Excessive Ventilation Research Articles

Effects of Chronic Hypoxemia on Chemosensitivity in Patients With Univentricular Heart

Objectives. We sought to compare the arterial blood gas chemosensitivity in relation to exercise ventilatory response in patients with univentricular heart and cyanosis and in patients with univentricular heart and Fontan-type circulation without cyanosis.Background. Patients with univentricular heart demonstrate excessive ventilation during exercise. Chronic hypoxemia may alter chemoreceptor function, affecting ventilation.Methods. Cardiopulmonary exercise testing was performed in 10 patients with rest or stress-induced cyanosis (cyanotic group: mean age ± SE 30.5 ± 2.3 years; 5 men), 8 patients without cyanosis with Fontan-type circulation (Fontan group: mean age 29.4 ± 1.5 years; 4 men) and 10 healthy control subjects (normal group: mean age 30.7 ± 1.9 years; 5 men). Hypoxic and hypercapnic chemosensitivity were assessed by using transient inhalations of pure nitrogen and the rebreathing of 7% CO2in 93% O2, respectively.Results. Peak O2consumption was comparable in both patient groups (21.7 ± 2.5 [cyanotic group] vs. 21.0 ± 1.9 ml/kg per min [Fontan group]) but was lower than that in the normal group (34.7 ± 1.9 ml/kg per min). The ventilatory response to exercise, characterized by the regression slope relating minute ventilation to CO2output, was higher in the cyanotic group (43.4 ± 4.0) than in the Fontan group (31.4 ± 3.0, p = 0.02) and the normal group (23.1 ± 1.1). Hypoxic chemosensitivity was blunted in the cyanotic group compared with that in the Fontan and normal groups (0.148 vs. 0.448 [p = 0.02] vs. 0.311 liter/min per percent arterial O2saturation, respectively) and did not correlate with the ventilatory response to exercise (r = −0.36, p = 0.29). In contrast, hypercapnic chemosensitivity represented by the slope of the hypercapnic-ventilatory response line was similar in the cyanotic, Fontan and normal groups (1.71 vs. 1.76 vs. 1.70 liter/min per mm Hg, respectively), but the response line had shifted to the left in the cyanotic group (x intercept = 31.9 vs. 39.9 mm Hg [p = 0.026]), compared with 45.2 mm Hg in normal subjects. These findings suggest that in the cyanotic group, ventilation is greater for a given level of arterial CO2tension and thus may partly explain the increased exercise ventilatory response in this group.Conclusions. Hypoxic chemosensitivity is blunted in patients with univentricular heart and cyanosis and does not determine the exercise ventilatory response. CO2elimination appears more important. The blunting of hypoxic chemosensitivity is reversible once chronic hypoxemia is relieved, as evident in the Fontan group.

Trickle ventilators: Field measurements in refurbished offices

Sununary This paper describes field measurements to assess the effectiveness of trickle ventilators in providing adequate and controlled background ventilation in office buildings during the heating season. The tests were at full-scale in two multi-storey office buildings. Both are located within a built-up area and recently refurbished. Carbon dioxide, air ventilation rates, temperatures and relative humidity were monitored for two weeks in one open-plan office in both buildings. It was concluded that resultant internal airspeeds are low, thus minimising the possibility of cold draughts. Metabolic carbon dioxide levels are not excessive and adequate ventilation is provided. It was also found that occupants use trickle ventilators regularly to control their environment once they are familiar with their operation.

The increased ventilatory response to exercise in chronic heart failure: relation to pulmonary pathology.

OBJECTIVE: To assess the exercise limitation of patients with chronic heart failure (CHF) and its relation to possible pulmonary and ventilatory abnormalities. SETTING: A tertiary referral centre for cardiology. METHODS:...

