Hemodynamic effects of resistive breathing

1986 ◽  
Vol 60 (3) ◽  
pp. 846-853 ◽  
Author(s):  
R. Olgiati ◽  
G. Atchou ◽  
P. Cerretelli
Keyword(s):  
Minute Ventilation ◽  
Intrathoracic Pressure ◽  
Normal Subjects ◽  
Systemic Arterial Pressure ◽  
O2 Consumption ◽  
Hemodynamic Effects ◽  
Mouth Pressure ◽  
Resistive Breathing ◽  
Myocardial O2 Consumption ◽  
End Tidal

To examine the acute hemodynamic effects induced by large swings in intrathoracic pressure such as may be generated by obstructive lung disease, airway obstruction was simulated by means of two different fixed external alinear resistances and the results were compared with those for unobstructed breathing (C). Eight normal subjects breathed through external resistances during inspiration (I), expiration (E), or both (IE) at rest (Re) and exercise (Ex). The resistances were chosen to induce similar mouth pressure (Pm) swings at Re and Ex. Pleural pressures (Ppl) were found to correlate closely with Pm. During IE resistive breathing mean swings in Pm were -31 and +19 cmH2O at Re and -38 and +22 cmH2O at Ex, with a corresponding decrease in minute ventilation (-30 and -18%) and an increase in end-tidal PCO2 (+5.6 and +4.2 Torr); these were associated with an increase in heart rate (delta HR = 4 and 6 beats/min) and systolic systemic arterial pressure (delta Psas = 10 and 14 Torr at Re and Ex, respectively). O2 consumption and cardiac output did not change. The myocardial O2 consumption, estimated from the product HR X (Psas--Ppl), increased by 17 and 20% at Re and Ex, respectively. Changes in mechanics, gas exchange, and hemodynamics were less pronounced during I or E resistive loading. It is concluded that breathing through a tight external resistance during IE at Re and Ex increases the metabolic load on the myocardium.

Ventilatory and occlusion pressure responses to helium breathing

1983 ◽  
Vol 54 (6) ◽  
pp. 1525-1531 ◽  
Author(s):  
E. L. DeWeese ◽  
T. Y. Sullivan ◽  
P. L. Yu
Keyword(s):  
Breathing Circuit ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Mouth Pressure ◽  
Partial Pressure Of Co2 ◽  
Lung Resistance ◽  
Balloon Technique ◽  
Resistive Loads ◽  
End Tidal ◽  
Airway Tone

To characterize the ventilatory response to resistive unloading, we studied the effect of breathing 79.1% helium-20.9% oxygen (He-O2) on ventilation and on mouth pressure measured during the first 100 ms of an occluded inspiration (P100) in normal subjects at rest. The breathing circuit was designed so that external resistive loads during both He-O2 and air breathing were similar. Lung resistance, measured in three subjects with an esophageal balloon technique, was reduced by 23 +/- 8% when breathing He-O2. Minute ventilation, tidal volume, respiratory frequency, end-tidal partial pressure of CO2, inspiratory and expiratory durations, and mean inspiratory flow were not significantly different when air was replaced by He-O2. P100, however, was significantly less during He-O2 breathing. We conclude that internal resistive unloading by He-O2 breathing reduces the neuromuscular output required to maintain constant ventilation. Unlike studies involving inhaled bronchodilators, this technique affords a method by which unloading can be examined independent of changes in airway tone.

Response of normal subjects to inspiratory resistive unloading

1989 ◽  
Vol 66 (3) ◽  
pp. 1113-1119 ◽  
Author(s):  
C. G. Gallagher ◽  
R. Sanii ◽  
M. Younes
Keyword(s):  
Average Rate ◽  
Minute Ventilation ◽  
Co2 Concentration ◽  
Normal Subjects ◽  
Resistive Load ◽  
Mouth Pressure ◽  
Inspiratory Resistance ◽  
Residual Capacity ◽  
Resistive Loads ◽  
End Tidal

