Effect of tonsillectomy and/or adenoidectomy on pulmonary arterial pressure in adults

Open Medicine ◽  
2008 ◽  
Vol 3 (4) ◽  
pp. 482-486
Author(s):  
Saeed Abdelwhab ◽  
Khaled. Dessoukey ◽  
Gamal Lotfy ◽  
Ashraf Alsaeed ◽  
Hesham Anwar
Keyword(s):  
Pulmonary Artery ◽  
Arterial Pressure ◽  
Pulmonary Artery Pressure ◽  
Pulmonary Arterial Pressure ◽  
Arterial Oxygen ◽  
Artery Pressure ◽  
Mean Pulmonary Arterial Pressure ◽  
Arterial Blood ◽  
Pulmonary Arterial ◽  
Group 1

AbstractThe aim of the study was to determine the mean pulmonary pressure in adult with hypertrophic tonsils and adenoids and to clarify whether tonsillectomy and adenoidectomy has any effect on mean pulmonary arterial pressure of these adult. The study was carried out on 50 patients with diagnosis of upper airway obstruction resulting from hypertrophied tonsils and adenoids (group1). 25 adults were assigned as control with similar age and sex distribution (group2). For study subjects Routine general Examinations, BMI, ECG, Chest X ray, Arterial blood gases and Echocardiography were done. Mean pulmonary arterial pressure was measured by using Doppler Echocardiography preoperatively and mean 3–4 months postoperatively in all subjects. Elevated PAP (pulmonary artery pressure) was found in 15 patients (30%) in group 1 preoperatively. Mean PAP was 28.34 ±5.11 mmHg preoperative in group 1 and 19.84 ± 5.0 mmHg in group 2 (p <0.001). PAP decrease to 22.38 ±4.28 mmHg postoperatively in group 1 (p <0.001). Arterial oxygen saturation (spo2%) increase from 93.5 ± 1.9% preoperatively to 95.3 ± 1.3% post operatively (p < 0.001). percent reduction of PAP postoperatively correlates to age (t=−2.3, p= 0.02), preoperative PAP (p =0.01) but no correlation was found with BMI. In conclusions, this Study showed that obstructed adenoid and hypertrophy of tonsils causes higher mean pulmonary artery pressure in adult & revealed that tonsil& adenoid is effective therapeutic measure in such patients. With early intervention is necessary to avoid progressive cardiopulmonary disease.

Effect of hypoxia on pulmonary artery pressure of dogs

1964 ◽  
Vol 207 (6) ◽  
pp. 1314-1318 ◽  
Author(s):  
Benson R. Wilcox ◽  
W. Gerald Austen ◽  
Harvey W. Bender
Keyword(s):  
Pulmonary Artery ◽  
Arterial Pressure ◽  
Pulmonary Artery Pressure ◽  
Pulmonary Arterial Pressure ◽  
Venous Pressure ◽  
Artery Pressure ◽  
Pulmonary Vasoconstriction ◽  
Systemic Hypoxia ◽  
Pump Output ◽  
Pulmonary Arterial

The mechanism by which the pulmonary artery pressure rises in response to hypoxia has never been clearly demonstrated. This problem was reinvestigated in experiments utilizing separate pulmonary and systemic perfusion systems. These vascular beds were perfused in such a fashion that a change in pulmonary artery pressure could only result from changes in vasomotor tone. Alveolar-pulmonary vein hypoxia was usually associated with a slight fall in pulmonary artery pressure. Systemic hypoxia resulted in elevation of pulmonary arterial pressure in 10 of the 12 animals tested with a constant-flow and constant-pulmonary venous pressure. In addition, all animals with systemic desaturation showed an increased venous return. When the "cardiac output" (pump output) was increased to match this return, the elevation in pulmonary artery pressure increased. It was concluded that the pulmonary arterial pressure elevation seen with hypoxia is the result of active pulmonary vasoconstriction coupled with an increased pulmonary blood flow.

