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BACKGROUND The output of carbon dioxide (VCO2) is controlled by both hemodynamics and ventilation. To understand VCO2 in patients who have chronic heart failure (CHF), we studied 14 patients who had New York Heart Association functional class III failure by measurements of hemodynamics, ventilation, and arterial and venous blood gases at rest and at 50 W of cycle ergometry exercise. METHODS AND RESULTS Fick principle analysis of VCO2 showed that because of a limited increase in cardiac output, CHF patients widened their venoarterial CO2 content difference from 4.9 +/- 3.5 ml/dl at rest to 11.1 +/- 4.0 ml/dl with exercise (p less than 0.05). This increase in CO2 content difference was achieved with no change in venous CO2 content (from 54.3 +/- 3.3 ml/dl at rest to 54.5 +/- 4.8 ml/dl at exercise, p = NS); however, there was a decrease of arterial CO2 content (from 49.4 +/- 3.7 ml/dl at rest to 43.4 +/- 2.3 ml/dl with exercise, p less than 0.05). Modeling of the CO2 tension-content relation showed that there would have been a small, nonproportional increase of venous CO2 content as venous CO2 tension increased from 43.2 +/- 1.8 mm Hg at rest to 55.3 +/- 4.2 mm Hg during exercise (p less than 0.05); however, the development of metabolic acidosis during exercise entirely blunted the increase of CO2 content. In contrast, both the shape of the tension-content relation and the acidosis of exercise further influenced the decrease of arterial CO2 content as arterial CO2 tension decreased from 37.0 +/- 2.9 mm Hg at rest to 32.0 +/- 3.4 mm Hg during exercise (p less than 0.05) as a result of excess ventilation. CONCLUSIONS In CHF patients during exercise, the circulatory limitations imposed by a low cardiac output on VCO2 are compensated by a widened venoarterial CO2 content difference. The content difference is not widened through an increase of venous CO2 content but rather by a decrease of arterial CO2 content caused by arterial hypocapnia and metabolic acidosis.

The ventilatory effects of beta-adrenergic blockade during steady-state exercise were studied in eight normal subjects using intravenous propranolol hydrochloride (0.2 mg/kg). Heart rate decreased in all subjects by an average of 17%. Coincident with the phase of decreasing heart rate was a significant decrease in both minute ventilation (VE) and CO2 output (VCO2), averaging 9.6 and 9.2%, respectively. Both functions returned to prepropranolollevels after heart rate had reached its reduced steady-state value. The change in VE was significantly correlated with the change in VCO2 (r = 0.85, Pless than 0.005), and was associated with negligible changes in endtidal CO2 tensions and ventilatory equivalents for CO2. We interpret these studies as showing that the transient isocapnic hypopnea concomitant with an acute reduction in cardiac output was secondary to a transient decrease in CO2 flux (cardiac output x mixed venous CO2 content). This decrease in VE appearsto be induced by the acute decrease in cardiac output (“cardiodynamic hypopnea”), in fashion similar to the previously described cardiodynamic hyperpnea.

Arterial oxygen transport (cardiac output x arterial oxygen content) may be decreased in heart failure. We studied the determinants of arterial oxygen transport in 15 patients with chronic, severe myocardial failure at rest and during cycle ergometry. During control therapy at rest, arterial oxygen tension was normal (81 +/- 8 mm Hg, mean +/- SD) and increased slightly during exercise (90 +/- 14 mm Hg). During hydralazine therapy at rest, arterial oxygen tension was slightly higher (87 +/- 9 mm Hg) and also increased during exercise (92 +/- 15 mm Hg). Hydralazine did not increase arterial oxygen tension (0.10 greater than p greater than 0.05), but exercise did (p less than 0.02). Arterial oxygen saturation and content were normal and did not change under any condition or treatment. During control therapy at rest, arterial oxygen transport was low (313 +/- 74 ml/min . m2) and remained abnormally low during exercise (434 +/- 124 ml/min . m2). During hydralazine therapy, arterial oxygen transport was higher at rest (457 +/- 100 ml/min . m2) and during exercise (577 +/- 131 ml/min . m2). Hydralazine increased arterial oxygen transport (p less than 0.01) because it increased stroke volume at rest and during exercise, but it did not change arterial oxygenation. Arterial oxygenation is normal in chronic heart failure patients at rest and during exercise. Hydralazine increases cardiac output and arterial oxygen transport without changing arterial oxygenation.

