Pulmonary Edema and Elevated Left Atrial Pressure: Four Hours and Beyond

Physiology ◽  
2002 ◽  
Vol 17 (6) ◽  
pp. 223-226 ◽  
Author(s):  
R. E. Drake ◽  
M. F. Doursout
Keyword(s):  
Connective Tissue ◽  
Pulmonary Edema ◽  
Left Atrial ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Cardiogenic Pulmonary Edema ◽  
Left Heart ◽  
Fluid Accumulation ◽  
Increased Pressure

Cardiogenic pulmonary edema is caused by the increase in left atrial pressure when the left heart fails. The increased pressure causes rapid fluid accumulation within the lung interstitial spaces. However, over the following days to weeks, additional fluid may accumulate due to the deposition of excess lung connective tissue.

β-Adrenergic agonist therapy accelerates the resolution of hydrostatic pulmonary edema in sheep and rats

2000 ◽  
Vol 89 (4) ◽  
pp. 1255-1265 ◽  
Author(s):  
James A. Frank ◽  
Yibing Wang ◽  
Oscar Osorio ◽  
Michael A. Matthay
Keyword(s):  
Pulmonary Edema ◽  
Left Atrial ◽  
Experimental Studies ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Adrenergic Agonist ◽  
Agonist Therapy ◽  
Arterial Blood ◽  
Alveolar Liquid Clearance ◽  
Alveolar Liquid

To determine whether β-adrenergic agonist therapy increases alveolar liquid clearance during the resolution phase of hydrostatic pulmonary edema, we studied alveolar and lung liquid clearance in two animal models of hydrostatic pulmonary edema. Hydrostatic pulmonary edema was induced in sheep by acutely elevating left atrial pressure to 25 cmH2O and instilling 6 ml/kg body wt isotonic 5% albumin (prepared from bovine albumin) in normal saline into the distal air spaces of each lung. After 1 h, sheep were treated with a nebulized β-agonist (salmeterol) or nebulized saline (controls), and left atrial pressure was then returned to normal. β-Agonist therapy resulted in a 60% increase in alveolar liquid clearance over 3 h ( P< 0.001). Because the rate of alveolar fluid clearance in rats is closer to human rates, we studied β-agonist therapy in rats, with hydrostatic pulmonary edema induced by volume overload (40% body wt infusion of Ringer lactate). β-Agonist therapy resulted in a significant decrease in excess lung water ( P < 0.01) and significant improvement in arterial blood gases by 2 h ( P < 0.03). These preclinical experimental studies support the need for controlled clinical trials to determine whether β-adrenergic agonist therapy would be of value in accelerating the resolution of hydrostatic pulmonary edema in patients.

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.

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.

scholarly journals Hemodynamics of the diastolic pressure gradients in acute heart failure: implications for the diagnosis of pre-capillary pulmonary hypertension in left heart disease

2018 ◽  
Vol 9 (1) ◽  
pp. 204589401881543 ◽  
Author(s):  
Doron Aronson ◽  
Emilia Hardak ◽  
Andrew J. Burger
Keyword(s):  
Heart Failure ◽  
Heart Disease ◽  
Acute Heart Failure ◽  
Left Atrial ◽  
Diastolic Pressure ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Left Heart ◽  
Left Heart Disease ◽  
Pulmonary Capillary

The diastolic pressure gradient (DPG) has been proposed as the metric of choice for the diagnosis of pulmonary vascular changes in left heart disease. We tested the hypothesis that this metric is less sensitive to changes in left atrial pressure and stroke volume (SV) than the transpulmonary gradient (TPG). We studied the effect of dynamic changes in pulmonary capillary wedge pressure (PCWP), SV, and pulmonary artery capacitance (PAC) on DPG and TPG in 242 patients with acute heart failure undergoing decongestive therapy with continuous hemodynamic monitoring. There was a close impact of PCWP reduction on TPG and DPG, with a 0.13 mmHg (95% confidence interval [CI] 0.07–0.19, P < 0.0001) and 0.21 mmHg (95% CI 0.16–0.25, P < 0.0001) increase for every 1 mmHg decrease in PCWP, respectively. Changes in SV had a negligible effect on TPG and DPG (0.19 and 0.13 mmHg increase, respectively, for every 10-mL increase in SV). Heart rate was positively associated with DPG (0.41-mmHg increase per 10 BPM [95% CI 0.22–0.60, P < 0.0001]). The resistance-compliance product was positively associated with both TPG and DPG (2.65 mmHg [95% CI 2.47–2.83] and 1.94 mmHg [95% CI 1.80–2.08] for each 0.1-s increase, respectively). In conclusion, DPG is not less sensitive to changes in left atrial pressure and SV compared with TPG. Although DPG was not affected by changes in PAC, the concomitant increase in the resistance-compliance product increases DPG.

