Response of pulmonary veins to increased intracranial pressure and pulmonary air embolization

1980 ◽  
Vol 48 (6) ◽  
pp. 957-964 ◽  
Author(s):  
B. T. Peterson ◽  
S. E. Grauer ◽  
R. W. Hyde ◽  
C. Ortiz ◽  
H. Moosavi ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Edema ◽  
Left Atrial ◽  
Venous Pressure ◽  
Pulmonary Veins ◽  
Venous Hypertension ◽  
Increased Intracranial Pressure ◽  
Anesthetized Dogs ◽  
Brain Compression ◽  
End Tidal

Brain compression with subdural air causes pulmonary hypertension and noncardiogenic pulmonary edema (A. B. Malik, J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 42: 335-343, 1977). To see whether air emboli to the lungs rather than brain compression caused these findings, anesthetized dogs received intravenous air infusions, subdural air infusions, or brain compression from balloons inflated in the subdural space. Subdural air and intravenous air resulted in similar vascular responses. Pulmonary artery pressure (Ppa) increased 160% (P less than 0.01) and pulmonary venous pressure transiently rose 13 +/- 5 Torr (P less than 0.05) without an increase in left atrial pressure or cardiac output (Q). The end-tidal PCO2 fell 55% (P less than 0.01) and the postmortem weight of the lungs increased 55% (P less than 0.05). Brain compression with a subdural balloon instead of air only caused a 20% rise in Ppa and Q without pulmonary edema. Thus, pulmonary air emboli rather than brain compression accounts for the edema and pulmonary hypertension caused by subdural air. Catheters in pulmonary veins and the left atrium showed that air emboli cause transient pulmonary venous hypertension as well as a reproducible form of noncardiogenic pulmonary endema.

THE PHYSIOLOGICAL MECHANISMS OF THE PULMONARY VENOUS HYPERTENSION

2018 ◽  
Vol 18 (2) ◽  
pp. 7-18
Author(s):  
V I Evlakhov ◽  
I Z Poyassov ◽  
V I Ovsyannikov
Keyword(s):  
Pulmonary Hypertension ◽  
Venous Pressure ◽  
Pulmonary Veins ◽  
Left Ventricular ◽  
Venous Hypertension ◽  
Physiological Mechanisms ◽  
Pulmonary Vasoconstriction ◽  
Pulmonary Arterial ◽  
Mechanisms Of Development ◽  
Trigger Mechanisms

In the review regulatory mechanisms of functions of pulmonary venous vessels have been considered as well as the signifi cance of their impairment in the development of the pulmonary hypertension, caused by the left ventricular cardiac failure. One of the trigger mechanisms of the development of the pulmonary hypertension as a result of the elevation of the left atrial and pulmonary venous pressure is the reflectory constriction of the pulmonary arterioles (Kitayev’s reflex). Further, the development of endothelial dysfunction and pulmonary vessels remodeling with the phenomenon of “arterializations” of the pulmonary veins take place. The exact evaluation of the pulmonary vascular resistance value in the clinical practice is a difficult task. This parameter, being integrated, does not allow to evaluate the resistance values of pulmonary arterial and venous vessels in the conditions of pulmonary hypertension and to give exact characteristics of their changes, as a result. The mechanisms of development of the pulmonary venous hypertension could not be explicated using the simplified model of the pulmonary vasoconstriction, because the main features of the pulmonary circulation are the presence of arteriovenous and bronchopulmonary shunts, and pulsatile character of the blood flow. To understand the exact pathogenesis of this pathology the further fundamental investigation not only on the cell level, but also on organ and system levels are needed.

