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.

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.

The pulmonary capillary wedge pressure accurately reflects both normal and elevated left atrial pressure

2014 ◽  
Vol 167 (6) ◽  
pp. 876-883 ◽  
Author(s):  
Anikó I. Nagy ◽  
Ashwin Venkateshvaran ◽  
Pravat Kumar Dash ◽  
Banajit Barooah ◽  
Béla Merkely ◽  
...  
Keyword(s):  
Pulmonary Capillary Wedge Pressure ◽  
Left Atrial ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Pulmonary Capillary ◽  
Wedge Pressure

Blunted hypoxic pulmonary vasoconstriction by increased lung vascular pressures

1975 ◽  
Vol 38 (5) ◽  
pp. 846-850 ◽  
Author(s):  
J. L. Benumof ◽  
E. A. Wahrenbrock
Keyword(s):  
Blood Flow ◽  
Left Atrial ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Main Pulmonary Artery ◽  
Lower Lobe ◽  
Respiratory Alkalosis ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Pulmonary Vasoconstriction ◽  
Lung Vessels

We tested the hypothesis that increased pressures within the lung vessels would inhibit hypoxic pulmonary vasoconstriction at all levels of alveolar CO2 tension. Selective hypoxia of the left lower lobe of the lung in open chested dogs caused the electromagnetically measured blood flow to the lobe to decrease 51 plus or minus 4 (SE) percent and its vascular resistance to increase 132 plus or minus 13 percent. Pressure and blood flow in the main pulmonary artery and left atrial pressure did not change during the hypoxic response. Stepwise increments in left artrial and pulmonary arterial pressures induced either by inflating a left atrial balloon or infusing dextran, progressively diminished the vasoconstrictive response to hypoxia. The response was usually abolished when left atrial pressure reached 25 mmHg. For all vascular pressures, hypoxic vasoconstriction was blunted by hypocapnic alkalosis but not enhanced by hypercapnia. We conclude that the redistribution of blood flow away from an hypoxic lobe of the lung to lobes with high Po2 was greatly attenuated by increasing pressures within lung vessels or by inducing respiratory alkalosis.

Longitudinal distribution of pulmonary vascular resistance with very high pulmonary blood flow

1987 ◽  
Vol 62 (1) ◽  
pp. 344-358 ◽  
Author(s):  
M. Younes ◽  
Z. Bshouty ◽  
J. Ali
Keyword(s):  
Blood Flow ◽  
Weight Gain ◽  
Left Atrial ◽  
Pulmonary Blood Flow ◽  
Lower Lobe ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Longitudinal Distribution ◽  
Flow Rates ◽  
Flow Threshold

Dog left upper lobes (LUL) were perfused in situ via the left lower lobe artery. Lobe weight was continuously monitored. Increasing lobar flow from normal to 10 times normal had little effect on left atrial pressure, which ranged from 1 to 5 mmHg. There was a flow threshold (Qth) below which lobar weight was stable. Qth ranged from 1.1 to 1.55 l/min (mean 1.27) corresponding to four times normal LUL blood flow. Above Qth, step increases in lobar flow resulted in progressive weight gain at a constant rate that was proportional to flow. The effective pressure at the filtration site (EFP) at different flow rates was estimated from the static vascular pressure that resulted in the same rate of weight gain. From this value and from mean pulmonary arterial (PA) and left atrial (LA) pressures, we calculated resistance upstream (Rus) and downstream (Rds) from filtration site. At Qth, Rds accounted for 60% of total resistance. This fraction increased progressively with flow, reaching 83% at Q of 10 times normal. We conclude that during high pulmonary blood flow EFP is closer to PA pressure than it is to LA pressure, and that this becomes progressively more so as a function of flow. As a result, the lung accumulates water at flow rates in excess of four times normal despite a normal left atrial pressure.

Effect of blood flow rate and blood flow history on newborn pulmonary microcirculation

1991 ◽  
Vol 261 (2) ◽  
pp. H271-H279 ◽  
Author(s):  
C. D. Fike ◽  
M. R. Kaplowitz
Keyword(s):  
Blood Flow ◽  
Flow Rate ◽  
Left Atrial ◽  
Total Pressure ◽  
Pulmonary Blood Flow ◽  
Blood Flow Rate ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Flow Rates ◽  
Pulmonary Arterial

The purpose of this study was to determine whether increased pulmonary blood flow and/or the history of pulmonary blood flow alters microvascular pressures in lungs of newborns. Using the direct micropuncture technique, we measured pressures in 20- to 60-microns-diameter arterioles and venules in isolated lungs of newborn rabbits at consecutive blood flow rates of 50 (baseline), 100, and/or 200 ml.min-1.kg-1. Then in some lungs we returned blood flow rate to baseline and repeated microvascular pressure measurements. We kept left atrial pressure the same at all blood flow rates. When blood flow rate increased and left atrial pressure was maintained constant, pulmonary arterial, 20- to 60-microns-diameter arteriolar, and 20- to 60-microns-diameter venular pressures increased such that the percentage of total pressure drop that occurred across veins increased. When we returned blood flow to baseline, venular pressure returned to baseline, but arteriolar and pulmonary arterial pressures returned to values less than baseline so that the percentage of the total pressure drop that occurred across microvessels decreased. Thus both blood flow rate and blood flow history are important determinants of the longitudinal distribution of pulmonary vascular pressures across newborn lungs. These findings also suggest that in newborn lungs venules greater than 60 microns diameter are poorly distensible such that higher blood flow rates result in increased microvascular pressures. Hence, under conditions of increased pulmonary blood flow, such as occurs with left to right shunts, the tendency for edema formation will increase in newborn lungs even if left atrial pressure does not increase.

Effect of hypoxia on lung lymph flow in newborn lambs with left atrial hypertension

1988 ◽  
Vol 254 (3) ◽  
pp. H487-H493
Author(s):  
J. U. Raj ◽  
T. A. Hazinski ◽  
R. D. Bland
Keyword(s):  
Blood Flow ◽  
Left Atrial ◽  
Control Period ◽  
Lymph Flow ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Fluid Filtration ◽  
Alveolar Hypoxia ◽  
Lung Lymph ◽  
Lung Lymph Flow

To determine the effect of left atrial hypertension on the vascular response to hypoxia in the newborn lung, we measured pulmonary artery and left atrial pressures, lung blood flow and lymph flow, and concentrations of protein in lymph and plasma of 13 lambs that spontaneously breathed air for 2-6 h (control period), followed by 8-11% O2 mixed with 3-5% CO2 and N2 for 2-4 h (experimental period). In eight studies, the lambs were made hypoxic first, after which we elevated their left atrial pressure by 10-12 Torr for 2-3 h. In 10 additional studies, we reversed the sequence by raising left atrial pressure first followed by addition of hypoxia. In lambs with normal left atrial pressure, alveolar hypoxia increased both pulmonary blood flow and lymph flow, with an associated reduction in lymph-to-plasma protein ratio (L/P). When left atrial pressure was increased in the presence of hypoxia, lymph flow increased by a small amount and L/P decreased further. In lambs with preexisting left atrial pressure elevation, addition of alveolar hypoxia increased both blood flow and lymph flow with no significant change in L/P. These results suggest that in newborn lambs with normal left atrial pressure, alveolar hypoxia increases lung lymph flow mainly by increasing microvascular filtration pressure, whereas in lambs with elevated left atrial pressure, hypoxia increases lymph flow by another mechanism, perhaps by increasing the perfused surface area for fluid filtration.

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