Johnson, Bruce D.

Our lab has demonstrated a lower cardiac output (Q) in patients with heart failure (HF) vs. controls (CTL) using acetylene rebreathing (ACET). This technique may be dependent on lung health, which is altered in HF. Therefore, we examined the relationship between Q from echocardiography (echo) and Q from ACET at rest and during exercise. Additionally, we examined the relationship between stroke volume (SV) estimated from O 2 pulse compared to SV by ACET (SV A ). 26 controls (CTL) and 18 HF patients with preserved ejection fraction (EF) completed an exercise test on a cycle ergometer. Lung conductance was measured by lung diffusion for carbon monoxide (DL CO ). Measures of Q (Q A , Acetylene rebreathe; Q E , transthoracic echo), heart rate (HR, 12‐lead ECG), and oxygen consumption (VO 2 , metabolic cart) were taken at rest and peak exercise. Stroke volume (SV) and O 2 pulse were calculated as Q/HR and VO 2 /HR, respectively. HF patients had lower DL CO compared to CTL (Rest: DL CO =11±0.5 vs 14±0.6 ml/min/mmHg, p<0.05). At rest and exercise, Q E was moderately correlated with Q A in CTL (Rest: r=0.47; Pk Ex: r=0.51, p<0.05) and HF (rest: r=0.47; Pk Ex: r=0.77, p<0.05). O 2 pulse was significantly related to SV A at rest and exercise in CTL (Rest: r=0.76; Pk Ex: r=0.81, p<0.05) and HF (Rest: r=0.81; Pk Ex: r=0.82, p<0.05). Cardiac function assessed via ACET is related to cardiac function by echo and O 2 pulse in patients with HF with preserved EF.

Purpose Oxygen pulse (O 2 pulse) is often used clinically as a surrogate for stroke volume during cardiopulmonary exercise testing; however, little data exists on the validity of this measure in patient populations (e.g. heart failure with preserved ejection fraction – HFpEF). Therefore, the purpose of this study was to examine the relationship between O 2 pulse and stroke volume (SV) measured using an accepted technique, echocardiography, at rest and during exercise. Methods Eighteen HFpEF (EF=62±1%) patients and 26 healthy controls (CTL) completed an exercise test on a cycle ergometer. Average measures of oxygen consumption (VO 2 , metabolic cart), heart rate (HR, 12‐lead ECG), and SV (transthoracic echocardiography) were taken at rest and peak exercise. O 2 pulse was calculated as VO 2 divided by HR. Results O 2 pulse was significantly correlated with SV at rest and at peak exercise in CTL (r=0.60 and r=0.55, p<0.05 for both respectfully). O 2 pulse was similarly significantly correlated with SV at rest in HFpEF (r=0.58, p<0.05) whereas this relationship demonstrated a trend at peak exercise (r=0.44, p=0.06). Conclusion Our results demonstrate a moderate relationship between O 2 pulse and SV measured using echocardiography in healthy control participants at rest and during exercise. There is a similar relationship at rest in patients with HFpEF; however, this relationship is less strong during exercise.

Asthma, chronic obstructive pulmonary disease, and other respiratory disorders often occur concurrently with heart failure (HF). HF patients with respiratory disease can improve lung function and, therefore, quality of life with β‐agonists. Beta‐agonist use remains controversial as it has been linked with increased mortality risk; however, recent studies that account for co‐morbidities find no association between β‐agonist use and mortality. Previous studies exploring the cardiovascular effect of β‐agonist use in HF are primarily retrospective and focus on heart rate (HR). We have previously demonstrated altered cardiovascular function in response to albuterol in healthy subjects. In the present study we sought to comprehensively assess the cardiovascular effects of albuterol sulfate using cardiac output (Q), stroke volume (SV), HR, systolic, diastolic, and mean arterial blood pressure (SBP, DBP, MAP, respectively) and systemic vascular resistance (SVR). We hypothesized that cardiovascular parameters would be altered 30‐minutes following albuterol administration, and that HF patients using β‐blockers would have an attenuated response. Twenty‐two healthy and twenty‐two HF subjects were recruited (age=56±13 vs. 62±12yrs; height=175±10 vs. 176±9cm; weight=78±15 vs. 93±20; BMI=26±4 vs. 30±6; and BSA=2.08±0 vs. 1.93±0m 2 , for healthy and HF, respectively, p<0.05 for weight, BMI, and BSA). We found that HR and Q increased in healthy but not HF subjects at 30min following albuterol. Patients who were not on β‐blockers (n=4, 18%) had an increase in SV and a decrease in SVR with albuterol, while there was no change in patients who were on β‐blockers (n=14, 64%). These data suggest that HF patients have an attenuated cardiovascular response to inhaled albuterol, particularly with concurrent β‐blocker usage.

