Relation of plain chest radiographic findings to pulmonary arterial pressure and arterial blood oxygen levels in patients with acute pulmonary embolism

1992 ◽  
Vol 69 (4) ◽  
pp. 394-396 ◽  
Author(s):  
Paul D. Stein ◽  
Christos Athanasoulis ◽  
Richard H. Greenspan ◽  
Jerald W. Henry
Keyword(s):  
Pulmonary Embolism ◽  
Arterial Pressure ◽  
Acute Pulmonary Embolism ◽  
Pulmonary Arterial Pressure ◽  
Blood Oxygen ◽  
Radiographic Findings ◽  
Arterial Blood ◽  
Plain Chest ◽  
Pulmonary Arterial ◽  
Arterial Blood Oxygen

Effects of inhaled nitric oxide in patients with hypoxemia and pulmonary hypertension after cardiac surgery

1997 ◽  
Vol 6 (2) ◽  
pp. 127-131 ◽  
Author(s):  
KA Bender ◽  
JA Alexander ◽  
JM Enos ◽  
JW Skimming
Keyword(s):  
Nitric Oxide ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Blood Oxygen ◽  
Mean Pulmonary Arterial Pressure ◽  
Arterial Blood ◽  
Pulmonary Arterial ◽  
Fraction Of Inspired Oxygen ◽  
Arterial Blood Oxygen ◽  
Inspired Oxygen

BACKGROUND: Cardiopulmonary bypass can increase pulmonary vascular tone and decrease ventilation-perfusion matching by impairing the pulmonary endothelial production of nitric oxide. OBJECTIVES: We tested the hypothesis that inhalation of exogenous nitric oxide decreases the ratio of mean pulmonary arterial pressure to mean system arterial pressure and the intrapulmonary shunt fraction and increases the ratio of arterial blood oxygen tension to fraction of inspired oxygen in patients in whom the ratio of mean pulmonary arterial pressure to mean systemic arterial pressure is more than 0.50, and the ratio of arterial blood oxygen tension to fraction of inspired oxygen is less than 300 mm Hg in the first 24 hours after cardiopulmonary bypass surgery. METHODS: Only those patients who had estimates of the ratio of mean pulmonary arterial pressure to mean systemic arterial pressure and the ratio of arterial blood oxygen tension to fraction of inspired oxygen determined preoperatively were enrolled. Hemodynamic variables were recorded, and blood samples were obtained for oximetric analysis 5 minutes before and 30 minutes after inhalation of nitric oxide began. The concentration of nitric oxide inhaled was maintained at 20 parts per million. The data were analyzed by using Friedman's repeated measures analysis of variance. RESULTS: Thirteen patients were enrolled in the study. The mean preoperative ratio of mean pulmonary arterial pressure to mean systemic arterial pressure was 0.63 +/- 0.08 (standard error of the mean), and the mean preoperative ratio of arterial blood oxygen tension to fraction of inspired oxygen was 131 +/- 15 mm Hg. No differences between preoperative and postoperative values were detected. Inhalation of nitric oxide decreased the ratio of mean pulmonary arterial pressure to mean systemic arterial from 0.53 +/- 0.07 to 0.39 +/- 0.5 and increased the ratio of arterial blood oxygen tension to fraction of inspired oxygen from 167 +/- 35 mm Hg to 235 +/- 45 mm Hg. Inhalation of nitric oxide also decreased the intrapulmonary shunt fraction from 0.29 +/- 0.05 to 0.19 +/- 0.04. CONCLUSIONS: Inhalation of nitric oxide selectively decreases pulmonary vascular tone and increases ventilation-perfusion matching in patients with persistent pulmonary hypertension and hypoxemia after surgery requiring cardiopulmonary bypass. Inhalation of nitric oxide may be a valuable adjunctive therapy for these patients.