Elevation of superior vena caval pressure increases extravascular lung water after endotoxemia

1987 ◽  
Vol 62 (3) ◽  
pp. 1006-1009 ◽  
Author(s):  
S. J. Allen ◽  
R. E. Drake ◽  
J. Katz ◽  
J. C. Gabel ◽  
G. A. Laine
Keyword(s):  
Pulmonary Hypertension ◽  
Central Venous Pressure ◽  
Pulmonary Edema ◽  
Left Atrial ◽  
Superior Vena ◽  
Venous Pressure ◽  
Weight Ratio ◽  
Central Venous ◽  
Superior Vena Caval ◽  
Extravascular Fluid

In many sheep Escherichia coli endotoxin results in pulmonary hypertension, increased microvascular permeability, pulmonary edema, and increased central venous pressure. Since lung lymph drains into the systemic veins, increases in venous pressure may impair lymph flow sufficiently to enhance the accumulation of extravascular fluid. We tested the hypothesis that, following endotoxin, elevating the venous pressure would increase extravascular fluid. Thirteen sheep were chronically instrumented with catheters to monitor left atrial pressure (LAP), pulmonary arterial pressure (PAP), and superior vena caval pressure (SVCP) as well as balloons to elevate LAP and SVCP. These sheep received 4 micrograms/kg endotoxin, and following the pulmonary hypertensive spike the left atrial balloon was inflated so that (PAP + LAP)/2 = colloid osmotic pressure. It was necessary to control PAP + LAP in this way to minimize the sheep-to-sheep differences in the pulmonary hypertension. We elevated the SVCP to 10 or 17 mmHg or allowed it to stay low (3.2 mmHg). After a 3-h period, we killed the sheep and removed the right lungs for determination of the extravascular fluid-to-blood-free dry weight ratio (EVF). Sheep with SVCP elevated to 10 or 17 mmHg had significant increases in EVF (5.2 +/- 0.1 and 5.6 +/- 1.2) compared with the sheep in which we did not elevate SVCP (EVF = 4.5 +/- 0.4). These results indicate that sustained elevation in central venous pressure in patients contributes to the amount of pulmonary edema associated with endotoxemia.

Effect of thoracic duct drainage on hydrostatic pulmonary edema and pleural effusion in sheep

1991 ◽  
Vol 71 (1) ◽  
pp. 314-316 ◽  
Author(s):  
S. J. Allen ◽  
R. E. Drake ◽  
G. A. Laine ◽  
J. C. Gabel
Keyword(s):  
Pleural Effusion ◽  
Central Venous Pressure ◽  
Pulmonary Edema ◽  
Thoracic Duct ◽  
Left Atrial ◽  
Venous Pressure ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Central Venous ◽  
Pulmonary Arterial

Positive end-expiratory pressure (PEEP) increases central venous pressure, which in turn impedes return of systemic and pulmonary lymph, thereby favoring formation of pulmonary edema with increased microvascular pressure. In these experiments we examined the effect of thoracic duct drainage on pulmonary edema and hydrothorax associated with PEEP and increased left atrial pressure in unanesthetized sheep. The sheep were connected via a tracheostomy to a ventilator that supplied 20 Torr PEEP. By inflation of a previously inserted intracardiac balloon, left atrial pressure was increased to 35 mmHg for 3 h. Pulmonary arterial, systemic arterial, and central venous pressure as well as thoracic duct lymph flow rate were continuously monitored, and the findings were compared with those in sheep without thoracic duct cannulation (controls). At the end of the experiment we determined the severity of pulmonary edema and the volume of pleural effusion. With PEEP and left atrial balloon insufflation, central venous and pulmonary arterial pressure were increased approximately threefold (P less than 0.05). In sheep with a thoracic duct fistula, pulmonary edema was less (extra-vascular fluid-to-blood-free dry weight ratio 4.8 +/- 1.0 vs. 6.1 +/- 1.0; P less than 0.05), and the volume of pleural effusion was reduced (2.0 +/- 2.9 vs. 11.3 +/- 9.6 ml; P less than 0.05). Our data signify that, in the presence of increased pulmonary microvascular pressure and PEEP, thoracic duct drainage reduces pulmonary edema and hydrothorax.

