Ventilatory Response In Patients Research Articles

Worth the risk? Effects of prolonged hypoxia and hypercapnia on ventilatory responses in patients with bilateral resection of the carotid bodies.

Worth the risk? Effects of prolonged hypoxia and hypercapnia on ventilatory responses in patients with bilateral resection of the carotid bodies.

Acute inorganic nitrate supplementation and the hypoxic ventilatory response in patients with obstructive sleep apnea.

Patients with obstructive sleep apnea (OSA) have increased cardiovascular disease risk largely attributable to hypertension. Heightened peripheral chemoreflex sensitivity (i.e., exaggerated responsiveness to hypoxia) facilitates hypertension in these patients. Nitric oxide blunts the peripheral chemoreflex, and patients with OSA have reduced nitric oxide bioavailability. We therefore investigated the dose-dependent effects of acute inorganic nitrate supplementation (beetroot juice), an exogenous nitric oxide source, on blood pressure and cardiopulmonary responses to hypoxia in patients with OSA using a randomized, double-blind, placebo-controlled crossover design. Fourteen patients with OSA (53 ± 10 yr, 29.2 ± 5.8 kg/m2, apnea-hypopnea index = 17.8 ± 8.1, 43%F) completed three visits. Resting brachial blood pressure and cardiopulmonary responses to inspiratory hypoxia were measured before, and 2 h after, acute inorganic nitrate supplementation [∼0.10 mmol (placebo), 4.03 mmol (low dose), and 8.06 mmol (high dose)]. Placebo increased neither plasma [nitrate] (30 ± 52 to 52 ± 23 μM, P = 0.26) nor [nitrite] (266 ± 153 to 277 ± 164 nM, P = 0.21); however, both increased following low (29 ± 17 to 175 ± 42 μM, 220 ± 137 to 514 ± 352 nM) and high doses (26 ± 11 to 292 ± 90 μM, 248 ± 155 to 738 ± 427 nM, respectively, P < 0.01 for all). Following placebo, systolic blood pressure increased (120 ± 9 to 128 ± 10 mmHg, P < 0.05), whereas no changes were observed following low (121 ± 11 to 123 ± 8 mmHg, P = 0.19) or high doses (124 ± 13 to 124 ± 9 mmHg, P = 0.96). The peak ventilatory response to hypoxia increased following placebo (3.1 ± 1.2 to 4.4 ± 2.6 L/min, P < 0.01) but not low (4.4 ± 2.4 to 5.4 ± 3.4 L/min, P = 0.11) or high doses (4.3 ± 2.3 to 4.8 ± 2.7 L/min, P = 0.42). Inorganic nitrate did not change the heart rate responses to hypoxia (beverage-by-time P = 0.64). Acute inorganic nitrate supplementation appears to blunt an early-morning rise in systolic blood pressure potentially through suppression of peripheral chemoreflex sensitivity in patients with OSA.NEW & NOTEWORTHY The present study is the first to examine the acute effects of inorganic nitrate supplementation on resting blood pressure and cardiopulmonary responses to hypoxia (e.g., peripheral chemoreflex sensitivity) in patients with obstructive sleep apnea (OSA). Our data indicate inorganic nitrate supplementation attenuates an early-morning rise in systolic blood pressure potentially attributable to blunted peripheral chemoreflex sensitivity. These data show proof-of-concept that inorganic nitrate supplementation could reduce the risk of cardiovascular disease in patients with OSA.

Applicability of Capnography in the Adult ICU During Physical Therapy: A Systematic Review