Effects of coronary flow reduction on lung vascular tissue transport in sheep

1983 ◽  
Vol 55 (6) ◽  
pp. 1906-1915 ◽  
Author(s):  
T. R. Harris ◽  
J. C. Collins ◽  
R. J. Roselli
Keyword(s):  
Left Atrial ◽  
Coronary Flow ◽  
Vascular Tissue ◽  
Lymph Flow ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Base Line ◽  
Flow Reduction ◽  
Second Period ◽  
Increased Pressure

This study was performed to measure the effects of a sustained reduction in coronary flow on lung lymph flow and protein content. Ten halothane-anesthetized sheep with cannulated lymphatic vessels were provided with a carotid-to-left anterior descending coronary artery cannula containing an electromagnetic flowmeter. One group of five animals was observed at base line and after coronary flow was reduced to 38% of base line. A second group of five animals acted as controls and was observed at base line, for 111 min of increased left atrial pressure, and a second period of normal pressures. Sustained coronary flow reduction led to significant increases in pulmonary arterial pressure, left atrial pressure, lymph flow, total protein lymph-to-plasma concentration ratio (L/P), and protein lymph clearance (L/P X lymph flow). Analysis of the pressure, lymph, protein, and indicator data with a two-pore model of the microvascular barrier showed that the observations were consistent with the concept that coronary flow reduction decreased functioning lung capillary surface but increased the size of the large pore and the number of small pores relative to the number of larger pores. Control studies showed increases in lymph flow and decreases in L/P with increased pressure but no significant changes in any variable between the first and second period of normal pressures. We conclude that coronary flow reduction increases lung vascular-tissue transport by decreasing the resistance of the microvascular barrier to protein and fluid movement. However, increased pressure secondary to left ventricular dysfunction plays a role in the magnitude of this response.

Mechanism of inhibition of renin secretion by increased left atrial pressure

1985 ◽  
Vol 248 (5) ◽  
pp. R641-R644
Author(s):  
M. E. Lee ◽  
T. N. Thrasher ◽  
D. J. Ramsay
Keyword(s):  
Left Atrial ◽  
Renal Perfusion ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Renin Release ◽  
Left Heart ◽  
Efferent Pathway ◽  
Mechanism Of Inhibition ◽  
Potent Inhibition ◽  
Aortic Cuff

Experiments were designed to elucidate the mechanism of the failure of systemic hypotension to stimulate renin release in the presence of elevated left heart pressure. We conducted a series of graded ascending aortic and suprarenal cuff inflations in dogs with bilateral renal denervation (n = 5). The renal perfusion pressure (RPP) was reduced by 10, 20, and 30% of control by inflation of either cuff. Comparison of the renin response with inflation of the ascending aortic to the suprarenal cuff revealed a clear increase in the threshold required to elicit a renin response to graded reduction of RPP after inflation of the ascending aortic cuff. These results may be explained by differential effects of the two maneuvers on left heart pressure. Left atrial pressure increased during inflation of the ascending aortic cuff but did not change during inflation of the suprarenal cuff. Since the kidneys were denervated, the shift in threshold must be caused by a humoral substance(s). In conclusion, our findings suggest that the efferent pathway of potent inhibition of renin release from the left heart is mediated, at least partially, by a humoral substance.

