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C Roussos

Publications and source records attributed to C Roussos.

At least 19 recordsLinked to original sources
PubMed1992

Round table conference on ventilatory failure, Brussels, Belgium, March 16-18, 1991.

It was possible to reach agreement on several important issues relating to VF. First, the phenomenon of CO2 retention may have both pathophysiologic and compensatory components. There is increased awareness of the nature, intensity, and significance of the cross-talk between the ventilatory control center and the pump itself, as expressed in breathing pattern and indices of ventilatory drive. We are learning to interpret that information more effectively to assess functional reserve. Second, knowledge concerning the relative importance of various muscle groups is still incomplete, and the impact of disease on muscle function, lung mechanics, and ventilatory control is not fully understood. Dynamic hyperinflation and sleep disturbances provide two clear examples of conditions whose wide-ranging influence on drive, workload, and muscle function was, until quite recently, under appreciated. Finally, there was a general consensus that our therapeutic approaches to VF should be modified to reflect improved understanding of the pathogenesis of CO2 retention and iatrogenic lung injury. In the acute setting, measures to limit alveolar distention, such as controlling airway pressure, revising blood gas targets, and/or using adjunctive methods for blood gas exchange may avoid barotraumatic edema and rupture. The potential for non-invasive ventilation to avert intubation, facilitate ventilator withdrawal, and help patients with chronic VF to achieve compensation without machine dependence is now being actively investigated. This two day conference proved a stimulating forum for interchange of ideas regarding the state of the field, and allowed many opportunities for scientific interaction, both during outside the formal program.(ABSTRACT TRUNCATED AT 250 WORDS)

Europe↗
PubMed1992

Effects of diaphragmatic ischemia on the inspiratory motor drive.

To assess the effect of diaphragmatic ischemia on the inspiratory motor drive, we studied the in situ isolated and innervated left diaphragm in anesthetized, vagotomized, and mechanically ventilated dogs. The arterial and venous vessels of the left diaphragm were catheterized and isolated from the systemic circulation. Inspiratory muscle activation was assessed by recording the integrated electromyographic (EMG) activity of the left and right costal diaphragms and parasternal intercostal and alae nasi muscles. Tension generated by the left diaphragm during spontaneous breathing attempts was also measured. In eight animals, left diaphragmatic ischemia was induced by occluding the phrenic artery for 20 min, followed by 10 min of reperfusion. This elicited a progressive increase in EMG activity of the left and right diaphragms and parasternal and alae nasi muscles to 170, 157, 152, and 128% of baseline values, respectively, an increase in the frequency of breathing efforts, and no change in left diaphragmatic spontaneous tension. Thus the ratio of left diaphragmatic EMG to tension rose progressively during ischemia. During reperfusion, only the frequency of breathing efforts and alae nasi EMG recovered completely. In four additional animals, left diaphragmatic ischemia was induced after the left phrenic nerve was sectioned. Neither EMG activity of inspiratory muscles nor respiratory timing changed significantly during ischemia. In conclusion, diaphragmatic ischemia increases inspiratory motor drive through activation of phrenic afferents. The changes in alae nasi activity and respiratory timing indicate that this influence is achieved through supraspinal pathways.

Afferent Pathways↗
PubMed1992

Effect of tidal volume and PEEP in ethchlorvynol-induced asymmetric lung injury.

We examined the effects of positive end-expiratory pressure (PEEP) and tidal volume on the distribution of ventilation and perfusion in a canine model of asymmetric lung injury. Unilateral right lung edema was established in 10 animals by use of a selective infusion of ethchlorvynol. Five animals were tested in the supine position (horizontal asymmetry) and five in the right decubitus position (vertical asymmetry). Raising PEEP from 5 to 12 cmH2O improved oxygenation despite a redistribution of blood flow toward the damage lung and a consistent decrease in total respiratory system compliance. This improvement paralleled a redistribution of tidal ventilation to the injured lung. This was effected primarily by a fall in the compliance of the noninjured lung due to hyperinflation. The effects of higher tidal volume were additive to those of PEEP. We propose that the major effect of PEEP in inhomogeneous lung injury is to restore tidal ventilation to a population of alveoli recruitable only at high airway pressures.