PurposeThe purpose of this review was three‐fold: first, evaluate the strength and quality of the current research evidence on usage of capnography, second, determine whether current evidence regarding the use capnography during physical therapy should be considered when making decisions regarding patient’s response to physical therapy; and third, identify weaknesses in the current evidence and area for continued research.Background/SignificanceCapnography is typically used in emergency departments and postoperatively but is not commonly used during physical therapy. Pulse oximetry is typically used to monitor oxygen desaturation and hypoxemia during physical therapy but does not predict or monitor respiratory depression. Capnography monitoring during exercise and mobility could have benefits for physical therapists monitoring patients during therapy as well as provide prognostic value of patient progress.Methods and MaterialsA literature search was completed using: Science Direct, IOP Science, PLOS one, Google scholar, Wiley, EBSCO Host, CINAHL Complete, Cochrane Library, and PubMed. Keywords: capnometry, capnography accuracy, physical therapy, application of capnography, mobility, monitoring. Articles selected for review were those of original research or systematic review published since 2009 and evaluated for quality using the Oxford Centre for Evidence‐Based Medicine 2011 levels of evidence system.ResultsTwenty‐seven articles are included for this study. Six articles were included in the introduction. Seven articles examined the current practices for use of capnography; six studies looked at the use of capnography in the intensive care unit. Three articles on pulse oximetry and capnography with mobility, two articles on the use of monitoring ventilation and oximetry during exercise, and three studies on biologically‐based assessment tools for physical therapy.ConclusionsEvidence suggests that monitoring partial pressure end‐tidal carbon dioxide (PETCO2) levels in patients during rest and exercise may provide more prognostic value of possible adverse events in patients with conditions such as heart failure. Monitoring ventilatory responses in patients is valuable in physical therapy as it indicates tolerance to activity. Evidence suggests there is a significant correlation between PETCO2 and cardiac output. Recent research also suggests regardless of mask or cannula used on patients, diagnostic accuracy of measuring PETCO2 is similar during normal and hyper‐ventilatory states. With increasing application of capnography in intensive care settings, studies involving usage in physical therapy are warranted.

The ventilatory response to muscle metaboreflex stimulation in patients with COPD

The role of skeletal muscle metaboreceptive afferents in human cardiorespiratory control can be examined using post exercise circulatory occlusion (PECO). We have shown that the ventilatory responses to PECO are augmented in humans during concurrent hypercapnia. We now aim to determine whether PECO produces ventilatory responses in COPD patients who do and do not retain CO2.With Ethical approval, 18 COPD patients and 9 aged matched controls performed 2 trials. In both trials participants rested for 2 minutes followed by 2 minutes of rhythmic handgrip exercise. Upon cessation of exercise in the PECO trial a cuff around the upper arm was inflated to 200mmHg for 2 minutes before cuff deflation.PECO maintained blood pressure significantly above baseline levels in COPD patients and control participants (+ 7 mmHg and + 8 mmHg respectively). However ventilation during PECO was only maintained above baseline levels in COPD patients (+2–3 l.min‐1). There was no difference in this response between retainers and non‐retainers of CO2.These results suggest that metaboreflex activation causes ventilatory responses in patients with COPD but not in healthy aged matched controls. However as there was no difference in the ventilatory response to PECO in CO2 retainers and non‐retainers it appears that chronic hypercapnia is not the underlying mechanism behind the response.

Autoregulation of ventilation with neurally adjusted ventilatory assist on extracorporeal lung support

Extracorporeal membrane oxygenation (ECMO) can support oxygenation and carbon dioxide elimination in severe lung failure. Usually it is accompanied by controlled mechanical ventilation. Neurally adjusted ventilatory assist (NAVA) is a new mode of ventilation triggered by the diaphragmatic electrical activity and controlled by the patient's respiratory centre, which may allow a close interaction between ventilation and extracorporeal perfusion. This pilot study intended to measure the physiologic ventilatory response in patients with severe lung failure treated with ECMO and NAVA. We hypothesized that the combination of both methods could automatically provide a protective ventilation with optimized blood gases. We report a case series of six patients treated with ECMO for severe lung failure. In the recovery phase of the disease, patients were ventilated with NAVA and ventilatory response and gas exchange parameters were measured under different sweep gas flows and temporarily inactivated ECMO. Tidal volumes on ECMO ranged between 2 and 5 ml/kg predicted body weight and increased up to 8 ml/kg with inactivated ECMO. Peak inspiratory pressure reached 19-29 cmH(2)O with active, and 21-45 cmH(2)O with inactivated ECMO. Ventilatory response to decreased sweep gas flow was rapid, and patients immediately regulated PaCO(2) tightly towards a physiological pH value. Increase in minute ventilation was a result of increased breathing frequency and tidal volumes, and protective ventilation was only abandoned if pH control was not achieved. With NAVA ventilatory response to decreased ECMO sweep gas flow was rapid, and patients immediately regulated PaCO(2) tightly towards a physiological pH value. Therefore, combination of NAVA and ECMO may permit a closed-loop ventilation with automated protective ventilation.