Abstract 17218: Reduced Left Atrial Compliance in Heart Failure With Preserved Ejection Fraction: New Insights Into Pathophysiology

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Rosita Zakeri ◽  
Qiang Chai ◽  
Gilles Moulay ◽  
Ozgur Ogut ◽  
Saad Hussain ◽  
...  
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Left Atrial ◽  
Pulmonary Veins ◽  
Venous Hypertension ◽  
Experimental Hypertension ◽  
Preserved Ejection Fraction ◽  
Stiffness Constant ◽  
Diastolic Stiffness ◽  
No Signaling

Background: Reduced left atrial (LA) compliance (LAC) contributes to pulmonary venous hypertension in heart failure with preserved ejection fraction (HFpEF); however the underlying mechanisms are poorly defined. We hypothesized that microvascular inflammation with rarefaction and impaired nitric oxide (NO) signaling, LA titin hypophosphorylation and fibrosis may each contribute to reduced LAC in HFpEF. Methods: Invasive LA pressure-volume (PV) analyses (open-chest; pericardiotomy; admittance catheter) were performed in 9 aged dogs with experimental hypertension (bilateral renal wrap + DOCA; HFpEF) compared to 13 sham-operated young adult dogs (control). LAC was measured at end-LA reservoir during acute preload reduction (cava occlusion). LA tissue and LA microvascular function were analyzed. Results: Compared to controls, the curvilinear end-LA reservoir PV relationship ( Fig A ) was shifted upward/leftward in HFpEF (LA diastolic stiffness constant 0.08 vs 0.16 mmHg/mL in controls, p=0.005). LA microvascular density (MVD; CD31 stain) tended to be lower in HFpEF than controls (2154±578 vs 2650±523 vessels/mm 2 , p=0.07) and LA MVD negatively correlated with the LA diastolic stiffness constant (r=-0.66, p=0.006). LA microvessels from HFpEF dogs showed impaired endothelium-dependent shear stress-mediated dilation compared to controls, consistent with impaired NO signaling ( Fig B ). Titin isoform expression was similar between groups, but isoform N2B (stiffer) was (p=0.03) and N2BA (compliant) tended to be (p=0.09) hypophosphorylated in HFpEF LA appendage (LAA) tissue. Fibrosis (Picrosirius Red) was similar between groups in the LA free wall and LAA, but increased in areas adjacent to the pulmonary veins in HFpEF (27±12% vs controls 15±8%, p=0.01). Conclusion: In experimental HFpEF, LAC was reduced in association with evidence of LA microvascular rarefaction and impaired NO signaling, titin hypophosphorylation and regional increases in LA fibrosis.

Pulmonary hypertension, pulmonary edema, and decreased pulmonary compliance produced by increased ICP in cats

1984 ◽  
Vol 60 (6) ◽  
pp. 1207-1213 ◽  
Author(s):  
Melvin M. Newman ◽  
Marta Kligerman ◽  
Mary Willcox
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Edema ◽  
Left Atrial ◽  
Pulmonary Ventilation ◽  
Systolic Pressure ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Sodium Pentobarbital ◽  
Left Heart Failure ◽  
Pulmonary Compliance

✓ Cats, anesthetized with sodium pentobarbital, were cannulated to measure pulmonary, systemic, and left atrial pressures and pulmonary ventilation, compliance, and resistance. Intracranial pressure was elevated to 30 mm Hg by injecting silicone oil into the extradural space. After an average time of 56 minutes, pulmonary systolic and diastolic pressures more than doubled, systemic systolic pressure sometimes rose and sometimes fell, and diastolic pressure rose 5%. Left atrial pressure never exceeded 8 cm of saline. Pulmonary compliance decreased by one-half, but airway resistance was unchanged. Pulmonary edema was estimated from histological sections. The pulmonary hypertension may be the result of a sympathetic discharge confined to the lung, since no remarkable changes in heart rate or systemic blood pressure occurred. The decrease in pulmonary compliance followed the rise in pulmonary arterial pressure, and is interpreted as the result of interstitial edema. There was no evidence that left heart failure or elevated left atrial pressure caused the pulmonary edema.