Animals↗
PubMed1992

Effect of phrenic afferent stimulation on pattern of respiratory muscle activation.

Ventilation and electromyogram (EMG) activities of the right hemidiaphragm, parasternal intercostal, triangularis sterni, transversus abdominis, genioglossus, and alae nasi muscles were measured before and during central stimulation of the left thoracic phrenic nerve in 10 alpha-chloralose anesthetized vagotomized dogs. Pressure in the carotid sinuses was fixed to maintain baroreflex activity constant. The nerve was stimulated for 1 min with a frequency of 40 Hz and stimulus duration of 1 ms at voltages of 5, 10, 20, and 30 times twitch threshold (TT). At five times TT, no change in ventilation or EMG activity occurred. At 10 times TT, neither tidal volume nor breathing frequency increased sufficiently to reach statistical significance, although the change in their product (minute ventilation) was significant (P less than 0.05). At 20 and 30 times TT, increases in both breathing frequency and tidal volume were significant. At these stimulus intensities, the increases in ventilation were accompanied by approximately equal increases in the activity of the diaphragm, parasternal, and alae nasi muscles. The increase in genioglossus activity was much greater than that of the other inspiratory muscles. Phrenic nerve stimulation also elicited inhomogeneous activation of the expiratory muscles. The transversus abdominis activity increased significantly at intensities from 10 to 30 times TT, whereas the activity of the triangularis sterni remained unchanged. The high stimulation intensities required suggest that the activation of afferent fiber groups III and IV is involved in the response. We conclude that thin-fiber phrenic afferent activation exerts a nonuniform effect on the upper airway, rib cage, and abdominal muscles and may play a role in the control of respiratory muscle recruitment.

Animals↗
PubMed1991

Diaphragmatic fatigue produced by constant or modulated electric currents.

In anesthetized rabbits the efficiency of phrenic nerve stimulation with trains of electric current was studied either when ventilation was effected entirely by bilateral nerve stimulation (electrophrenic ventilation) or during unilateral nerve stimulation when animals were ventilated with a pump and open chest. Trains of rectangular electric pulses (RPT) with constant amplitude and frequency or sine waves, both the amplitude and frequency of which were modulated and controlled by a computer (MSWT), were used with each animal. MSWT closely reproduced the physiological shape of transdiaphragmatic pressure waves. Diaphragm fatigue, as determined from the decrease in the maximal relaxation rate of twitches, occurred after 20 minutes of bilateral or unilateral nerve stimulation with RPT, but only after 60 min (unilateral stimulation) or 98 min (bilateral stimulation) with MSWT. These data show the importance of the motor signal pattern in long-lasting nerve stimulation.

Animals↗
PubMed1991

Respiratory muscle activation by limb muscle afferent stimulation in anesthetized dogs.

In 10 chloralose anaesthetized and spontaneously breathing dogs, we assessed the effect of limb muscle afferents on the peak integrated EMG activities of the genioglossus, alae nasi, costal diaphragm, parasternal intercostal, triangularis sterni, and transverse abdominis muscles. The influence of vagal and baroreceptor afferents were eliminated by vagotomy and perfusion of carotid sinuses at a constant pressure. Muscle afferents were activated by stimulating the central end of the gastrocnemius nerve for 1 min at 40 Hz and at different voltages. Stimulation at voltages equal to 5, 10 and 20 times twitch-threshold increased minute ventilation to 165, 216 and 250% of pre-stimulation values, respectively, which was achieved by increasing breathing frequency (shortening of the inspiratory and expiratory times) and tidal volume. The activity of the parasternal intercostal and alae nasi muscles increased by a similar degree to that of the diaphragm while the activities of the genioglossus and transverse abdominis were augmented to a greater degree than that of the diaphragm. On the other hand, the motor drive to triangularis sterni increased significantly only at 20 times twitch-threshold and to a lesser degree than that to the diaphragm. These results suggest that upper airway, inspiratory and expiratory rib cage and abdominal muscles may be independently regulated. Differences in the sensitivity of these muscles to the activation of limb muscle afferents can be explained by a complex pattern of central projections of these afferents on the central respiratory controllers or by intrinsic properties of the motor output of these controllers.

Animals↗
PubMed1991

Chemical activation of thin-fiber phrenic afferents. 2. Cardiovascular responses.

