Using a human cardiovascular-respiratory model to characterize cardiac tamponade and pulsus paradoxus

Ramachandran, Deepa; Luo, Chi‐Cheng; Tony, S.; Clark, John W.

doi:10.1186/1742-4682-6-15

Cited by 13 publications

(14 citation statements)

References 51 publications

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“…There are also many other studies using various models to simulate pulsus paradoxus and try to disclose its mechanism [22]–[26]. In common with our study, most of these studies have noticed the important role of septal swing in the occurance of pulsus paradoxus.…”

Section: Discussionsupporting

confidence: 82%

“…In common with our study, most of these studies have noticed the important role of septal swing in the occurance of pulsus paradoxus. Ramachandran et al [22] used their complex H-CRS model to simulate hemodynamic and respiratory changes associated with tamponade clinically, focusing particularly on the role of the interventricular septum. Their study showed that pulsus paradoxus was a multifactorial phenomenon which is related with septal motion, atrioventricular and right-left ventricular interactions, pulmonary blood pooling, and the depth of respiration.…”

Section: Discussionmentioning

confidence: 99%

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Mechanism Study of Pulsus Paradoxus Using Mechanical Models

et al. 2013

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Pulsus paradoxus is an exaggeration of the normal inspiratory decrease in systolic blood pressure. Despite a century of attempts to explain this sign consensus is still lacking. To solve the controversy and reveal the exact mechanism, we reexamined the characteristic anatomic arrangement of the circulation system in the chest and designed these mechanical models based on related hydromechanic principles. Model 1 was designed to observe the primary influence of respiratory intrathoracic pressure change (RIPC) on systemic and pulmonary venous return systems (SVR and PVR) respectively. Model 2, as an equivalent mechanical model of septal swing, was to study the secondary influence of RIPC on the motion of the interventriclar septum (IVS), which might be the direct cause for pulsus paradoxus. Model 1 demonstrated that the simulated RIPC had different influence on the simulated SVR and PVR. It increased the volume of the simulated right ventricle (SRV) when the internal pressure was kept constant (8.16 cmH2O), while it had the opposite effect on PVR. Model 2 revealed the three major factors determining the respiratory displacement of IVS in normal and different pathophysiological conditions: the magnitude of RIPC, the pressure difference between the two ventricles and the intrapericardial pressure. Our models demonstrate that the different anatomical arrangement of the two venous return systems leads to a different effect of RIPC on right and left ventricles, and thus a pressure gradient across IVS that tends to shift IVS left- and rightwards. When the leftward displacement of IVS reaches a considerable amplitude in some pathologic condition such as cardiac tamponade, the pulsus paradoxus occurs.

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Section: Discussionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Mechanism Study of Pulsus Paradoxus Using Mechanical Models

et al. 2013

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“…There are also many other studies using various models to simulate pulsus paradoxus and try to disclose its mechanism [22][23][24][25][26]. In common with our study, most of these studies have noticed the important role of septal swing in the occurance of pulsus paradoxus.…”

Section: Previous Studies and Theories About The Mechanism Of Pulsus supporting

confidence: 59%

Mechanism Study of Pulsus Paradoxus Using Mechanical Models

Cao

Xing

Yuan

et al. 2013

Ultrasound in Medicine & Biology

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Pulsus paradoxus is an exaggeration of the normal inspiratory decrease in systolic blood pressure. Despite a century of attempts to explain this sign consensus is still lacking. To solve the controversy and reveal the exact mechanism, we reexamined the characteristic anatomic arrangement of the circulation system in the chest and designed these mechanical models based on related hydromechanic principles. Model 1 was designed to observe the primary influence of respiratory intrathoracic pressure change (RIPC) on systemic and pulmonary venous return systems (SVR and PVR) respectively. Model 2, as an equivalent mechanical model of septal swing, was to study the secondary influence of RIPC on the motion of the interventriclar septum (IVS), which might be the direct cause for pulsus paradoxus. Model 1 demonstrated that the simulated RIPC had different influence on the simulated SVR and PVR. It increased the volume of the simulated right ventricle (SRV) when the internal pressure was kept constant (8.16 cmH 2 O), while it had the opposite effect on PVR. Model 2 revealed the three major factors determining the respiratory displacement of IVS in normal and different pathophysiological conditions: the magnitude of RIPC, the pressure difference between the two ventricles and the intrapericardial pressure. Our models demonstrate that the different anatomical arrangement of the two venous return systems leads to a different effect of RIPC on right and left ventricles, and thus a pressure gradient across IVS that tends to shift IVS left-and rightwards. When the leftward displacement of IVS reaches a considerable amplitude in some pathologic condition such as cardiac tamponade, the pulsus paradoxus occurs.

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“…Both parallel and series biventricular interdependence mechanisms should contribute to decrease left ventricle filling and hence to decrease LVSV at inspiration if the left ventricle is preload-dependent. RAMACHANDRAN et al [36] used a human cardiovascular-respiratory system model that simulates haemodynamic and respiratory changes associated with tamponade clinically. They showed that both the parallel and series interactions have an equal and significant contribution to LVSV respiratory variation, and hence to pulsus paradoxus.…”

Section: Pulsus Paradoxus In Cardiac Tamponadementioning

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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Using a human cardiovascular-respiratory model to characterize cardiac tamponade and pulsus paradoxus

Cited by 13 publications

References 51 publications

Mechanism Study of Pulsus Paradoxus Using Mechanical Models

Mechanism Study of Pulsus Paradoxus Using Mechanical Models

Mechanism Study of Pulsus Paradoxus Using Mechanical Models

Pulsus paradoxus

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