The purpose of this study was to examine the role of the normal inspiratory resistive load in the regulation of respiratory motor output in resting conscious humans. We used a recently described device (J. Appl. Physiol. 62: 2491–2499, 1987) to make mouth pressure during inspiration positive and proportional to inspiratory flow, thus causing inspiratory resistive unloading (IRUL); the magnitude of IRUL (delta R = -3.0 cmH2O.1(-1).s) was set so as to unload most (approximately 86% of the normal inspiratory resistance. Six conscious normal humans were studied. Driving pressure (DP) was calculated according to the method of Younes et al. (J. Appl. Physiol. 51: 963–1001, 1981), which provides the equivalent of occlusion pressure at functional residual capacity throughout the breath. IRUL resulted in small but significant changes in minute ventilation (0.6 1/min) and in end-tidal CO2 concentration (-0.11%) with no significant change in tidal volume or respiratory frequency. There was a significant shortening of the duration (neural inspiratory time) of the rising phase of the DP waveform and the shape of the rising phase became more convex to the time axis. There was no change in the average rate of rise of DP or in the duration or shape of the declining phase. We conclude that 1) the normal inspiratory resistance is an important determinant of the duration and shape of the rising phase of DP and 2) the neural responses elicited by the normal inspiratory resistance are similar to those observed with added inspiratory resistive loads.

Influence of inspiratory flow rate and frequency on O2 cost of resistive breathing in humans

1988 ◽  
Vol 65 (2) ◽  
pp. 760-766 ◽  
Author(s):  
D. S. Dodd ◽  
P. W. Collett ◽  
L. A. Engel
Keyword(s):  
Flow Rate ◽  
Duty Cycle ◽  
Normal Subjects ◽  
Work Rate ◽  
Inspiratory Flow ◽  
Inspiratory Flow Rate ◽  
Contraction Frequency ◽  
Mouth Pressure ◽  
Resistive Breathing ◽  
Residual Capacity

We examined the combined effect of an increase in inspiratory flow rate and frequency on the O2 cost of inspiratory resistive breathing (VO2 resp). In each of three to six pairs of runs we measured VO2 resp in six normal subjects breathing through an inspiratory resistance with a constant tidal volume (VT). One of each pair of runs was performed at an inspiratory muscle contraction frequency of approximately 10/min and the other at approximately 30/min. Inspiratory mouth pressure was 45 +/- 2% (SE) of maximum at the lower contraction frequency and 43 +/- 2% at the higher frequency. Duty cycle (the ratio of contraction time to total cycle time) was constant at 0.51 +/- 0.01. However, during the higher frequency runs, two of every three contractions were against an occluded airway. Because VT and duty cycle were kept constant, mean inspiratory flow rate increased with frequency. Careful selection of appropriate parameters allowed the pairs of runs to be matched both for work rate and pressure-time product. The VO2 resp did not increase, despite approximately threefold increases in both inspiratory flow rate and contraction frequency. On the contrary, there was a trend toward lower values for VO2 resp during the higher frequency runs. Because these were performed at a slightly lower mean lung volume, a second study was designed to measure the VO2 resp of generating the same inspiratory pressure (45% maximum static inspiratory mouth pressure at functional residual capacity) at the same frequency but at two different lung volumes. This was achieved with a negligibly small work rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of naloxone on the sensation of dyspnea during acute respiratory stress in normal adults

1993 ◽  
Vol 74 (2) ◽  
pp. 590-595 ◽  
Author(s):  
Y. Akiyama ◽  
M. Nishimura ◽  
S. Kobayashi ◽  
A. Yoshioka ◽  
M. Yamamoto ◽  
...  
Keyword(s):  
Minute Ventilation ◽  
Endogenous Opioids ◽  
Endogenous Opioid System ◽  
Endogenous Opioid ◽  
Specific Effects ◽  
Mouth Pressure ◽  
End Tidal ◽  
Visual Analogue Scaling ◽  
The Brain ◽  
Normal Adults