To assess the effects of groups III and IV (thin-fiber) phrenic afferents on arterial pressure, heart rate, and distribution of cardiac output, we injected capsaicin into phrenic arteries of in situ isolated and innervated left diaphragms of dogs anesthetized with chloralose, vagotomized, and mechanically ventilated. Blood flow in the ascending aorta, common carotid, renal, superior mesenteric, and femoral arteries was measured by electromagnetic and Doppler flow probes. Injection of 1 mg capsaicin into the left phrenic artery produced congruent to 15% increase in mean arterial pressure and congruent to 7% increase in heart rate with no change in aortic flow. Phrenic arterial flow decreased by 64%, renal arterial flow by 16%, and superior mesenteric arterial flow by 10%, whereas carotid flow increased by 13% and flow to the right gastrocnemius muscle did not change. Mean arterial pressure, heart rate, and blood flow distribution (with the exception of the decline in phrenic blood flow) returned to baseline within 60 s of the injection. Injection of 1.5 mg capsaicin into the right isolated and innervated gastrocnemius produced congruent to 35% increase in mean arterial pressure, 17% rise in heart rate, and no change in aortic blood flow. Phrenic and carotid arterial flow rose by 240 and 41%, respectively, whereas renal and superior mesenteric flow declined by 50 and 20%, respectively. In conclusion, thin-fiber phrenic afferents have an excitatory effect on arterial pressure and heart rate. They redistribute blood flow away from the renal and intestinal vascular beds and toward the carotid vascular bed. On the other hand, the cardiovascular reflex from thin-fiber phrenic afferents seems less potent than that from limb muscle afferents.

Afferent Pathways↗
PubMed1990

Assessment of respiratory muscle dysfunction in chronic obstructive lung disease.

In COLD, the inspiratory muscles are severely disadvantaged by virtue of the hyperinflation that accompanies this disorder. Such mechanical disadvantage will lead clinically, in the stable patient, to the active recruitment of the accessory muscles of inspiration and to a pattern of rapid, shallow breathing that may be due to either peripheral (muscle) or central (neurogenic) influences thought to be linked to a critical tension-time index of the inspiratory muscles. This pattern appears to be all the more pronounced in the patient with acute respiratory failure and is frequently accompanied by disordered rib cage-abdominal movements. While these movements may reflect the muscles' attempts to stave off fatigue, they may also imply that if the imposed mechanical stress is unrelieved, muscle failure will ensue. In the laboratory, mechanical disadvantage is marked by diminished inspiratory mouth pressures. Because of wide scatter, a low mouth pressure beyond that which can be explained by hyperinflation alone should be confirmed by an assessment of Pesosniff or by the measurement of transdiaphragmatic pressure. Muscle endurance, also compromised in this condition, can be assessed indirectly by the measurement of MVV or MSVC, or more directly by an invasive assessment of the tension-time index and endurance time of the diaphragm or noninvasively by the Endurance Index of McKenzie and Gandevia. And finally, once muscle failure is pending or has been established, a program of muscle rest, either complete or partial, pharmacotherapy, and goal-specific training should be instituted.

Acute Disease↗
PubMed1990

Chemical activation of thin-fiber phrenic afferents: respiratory responses.

In supine chloralose-anesthetized and mechanically ventilated dogs, we assessed the effects of group III and IV thin-fiber phrenic afferents on cardiorespiratory control by injecting capsaicin into the phrenic artery of an in situ isolated and innervated left diaphragm. Inspiratory motor drive was assessed by measuring the electromyogram of left and right diaphragm, left parasternal, and mylohyoid muscles in five protocols. 1) Three boluses (2 ml) of capsaicin (1, 10, and 50 micrograms/ml) were injected 30 min apart. Only the 50-micrograms/ml injection elicited a significant increase in arterial pressure, heart rate, and inspiratory motor drive. 2) Repeated doses of capsaicin were tested. The pressor and hyperpneic responses were weakened. 3) High doses of capsaicin (100 and 500 micrograms/ml) were given. Hyperpneic and pressor responses were similar to those elicited by the 50-micrograms/ml dose. 4) When the left phrenic nerve was sectioned, the pressor and hyperpneic responses to the 50-micrograms/ml injection were abolished. 5) Capsaicin (50 micrograms/ml) was infused into the arterial supply of the in situ vascularly isolated and innervated gastrocnemius. Arterial pressure, breathing frequency, and inspiratory motor drive to all inspiratory muscles increased significantly and to a greater degree than in the diaphragm. In conclusion, diaphragmatic thin-fiber afferents have an excitatory effect on the inspiratory motor drive and arterial pressure that is similar to that seen in limb muscles.

