Mechanism of hyperpnea induced by changes in pulmonary blood flow

1984 ◽  
Vol 56 (5) ◽  
pp. 1418-1422 ◽  
Author(s):  
J. F. Green ◽  
N. D. Schmidt
Keyword(s):  
Blood Flow ◽  
Pulmonary Blood Flow ◽  
Venous Return ◽  
Membrane Oxygenator ◽  
Co2 Gas ◽  
Ventilatory Drive ◽  
Systemic Venous Return ◽  
Pulmonary Arterial ◽  
The Right ◽  
Breathing Room

Increases in pulmonary blood flow can elicit hyperpnea. To examine the mechanisms responsible, we surgically isolated the systemic and pulmonary circulations in six dogs and independently controlled PCO2, PO2, and blood flow in each circuit. Anesthesia was induced with ketamine and maintained with halothane. Systemic venous return was drained from the right atrium and passed through a membrane oxygenator and heat exchanger; blood was returned to the ascending aorta (Qs). An identical bypass was established for the pulmonary circulation, draining blood from the left atrium and returning it to the pulmonary artery (Qp). The lungs were initially ventilated with room air. Qs and systemic arterial CO2 gas tension were maintained at approximately 0.080 1 X min-1 X kg-1 and 40 Torr, respectively. Pulmonary arterial CO2 gas tension was set near 55 Torr, and Qp varied. Ventilatory drive was assessed by minute integration (MI) of the activity recorded from the central end of the left C5 root of the phrenic nerve. MI increased as much as 160% above control as Qp was increased over the range of 0.025 (control) to 0.175 1 X min-1 X kg-1. When pulmonary CO2 gradients were eliminated by a rebreathing technique, MI was independent of Qp. These results suggest that CO2-sensitive pulmonary receptors respond to the change in pulmonary PCO2 gradients which occur when Qp is elevated (breathing room air) augmenting ventilation.

Evidence for pulmonary CO2 chemosensitivity: effects on ventilation

1982 ◽  
Vol 52 (5) ◽  
pp. 1192-1197 ◽  
Author(s):  
M. I. Sheldon ◽  
J. F. Green
Keyword(s):  
Blood Flow ◽  
Heat Exchanger ◽  
Venous Return ◽  
Median Sternotomy ◽  
Ascending Aorta ◽  
Partial Pressure Of Co2 ◽  
Systemic Venous Return ◽  
Flow Through ◽  
The Right ◽  
Co2 Chemosensitivity

To determine whether there is a pulmonary chemoreceptor for CO2 that influences spontaneous ventilation (VE), we separated the systemic and pulmonary circulations and controlled partial pressure of CO2 (PCO2) independently in each circuit under hyperoxic conditions and measured VE. Dogs were anesthetized with ketamine and maintained with 1% halothane. Systemic venous return was drained from the right atrium and passed through an oxygenator and heat exchanger; blood was returned to the ascending aorta. An identical bypass was established for the pulmonary circulation, draining blood from the left atrium and returning it to the pulmonary artery. The heart was fibrillated; all cannulas were brought through the chest wall; and the median sternotomy was closed. Blood flow through both circuits was maintained at 0.080 l . kg-1 . min-1. Systemic PCO2 (PSCO2) was held constant at three different nonoscillatory levels. At each level, pulmonary PCO2 (PpCO2) was randomly varied between approximately 7 and 85 Torr. With PSCO2 at 43.5 +/- 0.4 Torr, VE increased 2.67 +/- 0.61 l . min-1 as PpCO2 was varied between these limits. With PSCO2 at 63.8 +/- 2.5 Torr, VE increased 3.95 +/- 0.73 l . min-1 over these same limits of PpCO2. With PSCO2 below 25--30 Torr, the dogs were apneic and no longer responded to changes in PpCO2. The effect of PpCO2 on VE was abolished by vagotomy. These results suggest the presence of a CO2 chemoreceptor in the lung that interacts with the nonpulmonary chemoreceptors in the control of VE.