Persistence of lung edema and arterial pressure rise in dogs after lung emboli

1964 ◽  
Vol 207 (3) ◽  
pp. 641-646 ◽  
Author(s):  
H. Weisberg ◽  
J. F. Lopez ◽  
M. H. Luria ◽  
L. N. Katz
Keyword(s):  
Pulmonary Artery ◽  
Arterial Pressure ◽  
Pulmonary Edema ◽  
Pulmonary Artery Pressure ◽  
Pressure Rise ◽  
Significant Rise ◽  
Lung Edema ◽  
Artery Pressure ◽  
Acute Elevation ◽  
Pulmonary Arterial

Bilateral pulmonary edema was present in dogs autopsied 24 hr after pulmonary embolization. Mean pulmonary artery pressure remained elevated during this period. Most others, which survived up to the 3rd day and died spontaneously after embolization, showed edema at autopsy. Longer survivors showed no edema. Edema severity during the first 2 days was roughly related to the pressure rise during the 1st hr after embolization. Immediate significant pulmonary artery pressure rise, predominant in dogs succumbing by the 3rd day, was not as common in those surviving longer. Thus, survival time showed an inverse relationship to immediate pulmonary artery pressure elevation. In another 17 dogs followed as long as 10–23 months after embolization, 53% showed a significant rise in pressure at the end and some animals also had histologic pulmonary vascular changes. In some instances acute elevation of pulmonary artery pressure at embolization may anticipate chronic pulmonary arterial hypertension. The problem is the creation of embolism which elevates pulmonary arterial pressure without animals succumbing acutely to the associated pulmonary edema.

Effects of extracorporeal oxygenation of venous return on pulmonary artery pressure

1962 ◽  
Vol 202 (3) ◽  
pp. 510-514 ◽  
Author(s):  
William M. Chadduck
Keyword(s):  
Pulmonary Artery ◽  
Oxygen Saturation ◽  
Pulmonary Artery Pressure ◽  
Venous Return ◽  
Arterial Oxygen Saturation ◽  
Right Atrial ◽  
Arterial Oxygen ◽  
Artery Pressure ◽  
Pulmonary Arterial ◽  
Extracorporeal Oxygenation

Pulmonary arterial hyperoxemia was produced in anesthetized, open-chest dogs by means of an extracorporeal oxygenator with an inflow system which prevented right atrial pressure from exceeding 7–10 cm of blood. No significant changes in pulmonary artery pressure were found when pulmonary arterial oxygen saturation was elevated to 80–99%. The elevated pulmonary artery pressure associated with systemic arterial hypoxemia was reduced by extracorporeal oxygenation of venous return. The use of such a system for attainment of tolerable levels of systemic arterial oxygen saturation in patients with acute disorders of pulmonary alveolar-capillary gas exchange is discussed.

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.

The Effect of Aminophylline on the Respiration and Pulmonary Circulation

1970 ◽  
Vol 38 (5) ◽  
pp. 549-554 ◽  
Author(s):  
V. Ježek ◽  
A. Ouředník ◽  
J. Štěpánek ◽  
F. Boudík
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Chronic Bronchitis ◽  
Pulmonary Circulation ◽  
Pulmonary Arterial Pressure ◽  
Alveolar Ventilation ◽  
Arterial Oxygen ◽  
Bronchial Obstruction ◽  
Arterial Blood ◽  
Pulmonary Arterial

1. We have examined the effects of aminophylline on the respiration and pulmonary circulation of eleven patients with chronic bronchitis and six patients with peripheral bronchial carcinoma; the latter were free from bronchial obstruction at the time of study. 2. Aminophylline caused an increase in total and alveolar ventilation and a decrease in arterial carbon dioxide tension. Lung diffusing capacity was unaltered in subjects with marked respiratory insufficiency but increased slightly in an additional group of less severely affected patients, and in the control subjects. 3. Mean pulmonary arterial pressure decreased significantly in the patients with chronic bronchitis but not those with lung cancer. A positive correlation was observed between the level of pulmonary arterial pressure during the control period and the decrease after aminophylline. 4. For the group as a whole there was no significant change in cardiac output or arterial oxygen saturation or tension. However, in those subjects in whom the cardiac output was increased, the arterial blood oxygen was reduced despite an increase in alveolar ventilation. The data are interpreted as evidence for a disproportionate part of the increase in cardiac output being directed to poorly ventilated areas of the lung.