Animals↗
PubMed1990

Electromyographic study of respiratory muscles during human diving at 46 ATA.

Electromyographic (EMG) recordings of the 6th to 7th intercostal space (thoracic EMG) and abdominal muscles, ventilatory pattern, and the work of breathing were studied in 4 human subjects exposed for 12 days to 46 ATA of helium-oxygen (density = 8.7 g.liter-1) then of nitrogen-helium-oxygen gas mixture (ternary mixture) (density = 11.1 g.liter-1). We found that the respiratory muscle work necessary for eupneic ventilation was multiplied by 4 at 46 ATA. During quiet breathing as well as during forced inspiratory maneuvers, the power spectrum of thoracic EMG shifted to the left in three individuals during the sojourn at maximal pressure, whichever gas mixture was inhaled. This was corroborated by the decreased ratio of EMG power in a high to that in a low band of frequencies. These alterations disappeared at the end of the decompression period, suggesting the existence of inspiratory muscle fatigue at high pressure. Hyperbaric tremor was recorded on the thoracic EMG and was maximal with He-O2 inhalation. It disappeared at the end of the period at 46 ATA (He-N2-O2).

Adult↗
PubMed1989

Effects of tension, duty cycle, and arterial pressure on diaphragmatic blood flow in dogs.

We investigated the selective effects of changes in transdiaphragmatic pressure (Pdi) and duty cycle on diaphragmatic blood flow in supine dogs at normal arterial pressure (N), moderate hypotension (MH), and severe hypotension (SH) [mean arterial pressure (Part) of 116, 75, and 50 mmHg, respectively]. The diaphragm was paced at a rate of 12/min by bilateral phrenic nerve stimulation. Left phrenic (Qphr-T) and left internal mammary (Qim-T) arterial flows were measured by electromagnetic flow probes. Changes in Pdi and duty cycle were achieved by changing the stimulation frequencies and the duration of contraction, whereas Part changes were produced by bleeding. With N and at a duty cycle of 0.5, incremental increases in Pdi produced peaks in Qphr-T and Qim-T at 30% maximum diaphragmatic pressure (Pdimax) with a gradual decline at higher Pdi. With MH and SH, blood flow peaked at 10% Pdimax. At any given Pdi, blood flow was lower with MH and SH in comparison to N. The effect of duty cycle was tested at two levels of Pdi. With N and at low Pdi (25% Pdimax), blood flow rose progressively with increases in duty cycle, whereas at moderate Pdi level (50% Pdimax) blood flow peaked at a duty cycle of 0.3, with no increase thereafter. With MH, blood flow at low Pdi rose linearly with increasing duty cycle but to a lesser extent than with N, and at a moderate Pdi flow peaked at a duty cycle of 0.3. With SH, blood flow at low and moderate Pdi was limited at duty cycles greater than 0.3 and 0.1, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

In situ isolated perfused and innervated left hemidiaphragm preparation.

We developed a vascularly isolated in situ preparation of the left hemidiaphragm in which arterial blood was only provided through the left phrenic artery and the venous blood only drained through the phrenic vein. The costal margins were secured and connected to three force transducers. Muscle shortening was measured by sonomicrometry. The presence of arterial collaterals between the left hemidiaphragm and the systemic circulation was excluded by the systemic injection of a vital dye (Lissamine Green), a neuromuscular blocking agent (succinylcholine), and by the injection of epinephrine. Left phrenic nerve stimulation produced homogeneous shortening and tension. The degree of shortening in the isolated and intact left diaphragm at the same resting length was similar. The preparation was stable for 2 h with less than 10% decline in maximum tension. Two advantages of this preparation are particularly important. 1) Diaphragmatic energetics can be studied independently of systemic factors, and 2) the role of phrenic nerve afferents in the control of breathing and systemic circulation can easily be assessed without activating nonphrenic nerve afferents.