Dyspnea and exercise limitation are ubiquitous symptoms in heart failure; the role of pulmonary factors has not been defined. We studied patients with severe left ventricular dysfunction at upright rest and during cycle ergometry. Arterial oxygen tension and saturation were normal at rest and exercise despite mild abnormalities in Qs/Qt and P(A-a)O2, as well as the effects of low S-vO2. Ventilation was increased at rest and exercise because of increased VD/VT and alveolar hyperventilation. The basis of these abnormalities is unknown. We concluded that when considering the symptoms of dyspnea and exercise limitation, arterial oxygenation is probably not important, but excessive ventilation may be a contributing factor.

The value of a new oxygen concentrator was investigated in 20 patients with COPD. The oxygenating ability of the device was compared to that of piped-in oxygen at flows of 1, 2, 4, 6, 8, and 10 l/min by measuring arterial blood gases after 14 min of breathing through a nasal cannula. For flows up to 4 l/min, the concentrator produced increases in PaO2 that were comparable to the increases resulting from piped-in oxygen. At higher flows, the PaO2 achieved by each flow of 6-10 l/min was significantly less when using the concentrator as compared to piped-in oxygen. The device was reliable, easy to use, and well accepted. It was concluded that the concentrator provides a useful alternative to piped-in oxygen or cylinders of oxygen for patients requiring flows of up to 4 l/min.

A post-right pneumonectomy syndrome is described which manifests symptoms of exertional dyspnea and inspiratory stridor on rapid inspiration. These symptoms were associated with marked rightward and posterior deviation of the trachea, over-distention of the left lung with its herniation into the right side of the chest and kinking of the left lower lobe bronchus. At the time of surgery, the tracheal deviation, lung herniation and the kink in the left lower lobe bronchus were immediately corrected by releasing the adhesions between the malpositioned structures and the right chest wall. To maintain the corrected positions, Silastic implants totalling a volume of 990 ml were placed into the space created in the right chest. Following surgery, exertional dyspnea was present with only extraordinary activity, and inspiratory stridor was eliminated. The patient remains asymptomatic three years following surgical correction, and is able to carry on a normal and productive life. We conclude that a syndrome associated with marked exertional dyspnea and inspiratory stridor might develop in situations of marked tracheal shift and overdistention of the remaining lung following right pneumonectomy.

The effects of beta-adrenergic blockade induced by intravenous propranolol hydrochloride (0.2 mg/kg) on ventilatory and gas exchange responses to exercise were studied during tests in which the work rate was either increased progressively or maintained at a constant load in six healthy young male subjects. Heart rate during exercise decreased by about 20% and cardiac output, as estimated by a modification of the method of Kim et al. (J. Appl. Physiol. 21: 1338–1344, 1966), by about 15%. The relation between work rate and O2 uptake (VO2) was unaffected by propranolol, whereas maximal O2 uptake (VO2max) decreased by 5% and the anaerobic threshold, estimated noninvasively, was lowered by 23%. The relations between CO2 output (VCO2) and end-tidal CO2 partial pressure (PCO2) and between VCO2 and minute ventilation (VE) were both unaffected. The time constants for changes of VO2, VCO2, and VE during on-transients from unloaded pedaling to either a moderate (ca. 50% VO2max) or a heavy (ca. 67% VO2max) work rate in the control studies were in agreement with previously reported values, i.e., 42, 60, and 69 s, respectively. beta-Blockade was associated with a significantly increased time constant for VO2 of 61 s but with less consistent and insignificant changes for VCO2 and VE. There was a small but significant increase of the time constant for heart rate from 40 to 45 s. It is concluded that propranolol exerts its primary influence during exercise on the cardiovascular system without any discernible effect on ventilatory control.

An attempt was made to discover whether, in conditions similar to those of Michotte, the number of causal responses given by subjects was influenced by stimulation during the period just before the main experiment. Time-intervals between the arrival of object A and the departure of object B were systematically varied within the range 60 to 390 msec. Those who had earlier been exposed to shorter time-intervals (60 to 210 msec.) gave fewer causal responses than those who had been exposed to longer ones (150 to 300 msec. and 240 to 390 msec.). A possible explanation is offered in terms of the modification of existing “schemata.”