Intrathoracic Pressure Swings Research Articles

Exploring the complexity of obstructive sleep apnea: findings from machine learning on diagnosis and predictive capacity of individual factors.

Obstructive sleep apnoea (OSA) is a prevalent sleep disorder characterized by pharyngeal airway collapse during sleep, leading to intermittent hypoxia, intrathoracic pressure swings, and sleep fragmentation. OSA is associated with various comorbidities and risk factors, contributing to its substantial economic and social burden. Machine learning (ML) techniques offer promise in predicting OSA severity and understanding its complex pathogenesis. This study aims to compare the accuracy of different ML techniques in predicting OSA severity and identify key associated factors contributing to OSA. Adult patients suspected of OSA underwent clinical assessments and polysomnography. Demographic, anthropometric and clinical data were collected. Five supervised ML models (logistic regression, decision tree, random forest, extreme gradient boosting, support vector machine) were employed, optimized through grid search and cross-validation. ML models exhibited varied performance across OSA severity levels. SVM demonstrated the highest accuracy for mild OSA, XGBoost for moderate OSA, and random forest for severe OSA. Logistic regression showed the highest AUC for moderate and severe OSA. Anthropometric measures, gender, and hypertension were significant predictors of OSA severity. ML models offer valuable insights into predicting OSA severity and identifying associated factors. Our findings support the relevant potential clinical utility of ML in OSA management, although further validation and refinement are warranted.

Incorporating intrathoracic pressure fluctuation can improve noninvasive prediction of left ventricular end-diastolic pressure

Abstract Introduction Heart failure (HF) is a leading cause of mortality and morbidity, with a prevalence above 10% in elderly population (1). Left ventricular end-diastolic pressure (LVEDP) is a known indicator for all types of HF. An invasive pressure catheter is the gold standard for measuring LVEDP (2). However, it involves an in-hospital procedure and is costly, which limits the accessibility. A noninvasive strategy would improve early diagnosis and reduce the burden on secondary care. Several noninvasive classifiers are able to detect elevated LVEDP (3-5), with some receiving FDA clearance (6). While beneficial for triaging patients, these classifiers cannot quantify the severity and track disease progression. Developing a noninvasive LVEDP regression model requires accounting for respiration dynamics. Even invasively, the dynamics make measuring LVEDP challenging. This study uses an error metric from ANSI/AAMI/ISO 81060-2:2019 (AAMI) (7) to evaluate the effect of respiration on noninvasive LVEDP regression results. Methods The dataset (147 patients, 21+ yrs old, mean 65 ± 10 yrs; 68% male) consisted of patients referred for nonemergent left heart catheterisation inclusive of direct assessment of LVEDP. Noninvasive data was collected by a modified brachial cuff with a single-lead electrocardiogram (ECG). Invasive data was acquired using a Millar pressure catheter. LVEDP was derived based on the time of the R-wave of the ECG (8). For each patient, 40 secs of noninvasive data with synchronised catheter signals were analysed to build an LVEDP regression model. Inputs were generated from the ECG and brachial pressure waves based on fiducials identified in both signals. Leave-one-subject-out cross-validation (LOSO CV) was used to train and test the algorithm. The impact of respirophasic variation on the model was analysed by comparing the prediction with the mean LVEDP and the range of the mean ± standard deviation (std) (i.e. AAMI error metric). Results The results, evaluated using Bland-Altman and correlation analysis, showed a decrease in the mean absolute error (MAE) from 3.6 mmHg to 1.4 mmHg, the std from 4.9 mmHg to 3.0 mmHg, and the correlation (r) from 0.57 to 0.77 when incorporating intrathoracic pressure swings (Fig.1 and Fig.2). A Levene test on the residuals of the two error determinations showed a significant difference (p-value < 0.01). Conclusion Irrespective of the error metric, the model performance meets the AAMI standard for blood pressure (BP) measurement. Moreover, when respiratory motion is included, agreement with invasive LVEDP improves considerably. From a clinical perspective, this emphasises the importance of targeting end-expiratory LVEDP. With respect to noninvasive BP measurement, it suggests that both brachial BP evaluation and LVEDP prediction should attempt to quantify fluctuations. While the challenge remains, these results indicate that noninvasive LVEDP prediction could be realised in the near future.Fig.1 Prediction vs mean LVEDP.Fig. 2 Prediction vs mean +/- std.