Relationship of pulmonary arterial and venous pressure to diffusing capacity

1964 ◽  
Vol 19 (3) ◽  
pp. 381-386 ◽  
Author(s):  
W. H. Lawson ◽  
Helen N. Duke ◽  
Richard W. Hyde ◽  
Robert E. Forster
Keyword(s):  
Blood Flow ◽  
Pulmonary Edema ◽  
Vascular Resistance ◽  
Venous Pressure ◽  
Pulmonary Veins ◽  
Diffusing Capacity ◽  
Arterial Perfusion ◽  
Single Breath ◽  
Capillary Bed ◽  
Relationship Of

Single-breath carbon monoxide diffusing capacity (DlCO) was determined in ten isolated perfused cat lungs at 37 C during a) forward (arterial) perfusion through the pulmonary artery and b) reverse (venous) perfusion through the left atrium. Blood flow, inflow and outflow pressure, lung volume, and transpulmonary ventilating pressure were approximately equal in a and b, but in all ten lungs DlCO was greater in b than a. In five lungs during forward (arterial) perfusion blood flow was increased from a mean of 62–180 ml/min while left atrial outflow pressure was maintained about zero mm Hg. At the higher blood flow DlCO was not significantly changed although vascular resistance decreased a mean of 34% and arterial pressure increased a mean of 98%. We conclude that a) transmural pressure in the pulmonary veins is more important than that in the arteries in determining the size of the capillary bed as measured by DlCO, and b) the size of the capillary bed and total vascular resistance can vary independently. When pulmonary edema occurred in five lungs DlCO did not change significantly. pulmonary capillary bed size; pulmonary edema and lung diffusing capacity; pulmonary blood flow and lung diffusing capacity Submitted on February 11, 1963

Effect of a left atrium-pulmonary vein baroreflex on peripheral vascular beds

1977 ◽  
Vol 233 (5) ◽  
pp. H587-H591 ◽  
Author(s):  
T. C. Lloyd ◽  
J. J. Fried
Keyword(s):  
Left Atrial ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Radioactive Microspheres ◽  
Peripheral Vascular ◽  
Blood Flows ◽  
Arterial Blood ◽  
Anesthetized Dogs ◽  
Response Peak ◽  
Vascular Beds

A step increase of left atrial and pulmonary venous pressure from 0 to 25 mmHg was used in anesthetized dogs with controlled arterial blood pressure to generate reflex systemic vasodilation. The resultant response of total peripheral resistance was an initial transient fall of about 40% which spontaneously regressed while the stimulus was maintained. Injections of differently tagged radioactive microspheres were used to measure selected organ blood flows prior to raising atrial pressure, at the response peak, during the steady state, and after recovery. Resistances of skin, skeletal muscle, kidney, and large intestine significantly fell upon atriovenous distention. The response in muscle, which greatly exceeded that of the other organs, was not sustained, whereas resistances of other responding beds remained depressed until the stimulus was removed. No significant responses occurred in small intestine, liver (hepatic artery), or adrenal gland.

Left atrial hypertension causes pleural effusion formation in unanesthetized sheep

1989 ◽  
Vol 257 (2) ◽  
pp. H690-H692 ◽  
Author(s):  
S. Allen ◽  
J. Gabel ◽  
R. Drake
Keyword(s):  
Pleural Effusion ◽  
Pulmonary Artery ◽  
Pulmonary Edema ◽  
Left Atrium ◽  
Left Atrial ◽  
Protein Concentration ◽  
Venous Pressure ◽  
Recovery Period ◽  
Pleural Effusions ◽  
The Right

