Operation Everest II: Cardiac filling pressures during cycle exercise at sea level

Reeves, John Τ.; Groves, Bertron Μ.; Cymerman, Allen; Sutton, John R.; Wagner, Peter D.; Turkevich, Darya; Houston, C. Stuart

doi:10.1016/0034-5687(90)90078-d

Cited by 113 publications

(76 citation statements)

References 19 publications

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“…The increase in PCWP calculated as a ratio to the increase in RAP, as previously suggested [26], is unaffected by intrathoracic pressure swings. This ratio might therefore be of potential help in the difficult situation of a high PCWP with exercise in the presence of intrathoracic pressure swings, a situation that is common in COPD patients.…”

Section: Discussionmentioning

confidence: 74%

Measuring central pulmonary pressures during exercise in COPD: how to cope with respiratory effects

et al. 2013

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Respiratory influences are major confounders when evaluating central haemodynamics during exercise. We studied four different methods to assess mean pulmonary artery pressure (mPAP) and pulmonary capillary wedge pressure (PCWP) in cases of respiratory swings.Central haemodynamics were measured simultaneously with oesophageal pressure during exercise in 30 chronic obstructive pulmonary disease (COPD) patients. mPAP and PCWP were assessed at the end of expiration, averaged over the respiratory cycle and corrected for the right atrial pressure (RAP) waveform estimated intrathoracic pressure, and compared with the transmural pressures.Bland-Altman analyses showed the best agreement of mPAP averaged over the respiratory cycle (bias (limits of agreement) 2.5 (-6.0-11.8) mmHg) and when corrected with the nadir of RAP (-3.6 (-11.2-3.9) mmHg). Measuring mPAP at the end of expiration (10.3 (0.5-20.3) mmHg) and mPAP corrected for the RAP swing (-9.3 (-19.8-2.1) mmHg) resulted in lower levels of agreement. The respiratory swings in mPAP and PCWP were similar (r 2 50.82, slope¡SE 0.95¡0.1). Central haemodynamics measured at the end of expiration leads to an overestimation of intravascular pressures in exercising COPD patients. Good measurement can be acquired even when oesopghageal pressure is omitted, by averaging pressures over the respiratory cycle or using the RAP waveform to correct for intrathoracic pressure. Assessment of the pulmonary gradient is unaffected by respiratory swings. @ERSpublications Measurement of intravascular pressures in exercising COPD patients requires correction for intrathoracic pressure

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Section: Discussionmentioning

confidence: 74%

Measuring central pulmonary pressures during exercise in COPD: how to cope with respiratory effects

et al. 2013

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“…Moreover, PAWP was increasing during exercise after PEA, which can be interpreted both as a physiological response to the increased CO but partially also as a response unmasking previously unknown left ventricular diastolic dysfunction. With the latter in mind, it is interesting to observe PAWP values >20 mm Hg throughout exercise in elderly subjects [23,48] . Nevertheless, we conclude that our patients mainly exhibited precapillary PH as (1) the steep TPG/CO slope of our patients before PEA was reflecting a disproportionate increase in mPAP during exercise and (2) mean DPG at baseline was >5 mm Hg indicating a predominantly precapillary PH [44] .…”

Section: Discussionmentioning

confidence: 99%

Pulmonary Hemodynamic Response to Exercise in Chronic Thromboembolic Pulmonary Hypertension before and after Pulmonary Endarterectomy

Richter

Sommer²,

Gall³

et al. 2015

Respiration

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put (CO) from 4.4 ± 0.8 to 6.5 ± 1.9 l/min and diastolic pulmonary gradient (DPG) from 14.6 ± 4.9 to 20.7 ± 12.7 mm Hg. Post-PEA mPAP increased from 23.7 ± 6.6 at rest to 43.2 ± 7.1 mm Hg, while CO increased to a higher extent from 5.1 ± 0.9 to 8.4 ± 1.9 l/min. There were significant correlations between pre-PEA DPG/CO and dPAP/CO slopes with the pulmonary vascular resistance (Spearman r = 0.578, p = 0.019, and r = 0.547, p = 0.028) and mPAP at rest after PEA (Spearman r = 0.581, p = 0.018, and r = 0.546, p = 0.028). Conclusions: In CTEPH, the presurgical dynamic DPG/CO and dPAP/ CO slopes during submaximal exercise are associated with the hemodynamic outcome 1 year after PEA.

