Paul R. Woods

Causes of breathing inefficiency during exercise in heart failure.

BACKGROUND Patients with heart failure (HF) develop abnormal pulmonary gas exchange; specifically, they have abnormal ventilation relative to metabolic demand (ventilatory efficiency/minute ventilation in relation to carbon dioxide production [V(E)/VCO₂]) during exercise. The purpose of this investigation was to examine the factors that underlie the abnormal breathing efficiency in this population. METHODS AND RESULTS Fourteen controls and 33 moderate-severe HF patients, ages 52 ± 12 and 54 ± 8 years, respectively, performed submaximal exercise (∼65% of maximum) on a cycle ergometer. Gas exchange and blood gas measurements were made at rest and during exercise. Submaximal exercise data were used to quantify the influence of hyperventilation (PaCO₂) and dead space ventilation (V(D)) on V(E)/VCO₂. The V(E)/VCO₂ relationship was lower in controls (30 ± 4) than HF (45 ± 9, P < .01). This was the result of hyperventilation (lower PaCO₂) and higher V(D)/V(T) that contributed 40% and 47%, respectively, to the increased V(E)/VCO₂ (P < .01). The elevated V(D)/V(T) in the HF patients was the result of a tachypneic breathing pattern (lower V(T), 1086 ± 366 versus 2003 ± 504 mL, P < .01) in the presence of a normal V(D) (11.5 ± 4.0 versus 11.9 ± 5.7 L/min, P = .095). CONCLUSIONS The abnormal ventilation in relation to metabolic demand in HF patients during exercise was due primarily to alterations in breathing pattern (reduced V(T)) and excessive hyperventilation.

The usefulness of submaximal exercise gas exchange to define pulmonary arterial hypertension

BACKGROUND The 6-minute walk test is widely used to characterize activity tolerance and response to therapy in pulmonary arterial hypertension (PAH) but provides little information about cardiopulmonary pathophysiology. The aim of the present study was to determine whether measures of pulmonary gas exchange during relatively light exercise could differentiate between PAH patients and healthy individuals and also stratify disease severity. METHODS The study comprised 40 PAH patients and 25 matched controls. Each completed a sub-maximal exercise test, consisting of 2 minutes of rest, 3 minutes of exercise, and 1 minute of recovery. Ventilation, pulmonary gas exchange, arterial oxygen saturation (Sao(2)), and heart rate were measured throughout using a simplified gas analysis system. RESULTS A number of gas exchange variables differentiated PAH patients and controls. End-tidal CO(2) (P(ET)co(2)) and Sao(2) were lower in PAH vs controls (31 ± 7 vs 39 ± 3 mm Hg and 89% ± 5% vs 95% ± 2%, respectively, p < 0.05). Breathing efficiency (V(E)/Vco(2) ratio) was poorer in PAH vs controls (42 ± 10 vs 33 ± 5, p < 0.05). In addition, P(ET)co(2) and V(E)/Vco(2) discriminated between different severities of PAH. CONCLUSIONS Gas exchange variables obtained during light sub-maximal exercise differentiated PAH patients from healthy controls and also between different severities of PAH. Sub-maximal exercise gas exchange may be a useful end point measure in a PAH population.

Submaximal exercise gas exchange is an important prognostic tool to predict adverse outcomes in heart failure

Traditionally, VO2peak has been used to determine prognosis in heart failure; however, this measure has limitations. Hence, other exercise and gas exchange parameters measured submaximally, e.g. breathing efficiency (VE/VCO2), end‐tidal CO2 (PETCO2), oxygen uptake efficiency slope (OUES), and circulatory power [ systolic blood pressure (SBP)], have been investigated. The aim of this study was to investigate the prognostic relevance of submaximal exercise gas exchange in heart failure patients.

