Respiratory Muscle Blood Flow Research Articles

Last Word on Point:Counterpoint: Exercise-induced intrapulmonary shunting is imaginary vs. real

to the editor: We completely agree with the letter writers ([3][1]) that it is important to apply quantitative techniques for the measurement of intrapulmonary shunt before drawing conclusions. Both MIGET and the 100% oxygen technique are quantitative and have consistently shown insignificant

Influence of Respiratory Muscle Blood Flow and Hypoxemia on Exercise Induced Diaphragmatic Fatigue in Humans

Influence of Respiratory Muscle Blood Flow and Hypoxemia on Exercise Induced Diaphragmatic Fatigue in Humans

The underwater environment: cardiopulmonary, thermal, and energetic demands

Water covers over 75% of the earth, has a wide variety of depths and temperatures, and holds a great deal of the earth's resources. The challenges of the underwater environment are underappreciated and more short term compared with those of space travel. Immersion in water alters the cardio-endocrine-renal axis as there is an immediate translocation of blood to the heart and a slower autotransfusion of fluid from the cells to the vascular compartment. Both of these changes result in an increase in stroke volume and cardiac output. The stretch of the atrium and transient increase in blood pressure cause both endocrine and autonomic changes, which in the short term return plasma volume to control levels and decrease total peripheral resistance and thus regulate blood pressure. The reduced sympathetic nerve activity has effects on arteriolar resistance, resulting in hyperperfusion of some tissues, which for specific tissues is time dependent. The increased central blood volume results in increased pulmonary artery pressure and a decline in vital capacity. The effect of increased hydrostatic pressure due to the depth of submersion does not affect stroke volume; however, a bradycardia results in decreased cardiac output, which is further reduced during breath holding. Hydrostatic compression, however, leads to elastic loading of the chest wall and negative pressure breathing. The depth-dependent increased work of breathing leads to augmented respiratory muscle blood flow. The blood flow is increased to all lung zones with some improvement in the ventilation-perfusion relationship. The cardiac-renal responses are time dependent; however, the increased stroke volume and cardiac output are, during head-out immersion, sustained for at least hours. Changes in water temperature do not affect resting cardiac output; however, maximal cardiac output is reduced, as is peripheral blood flow, which results in reduced maximal exercise performance. In the cold, maximal cardiac output is reduced and skin and muscle are vasoconstricted, resulting in a further reduction in exercise capacity.

Contribution of respiratory muscle blood flow to exercise‐induced diaphragmatic fatigue in trained cyclists

We investigated whether the greater degree of exercise-induced diaphragmatic fatigue previously reported in highly trained athletes in hypoxia (compared with normoxia) could have a contribution from limited respiratory muscle blood flow. Seven trained cyclists completed three constant load 5 min exercise tests at inspired O(2) fractions (FIO2) of 0.13, 0.21 and 1.00 in balanced order. Work rates were selected to produce the same tidal volume, breathing frequency and respiratory muscle load at each FIO2 (63 +/- 1, 78 +/- 1 and 87 +/- 1% of normoxic maximal work rate, respectively). Intercostals and quadriceps muscle blood flow (IMBF and QMBF, respectively) were measured by near-infrared spectroscopy over the left 7th intercostal space and the left vastus lateralis muscle, respectively, using indocyanine green dye. The mean pressure time product of the diaphragm and the work of breathing did not differ across the three exercise tests. After hypoxic exercise, twitch transdiaphragmatic pressure fell by 33.3 +/- 4.8%, significantly (P < 0.05) more than after both normoxic (25.6 +/- 3.5% reduction) and hyperoxic (26.6 +/- 3.3% reduction) exercise, confirming greater fatigue in hypoxia. Despite lower leg power output in hypoxia, neither cardiac output nor QMBF (27.6 +/- 1.2 l min(-1) and 100.4 +/- 8.7 ml (100 ml)(-1) min(-1), respectively) were significantly different compared with normoxia (28.4 +/- 1.9 l min(-1) and 94.4 +/- 5.2 ml (100 ml)(-1) min(-1), respectively) and hyperoxia (27.8 +/- 1.6 l min(-1) and 95.1 +/- 7.8 ml (100 ml)(-1) min(-1), respectively). Neither IMBF was different across hypoxia, normoxia and hyperoxia (53.6 +/- 8.5, 49.9 +/- 5.9 and 52.9 +/- 5.9 ml (100 ml)(-1) min(-1), respectively). We conclude that when respiratory muscle energy requirement is not different between normoxia and hypoxia, diaphragmatic fatigue is greater in hypoxia as intercostal muscle blood flow is not increased (compared with normoxia) to compensate for the reduction in PaO2, thus further compromising O(2) supply to the respiratory muscles.

