Hyperinflation with intrinsic PEEP and respiratory muscle blood flow

1994 ◽  
Vol 77 (5) ◽  
pp. 2440-2448 ◽  
Author(s):  
Y. Kawagoe ◽  
S. Permutt ◽  
H. E. Fessler

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.

2008 ◽  
Vol 104 (4) ◽  
pp. 1202-1210 ◽  
Author(s):  
Jordan A. Guenette ◽  
Ioannis Vogiatzis ◽  
Spyros Zakynthinos ◽  
Dimitrios Athanasopoulos ◽  
Maria Koskolou ◽  
...  

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.


1988 ◽  
Vol 64 (4) ◽  
pp. 1624-1628 ◽  
Author(s):  
J. R. Coast ◽  
R. A. Jensen ◽  
S. S. Cassidy ◽  
M. Ramanathan ◽  
R. L. Johnson

In this study, noninvasive measurements of cardiac output and O2 consumption were performed to estimate the blood flow to and efficiency of the respiratory muscles that are used in elevated inspiratory work loads. Five subjects were studied for 4.5 min at a respiratory rate of 18 breaths/min and a duty cycle of 0.5. Studies were performed at rest without added respiratory loads and at elevated inspiratory work loads with the use of an inspiratory valve that permitted flow only when a threshold pressure was maintained. Cardiac output and O2 consumption were calculated using a rebreathing technique. Respiratory muscle blood flow and O2 consumption were estimated as the difference between resting and loaded breathing. Work of breathing was calculated by integrating the product of mouth pressure and volume. Increases in cardiac output and O2 consumption in response of 4.5 min loaded breathing averaged 1.84 l/min and 108 ml/min, respectively. No increases were seen in response to 20-s loaded breathing. In a separate series of experiments on four subjects, though, cardiac output increased for the first 2 min then leveled off. These results indicate that the increase in cardiac output was a metabolic effect of the increased work load and was not caused primarily by the influence of the highly negative intrathoracic pressure on venous return. Efficiency of the respiratory muscles during inspiratory threshold loading averaged 5.9%, which was similar to measurements of efficiency of respiratory muscles using whole-body O2 consumption that have been reported previously in humans and in dogs.


1986 ◽  
Vol 60 (5) ◽  
pp. 1759-1764 ◽  
Author(s):  
A. W. Bell ◽  
J. R. Hales ◽  
A. A. Fawcett ◽  
R. B. King

Radioactive microspheres were used to measure cardiac output and blood flow to most major tissues, including those in the pregnant uterus, in late-pregnant ewes at rest and during treadmill exercise (approximately 3-fold increase in metabolic rate for 30 min) in thermoneutral (TN) (dry bulb temperature (Tdb) = 13 degrees C, wet bulb temperature (Twb) = 10 degrees C) and mildly hot (MH) (Tdb = 40 degrees C, Twb = 27 degrees C) environments. Exercise caused major increases in blood flow to respiratory muscles, nonrespiratory limb muscles, and adipose tissue, and flow was decreased to some gastrointestinal tissues, spleen, pancreas, and to placental and nonplacental tissues in the pregnant uterus. Heat exposure had relatively little effect on these exercise-induced changes, except that flow was further increased in the respiratory muscles. Results are compared with those of a similar study on nonpregnant sheep in which changes in muscle, skin, and visceral flows during exercise were attenuated by heat exposure. It is suggested that redistribution of blood flow from the pregnant uterus, which in resting ewes took 22% of cardiac output, is a significant buffer against the potentially deleterious effects of combined exercise and heat stress on blood flow to exercising muscles and thermoregulatory tissues.


1987 ◽  
Vol 63 (1) ◽  
pp. 181-187 ◽  
Author(s):  
J. D. Anholm ◽  
R. L. Johnson ◽  
M. Ramanathan

To determine the increment in cardiac output and in O2 consumption (Vo2) from quiet breathing to maximal sustained ventilation, Vo2 and cardiac output were measured using an acetylene rebreathing technique in five subjects. Cardiac output and Vo2 were measured multiple times in each subject at rest and during sustained maximal ventilation. During maximal ventilation subjects breathed 5% CO2 to prevent hypocapnia. The increase in cardiac output from rest to maximal breathing was taken as an estimate of respiratory muscle blood flow and was used to calculate the arteriovenous O2 content difference across the respiratory muscles from the Fick equation. Cardiac output increased by 4.3 +/- 1.0 l/min (mean +/- SD), from 5.6 +/- 0.7 l/min at rest to 9.9 +/- 1.1 l/min, during maximal ventilations ranging from 127 to 193 l/min. Vo2 increased from 312 +/- 29 to 723 +/- 69 ml/min during maximal ventilation. O2 extraction across the respiratory muscles during maximal breathing was 9.6 +/- 1.0 vol% (range 8.5 to 10.7 vol%). These values suggest an upper limit of respiratory muscle blood flow of 3–5 l/min during unloaded maximal sustained ventilation.