To clarify whether endogenous opioids modulate the dyspnea intensity and, if so, by what mechanism they act on it, we examined 12 healthy male volunteers aged 19–27 yr for ventilatory and peak mouth pressure (Pm) responses to hypoxic progressive hypercapnia with inspiratory flow-resistive loading after the intravenous infusion of 3 mg of naloxone or saline. The intensity of dyspnea was simultaneously assessed by visual analogue scaling every 15 s. Naloxone administration increased both ventilatory and Pm responses to hypoxic progressive hypercapnia (P < 0.05 for both). The increase in dyspnea intensity for a given increase in end-tidal PCO2 was significantly greater after naloxone infusion than after saline (P < 0.05). However, there were no differences in the increase in dyspnea intensity for a given increase in minute ventilation or Pm. These results suggest that the endogenous opioid system suppresses the respiratory output under a strong, acute respiratory stress in normal adults and that this system may relieve the dyspnea sensation secondary to the suppression of the brain stem respiratory center without specific effects on the processing of respiratory sensations in the higher brain.

Assessment of rebreathing O2 consumption in humans with normal and diseased lungs

1990 ◽  
Vol 68 (4) ◽  
pp. 1443-1452 ◽  
Author(s):  
M. C. Kallay ◽  
R. W. Hyde ◽  
R. J. Smith
Keyword(s):  
Steady State ◽  
Pulmonary Function ◽  
Lung Disease ◽  
Pulse Rate ◽  
Obstructive Lung Disease ◽  
Pulmonary Function Tests ◽  
Normal Subjects ◽  
O2 Consumption ◽  
O2 Uptake ◽  
End Tidal

We investigated sources of error in estimating steady-state O2 consumption (VO2ss) by calculating O2 uptake from an anesthesia bag containing O2, He, and N2 during 10-20 s of rebreathing (VO2rb). In 11 normal resting subjects, VO2rb calculated with end-tidal sampling overestimated VO2ss by 16 +/- 15% (SD) (P less than 0.003). This error was proportional to the increase in pulse rate during rebreathing, so that pulse-corrected VO2rb slightly underestimated VO2ss by 2.1 +/- 12.2% (P = 0.66) in the six subjects who rebreathed 28% O2 in the rebreathing bag but significantly underestimated VO2ss by 7.5 +/- 6.7% (P less than 0.04) in the six subjects who rebreathed 21% O2 in the rebreathing bag. During exercise, VO2rb underestimated VO2ss by 4 +/- 12% (P less than 0.001) and by 7 +/- 6% at O2 consumptions greater than 2,000 ml/min if O2 in the rebreathing bag was kept above 20% throughout rebreathing. We found that VO2rb calculated with end-tidal gas concentrations underestimated VO2ss by 1-43% in patients with moderate-to-severe obstructive lung disease, with even greater errors when mixed expired samples were used. The magnitude of the discrepancy correlated poorly with abnormalities in standard pulmonary function tests. Based on these data, VO2rb closely approximates VO2ss in normal subjects, provided hypoxia during rebreathing is avoided and cardiac acceleration from rebreathing is taken into account during resting measurement.

Pressure-time product, work rate, and endurance during resistive breathing in humans

1988 ◽  
Vol 64 (4) ◽  
pp. 1397-1404 ◽  
Author(s):  
D. S. Dodd ◽  
S. Kelly ◽  
P. W. Collett ◽  
L. A. Engel
Keyword(s):  
Blood Flow ◽  
Respiratory Muscle ◽  
Muscle Blood Flow ◽  
Normal Subjects ◽  
Work Rate ◽  
Available Energy ◽  
Pressure Time ◽  
Mouth Pressure ◽  
Resistive Breathing ◽  
Pressure Time Product