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“…Thus the power output generated by the muscle is less, and the stimulus for muscle hypertrophy and myosin synthesis must be equivalently less. Moreover, although submaximal heart rates and lactates are higher during hypoxic exercise compared to normoxic exercise, maximal heart rate, cardiac output, and peak lactate during high-intensity exercise are reduced (Sutton et al, 1988Cymerman et al, 1989;Hochachka, 1989;Reeves et al, 1990Reeves et al, , 1991Reeves et al, , 1992Reeves, 1999), arguing that neither the cardiovascular system nor the metabolic state of skeletal muscle are "stressed" to a greater degree (McClelland et al, 1998).…”

Section: Levinementioning

confidence: 99%

Intermittent Hypoxic Training: Fact and Fancy

Levine

2002

High Altitude Medicine & Biology

163

142

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LTITUD E TRAINING has been used frequently by endurance athletes to enhance performance. However, not all athletes or teams have the resources to travel to high altitude environments on a regular basis. Moreover, issues such as availability of adequate training facilities have limited the use of mountain-based altitude training. In the last few years, there has been a remarkable increase in the number of techniques designed to "bring the mountain to the athlete." Nitrogen houses, hypoxia tents, and special breathing apparatuses to provide inspired hypoxia at rest and during exercise, all have been developed and promoted to simulate what are perceived as the critical elements of altitude training.Intermittent hypoxic training (IHT) refers to the discontinuous use of normobaric or hypobaric hypoxia, in an attempt to reproduce some of these key features of altitude acclimatization, with the ultimate goal to improve sea-level athletic performance. In general, IHT can be divided into two different strategies: (1) providing hypoxia at rest with High Alt Med Biol. 3:177-193, 2002.-Intermittent hypoxic training (IHT) refers to the discontinuous use of normobaric or hypobaric hypoxia, in an attempt to reproduce some of the key features of altitude acclimatization, with the ultimate goal to improve sea-level athletic performance. In general, IHT can be divided into two different strategies: (1) providing hypoxia at rest with the primary goal being to stimulate altitude acclimatization or (2) providing hypoxia during exercise, with the primary goal being to enhance the training stimulus. Each approach has many different possible application strategies, with the essential variable among them being the "dose" of hypoxia necessary to achieve the desired effect. One approach, called living high-training low, has been shown to improve sea-level endurance performance. This strategy combines altitude acclimatization (2500 m) with low altitude training to ensure high-quality training. The opposite strategy, living low-training high, has also been proposed by some investigators. The primacy of the altitude acclimatization effect in IHT is demonstrated by the following facts: (1) living high-training low clearly improves performance in athletes of all abilities, (2) the mechanism of this improvement is primarily an increase in erythropoietin, leading to increased red cell mass, V O 2max , and running performance, and (3) rather than intensifying the training stimulus, training at altitude or under hypoxia leads to the opposite effect-reduced speeds, reduced power output, reduced oxygen flux-and therefore is not likely to provide any advantage for a well-trained athlete.

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Operation Everest II: Cardiac filling pressures during cycle exercise at sea level

Cited by 113 publications

References 19 publications

Measuring central pulmonary pressures during exercise in COPD: how to cope with respiratory effects

Measuring central pulmonary pressures during exercise in COPD: how to cope with respiratory effects

Pulmonary Hemodynamic Response to Exercise in Chronic Thromboembolic Pulmonary Hypertension before and after Pulmonary Endarterectomy

Intermittent Hypoxic Training: Fact and Fancy

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