Echocardiographic study of the paradoxical arterial pulse in chronic obstructive lung disease.

Settle, Harold P.; Engel, Peter J.; Fowler, Noble O.; Allen, J. M.; Vassallo, Charles L.; Hackworth, J N; Adolph, Robert J.; Eppert, D. C.

doi:10.1161/01.cir.62.6.1297

Cited by 45 publications

(16 citation statements)

References 28 publications

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“…SETTLE et al [30], studying stable COPD patients, observed an increase in RV dimension during inspiration associated with a reduction in LV dimensions. Similarly, JARDIN and co-workers [31], studying mild acute exacerbation of COPD, found increased RV dimensions when compared to a control group.…”

Section: Effects Of Peepi On Cardiopulmonary Interaction During Weaningmentioning

confidence: 98%

Intrinsic PEEP and cardiopulmonary interaction in patients with COPD and acute ventilatory failure

Dambrosio¹,

Brienza²

1996

Eur Respir J

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Intrinsic PEEP and cardiopulmonary interaction in patients with COPD and acute ventilatory failure. V.M. Ranieri, M. Dambrosio, N. Brienza. ERS Journals Ltd 1996. ABSTRACT: Deviation of end-expiratory lung volume from the elastic equilibrium volume of the respiratory system is recognized as a cardinal feature in mechanically-ventilated patients with severe chronic obstructive pulmonary disease (COPD) and acute ventilatory failure (AVF). The presence of dynamic hyperinflation implies that alveolar pressure remains positive throughout expiration. At the end of the expiration, this positive pressure is named intrinsic positive end-expiratory pressure (PEEPi).Recent studies have suggested that, in COPD patients with expiratory flow limitation, the application of external PEEP during assisted mechanical ventilation, or the use of continuous positive airway pressure (CPAP) in spontaneously breathing patients, can counterbalance and reduce the inspiratory threshold load imposed by PEEPi, without causing further increase in lung volume and alveolar and intrathoracic pressures until a critical value of PEEP (Pcrit) is reached. Above this critical limit further hyperinflation is observed.A specific and characteristic role of PEEPi in compromising the heart function in COPD patients during AVF may be identified based on: 1) an increase in right ventricular impedance due to lung hyperinflation; 2) an increase in the venous return to the right ventricle and, consequently, a leftward shift of the septum caused by the large negative deflections in intrathoracic pressure due to the inspiratory threshold load; 3) a further increase in venous return to the right ventricle, with the eventual collapse of the vena cava caused by the expiratory recruitment of abdominal muscles; and 4) hypoxia and hypercapnia consequent to acute ventilatory failure, which may further increase right ventricular impedance and venous return to the right ventricle.All these phenomenon are directly correlated to the large negative intrathoracic pressure developed by the respiratory muscles to overcome the inspiratory threshold caused by intrinsic positive end-expiratory pressure (preload effect), and to the increase in lung volume (afterload effect). Application of positive end-expiratory pressure/continuous positive airway pressure in chronic obstructive pulmonary disease patients during acute ventilatory failure may, hence, unload the respiratory muscles as well as the heart. Eur Respir J., 1996Respir J., , 9, 1283Respir J., -1292

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Section: Effects Of Peepi On Cardiopulmonary Interaction During Weaningmentioning

confidence: 98%

Intrinsic PEEP and cardiopulmonary interaction in patients with COPD and acute ventilatory failure

Dambrosio¹,

Brienza²

1996

Eur Respir J

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“…In addition, right ventricular afterload should increase during inspiration (breathing at high lung volume). During acute exacerbation of COPD, where the right ventricle can already be enlarged, combination of increased right ventricular preload and increased right ventricular afterload during inspiration should result in a marked parallel biventricular interdependence phenomenon, as demonstrated by SETTLE et al [32] in an electrocardiographic study. This can contribute to the development of pulsus paradoxus during acute exacerbation of COPD.…”

Section: Pulsus Paradoxus In Acute Asthmamentioning

confidence: 88%

“…The reduction in left ventricular preload during inspiration, which is thus the most plausible explanation, could be due: either to 1) series ventricular interaction (see above), making the right and left ventricles 180u out of phase; 2) reduction in left ventricular diastolic time related to the increased heart rate accompanying inspiration; or 3) the parallel ventricular interdependence phenomenon. However, it is unlikely that the latter mechanism is significant in the absence of pericardial constraint or of right ventricle overdistension during normal inspiration [32]. Another possible mechanism could be an inspiratory pulmonary venous blood pooling, related to the fact that pulmonary vessels are supposed to be more compliant than the left ventricle [25,33].…”