A quick and easy method of measuring the hypercapnic ventilatory response in patients with COPD

Hypercapnic ventilatory response (HCVR) techniques have not previously been adequately validated in patients with chronic obstructive pulmonary disease (COPD). We have tested the hypothesis that end-tidal PCO(2) may be used to test the HCVR in COPD during non-steady-state rebreathing, despite the fact that large (arterial-end-tidal) PCO(2) differences (P(a-et)CO(2)) exist during air breathing. Eight patients and 11 healthy volunteers underwent steady-state HCVR testing and non-steady-state rebreathing HCVR testing, using Pa and PetCO(2). In COPD patients, PetCO(2) was lower than PaCO(2) by a constant amount throughout steady-state HCVR, but equalised with PaCO(2) during non-steady-state HCVR. Consequently there were no differences in HCVR slope using either method (steady-state p=0.91; rebreathing p=0.73), or HCVR intercept in rebreathing (p=0.68) whether PaCO(2) or PetCO(2) was used. The steady-state HCVR intercept using PetCO(2) was greater than that using PaCO(2) (p=0.02). In healthy volunteers PetCO(2) equalised with PaCO(2) during steady-state HCVR, but was progressively greater than PaCO(2) during non-steady-state. Consequently, there was no difference in HCVR slope (p=0.21) or intercept (p=0.46) whether PaCO(2) or PetCO(2) was used. During non-steady-state there was a P(a-et)CO(2) difference in slope (p=0.03) and intercept (p=0.04). In COPD patients non-steady-state HCVR using PetCO(2) is well tolerated, which is as accurate as PaCO(2). HCVR slope may be derived using PetCO(2) during steady-state testing, though there may be errors in intercept compared to use of PaCO(2). In healthy volunteers PetCO(2) may be used to estimate PaCO(2) during steady-state but not rebreathing HCVR.

275: Preferential Improvement in Exercise Time, Oxygen Consumption and Ventilatory Response in Patients Supported with Pneumatic Versus Electric LVADs

275: Preferential Improvement in Exercise Time, Oxygen Consumption and Ventilatory Response in Patients Supported with Pneumatic Versus Electric LVADs

Exercise Capacity, Breathing Pattern, and Gas Exchange During Exercise for Patients with Isolated Diastolic Dysfunction

Left ventricular diastolic dysfunction (DiaD) is as common as left ventricular systolic dysfunction. Whether these causes of heart failure lead to similar breathing pattern and gas exchange responses to exercise remains unclear. Participants (control subjects [n = 47], systolic dysfunction [n = 46], and DiaD [n = 40]) underwent resting echocardiograms and cardiopulmonary exercise testing. Patients demonstrated lower peak oxygen consumption and tidal volume than control subjects (P < .05). Ventilation tended to be highest in DiaD. The submaximal ventilatory equivalent for carbon dioxide was highest in DiaD. Left atrial volume (all groups) was correlated with peak oxygen consumption (r = -0.38) whereas the ratio of early mitral inflow velocity to early mitral annular velocity was related to peak oxygen consumption (r = -0.36) and treadmill time (r = -0.35). Isolated DiaD is associated with altered breathing pattern and gas exchange similar to systolic dysfunction. Elevated left atrial volume, higher early mitral inflow velocity to early mitral annular velocity ratio, or both are predictive of exercise capacity and elevated ventilatory responses in patients with DiaD suggesting a role for dysfunctional ventricular relaxation.

1138 Assessment of right ventricular function during exercise by strain or strain rate imaging and ventilatory response in patients with severe pulmonary arterial hypertension

1138 Assessment of right ventricular function during exercise by strain or strain rate imaging and ventilatory response in patients with severe pulmonary arterial hypertension

Ventilatory Markers During Exercise for Congestive Heart Failure

The exaggerated ventilatory response in patients with heart failure is clearly multifactorial and complex beyond a mere reduction in pulmonary blood flow. Pulmonary dysfunction, including ventilation-perfusion mismatching, decreased lung compliance, restriction, airway obstruction, decreased diffusion capacity, and decreases in respiratory muscle strength and endurance, contributes to an inefficient breathing pattern and increased work of breathing. This is further compounded by the limited ability of the failing heart to meet the metabolic demands of the respiratory muscles, leading to underperfusion and ischemia.Although VO2max has important implications with regard to functional capacity, exercise test personnel must be knowledgeable concerning the clinical physiology of ventilation during exercise in the patient with heart failure. Ventilatory markers, as Arena and coworkers have demonstrated, are most indicative of disease severity and enhance the prognostic value of the test results.

