to pre‐intervention values (P = 0.064 and P = 0.838, respectively) and were significantly lower compared with post‐intervention (P = 0.016 and P = 0.018, respectively). The decline in VO2max after phlebotomy was linear to the amount of blood removed (P = 0.007, R = −0.82). The causal relationship between BV, Qmax and VO2max shows that the hypervolemic response is a key mediator of the increases in VO2max following SIT.
Key points
Sprint‐interval training (SIT) is an exercise model involving supramaximal bouts of exercise interspersed with periods of rest known for its efficiency in improving maximal oxygen uptake (VO2max).
In contrast to the commonly accepted view where central haemodynamic adaptations are considered to be the key mediators of increases in VO2max there have been propositions highlighting peripheral adaptations as the main mediators in the context of SIT‐induced changes in VO2max.
By combining right heart catheterization, carbon monoxide rebreathing and phlebotomy, this study shows that increases in maximal cardiac output due to the expansion of the total blood volume is a major explanatory factor for the improvement in VO2max following SIT, with a smaller contribution from improved systemic oxygen extraction.
The present work not only clarifies a controversy in the field by using state‐of‐the‐art methods, but also encourages future research to investigate regulatory mechanisms that could explain how SIT can lead to improvements in VO2max and maximal cardiac output similar to those that have previously been reported for traditional endurance exercise.
figure legend This study aimed to understand the factors contributing to increases in maximal oxygen uptake (VO2max) after sprint‐interval training (SIT). The study involved nine healthy subjects who completed 6 weeks of SIT. Measurements were taken before and after the intervention to assess factors such as maximal cardiac output (Qmax), arterial and mixed venous oxygen content (caO2 and cvO2), blood volume (BV) and VO2max. To determine the importance of the hypervolemic response on Qmax and VO2max, BV was reduced to pre‐training levels through phlebotomy. Following the intervention, VO2max, BV and Qmax increased, while cvO2 decreased, and systemic O2 extraction increased. After phlebotomy, VO2max and Qmax decreased to pre‐intervention levels, and were significantly lower than post‐intervention values. The study suggests that the hypervolemic response is a key factor in the increases in VO2max following SIT.
Full text
Available for:
FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SAZU, SBCE, SBMB, UL, UM, UPUK
Recent studies have challenged the reported causal association between acute kidney injury and iodinated contrast administration, ascribing some cases to changes in renal function that are ...independent of contrast administration.
We studied 1779 consecutive patients undergoing right heart catheterization (RHC) at a Veterans Administration Medical Center. We compared the incidence of acute kidney injury and of nephropathy at 3 months in veterans undergoing right and left heart catheterization and coronary angiography (R&LHC) to the incidence of acute kidney injury and of nephropathy at 3 months in patients undergoing RHC only.
The incidence of acute kidney injury at 3 days was 47 (9.7%) in the R&LHC group and 58 (9.6%) in the RHC group (P = .99). The incidence of nephropathy at 3 months was 115 (17%) in the L&RHC group and 141 (19.2%) in the RHC group (P = 0.31). In a propensity score-paired analysis of 782 patients and after adjustment for baseline characteristics, the odds ratio for acute kidney injury at 3 days among patients undergoing R&LHC was 1.25 (95% confidence interval, 0.65-2.42; P = .50), and the odds ratio for nephropathy at 3 months was 0.69 (95% confidence interval, 0.46-1.04; P = .08).
The incidence of changes in creatinine consistent with acute kidney injury at 3 days and of nephropathy at 3 months was not significantly different in patients undergoing R&LHC compared with patients undergoing RHC only. This supports the thesis that not all changes in creatinine after procedures involving administration of contrast are caused by the contrast.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
57.
Exercise Pulmonary Hypertension Katarina Zeder; Horst Olschewski; Gabor Kovacs
Barcelona Respiratory Network Reviews,
04/2022, Volume:
8, Issue:
2
Journal Article
Peer reviewed
Open access
The clinical value of pulmonary hemodynamics during exercise has not been fully explored. In the last decade, several studies investigated the prognostic and diagnostic relevance of exercise ...hemodynamics and novel hemodynamic variables including the mean pulmonary arterial pressure (mPAP)/cardiac output (CO) slope and the pulmonary arterial wedge pressure (PAWP)/CO slope have been analyzed. These parameters describe the effects of pulmonary blood flow on the pulmonary pressure and were shown to be of prognostic relevance. In addition, they may also serve as tools to differentiate early forms of pulmonary vascular from left heart diseases. Right heart catheterization remains the gold standard to assess pulmonary hemodynamics both at rest and during exercise, while exercise echocardiography represents a promising non-invasive research tool. In this review, we provide an overview of the growing body of evidence on the clinical relevance of pulmonary hemodynamics during exercise and discuss its potential future role.