Discovering the Clinical Relevance of Heart-Lung Interactions.

In 1978, Dr. Pinsky's scientific career became firmly directed toward understanding the deeper meaning of heart-lung interactions. This would define his focus for the next 45 yr. At the time, he and colleagues studied the effects of changes in intrathoracic pressure on left ventricular performance in humans, documenting that the primary effect of large negative swings in intrathoracic pressure was to increase left ventricular transmural ejection pressure, and thus left ventricular afterload, selectively. They concluded that large intrathoracic pressure changes directly influence cardiac performance. This fundamental observation was followed by many additional observations in both highly invasive animal studies supported by less invasive clinical studies, which showed that intrathoracic pressure-induced changes in the gradients for venous return to the heart and left ventricular ejection from the heart disproportionately affected both right ventricular and left ventricular function. The direct clinical implications of these results form the rationale for use of continuous positive airway pressure as a primary treatment of acute cardiogenic pulmonary edema and immediate endotracheal intubation for acute upper airway obstruction. These findings subsequently led to the practical use of dynamic changes in left ventricular stroke volume and the associated arterial pulse pressure during positive-pressure ventilation to identify volume responsiveness and, thus, to personalize resuscitation efforts in the treatment of acute cardiovascular insufficiency.

Cardio-respiratory interactions in acute asthma.

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

Cardiopulmonary interactions in left heart failure.

The primary impact of ventilation and ventilatory efforts on left ventricular (LV) function in left ventricular dysfunction relate to how changes in intrathoracic pressure (ITP) alter the pressure gradients for venous return into the chest and LV ejection out of the chest. Spontaneous inspiratory efforts by decreasing ITP increase both of these pressure gradients increasing venous blood flow and impeding LV ejection resulting in increased intrathoracic blood volume. In severe heart failure states when lung compliance is reduced, or airway resistance is increased these negative swings in ITP can be exacerbated leading to LV failure and acute cardiogenic pulmonary edema. By merely reversing these negative swings in ITP by the use of non-invasive continuous positive airway pressure (CPAP), these profoundly detrimental forces can be immediately reversed, and cardiovascular stability can be restored in moments. This forms the clinical rationale for the immediate use of CPAP for the treatment of acute cardiogenic pulmonary edema. Increasing ITP during positive pressure ventilation decreases the pressure gradients for venous return and LV ejection decreasing intrathoracic blood volume. In a hypovolemic patient even with LV dysfunction this can result in hypotension due to inadequate LV preload. Minor increases in ITP as occur using pressure-limited positive-pressure ventilation primarily reverse the increased LV afterload of negative swings in ITP and if fluid overload was already present, minimally alter cardiac output. The effect of changes in lung volume on LV function are related primarily to its effects on right ventricular (RV) function through changes in pulmonary vascular resistance and overdistention (hyperinflation). In acute lung injury with alveolar collapse, positive pressure ventilation may reduce pulmonary vascular resistance if alveolar recruitment predominates. Hyperinflation, however, impedes diastolic filling while simultaneously increasing pulmonary vascular resistance. Thus, increasing lung volume can reduce RV afterload by reversing hypoxic pulmonary vasoconstriction or increase afterload by overdistention. Hyperinflation can also impede RV filling. All of these processes can be readily identified at the bedside using echocardiography.

Effect of Continuous Positive Airway Pressure Therapy in Patient with Obstructive Sleep Apnea and Pulmonary Hypertension: A literature review.