Measurement of Respiratory Muscle Blood Flow in Humans Using Near Infrared Spectroscopy and Indocyanine Green

It has been difficult to measure respiratory muscle blood flow (RMBF) in humans because of the highly invasive measurement techniques and the need to anesthetize patients. To our knowledge, there are no methods available to accurately measure RMBF in conscious humans. PURPOSE: To develop an indicator-dilution approach to measure RMBF using near-infrared spectroscopy (NIRS) to detect indocyanine green dye (ICG) over the respiratory muscles in spontaneously breathing humans. METHODS: NIRS optodes were placed on the left 7th intercostal space at the apposition of the costal diaphragm and on an inactive control muscle (vastus lateralis) in 5 healthy male cyclists. Intravenous injection of ICG allowed cardiac output (by the conventional dye-dilution method with arterial sampling) and RMBF to be measured simultaneously. Esophageal and gastric pressures were also measured to calculate the mechanical work of breathing and trans-diaphragmatic pressure. Measurements were obtained during both resting breathing and three separate 5 minute bouts of constant isocapnic hyperventilation at 27.1±3.2, 56.0±6.1 and 75.9±5.7% of maximum minute ventilation as determined on a previous maximal exercise test. RESULTS: RMBF progressively increased (9.9±0.6, 14.8±2.7, 29.9±5.8 and 50.1±12.5 ml·100ml−1·min) with increasing levels of ventilation while blood flow to the inactive control muscle remained constant (10.39±1.4, 8.7±0.7, 12.9±1.7 and 12.2±1.8 ml·100ml−1·min−1). As ventilation rose, RMBF was closely and significantly correlated with cardiac output (r = 0.994, P = 0.006), the work of breathing (r = 0.995, P= 0.005) and trans-diaphragmatic pressure (r = 0.998, P= 0.002). CONCLUSION: To our knowledge, this is the first study to quantify RMBF in conscious humans during spontaneous hyperventilation. These data suggest that the NIRS-ICG method provides a feasible and sensitive index of respiratory muscle blood flow in humans that should be applicable to rest, light, moderate and heavy exercise.

The major limitation to exercise performance in COPD is inadequate energy supply to the respiratory and locomotor muscles

No doubt dynamic hyperinflation and lack of oxidative capacity of skeletal muscles are important causes of exercise limitation in COPD. O'Donnell and Webb and Debigare and Maltais will convince the reader of this by the elegant experiments they have performed. The thesis we will put forward is that

Respiratory muscle blood flow steal during exercise in heart failure

Heart failure (HF) patients have reduced cardiac reserve and increased work of breathing (WOB)., Increased demand for locomotor muscle blood flow (i.e. activities of daily living) may result in competition between respiratory and locomotor vascular beds. We hypothesized that HF patients would demonstrate improved locomotor blood flow with respiratory muscle unloading during moderate activity. We studied 10 HF patients (EF=30±8%) and 10 controls during two 10 min. cycling sessions at 60% VO2max. Session 1 (S1): 5 min of normal breathing (NB) and 5 min respiratory muscle unloading with a ventilator. Session 2 (S2): 5 min NB and 5 min of respiratory muscle loading with inspiratory resistance. Measurements included: leg blood flow (LBF), cardiac output (CO), and inspiratory pleural pressure time integral as an index of the WOB. During S1, WOB was reduced similarly in both groups (HF: 50±60%; CTL: 50±56%, p&lt;0.05 for both). In HF, CO was reduced (9.6±1.4 vs 8.2±2.1 L/min, p&lt;0.05) and LBF increased (4.9±2.6 vs 6.2±2.9 L/min, p&lt;0.01). In CTL, there was no change in CO (14.7±3.1 vs 14.8±5.0 L/min) or LBF (10.9±5.6 vs 10.3±5.2 L/min). During S2, WOB was increased similarly in both groups (HF: 111±75%, CTL: 110±85%, p&lt;0.01 for both). In HF, there was no change in CO (10.0±1.3 vs 10.3±2.5 L/min) or LBF (5.0±1.8 vs 4.9±1.4 L/min). In CTL, CO increased (15.4±4.3 vs 16.9±4.7 L/min, p&lt;0.01) with no change in LBF (10.7±5.3 vs 10.3±5.6 L/min). These data suggest that the respiratory muscles of HF patients preferentially recruit blood flow away from the locomotor muscles during moderate intensity, whole body exercise.