Pulmonary artery rupture is a rare complication of right heart catheterization characterized by a rapid clinical deterioration and high mortality rate. We present the case of an 89-year-old woman ...with severe symptomatic aortic stenosis who underwent cardiac catheterization prior to aortic valve replacement. The patient had acute cardiopulmonary deterioration due to pulmonary artery rupture at the time of right heart catheterization, that was successfully sealed by balloon tamponade.
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NUK, OILJ, SAZU, UKNU, UL, UM, UPUK
Guidelines recommend using end-expiration pulmonary pressure measurements to determine the hemodynamic subgroups in pulmonary hypertension. Pulmonary artery wedge pressure (PAWP) determinations ...averaged across the respiratory cycle (PAWPav) instead of PAWP at end-expiration (PAWPee) and cardiac output (CO) measured by Fick (CO
) instead of thermodilution (CO
) may affect the hemodynamic classification of pulmonary hypertension.
To assess the impact on the pulmonary hypertension hemodynamic classification of the use of PAWPee versus PAWPav as well as CO
versus CO
.
This was a single-center retrospective study of consecutive patients (
= 151) who underwent right heart catheterization with CO
, CO
, PAWPee, and PAWPav. A secondary cohort consisted of consecutive patients (
= 71) who had mean pulmonary artery pressure at end-expiration (mPAPee) and mPAP averaged across the respiratory cycle (mPAPav) measured, as well as PAWPee and PAWPav.
The PAWPee and PAWPav were 16.8 ± 6.4 and 15.1 ± 6.8 mm Hg, respectively, with a mean difference of 1.7 ± 2.1 mm Hg. The CO
and CO
determinations were 5.0 ± 2.4 and 5.3 ± 2.5 L/min, respectively, with a mean difference of -0.4 ± 1.3 L/min. The hemodynamic group distribution was significantly different when using PAWPee versus PAWPav, when using either CO
or CO
(
< 0.001 for both comparisons), and these results were consistent in our secondary cohort. The pulmonary hypertension hemodynamic group distribution was not significantly different between CO
and CO
when using either PAWPee or PAWPav.
The methodology used to measure PAWP, either at end-expiration or averaged across the respiratory cycle, significantly impacts the hemodynamic classification of pulmonary hypertension.
Pulmonary hypertension (PH) is quite infrequent in pediatric age and its most common etiologies include idiopathic pulmonary arterial hypertension, PH related to congenital heart diseases, ...bronchopulmonary dysplasia (chronic lung disease), persistence of pulmonary hypertension of the newborn, and congenital diaphragmatic hernia. The developed for adult patients PH classification shows limitations when applied to pediatric subjects since the underlying causes are markedly different between the two ages. In 2011, the Pulmonary Vascular Research Institute Panama Task Force outlined the first specific pediatric pulmonary hypertensive vascular disease diagnostic classification, including 10 main categories and 109 subcategories, thus testifying PH complex pathophysiology during newborns/children growth and development. The unique, distinctive features of pediatric PH were recognized also during the fifth World Symposium on pulmonary hypertension in 2013 and then confirmed in the recent 2018 sixth World Symposium. For the sake of uniformity, an attempt to adapt the adult classification to pediatric patients was made. However, all these commendable classifications are very complex and maybe not of quick comprehension for clinicians. A clinical simpler and simplified method is now suggested, comprising only five groups: neonatal, cardiac, developmental, idiopathic, and syndromic PH. This approach is not aimed at replacing the already existing classifications but is mainly based on the kind of specialized physician (neonatologist, pediatric cardiologist, pediatrician, pulmonologist, general practitioner) who first faces and looks after the child with suspected PH. What is dramatically known is that pediatric PH is a severe disease which, when untreated or undertreated, may lead to increased morbidity and mortality.
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