Regulation of Breathing and Perception of Dyspnea in Healthy Pregnant Women

To examine if the perception of dyspnea during normal pregnancy may be related to an inappropriate ventilatory response to the increased metabolic rate, due to a higher chemosensitivity. At weeks 12, 24, and 36 of gestation and 4 months after delivery, 11 healthy pregnant women with dyspnea and 12 asymptomatic pregnant women were studied. Progesterone plasma levels, lung volumes, diffusion capacity, maximal respiratory pressures, rest oxygen uptake, breathing pattern, and mouth occlusion pressure (P0.1) were measured. Progressive isocapnic hypoxic stimulation and progressive hyperoxic hypercapnic stimulation were performed. Oxygen ventilation equivalent during pregnancy was significantly higher for the dyspneic group than for nondyspneic pregnant women. Dyspneic patients exhibited greater minute ventilation, tidal volume, and P0.1 than the nondyspneic group. The mean values of ventilatory and P0.1 slopes to hypoxia and CO2 during pregnancy were significantly greater in the patients with dyspnea than in asymptomatic subjects. These changes were not due to differences in progesterone plasma levels. A significant relation among the Borg score, inspiratory drive, and chemosensitivity was found. In some pregnant women, a higher sensitivity to CO2 and hypoxia may induce excessive ventilation to metabolic demand, which would contribute to dyspnea.

Leg blood flow, metabolism and exercise capacity in chronic stable heart failure

Objectives: To assess the metabolic state of skeletal muscle during exercise in patients with chronic heart failure (CHF) and relate this to exercise capacity. Background: During exercise in CHF, there is little relation between exercise capacity and central haemodynamic function. Skeletal muscle and limb blood flow are abnormal in CHF. We investigated the relationship between leg blood flow, metabolism and exercise capacity and ventilation in 10 patients (average age 63.3 ± 6.0 years; 3 female) with stable CHF. Methods: Patients undertook maximal exercise testing. Peak oxygen consumption (V̇O 2) and the slope of the relationship between ventilation and carbon dioxide production V̇E/V̇CO 2 slope) were derived. During a supine cycle exer cardiac output (CO) by Doppler echocardiography, femoral blood flow (FBF) by thermodilution, pulse and blood pressure were recorded, and radial arterial and femoral venous blood samples taken for catecholamine, lactate and potassium estimation every 3 min. Results: The average peak V̇O 2 was 19.7 (± 5.2; range 11.3–29.0) ml/kg/min. The proportion of CO to the right leg increased from 0.08 (± 0.03) to 0.22 (± 0.06) ( P < 0.001) at 3 min, with no further significant change thereafter. There was a linear increase in leg V̇O 2 reaching a plateau towards peak. At peak, femoral venous saturation was 22.79% ± 7.20%. Venous lactate and potassium were higher than arterial ( P < 0.001 for each comparison). There was no correlation between exercise performance and any of the measured metabolites either in absolute measurements, expressed as change from rest to peak exercise or as arterio-venous difference. The closest correlate of leg V̇O 2 was leg hydrogen ion production, V̇[H + Change in femoral venous lactate from rest to peak exercise correlated with V ̇ E V ̇ CO 2 slope before the anaerobic threshold ( r = − 0.80; P = 0.025). Conclusions: In CHF, exercise capacity is not determined by individual haemodynamic events, and does not seem to be determined by the possible humoral signals we investigated. Ventilation is abnormal before anaerobic threshold, and predicts subsequent lactate rise, suggesting that skeletal muscle is the origin of excessive ventilation.

Dissociation between exertional symptoms and circulatory function in patients with heart failure.