1993 ◽  
Vol 183 (1) ◽  
pp. 301-321 ◽  
Author(s):  
A. S. Kolok ◽  
M. R. Spooner ◽  
A. P. Farrell

Cardiac output (Q.) and blood flow distribution were measured in adult largescale suckers at rest and while swimming. Cardiac output was directly measured using an ultrasonic flowprobe in fish during the summer (16°C), fall (10°C) and winter (5°C). Largescale suckers were adept at holding station against a current without swimming and, when engaged in this behavior, they did not significantly increase Q. relative to that found in fish in still water. When fish began to swim, Q. increased significantly. From 16 to 10°C, the critical swimming speed (Ucrit), maximum Q. and scope for Q. of the suckers did not change. However, from 10 to 5°C all three traits were significantly reduced. Thus, these fish respond to variation in water temperature in two different ways. From 16 to 10°C, the fish compensate perfectly for the change in temperature with respect to cardiac and swimming performance. From 10 to 5°C, however, largescale suckers experience a dramatic decline in cardiac and swimming performance that may be associated with a quiescent overwintering strategy. Blood flow distribution in the fish at rest and while swimming was measured at 16°C using injection of colored microspheres. In the resting fish, over 10 % of the microspheres were recovered from the kidney and over 43 % were recovered from white muscle. When the fish were swimming, there was a 60-fold increase in blood flow to the red muscle while blood flow to all other tissues remained consistent with that at rest.


1990 ◽  
Vol 69 (3) ◽  
pp. 1117-1122 ◽  
Author(s):  
D. A. White ◽  
G. H. Parsons

Tracheal blood flow increases greater than twofold in response to eucapnic hyperventilation of dry gas in anesthetized sheep. To determine whether this occurs at normal minute ventilation, we studied sheep in which tracheal blood flow was measured in response to humid and dry gas ventilation while 1) awake and spontaneously breathing and 2) anesthetized and intubated during isocapnic mechanical ventilation. In additional sheep, three tracheal mucosal temperatures were measured during humid and dry gas mechanical ventilation to measure airway tissue cooling. Tracheal blood flow was determined by use of a left atrial injection of 15-microns-diam radiolabeled microspheres. Previously implanted flow probes on the pulmonary artery and the common bronchial artery allowed continuous recording of cardiac output and bronchial blood flow. Tracheal blood flow in awake spontaneously breathing sheep was 10.8 +/- 5.6 (SD) ml.min-1.100 g wet wt-1 while humid gas was breathed, and it was unchanged with dry gas. In contrast, isocapnic ventilation of intubated animals with dry gas resulted in a 10-fold increase in blood flow to the most proximal two-ring tracheal segment compared with that seen while humid gases were spontaneously ventilated [101 +/- 75 vs. 11 +/- 6 (SD) ml.min-1.100 g-1, P less than 0.05]. Despite a 10-fold increase in proximal tracheal blood flow, there was no response in distal tracheal and bronchial blood flow, as indicated by no change in the common bronchial artery blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)


1985 ◽  
Vol 58 (4) ◽  
pp. 1148-1156 ◽  
Author(s):  
S. Magder ◽  
D. Lockhat ◽  
B. J. Luo ◽  
C. Roussos

