142 research outputs found
Does phase 2 of the expiratory PCO2 versus volume curve have diagnostic value in emphysema patients?
It has been postulated that serial inhomogeneity of ventilation in the
peripheral airways in emphysema is represented by the shape of expiratory
carbon dioxide tension versus volume curve. We examined the diagnostic
value of this test in patients with various degrees of emphysema. The
volumes between 25-50% (V25-50) and 25-75% (V25-75) of the expiratory
carbon dioxide tension versus volume curve were determined in 29
emphysematous patients (20 severely obstructed and 9 moderately
obstructed), 12 asthma patients in exacerbation of symptoms, and 28
healthy controls. Discriminant analysis was used to examine whether these
diagnostic groups could be separated. With regard to phase 2 of the
expiratory CO2 versus volume curve (mixture of anatomic deadspace and
alveolar air), a plot of intercept versus slope of the relationships of
(V25-50) and (V25-75) versus inspiratory volume (VI) from functional
residual capacity (FRC), obtained during natural breathing frequency,
proved to be most discriminating in the separation between healthy
controls and severely obstructed emphysema patients. Separating healthy
controls and severely obstructed emphysema patients on the basis of the
discriminant line for V25-50, 9 of the 12 asthma patients in exacerbation
were classified as normal, and only 5 of the 9 moderately obstructed
emphysema patients as emphysematous. For V25-75 involvement of phase 3 of
the curve (alveolar plateau) in asthma patients in exacerbation caused a
marked overlap with the severely obstructed emphysema patients. In the
healthy controls, a fixed breathing frequency of 20 breaths.min-1 led to
an increase of both volumes.(ABSTRACT TRUNCATED AT 250 WORDS
Dead space and slope indices from the expiratory carbon dioxide tension-volume curve
The slope of phase 3 and three noninvasively determined dead space
estimates derived from the expiratory carbon dioxide tension (PCO2) versus
volume curve, including the Bohr dead space (VD,Bohr), the Fowler dead
space (VD,Fowler) and pre-interface expirate (PIE), were investigated in
28 healthy control subjects, 12 asthma and 29 emphysema patients (20
severely obstructed and nine moderately obstructed) with the aim to
establish diagnostic value. Because breath volume and frequency are
closely related to CO2 elimination, the recording procedures included
varying breath volumes in all subjects during self-chosen/natural
breathing frequency, and fixed frequencies of 10, 15 and 20 breaths x
min(-1) with varying breath volumes only in the healthy controls. From the
relationships of the variables with tidal volume (VT), the values at 1 L
were estimated to compare the groups. The slopes of phase 3 and VD,Bohr at
1 L VT showed the most significant difference between controls and
patients with asthma or emphysema, compared to the other two dead space
estimates, and were related to the degree of airways obstruction.
Discrimination between no-emphysema (asthma and controls) and emphysema
patients was possible on the basis of a plot of intercept and slope of the
relationship between VD,Bohr and VT. A combination of both the slope of
phase 3 and VD,Bohr of a breath of 1 L was equally discriminating. The
influence of fixed frequencies in the controls did not change the results.
The conclusion is that Bohr dead space in relation to tidal volume seems
to have diagnostic properties separating patients with asthma from
patients with emphysema with the same degree of airways obstruction.
Equally discriminating was a combination of both phase 3 and Bohr dead
space of a breath of 1 L. The different pathophysiological mechanisms in
asthma and emphysema leading to airways obstruction are probably
responsible for these results
Pulmonary hypertension after transjugular intrahepatic portosystemic shunt (TIPS)
We reported the case of a patient in whom severe, and ultimately fatal,
pulmonary hypertension developed 1.5 yrs after transjugular intrahepatic
portosystemic shunt (TIPS). Pulmonary artery pressures were not affected
by 100% oxygen, prostacyclin or nifedipine. Postmortem examinations showed
pulmonary and vascular abnormalities typical of pulmonary hypertension.
Pulmonary artery pressures should be measured in each patient with
otherwise not readily explained dyspnoea following transjugular
intrahepatic portosystemic shunt
Identifying risk factors for COPD and adult-onset asthma: an umbrella review
BACKGROUND: COPD and adult-onset asthma (AOA) are the most common noncommunicable respiratory diseases. To improve early identification and prevention, an overview of risk factors is needed. We therefore aimed to systematically summarise the nongenetic (exposome) risk factors for AOA and COPD. Additionally, we aimed to compare the risk factors for COPD and AOA. METHODS: In this umbrella review, we searched PubMed for articles from inception until 1 February 2023 and screened the references of relevant articles. We included systematic reviews and meta-analyses of observational epidemiological studies in humans that assessed a minimum of one lifestyle or environmental risk factor for AOA or COPD. RESULTS: In total, 75 reviews were included, of which 45 focused on risk factors for COPD, 28 on AOA and two examined both. For asthma, 43 different risk factors were identified while 45 were identified for COPD. For AOA, smoking, a high body mass index (BMI), wood dust exposure and residential chemical exposures, such as formaldehyde exposure or exposure to volatile organic compounds, were amongst the risk factors found. For COPD, smoking, ambient air pollution including nitrogen dioxide, a low BMI, indoor biomass burning, childhood asthma, occupational dust exposure and diet were amongst the risk factors found. CONCLUSIONS: Many different factors for COPD and asthma have been found, highlighting the differences and similarities. The results of this systematic review can be used to target and identify people at high risk for COPD or AOA
The Cloning and Expression of Human Monoclonal Antibodies: Implications for Allergen Immunotherapy
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