Patients with heart failure frequently report exertional dyspnea and fatigue. These symptoms are usually attributed to circulatory dysfunction and therefore are typically treated with cardiovascular medications. Serial assessment of exertional symptoms has also become the principal method used to assess drug efficacy in heart failure. Nevertheless, the relation between exertional symptoms in heart failure and circulatory dysfunction remains uncertain. This study was undertaken to investigate the relation between exertional symptoms, ventilatory and skeletal muscle dysfunction, and circulatory function in patients with heart failure. To this end, 52 ambulatory patients with heart failure underwent hemodynamic monitoring during maximal treadmill exercise testing. During exercise, the severity of dyspnea and fatigue was evaluated on a scale of 6 to 20 (Borg scale). The level of perceived exercise intolerance during daily activities was evaluated with the Minnesota Living With Heart Failure Questionnaire and the Yale Dyspnea-Fatigue Index. Maximal treadmill exercise increased the VO2 to 13.4 +/- 2.8 mL.min-1.kg-1, the dyspnea score to 15.7 +/- 2.3, the fatigue score to 14.8 +/- 3.4, the pulmonary wedge pressure to 28 +/- 11 mm Hg, and the pulmonary artery lactate concentration to 34.5 +/- 16.3 mg/dL and decreased the pulmonary artery hemoglobin oxygen saturation to 30 +/- 9%. The level of perceived dyspnea had no relation to the pulmonary wedge pressure and correlated only minimally with the level of excessive ventilation (r = 39). The level of perceived fatigue correlated only weakly with blood lactate concentration (r = .55). Eleven patients (21%) exhibited a normal cardiac output and wedge pressure < 20 mm Hg during exercise, 22 (42%) exhibited a normal cardiac output but wedge pressure > 20 mm Hg during exercise, and 19 (37%) exhibited reduced cardiac output and wedge pressure > 20 mm Hg during exercise. Despite these markedly different hemodynamic responses, all three groups exhibited similar levels of fatigue and dyspnea at comparable workloads and had comparable total scores for the Minnesota Living With Heart Failure Questionnaire and the Yale Dyspnea-Fatigue Index. There was no relation between the Living With Heart Failure Questionnaire and peak exercise VO2 and only a weak correlation between the Dyspnea-Fatigue Index and peak VO2 (r = .48). The level of exercise intolerance perceived by patients with heart failure has little or no relation to objective measures of circulatory, ventilatory, or metabolic dysfunction during exercise. In patients who report severe exertional symptoms, it may be desirable to directly measure hemodynamic response to exercise to ensure that these symptoms are due to circulatory dysfunction.

Ventilation-perfusion matching in chronic heart failure

Background: The exercise limitation of patients with chronic heart failure is associated with an increased ventilatory response during exercise. This is thought to be due, at least in part, to excessive dead space ventilation. Methods: To assess ventilation perfusion matching, 20 patients with chronic heart failure and eight controls with asymptomatic left ventricular dysfunction underwent symptom limited treadmill exercise with arterial blood sampling. Metabolic gas exchange was determined by expired gas analysis. Fractional dead space ventilation and the alveolar arterial oxygen difference were derived. Results: There was a fall in fractional dead space ventilation (0.43 to 0.28; P < 0.001), more marked in the controls (peak dead space fraction 0.19 (controls), 0.32 (patients); P = 0.002). There was a rise in alveolar arterial difference in all patients (1.59 to 2.55 kPa; P = 0.006) with no difference between patients and controls. Arterial carbon dioxide tension fell during exercise (4.89 to 4.63 kPa; P < 0.001), with no difference between patients and controls. There was no significant change in arterial oxygen tension. Conclusions: The fall in arterial carbon dioxide was the same in both patients and controls. The modest increase in alveolar-arterial oxygen difference tension was the same in both groups, which, coupled with the stable arterial oxygen tension makes it unlikely that a primary change in ventilation-perfusion matching is the cause of increased ventilatory response to exercise in chronic heart failure.