We examined the effect of increasing work rate, without a corresponding increase in the pressure-time product, on energy cost and inspiratory muscle endurance (Tlim) in five normal subjects during inspiratory resistive breathing. Tidal volume, mean inspiratory mouth pressure, duty cycle, and hence the pressure-time product were kept constant, whereas work rate was varied by changing the frequency of breathing. There was a linear decrease in Tlim of -2.1 ± 0.5 s.J-1.min-1 (r = 0.87 ± 0.06) with increasing work rate. The data satisfied a model of energy balance during fatiguing runs (Monod and Scherrer. Ergonomics 8: 329-337, 1965) and were consistent with the hypothesis that the rate of energy supply, or respiratory muscle blood flow, is fixed when the pressure-time product is constant. Our results indicate that during inspiratory resistive breathing against fatiguing loads, work rate determines endurance independently of the pressure-time product. On the basis of the model, our results lead to estimates of respiratory muscle blood flow and available energy stores under the conditions of our experiment.

Measurement and analysis of gas exchange during exercise using a programmable calculator

1980 ◽  
Vol 49 (3) ◽  
pp. 456-461 ◽  
Author(s):  
D. Y. Sue ◽  
J. E. Hansen ◽  
M. Blais ◽  
K. Wasserman
Keyword(s):  
Gas Exchange ◽  
Respiratory Exchange Ratio ◽  
Minute Ventilation ◽  
Co2 Production ◽  
O2 Consumption ◽  
Exercise Tests ◽  
Programmable Calculator ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
End Tidal

Although exercise testing is useful in the diagnosis and management of cardiovascular and pulmonary diseases, a rapid comprehensive method for measurement of ventilation and gas exchange has been limited to expensive complex computer-based systems. We devised a relatively inexpensive, technically simple, and clinically oriented exercise system built around a desktop calculator. This system automatically collects and analyzes data on a breath-by-breath basis. Our calculator system overcomes the potential inaccuracies of gas exchange measurement due to water vapor dilution and mismatching of expired flow and gas concentrations. We found no difference between the calculator-derived minute ventilation, CO2 production, O2 consumption, and respiratory exchange ratio and the values determined from simultaneous mixed expired gas collections in 30 constant-work-rate exercise studies. Both tabular and graphic displays of minute ventilation, CO2 production, O2 consumption, respiratory exchange ratio, heart rate, end-tidal O2 tension, end-tidal CO2 tension, and arterial blood gas value are included for aid in the interpretation of clinical exercise tests.

scholarly journals Control of breathing during sleep assessed by proportional assist ventilation

1998 ◽  
Vol 84 (1) ◽  
pp. 3-12 ◽  
Author(s):  
S. Meza ◽  
E. Giannouli ◽  
M. Younes
Keyword(s):  
Rem Sleep ◽  
Slow Wave Sleep ◽  
Minute Ventilation ◽  
Upper Airway ◽  
Normal Subjects ◽  
Progressive Increase ◽  
Control Of Breathing ◽  
Respiratory Drive ◽  
Proportional Assist Ventilation ◽  
End Tidal

Meza, S., E. Giannouli, and M. Younes. Control of breathing during sleep assessed by proportional assist ventilation. J. Appl. Physiol. 84(1): 3–12, 1998.—We used proportional assist ventilation (PAV) to evaluate the sources of respiratory drive during sleep. PAV increases the slope of the relation between tidal volume (Vt) and respiratory muscle pressure output (Pmus). We reasoned that if respiratory drive is dominated by chemical factors, progressive increase of PAV gain should result in only a small increase in Vt because Pmus would be downregulated substantially as a result of small decreases in[Formula: see text]. In the presence of substantial nonchemical sources of drive [believed to be the case in rapid-eye-movement (REM) sleep] PAV should result in a substantial increase in minute ventilation and reduction in [Formula: see text] as the output related to the chemically insensitive drive source is amplified severalfold. Twelve normal subjects underwent polysomnography while connected to a PAV ventilator. Continuous positive air pressure (5.2 ± 2.0 cmH2O) was administered to stabilize the upper airway. PAV was increased in 2-min steps from 0 to 20, 40, 60, 80, and 90% of the subject’s elastance and resistance. Vt, respiratory rate, minute ventilation, and end-tidal CO2pressure were measured at the different levels, and Pmus was calculated. Observations were obtained in stage 2 sleep ( n = 12), slow-wave sleep ( n = 11), and REM sleep ( n = 7). In all cases, Pmus was substantially downregulated with increase in assist so that the increase in Vt, although significant ( P < 0.05), was small (0.08 liter at the highest assist). There was no difference in response between REM and non-REM sleep. We conclude that respiratory drive during sleep is dominated by chemical control and that there is no fundamental difference between REM and non-REM sleep in this regard. REM sleep appears to simply add bidirectional noise to what is basically a chemically controlled respiratory output.