A Pulmonary Hypertension Gas Exchange Severity (PH-GXS) Score to Assist With the Assessment and Monitoring of Pulmonary Arterial Hypertension

Submaximal exercise gas analysis may be a useful method to assess and track pulmonary arterial hypertension (PAH) severity. The aim of the present study was to develop an algorithm, using exercise gas exchange data, to assess and monitor PAH severity. Forty patients with PAH participated in the study, completing a range of clinical tests and a novel submaximal exercise step test, which lasted 6 minutes and incorporated rest (2 minutes), exercise (3 minutes), and recovery (1 minute) ventilatory gas analysis. Using gas exchange data, including breathing efficiency, end-tidal carbon dioxide, oxygen saturation, and oxygen pulse, a pulmonary hypertension gas exchange severity (PH-GXS) score was developed. Patients were retested after about 6 months. There was significant separation between healthy controls and patients with moderate PAH (World Health Organization [WHO] class I/II) and those with more severe PAH (WHO class III/IV) for breathing efficiency, end-tidal carbon dioxide, oxygen saturation, and oxygen pulse. The PH-GXS score was significantly correlated with WHO class (r = 0.51), 6-minute walking distance (r = -0.59), right ventricular systolic pressure (r = 0.49), log N-terminal pro-B-type natriuretic peptide (r = 0.54), and pulmonary vascular resistance (r = 0.71). The PH-GXS score remained unchanged in 22 patients retested (1.50 ± 0.92 vs 1.48 ± 0.94), as did WHO class (2.3 ± 0.8 vs 2.3 ± 0.8) and 6-minute walking distance (455 ± 120 vs 456 ± 103 m). Small individual changes were observed in the PH-GXS score, with 8 patients improving and 8 deteriorating. In conclusion, the PH-GXS score differentiated between patients with PAH and was correlated with traditional clinical measures. The PH-GXS score was unchanged in our cohort after 6 months, consistent with traditional clinical metrics, but individual differences were evident. A PH-GXS score may be a useful way to track patient responses to therapy.

Validation of a Simplified, Portable Cardiopulmonary Gas Exchange System for Submaximal Exercise Testing~!2009-10-25~!2010-01-09~!2010-03-17~!

Shape Medical Systems, Inc. has developed a new miniaturized, simplified system for non-invasive cardiopulmonary gas exchange quantification and has targeted their system for submaximal clinical exercise testing in order to abbreviate testing in an expanding clinical market during a climate of escalating health care costs. The focus of the present study was to compare this new device to a validated, standardized system for measures of cardiopulmonary gas exchange. Eighteen healthy adults (10 male/8 female, age 29±7 yr, BMI 23.8±2.4 kg/m 2 ) were brought to the laboratory and instrumented with both measurement systems via in-series pneumotachs. Additionally, the Shape system included a pulse oximeter for heart rate (HR) and oxygen saturation (SaO2), while the standard system included separate 12-lead ECG and oximetry devices. The protocol included 2-min resting breathing, followed by 3-min at each of 3 workloads (50, 70, 125 watts) on a cycle ergometer. Data were collected breath-by-breath and averaged the last 30-sec of each workload. After a 15-min rest period, the pneumotach order was reversed and the study repeated. Since gas exchange data were similar (p>0.05) within a given metabolic testing system between sessions the data were pooled for comparing the Shape and Standard systems. There were no differences (p>0.05) between the systems for oxygen consumption-VO2, carbon dioxide production-VCO2, ventilation-VE, end tidal CO2-PetCO2, tidal volume-VT, respiratory rate-fb, and HR at rest or any work load. SaO2 was slightly, but significantly lower using the Shape embedded oximeter (p 0.05). These data suggest that the new, simplified metabolic system developed by Shape Medical Systems, Inc. accurately quantifies key cardiopulmonary variables over a range of workloads, has a coefficient of variation similar to a well validated system and can be used with mouthpiece or mask.

Modulation of the central chemoreflex magnitude by the peripheral chemoreceptors: a hyperadditive effect or are we barking up the wrong tree?

Ventilation is required to precisely maintain arterial blood gases and acid–base balance within normal limits. Matching of breathing to metabolic demand involves complex integration of chemically and mechanically mediated afferent feedback to the respiratory control centre in the brain stem. At rest, ventilation is primarily controlled via detection of perturbations in arterial levels of CO2, O2 and H+ by two distinct chemoreceptive elements situated peripherally (primarily the carotid bodies, CB) and centrally (medulla oblongata). Although it is commonly accepted that both the peripheral and central chemoreceptors are important mediators of ventilatory responsiveness, it remains unclear how these receptors interact to provide coordinated control of ventilation.