Cardiorespiratory Responses to Incremental Exercise in Sarcoidosis Patients With Normal Spirometry

Patients with sarcoidosis are known to have histologic pulmonary abnormalities despite normal lung fields or conventional pulmonary function or both. These patients permit a useful assessment of the alleged greater sensitivity of the various measurements made during incremental cardiorespiratory exercise testing. Abnormal responses on such testing may provide insight into such complaints as dyspnea in these patients. Incremental exercise testing was performed on 30 patients with biopsy-proven sarcoidosis who had normal spirometry; 13 had clear lung fields radiographically. Of these patients, the 21 who had normal single-breath diffusing capacity for carbon monoxide (Dsb; [group A]) were compared with the 9 who had decreased Dsb (group B). Half of the group A patients had excessive ventilation and 38% had increased dead space to tidal volume ratio (Vd/Vt), but frequencies of these abnormalities were greater in group B, 89 and 78%, respectively. Ventilatory response, as minute ventilation to oxygen consumption ratios ventilatory equivalents, and deadspace to tidal volume ratio (Vd/Vt) ratios were higher in group B. Widened alveolar-arterial oxygen pressure differences were seen in 7 of 9 group B patients but only 1 of 17 group A patients. This study supports the clinical impression that occult pulmonary impairment may be present in patients (in this case, sarcoidosis patients) with normal pulmonary function, and corroborates the utility of exercise testing in demonstrating such impairment. Reduction in Dsb predicted greater frequency of abnormal exercise responses, especially in oxygenation.

Factors contributing to the exercise limitation of heart failure

Exertional intolerance is a major clinical problem in ambulatory patients with chronic heart failure and is associated with both muscle fatigue and dyspnea. The increased muscle fatigability is most likely caused by a combination of muscle underperfusion and muscle deconditioning; patients frequently exhibit skeletal muscle atrophy, altered muscle metabolism and reduced mitochondrialbased enzyme levels, consistent with deconditioning. The muscle underperfusion is largely due to impaired arteriolar vasodilation within exercising muscle. Exertional dyspnea appears to be due to increased respiratory muscle work mediated by excessive ventilation and decreased lung compliance. Both excessive carbon dioxide production, secondary to increased muscle lactate release, and increased lung dead space contribute to the excessive ventilation. Decreased lung compliance is caused by chronic pulmonary congestion and fibrosis. Optimal management of exercise intolerance in patients with heart failure requires an understanding of the role of these multiple potential contributors to exertional fatigue and dyspnea.

Acute effects of inhaled salbutamol on the metabolic rate of normal subjects.

This study was designed to investigate the contribution of inhaled salbutamol to the increase in resting metabolic rate found in patients with chronic airflow limitation who were receiving bronchodilator therapy. The resting metabolic rate of 10 normal subjects (age 20-47 years, weight 42-105 kg, seven men) was studied after inhalations of salbutamol or placebo. An open canopy method of indirect calorimetry was used to measure resting oxygen consumption (VO2) and resting carbon dioxide production (VCO2). Subjects inhaled two, four, eight, or 12 puffs (100 micrograms/puff) of salbutamol or placebo in a double blind manner. Recordings of VO2 and VCO2 were made after inhalation of the four doses of salbutamol or placebo, integrated over one hour, and compared. VO2 and VCO2 increased in a dose dependent manner after inhaled salbutamol with a maximum effect at five minutes after inhalation. After four puffs, VO2 was 203 and 188 ml/kg/h for salbutamol and placebo respectively. After eight puffs, VO2 was 207 and 185 and VCO2 was 167 and 155 ml/kg/h. After 12 puffs, VO2 was 220 and 190 with a VCO2 of 181 and 168 ml/kg/h. Twelve puffs of salbutamol increased the mean (SE) respiratory quotient from 0.85 (0.01) to 0.93 (0.04) at five minutes indicating an increase in ventilation in excess of metabolic demand. Mean heart rate increased in parallel with VO2. Inhaled salbutamol significantly increases resting metabolic rate in a dose dependent manner.

