Late-Presenting Swimming-Induced Pulmonary Edema: A Case Report Series from the Norseman Xtreme Triathlon

Swimming-induced pulmonary edema (SIPE) may develop during strenuous physical exertion in water. This case series reports on three cases of suspected late-presenting SIPE during the Norseman Xtreme Triathlon. A 30-year-old male professional (PRO) triathlete, a 40-year-old female AGE GROUP triathlete and a 34-year-old male AGE GROUP triathlete presented with shortness of breath, chest tightness and coughing up pink sputum during the last part of the bike phase. All three athletes reported an improvement in breathing during the first major uphill of the bike phase and increasing symptoms during the downhill. The PRO athlete had a thoracic computed tomography, and the scan showed bilateral ground glass opacity in the peripheral lungs. The male AGE GROUP athlete had a normal chest x-ray. Both athletes were admitted for further observation and discharged from hospital the following day, with complete regression of symptoms. The female athlete recovered quickly following pre-hospital oxygen treatment. Non-cardiogenic pulmonary edema associated with endurance sports is rare but potentially very dangerous. Knowledge and awareness of possible risk factors and symptoms are essential, and the results presented in this report emphasize the importance of being aware of the possible delayed development of symptoms. To determine the presence of pulmonary edema elicited by strenuous exercise, equipment for measuring oxygen saturation should be available for the medical staff on site

Exercise capacity in COPD patients with exercise-induced pulmonary hypertension

Background: Pulmonary hypertension (PH) in patients with COPD is associated with reduced exercise capacity. A subgroup of COPD patients has normal mean pulmonary artery pressure (mPAP) at rest, but develops high mPAP relative to cardiac output (CO) during exercise, a condition we refer to as exercise-induced pulmonary hypertension (EIPH). We hypothesized that COPD patients with EIPH could be identified by cardiopulmonary exercise test (CPET) and that these patients have lower exercise capacity and more abnormal CPET parameters compared to COPD patients with normal hemodynamic exercise response. Methods: Ninety-three stable outpatients with COPD underwent right heart catheterization with the measurement of mPAP, CO, and capillary wedge pressure at rest and during supine exercise. Resting mPAP <25 mmHg with ΔmPAP/ΔCO slope above or below 3 mmHg/L/min were defined as COPD-EIPH and COPD-normal, respectively. Pulmonary function tests and CPET with arterial blood gases were performed. Linear mixed models were fitted to estimate differences between the groups with adjustment for gender, age, and airflow obstruction. Results: EIPH was observed in 45% of the study population. Maximal workload was lower in COPD-EIPH compared to COPD-normal, whereas other CPET measurements at peak exercise in % predicted values were similar between the two groups. After adjustment for gender, age, and airflow obstruction, patients with COPD-EIPH showed significantly greater increase in oxygen uptake, ventilation, respiratory frequency, heart rate, and lactate with increasing work load, as well as more reduction in pH compared to those with normal hemodynamic responses. Conclusion: COPD-EIPH could not be discriminated from COPD-normal by CPET. However, COPD-EIPH experienced a higher cost of exercise in terms of higher oxygen uptake, ventilation, respiratory frequency, heart rate, and lactate for a given increase in workload compared to COPD-normal

Mechanisms of ECG signs in chronic obstructive pulmonary disease.