We studied the effect of left atrial pressure (LAP) elevation on the formation of pleural effusion in unanesthetized sheep. We prepared the animals by placing catheters in the left atrium, pulmonary artery, femoral artery, and vein. We also placed a balloon catheter in the left atrium. After a recovery period of at least 1 wk, we measured LAP, pulmonary artery pressure (PAP), systemic arterial pressure, systemic venous pressure, cardiac output, plasma protein concentration, and plasma colloid osmotic pressure (pi c). We calculated capillary pressure (Pc) as 0.5(PAP - LAP). We then elevated LAP such that Pc-pi c was between -10 and 19.5 mmHg for 6-24 h. At the end of the experiment, we killed the sheep and measured the volume and protein concentration of the right pleural effusion. We also determined the extravascular fluid to blood free dry weight of the right lung. We found that pleural effusions and pulmonary edema formed when Pc-pi c greater than 5 mmHg. We also found that the pleural effusion volume correlated with the amount of pulmonary edema. Our data show that elevated LAP may cause pleural effusions, but only after pulmonary edema has developed.

Effect of increased left atrial pressure on breathing frequency in anesthetized dog

1990 ◽  
Vol 69 (6) ◽  
pp. 1973-1980 ◽  
Author(s):  
T. C. Lloyd
Keyword(s):  
Atrial Fibrillation ◽  
Left Atrium ◽  
Left Atrial ◽  
Pulmonary Veins ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Left Heart ◽  
Breathing Frequency ◽  
Anesthetized Dogs ◽  
The Right

Distension or loading of the isolated canine left heart caused reflex tachypnea in prior studies. The object of the present effort was to explore the possibility that this depended primarily on atrial distension. Cardiopulmonary bypass perfusion and ligation of pulmonary veins were used to isolate the left-heart chambers of anesthetized dogs. Simultaneous distension of the beating left atrium and fibrillating ventricle stimulated breathing frequency (f), whereas isolated ventricular distension did not. At other times, intervals of atrial fibrillation were imposed under two different conditions: 1) while the right heart and lungs were bypassed and systemic perfusion was provided by the left ventricle using blood returned to the left atrium by pump and 2) while the ventricles fibrillated and systemic perfusion was supplied directly by the pump. Atrial fibrillation increased left atrial pressure and stimulated f in condition 1. In condition 2, f increased only if fibrillation was associated with a rise in left atrial pressure. Vagal cooling blocked the effect of fibrillation. I conclude that left atrial distension may initiate reflex tachypnea.

Wedge pressure in large vs. small pulmonary arteries to detect pulmonary venoconstriction

1985 ◽  
Vol 59 (4) ◽  
pp. 1329-1332 ◽  
Author(s):  
A. Zidulka ◽  
T. S. Hakim
Keyword(s):  
Blood Flow ◽  
Left Atrial ◽  
Venous Pressure ◽  
Pulmonary Veins ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Large Artery ◽  
Small Artery ◽  
Proximal Site ◽  
Wedge Pressure

Pulmonary arterial wedge pressure measures the pressure where blood flow resumes on the venous side. By occlusion of a large artery, the point where blood flow resumes will be in or near the left atrium. However, by occlusion of a small artery, it is possible to shift the point where flow resumes to a more proximal site in the veins and thus measure a pressure within the small veins. Increased pulmonary venous pressure, as a result of partial obstruction in the large veins, may not be detected by wedging a Swan-Ganz catheter in a large artery but may be detected by wedging in a small artery. We demonstrated this phenomenon in open-chest dogs by mechanically obstructing the left lower lobar vein or by infusing histamine to cause a generalized pulmonary venoconstriction. The wedge pressure measured by a 7-F Swan-Ganz catheter, with its balloon inflated in the main left lower lobar artery, nearly equaled left atrial pressure. On the other hand, the wedge pressure measured with a 7-F, 5-F, or a PE-50 catheter advanced into a small artery (without a balloon) was considerably higher than left atrial pressure. These results suggest that high resistance in the pulmonary veins can be demonstrated with the Swan-Ganz catheter by comparing the pressures obtained with the catheter wedged in a small and large artery.

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