Cardiorespiratory Responses to Incremental Exercise in Patients With Asbestos-related Pleural Thickening and Normal or Slightly Abnormal Lung Function

An increasing number of patients with asbestos exposure are being identified with pleural thickening (PT) alone, with little or no impairment in standard tests of lung function despite their frequent complaint of dyspnea. We have employed incremental cardiorespiratory exercise testing to evaluate the types and mechanisms of impairment in 23 such patients. All had normal lung fields on radiographic examinations and normal (group 1, n = 12) or minimally reduced (group 2A slight restriction, n = 5, group 2B, slight obstruction, n = 6), lung function. Excessive ventilation was common in all groups, but especially in group 2B. Abnormal dead space ventilation (VD/VT) was more frequent in groups 2A (4/5) and 2B (4/6) than in group 1 (3/12). It was associated with O2 desaturation in three patients in groups 2A and B. Cardiovascular abnormalities were rare (1/23). Excessive ventilation and dead space provide a basis for the symptom of dyspnea in these patients.

Pulmonary Function in Asbestosis and Asbestos-Related Pleural Disease

This review begins with the classic physiologic syndrome of interstitial lung disease (ILD) described in established asbestosis in the 1950s: reduced VC and pulmonary compliance, maintenance of airflow (measured indirectly), decreased diffusing capacity (a laborious undertaking in those years), and hyperventilation, increased dead space (VD/VT), and desaturation on exercise. Small airways dysfunction (SAD) was recognized in the 1960s and 1970s as the physiologic counterpart of the early peripheral bronchiolar inflammatory and fibrotic narrowing reported in experimental animals and in asbestos workers. SAD is nonspecific and is often overshadowed by more severe obstruction caused by smoking or by the countervailing effects of increased lung recoil caused by interstitial fibrosis. Airtrapping secondary to SAD may explain some of the reduction in VC in asbestos exposed workers whose FEV1/FVC is normal. There may be a greater frequency of obstructive airways disease in asbestos workers who smoke than in other smokers, suggesting an interaction between these two noxious inhalants. An interaction is seen in the greater frequency and severity of radiographic asbestosis in smokers at equivalent durations of exposure and in the greater reduction in FVC in smokers at equivalent ILO profusion scores. The functional importance of PT is well documented by lower values for FVC at equivalent profusions of parenchymal disease. This is true of circumscribed PT but much more so of diffuse PT, which can occasionally result in ventilatory failure and death. Incremental exercise testing often reveals evidence of excessive ventilation and abnormal gas exchange (VD/VT) attributable to ILD, when standard tests of pulmonary function and chest radiography are normal. These abnormalities help explain dyspnea in such patients.

Importance of abnormal lung perfusion in excessive exercise ventilation in chronic heart failure

Whether excessive ventilatory response to exercise is related to the maldistribution of pulmonary blood flow was examined in 23 patients with chronic heart failure and nine age-matched normal subjects. With the use of technetium 99m macroaggregated albumin, the resting distribution of pulmonary blood flow was assessed by the scintigraphic counts ratio of upper to lower lung fields. The ventilatory response to exercise was assessed by the slope of the relationship between minute ventilation and carbon dioxide production during exercise. Eight patients (group A) had slope less than 33, the upper limit of the normal range, and 15 patients had slope of 33 or greater (group B). In group B pulmonary blood flow was distributed more to the upper lung, which made the counts ratio (60%) higher than in normal subjects (34%) or in patients in group A (38%). There was no significant difference in pulmonary flow distribution between normal subjects and patients in group A. In group B tidal volume did not increase during exercise as much as it did in normal subjects and in patients in group A; therefore, the respiratory pattern was rapid and shallow. Although the ratio of physiologic dead space to tidal volume fell by 20% during exercise in normal subjects and by 23% in patients in group A, it failed to decrease in patients in group B (−1%), which indicates a relative increase in dead space respiration during exercise. These data indicate that decreased lung compliance and regional ventilation-perfusion mismatch caused by pulmonary vascular and parenchymal abnormalities would play an important role in the excessive exercise ventilation in chronic heart failure.