Since respiratory muscles fail when blood flow is inadequate, we asked whether their blood flow would be maintained in severe hypotensive states at the expense of other vital organs (brain, heart, kidney, gut, spleen). We measured blood flow (radiolabeled microspheres) to respiratory muscles and vital organs in 11 dogs breathing against an inspiratory elastic load, first with normal blood pressure (BP) and then hypotension produced by cardiac tamponade. With the elastic load alone, there was no change in BP or cardiac output; diaphragmatic blood flow (Qdi) increased from 12.8 +/- 7.0 to 34.1 +/- 15.6 ml/100 g, and total respiratory muscle flow (QTR) increased from 56.5 +/- 19.1 to 97.4 +/- 36.5 ml/100 g, but except for the brain, there was no change in blood flow to other organs. With tamponade (mean BP = 79 +/- 16 mmHg), flow decreased to all organs, whereas Qdi (39.0 +/- 19.4) did not change. QTR decreased, but not significantly, to 88.6 +/- 49.5. With more tamponade (mean BP = 53 +/- 13 mmHg), flow to all vital organs decreased as well as QTR (57.9 +/- 47.18), but Qdi did not significantly decrease and had the same relationship to respiratory force as with normal BP. Thus, with severe inspiratory elastic loading and severe hypotension, the diaphragm and external intercostal muscles did most of the respiratory work, and their flow was maintained at the expense of other vital organs.


1981 ◽  
Vol 59 (2) ◽  
pp. 204-208 ◽  
Author(s):  
R. Keeler ◽  
Anamaria Barrientos ◽  
K. Lee

A study was made of the effects of acute (4 h) or chronic (4 days) infusion of Escherichia coli endotoxin on cardiovascular function in rats. Rats with acute endotoxemia had a reduced cardiac output but maintained their arterial blood pressure. Fractional distribution of the cardiac output was increased to the liver and reduced to the gastrointestinal tract and skin. No changes in fractional distribution to the kidneys, lungs, or heart were observed although absolute blood flow to these areas was reduced.Rats with chronic endotoxemia had a reduced cardiac output and hypotension with no change in peripheral resistance. Other changes resembled those seen in acute endotoxemia apart from a low renal fraction of the cardiac output. Calculation and interpretation of blood flow changes in these animals was difficult because of a large fall in hematocrit and changes in organ weight.


1963 ◽  
Vol 204 (6) ◽  
pp. 963-968 ◽  
Author(s):  
John F. Murray ◽  
I. Maureen Young

The circulatory effects of breathing low concentrations of oxygen were studied in ten anesthetized dogs. Simultaneous measurements were made of cardiac output (indicator dilution technique) and blood flow to the head, kidney, and hind limb (electromagnetic flowmeters). Four experiments were performed with the addition of succinylcholine to inhibit the ventilatory response to hypoxia and maintain pCO2 constant. A rise in cardiac output and mean arterial pressure occurred which was significantly correlated to the decrease in arterial oxygen saturation. No threshold for these responses was found. Blood flow tended to increase during hypoxia in the regions studied but the responses were variable and only the change in renal blood flow had a significant correlation to arterial oxygen unsaturation. Systemic and regional vascular resistances during hypoxia varied both in direction and magnitude of change. The preponderant effects of hypoxia influence cardiac output more than peripheral vascular resistance.


2003 ◽  
Vol 95 (3) ◽  
pp. 1159-1169 ◽  
Author(s):  
Joshua R. Rodman ◽  
Kathleen S. Henderson ◽  
Curtis A. Smith ◽  
Jerome A. Dempsey

In awake dogs, lactic acid was injected into the phrenic and deep circumflex iliac arteries to elicit the diaphragm and abdominal muscle metaboreflexes, respectively. At rest, injections into the phrenic or deep circumflex iliac arteries significantly increased mean arterial blood pressure 21 ± 7% and reduced cardiac output 6 ± 2% and blood flow to the hindlimbs 20 ± 9%. Simultaneously, total systemic, hindlimb, and abdominal expiratory muscle vascular conductances were reduced. These cardiovascular responses were not accompanied by significant changes in the amplitude or timing of the diaphragm electromyogram. During treadmill exercise that increased cardiac output, hindlimb blood flow, and vascular conductance 159 ± 106, 276 ± 309, and 299 ± 90% above resting values, lactic acid injected into the phrenic or deep circumflex iliac arteries also elicited pressor responses and reduced hindlimb blood flow and vascular conductance. Adrenergic receptor blockade at rest eliminated the cardiovascular effects of the respiratory muscle metaboreflex. We conclude that the cardiovascular effects of respiratory muscle metaboreflex activation are similar to those previously reported for limb muscles. When activated via metabolite production, the respiratory muscle metaboreflex may contribute to the increased sympathetic tone and redistribution of blood flow during exercise.


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