Patients with obstructive sleep apnea (OSA) and pulmonary hypertension (PH) have a reduced functional capacity and potential survival. Continuous positive airway pressure (CPAP) is the primary treatment for OSA, and this improves sleep parameters, functional activity, and possibly pulmonary artery pressures (PAPs). This literature review summarizes the available studies that have measured changes in PAPs in patients with sleep apnea following the institution of CPAP. The PubMed.gov database was searched with a combination of keywords including: "Pulmonary Hypertension," "Obstructive Sleep Apnea," and "Continuous Positive Airway Pressure." Specific inclusion and exclusion criteria were applied to select prospective studies, and data were carefully extracted from each study. Seven unique studies were identified from a list of 272 search results. The studies included a range of CPAP treatments; all showed significant improvement in PAP. The average improvement in PAP across all studies when weighted for a number of participants was 9.33 ± 7.71 mm Hg. This systematic literature review demonstrates that CPAP treatment reduces PAPs in patients with OSA. The study intervals ranged from 48 hours to 6 months to determine the effects of CPAP on PH in these patients. The literature review undertaken during the analysis of these original studies on OSA and PH provides information about vascular remodeling during OSA and the effect of apnea on O2 saturation, intrathoracic pressure swings, and sympathetic surges post apnea. Patients with OSA frequently have significant comorbidity, including hypertension, obesity, and overlap syndromes with other pulmonary disorders and/or cardiac disorders. This comorbidity increases the complexity of management and likely contributes to poor outcomes. The gold standard for making a diagnosis of PH requires right heart catheterization, but practical issues dictate the need for frequent echocardiograms to evaluate right ventricular systolic pressures and right atrial and ventricle chamber sizes. A better understanding of the association between OSA and PH and its treatment with CPAP will require long-term perspective studies.

Differences in the respiratory swings in COPD and ILD candidates for lung transplantation: a critical concern interpreting central pulmonary pressures

Abstract Background In different clinical scenarios (i.e., obesity, COPD, exercise, mechanical ventilation), the swings in intrathoracic pressure are much larger, and end-expiratory (Pee) pressure can be significantly greater than atmospheric pressure. In these scenarios, the intravascular (Piv) pulmonary pressure can overestimate the true transmural (tm) value and it is recommended to read the average of Piv over a few respiratory cycles (Pmrc) [1–3]. Purpose To analyze the respiratory swings and the effect of esophageal pressure (PES) (as a surrogate of intrathoracic pressure) on the reading of Piv tracings during the RHC at rest in COPD and interstitial lung disease (ILD) candidates for lung transplantation (LTx). Methods Thirty-one COPD (15) and ILD (16) candidates for LTx underwent RHC. End-expiratory and mean respiratory cycle measurements were obtained. The respiratory swing was estimated as the difference between maximum-minimum values of Piv. Ten patients (5 COPD/5 ILD) underwent simultaneous RHC and PES (Micro-balloon Esophageal Catheter, LATITUDE) to assess the Ptm (Piv − PES) [4]. Results Both demographic (11F/20M, 60±7 yrs, 25±4 kg/m2) and hemodynamic data (mPAP 24±9 mmHg, pulmonary arterial occlusion pressure [PAOP] 8.6±4 mmHg, right atrial pressure [RAP] 5.2±3.9 mmHg, pulmonary vascular resistance 3.5±2.6 Wu) did not show significant differences between ILD and COPD except the cardiac index (ILD: 2.8±0.8 vs. COPD: 2.4±0.3 L/min/m2). Intravascular RAPee and PAOPee were higher than mrc values in both groups (Fig 1). However, transmural RAPee and PAOPee were similar to and correlated with (r=0.62 and 0.69, respectively; p<0.05) transmural Pmrc values. PESee values were positive in COPD and ILD (3.0±2.2 vs. 3.3±2.0 mmHg, NS). All ILD had negative PESmrc values and were lower than COPD patients (−1.76±1.7 vs. 0.78±1.6 mmHg, p<0.05). ILD PES swings were higher than COPD (10.9±3.7 vs. 8.3±1.4 mmHg), although it did not reach statistical significance (p=0.08). The lower forced vital capacity (%), the more negative the PESmrc (Fig 2A). ILD pts showed higher transmural to intravascular Pmrc (p<0.05) (Fig 2B). Conclusion End-expiratory intravascular RAP and PAOP overestimates the mean respiratory cycle pressures in COPD and ILD candidates for LTx. Averaging pulmonary vascular pressure tracings over the respiratory cycle would be accurate in COPD but could underestimate transmural values in ILD candidates for LTx. The reading of mean respiratory cycle pressure could not be enough to correct the pulmonary pressures measurement error associated with the presence of large swings of intrathoracic pressure. Funding Acknowledgement Type of funding sources: None.