Concealed pulmonary venous obstruction in right atrial isomerism with pulmonary outflow tract obstruction—surgical management following modified Blalock-Taussig shunt

1992 ◽  
Vol 2 (1) ◽  
pp. 95-99 ◽  
Author(s):  
Ing-Sh Chiu ◽  
Nan-Koong Wang ◽  
Mei-Hwan Wu ◽  
Fen-Fen Wu ◽  
Chi-Ren Hung
Keyword(s):  
Blood Flow ◽  
Pulmonary Edema ◽  
Cardiac Catheterization ◽  
Pulmonary Blood Flow ◽  
Venous Return ◽  
Balloon Catheter ◽  
Right Atrial ◽  
Initial Surgery ◽  
The Right ◽  
Blalock Taussig Shunt

SummaryObstruction to the pulmonary venous return is a frequent associated anomaly in patients with isomerism of the right atrial appendages. Yet, preoperative diagnosis by means of either cross-sectional echocardiography or cardiac catheterization can be intriguing. Indeed, the presence of two morphologically right lungs reduce considerably the size of window for precordial echocardiography. Also, in the presence of severe pulmonary stenosis or atresia, it can be difficult at cardiac catheterization to enter the pulmonary trunk. In these patients, construction of a systemic-to-pulmonary artery anastomosis will almost inevitably result in pulmonary edema. Between May 1984 and December 1988, five patients with isomerism of the right atrial appendages, severely decreased pulmonary blood flow and concealed obstruction to the pulmonary venous return were admitted to our hospital. A modified Blalock Taussig shunt by interposition of a polytetrafluoroethylene prosthesis was performed in each patients and all of them developed pulmonary edema. Three patients died despite appropriate medical treatment. The remaining two patients were successfully treated by banding of the Blalock shunt. This was performed in the first patient at the time of the initial surgery, when prior to closure of chest, pulmonary edema became manifest. The second patient who developed pulmonary edema early postoperatively, underwent cardiac catheterization to confirm the clinical diagnosis of obstruction to the pulmonary venous return. Reduction of blood flow through the Blalock shunt with resolution of edema was initially achieved by means of a partially occluding balloon catheter. Pulmonary edema recurred one week later because of rupture of the balloon and the patient eventually underwent a successful banding of the Blalock shunt through a left thoracotomy. We conclude that preoperative assessment of the pulmonary venous return is mandatory in patients with right isomerism and reduced pulmonary blood flow. Construction of a modified Blalock-Taussig shunt in the presence of concealed obstruction to the pulmonary venous return will almost inevitably cause pulmonary edema. Banding of the Blalock shunt can be successful, as observed in our experience, for the management of this serious complication.

scholarly journals CLOSING OF INTERVENTRICULAR SEPTUM DEFECT IN ONE-STEP AND STEPWISE SURGICAL TREATMENT IN PATIENTS WITH PULMONARY ATRESIA AND AORTO-PULMONARY COLLATERALS

2015 ◽  
Vol 174 (4) ◽  
pp. 9-12
Author(s):  
A. A. Morozov ◽  
R. R. Movsesyan ◽  
V. G. Lyubomudrov
Keyword(s):  
Blood Flow ◽  
Surgical Treatment ◽  
Pulmonary Blood Flow ◽  
Interventricular Septum ◽  
Pulmonary Arteries ◽  
Pulmonary Atresia ◽  
Definitive Repair ◽  
One Step ◽  
Pulmonary Arterial ◽  
The Right

Pulmonary atresia with defect of interventricular septum and collateral pulmonary blood flow refers to complicated congenital malformation of the heart. Surgical treatment represents itself as very difficult task because of anatomical variability of this abnormality. The main problem of surgery is a definitive repair of the defect including correction of maldistributions of pulmonary arterial bed (unifocalization of pulmonary blood flow), reconstruction of outflow tract of the right ventricle and closing of interventricular septum defect. The performance of closing interventricular septum defect could be successful in patients with pulmonary atresia and collateral pulmonary blood flow in case of stepwise and one-step surgical treatment. The combination of maximal number of pulmonary segments and sufficient development of central pulmonary arteries facilitates to progress of assigned task. Patients with the level of pulmonary-arterial index more than 170 mm/m² and integrity of pulmonary arterial bed, centralization of pulmonary segments (minimum 15) could be considered as a candidate for definite repair of the defect.

Regional pulmonary blood flow during 96 hours of hypoxia in conscious sheep

1986 ◽  
Vol 61 (6) ◽  
pp. 2136-2143 ◽  
Author(s):  
D. C. Curran-Everett ◽  
K. McAndrews ◽  
J. A. Krasney
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Pulmonary Blood Flow ◽  
Pulmonary Arterial Pressure ◽  
Pressor Response ◽  
Superior Vena ◽  
Acute Hypoxia ◽  
Vena Cava ◽  
Normobaric Hypoxia ◽  
Pulmonary Arterial

