Pulsus Paradoxus as a Valuable Sign Indicating Severity of Asthma

Knowles, G.K.; Clark, Timothy

doi:10.1016/s0140-6736(73)93324-2

Cited by 102 publications

(32 citation statements)

References 7 publications

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“…A common radiologic finding in infants with severe RSV disease is pulmonary air trapping (49). A correlate of pulmonary obstruction and air trapping in humans is pulsus paradoxus, an exaggeration of normal variation in the pulse volume with respiration that can be caused by labored breathing (22,30,57). We observed labored breathing in RSV 2-20-infected mice (data not shown).…”

Section: Rsv Clinical Isolates Caused Differential Disease Severitymentioning

confidence: 65%

Differential Pathogenesis of Respiratory Syncytial Virus Clinical Isolates in BALB/c Mice

Stokes

Michael

Sakamoto

et al. 2011

J Virol

166

240

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Airway mucus is a hallmark of respiratory syncytial virus (RSV) lower respiratory tract illness. Laboratory RSV strains differentially induce airway mucus production in mice. Here, we tested the hypothesis that RSV strains differ in pathogenesis by screening six low-passage RSV clinical isolates for mucogenicity and virulence in BALB/cJ mice. The RSV clinical isolates induced variable disease severity, lung interleukin-13 (IL-13) levels, and gob-5 levels in BALB/cJ mice. We chose two of these clinical isolates for further study. Infection of BALB/cJ mice with RSV A2001/2-20 (2-20) resulted in greater disease severity, higher lung IL-13 levels, and higher lung gob-5 levels than infection with RSV strains A2, line 19, Long, and A2001/3-12 (3-12). Like the line 19 RSV strain, the 2-20 clinical isolate induced airway mucin expression in BALB/cJ mice. The 2-20 and 3-12 RSV clinical isolates had higher lung viral loads than laboratory RSV strains at 1 day postinfection (p.i.). This increased viral load correlated with higher viral antigen levels in the bronchiolar epithelium and greater histopathologic changes at 1 day p.i. The A2 RSV strain had the highest peak viral load at day 4 p.i. RSV 2-20 infection caused epithelial desquamation, bronchiolitis, airway hyperresponsiveness, and increased breathing effort in BALB/cJ mice. We found that RSV clinical isolates induce variable pathogenesis in mice, and we established a mouse model of clinical isolate strain-dependent RSV pathogenesis that recapitulates key features of RSV disease.Respiratory syncytial virus (RSV) is the most important cause of bronchiolitis and viral pneumonia in children. Each year in the United States, RSV causes lower respiratory tract illness (LRI) in 20 to 30% of infants and leads to the hospitalization of approximately 1% of infants at a cost of $300 to $400 million (19,21,27). The incidence and disease severity of RSV can vary from year to year (47). Dominant circulating RSV strains are generally replaced each year, likely by a process involving immune selection (5,6,53,54). RSV strain differences may contribute to year-to-year and/or patient-topatient variations in clinical severity.In BALB/cJ mice, laboratory RSV strains (A2, Long, and line 19) differ in their ability to cause pulmonary interleukin-13 (IL-13) and mucin expression (34, 41). We are interested in RSV-induced mucin expression in mice because mucus overabundance contributes to airway obstruction in severe RSV disease in children (2,33,44,56). IL-13 is a cytokine linked to mucus production (71). The line 19 RSV strain induces lung IL-13 and airway mucin expression in BALB/cJ mice, whereas the A2 and Long RSV strains do not (34, 41). However, the in vitro passage histories of RSV strains A2, Long, and line 19 are not defined and involve many serial passages. Thus, it is possible that mutations in these RSV laboratory strains determine pathogenesis phenotypes in the mouse model. RSV clinical isolates have not been studied extensively in vivo, and the role of RSV strain differences in...

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Section: Rsv Clinical Isolates Caused Differential Disease Severitymentioning

confidence: 65%

Differential Pathogenesis of Respiratory Syncytial Virus Clinical Isolates in BALB/c Mice

Stokes

Michael

Sakamoto

et al. 2011

J Virol

166

240

View full text Add to dashboard Cite

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“…Pulsus paradoxus is a valuable sign indicating severe asthma and correlates well with other objective and clinical assessments. 6 Woolcock and Reid7 showed that a reduction in lung volumes and a consequent reduction in the elastic work of inspiration after administration of bronchodilator drugs to patients with acute asthma may precede improvement in the forced expiratory volume. Our results suggest that relief of pulsus paradoxus may be a more sensitive index of improvement in acute asthma than simple measurements of ventilatory function such as PEFR and forced expiratory volume.…”

Section: Methodsmentioning

confidence: 99%

Comparison of salbutamol given intravenously and by intermittent positive-pressure breathing in life-threatening asthma.

