Pressure-Flow Studies in Man: Effect of Respiration on Left Ventricular Stroke Volume

Ruskin, Jerome; Bache, Robert J.; Rembert, Judith C.; Greenfield, Joseph C.

doi:10.1161/01.cir.48.1.79

Cited by 126 publications

(61 citation statements)

References 18 publications

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“…Collapse of the inferior vena cava during inspiration decreases venous return from the lower extremities and is associated with a decrease in splanchnic blood flow (Abel and Waldhausen, 1969;Rabinovici and Navot, 1980;Willeput et al, 1984). Left ventricular stroke volume can also be reduced during inspiration in mammals (Charlier et al, 1974;Hoffman et al, 1965;Ruskin et al, 1973;Schrijen et al, 1975) due to a fall in effective ejection pressure of the left ventricle (Olsen et al, 1985). Contraction of the abdominal muscles during expiration aids venous return in mammals (Abel and Waldhausen, 1969;Youmans et al, 1963).…”

Section: Discussionmentioning

confidence: 99%

Terrestrial locomotion does not constrain venous return in the American alligator,Alligator mississippiensis

Munns

Hartzler

Bennett

et al. 2005

Journal of Experimental Biology

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SUMMARY The effects of treadmill exercise on components of the cardiovascular(heart rate, mean arterial blood pressure, central venous pressure, venous return) and respiratory (minute ventilation, tidal volume, breathing frequency, rate of oxygen consumption, rate of carbon dioxide production)systems and on intra-abdominal pressure were measured in the American alligator, Alligator mississippiensis, at 30°C. Alligators show speed-dependent increases in tidal volume and minute ventilation,demonstrating that the inhibition of ventilation during locomotion that is present in some varanid and iguanid lizards was not present in alligators. Exercise significantly increases intra-abdominal pressure; however,concomitant elevations in central venous pressure acted to increase the transmural pressure of the post caval vein and thus increased venous return. Therefore, despite elevated intra-abdominal pressure, venous return was not limited during exercise in alligators, as was the case in Varanus exanthematicus and Iguana iguana. Respiratory cycle variations in intra-abdominal pressure, central venous pressure and venous return indicate that, at high tidal volumes, inspiration causes a net reduction in venous return during active ventilation and thus may act to limit venous return during exercise. These results suggest that, while tonically elevated intra-abdominal pressure induced by exercise does not inhibit venous return,phasic fluctuations during each breath cycle may contribute to venous flow limitation during exercise.

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Section: Discussionmentioning

confidence: 99%

Terrestrial locomotion does not constrain venous return in the American alligator,Alligator mississippiensis

Munns

Hartzler

Bennett

et al. 2005

Journal of Experimental Biology

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“…The mechanism of pulsus paradoxus in cardiac tamponade has been extensively studied, using a variety of techniques over many years. While the details differ, two major pathophysiologic alterations emerge from the published data: 1) a limitation of ventricular volume expansion so that inspiratory increases in right ventricular filling tend to decrease that of the left,14, 18,20,22,23 and 2) an inspiratory decrease in pulmonary venous below pericardial and left atrial pressure impeding filling of the left ventricle.8' 15,16 Our data are compatible with the following hypothesis for pulsus paradoxus production, and suggest the above theories are complementary rather than mutually exclusive. When cardiac tamponade is severe enough to embarrass both ventricles, the operative portion of the pericardial volume-pressure curve is steeper than that of either ventricle; therefore, flow into both ventricles takes place against a common stiffness.…”

Section: Resultsmentioning

confidence: 99%

Cardiac tamponade: hemodynamic observations in man.

Reddy¹,

Curtiss²,

O'Toole³

et al. 1978

Circulation

259

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SUMMARY Hemodynamic studies were performed before and after pericardiocentesis in 19 patients with pericardial effusion. Right atrial pressure decreased significantly, from 16 ± 4 mm Hg (mean ± SD) to 7 ± 5 mm Hg in 14 patients with cardiac tamponade. This change was accompanied by significant increases in cardiac output (3.87 ± 1.77 to 7 ± 2.2 I/min) and inspiratory systemic arterial pulse pressure (45 ± 29 to 81 ± 23 mm Hg). The remaining five patients did not demonstrate cardiac tamponade, as evidenced by lack of significant change in these hemodynamic parameters.In all patients with tamponade, right ventricular end-diastolic pressure (RVEDP) was elevated and equal to pericardial pressure; equilibration was uniformly absent in patients without tamponade. During gradual fluid withdrawal in the tamponade group, significant hemodynamic improvement was largely confined to the period when right ventricular filling pressure remained equilibrated with pericardial pressure. In 10 patients with tamponade and pulsus paradoxus, pulmonary arterial wedge pressure (PAW) was equal to pericardial pressure except during early inspiration and expiration when it was transiently less and greater, respectively; however, inspiratory right atrial pressure never fell below pericardial pressure. In these 10 patients, PAW decreased significantly following pericardiocentesis (P < 0.001). In the remaining four patients with tamponade but without pulsus paradoxus, all of whom had chronic renal failure, PAW was consistently higher than pericardial pressure or RVEDP and did not decrease after pericardiocentesis.These data tend to confirm the hypothesis that in patients with tamponade, the venous pressure required to maintain any given cardiac volume is determined by pericardial rather than ventricular compliance. When pericardial compliance determines diastolic pressure in both ventricles, relative filling of the ventricles will be competitive and determined by their respective venous pressures (pulmonary vs systemic), which vary with respiration and alternately favor right and left ventricular filling. This results in pulsus paradoxus. However, if pulmonary arterial wedge pressure is markedly elevated before the onset of tamponade, as in patients with chronic renal failure, then pericardial compliance may only determine right ventricular filling pressure. In such cases, pulsus paradoxus may be absent. MUCH OF OUR

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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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Pressure-Flow Studies in Man: Effect of Respiration on Left Ventricular Stroke Volume

Cited by 126 publications

References 18 publications

Terrestrial locomotion does not constrain venous return in the American alligator,Alligator mississippiensis

Terrestrial locomotion does not constrain venous return in the American alligator,Alligator mississippiensis

Cardiac tamponade: hemodynamic observations in man.

Mechanism Study of Pulsus Paradoxus Using Mechanical Models

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