Respiratory Variation in Mitral Flow Velocity in Pericardial Effusion and Cardiac Tamponade

Simeonidou, Eftihia; Hamouratidis, Nikolaos; Tzimas, Konstantinos; Tsounos, J. P.; Roussis, Stefanos

doi:10.1177/000331979404500306

Cited by 9 publications

(3 citation statements)

References 13 publications

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“…Only recently, increased respiratory variations in Doppler tracings [8, 10]have been shown not to correlate with the hemodynamic severity of tamponade [22], possibly because this phenomenon is influenced by the degree of respiratory effort itself. In addition, it can occur in pathophysiologic conditions other than tamponade, such as acute pulmonary embolism, which it may even resemble in its clinical presentation.…”

Section: Discussionmentioning

confidence: 99%

Assessment of Pseudohypertrophy as a Measure of Left-Ventricular Compression in Patients with Cardiac Tamponade

Feinberg¹,

Popescu²,

Popescu³

et al. 2000

Cardiology

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Background: Left-ventricular pseudohypertrophy reflecting left-ventricular compression was reported in a selected group of patients with cardiac tamponade. Hypothesis: Criteria for the presence of pseudohypertrophy can be established to guide its use as a sign of left-ventricular compression in patients with cardiac tamponade. Methods: Left-ventricular wall thickness, diameters, relative diastolic wall thickness (%) = (posterior wall thickness/end diastolic radius) x 100 and estimated left-ventricular mass were measured in patients with small, moderate and large pericardial effusion, in patients with cardiac tamponade before and after pericardiocentesis (16 patients in each group) and in 30 control subjects with normal echocardiograms. Results: Left-ventricular posterior wall thickness was increased (12 ± 2 vs. 9 ± 1 mm, p < 0.001), left-ventricular end-diastolic diameter was reduced (3.9 ± 0.5 vs. 4.6 ± 0.3 cm, p < 0.001) and relative left-ventricular diastolic wall thickness was increased (61 ± 13 vs. 41 ± 4.5%, p < 0.001) only in patients with cardiac tamponade compared to controls, but not in patients with small, moderate and large effusions, respectively (relative wall thickness: 42 ± 5, 41 ± 7 and 44 ± 7%, p = NS). Mean values of the estimated left-ventricular mass were similar in all groups. Following pericardiocentesis all parameters were normal. Conclusions: Despite normal left-ventricular mass, relative left-ventricular diastolic wall thickness is elevated in patients with cardiac tamponade. In contrast it is normal in patients with various degrees of pericardial effusion supporting its use as a quantitative measure of left-ventricular compression in patients with suspected cardiac tamponade.

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Section: Discussionmentioning

confidence: 99%

Assessment of Pseudohypertrophy as a Measure of Left-Ventricular Compression in Patients with Cardiac Tamponade

Feinberg¹,

Popescu²,

Popescu³

et al. 2000

Cardiology

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“…Some studies contributed to the mechanism of normal respiratory hemodynamic variations [15], [16], and others focused on the mechanism of pulsus paradoxus in cardiac tamponade [17]–[19]. However, none of the previous studies has fully elucidated the true mechanism.…”

Section: Discussionmentioning

confidence: 99%

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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“…Some studies contributed to the mechanism of normal respiratory hemodynamic variations [15,16], and others focused on the mechanism of pulsus paradoxus in cardiac tamponade [17][18][19]. However, none of the previous studies has fully elucidated the true mechanism.…”

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

confidence: 99%

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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Respiratory Variation in Mitral Flow Velocity in Pericardial Effusion and Cardiac Tamponade

Cited by 9 publications

References 13 publications

Assessment of Pseudohypertrophy as a Measure of Left-Ventricular Compression in Patients with Cardiac Tamponade

Assessment of Pseudohypertrophy as a Measure of Left-Ventricular Compression in Patients with Cardiac Tamponade

Mechanism Study of Pulsus Paradoxus Using Mechanical Models

Mechanism Study of Pulsus Paradoxus Using Mechanical Models

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