[Show abstract][Hide abstract] ABSTRACT: The healthy human respiratory system has impressive ventilatory reserve and can easily meet the demands placed upon it by strenuous exercise. Several acute physiological adaptations during exercise ensure harmonious neuromechanical coupling of the respiratory system, which allow healthy humans to reach high levels of ventilation without perceiving undue respiratory discomfort (breathlessness). However, in certain circumstances, such as pregnancy, obesity and natural aging, ventilatory reserve becomes diminished and exertional breathlessness is present. In this review, we focus on what is known about the mechanisms of increased activity-related breathlessness in these populations. Notwithstanding the obvious physiological differences between the three conditions, they share some common perceptual and ventilatory responses to exercise. Breathlessness intensity ratings (described as an increased "sense of effort") are consistently higher than normal at any given submaximal power output; and central motor drive to the respiratory muscles is consistently increased, reflecting increased ventilatory stimulation. The increased contractile respiratory muscle effort required to support the increased ventilatory requirements of exercise remains the most plausible source of increased activity-related breathlessness in pregnant, obese and elderly humans. In all three conditions, static and dynamic respiratory mechanical/muscular function is, to some extent, altered or impaired. Nevertheless, breathlessness intensity ratings are not significantly increased (compared to normal) at any given exercise ventilation in any of these three conditions. This strongly suggests that respiratory mechanical/muscular factors, per se, may be less important in the genesis of breathlessness. Moreover, in pregnancy and obesity, we present evidence that effective physiological adjustments exist to counterbalance the potentially negative sensory consequences of the altered respiratory mechanical/muscular function peculiar to these conditions.
[Show abstract][Hide abstract] ABSTRACT: To record any physiological changes in lung function during healthy pregnancies, and evaluate the influence of parity, pregestational overweight, and excessive weight gain.
Longitudinal cohort study.
Antenatal clinic at Oslo University Hospital.
One hundred healthy white women with singleton pregnancies.
The women were studied with repeated measures of lung function using spirometry at a gestational age of 14-16, 22-24, 30-32, and 36 weeks, and at 6 months postpartum.
Forced vital capacity (FVC), forced expiratory volume in 1 second (FEV1), and peak expiratory flow (PEF), also expressed as a percentage of predicted values according to age and height: i.e. FVC%, FEV1%, and PEF%.
Both FVC and FVC% increased significantly after 14-16 weeks of gestation (P=0.001), as was the case for both PEF and PEF% (P<0.001). FVC, FVC%, PEF, and PEF% in early and mid-pregnancy were significantly lower compared with the postpartum value (all P<0.05). Nulliparous women had an overall 4.4% lower value of FVC% than parous women (P=0.039). There were no differences in FVC, FEV1, or PEF dependent upon pregestational overweight or excessive weight gain.
Forced vital capacity (FVC) increases significantly after 14-16 weeks of gestation. The FVC% is significantly higher in parous compared with primigravida women, suggesting that the changes in FVC occurring during pregnancy persist postpartum. PEF increases significantly during healthy pregnancies, and should be interpreted cautiously in pregnant women with impaired lung function.
BJOG An International Journal of Obstetrics & Gynaecology 01/2012; 119(1):94-101. · 3.76 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: To study longitudinally changes in blood pressure (BP) and heart rate (HR) during healthy pregnancies and to evaluate the influence of parity, pregestational overweight, and excessive weight gain.
A prospective longitudinal cohort study of 57 healthy white women with singleton pregnancies. BP and HR were measured repeatedly at gestational age 14-16 weeks, 22-24 weeks, 30-32 weeks, 36 weeks, and 6 months postpartum using both an oscillometric measurement device (Dinamap) and finger arterial pressure (Finometer PRO).
SBP, DBP, and mean arterial pressure (MAP) reached a statistically significant trough at gestational age 22-24 weeks using both measurement devices. When compared with the nonpregnant measurement, SBP at gestational age 22-24 weeks was 6.2 mmHg [95% confidence interval (95% CI) 1.3-11.2] lower measured by Finometer and 7.2 mmHg (95% CI 4.2-10.1) lower measured by Dinamap. DBP and MAP were 8.9 mmHg (95% CI 4.6-13.2) and 9.8 mmHg (95% CI 5.3-14.2) lower measured by Finometer. Measured by Dinamap, DBP and MAP were 4.5 mmHg (95% CI 1.7-7.3) and 5.4 mmHg (95% CI 2.8-7.9) lower at gestational age 22-24 weeks when compared with the nonpregnant state. SBP was significantly higher in women with pregestational BMI at least 25 kg/m with both measurement devices (both P < 0.05). There were no differences in SBP, DBP, or MAP depending on parity or excessive weight gain.
BP measured repeatedly by two different noninvasive devices during pregnancy and postpartum showed a statistically significant drop in mid-pregnancy, followed by a progressive increase until term.
Journal of Hypertension 12/2011; 30(2):342-50. · 4.22 Impact Factor
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