Human respiratory muscle blood flow measured by near-infrared spectroscopy and indocyanine green

Measurement of respiratory muscle blood flow (RMBF) in humans has important implications for understanding patterns of blood flow distribution during exercise in healthy individuals and those with chronic disease. Previous studies examining RMBF in humans have required invasive methods on anesthetized subjects. To assess RMBF in awake subjects, we applied an indicator-dilution method using near-infrared spectroscopy (NIRS) and the light-absorbing tracer indocyanine green dye (ICG). NIRS optodes were placed on the left seventh intercostal space at the apposition of the costal diaphragm and on an inactive control muscle (vastus lateralis). The primary respiratory muscles within view of the NIRS optodes include the internal and external intercostals. Intravenous bolus injection of ICG allowed for cardiac output (by the conventional dye-dilution method with arterial sampling), RMBF, and vastus lateralis blood flow to be quantified simultaneously. Esophageal and gastric pressures were also measured to calculate the work of breathing and transdiaphragmatic pressure. Measurements were obtained in five conscious humans during both resting breathing and three separate 5-min bouts of constant isocapnic hyperpnea at 27.1 +/- 3.2, 56.0 +/- 6.1, and 75.9 +/- 5.7% of maximum minute ventilation as determined on a previous maximal exercise test. RMBF progressively increased (9.9 +/- 0.6, 14.8 +/- 2.7, 29.9 +/- 5.8, and 50.1 +/- 12.5 ml 100 ml(-1) min(-1), respectively) with increasing levels of ventilation while blood flow to the inactive control muscle remained constant (10.4 +/- 1.4, 8.7 +/- 0.7, 12.9 +/- 1.7, and 12.2 +/- 1.8 ml 100 ml(-1) min(-1), respectively). As ventilation rose, RMBF was closely and significantly correlated with 1) cardiac output (r = 0.994, P = 0.006), 2) the work of breathing (r = 0.995, P = 0.005), and 3) transdiaphragmatic pressure (r = 0.998, P = 0.002). These data suggest that the NIRS-ICG technique provides a feasible and sensitive index of RMBF at different levels of ventilation in humans.

Effects of hypoxia on diaphragmatic fatigue in highly trained athletes

Previous work suggests that exercise-induced arterial hypoxaemia (EIAH), causing only moderate arterial oxygen desaturation (SaO2 : 92 +/- 1%), does not exaggerate diaphragmatic fatigue exhibited by highly trained endurance athletes. Since changes in arterial O2 tension have a significant effect on the rate of development of locomotor muscle fatigue during strenuous exercise, the present study investigated whether hypoxia superimposed on EIAH exacerbates the exercise-induced diaphragmatic fatigue in these athletes. Eight trained cyclists (VO2max : 67.0 +/- 2.6 ml kg(-1) min(-1); mean +/- S.E.M.) completed in balanced order four 5 min exercise tests leading to different levels of end-exercise SaO2 (64 +/- 2, 83 +/- 1, 91 +/- 1 and 96 +/- 1%) via variations in inspired O2 fraction (FiO2 : 0.13, 0.17, 0.21 and 0.26, respectively). Measurements were made at corresponding intensities (65 +/- 3, 80 +/- 3, 85 +/- 3 and 90 +/- 3% of normoxic maximal work rate, respectively) in order to produce the same tidal volume, breathing frequency and respiratory muscle load at each FiO2. The mean pressure time product of the diaphragm did not differ across the four exercise tests and ranged between 312 +/- 28 and 382 +/- 22 cmH2O s min(-1). Ten minutes into recovery, twitch transdiaphragmatic pressure (P(di,tw)) determined by bilateral phrenic nerve stimulation, was significantly (P = 0.0001) reduced after all tests. After both hypoxic tests (FiO2 : 0.13, 0.17) the degree of fall in P(di,tw) (by 26.9 +/- 2.7 and 27.4 +/- 2.6%, respectively) was significantly greater (P < 0.05) than after the normoxic test (by 20.1 +/- 3.4%). The greater amount of diaphragmatic fatigue in hypoxia at lower leg work rates (presumably requiring smaller leg blood flow compared with normoxia at higher leg work rates), suggests that when ventilatory muscle load is similar between normoxia and hypoxia, hypoxia exaggerates diaphragmatic fatigue in spite of potentially greater respiratory muscle blood flow availability.

