A comparison of the acute haemodynamic response to aerobic and resistance exercise in subjects with exercise-induced pulmonary arterial hypertension.

BACKGROUND: Exercise-induced pulmonary arterial hypertension (EIPAH) is associated with reduced exercise capacity and abnormal central haemodynamic responses to maximal aerobic exercise. Aerobic and resistance exercise training are commonly employed to treat reduced exercise capacity; however, the haemodynamic response to aerobic and resistance exercise, at training intensities, in subjects with EIPAH is unknown. METHODS: Fourteen subjects (11 with scleroderma, 12 females) with EIPAH underwent cardiopulmonary exercise testing on a cycle ergometer, a one-repetition maximum (1RM) strength test and resistance exercise at 40% and 60% of maximum on a bilateral leg press machine. All tests were performed with a pulmonary artery catheter in situ. Haemodynamic and symptomatic responses to aerobic and resistance exercise, performed at 40% of peak oxygen consumption and 40% of 1RM, and at 60% of peak oxygen consumption and 60% of 1RM, were compared. For maximal exercise, the highest haemodynamic responses recorded during the cycling and 1RM tests were compared. RESULTS: There were no differences in haemodynamic or symptomatic responses between the two modalities of submaximal exercise. At maximal exercise, all haemodynamic and symptomatic responses were lower during resistance compared with aerobic exercise (p < 0.05). CONCLUSIONS: At the intensities studied, lower-limb resistance exercise was well tolerated and was mostly associated with similar or lower haemodynamic responses compared with aerobic exercise, in subjects with EIPAH.

Exercise intolerance in pulmonary arterial hypertension.

Pulmonary arterial hypertension (PAH) is associated with symptoms of dyspnea and fatigue, which contribute to exercise limitation. The origins and significance of dyspnea and fatigue in PAH are not completely understood. This has created uncertainly among healthcare professionals regarding acceptable levels of these symptoms, on exertion, for patients with PAH. Dysfunction of the right ventricle (RV) contributes to functional limitation and mortality in PAH; however, the role of the RV in eliciting dyspnea and fatigue has not been thoroughly examined. This paper explores the contribution of the RV and systemic and peripheral abnormalities to exercise limitation and symptoms in PAH. Further, it explores the relationship between exercise abnormalities and symptoms, the utility of the cardiopulmonary exercise test in identifying RV dysfunction, and offers suggestions for further research.

Effects of high-intensity inspiratory muscle training following a near-fatal gunshot wound.

BACKGROUND AND PURPOSE: Severe injuries sustained during combat may classify individuals as undeployable for active service. It is imperative that every effort is made to optimize physical function following such injuries. CASE DESCRIPTION: A 38-year-old man sustained a gunshot wound during armed combat. The bullet entered via the left axilla and exited from the right side of the abdomen, resulting in severe thoracic and abdominal injuries. Five months later, he continued to describe severe dyspnea on exertion. During a cardiopulmonary exercise test on a cycle ergometer, he achieved a maximum rate of oxygen uptake of 2,898 mL·min(-1) (114% predicted) and maximum power of 230 W (114% predicted). His maximum forced inspiratory flow was 5.95 L·s(-1), and inspiratory reserve volume at test end was ∼80 mL. The test was terminated by the patient due to dyspnea that was too severe to tolerate. Video fluoroscopy demonstrated impaired right hemidiaphragm function. The main goals of therapy were to reduce dyspnea on exertion and to enable return to full work duties. A program of high-intensity, interval-based threshold inspiratory muscle training (IMT) was undertaken. OUTCOMES: An average of 5 sessions of IMT were completed each week for 10 weeks. During a repeat cardiopulmonary exercise test, the patient achieved a similar power and maximum rate of oxygen uptake. His maximum forced inspiratory flow increased by 48% to 8.83 L·s(-1), and he was limited by leg fatigue. DISCUSSION: High-intensity IMT was safe and well tolerated. It was associated with improvements in maximum forced inspiratory flow and changed the locus of symptom limitation during high-intensity exercise from dyspnea to leg fatigue.

Implications of exercise-induced pulmonary arterial hypertension.

PURPOSE: To characterize the hemodynamic and ventilatory responses to exercise in a group of patients with unexplained dyspnea, increased risk for pulmonary arterial hypertension (PAH), and an elevated mean pulmonary artery pressure (mPAP; >30 mm Hg) on exercise. METHODS: A total of 37 symptomatic patients at risk of PAH and 20 healthy controls underwent a cardiopulmonary exercise test and were assessed for quality of life (QOL). Patients had a pulmonary artery catheter in situ during the exercise test. RESULTS: Seventeen subjects had exercise-induced PAH (EIPAH), which we defined as mPAP ≤ 25 mm Hg at rest, and mPAP > 30 mm Hg and pulmonary artery wedge pressure <20 mm Hg on exercise. These subjects had reduced peak exercise cardiac output (72% ± 19% predicted). Further, compared with matched controls, subjects with EIPAH had reduced peak oxygen consumption (1.2 ± 0.4 vs 1.7 ± 0.5 L · min, P < 0.05), an elevated ventilatory equivalent for carbon dioxide (41.0 ± 7.3 vs 31.0 ± 2.9, P < 0.05) and reduced end-tidal carbon dioxide tension (32.6 ± 3.6 vs 39.4 ± 2.7 mm Hg, P < 0.05) at the anaerobic threshold. These exercise abnormalities were associated with impaired QOL (P < 0.05). CONCLUSIONS: Elevated pulmonary artery pressure on exercise can be associated with hemodynamic and ventilatory abnormalities typical of PAH, along with impaired exercise capacity and reduced QOL.

Continuous positive airway pressure titration for obstructive sleep apnoea: automatic versus manual titration.

BACKGROUND AND AIMS: Manual laboratory continuous positive airway pressure (CPAP) titration for obstructive sleep apnoea (OSA) is costly, time intensive and delays access to treatment. Automatic positive airway pressure (APAP) titration has the potential to reduce cost and improve access to treatment. The aim of this study was to assess the clinical efficacy and costs of APAP titration compared with manual titration in moderate-severe OSA. METHODS: Patients with moderate-severe OSA (apnoea/hypopnoea index >15 and Epworth Sleepiness Score > or = 8) who were free of co-morbidities that could impair APAP titration were eligible. 249 participants were randomised to manual titration, home APAP or laboratory APAP titration to determine a fixed pressure for CPAP. Clinical and direct cost outcomes were assessed after 4 weeks of treatment. RESULTS: Average nightly CPAP use, subjective sleepiness, SF36 quality of life, Trails A and B cognitive function and polysomnographic outcomes were similar among the per-protocol groups. Non-hypertensive patients had a lower resting heart rate (and greater reduction in heart rate) at 4 weeks after laboratory APAP titration compared with home APAP titration. Costs per patient were highest in manual (AU$817.84), followed by laboratory (AU$647.56) and home (AU$132.09) APAP titration. An intention-to-treat analysis confirmed the effectiveness of APAP titration compared with manual titration in the standard clinical setting. CONCLUSIONS: Among patients with moderate-severe OSA without serious co-morbidities, outcomes at 1 month indicate that APAP titration is more cost-effective than manual laboratory titration to determine an appropriate pressure for CPAP for long-term use; with the largest savings occurring in the home APAP patients.