Association between obstructive sleep apnea and cardiovascular diseases.

Obstructive sleep apnea (OSA) is a common respiratory disorder characterized by partial obstruction of upper respiratory tract and repetitive cessation of breathing during sleep. The etiology behind OSA is associated with the occurrence of intermittent hypoxemia, recurrent arousals and intrathoracic pressure swings. These contributing factors may turn on various signaling mechanisms including elevated sympathetic tone, oxidative stress, inflammation, endothelial dysfunction, cardiovascular variability, abnormal coagulation and metabolic defect ( e.g., insulin resistance, leptin resistance and altered hepatic metabolism). Given its close tie with major cardiovascular risk factors, OSA is commonly linked to the pathogenesis of a wide array of cardiovascular diseases (CVDs) including hypertension, heart failure, arrhythmias, coronary artery disease, stroke, cerebrovascular disease and pulmonary hypertension (PH). The current standard treatment for OSA using adequate nasal continuous positive airway pressure (CPAP) confers a significant reduction in cardiovascular morbidity. Nonetheless, despite the availability of effective therapy, patients with CVDs are still deemed highly vulnerable to OSA and related adverse clinical outcomes. A better understanding of the etiology of OSA along with early diagnosis should be essential for this undertreated disorder in the clinical setting.

0854 A case of complete heart block in a patient with severe obstructive sleep apnea

Abstract Introduction Obstructive sleep apnea (OSA) has been associated with bradycardic arrythmias and cases of transient heart block. Heart block occurring during sleep has been described in up to 10% of patients with obstructive sleep apnea, most commonly during stage R sleep and through a mechanism known as vagal activation. Stage R sleep is associated with desynchronization of respiratory and cardiovascular functions, and the excessive autonomic response (vagal activation) occurs due to the stronger stimulation of chemoreceptors and baroreceptors induced by hypoxemia, intrathoracic pressure swings, and hemodynamic alterations. Treatment of the underlying sleep-disordered breathing will typically treat the bradycardic arrythmia as well. Report of Cases: A 49-year-old male with a BMI of 30 kg/m , neck circumference of 16 inches, and obstructive sleep apnea presented to the sleep center to establish care for management of his preexisting OSA. He was previously diagnosed with moderate OSA in 2007 but had discontinued therapy shortly after due to Continuous Positive Airway Pressure (CPAP) intolerance. The patient complained of snoring, nocturia, and excessive daytime sleepiness (18/24 on Epworth Sleepiness Scale). During the split night study, the patient was noted to have 2:1 second degree heart block followed by a transient episode of complete heart block, manifested by 4 non-conducted p-waves. The patient remained asymptomatic throughout the night. Upon study completion, the patient denied any prior chest pain, presyncope, syncope, or medications that might cause heart block. Conclusion Bradyarrythmias can be seen in severe obstructive sleep apnea in the setting of excessive vagal stimulation through increased stimulation of chemoreceptors and baroreceptors. Treatment with PAP therapy can lead to prevention of heart block in 80-90% of these patients. Support (If Any)

OSA and Chronic Respiratory Disease: Mechanisms and Epidemiology.