Regional Blood Flow in Respiratory Muscles During Partial Ventilatory Assistance in Rabbits

We tested the hypothesis that even partial ventilatory assistance would reduce respiratory muscle blood flow to levels similar to those found during control mechanical ventilation (CMV). Three levels of pressure support ventilation (PSV) and 2 CMV settings were compared in 10 rabbits. PSV 0, 6, and 12 cm H2O, under continuous positive airway pressure mode, were applied, and then pressure control ventilation (PCV) values of 6 (36 breaths/min) and 12 cm H2O (18 per breaths/min) were applied to each CMV setting with a muscle relaxant. Using colored microspheres, we measured regional tissue blood flow in respiratory muscles, lower extremities, kidney, and liver. Regional tissue blood flow in the diaphragm during PSV6, PCV6, and PCV12 were less than those during PSV0. During PSV12, blood flow in the crural diaphragm was more than that during PCV12 and similar to that during PSV0. Whereas the transdiaphragmatic pressure of PSV6 was -0.8 +/- 1.6 cm H2O, that of PSV12 was -3.1 +/- 2.4 cm H2O. Inspiratory asynchrony, arising from an ineffective triggering effort, was observed in PSV12. The ventilatory settings did not affect blood flow of the lower extremities, liver, and kidney. In conclusion, ventilatory settings affected blood flow in the diaphragm. At certain PSV settings, blood flow in the diaphragm was minimal.

Effects of Spontaneous Breathing During Airway Pressure Release Ventilation on Respiratory Work and Muscle Blood Flow in Experimental Lung Injury

To evaluate the effects of spontaneous breathing at ambient airway pressure (Paw) and during airway pressure release ventilation (APRV) on respiratory work and respiratory muscle blood flow (RMBF) in experimental lung injury. Prospective experimental study. Research laboratory of a university hospital. Twelve hemodynamically stable, analgosedated, and tracheotomized domestic pigs. Respiratory work was estimated by the inspiratory pressure time product (PTPinsp) of esophageal pressure, and RMBF was measured with colored microspheres. Lung injury was induced with IV boli of oleic acid. The first set of measurements was performed before induction of lung injury while pigs were breathing spontaneously at ambient Paw, the second after induction of lung injury while breathing spontaneously at ambient Paw, and the third with lung injury and spontaneous breathing with APRV. After induction of lung injury PTPinsp increased from 138 +/- 14 to 214 +/- 32 cm H2O s/min when pigs breathed spontaneously at ambient Paw (p < 0.05) and returned to 128 +/- 27 cm H2O s/min during APRV. While systemic hemodynamics and blood flow to the psoatic and intercostal muscles did not change, diaphragmatic blood flow increased from 0.34 +/- 0.05 before to 0.54 +/- 0.08 mL/g/min after induction of lung injury and spontaneous breathing at ambient Paw (p < 0.05) and returned to 0.32 +/- 0.05 mL/g/min during APRV (p < 0.05 vs spontaneous breathing at ambient Paw [lung injury]). Respiratory work and RMBF are increased in acute lung injury when subjects breathe spontaneously at ambient Paw. Supporting spontaneous breathing with APRV decreases respiratory work and RMBF to physiologic values.

Respiratory muscle blood flows during physiological and chemical hyperpnea in the rat.