scholarly journals A scoring system to predict the elevation of mean pulmonary arterial pressure in idiopathic pulmonary fibrosis

2018 ◽  
Vol 51 (1) ◽  
pp. 1701311 ◽  
Author(s):  
Taiki Furukawa ◽  
Yasuhiro Kondoh ◽  
Hiroyuki Taniguchi ◽  
Mitsuaki Yagi ◽  
Toshiaki Matsuda ◽  
...  
Keyword(s):  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Arterial Pressure ◽  
Scoring System ◽  
Screening Tool ◽  
Pulmonary Arterial Pressure ◽  
Arterial Oxygen Tension ◽  
Arterial Oxygen ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Arterial

Elevated mean pulmonary arterial pressure (MPAP; ≥21 mmHg) is sometimes seen in patients with idiopathic pulmonary fibrosis (IPF) and has an adverse impact upon survival. Although early diagnosis is crucial, there is no established screening tool that uses a combination of noninvasive examinations.We retrospectively analysed IPF patients at initial evaluation from April 2007 to July 2015 and, using logistic regression analysis, created a screening tool to identify elevated MPAP. Internal validation was also assessed for external validity using a bootstrap method.Using right-heart catheterisation (RHC), elevation of MPAP was determined to be present in 55 out of 273 patients. Multivariate models demonstrated that % predicted diffusing capacity of the lung for carbon monoxide (DLCO) <50%, ratio of pulmonary artery diameter to aorta diameter (PA/Ao) on computed tomography (CT) ≥0.9 and arterial oxygen tension (PaO2) <80 Torr were independent predictors. When we assigned a single point to each variable, the prevalence of elevation of MPAP with a score of zero, one, two or three points was 6.7%, 16.0%, 29.1% and 65.4%, respectively. The area under curve (AUC) for the receiver operating characteristic (ROC) curve was good at 0.757 (95% CI 0.682–0.833).A simple clinical scoring system consisting of % predicted DLCO, PA/Ao ratio on CT and PaO2 can easily predict elevation of MPAP in patients with IPF.

Effect of RBC shape and deformability on pulmonary O2 diffusing capacity and resistance to flow in rabbit lungs

1995 ◽  
Vol 78 (3) ◽  
pp. 778-783 ◽  
Author(s):  
D. C. Betticher ◽  
W. H. Reinhart ◽  
J. Geiser
Keyword(s):  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Oxygen Transfer ◽  
Sodium Salicylate ◽  
Pulmonary Arterial Pressure ◽  
Diffusing Capacity ◽  
Artery Pressure ◽  
Human Red Blood Cells ◽  
Pulmonary Arterial ◽  
The Mean

Isolated rabbit lungs were perfused with washed and resuspended human red blood cells (RBCs) in the presence of drugs known to change the shape and deformability of RBCs. With sodium salicylate (0.5–2 g/l), which causes echinocytosis and increases RBC deformability, lung diffusing capacity for O2 (DLO2) increased by 21%. When chlorpromazine, which induces stomatocytosis and stiffens RBCs, was given (50 mg/l), DLO2 decreased by 18%. With sodium salicylate, the mean pulmonary artery pressure dropped by 14% from control values, whereas it increased by 18% under chlorpromazine. Comparative experiments with hemoglobin solutions did not reveal any effect of those two drugs either on DLO2 or on pulmonary arterial pressure, which indicates that the effects of sodium salicylate and chlorpromazine were due to changes in RBC shape and deformability. It is concluded that RBC shape and deformability affect pulmonary artery pressure and oxygen diffusing capacity, which may have an influence on oxygen transfer to tissue and hence be of clinical relevance.