The effects of acute hypoxia on regional pulmonary perfusion have been studied previously in anesthetized, artificially ventilated sheep (J. Appl. Physiol. 56: 338–342, 1984). That study indicated that a rise in pulmonary arterial pressure was associated with a shift of pulmonary blood flow toward dorsal (nondependent) areas of the lung. This study examined the relationship between the pulmonary arterial pressor response and regional pulmonary blood flow in five conscious, standing ewes during 96 h of normobaric hypoxia. The sheep were made hypoxic by N2 dilution in an environmental chamber [arterial O2 tension (PaO2) = 37–42 Torr, arterial CO2 tension (PaCO2) = 25–30 Torr]. Regional pulmonary blood flow was calculated by injecting 15-micron radiolabeled microspheres into the superior vena cava during normoxia and at 24-h intervals of hypoxia. Pulmonary arterial pressure increased from 12 Torr during normoxia to 19–22 Torr throughout hypoxia (alpha less than 0.049). Pulmonary blood flow, expressed as %QCO or ml X min-1 X g-1, did not shift among dorsal and ventral regions during hypoxia (alpha greater than 0.25); nor were there interlobar shifts of blood flow (alpha greater than 0.10). These data suggest that conscious, standing sheep do not demonstrate a shift in pulmonary blood flow during 96 h of normobaric hypoxia even though pulmonary arterial pressure rises 7–10 Torr. We question whether global hypoxic pulmonary vasoconstriction is, by itself, beneficial to the sheep.

The pulmonary vasculature in a neonatal porcine model with increased pulmonary blood flow and pressure

2001 ◽  
Vol 11 (4) ◽  
pp. 420-430 ◽  
Author(s):  
Elisabeth V. Stenbøg ◽  
Daniel A. Steinbrüchel ◽  
Anne Bloch Thomsen ◽  
Ulrik Baandrup ◽  
Lene Heickendorff ◽  
...  
Keyword(s):  
Blood Flow ◽  
Pulmonary Artery ◽  
Vascular Disease ◽  
Pulmonary Blood Flow ◽  
Left Pulmonary Artery ◽  
Pulmonary Vasculature ◽  
Pulmonary Vascular Disease ◽  
Systolic Pulmonary Arterial Pressure ◽  
Pulmonary Arterial ◽  
Circulating Levels

Introduction: Hypertension and hyperperfusion of the pulmonary vascular bed in the setting of congenital cardiac malformations may lead to progressive pulmonary vascular disease. To improve the understanding of the basic mechanisms of this disease, there is a need for clinically relevant animal models which reflect the disease process. Material and Results: We randomly allocated 45 newborn pigs, at the age of 48 hrs, to groups in which there was either construction of a 3 mm central aorto-pulmonary shunt, undertaken in 9, or ligation of the left pulmonary artery, achieved in 13. Controls included sham operations in 13, or no operations in 10 pigs. Follow-up was continued for three months. The interventions were compatible with survival in most pigs. The shunts resulted in an acute 85% increase in systolic pulmonary arterial pressure, and a more than twofold increase in pulmonary blood flow. By three months of age, nearly all shunts had closed spontaneously, and haemodynamics were normal. Ligation of the left pulmonary artery resulted in a normal total pulmonary blood flow, despite only the right lung being perfused, and a 33% increase in systolic pulmonary arterial pressure. These haemodynamic changes were maintained throughout the period of study. In both groups, histomorphometry revealed markedly increased muscularity of the intra-acinar pulmonary arteries. Circulating levels of endothelin were normal in the shunted animals, and elevated in those with ligation of the left pulmonary artery. Conclusion: In neonatal porcine models of pulmonary vascular disease, created by construction of 3 mm central aorto-pulmonary shunts and ligation of one pulmonary artery, we observed histopathological changes of the pulmonary vasculature similar to early hypertensive pulmonary vascular disease in humans. Elevated circulating levels of endothelin were associated with abnormal haemodynamics rather than abnormal pathology. These findings could be valuable for future studies on the pathogenesis of hypertensive pulmonary vascular disease associated with congenital cardiac malformations.

Effect of a regional increase in alveolar pressure on pulmonary blood flow

1992 ◽  
Vol 73 (4) ◽  
pp. 1291-1296 ◽  
Author(s):  
L. E. Olson ◽  
R. L. Wardle
Keyword(s):  
Blood Flow ◽  
Pulmonary Blood Flow ◽  
Left Lung ◽  
Dry Weight ◽  
Test Lung ◽  
Test Segment ◽  
Control Segment ◽  
Lung Segment ◽  
Lung Blood Flow ◽  
The Right