Whether the diaphragm retains a vasodilator reserve at maximal exercise is controversial. To address this issue, we measured respiratory and hindlimb muscle blood flows and vascular conductances using radiolabeled microspheres in rats running at their maximal attainable treadmill speed (96 +/- 5 m/min; range 71-116 m/min) and at rest while breathing either room air or 10% O(2)-8% CO(2) (balance N(2)). All hindlimb and respiratory muscle blood flows measured increased during exercise (P < 0.001), whereas increases in blood flow while breathing 10% O(2)-8% CO(2) were restricted to the diaphragm only. During exercise, muscle blood flow increased up to 18-fold above rest values, with the greatest mass specific flows (in ml. min(-1). 100 g(-1)) found in the vastus intermedius (680 +/- 44), red vastus lateralis (536 +/- 18), red gastrocnemius (565 +/- 47), and red tibialis anterior (602 +/- 44). During exercise, blood flow was higher (P < 0.05) in the costal diaphragm (395 +/- 31 ml. min(-1). 100 g(-1)) than in the crural diaphragm (286 +/- 17 ml. min(-1). 100 g(-1)). During hypoxia+hypercapnia, blood flows in both the costal and crural diaphragms (550 +/- 70 and 423 +/- 53 ml. min(-1). 100 g(-1), respectively) were elevated (P < 0.05) above those found during maximal exercise. These data demonstrate that there is a substantial functional vasodilator reserve in the rat diaphragm at maximal exercise and that hypoxia + hypercapnia-induced hyperpnea is necessary to elevate diaphragm blood flow to a level commensurate with its high oxidative capacity.

Respiratory, cardiovascular, and metabolic adjustments to hypoxemia during sleep in piglets

The influence of sleep on ventilation, metabolic rate, cardiovascular function, and regional distribution of blood flow during hypoxemia (PaO2 of 45-50 mmHg (1 mmHg = 133.3 Pa)) was studied in piglets at 6 ± 1 and 34 ± 5 days (mean ± SD). Measurement of ventilation and metabolic rate was done in a metabolic chamber, and blood flow was measured using the microsphere technique. A subgroup of animals was instrumented for cardiac output measurement (dye-dilution technique) and continuous monitoring of the hemoglobin saturation in oxygen (SaO2) We found that although sleep did not influence the metabolic and cardiac output response to hypoxemia, it affected the ventilatory response as well as the brain and the respiratory muscle blood flows. During active sleep in the older animals, the ventilatory response to hypoxemia was smaller than in the other two states; marked drops in SaO2 occurred with changes in the breathing pattern; and that state was associated with the highest rate of brain blood flow. As well, age affected the ventilatory and metabolic response, but not the cardiovascular response to hypoxemia. The age-dependent ventilatory changes with hypoxemia (smaller ventilatory response in the young than in the older animals) were related to the different levels of oxygen consumption. In summary, active sleep was responsible for all the sleep-dependent changes in the response to a moderate degree of hypoxemia.Key words: breathing pattern, metabolic rate, blood flow, microspheres, maturation.

Respiratory muscle work compromises leg blood flow during maximal exercise.

We hypothesized that during exercise at maximal O2 consumption (VO2max), high demand for respiratory muscle blood flow (Q) would elicit locomotor muscle vasoconstriction and compromise limb Q. Seven male cyclists (VO2max 64 +/- 6 ml.kg-1.min-1) each completed 14 exercise bouts of 2.5-min duration at VO2max on a cycle ergometer during two testing sessions. Inspiratory muscle work was either 1) reduced via a proportional-assist ventilator, 2) increased via graded resistive loads, or 3) was not manipulated (control). Arterial (brachial) and venous (femoral) blood samples, arterial blood pressure, leg Q (Qlegs; thermodilution), esophageal pressure, and O2 consumption (VO2) were measured. Within each subject and across all subjects, at constant maximal work rate, significant correlations existed (r = 0.74-0.90; P < 0.05) between work of breathing (Wb) and Qlegs (inverse), leg vascular resistance (LVR), and leg VO2 (VO2legs; inverse), and between LVR and norepinephrine spillover. Mean arterial pressure did not change with changes in Wb nor did tidal volume or minute ventilation. For a +/-50% change from control in Wb, Qlegs changed 2 l/min or 11% of control, LVR changed 13% of control, and O2 extraction did not change; thus VO2legs changed 0.4 l/min or 10% of control. Total VO2max was unchanged with loading but fell 9.3% with unloading; thus VO2legs as a percentage of total VO2max was 81% in control, increased to 89% with respiratory muscle unloading, and decreased to 71% with respiratory muscle loading. We conclude that Wb normally incurred during maximal exercise causes vasoconstriction in locomotor muscles and compromises locomotor muscle perfusion and VO2.