1165-103 Effect of beta-blocker therapy on ventilatory responses in patients with heart failure

1165-103 Effect of beta-blocker therapy on ventilatory responses in patients with heart failure

Hypercapnic Ventilatory Response in Patients With and Without Obstructive Sleep Apnea: Do Age, Gender, Obesity, and Daytime Paco2 Matter?

To evaluate the relationship between obstructive sleep apnea (OSA) and ventilatory responsiveness to carbon dioxide in both men and women. An analysis of 219 patients referred to an university-based sleep center between 1989 to 1994 was conducted (104 with OSA and 115 without OSA; 43 women and 176 men). These patients had spirometry and a daytime hypercapnic ventilatory response (HCVR) test that was corrected to the patient's ability to attain maximal ventilation. Comparisons between OSA and no-OSA groups, as well as between men and women, were made using multivariate modeling techniques. There was no significant difference in the slope of correlated HCVR (cHCVR) between those with and without OSA (1.57 +/- 0.57 vs 1.63 +/- 0.66; p = 0.48). In men, an inverse correlation between daytime PCO(2) and cHCVR was observed in both crude and multivariate analyses (crude beta-coefficient = - 0.04 +/- 0.02, p = 0.02; adjusted beta-coefficient = 0.07 +/- 0.02, p < 0.01). Although age and cHCVR did not share a significant relationship in the crude analysis (crude beta-coefficient = - 0.01 +/- 0.01, p = 0.10), with adjustments for confounding variables, a significant inverse relationship between age and cHCVR was observed (beta-coefficient = - 0.02 +/- 0.01, p = 0.04). On the other hand, in women, only body mass index (BMI) was positively correlated with cHCVR (crude beta-coefficient = 0.03 +/- 0.01, p = 0.01; adjusted beta-coefficient = 0.04 +/- 0.01, p < 0.01). OSA disorder is not associated with a blunted ventilatory chemoresponsiveness to carbon dioxide. Elevated PaCO(2) and older age are significant correlates for a low cHCVR in men. For women only, BMI was associated with cHCVR. These findings suggest that men and women may have different ventilatory control mechanisms.

Effects of nasal continuous positive airway pressure on awake ventilatory responses to hypoxia and hypercapnia in patients with obstructive sleep apnea.

This study was aimed to examine the short- and long-term effects of nasal continuous positive airway pressure (CPAP) on the chemosensitivity to hypoxia and hypercapnia in the patients with obstructive sleep apnea (OSA). Awake ventilatory responses to hypoxia and hypercapnia were examined in 28 patients (3 female) with moderate to severe OSA. All these tests were examined before and after 2 weeks of nasal CPAP. In 10 patients these tests were repeated after 3-6 months of nasal CPAP. All were also tested for spirometry and arterial blood gas analysis. Patients were middle-aged (48.9 +/- 9.9 years) and their mean apnea-hypopnea index was 58.3 +/- 20.4/hour. After 2 week of nasal CPAP, PaO2 significantly increased (77.7 +/- 11.8 vs. 84.6 +/- 9.8 mmHg) and PaCO2 significantly decreased (44.9 +/- 3.8 vs. 42.3 +/- 3.7 mmHg). The ventilatory response to hypoxia significantly decreased (0.80 +/- 0.51 vs. 0.61 +/- 0.51 liter/min/%) whereas the ventilatory response to hypercapnia significantly increased after 2 weeks (1.47 +/- 0.73 vs. 1.80 +/- 0.76 liter/min/mmHg). Similar findings were also observed after 3-6 months of nasal CPAP in 10 OSA patients. Nasal CPAP treatment can alter the ventilatory responses in patients with OSA.

Abnormal ventilatory responses in patients with Prader-Willi syndrome.

Abnormal ventilatory control in patients with Prader-Willi syndrome when awake and sleeping include abnormal responses to hyperoxia, hypoxia and hypercarbia. Lindgren et al., report similar results regarding response to hypoxia; however, they have demonstrated significant minute ventilation and carbon dioxide responses in their patients treated with growth hormone irrespective of body mass index. It is possible that the explanation for the abnormal respiratory control in this syndrome is located in central rather than peripheral structures. The hypothalamus stands out as the possible location that links their abnormal ventilatory control with the other features. Further investigations to correlate this finding are warranted.

Relationship between exercise capacity and ventilatory equivalent for carbon dioxide in patients with stable old myocardial infarction.