We examined whether wedging a catheter (0.5 cm OD) into a subsegmental airway in dog (n = 6) or pig lungs (n = 5) and increasing pressure in the distal lung segment affected pulmonary blood flow. Dogs and pigs were anesthetized and studied in the prone position. Pulmonary blood flow was measured by injecting radiolabeled microspheres (15 microns diam) into the right atrium when airway pressure (Pao) was 0 cmH2O and pressure in the segment distal to the wedged catheter (Ps) was 0, 5, or 15 cmH2O and when Pao = Ps = 15 cmH2O. The lungs were excised, air-dried, and sectioned. Blood flow per gram dry weight normalized to cardiac output to the right or left lung, as appropriate, was calculated for the test segment, a control segment in the opposite lung corresponding anatomically to the test segment, the remainder of the lung containing the test segment (test lung), and the remainder of the lung containing the control segment (control lung). The presence of the catheter reduced blood flow in the test segment compared with that in the control segment and in the test lung. Blood flow was not affected by increasing pressure in the test segment. We conclude that, in studies designed to measure collateral ventilation in dog lungs, the presence of the wedged catheter is likely to have a greater effect on blood flow than the increase in pressure associated with measuring collateral airway resistance.

CLINICAL CONFERENCE

PEDIATRICS ◽  
1957 ◽  
Vol 19 (6) ◽  
pp. 1139-1147
Author(s):  
Mary Allen Engle
Keyword(s):  
Blood Flow ◽  
Right Ventricle ◽  
Right Ventricular ◽  
Pulmonary Blood Flow ◽  
Ventricular Hypertrophy ◽  
Pulmonary Valve ◽  
Muscular Tissue ◽  
Pulmonic Stenosis ◽  
Infundibular Stenosis ◽  
The Right

Dr. Engle: When pulmonic stenosis occurs as an isolated congenital malformation of the heart, it usually is due to fusion of the valve cusps into a dome with a small hole in the center. In Figure 1 the pulmonary artery has been laid open so that one can see the three leaflets of the pulmonary valve are completely fused, and that there is only a small, central, pinpoint opening which permits blood to leave the right ventricle and enter the pulmonary circulation. Valvular pulmonic stenosis is much more common than subvalvular or infundibular stenosis, where the obstruction to pulmonary blood flow lies within the substance of the right ventricle. There it may be due to a diaphragm of tissue which obstructs the outflow of the right ventricle, or to an elongated narrow tunnel lined with thickened endocardium, or to a ridge of fibrous or muscular tissue just beneath the pulmonary valve. The changes in the cardiovascular system which result from obstructed pulmonary blood flow are so characteristic that they permit the ready recognition of this condition. Proximal to the constriction, these changes manifest the burden placed on the right ventricle, which enlarges and hypertrophies. On physical examination this is demonstrated by the precordial bulge and tapping impulse just to the left of the sternum, where the rib cage overlies the anterior (right) ventricle. Radiographically, both by fluoroscopy and in roentgenograms in the frontal and both oblique views, right ventricular enlargement is seen. In the electrocardiogram, the precordial leads show a pattern of right ventricular hypertrophy.

Effect of furosemide on pulmonary blood flow distribution in resting and exercising horses

1999 ◽  
Vol 86 (6) ◽  
pp. 2034-2043 ◽  
Author(s):  
Howard H. Erickson ◽  
Susan L. Bernard ◽  
Robb W. Glenny ◽  
M. Roger Fedde ◽  
Nayak L. Polissar ◽  
...  
Keyword(s):  
Blood Flow ◽  
Pulmonary Blood Flow ◽  
Flow Distribution ◽  
Thoroughbred Horses ◽  
Dorsal Portion ◽  
Primary Finding ◽  
Pulmonary Arterial ◽  
Relationship Of ◽  
The Relationship ◽  
Rest And Exercise

We determined the spatial distribution of pulmonary blood flow (PBF) with 15-μm fluorescent-labeled microspheres during rest and exercise in five Thoroughbred horses before and 4 h after furosemide administration (0.5 mg/kg iv). The primary finding of this study was that PBF redistribution occurred from rest to exercise, both with and without furosemide. However, there was less blood flow to the dorsal portion of the lung during exercise postfurosemide compared with prefurosemide. Furosemide did alter the resting perfusion distribution by increasing the flow to the ventral regions of the lung; however, that increase in flow was abated with exercise. Other findings included 1) unchanged gas exchange and cardiac output during rest and exercise after vs. before furosemide, 2) a decrease in pulmonary arterial pressure after furosemide, 3) an increase in the slope of the relationship of PBF vs. vertical height up the lung during exercise, both with and without furosemide, and 4) a decrease in blood flow to the dorsal region of the lung at rest after furosemide. Pulmonary perfusion variability within the lung may be a function of the anatomy of the pulmonary vessels that results in a predominantly fixed spatial pattern of flow distribution.

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