Hyperinflation with intrinsic PEEP and respiratory muscle blood flow

Increased end-expiratory lung volume and intrinsic positive end-expiratory pressure (PEEP) are common in obstructive lung disease, especially during exacerbations or exercise. This loads the respiratory muscles and may also stress the circulatory system, causing a reduction or redistribution of cardiac output. We measured the blood flow to respiratory muscles and systemic organs using colored microspheres in 10 spontaneously breathing anesthetized tracheotomized dogs. Flows during baseline breathing (BL) were compared with those during hyperinflation (HI) induced by a mechanical analogue of airway closure and with those during an inspiratory resistive load (IR) that produced an equivalent increase in inspiratory work and time-integrated transdiaphragmatic pressure. Cardiac output was unchanged during IR (3.19 +/- 0.27 l/min at BL, 3.09 +/- 0.34 l/min during IR) but was reduced during HI (2.14 +/- 0.29 l/min; P < 0.01). Among the organs studied, flow was unaltered by IR but decreased to the liver and pancreas and increased to the brain during HI. For the respiratory muscles, flow to the diaphragm increased during IR. However, despite a 1.9-fold increase in inspiratory work per minute and a 2.5-fold increase in integrated transdiaphragmatic pressure during HI, blood flow to the diaphragm was unchanged and flow to the scalenes and sternomastoid fell. The only respiratory muscle to which flow increased during HI was the transversus abdominis, an expiratory muscle. We conclude that the circulatory effects of hyperinflation in this model impair inspiratory muscle perfusion and speculate that this may contribute to respiratory muscle dysfunction in hyperinflated states.

Theophylline alters distribution of blood flow to respiratory muscles.

This study was designed to examine the effects of theophylline on respiratory muscle blood flow in 11 lightly anesthetized and spontaneously breathing dogs using the radioactive microsphere tracer technique. During quiet breathing, blood flow to the costal diaphragm (25.1 +/- 13.9 ml/100 g/min) exceeded blood flow to the parasternal intercostals (18.0 +/- 10.2 ml/100 g/min, p < 0.05). Inspiratory resistive loading abolished these differences by increasing blood flow to the parasternal intercostals more than to the diaphragm. Aminophylline (40 mg/kg) significantly increased minute ventilation and tidal transdiaphragmatic pressure (Pdi) swing during quiet breathing but not during inspiratory resistive loading. Theophylline did not affect diaphragmatic blood flow during inspiratory resistive loading while the same Pdi swing and tension-time index (TTdi) were reached. During quiet breathing, however, theophylline significantly (p < 0.05) increased blood flow to the triangularis sterni from 7.9 +/- 5.6 to 18.1 +/- 25.6 ml/100 g/min and to the transversus abdominis from 10.8 +/- 8.4 to 14.6 +/- 10.5 ml/100 g/min and tended to increase blood flow to the costal diaphragm and the parasternals. We conclude that (1) during quiet breathing, but not during inspiratory resistive loading, blood flow to the costal diaphragm exceeded flow to the parasternal intercostals; (2) during quiet breathing, theophylline increased blood flow to the expiratory muscles as it promoted recruitment of expiratory muscles; and (3) theophylline did not affect diaphragmatic blood flow for a given TTdi.

Respiratory muscle blood flow in the fetal lamb during apnoea and breathing

We measured blood flow to the respiratory muscles of the fetal lamb using the radioactively-labelled microsphere technique in order to assess whether fetal breathing is an energetically costly activity as has been reported. Diaphragm flow ranged from 6.4–35.2 ml·min −1·100 g −1 during fetal apnoea and rose to 21.1–615 ml·min −1·100 g −1 during fetal breathing ( P<0.02; n = 7). Parasternal muscle flow also increased significantly ( P<0.02) between fetal apnoea and breathing while external and internal intercostal flows did not change. Expressed as a percentage of cardiac output the diaphragm received 0.08–0.28% during apnoea and 0.22–2.2% during fetal breathing. Neither placental blood flow nor fetal O 2 consumption increased significantly between fetal apnoea and breathing. We conclude that the levels of perfusion required by the respiratory muscles for breathing in the fetus are inconsistent with fetal breathing costing a large proportion of the fetal O 2 budget.