Feedback from active locomotor muscles contributes to the pressor response and may be more prominent in heart failure (HF) due to muscle myopathy, greater metabolite production and/or heightened sensitivity of receptors. We sought to examine the influence of metaboreflex stimulation on mean arterial pressure (MAP) in HF. Eleven HF patients (51±15yrs, NYHA Class I/II, LVEF 32±9%) and 11 controls (CTL) (42±9yrs) were recruited. Participants completed 3 study visits; 1) maximal cycle ergometry, 2) and 3) constant‐work cycling (60% peak power) for 4 min with 2 min recovery. Recovery was randomized to normal or regional circulatory occlusion (metaboreflex stimulation). Oxygen consumption (VO 2 ), carbon dioxide production (VCO 2 ), blood pressure and heart rate (HR) were measured at rest, end‐exercise and recovery. With metaboreflex stimulation, MAP and systolic blood pressure (SBP) increased in HF compared to CTL (6.8±5.8% vs −3.0±7.8%, p <0.01 and 3.4±6.4% vs −12.7±10.4%, p <0.01, respectively), with no difference in diastolic pressure ( p =0.61). HR and O 2 pulse demonstrated an attenuated return to baseline in HF (6.7±5.9% vs 1.0±6.6%, p <0.01 and −50.4±15.6 vs −72.4±6.9%, p <0.01, respectively). Metaboreflex stimulation resulted in a marked pressor response in HF relative to CTL due primarily to an influence of SBP and attenuated cardiac recovery as suggested by the persistent elevation in HR and O 2 pulse.

Background Patients with heart failure (HF) often develop pulmonary system abnormalities. Specifically, an abnormal ventilation relative to metabolic demand (V E /VCO 2 , ventilatory efficiency) during exercise has been shown to be an important marker of disease severity and prognosis. The purpose of this investigation was to focus on the factors that underlie the abnormal breathing efficiency in this population. Methods 14 controls (10 male) and 40 (36 male) mod‐severe HF patients, age 52±12 and 56±8 yrs, respectively, performed graded exercise on a cycle ergometer. Gas exchange and blood gas measurements were made during submaximal exercise (~65% peak VO 2 ) and used to quantify the influence of hyperventilation (PaCO 2 ) and dead space ventilation (V D ) on V E /VCO 2 . Results The V E /VCO 2 ratio was lower in controls (30±4) than in HF (45±9, p<0.001) due to a lower PaCO 2 and higher V D /V T that contributed an estimated 29% and 71%, respectively, to the increased V E /VCO 2 (p<0.05). The elevated V D /V T in HF was in turn the result of a tachypneic breathing pattern (lower V T , 877±306 vs 2003±504ml, p<0.01) in the presence of a relatively normal V D (9.6±3.8 vs 11.9±5.7 L/min, p=0.094). Conclusion The abnormal ventilation in relation to metabolic demand in HF during exercise is predominantly due to alterations in breathing pattern, rather than hyperventilation or changes in ventilation/perfusion relationships. HL71478