Changes in microvascular permeability with acceleration of edema in dog lungs

1990 ◽  
Vol 258 (2) ◽  
pp. H395-H399 ◽  
Author(s):  
B. D. Butler ◽  
R. E. Drake ◽  
W. D. Sneider ◽  
S. J. Allen ◽  
J. C. Gabel
Keyword(s):  
Weight Gain ◽  
Pulmonary Edema ◽  
Membrane Permeability ◽  
Left Atrial ◽  
Membrane Filtration ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Base Line ◽  
Edema Formation ◽  
Before And After

Elevation of left atrial pressure to 25–40 mmHg causes continuous pulmonary edema formation in dog lungs. However, after 5–120 min, the rate of edema formation often increases (acceleration of edema). Acceleration of edema could be associated with an increase in microvascular membrane permeability because an increase in permeability would cause fluid to filter through the microvascular membrane more rapidly. To test the hypothesis that acceleration is associated with increased permeability, we used the continuous weight-gain technique to estimate the pulmonary microvascular membrane filtration coefficient (Kf) before and after acceleration of edema in 10 dogs. Acceleration occurred 36 +/- 38 (SD) min after elevation of left atrial pressure to 35.2 +/- 5.4 mmHg. Rate of weight gain increased from 0.47 +/- 0.17 g/min before acceleration to 0.88 +/- 0.26 g/min (P less than 0.05) after acceleration of pulmonary edema. Kf was increased from initial values of 0.058 +/- 0.027 to 0.075 +/- 0.029 ml.min-1.mmHg-1 (P less than 0.05) after acceleration. In five additional dogs we cannulated lung lymphatics and determined the lymph to plasma protein concentration ratio (CL/CP) before and after acceleration. CL/CP increased from base-line values of 0.37 +/- 0.07 to 0.44 +/- 0.06 (P less than 0.05) after acceleration. Both the increase in Kf and CL/CP data support the hypothesis that acceleration of edema is due, in part, to a slight increase in microvascular membrane permeability. However, the findings could also have been caused by an increase in interstitial conductance, washout of interstitial proteins, or alveolar flooding.

scholarly journals Alveolar fluid reabsorption is impaired by increased left atrial pressures in rats

2001 ◽  
Vol 281 (3) ◽  
pp. L591-L597 ◽  
Author(s):  
F. J. Saldı́as ◽  
Z. S. Azzam ◽  
K. M. Ridge ◽  
A. Yeldandi ◽  
D. H. Rutschman ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
Pulmonary Circulation ◽  
Left Atrial ◽  
Passive Movement ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Control Group ◽  
Experimental Protocol ◽  
Fluid Reabsorption ◽  
Rat Lungs

Cardiogenic pulmonary edema results from increased hydrostatic pressures across the pulmonary circulation. We studied active Na+ transport and alveolar fluid reabsorption in isolated perfused rat lungs exposed to increasing levels of left atrial pressure (LAP; 0–20 cmH2O) for 60 min. Active Na+ transport and fluid reabsorption did not change when LAP was increased to 5 and 10 cmH2O compared with that in the control group (0 cmH2O; 0.50 ± 0.02 ml/h). However, alveolar fluid reabsorption decreased by ∼50% in rat lungs in which the LAP was raised to 15 cmH2O (0.25 ± 0.03 ml/h). The passive movement of small solutes (22Na+ and [3H]mannitol) and large solutes (FITC-albumin) increased progressively in rats exposed to higher LAP. There was no significant edema in lungs with a LAP of 15 cmH2O when all active Na+ transport was inhibited by hypothermia or amiloride (10−4 M) and ouabain (5 × 10−4 M). However, when LAP was increased to 20 cmH2O, there was a significant influx of fluid (−0.69 ± 0.10 ml/h), precluding the ability to assess the rate of fluid reabsorption. In additional studies, LAP was decreased from 15 to 0 cmH2O in the second and third hours of the experimental protocol, which resulted in normalization of lung permeability to solutes and alveolar fluid reabsorption. These data suggest that in an increased LAP model, the changes in clearance and permeability are transient, reversible, and directly related to high pulmonary circulation pressures.

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