Mechanisms of pulsus paradoxus during resistive respiratory loading and asthma

Blaustein, Alvin S.; Risser, Thomas A.; Weiss, J. Woodrow; Parker, J. Anthony; Holman, B. Leonard; McFadden, E. R.

doi:10.1016/s0735-1097(86)80179-6

Cited by 40 publications

(42 citation statements)

References 19 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][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: 82%

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

confidence: 82%

Mechanism Study of Pulsus Paradoxus Using Mechanical Models

Cao

Xing

Yuan

et al. 2013

Ultrasound in Medicine & Biology

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“…Such an increase could be consequent to an increase in right ventricular preload [21] and output [21,22], or to an increase in left ventricular afterload [18][19][20]23]. However, PODSZUS and co-workers [6] considered negative intrathoracic pressure as a possible cause for a decrease, and not for an increase, in Ppa, due to possible extrathoracic vein collapse and venous return limitation; in fact, venous return was found to be limited by extrathoracic vein collapse when threshold negative intrathoracic pressure levels were exceeded [24].…”

Section: Discussionmentioning

confidence: 99%

Slow and fast changes in transmural pulmonary artery pressure in obstructive sleep apnoea

Marrone¹,

Mr²,

Romano³

et al. 1994

Eur Respir J

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S Sl lo ow w a an nd d f fa as st t c ch ha an ng ge es s i in n t tr ra an ns sm mu ur ra al l p pu ul lm mo on na ar ry y a ar rt te er ry y p pr re es ss su ur re e i in n o ob bs st tr ru uc ct ti iv ve e s sl le ee ep p a ap pn no oe ea a Transmural systolic pulmonary artery pressure (Ppa,STM), oxyhaemoglobin saturation (SaO 2 ) and oesophageal pressure were analysed in two samples of consecutive obstructive apnoeas in each of four patients.In the first samples (samples A; probably recorded during non-rapid eye movement (NREM) sleep), SaO 2 swings were small and repetitive. In the second samples (samples B; probably recorded during rapid eye movement (REM) sleep), they were large and more variable. Oesophageal pressure oscillated similarly in the two groups of samples. In all cases, transmural systolic pulmonary artery pressure progressively increased throughout apnoeas, and subsequently decreased in the interapnoeic periods. However, both early and end-apnoeic transmural systolic pulmonary artery pressure, remained stable in samples A; whilst they progressively increased in samples B. Transmural systolic pulmonary artery pressure at the beginning of each apnoea was inversely correlated with SaO 2 at the end of the preceding apnoea. These results suggest that transmural systolic pulmonary artery pressure is influenced by SaO 2 , but does not vary at the same speed as SaO 2 . In all cases, beat-by-beat analysis showed, as expected, that the lower the oesophageal pressure, the higher the transmural systolic pulmonary artery pressure however, at each oesophageal pressure level, transmural systolic pulmonary artery pressure was more variable and higher, in samples B.In conclusion, transmural systolic pulmonary artery pressure in obstructive apnoeas shows rapid changes, which reflect oesophageal pressure variations, and slower changes, which are likely to be caused by SaO 2 .

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“…Moreover, right ventricular stroke area and pulmonary artery pulse pressure decrease during inspiration, findings that are the opposite of what is expected in normal subjects [4]. However, divergent findings were reported in a clinical study including asthmatic patients with cold air bronchial hyperreactivity before and during a bronchial challenge with cold air mimicking an asthmatic attack [41]. In this study, right ventricle and left ventricle volumes and ejection fractions were measured using radionuclide angiography during inspiration and expiration [41].…”

Section: Pulsus Paradoxus In Acute Asthmamentioning

confidence: 67%

“…However, divergent findings were reported in a clinical study including asthmatic patients with cold air bronchial hyperreactivity before and during a bronchial challenge with cold air mimicking an asthmatic attack [41]. In this study, right ventricle and left ventricle volumes and ejection fractions were measured using radionuclide angiography during inspiration and expiration [41]. The bronchial challenge produced pulsus paradoxus and changes in oesophageal pressure (measuring ITP) that were significantly greater than those during quiet breathing [41].…”

Section: Pulsus Paradoxus In Acute Asthmamentioning

confidence: 72%

“…In this study, right ventricle and left ventricle volumes and ejection fractions were measured using radionuclide angiography during inspiration and expiration [41]. The bronchial challenge produced pulsus paradoxus and changes in oesophageal pressure (measuring ITP) that were significantly greater than those during quiet breathing [41]. These changes were accompanied by a decrease in left ventricle diastolic volume and in LVSV during inspiration and an increase in these variables during expiration; right ventricular diastolic volume and RVSV demonstrated changes reciprocal to those seen in the left ventricle [40].…”

Section: Pulsus Paradoxus In Acute Asthmamentioning

confidence: 99%

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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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Mechanisms of pulsus paradoxus during resistive respiratory loading and asthma

Cited by 40 publications

References 19 publications

Mechanism Study of Pulsus Paradoxus Using Mechanical Models

Mechanism Study of Pulsus Paradoxus Using Mechanical Models

Slow and fast changes in transmural pulmonary artery pressure in obstructive sleep apnoea

Pulsus paradoxus

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