Gastric intramucosal acidosis during weaning from mechanical ventilation.

Hussain and Roussosl showed that during endotoxic shock, respiratory muscle blood flow in spontaneously breathing dogs increases significantly from baseline values, and in the animals who are mechanically ventilated, respiratory muscle perfusion decreases to control values. Similarly, blood flow in organs like brain, gut, and skeletal muscles, in the mechanically ventilated group was significantly higher than the spontaneously breathing group. Therefore, during mechanical ventilation, a fraction of the cardiac output used by the respiratory muscles can be made available to the other organs and, conversely, during spontaneous ventilation, organs such as skeletal muscles, brain and gut fall under the disadvantage of losing out to respiratory muscles. The magnitude of increase in respiratory blood flow in the spontaneously breathing group was from 51 ml/min to 101 ml/min at 60 minutes of shock. Mohsenifar et al.2 tested the hypothesis that gastric intramucosal pH can be used as a trend indicator of gut and/or splanchnic ischemia in patients with chronic obstructive lung disease, respiratory failure, during weaning from mechanical ventilation. This chapter will summarize the data on the role of gastric intramucosal pH as an indicator of weaning success or failure in these patients.

Blood flow to respiratory muscles and major organs during inspiratory flow resistive loads.

To determine whether diaphragmatic fatigue in the intact animal subjected to loaded breathing is associated with a decrease in diaphragmatic blood flow, seven unanesthetized sheep were subjected to severe inspiratory flow resistive (IFR) loads that led to a decrease in transdiaphragmatic pressure (Pdi) and a rise in arterial PCO2 (PaCO2). Blood flow to the diaphragm, other respiratory muscles, limb muscles, and major organs was measured using the radionuclide-labeled microsphere method. With these loads blood flow increased to the diaphragm (621 +/- 242%) and all the other inspiratory and expiratory diaphragm (621 +/- 242%) and all the other inspiratory and expiratory muscles; there was no statistically significant change in blood flow to these muscles at the time when Pdi decreased and PaCO2 rose. Blood flow also increased to the heart (103 +/- 34%), brain (212 +/- 39%), and adrenals (76 +/- 9%), whereas pancreatic flow decreased (-66 +/- 14%). Limb muscle blood flow remained unchanged. We conclude that in unanesthetized sheep subjected to IFR loads 1) we did not demonstrate a decrease in respiratory muscle blood flow associated with diaphragmatic fatigue and ventilatory failure, and 2) there is a redistribution of blood flow among major organs.

Respiratory muscle blood flow in exercising dogs after pneumonectomy.

In three foxhounds after left pneumonectomy, the relationships of ventilatory work and respiratory muscle (RM) blood flow to ventilation (VE) during steady-state exercise were examined. VE was measured using a specially constructed respiratory mask and a pneumotach; work of breathing was measured by the esophageal balloon technique. Blood flow to RM was measured by the radionuclide-labeled microsphere technique. Lung compliance after pneumonectomy was 55% of that before pneumonectomy; compliance of the thorax was unchanged. O2 uptake (VO2) of RM comprised only 5% of total body VO2 at exercise. At rest, inspiratory muscles received 62% and expiratory muscles 38% of the total O2 delivered to the RM (QO2RM). During exercise, inspiratory muscles received 59% and expiratory muscles 41% of total QO2RM. Blood flow per gram of muscle to the costal diaphragm was significantly higher than that to the crural diaphragm. The diaphragm, parasternals, and posterior cricoarytenoids were the most important inspiratory muscles, and internal intercostals and external obliques were the most important expiratory muscles for exercise. Up to a VE of 120 l/min through one lung, QO2RM constituted only a small fraction of total body VO2 during exercise and maximal vasodilation in the diaphragm was never approached.