Inflammation and Congenital Heart Disease Associated Pulmonary Hypertension

2015 ◽  
Vol 18 (1) ◽  
pp. 038 ◽  
Author(s):  
Mete Gursoy ◽  
Ece Salihoglu ◽  
Ali Can Hatemi ◽  
A. Faruk Hokenek ◽  
Suleyman Ozkan ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Neutrophil To Lymphocyte Ratio ◽  
Cell Distribution ◽  
Inflammation Markers ◽  
Distribution Width ◽  
Artery Pressure ◽  
Lymphocyte Ratio ◽  
Mean Pulmonary Artery Pressure ◽  
Pulmonary Arterial

<strong>Background:</strong> Increased blood flow may trigger pulmonary arterial wall inflammation, which may influence progression of pulmonary artery hypertension in patients with congenital heart disease. In this study, we aimed to investigate the correlation between preoperative inflammation markers and pulmonary arterial hypertension. <br /><strong>Methods:</strong> A total of 201 patients with pulmonary hypertension were enrolled in this study retrospectively; they had undergone open heart surgery between January 2012 and December 2013. Patients’ preoperative C-reactive protein (CRP), neutrophil to lymphocyte ratio, red blood cell distribution width, pulmonary pressures, and postoperative outcomes were evaluated.<br /><strong>Results:</strong> Patient age, neutrophil to lymphocyte ratio, red blood cell distribution width, and CRP were found to be significantly correlated with both preoperative peak and mean pulmonary artery pressures. These data were entered into a linear logistic regression analysis. Patient age, neutrophil to lymphocyte ratio, and CRP were found to be independently correlated with peak pulmonary pressure (P &lt; .001, P &lt; .001, and P = .004) and mean pulmonary artery pressure (P &lt; .001, P &lt; .001, and P = .001), whereas preoperative mean pulmonary artery pressure was found to be independently correlated with intensive care unit stay (P &lt; .001). No parameter was found to be significantly correlated with extubation time and mortality. Eighteen patients had experienced pulmonary hypertensive crisis; in this subgroup, patients’ mean pulmonary artery pressure and neutrophil to lymphocyte ratio were found to be significant (P = .047, P = .003). <br /><strong>Conclusion:</strong> Preoperative inflammation markers may be correlated with the progression of pulmonary hypertensive disease, but further studies with larger sample size are needed to determine the predictive role of these markers for postoperative outcomes.<br /><br />

A Comparison of the Acute Haemodynamic Effects of Propranolol and Pindolol at Rest and during Supine Exercise in Man

1980 ◽  
Vol 59 (s6) ◽  
pp. 465s-468s ◽  
Author(s):  
T. L. Svendsen ◽  
J. E. Carlsen ◽  
O. Hartling ◽  
A. McNair ◽  
J. Trap-Jensen
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Response Curves ◽  
Receptor Blocking ◽  
Artery Pressure ◽  
Arterial Blood ◽  
Β Receptor

1. Dose-response curves for heart rate, cardiac output, arterial blood pressure and pulmonary artery pressure were obtained in 16 male patients after intravenous administration of three increasing doses of pindolol, propranolol or placebo. All patients had an uncomplicated acute myocardial infarction 6–8 months earlier. 2. The dose-response curves were obtained at rest and during repeated bouts of supine bicycle exercise. The cumulative dose amounted to 0.024 mg/kg body weight for pindolol and to 0.192 mg/kg body weight for propranolol. 3. At rest propranolol significantly reduced heart rate and cardiac output by 12% and 15% respectively. Arterial mean blood pressure was reduced by 9.2 mmHg. Mean pulmonary artery pressure increased significantly by 2 mmHg. Statistically significant changes in these variables were not seen after pindolol or placebo. 4. During exercise pindolol and propranolol both reduced cardiac output, heart rate and arterial blood pressure to the same extent. After propranolol mean pulmonary artery pressure was increased significantly by 3.6 mmHg. Pindolol and placebo did not change pulmonary artery pressure significantly. 5. The study suggests that pindolol may offer haemodynamic advantages over β-receptor-blocking agents without intrinsic sympathomimetic activity during low activity of the sympathetic nervous system, and may be preferable in situations where the β-receptor-blocking effect is required only during physical or psychic stress.

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