Relation between ventilation and carbon dioxide production in patients with chronic heart failure

Objectives. The aim of this study was to analyze the relation between ventilation and carbon dioxide production and the control of ventilation in patients with chronic heart failure.Background. Patients with chronic heart failure exhibit an increased ventilatory response to exercise. Ventilation is closely linked to carbon dioxide production, producing a high correlation between the two variables. This relation is nonlinear at high levels of exercise.Methods. The ventilation/carbon dioxide production ratio during exercise was examined in 29 patients with chronic heart failure and 9 normal volunteers.Results. In the patients with heart failure, there were three patterns: in the least severely affected patients, the pattern was similar to that of the normal subjects, with an initial decrease in the ventilation/carbon dioxide production ratio to a plateau maintained during exercise; in more severely affected patients, there was an increase in the ratio at the end of exercise, and in the most severely affected patients, the ratio increased from the outset of exercise. The ventilation/carbon dioxide relation is not adequately described by a straight line relation.Conclusions. The ventilation/carbon dioxide ratio is not fixed, and the changes that occur in this ratio reflect either a noncarbon dioxide-driven ventilatory stimulus or an increase in ventilation-perfusion mismatch due to increased dead space ventilation. The different patterns of this ratio may provide clues to the pathophysiologic mechanisms of the excessive ventilation and breathlessness seen during exercise in chronic heart failure.

Ventilatory mechanisms of exercise intolerance in chronic heart failure

Mechanisms that have been suggested to underlie the abnormal ventilatory response to exercise in patients with chronic congestive heart failure (CHF) include high pulmonary pressures, ventilation-perfusion mismatching, early metabolic acidosis, and abnormal respiratory control. To evaluate the role that ventilation and gas exchange play in limiting exercise capacity in patients with CHF, data from 33 patients with CHF and 34 normal subjects of similar age who underwent maximal exercise testing were analyzed. Maximal oxygen uptake was higher among normal subjects (31.7 ± 6 ml/kg/min) than among patients with CHF (17.7 ± 4 ml/kg/min; p < 0.001). The ventilatory equivalent for oxygen, expressed as a percentage of maximal oxygen uptake, was 25% to 35% higher among patients with CHF compared with normal subjects throughout exercise ( p < 0.01). A steeper component effect of ventilation on maximal oxygen uptake was observed among normal subjects compared with patients with CHF, which suggests that a significant portion of ventilation in CHF is wasted. Maximal oxygen uptake was inversely related to the ratio of maximal estimated ventilatory dead space to maximal tidal volume ( VD VT ) in both groups ( r = −0.73, p < 0.001). Any given oxygen uptake at high levels of exercise among patients with CHF was accompanied by a higher VD VT , lower tidal volume, and higher respiratory rate compared with normal subjects ( p < 0.01). Relative hyperventilation in patients with CHF started at the beginning of exercise and was observed both below and above the ventilatory threshold, which suggests that the excess ventilation was not directly related to earlier than normal metabolic acidosis. Thus abnormal ventilatory mechanisms contribute to exercise intolerance in CHF, and excess ventilation is associated with both a higher physiologic dead space and an abnormal breathing pattern. The high dead space is most likely due to ventilation-perfusion mismatching in the lungs, which is related to poor cardiac output, and the abnormal breathing pattern appears to be an effort to reduce the elevated work of breathing that is caused by high pulmonary pressures and poor lung compliance.

Improvement in Exercise Capacity after Nocturnal Positive Pressure Ventilation and Tracheostomy in a Postpoliomyelitis Patient

Progressive neuromuscular symptoms years after recovery from acute paralytic poliomyelitis have been termed the PPS. We describe a 52-year-old man who contracted poliomyelitis at age 9 years who fully recovered and 33 years later developed progressive dyspnea. Neurologic evaluation revealed bilateral paralysis of the vocal cords, generalized weakness, and accentuated mouth occlusion pressure and ventilatory responses to hypercapnic, hyperoxic breathing. An EMG and muscle biopsy showed changes consistent with acute and chronic denervation. Cardiopulmonary exercise evaluation demonstrated a pulmonary mechanical limit with excessive ventilation relative to CO2 output. Tracheostomy and nocturnal positive pressure ventilation resulted in increased respiratory muscle strength, normalization of ventilatory drive and marked improvement in exercise capacity.