Section: Mechanisms Of Pulsus Paradoxusmentioning

confidence: 99%

Pulsus paradoxus

2012

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Systolic blood pressure normally falls during quiet inspiration in normal individuals. Pulsus paradoxus is defined as a fall of systolic blood pressure of .10 mmHg during the inspiratory phase. Pulsus paradoxus can be observed in cardiac tamponade and in conditions where intrathoracic pressure swings are exaggerated or the right ventricle is distended, such as severe acute asthma or exacerbations of chronic obstructive pulmonary disease. Both the inspiratory decrease in left ventricular stroke volume and the passive transmission to the arterial tree of the inspiratory decrease in intrathoracic pressure contribute to the occurrence of pulsus paradoxus. During cardiac tamponade and acute asthma, biventricular interdependence (series and parallel) plays an important role in the inspiratory decrease in left ventricular stroke volume.Early recognition of pulsus paradoxus in the emergency room can help to diagnose rapidly cardiac tamponade. Measurement of pulsus paradoxus is also useful to assess the severity of acute asthma as well as its response to therapy. Recent development of noninvasive devices capable of automatic calculation and display of arterial pressure variation or derived indices should help improve the assessment of pulsus paradoxus at the bedside.

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“…Moreover, it was previously demonstrated via magnetic resonance angiography that the pulmonic vein area of patients with COPD is smaller, suggesting underfilling of their LA [20]. Proposed mechanisms for decreased left side filling in patients with COPD include an altered intrathoracic pressure, increased pulmonary veins resistance, compression of alveolar vessels [20], increased heart rate [19], systemic vasodilation [21], and bulging of the septum due to right heart dilatation [22,23]. Investigating the etiologies of small LA size on CT, Cassagnes et al [6] reported that patients with emphysema had an inverse correlation between LA volume and the severity of emphysema.…”

Section: Discussionmentioning

confidence: 99%

Very Small Left Atrial Volume as a Marker for Mortality in Patients Undergoing Nongated Computed Tomography Pulmonary Angiography

Rozenbaum

Granot²,

Turkeltaub³

et al. 2017

Cardiology

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Objectives: To evaluate the association between very small left atria (VSLA) on nongated computed tomography pulmonary angiography (CTPA) and mortality in patients without pulmonary embolism (PE). Methods: Patients who underwent nongated CTPA between 2011 and 2015 in order to rule out PE, and had an echocardiogram within 24 h of the CTPA, were retrospectively identified. The left atrial volume of nongated CTPA was calculated using automatic 4-chamber volumetric analysis software. The association between the lowest 5th percentile of the left atrial volume index, referred to as the VSLA group, and mortality was investigated after adjustment for age, gender, background diseases, and laboratory values. Results: The study cohort included 241 patients. Patients with VSLA had a left atrial volume index <24 mL/m² (n = 11). Demographics and background diseases did not differ between the study groups. The median follow-up was 22.7 months (IQR 0.03-54.3). VSLA was an independent predictor of mortality (HR_adj = 3.6; 95% CI 1.46-8.87; p = 0.005), along with malignancy (HR_adj = 2.28; 95% CI 1.32-3.93; p = 0.003) and lower hemoglobin (HR_adj = 0.86; 95% CI 0.76-0.99; p = 0.032). Conclusions: Our findings suggest that VSLA on nongated CTPA may serve as a marker for mortality. The use of CTPA volumetric analysis can help risk stratification in patients with dyspnea and no PE.

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Echocardiographic study of the paradoxical arterial pulse in chronic obstructive lung disease.

Cited by 45 publications

References 28 publications

Intrinsic PEEP and cardiopulmonary interaction in patients with COPD and acute ventilatory failure

Intrinsic PEEP and cardiopulmonary interaction in patients with COPD and acute ventilatory failure

Pulsus paradoxus

Very Small Left Atrial Volume as a Marker for Mortality in Patients Undergoing Nongated Computed Tomography Pulmonary Angiography

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