Exercise gas exchange, breath-by-breath.
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Biomedical subjects
Publications and source records attributed to Karlman Wasserman.
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BACKGROUND: Because of high pulmonary vascular resistance in patients with primary pulmonary hypertension (PPH), right atrial pressure may exceed left atrial pressure during exercise, resulting in a right-to-left shunt via a patent foramen ovale (PFO). This shunting would disturb arterial PCO2 and H+ homeostasis if the pulmonary blood were not simultaneously hyperventilated to compensate for the high CO2 and H+ in the shunted blood. This article first hypothesizes and then describes unique changes in gas exchange when right-to-left exercise-induced shunting (EIS) occurs. METHODS AND RESULTS: Retrospectively, the cardiopulmonary exercise tests of 71 PPH patients were studied. Criteria postulated to document hyperventilation of the pulmonary blood flow due to a right-to-left EIS were (1) an abrupt and sustained increase in end-tidal O2 with a simultaneous sustained decrease in end-tidal CO2; (2) an abrupt and sustained increase in the respiratory exchange ratio; and (3) usually, an associated decline in pulse oximetry saturation. Each patient was evaluated for a PFO with resting echocardiography. The investigators interpreting the gas exchange evidence of EIS were blinded to the echocardiographic readings. Forty-five percent of the patients had demonstrable EIS by gas exchange criteria. Almost all were also positive for a PFO by echocardiography. Using the resting echocardiograph as the reference, the sensitivity, specificity, positive and negative predictive values, and accuracy were all between 90% to 96%. CONCLUSIONS: Exercise-induced right-to-left shunting can be detected by noninvasive, cardiopulmonary exercise testing in patients with PPH.
PURPOSE: The kinetics of the decrease in venous O(2) content in response to constant work rate exercise below the lactic acidosis threshold (LAT) is very rapid, reaching a constant value by approximately 1 min. However, for work rates above the LAT, a slow further decrease in venous O(2) content takes place that is attributable to the Bohr effect rather than further decrease in end capillary PO. We hypothesized that similar differences, with respect to the LAT, will be observed in muscle deoxygenation kinetics when studied with near-infrared spectroscopy (NIRS). METHODS: Twelve normal subjects performed three constant work rate tests from unloaded cycling at 60% of LAT, 80% LAT, each with four repetitions, and above LAT (LAT + 35% between LAT and VO(2max) three times, on a cycle ergometer for 6 min. We measured tissue deoxygenation with NIRS, with the probe over the vastus lateralis muscle, time-averaging the repetitions. Gas exchange and heart rate (HR) were measured breath-by-breath and beat-by-beat. RESULTS: Tissue deoxygenation kinetics were significantly faster than VO(2) and HR at 60%- and 80%-LAT work rates. By 1 min of exercise, deoxygenation was constant for the work rate below the LAT. At 30 s, tissue deoxygenation was 70-95% complete, whereas VO(2) and HR were only 30-60% complete. For the work rate above the LAT, a steady state for muscle deoxygenation was not reached during the 6 min of exercise. After 1 min of above-LAT exercise, either one of two patterns of slow change in tissue oxygenation developed, deoxygenation or reoxygenation. It is postulated that these different responses might be due to effects of the exercise lactic acidosis. H accompanying lactate increase might cause further deoxygenation due to the Bohr effect, and acidosis-induced vasodilatation might cause reoxygenation after the initial deoxygenation. CONCLUSION: 1) The kinetics of tissue deoxygenation are significantly more rapid than VO(2) and HR kinetics at all work rates studied, and 2) steady-state in tissue deoxygenation is seen by 1 min of constant work rate exercise below the LAT, but this is much delayed for work rates above the LAT.