Respiratory and circulatory analysis of CO2 output during exercise in chronic heart failure.

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. 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. 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.

Components of excess ventilation in patients initiated on mechanical ventilation

To determine the causes of excess minute ventilation in patients initiated on mechanical ventilation. Prospective study of recently intubated, mechanically ventilated patients. The medical ICU in a county hospital. Fifty-two mechanically ventilated medical ICU patients were studied within 36 hrs of intubation. Patients were all supported with volume-cycled ventilation in the assist-control mode. Timed expired gas collection and an arterial blood gas. Measurements of minute ventilation and CO2 production (VCO2) were made from a timed expired gas collection. PaCO2 was sampled during the gas collection and deadspace was determined. Minute ventilation, VCO2, deadspace, and PaCO2 values in the patients were compared with predicted normal values, and excess minute ventilation due specifically to each component was calculated. Patients were separated clinically into groups: adult respiratory distress syndrome (ARDS), sepsis, obstructive lung disease, pneumonia, and drug overdose. Comparisons were then made between groups. Excess minute ventilation for the entire study population was secondary to increased deadspace (39%), low PaCO2 (36%), increased VCO2 (15%), and the interactive effect of deadspace and VCO2 (10%). VCO2 contributed little to excess minute ventilation early in respiratory failure, even in the ARDS and sepsis groups. Deadspace contributed significantly to excess minute ventilation in all groups, especially in the ARDS group, where it accounted for 53% of the excess ventilation. Low PaCO2 set-point was the predominant cause of excess minute ventilation in the sepsis group, where it contributed to 57% of their total excess minute ventilation. Although all groups initiated on mechanical ventilation had an excess ventilatory requirement, the contribution of individual components varied considerably between clinical groups.

Resting energy expenditure in chronic cardiac failure.

1. Resting energy expenditure has previously been shown to be elevated in the acute phase of heart failure, but the situation in the compensated state of chronic cardiac failure is unclear. Resting energy expenditure was assessed in 14 patients with stable chronic cardiac failure and 14 matched control subjects by using indirect calorimetry. 2. Resting energy expenditure was significantly elevated in the patients with chronic cardiac failure (112.6 +/- 18.1 versus 87.1 +/- 12.2 kJ day-1 kg-1 total body weight, P less than 0.0002; mean +/- SD) as were resting O2 consumption (3.88 +/- 0.64 versus 3.00 +/- 0.43 ml min-1 kg-1, P less than 0.0002), ventilation (164 +/- 40.3 versus 104 +/- 16.2 ml min-1 kg-1, P less than 0.0001) and heart rate (85.8 +/- 16.9 versus 66.6 +/- 6.9 beats/min, P less than 0.001). Both the resting plasma concentration of noradrenaline (4.48 +/- 1.52 versus 2.28 +/- 0.96 nmol/l, P less than 0.0001) and the serum concentration of free fatty acids (0.78 +/- 0.21 versus 0.57 +/- 0.27 mmol/l, P less than 0.03) were greater in the patients with chronic cardiac failure. Analysis of covariance indicated that most of the difference in resting energy expenditure could be accounted for by the elevated ventilation in the patients with chronic cardiac failure. Arm muscle area, an index of wasting, was lower in the patients with chronic cardiac failure (39.1 +/- 13.1 versus 50.5 +/- 9.4 cm2, P less than 0.02) and resting energy expenditure was found to account for some of this difference. 3. We conclude that an elevated basal metabolism occurs in chronic cardiac failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Importance of abnormal lung perfusion in excessive exercise ventilation in chronic heart failure

Importance of abnormal lung perfusion in excessive exercise ventilation in chronic heart failure