Coupling of ventilation to pulmonary gas exchange during nonsteady-state work in men

1983 ◽  
Vol 54 (2) ◽  
pp. 587-593 ◽  
Author(s):  
D. H. Wasserman ◽  
B. J. Whipp
Keyword(s):  
Gas Exchange ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Load Cycle ◽  
Constant Load ◽  
Response Dynamics ◽  
Co2 Output ◽  
Exercise Ventilation ◽  
Nonsteady State ◽  
End Tidal

During steady-state exercise, ventilation increases in proportion to CO2 output (VCO2), regulating arterial PCO2. To characterize the dynamics of ventilatory coupling to VCO2 and O2 uptake (VO2) in the nonsteady-state phase, seven normal subjects performed constant-load cycle ergometry to a series of subanaerobic threshold work rates. Each bout consisted of eight 6-min periods of alternating loaded and unloaded cycling. Ventilation and gas exchange variables were computed breath by breath, with the time-averaged response dynamics being established off-line. Ventilation increased as a linear function of VCO2 in all cases, the relationship being identical in the steady- and the nonsteady-state phases. Ventilation, however, bore a curvilinear relation to VO2, the kinetics of the latter being more rapid. Owing to the kinetic disparity between expired minute ventilation (VE) and VO2, there was an overshoot in the direction of change in VE/VO2 and end-tidal PO2 during the work-rate transition. In contrast, there was no overshoot in the direction of change in VE/VCO2 and end-tidal PCO2 throughout the nonsteady-state period. These data suggest that the exercise hyperpnea is coupled to metabolism in men via a signal proportional to VCO2 in both the nonsteady and steady states of moderate exercise.

Exercise hyperventilation in patients with McArdle's disease

1982 ◽  
Vol 52 (4) ◽  
pp. 991-994 ◽  
Author(s):  
J. M. Hagberg ◽  
E. F. Coyle ◽  
J. E. Carroll ◽  
J. M. Miller ◽  
W. H. Martin ◽  
...  
Keyword(s):  
Blood Lactate ◽  
Normal Subjects ◽  
O2 Consumption ◽  
Intense Exercise ◽  
Mcardle's Disease ◽  
Normal Individuals ◽  
Mcardle’S Disease ◽  
Muscle Phosphorylase ◽  
Lactate Levels ◽  
End Tidal

This study was undertaken to determine if patients who lack muscle phosphorylase (i.e., McArdle's disease), and therefore the ability to produce lactic acid during exercise, demonstrate a normal hyperventilatory response during progressive incremental exercise. As expected these patients did not increase their blood lactate above resting levels, whereas the blood lactate levels of normal subjects increased 8- to 10-fold during maximal exercise. The venous pH of the normal subjects decreased markedly during exercise that resulted in hyperventilation. The patients demonstrated a distinct increase in ventilation with respect to O2 consumption similar to that seen in normal individuals during submaximal exercise. However their hyperventilation resulted in an increase in pH because there was no underlying metabolic acidosis. End-tidal partial pressures of O2 and CO2 also reflected a distinct hyperventilation in both groups at approximately 70–85% maximal O2 consumption. These data show that hyperventilation occurs during intense exercise, even when there is no increase in plasma [H+]. Since arterial CO2 levels were decreasing and O2 levels were increasing during the hyperventilation, it is possible that nonhumoral stimuli originating in the active muscles or in the brain elicit the hyperventilation observed during intense exercise.

Sign in / Sign up

Export Citation Format

Share Document