Right ventricular adaptation in the critical phase after acute intermediate-risk pulmonary embolism

2020 ◽  
pp. 204887262092525 ◽  
Author(s):  
Mads Dam Lyhne ◽  
Jacob Gammelgaard Schultz ◽  
Anders Kramer ◽  
Christian Schmidt Mortensen ◽  
Jens Erik Nielsen-Kudsk ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Arterial Pressure ◽  
Right Ventricular ◽  
Acute Pulmonary Embolism ◽  
Pulmonary Arterial Pressure ◽  
Intermediate Risk ◽  
Right Ventricular Afterload ◽  
Mean Pulmonary Arterial Pressure ◽  
Ventricular Afterload ◽  
Pulmonary Arterial

Background The haemodynamic response following acute, intermediate-risk pulmonary embolism is not well described. We aimed to describe the cardiovascular changes in the initial, critical phase 0–12 hours after acute pulmonary embolism in an in-vivo porcine model. Methods Pigs were randomly allocated to pulmonary embolism ( n = 6) or sham ( n = 6). Pulmonary embolism was administered as autologous blood clots (20 × 1 cm) until doubling of mean pulmonary arterial pressure or mean pulmonary arterial pressure was greater than 34 mmHg. Sham animals received saline. Cardiopulmonary changes were evaluated for 12 hours after intervention by biventricular pressure–volume loop recordings, invasive pressure measurements, arterial and central venous blood gas analyses. Results Mean pulmonary arterial pressure increased ( P < 0.0001) and stayed elevated for 12 hours in the pulmonary embolism group compared to sham. Pulmonary vascular resistance and right ventricular arterial elastance (right ventricular afterload) were increased in the first 11 and 6 hours, respectively, after pulmonary embolism ( P < 0.01 for both) compared to sham. Right ventricular ejection fraction was reduced ( P < 0.01) for 8 hours, whereas a near-significant reduction in right ventricular stroke volume was observed ( P = 0.06) for 4 hours in the pulmonary embolism group compared to sham. Right ventricular ventriculo–arterial coupling was reduced ( P < 0.05) for 6 hours following acute pulmonary embolism despite increased right ventricular mechanical work in the pulmonary embolism group ( P < 0.01) suggesting right ventricular failure. Conclusions In a porcine model of intermediate-risk pulmonary embolism, the increased right ventricular afterload caused initial right ventricular ventriculo–arterial uncoupling and dysfunction. After approximately 6 hours, the right ventricular afterload returned to pre-pulmonary embolism values and right ventricular function improved despite a sustained high pulmonary arterial pressure. These results suggest an initial critical and vulnerable phase of acute pulmonary embolism before haemodynamic adaptation.

Evaluation of Pulmonary Arterial Pressure in Acute Pulmonary Embolism

Angiology ◽  
1994 ◽  
Vol 45 (2) ◽  
pp. 149-154 ◽  
Author(s):  
Hiroyuki Shimizu ◽  
Junko Tanaka ◽  
Norikazu Yamada ◽  
Takahiro Ohnishi ◽  
Mashio Nakamura ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Arterial Pressure ◽  
Acute Pulmonary Embolism ◽  
Pulmonary Arterial Pressure ◽  
Pulmonary Arterial

Terlipressin Increases Systemic and Lowers Pulmonary Arterial Pressure in Experimental Acute Pulmonary Embolism

2020 ◽  
Vol 48 (4) ◽  
pp. e308-e315 ◽  
Author(s):  
Jacob Schultz ◽  
Asger Andersen ◽  
Mads D. Lyhne ◽  
Daniel D. R. Arcanjo ◽  
Benedict Kjaergaard ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Arterial Pressure ◽  
Acute Pulmonary Embolism ◽  
Pulmonary Arterial Pressure ◽  
Pulmonary Arterial

Echocardiographic assessment of pulmonary arterial pressure in the follow-up of patients with pulmonary embolism

2011 ◽  
Vol 127 (4) ◽  
pp. 303-308 ◽  
Author(s):  
Remedios Otero ◽  
Mikel Oribe ◽  
Aitor Ballaz ◽  
David Jimenez ◽  
Fernando Uresandi ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Echocardiographic Assessment ◽  
Pulmonary Arterial

Thromboxane does not mediate pulmonary hypertension in phorbol ester-induced acute lung injury in dogs

