Dyspnea Postpulmonary Embolism From Physiological Dead Space Proportion and Stroke Volume Defects During Exercise

Fernandes, Timothy; Alotaibi, Mona; Strozza, Danielle M.; Stringer, William W.; Pórszász, János; Faulkner, Garner George; Castro, Cara F.; Tran, Don A.; Morris, Timothy A.

doi:10.1016/j.chest.2019.10.047

Cited by 32 publications

(46 citation statements)

References 28 publications

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“…32 In a fourth recently published retrospective cohort study, 40 PE patients with persistent exertional dyspnea were subjected to CPET. 33 Increased dead-space ventilation (Vd/Vt), decreased stroke volume reserve (oxygen pulse, indicating an insufficient stroke volume for the demand imposed), or both were evident in two-thirds of the study population during incremental exercise. 34 These responses have repeatedly been found in small case series studying specific patients with chronic emboli.…”

Section: Cardiopulmonary Responses To Exercisementioning

confidence: 95%

Determinants and Management of the Post–Pulmonary Embolism Syndrome

Boon

Huisman

Klok

2021

Semin Respir Crit Care Med

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Acute pulmonary embolism (PE) is not only a serious and potentially life-threatening disease in the acute phase, in recent years it has become evident that it may also have a major impact on a patient's daily life in the long run. Persistent dyspnea and impaired functional status are common, occurring in up to 50% of PE survivors, and have been termed the post-PE syndrome (PPES). Chronic thromboembolic pulmonary hypertension is the most feared cause of post-PE dyspnea. When pulmonary hypertension is ruled out, cardiopulmonary exercise testing can play a central role in investigating the potential causes of persistent symptoms, including chronic thromboembolic pulmonary disease or other cardiopulmonary conditions. Alternatively, it is important to realize that post-PE cardiac impairment or post-PE functional limitations, including deconditioning, are present in a large proportion of patients. Health-related quality of life is strongly influenced by PPES, which emphasizes the importance of persistent limitations after an episode of acute PE. In this review, physiological determinants and the diagnostic management of persistent dyspnea after acute PE are elucidated.

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Section: Cardiopulmonary Responses To Exercisementioning

confidence: 95%

Determinants and Management of the Post–Pulmonary Embolism Syndrome

Boon

Huisman

Klok

2021

Semin Respir Crit Care Med

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“…16,17,30,31 Another prevalent condition causing the post-PE syndrome however is deconditioning after the acute cardiovascular event. 24,25,[32][33][34][35] Clinical presentation of CTEPH Diagnosing CTEPH is challenging because signs of right heart failure only become evident in advanced disease stages and earlier disease stages are characterised by non-specific or even absence of symptoms. In the International CTEPH Registry, the most common presenting symptom was dyspnoea (99%), followed by oedema (41%), fatigue (32%), chest pain (15%) and syncope (14%).…”

Section: Who and When To Test For Cteph?mentioning

confidence: 99%

Diagnosis of chronic thromboembolic pulmonary hypertension after acute pulmonary embolism

et al. 2020

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Chronic thromboembolic pulmonary hypertension (CTEPH) is the most severe long-term complication of acute pulmonary embolism (PE). Untreated CTEPH is fatal, but, if diagnosed in time, successful surgical (pulmonary endarterectomy), medical (pulmonary hypertension drugs) and/or interventional (balloon pulmonary angioplasty) therapies have been shown to improve clinical outcomes, especially in case of successful pulmonary endarterectomy. Early diagnosis has however been demonstrated to be challenging. Poor awareness of the disease by patients and physicians, high prevalence of the post-PE syndrome (i.e. persistent dyspnoea, functional limitations and/or decreased quality of life following an acute PE diagnosis), lack of clear guideline recommendations as well as inefficient application of diagnostic tests in clinical practice lead to a reported staggering diagnostic delay >1 year. Hence, there is a great need to improve current clinical practice and diagnose CTEPH earlier. In this review, we will focus on the clinical presentation of and risk factors for CTEPH, and provide best practices for PE follow-up programmes from expert centres, based on a clinical case.

