BACKGROUND
 
Pulmonary function tests (PFTs) are highly sensitive to derangements in the cardiopulmonary unit. Recognizing the effects of cardiac disease on PFTs is paramount to proper testing interpretation, a task particularly challenging in the presence of coexisting respiratory disorders.
 
OVERVIEW
 
A 72-year-old former smoker underwent PFTs due to out-of-proportion dyspnea after treatment optimization for heart failure with reduced ejection fraction (HFrEF). RV and functional residual capacity (FRC) were markedly increased (~160%) despite only a mild and proportional decrease in post-bronchodilator (BD) FEV1 and FVC with preserved TLC. Given air trapping and smoking history, long-acting BDs were initiated with rapid improvement in dyspnea (case #1). An 81-year-old former smoker admitted to the hospital due to HFrEF decompensation showed “fixed” obstruction with a low DLCO a week after discharge. The patient refused BD treatment for potential COPD. Two months later, all PFTs were within normal range (case #2).
 
Clinical interpretation of PFTs in cardiac disease associated with lung congestion and/or low cardiac output is full of pitfalls.(1,2) In chronic HFrEF, decrements in lung volumes (low lung compliance, alveolar filling, cardiomegaly) and, in some patients, inspiratory muscle weakness might cause restriction. If severe enough, this may “normalize” spirometry and counterbalance any hyperinflation in coexisting COPD.(3) Air trapping is not commonly seen in stable HFrEF and, in the proper clinical context, might signal underlying airway disease (case #1; Figure 1A). Exaggerated ventilation(4) coupled with poor muscle O2 delivery on cardiopulmonary exercise testing might suggest that HFrEF contributes to exertional dyspnea in COPD. Overt obstruction with reduced mid-expiratory flows due to peribronchiolar cuffing, mucosal swelling, and vagal reflexes may occur in acute decompensated HFrEF (“cardiac asthma”; Figure 1B). These abnormalities may take weeks to resolve (case #2), frequently accompanied by airway hyperresponsiveness.(5) Although higher capillary blood volume may increase the “vascular” conductance to gas transfer, this is superseded by increases in the “membrane” resistance. Thus, mild-moderate decreases in DLCO—worsening with HFrEF progression—may make it difficult to portion out the contribution of any underlying lung disease (e.g., COPD, interstitial lung disease) to a low DLCO (Figure 1B).
 

 
In contrast with HFrEF, mild decrement in FEV1/(F)VC and increases in RV are frequently seen in patients with stable moderate-to-severe mitral valve disease, likely because of the congested vessels in alveolar walls impeding their complete deflation. Congenital heart disease associated with left (L)-to-right (R) shunt and increased capillary blood volume may increase DLCO and carbon monoxide transfer coefficient (KCO). Mild hypoxemia and an increased alveolar-arterial O2 gradient may occur due to ventilation/perfusion mismatch. Severe hypoxemia is the hallmark of patients with R-to-L shunt (e.g., tetralogy of Fallot, Eisenmenger syndrome), the shunted fraction being estimated by the 100% O2 inhalation test.(6)
 
CLINICAL MESSAGE
 
Given that respiratory and cardiac disease often coexist and given the overlapping consequences to lung function, the pulmonologist should recognize the “shades of gray” when interpreting PFTs in these patients. Frequently, little is known about the pre-test likelihood of disease or disease severity/stability in patients with known cardiac disease. Thus, the report should cautiously state that testing results should be analyzed considering the individual’s clinical context.
 
AUTHOR CONTRIBUTIONS
 
All authors contributed to conceptualization, writing, reviewing, and editing.
 
CONFLICTS OF INTEREST
 
None declared.
 
REFERENCES
 
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2.Neder JA, Rocha A, Alencar MCN, Arbex F, Berton DC, Oliveira MF, et al. Current challenges in managing comorbid heart failure and COPD. Expert Rev Cardiovasc Ther. 2018;16(9):653-673. https://doi.org/10.1080/14779072.2018.1510319
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6.Neder JA, Berton DC, O’Donnell DE. Integrating measurements of pulmonary gas ex-change to answer clinically relevant questions. J Bras Pneumol. 2020;46(1):e20200019. https://doi.org/10.1590/1806-3713/e20200019