Echocardiographic study of cardiac tamponade.

Settle, Harold P.; Adolph, Robert J.; Fowler, Noble O.; Engel, Peter J.; Agruss, Neil S.; Levenson, Norman I.

doi:10.1161/01.cir.56.6.951

Cited by 119 publications

(29 citation statements)

References 32 publications

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“…Such overlap is evident on examining the mitral valve data of Settle et al 4 Vignola et al13 described a systolic notch in the right ventricular motion in four tamponade patients, but we did not encounter this in our dogs.…”

Section: Resultsmentioning

confidence: 57%

Can cardiac tamponade be diagnosed by echocardiography? Experimental studies.

Martins¹,

Kerber²

1979

Circulation

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The purpose of this study was to determine if echocardiography could be used to predict the presence and/or severity of cardiac tamponade in an experimental model. Methods Animal PreparationNine mongrel dogs that weighed 15-35 kg were lightly anesthetized with a mixture of chloralose and urethane, 100 mg/kg and 1000 mg/kg, respectively. The left chest was entered through the fourth intercostal space and the pericardium was cannulated with a #8 polyethylene pigtail catheter through a stab incision. Two 00 silk ties were placed around the catheter using a pursestring suture and a cyanoacrylate ester glue was placed over the suture and surrounding areas to achieve a seal. The chest was closed, and a chest tube to an underwater seal was left in place to remove air and prevent atelectasis. Spontaneous respiration resumed after surgery was completed and the chest closed. We measured right atrial, aortic arch and left ventricular pressures using a Statham P23Db transducer at the midchest level. Cardiac output was measured by the dye-dilution principle. Indocyanine green dye (2.5 mg) was injected into the right atrium, and dye concentrations in right brachial artery blood were recorded from duplicate curves with exponential decay. Echocardiographic StudiesEchocardiographic studies were obtained using a commercially available ultrasonoscope and a 2.25-MHz transducer focused at 7.5 cm. The dogs were examined during spontaneous respiration in the right lateral decubitus position.8 The hand-held transducer was placed in the fourth or fifth right intercostal space approximately 5 cm from the midsternal line and angled slightly inferiorly and anteriorly. An M-mode sweep was initially performed to identify the septum and posterior wall of the left ventricle just below the mitral valve for left ventricular diameter measurements. In addition, a minor sweep was initially done in order to identify the largest end-diastolic dimension measured at the R wave of the QRS complex of the simultaneous electrocardiographic tracing. After the optimal transducer position and beam angulation were initially identified, the transducer was subsequently moved as little as possible to minimize artifacts caused by changing transducer position or beam direction. Measurements were taken during expiration and inspiration in the control state, and during various levels of tamponade ( figs. 1 and 2). The phases of the respiratory cycle were identified by visual inspection of the records; this was verified in some of the dogs by simultaneously recording intrapleural pressures as well. Measurements of the ven-

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Section: Resultsmentioning

confidence: 57%

Can cardiac tamponade be diagnosed by echocardiography? Experimental studies.

Martins¹,

Kerber²

1979

Circulation

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“…After removal of the maximal amount of pericardial 16 We found a marked stepwise increase in left ventricular diastolic volume during relief of cardiac tamponade. This incremental increase in end-diastolic volume paralleled the increase in stroke volume demonstrated by us and others.…”

Section: Hemodynamic Measurements and Calculationsmentioning

confidence: 81%

Left ventricular volume and function during relief of cardiac tamponade in man.

Grose

Greenberg²,

Steingart

et al. 1982

Circulation

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SUMMARY To determine the causes of cardiac failure during cardiac tamponade in man, we studied left ventricular volume and function in eight patients during pericardiocentesis using gated equilibrium radionuclide ventriculography. In the seven patients with clinical and hemodynamic evidence of cardiac tamponade, end-diastolic and end-systolic volumes increased progressively as the initial 500 ml offluid were removed; the most marked increase occurred during the removal of the first 200 ml of pericardial fluid. After removal of 500 ml of pericardial fluid, end-diastolic volume increased from 52 ± 8 ml to 111 ± 13 ml (p < 0.05) and end-systolic volume from 17 ± 5 ml to 34 ± 7 ml (p < 0.05). Right-heart catheterization was performed at the bedside using a #7F triple-lumen thermodilution balloon catheter. Arterial pressure was obtained with a #18 or #20 Teflon catheter inserted percutaneously into a radial or brachial artery. Percutaneous pericardiocentesis was performed by puncturing the pericardial sac with a stainless-steel needle. The needle was used as an exploring electrode to achieve continuous electrocardiographic monitoring by connecting it to the V lead of a standard electrocardiograph. A 5.5-inch #19 Teflon catheter with four side holes was then advanced over the rigid needle so that all side holes were within the pericardial cavity and no damage was done to the cardiac structures. The needle was then withdrawn. There were no complications of the pericardiocentesis, and the initial insertion was performed with a single puncture in all cases. In patient 6, mechanical problems with the catheter necessitated repeat puncture after 200 ml of pericardial fluid had been withdrawn. In patient 5, withdrawal of pericardial fluid was halted after 500 ml because of unsustained ventricular tachycardia related to negative pressure applied to the pericardial catheter.Pressures were measured with Statham P231D transducers and recorded along with a bipolar electrocardiographic lead on an Electronics for Medicine VR6 recorder. To ensure precise linearity of response, the transducers were connected to a single manifold, which allowed them to be calibrated simultaneously. Thermodilution cardiac output was calculated by a computer from the curve generated by hand injection of 10 ml of room temperature 5% dextrose solution.

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“…Based on this theory, the pulmonary arterial pressure and flow would be nearly reciprocal to the aortic pressure and flow [8]. Settle et al [21] also proposed that the increase in venous return flow during inspiration results in a marked and exaggerated increase in right ventricular dimensions accompanied by a reduction in left ventricular dimensions and flattening and displacement of the septum toward the left ventricle and thus decreases the hemodynamics of the left heart. However, this theory doesn't reveal the mechanism but a description of the observed phenomenon.…”

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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Echocardiographic study of cardiac tamponade.

Cited by 119 publications

References 32 publications

Can cardiac tamponade be diagnosed by echocardiography? Experimental studies.

Can cardiac tamponade be diagnosed by echocardiography? Experimental studies.

Left ventricular volume and function during relief of cardiac tamponade in man.

Mechanism Study of Pulsus Paradoxus Using Mechanical Models

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