Bloomfield¹,

Carmichael²,

Petrie³

et al. 1979

BMJ

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procedure for climacteric women receiving hormone replacement therapy or to monitor the reversal of endometrial hyperplasia with oral progestogens.8 One cytologist felt that a confident diagnosis was possible only when a piece of endometrial tissue had been obtained, allowing a histological diagnosis to be made.We believe that cytology will not be a useful means of detecting endometrial abnormalities and that efforts should be directed towards establishing the correct dose and duration of treatment with an oestrogen-progestogen preparation to avoid overstimulating the endometrium. Medical_Journal, 1978, 1, 947. 3Smith, D G, et al, New England Journal of Medicine, 1975, 293, 1164 Comparison of salbutanmol given intravenously and by intermittent positive-pressure breathing in life-threatening asthma P BLOOMFIELD, J CARMICHAEL, G R PETRIE, N P JEWELL, G K CROMPTON British Medical_Journal, 1979, 1, 848-850 Summary and conclusions A double-blind crossover trial was carried out during 22 episodes of life-threatening asthma in 19 patients to compare salbutamol given as a 500 ,ug intravenous injection and as a 0 5% solution administered by intermittent positive-pressure breathing (IPPB) for three minutes. Relief of pulsus paradoxus was significantly better after IPPB than the intravenous treatment. Both treatments significantly improved the peak expiratory flow rate. Salbutamol given intravenously produced a mean increase in heart rate of over 20 beats/min five minutes after treatment compared with the relief of tachycardia that occurred after administration by IPPB. Four patients had noticeable cardiovascular side effects after salbutamol given intravenously, but no such effects were noticed after administration by IPPB. Two patients withdrawn shortly after entry into the trial because of a worsening clinical condition had received intravenous salbutamol. It is concluded that salbutamol given by IPPB is better than that given by slow intravenous injection in severe acute asthma. IntroductionBronchodilators are essential in treating severe acute asthma in the critical initial period before corticosteroids have had time to

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“…Often noted in the past,' this inspiratory increase in arterial pulse during positive pressure lung inflation has been called "reversed pulsus paradoxus,'2 in contrast with the inspiratory decline in arterial pulse (paradoxical pulse) sometimes observed during spontaneous breathing in cardiac tamponade3 or status asthmaticus. 4 Such an inspiratory increase in arterial pulse during positivepressure breathing is quite unexpected since positivepressure lung inflation, by increasing pleural pressure and lung volume, should act to decrease aortic flow, decrease venous return to the right atrium,5 and increase right ventricular afterload. 6 On the other hand, the observed inspiratory increase in blood pressure involves not only the systolic and diastolic pressures, but also the pulse pressure.…”

mentioning

confidence: 99%

Cyclic changes in arterial pulse during respiratory support.

Jardin¹,

Farcot²,

Guéret³

et al. 1983

Circulation

223

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In 13 patients on respiratory support we combined two-dimensional echocardiography with hemodynamic monitoring to determine the mechanism of cyclic changes in arterial pulse, defined as an inspiratory rise in radial artery pulse pressure. Beat-to-beat evaluation of cardiac performance was obtained during the following three distinct consecutive phases of the controlled respiratory cycle: exhalation (phase I), preinspiratory pause (phase LI), and lung inflation (phase III). Airway pressure, left ventricular filling pressure (i.e., pulmonary capillary wedge minus esophageal pressure), and pulmonary artery and radial artery pressures were simultaneously recorded during mechanical ventila-'tion along with beat-to-beat two-dimensional echocardiographic left ventricular end-systolic and enddiastolic dimensions. From a reference value for pulmonary artery and radial artery pulse contour obtained during a brief period of imposed apnea, beat-to-beat measurements of left and right ventricular stroke output were also performed during the controlled respiratory cycle with the pulse contour method. Cyclic changes in arterial pulse appeared to result directly from a transitory increase in left ventricular stroke output during lung inflation (41.4 + 14.6 ml/m2), whereas right ventricular stroke output exhibited a steep fall (31.7 ± 12.4 ml/m2) at this time. An opposite variation was also observed during exhalation, during which a fall in left ventricular stroke output (31.9 ± 11.2 mI/i2) was accompanied by a rise in right ventricular stroke output (38.6 11.9 ml/m2). Both stroke outputs reached an identical level during preinspiratory pause (37.4 + 14. 1 ml/m2 for left ventricle and 39.1 ±-13.8 ml/m2 for right ventricle

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Pulsus Paradoxus as a Valuable Sign Indicating Severity of Asthma

Cited by 102 publications

References 7 publications

Differential Pathogenesis of Respiratory Syncytial Virus Clinical Isolates in BALB/c Mice

Differential Pathogenesis of Respiratory Syncytial Virus Clinical Isolates in BALB/c Mice

Comparison of salbutamol given intravenously and by intermittent positive-pressure breathing in life-threatening asthma.

Cyclic changes in arterial pulse during respiratory support.

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