Commentary

Commentary on “Mechanism of augmented exercise hyperpnea in chronic heart failure and dead space loading” by Poon and Tin

Dyspnea on exertion is common to both heart failure (HF) and chronic obstructive pulmonary disease (COPD), and it is important to discriminate whether symptoms are caused by HF or COPD in clinical practice. The ventilatory equivalent for carbon dioxide (V̇_E/V̇CO₂) slope and V̇_E intercept (a reflection of pulmonary dead space) are two candidate non-invasive indices that could be used for this purpose. Thus, we compared non-invasive indexes of ventilatory efficiency in patients with HF and preserved or reduced ejection fraction (HFpEF and HFrEF, respectively) or COPD.

Patients with HFpEF (n = 21), HFrEF (n = 20), and COPD (n = 22) patients performed cardiopulmonary exercise testing to volitional fatigue. V̇_E and gas exchange were measured via breath-by-breath open circuit spirometry. All data from rest to peak exercise were used to calculate V̇_E/V̇CO₂ slope and V̇_E intercept using linear regression. Receiver operating characteristic (ROC) curves were constructed to determine optimized cutoffs for V̇_E/V̇CO₂ slope and V̇_E intercept to discriminate HFpEF and HFrEF from COPD.

HFrEF patients had a greater V̇_E/V̇CO₂ slope than HFpEF and COPD patients (HFrEF: 40 ± 9; HFpEF: 32 ± 7; COPD: 32 ± 7) (p < 0.01). COPD patients had a greater V̇_E intercept than HFpEF and HFrEF patients (COPD: 3.32 ± 1.66; HFpEF: 0.77 ± 1.23; HFrEF: 1.28 ± 1.19 L/min) (p < 0.01). A V̇_E intercept of 2.64 L/min discriminated COPD from HF patients (AUC: 0.88, p < 0.01), while V̇_E/V̇CO₂ slope did not (p = 0.11).

These findings demonstrate that V̇_E intercept, not V̇_E/V̇CO₂ slope, may discriminate COPD from both HFpEF and HFrEF patients.

The use of perioperative cardiopulmonary exercise testing (CPET) to evaluate the risk of adverse perioperative events and inform the perioperative management of patients undergoing surgery has increased over the last decade. CPET provides an objective assessment of exercise capacity preoperatively and identifies the causes of exercise limitation. This information may be used to assist clinicians and patients in decisions about the most appropriate surgical and non-surgical management during the perioperative period. Information gained from CPET can be used to estimate the likelihood of perioperative morbidity and mortality, to inform the processes of multidisciplinary collaborative decision making and consent, to triage patients for perioperative care (ward vs critical care), to direct preoperative interventions and optimization, to identify new comorbidities, to evaluate the effects of neoadjuvant cancer therapies, to guide prehabilitation and rehabilitation, and to guide intraoperative anaesthetic practice. With the rapid uptake of CPET, standardization is key to ensure valid, reproducible results that can inform clinical decision making. Recently, an international Perioperative Exercise Testing and Training Society has been established (POETTS www.poetts.co.uk) promoting the highest standards of care for patients undergoing exercise testing, training, or both in the perioperative setting. These clinical cardiopulmonary exercise testing guidelines have been developed by consensus by the Perioperative Exercise Testing and Training Society after systematic literature review. The guidelines have been endorsed by the Association of Respiratory Technology and Physiology (ARTP).

Patients with late-stage chronic obstructive pulmonary disease (COPD) are prone to CO₂ retention, a condition which has been often attributed to increased ventilation–perfusion mismatch particularly during oxygen therapy. However, patients with mild-to-moderate COPD or chronic heart failure (CHF) also suffer similar ventilatory inefficiency but they remain near-normocapnic at rest and during exercise with an augmented respiratory effort to compensate for the wasted dead space ventilation. In severe COPD, the augmented exercise ventilation progressively reverses as the disease advances, resulting in hypercapnia at peak exercise as ventilatory limitation due to increasing expiratory flow limitation and dynamic lung hyperinflation sets in. Submissive hypercapnia is an emerging paradigm for understanding optimal ventilatory control and cost/benefit decision-making under prohibitive respiratory chemical–mechanical constraints, where the need to maintain normocapnia gives way to the mounting need to conserve the work of breathing. In severe/very severe COPD, submissive hypercapnia epitomizes the respiratory controller's ‘can’t breathe, so won’t breathe’ say-uncle policy when faced with insurmountable ventilatory limitation. Even in health, submissive hypercapnia ensues during CO₂ breathing/rebreathing when the inhaled CO₂ renders normocapnia difficult to restore even with maximal respiratory effort, hence the respiratory controller's ‘ain’t fresh, so won’t breathe’ modus operandi. This ‘wisdom of the body’ with a principled decision to tolerate hypercapnia when faced with prohibitive ventilatory or gas exchange limitations rather than striving for untenable normocapnia at all costs is analogous to the notion of permissive hypercapnia in critical care, a clinical strategy to minimize the risks of ventilator-induced lung injury in patients receiving mechanical ventilation.