Obstructive sleep apnea (OSA) is a highly prevalent disorder that has profound implications on the outcomes of patients with chronic lung disease. The hallmark of OSA is a collapse of the oropharynx resulting in a transient reduction in airflow, large intrathoracic pressure swings, and intermittent hypoxia and hypercapnia. The subsequent cytokine-mediated inflammatory cascade, coupled with tractional lung injury, damages the lungs and may worsen several conditions, including chronic obstructive pulmonary disease, asthma, interstitial lung disease, and pulmonary hypertension. Further complicating this is the sleep fragmentation and deterioration of sleep quality that occurs because of OSA, which can compound the fatigue and physical exhaustion often experienced by patients due to their chronic lung disease. For patients with many pulmonary disorders, the available evidence suggests that the prompt recognition and treatment of sleep-disordered breathing improves their quality of life and may also alter the course of their illness. However, more robust studies are needed to truly understand this relationship and the impacts of confounding comorbidities such as obesity and gastroesophageal reflux disease. Clinicians taking care of patients with chronic pulmonary disease should screen and treat patients for OSA, given the complex bidirectional relationship OSA has with chronic lung disease.

Sleep apnea and atrial fibrillation: the spell of Groundhog Day.

Sleep apnea and atrial fibrillation: the spell of Groundhog Day.

Chapter 15 - Sleep and breathing disorders in heart failure

Sleep disorders are prevalent in heart failure and include insomnia, poor sleep architecture, periodic limb movements and periodic breathing, and encompass both obstructive (OSA) and central sleep apnea (CSA). Polysomnographic studies show excess light sleep and poor sleep efficiency particularly in those with heart failure. Multiple studies of consecutive patients with heart failure show that about 50% of patients suffer from either OSA or CSA. While asleep, acute pathological consequences of apneas and hypopneas include altered blood gases, sleep fragmentation, and large negative swings in intrathoracic pressure. These pathological consequences are qualitatively similar in both types of sleep apnea, though worse in OSA than CSA. Sleep apnea results in oxidative stress, inflammation, and endothelial dysfunction, best documented in OSA. Multiple studies show that both OSA and CSA are associated with excess hospital readmissions and premature mortality. However, no randomized controlled trial (RCT) has been reported for OSA, but sensitivity analysis of two randomized controlled trials has concluded that use of positive airway pressure devices is associated with excess mortality in patients with heart failure and CSA. Phrenic nerve stimulation has shown improvement in sleep apnea events and daytime sleepiness; however, no randomized controlled trials have demonstrated improvement in survival in patients with heart failure. The correct identification and treatment of heart failure patients with sleep and breathing disorders could affect the long-term outcomes of these patients.

Cardiovascular manifestations in obstructive sleep apnea: current evidence and potential mechanisms.

Obstructive sleep apnea (OSA) is an increasingly prevalent health concern characterized by repeated episodes of pharyngeal collapse during sleep. It is frequently associated with daytime sleepiness and impaired functional capacity, but it is also linked to cardiovascular disease by a growing body of epidemiological, clinical, and translational research. The severity of OSA is traditionally evaluated by the apnea‑hypopnea index (AHI), but the value of this marker as a predictor of cardiovascular outcomes is limited. Thus, there is an increasing focus on alternative classification methods such as the hypoxic burden, other polysomnographic traits, and phenotypic subgroups based on clinical symptoms. There is a need to identify subgroups of patients with OSA who will benefit most from treatment, as recent large randomized controlled trials in selected populations have failed to show benefit in reducing overall cardiovascular mortality. Obstructive sleep apnea adversely affects cardiovascular structure and function by several distinct mechanisms such as intermittent hypoxia, sleep fragmentation, and intrathoracic pressure swings. These mechanisms lead to sympathetic activation, inflammation, and oxidative stress, which may result in the clinical consequences of OSA such as hypertension, coronary artery disease, heart failure, and cerebrovascular disease. This review focuses on the epidemiology and potential mechanisms of cardiovascular diseases in OSA. Furthermore, we will briefly discuss the role of personalized medicine, alternative treatment options, and precise phenotyping to optimize treatment of this complex condition and its associated cardiovascular risk.