The aim of the present study was to evaluate the relationship between exercise capacity and ventilatory response in patients with stable old myocardial infarction. We performed cardiopulmonary exercise test in 61 patients with stable old myocardial infarction and in 30 healthy men. Each subject exercised on a bicycle ergometer until exhaustion. Patients who had anginal pain or electrocardiographic ischemic changes during exercise were excluded. The patients were classified into three groups according to peakVO2 achieved during exercise, using Weber's method: group A, peakVO2 > or = 21 ml/min/kg (n = 4); group B, 14 < or = peakVO2 < 21 ml/min/kg (n = 45); and group C, peakVO2 < 14 ml/min/kg (n = 12). With progressive increases in VCO2, VE increased linearly below the anaerobic threshold (AT) level. The slope of the linear regression line between VCO2 and VE (SLOPE) was calculated in each subject. The mean SLOPE of the healthy men (group N) and groups A, B and C were 25.8 +/- 0.5, 25.1 +/- 0.5, 28.9 +/- 0.8 and 37.1 +/- 1.7 (x 10(-3), respectively. Thus, the SLOPE was steeper in patients with lower peakVO2. It is difficult to perform a maximal exercise tolerance test on patients with chronic heart failure to evaluate their exercise capacity. We can assess exercise capacity by the slope of the linear regression line between VCO2 and VE (SLOPE) at the lower exercise level.

Nocturnal oxygen and hypercapnic ventilatory response in patients with congestive heart failure

Patients with congestive heart failure and Cheyne-Stokes respiration have a low arterial oxygen saturation, especially during sleep, which can be increased by breathing oxygen. Chronic alterations in blood gases are known to modulate the hypercapnic ventilatory response (HCVR). We therefore evaluated whether the HCVR is influenced by nocturnal nasal oxygen in patients with heart failure and Cheyne-Stokes respiration. Twenty patients with chronic congestive heart failure and a left ventricular ejection fraction ≤35% (mean 18·3% ± sd 6·0%) as well as 25 healthy control subjects were studied. The patients were assigned to 1 week each of nocturnal nasal oxygen and room air with a flow of 4 l min −1 in a randomized cross-over fashion. After each week resting ventilation and HCVR were evaluated by the rebreathing technique. Breathing oxygen during the night for 1 week increased the basal nocturnal oxygen saturation from 92·5 ± 1·6% to 96·5% ± 0·9% ( P<0·000 01) and reduced Cheyne-Stokes respiration. HCVR was 1·22 ± 0·90 l min −1 mmHg −1 after nocturnal room air and did not differ from that in the control subjects (1·31 ± 0·62 l min −1 mmHg −1). In the patients HCVR decreased to 0·91 ± 0·52 l min −1 mmHg −1 after nocturnal oxygen ( P=0·019). There were no significant changes with nocturnal oxygen in resting minute ventilation, respiratory rate or end-tidal PCO 2. We conclude that nocturnal nasal oxygen reduces HCVR in patients with congestive heart failure and Cheyne-Stokes respiration.

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.

Evaluation of ventilatory responses in severe acidemia in diabetic ketoacidosis.

Ventilatory response in patients with severe acidemia in diabetic ketoacidosis (DKA) was unresolved. Thus, 83 patients with uncomplicated DKA were studied for the relation between arterial blood pH, calculated bicarbonate concentration (HCO3) and carbon dioxide tension (PCO2). The equation for the PCO2/HCO3 pair was: PCO2 = 1.58 x HCO3 + 7.6 (SE 2.55, r = 0.95, p < 0.01); for the PCO2/pH pair was: PCO2 = 43.8 x pH-293 (SE 6.23, r = 0.66, p < 0.01). The correlation coefficient for the PCO2/HCO3 pair was significantly greater compared to the PCO2/pH pair (p < 0.001). Multiple regression analysis showed that severe acidemia (pH < or = 7.10) per se was independently associated with PCO2 for the PCO2/HCO3 pair, but not for the PCO2/pH pair. Thus, our patients were divided into 2 groups for the PCO2/HCO3 pair: group 1 with pH < or = 7.10 (n = 25) and group 2 with pH > 7.10 (n = 58). The equations were: group 1:PCO2 = 3.18 x HCO3 + 2.88 (SE 1.72, r = 0.87, p < 0.01); group 2:PCO2 = 1.65 x HCO3 + 6.6 (SE 2.6, r = 0.95, p < 0.01). There was a significant difference between these 2 equations (p < 0.01). Mathematical simulations with 10 sets of 25 or 58 random pH/PCO2 pairs (and calculated HCO3) for "group 1' and "group 2' also showed similar results, albeit with less precision. Hence, ventilatory response in DKA varies between patients with severe acidemia and those with moderate acidemia by the PCO2/HCO3 pair, but not by the PCO2/pH pair.