Pulse Decomposition Analysis (PDA) offers new insights into factors altering the arterial pressure pulse contour. PDA premise is that peripheral arterial pressure pulse envelope consists of distinct component pressure pulses, a left ventricular ejection and its reflections. Two PDA parameters appear to be particularly useful in quantifying the pulse contour. P2P1 is the ratio of second component pulse and primary ejection pulse amplitudes. T13 is the temporal delay between the third component pulse and the primary ejection pulse. P2P1 and T13 parameters were used to examine pressure pulse contour changes in 81 healthy subjects (18–27 yrs; BMI 27.5 ± 2.6) undergoing a Stroop mental stress test, cycle ergometer stress tests (3 min; 50W and 100W), and post‐exercise recovery. Digital pressure pulse contours were recorded/quantified using PDA formalism. Relative to baseline, P2P1 increased 8% post‐Stroop (individual variation 0% to 15%), T13 increased 4%, (individual variation 0% to 8%). Exercise decreased P2P1 21 ± 14%, while the T13 change was 19 ± 15%. PDA‐based pulse propagation model quantifies physical changes that arterial pulse reflection sites undergo. Peripheral arterial pressure pulse appears to be due to the primary ejection pulse and two major reflections. Two reflection sites in the central arteries appear to be responsible for the “reflected” wave part of the pulse contour.

BACKGROUND: Peak flow testing is a common procedure performed in ambulatory care. There are currently no data regarding aerosol generation during this procedure. Given the ongoing debate regarding the potential for aerosol transmission of SARS-CoV-2, we aimed to quantify and characterize aerosol generation during peak flow testing. METHODS: Five healthy volunteers performed peak flow maneuvers in a particle-free laboratory space. Two devices continuously sampled the ambient air during the procedure. One device can detect ultrafine particles 0.02–1 μ m in diameter, while the second device can detect particles 0.3, 0.5, 1.0, 2.0, 5.0, and 10 μ m in diameter. Five different peak flow meters were compared to ambient baseline during masked and unmasked tidal breathing. RESULTS: Ultrafine particles (0.02–1 μ m) were generated during peak flow measurement. There was no significant difference in ultrafine particle mean concentration between peak flow meters ( P = .23): Respironics (1.25 ± 0.47 particles/mL), Philips (3.06 ± 1.22), Clement Clarke (3.55 ± 1.22 particles/mL), Respironics Low Range (3.50 ± 1.52 particles/mL), and Monaghan (3.78 ± 1.31 particles/mL). Ultrafine particle mean concentration with peak flow testing was significantly higher than masked (0.22 ± 0.29 particles/mL) and unmasked tidal breathing (0.15 ± 0.18 particles/mL, P = .01), but the ultrafine particle concentrations were small compared to ambient particle concentrations in a pulmonary function testing room (89.9 ± 8.95 particles/mL). CONCLUSIONS: In this study, aerosol generation was present during peak flow testing, but concentrations were small compared to the background particle concentration in the ambient clinical environment. Surgical masks and eye protection are likely sufficient infection control measures during peak expiratory flow testing in asymptomatic patients with well controlled respiratory symptoms, but COVID-19 testing remains prudent in patients with acute respiratory symptoms prior to evaluation and peak expiratory flow assessment while the community prevalence of SARS-CoV-2 cases remains high.

There are growing concerns that the COVID-19 pandemic has facilitated a sedentary shift in our physical activity habits. A reduction in physical activity during the pandemic may be secondary to restrictive policies implemented at the government-level, typically those policies which limit interpersonal contact; for example, physical/social distancing. It is without question that social distancing is a necessary measure to mitigate community transmission of the novel virus; however, these policies often limit the public’s opportunities to engage in physical activity. The strictest enforcement of social distancing occurs during an authority-mandated ‘lockdown’ (also known as a ‘shelter-in-place’ or ‘stay-at-home’ order). This Viewpoint focuses on the current evidence demonstrating that physical activity declines during a COVID-19 ‘lockdown’. We highlight the point that most of the available evidence stems from investigations using non-validated, self-reported measures of physical activity and discuss the caveats therewith. This Viewpoint explores whether current evidence reflects an ‘actual’ or rather a ‘perceived’ reduction in physical activity, and raises the question of whether this distinction matters in the end.