Priming the cardiodynamic phase of pulmonary oxygen uptake through voluntary modulations of the respiratory pump at the onset of exercise.

What is the central question of this study? The initial increase in oxygen uptake ( ) at exercise onset results from pulmonary perfusion changes secondary to an increased venous return. Breathing mechanics contribute to venous return through abdominal and intrathoracic pressures variation. Can voluntary breathing techniques (abdominal or rib cage breathing) increase venous return and improve at exercise onset? What is the main finding and its importance? Abdominal and rib cage breathing increase venous return and at exercise onset. This mechanism could be clinically relevant in patients with impaired cardiac function limiting oxygen transport. We examined how different breathing patterns can modulate venous return and alveolar gas transfer during exercise transients in humans. Ten healthy men transitioned from rest to moderate cycling while breathing spontaneously (SP) or with voluntary increases in abdominal (AB) or intrathoracic (RC) pressure swings. We used double body plethysmography to determine blood displacements between the trunk and the extremities (Vbs ). From continuous signals of airflow and O2 fraction, we calculated breath-by-breath oxygen uptake at the mouth and used optoelectronic plethysmography to correct for lung O2 store changes and calculate alveolar O2 transfer ( ). Oesophageal (Poes ) and gastric (Pga ) pressures were monitored using balloon-tipped catheters. Cardiac stroke volume was measured using impedance cardiography. During the cardiodynamic phase (Φ1) of -on kinetics (20s following exercise onset), AB and RC increased total alveolar oxygen transfer compared to SP (227±32, P=0.019 vs. 235±27, P=0.001 vs. 206±20ml, mean±SD). Pga and Poes swings increased with AB (by 24.4±9.6cmH2 O, P<0.001) and RC (by 14.5±5.7cmH2 O, P<0.001), respectively. AB yielded a greater increase in intra-breath Vbs swings compared with RC and SP (+0.30±0.14 vs. +0.16±0.11, P<0.001 vs. +0.10±0.05ml, P=0.006) and increased the sum of stroke volumes compared to SP (4.47±1.28 vs. 3.89±0.96litres, P=0.053), while RC produced significant central blood translocation from the extremities compared with SP (by 493±311ml, P<0.001). Our findings indicate that combining exercise onset with AB or RC increases venous return, thus increasing mass oxygen transport above metabolic consumption during Φ1 and limiting the oxygen deficit incurred.

When will we ditch the AHI?

When will we ditch the AHI?

Obstructive sleep apnoea but not central sleep apnoea is associated with left ventricular remodelling after acute myocardial infarction

ObejctiveObstructive sleep apnoea (OSA) increases left ventricular transmural pressure more than central sleep apnoea (CSA) owing to negative intrathoracic pressure swings. We tested the hypothesis that the severity of OSA, and not CSA, is therefore associated with spheric cardiac remodelling after acute myocardial infarction.MethodsThis sub-analysis of a prospective observational study included 24 patients with acute myocardial infarction who underwent primary percutaneous coronary intervention. Spheric remodelling, calculated according to the sphericity index, was assessed by cardiac magnetic resonance imaging at baseline and 12 weeks after acute myocardial infarction. OSA and CSA [apnoea-hypopnoea index (AHI) ≥ 5/hour] were diagnosed by polysomnography.ResultsWithin 12 weeks after acute myocardial infarction, patients with OSA exhibited a significant increase in systolic sphericity index compared to patients without sleep-disordered breathing (no SDB) and patients with CSA (OSA vs. CSA vs. no SDB: 0.05 ± 0.04 vs. 0.01 ± 0.04 vs. − 0.03 ± 0.03, p = 0.002). In contrast to CSA, the severity of OSA was associated with an increase in systolic sphericity index after accounting for TIMI-flow before percutaneous coronary intervention, infarct size, pain-to-balloon-time and systolic blood pressure [OSA: B (95% CI) 0.443 (0.021; 0.816), p = 0.040; CSA: 0.193 (− 0.134; 0.300), p = 0.385].ConclusionIn contrast to CSA and no SDB, OSA is associated with spheric cardiac remodelling within the first 12 weeks after acute myocardial infarction. Data suggest that OSA-related negative intrathoracic pressure swings may contribute to this remodelling after acute myocardial infaction.Graphic abstract