Animals↗
PubMed1989

Effects of furosemide on pulmonary shunts.

In 23 mechanically ventilated anuric (six) or oliguric (17) patients (less than 16 ml/h of urine output) with severe gas exchange abnormality, we investigated the effect of furosemide on intrapulmonary shunt (Qs/QT). Before and after 0.5, 1, and 2 h of IV administration of 200 mg of furosemide, we assessed the intrapulmonary shunt and PaO2 while patients' hemodynamic measurements were monitored. Ventilatory parameters remained constant throughout the study. While the urine output was minimal and no alteration in hemodynamic values was found, the Qs/QT decreased from 27.7 +/- 2.3 percent (mean +/- SEM) at control to 24.3 +/- 2.1 percent (p less than 0.01) at 0.5 h, 21.7 +/- 2.1 percent (p less than 0.001) at 1 h, and 18.1 +/- 1.8 percent (p less than 0.001) at 2 h. The PaO2 showed no significant difference at 0.5 h but rose significantly from 96 +/- 14 to 105 +/- 14 mm Hg (p less than 0.05) and 111 +/- 14 mm Hg (p less than 0.01) at 1 and 2 h, respectively. Since we observed no changes in hemodynamics, we speculate a direct effect of furosemide in the pulmonary vasculature affecting the ventilation-perfusion mismatch and, therefore, the Qs/QT and PaO2.

Acute Kidney Injury↗
PubMed1988

Autoregulation of diaphragmatic blood flow in dogs.

In eight anesthetized spontaneously breathing dogs, we determined whether diaphragmatic blood flow is dependent on arterial blood pressure (Pa) or whether it is autoregulated. We also determined whether diaphragmatic muscular activity affects the degree of autoregulation. We measured blood flow through the left phrenic artery (Qphr) with an electromagnetic flow probe and decreased Pa in steps by controlled hemorrhage. Phrenic venous blood was sampled to allow the calculation of diaphragmatic O2 consumption (VO2phr). Diaphragmatic energy demands were varied by using three inspiratory resistances (R1, R2, and R3), which increased peak transdiaphragmatic pressure two-, three-, and fourfold, respectively. During quiet breathing, Qphr was independent of Pa between Pa of 90 and 120 mmHg (i.e., plateau of pressure-flow relation), but at lower Pa, Qphr was directly related to Pa. During inspiratory loading, the Qphr plateau ended at a higher Pa than with quiet breathing, but within the normal ranges of Pa there still was a plateau. VO2phr at a given work load was constant between Pa of 70 and 120 mmHg, but at Pa of 50-55 mmHg, VO2phr declined with all work loads. We conclude that in spontaneously breathing dogs 1) Qphr is autoregulated over the normal range of blood pressures and 2) VO2phr is maintained over wider ranges of Pa than Qphr.

Animals↗
PubMed1988

Interaction of fatigue and hypercapnia in the canine diaphragm.

We studied 10 open-chest dogs and measured the pressure across the diaphragm (Pdi) in each period of the protocol during stimulation at frequencies of 1, 20, 50, and 80 Hz. Three ranges of arterial PCO2 (PaCO2) were examined: less than or equal to 26, 36-50, and greater than or equal to 89 Torr. The diaphragm was fatigued with repetitive phrenic stimulation (30 Hz). During the fatiguing activity, five of the animals were subjected to hypercapnia and the other five to hypocapnia. A frequency-Pdi curve was generated for each period in the protocol. The data show that 1) fatiguing to 50% of the initial Pdi value during hypercapnia was significantly more rapid than during hypocapnia; 2) both the prefatigue and postfatigue mean Pdi values over all interactions of frequency, fatigue, and PaCO2 were unaffected by the fatiguing environment (hypercapnia vs. hypocapnia); 3) the percent reduction of Pdi by hypercapnia was the same at all four frequencies; 4) hypocapnia did not alter either the pre- or postfatigue frequency-Pdi curve; and 5) one-half relaxation time, unaffected by PaCO2, was prolonged by fatigue. We conclude that the hypercapnic diaphragm has less endurance than the hypocapnic diaphragm and that although both fatigue and hypercapnia decrease Pdi, they appear to be separate entities working through different mechanisms.

Animals↗