Relationship between breathlessness and hypoxic and hypercapnic ventilatory response in patients with COPD.

The purpose of this study is to examine the relationship between breathlessness and the ventilatory response to hypercapnia or hypoxia in patients with chronic obstructive pulmonary disease (COPD). Fifteen male patients (mean forced expiratory volume in one second (FEV1): 1.13 L) underwent tests to determine hyperoxic hypercapnic ventilatory response (HCVR) and isocapnic hypoxic ventilatory response (HVR) with simultaneous quantification of breathlessness by modified Borg scale. The ventilatory output was evaluated by the ratio of minute ventilation (V'E) divided by measured maximal voluntary ventilation (MVV). The magnitude of HCVR or HVR was assessed as the slope value of the V'E/MVV-end-tidal carbon dioxide pressure (PET,CO2) or arterial oxygen saturation (Sa,O2) regression line, respectively. The breathlessness during the tests was evaluated not only linearly in relation to V'E/MVV, but also at given levels of PET,CO2 or Sa,O2. The mean value of the breathlessness at two different levels of ventilation was greater during HVR than during HCVR, suggesting that hypoxia is dyspnogenic independently of ventilatory stimulation. The HCVR was inversely correlated with the breathlessness response to ventilation, while similar correlation was partly present for HVR. The HVR was positively correlated with the breathlessness at an Sa,O2 of 80%, whilst there was no such correlation between the HCVR and the breathlessness related to PET,CO2. Therefore, patients with a higher breathlessness related to increased ventilation had a lower HCVR and HVR, whilst those with a higher breathlessness with desaturation, which might include a direct influence of hypoxia, had a higher HVR. These findings suggest an interaction between ventilatory response and breathlessness during the test, which may partly include behavioural modulation of HCVR and HVR through the breathlessness in various ways, depending on the origin and nature of the sensation.

Cardiopulmonary exercise response in patients with left ventricular dysfunction or heart failure: a noninvasive study by gas exchange and impedance cardiography monitoring.

We investigated the upright bicycle exercise cardiopulmonary response in 20 patients with left ventricular dysfunction (LVD, secondary to previous myocardial infarction, left ventricular ejection fraction range 18-44%). Ten patients (48 +/- 7 years) asymptomatic (I NYHA class) without drug treatment (LVD group). The others (n = 10) (50 +/- 1 years) complained of dyspnea and/or fatigue despite therapy (NYHA II-III). They represented the heart failure (HF) group. Eight sedentary men (40 +/- 10 years) served as controls. Controls and patients performed stress testings under drug treatment, when administered. Anaerobic ventilatory threshold (ATge) was considered as an index of submaximal exercise while peak exercise VO2 (Peak VO2) was considered the maximal volitional exercise capacity. The ratio between minute ventilation (VE) to carbon dioxide release (VCO2) (VE/VCO2) was assessed to evaluate the ventilatory response during exercise. We coupled gas exchange assessment (2001, MGC) with noninvasive monitoring of stroke volume (SV) by impedance cardiography (NCCOM3, BOMED) and total systemic vascular resistances (TSVR; by auscultatory blood pressure measurement). In controls VO2 increase during exercise was related to higher heart rate (HR) and SV both from resting to ATge and from this point to the peak. TSVR declined during both steps. In patients with HF VO2 rose from resting to ATge (by faster HR and unchanged SV). VO2 increased slightly from this point to Peak VO2. This result was related to flat HR increase and unchanged SV as well as TSVR. In patients with LVD VO2 increased similarly to controls from resting to ATge and less above the threshold. In these patients both HR and SV increased during submaximal exercise. From ATge to Peak VO2 only HR increased. TSVR declined significantly similarly to controls. The VE/VCO2 ratio was higher at peak exercise in patients with HF compared to controls. Different determinants were demonstrated in patients with left ventricular dysfunction with mild or symptomatic chronic heart failure (CHF). These findings and the increased ventilatory response in patients with CHF can explain different changes of VO2 in these patients during submaximal and maximal voluntary exercise and contribute to explain exercise-induced exertion in these subjects.