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Mechanism study of pulsus paradoxus using mechanical models.

Xing CY, Cao TS, Yuan LJ, Wang Z, Wang K, Ren HR, Yang Y, Duan YY - PLoS ONE (2013)

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Ultrasound Diagnostics, Tangdu Hospital, Fourth Military Medical University, Xi'an, China.

ABSTRACT
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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The influence of simulated RIPC on the motion of the simulated IVS.Under the simulated RIPC, the simulated IVS is swinging left- and rightwards (down and up in the figure) to correspond the pressure change in SCC. To simulate the in vivo condition where the right ventricle anterior wall and the left ventricle posterior walls are kept in touch with the chest wall, the pressures in SRV, SLV, SCC and SP are adjusted to 4 mmHg, 9 mmHg, 0 mmHg and 0 mmHg respectively. Acuson’s Sequoia 512 ultrasonographic system was used to record the M-mode and two-dimensional cineloops of the simulated IVS’s motion under the simulated RIPC. Total of 150 frames were captured. A. With rhythmic pressure change in SCC, or under the simulated RIPC of 0 to −4mmHg, the IVS swung left- and rightwards at amplitude of 2.2 mm. B and C. These two of the total 150 frames demonstrate the 2D echocardiograms of the end-expiration (B) and end-inspiration (C) phases. Their internal LV diameters are 35.0 and 32.8 mm, respectively. RIPC = respiratory intrathoracic pressure change; PVR = pulmonary venous return system; SVR = systemic venous return system, SCC = simulated chest cavity; SRV = simulated right ventricle, SLV = simulated left ventricle; SP = simulated pericardium, IVS: interventricular septum.
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pone-0057512-g004: The influence of simulated RIPC on the motion of the simulated IVS.Under the simulated RIPC, the simulated IVS is swinging left- and rightwards (down and up in the figure) to correspond the pressure change in SCC. To simulate the in vivo condition where the right ventricle anterior wall and the left ventricle posterior walls are kept in touch with the chest wall, the pressures in SRV, SLV, SCC and SP are adjusted to 4 mmHg, 9 mmHg, 0 mmHg and 0 mmHg respectively. Acuson’s Sequoia 512 ultrasonographic system was used to record the M-mode and two-dimensional cineloops of the simulated IVS’s motion under the simulated RIPC. Total of 150 frames were captured. A. With rhythmic pressure change in SCC, or under the simulated RIPC of 0 to −4mmHg, the IVS swung left- and rightwards at amplitude of 2.2 mm. B and C. These two of the total 150 frames demonstrate the 2D echocardiograms of the end-expiration (B) and end-inspiration (C) phases. Their internal LV diameters are 35.0 and 32.8 mm, respectively. RIPC = respiratory intrathoracic pressure change; PVR = pulmonary venous return system; SVR = systemic venous return system, SCC = simulated chest cavity; SRV = simulated right ventricle, SLV = simulated left ventricle; SP = simulated pericardium, IVS: interventricular septum.

Mentions: In Test 1, with the pressure in the SRV and SLV kept constant (standard pressure condition for model 2), each step of pressure decrease in the SCC from 0 mmHg to −5 mmHg, the simulated IVS moved leftwards (to the SLV direction) in a corresponding position and from 0 mmHg to +5 mmHg, rightwards correspondingly, i.e., it is a corresponding relationship between the pressure in SCC and the position of simulated IVS which we called pressure-position relationship. With rhythmic pressure change in SCC, or under the simulated RIPC of 0 – −4mmHg, the SIVS swung left- and rightwards at amplitude of 2.2 mm (Figure 4).


Mechanism study of pulsus paradoxus using mechanical models.

Xing CY, Cao TS, Yuan LJ, Wang Z, Wang K, Ren HR, Yang Y, Duan YY - PLoS ONE (2013)

The influence of simulated RIPC on the motion of the simulated IVS.Under the simulated RIPC, the simulated IVS is swinging left- and rightwards (down and up in the figure) to correspond the pressure change in SCC. To simulate the in vivo condition where the right ventricle anterior wall and the left ventricle posterior walls are kept in touch with the chest wall, the pressures in SRV, SLV, SCC and SP are adjusted to 4 mmHg, 9 mmHg, 0 mmHg and 0 mmHg respectively. Acuson’s Sequoia 512 ultrasonographic system was used to record the M-mode and two-dimensional cineloops of the simulated IVS’s motion under the simulated RIPC. Total of 150 frames were captured. A. With rhythmic pressure change in SCC, or under the simulated RIPC of 0 to −4mmHg, the IVS swung left- and rightwards at amplitude of 2.2 mm. B and C. These two of the total 150 frames demonstrate the 2D echocardiograms of the end-expiration (B) and end-inspiration (C) phases. Their internal LV diameters are 35.0 and 32.8 mm, respectively. RIPC = respiratory intrathoracic pressure change; PVR = pulmonary venous return system; SVR = systemic venous return system, SCC = simulated chest cavity; SRV = simulated right ventricle, SLV = simulated left ventricle; SP = simulated pericardium, IVS: interventricular septum.
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Related In: Results  -  Collection

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pone-0057512-g004: The influence of simulated RIPC on the motion of the simulated IVS.Under the simulated RIPC, the simulated IVS is swinging left- and rightwards (down and up in the figure) to correspond the pressure change in SCC. To simulate the in vivo condition where the right ventricle anterior wall and the left ventricle posterior walls are kept in touch with the chest wall, the pressures in SRV, SLV, SCC and SP are adjusted to 4 mmHg, 9 mmHg, 0 mmHg and 0 mmHg respectively. Acuson’s Sequoia 512 ultrasonographic system was used to record the M-mode and two-dimensional cineloops of the simulated IVS’s motion under the simulated RIPC. Total of 150 frames were captured. A. With rhythmic pressure change in SCC, or under the simulated RIPC of 0 to −4mmHg, the IVS swung left- and rightwards at amplitude of 2.2 mm. B and C. These two of the total 150 frames demonstrate the 2D echocardiograms of the end-expiration (B) and end-inspiration (C) phases. Their internal LV diameters are 35.0 and 32.8 mm, respectively. RIPC = respiratory intrathoracic pressure change; PVR = pulmonary venous return system; SVR = systemic venous return system, SCC = simulated chest cavity; SRV = simulated right ventricle, SLV = simulated left ventricle; SP = simulated pericardium, IVS: interventricular septum.
Mentions: In Test 1, with the pressure in the SRV and SLV kept constant (standard pressure condition for model 2), each step of pressure decrease in the SCC from 0 mmHg to −5 mmHg, the simulated IVS moved leftwards (to the SLV direction) in a corresponding position and from 0 mmHg to +5 mmHg, rightwards correspondingly, i.e., it is a corresponding relationship between the pressure in SCC and the position of simulated IVS which we called pressure-position relationship. With rhythmic pressure change in SCC, or under the simulated RIPC of 0 – −4mmHg, the SIVS swung left- and rightwards at amplitude of 2.2 mm (Figure 4).

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Ultrasound Diagnostics, Tangdu Hospital, Fourth Military Medical University, Xi'an, China.

ABSTRACT
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.

Show MeSH
Related in: MedlinePlus