1990 ◽  
Vol 69 (1) ◽  
pp. 345-352 ◽  
Author(s):  
A. H. Stephenson ◽  
R. S. Sprague ◽  
T. E. Dahms ◽  
A. J. Lonigro
Keyword(s):  
Pulmonary Hypertension ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Pressor Response ◽  
H2 Receptor Antagonist ◽  
Arterial Blood ◽  
Pulmonary Arterial ◽  
The Relationship

Thromboxane (Tx) has been suggested to mediate the pulmonary hypertension of phorbol myristate acetate- (PMA) induced acute lung injury. To test this hypothesis, the relationship between Tx and pulmonary arterial pressure was evaluated in a model of acute lung injury induced with PMA in pentobarbital sodium-anesthetized male mongrel dogs. Sixty minutes after administration of PMA (20 micrograms/kg iv, n = 10), TxB2 increased 10-fold from control in both systemic and pulmonary arterial blood and 8-fold in bronchoalveolar lavage (BAL) fluid. Concomitantly, pulmonary arterial pressure (Ppa) increased from 14.5 +/- 1.0 to 36.2 +/- 3.5 mmHg, and pulmonary vascular resistance (PVR) increased from 5.1 +/- 0.4 to 25.9 +/- 2.9 mmHg.l-1.min. Inhibition of Tx synthase with OKY-046 (10 mg/kg iv, n = 6) prevented the PMA-induced increase in Tx concentrations in blood and BAL fluid but did not prevent or attenuate the increase in Ppa. OKY-046 pretreatment did, however, attenuate but not prevent the increase in PVR 60 min after PMA administration. Pretreatment with the TxA2/prostaglandin H2 receptor antagonist ONO-3708 (10 micrograms.kg-1.min-1 iv, n = 7) prevented the pressor response to bolus injections of 1-10 micrograms U-46619, a Tx receptor agonist, but did not prevent or attenuate the PMA-induced increase in Ppa. ONO-3708 also attenuated but did not prevent the increase in PVR. These results suggest that Tx does not mediate the PMA-induced pulmonary hypertension but may augment the increases in PVR in this model of acute lung injury.

Effects of lung inflation on pulmonary arterial blood volume in intact dogs

1975 ◽  
Vol 38 (4) ◽  
pp. 675-680 ◽  
Author(s):  
A. Wanner ◽  
S. Zarzecki ◽  
M. A. Sackner
Keyword(s):  
Arterial Pressure ◽  
Blood Volume ◽  
Lung Volume ◽  
Pulmonary Arterial Pressure ◽  
Valsalva Maneuver ◽  
Lung Inflation ◽  
Arterial Blood ◽  
Mueller Maneuver ◽  
Pulmonary Arterial ◽  
Arterial Blood Volume

The isolated effects of alterations of lung inflation and transmural pulmonary arterial pressure (pressure difference between intravascular and pleural pressure) on pulmonary arterial blood volume (Vpa) were investigated in anesthetized intact dogs. Using transvenous phrenic nerve stimulation, changes in transmural pulmonary arterial pressure (Ptm) at a fixed transpulmonary pressure (Ptp) were produced by the Mueller maneuver, and increases in Ptp at relatively constant Ptm by a quasi-Valsalva maneuver. Also, both Ptm and Ptp were allowed to change during open airway lung inflation. Vpa was determined during these three maneuvers by multiplying pulmonary blood flow by pulmonary arterial mean transit time obtained by an ether plethysmographic method. During open airway lung inflation, mean (plus or minus SD) Ptp increased by 7.2 (plus or minus 3.7) cmH2O and Ptm by 4.3 (plus or minus 3.4) cmH2O for a mean increase in Vpa by 26.2 (plus or minus 10.7) ml. A pulmonary arterial compliance term (Delta Vpa/Delta Ptm) calculated from the Mueller maneuver was 3.9 ml/cmH2O and an interdependence term (Delta Vpa/Delta Ptp) calculated from the quasi-Valsalva maneuver was 2.5 ml/cmH2O for a 19% increase in lung volume, and 1.2 ml/cmH2O for an increase in lung volume from 19% to 35%. These findings indicate that in normal anesthetized dogs near FRC for a given change in Ptp and Ptm the latter results in a greater increase of Vpa.

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