Objective: Patients with chronic obstructive pulmonary disease (COPD) often have abnormal ECGs. Our aim was to separate the effects on ECG by airway obstruction, emphysema and right ventricular (RV) afterload in patients with COPD. Methods: A cross-sectional study was performed on 101 patients with COPD without left heart disease and 32 healthy age-matched controls. Body mass index (BMI) was measured, and pulmonary function tests, ECG, echocardiography and right heart catheterisation (only patients) were performed. Variables were grouped into (1) airway obstruction by FEV% (percentage of forced expiratory volume)_predicted, (2) emphysema by residual volume/total lung capacity and residual volume (percent of predicted) and (3) RV afterload by mean pulmonary pressure, artery compliance, vascular resistance and RV wall thickness. Results: In multivariate regression analysis, emphysema correlated negatively to R+S amplitudes in horizontal and frontal leads, RV/left ventricle (LV) end-diastolic volume ratio to horizontal amplitudes and BMI negatively to frontal amplitudes. Increased airway obstruction, RV afterload and BMI correlated with horizontal QRS-axis clockwise rotation. Airway obstruction, RV afterload, RV/LV end-diastolic volume ratio and BMI correlated to the Sokolow-Lyon Index for RV, and RV afterload negatively to Sokolow-LyonIndex for LV. Several classical ECG changes could, however, not be ascribed to specific mechanisms. Conclusions: In COPD, the various pathophysiological mechanisms modify the ECG differently. Increased airway obstruction and RV afterload mainly increase the Sokolow-Lyon Index for RV mass and associate with clockwise rotation of the horizontal QRS-axis, whereas emphysema reduces the QRS amplitudes. BMI is an equally important determinant for the majority of the ECG changes

Cardiopulmonary exercise test and PaO2 in evaluation of pulmonary hypertension in COPD

Background: Exercise tolerance decreases as COPD progresses. Pulmonary hypertension (PH) is common in COPD and may reduce performance further. COPD patients with and without PH could potentially be identified by cardiopulmonary exercise test (CPET). However, results from previous studies are diverging, and a unified conclusion is missing. We hypothesized that CPET combined with arterial blood gases is useful to discriminate between COPD outpatients with and without PH. Methods: In total, 93 COPD patients were prospectively included. Pulmonary function tests, right heart catheterization, and CPET with blood gases were performed. The patients were divided, by mean pulmonary artery pressure, into COPD-noPH (<25 mmHg) and COPD-PH (≥25 mmHg) groups. Linear mixed models (LMMs) were fitted to estimate differences when repeated measurements during the course of exercise were considered and adjusted for gender, age, and airway obstruction. Results: Ventilatory and/or hypoxemic limitation was the dominant cause of exercise termination. In LMM analyses, significant differences between COPD-noPH and COPD-PH were observed for PaO2, SaO2, PaCO2, ventilation, respiratory frequency, and heart rate. PaO2 <61 mmHg (8.1 kPa) during unloaded pedaling, the only load level achieved by all the patients, predicted PH with a sensitivity of 86% and a specificity of 78%. Conclusion: During CPET, low exercise performance and PaO2 strongly indicated PH in COPD patients

Left ventricular dysfunction in COPD without pulmonary hypertension

Objectives We aimed to assess prevalence of left ventricular (LV) systolic and diastolic function in stable cohort of COPD patients, where LV disease had been thoroughly excluded in advance. Methods 100 COPD outpatients in GOLD II-IV and 34 controls were included. Patients were divided by invasive mean pulmonary artery pressure (mPAP) in COPD-PH (≥25 mmHg) and COPD-non-PH (<25 mmHg), which was subdivided in mPAP ≤20 mmHg and 21–24 mmHg. LV myocardial performance index (LV MPI) and strain by tissue Doppler imaging (TDI) were used for evaluation of LV global and systolic function, respectively. LV MPI ≥0.51 and strain ≤-15.8% were considered abnormal. LV diastolic function was assessed by the ratio between peak early (E) and late (A) velocity, early TDI E´, E/E´, isovolumic relaxation time, and left atrium volume. Results LV MPI ≥0.51 was found in 64.9% and 88.5% and LV strain ≤-15.8% in 62.2.% and 76.9% in the COPD-non-PH and COPD-PH patients, respectively. Similarly, LV MPI and LV strain were impaired even in patients with mPAP <20 mmHg. In multiple regression analyses, residual volume and stroke volume were best associated to LV MPI and LV strain, respectively. Except for isovolumic relaxation time, standard diastolic echo indices as E/A, E´, E/E´ and left atrium volume did not change from normal individuals to COPD-non-PH. Conclusions Subclinical LV systolic dysfunction was a frequent finding in this cohort of COPD patients, even in those with normal pulmonary artery pressure. Evidence of LV diastolic dysfunction was hardly present as measured by conventional echo indices