Prolonged respiratory failure due to pulmonary embolism in a young woman: a case report

BackgroundThe pathophysiology of pulmonary edema is generally considered to result from elevated pulmonary capillary hydrostatic pressure due to increased left atrial pressure in consequence of a failing left ventricle.Case presentationWe present a case of pulmonary edema secondary to severe hypalbuminemia under excessive respiratory drive in a 29-year-old Caucasian woman in respiratory distress with detected bilateral central pulmonary embolism.ConclusionIn conjunction with severe hypalbuminemia, even the negative intrathoracic pressure swings of respiratory distress may cause pulmonary edema. Detrimental consequences of non-invasive ventilation due to uncontrolled tidal volume and pressure swings need to be considered when treating patients in hypoxemic respiratory failure with low serum albumin.

Sleep Disordered Breathing and Cardiovascular Diseases.

Sleep disordered breathing (SDB), which causes sleep deprivation, intermittent hypoxia, and negative intrathoracic pressure swings, can be accompanied by other harmful pathophysiologies relating to cardiovascular diseases (CVD), including sudden death, atrial fibrillation, stroke, and coronary artery disease leading to heart failure. Continuous positive airway pressure (CPAP) therapy for SDB has been reported to provide favorable effects such as lowered systemic blood pressure and improved endothelial function. However, in recent randomized controlled trials, CPAP has failed to demonstrate its beneficial prognostic impact on the primary or secondary setting of CVD. In this review article, we describe the characteristics of SDB complicated with CVD, the prognostic impacts of SDB in CVD, and the beneficial effects of CPAP on CVD.

CON: Persistent Central Sleep Apnea/Hunter-Cheyne-Stokes Breathing, Despite Best Guideline-Based Therapy of Heart Failure With Reduced Ejection Fraction, Is Not a Compensatory Mechanism and Should Be Suppressed.

CON: Persistent Central Sleep Apnea/Hunter-Cheyne-Stokes Breathing, Despite Best Guideline-Based Therapy of Heart Failure With Reduced Ejection Fraction, Is Not a Compensatory Mechanism and Should Be Suppressed.

Expiratory central airway collapse in stable COPD and during exacerbations

BackgroundTracheal obstruction resulting from expiratory tracheal deformation has been associated with respiratory symptoms and severe airway exacerbations. In chronic obstructive pulmonary disease (COPD), acute exacerbations (AECOPD) create large intrathoracic pressure swings which may increase tracheal deformation. Excessive central airway collapse (ECAC) may be diagnosed when the tracheal area on expiration is less than 50% of that on inspiration. The prevalence of ECAC in AECOPD and its temporal course have not been systematically studied.MethodsWe prospectively recruited healthy volunteers (n = 53), stable outpatients with COPD (n = 40) and patients with hospitalised acute exacerbations of COPD (AECOPD, n = 64). 17 of the AECOPD group returned for repeat evaluation when clinically well at 6–12 weeks. All subjects underwent dynamic 320-slice computed tomography of the larynx and trachea during tidal breathing, enabling quantitation of tracheal area and dimensions (mean ± SD).ResultsNo healthy individuals had ECAC. The prevalence of ECAC in stable COPD and AECOPD was 35% and 39% respectively. Mean tracheal collapse did not differ between stable COPD (57.5 ± 19.8%), AECOPD (53.8 ± 19.3%) and in the subset who returned when convalescent (54.9 ± 17.2%). AECOPD patients with and without ECAC had similar clinical characteristics.ConclusionsTracheal collapse in both stable and AECOPD is considerably more prevalent than in healthy individuals. ECAC warrants assessment as part of comprehensive COPD evaluation and management. Further studies should evaluate the aetiology of ECAC and whether it predisposes to exacerbations.