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“…Prior studies to compare TcPCO 2 with PaCO 2 during exercise in patients have often failed to obtain simultaneous measurements, have required at least one PaCO 2 measurement, or have not calculated V D /V T [11][12][13][14]. Recently, Fernandes et al compared TcPCO 2 with PaCO 2 , but the validation was only during rest and was not extended into exercise [15]. The most rigorous prior exercise study in 14 patients (including COPD, ischemic heart disease and hyperventilation syndrome) found narrow limits of agreement between V D /V T calculated from TcPCO 2 and PaCO 2 (mean bias: 0; CI À0.02 to þ0.02), but used an "in vivo calibration" method where the TcPCO 2 values were calibrated using a resting PaCO 2 measurement prior to the exercise test [16].…”

Section: Introductionmentioning

confidence: 99%

Transcutaneous PCO₂ for Exercise Gas Exchange Efficiency in Chronic Obstructive Pulmonary Disease

Cao

Stringer

Corey

et al. 2021

COPD: Journal of Chronic Obstructive Pulmonary Disease

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Gas exchange inefficiency and dynamic hyperinflation contributes to exercise limitation in chronic obstructive pulmonary disease (COPD). It is also characterized by an elevated fraction of physiological dead space (V D /V T). Noninvasive methods for accurate V D /V T assessment during exercise in patients are lacking. The current study sought to compare transcutaneous PCO 2 (TcPCO 2) with the gold standard-arterial PCO 2 (PaCO 2)-and other available methods (end tidal CO 2 and the Jones equation) for estimating V D /V T during incremental exercise in COPD. Ten COPD patients completed a symptom limited incremental cycle exercise. TcPCO 2 was measured by a heated electrode on the ear-lobe. Radial artery blood was collected at rest, during unloaded cycling (UL) and every minute during exercise and recovery. Ventilation and gas exchange were measured breath-bybreath. Bland-Altman analysis examined agreement of PCO 2 and V D /V T calculated using PaCO 2 , TcPCO 2 , end-tidal PCO 2 (P ET CO 2) and estimated PaCO 2 by the Jones equation (PaCO 2-Jones). Lin's Concordance Correlation Coefficient (CCC) was assessed. 114 measurements were obtained from the 10 COPD subjects. The bias between TcPCO 2 and PaCO 2 was 0.86 mmHg with upper and lower limit of agreement ranging À2.28 mmHg to 3.99 mmHg. Correlation between TcPCO 2 and PaCO 2 during rest and exercise was r 2 ¼0.907 (p < 0.001; CCC ¼ 0.941) and V D /V T using TcPCO 2 vs. PaCO 2 was r 2 ¼0.958 (p < 0.0001; CCC ¼ 0.967). Correlation between PaCO 2-Jones and P ET CO 2 vs. PaCO 2 were r 2 ¼0.755, 0.755, (p < 0.001; CCC ¼ 0.832, 0.718) and for V D /V T calculation (r 2 ¼0.793, 0.610; p < 0.0001; CCC ¼ 0.760, 0.448), respectively. The results support the accuracy of TcPCO 2 to reflect PaCO 2 and calculate V D /V T during rest and exercise, but not in recovery, in COPD patients, enabling improved accuracy of noninvasive assessment of gas exchange inefficiency during incremental exercise testing.

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Dyspnea Postpulmonary Embolism From Physiological Dead Space Proportion and Stroke Volume Defects During Exercise

Cited by 32 publications

References 28 publications

Determinants and Management of the Post–Pulmonary Embolism Syndrome

Determinants and Management of the Post–Pulmonary Embolism Syndrome

Diagnosis of chronic thromboembolic pulmonary hypertension after acute pulmonary embolism

Transcutaneous PCO₂ for Exercise Gas Exchange Efficiency in Chronic Obstructive Pulmonary Disease

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Dyspnea Postpulmonary Embolism From Physiological Dead Space Proportion and Stroke Volume Defects During Exercise

Cited by 32 publications

References 28 publications

Determinants and Management of the Post–Pulmonary Embolism Syndrome

Determinants and Management of the Post–Pulmonary Embolism Syndrome

Diagnosis of chronic thromboembolic pulmonary hypertension after acute pulmonary embolism

Transcutaneous PCO2 for Exercise Gas Exchange Efficiency in Chronic Obstructive Pulmonary Disease

Contact Info

Product

Resources

About

Transcutaneous PCO₂ for Exercise Gas Exchange Efficiency in Chronic Obstructive Pulmonary Disease