HRCT score in bronchiectasis: Correlation with pulmonary function tests and pulmonary artery pressure

Alterations in pulmonary function and in hemodynamics were studied in dogs with high pulmonary blood flow resulting from systemic pulmonary artery shunts. In order to facilitate elevation in pulmonary artery pressure, the vascular bed was reduced in some cases by obstructing branches of the pulmonary artery with Teflon clips or by lobectomy. Results in 30 control dogs and in 30 animals that survived 5–36 months (average 16) following creation of shunts indicated that pulmonary function was not significantly altered by increased pulmonary blood flow until pulmonary artery hypertension developed. When systolic pulmonary artery pressure exceeded 40 mm Hg, there was a decrease in arterial Po2, an increase in venous admixture percentage of cardiac output, and an increase in the A-a O2 difference during three levels of O2 breathing, indicating both abnormal venous admixture and abnormal diffusion. Possible explanations for these findings are presented. Evidence in one dog suggests that these alterations are reversible. Submitted on August 10, 1960

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Sarcoidosis-Associated Pulmonary Hypertension

Seminars in Respiratory and Critical Care Medicine ◽

10.1055/s-0040-1713615 ◽

2020 ◽

Vol 41 (05) ◽

pp. 659-672

Author(s):

Marloes P. Huitema ◽

Harold Mathijssen ◽

Johannes J. Mager ◽

Repke J. Snijder ◽

Jan C. Grutters ◽

...

Keyword(s):

Pulmonary Hypertension ◽

Pulmonary Artery ◽

Pulmonary Artery Pressure ◽

Lung Transplant ◽

Pulmonary Function Tests ◽

High Morbidity ◽

Artery Pressure ◽

Extrinsic Compression ◽

Tertiary Center ◽

Parenchymal Disease

AbstractPulmonary hypertension (PH) is a well-known complication of sarcoidosis, defined by a mean pulmonary artery pressure of ≥25 mm Hg. Since both PH and sarcoidosis are rare diseases, data on sarcoidosis-associated PH (SAPH) is retrieved mostly from small retrospective studies. Estimated prevalence of SAPH ranges from 3% in patients referred to a tertiary center up to 79% in patients awaiting lung transplant. Most patients with SAPH show advanced parenchymal disease as the underlying mechanism. However, some patients have disproportional elevated pulmonary artery pressure, and PH can occur in sarcoidosis patients without parenchymal disease. Other mechanisms such as vascular disease, pulmonary embolisms, postcapillary PH, extrinsic compression, and other sarcoidosis-related comorbidities might contribute to SAPH. The diagnosis of PH in sarcoidosis is challenging since symptoms and signs overlap. Suspicion can be raised based on symptoms or tests, such as pulmonary function tests, laboratory findings, electrocardiography, or chest CT. PH screening mainly relies on transthoracic echocardiography. Right heart catheterization should be considered on a case-by-case basis in patients with clinical suspicion of PH, taking into account clinical consequences. Treatment options are considered on patient level in a PH expert center, and might include oxygen therapy, immunosuppressive, or PH-specific therapy. However, qualitative evidence is scarce. Furthermore, in a subset of patients, interventional therapy or eventually lung transplant can be considered. SAPH is associated with high morbidity. Mortality is higher in sarcoidosis patients with PH compared with those without PH, and increases in patients with more advanced stages of sarcoidosis and/or PH.

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Pulmonary hypertension after ventriculoatrial shunt implantation

Journal of Neurosurgery ◽

10.3171/2010.6.jns091541 ◽

2010 ◽

Vol 113 (6) ◽

pp. 1279-1283 ◽

Cited By ~ 22

Author(s):

Stefan Kluge ◽

Hans Jörg Baumann ◽

Jan Regelsberger ◽

Uwe Kehler ◽

Jan Gliemroth ◽

...

Keyword(s):

Pulmonary Hypertension ◽

Pulmonary Artery ◽

Pulmonary Function ◽

Pulmonary Function Tests ◽

Significant Proportion ◽

Systolic Pressure ◽

Chronic Thromboembolic Pulmonary Hypertension ◽

Doppler Velocity ◽

Systolic Pulmonary Artery Pressure ◽

Function Tests

Object Ventriculoatrial (VA) shunts inserted for the treatment of hydrocephalus are known to be a risk factor for pulmonary hypertension. The aim of this study was to evaluate the incidence of pulmonary hypertension among adult patients with VA shunts. Methods All patients who had received a VA shunt at one of two institutions between 1985 and 2000 were invited for a cardiopulmonary evaluation. The investigation included a thorough history taking, clinical examination, echocardiography, and pulmonary function testing including diffusing capacity of the lung for carbon monoxide (DLCO). Pulmonary hypertension was defined as systolic pulmonary artery pressure > 35 mm Hg at rest. Results The study group consisted of 86 patients, of whom 38 (44%) could be examined. The patients' mean age was 47.1 ± 18.4 years; the median interval between shunt insertion and cardiopulmonary evaluation was 15 years (range 5–20 years). Of the 38 patients, 20 (53%) had Doppler velocity profiles of tricuspid regurgitation that were adequate for the estimation of pulmonary artery systolic pressure. Doppler-defined pulmonary hypertension was observed in 3 patients (8%), 2 of whom underwent right heart catheterization. Chronic thromboembolic pulmonary hypertension was confirmed in both patients, and medical therapy, including anticoagulation, was started. The VA shunt was removed in both cases and replaced with a different type of device. Pulmonary function tests revealed a restrictive pattern in 15% and typical obstructive findings in 9% of patients. In 30% of patients the DLCO was less than 80% of predicted, and blood gas analysis showed hypoxemia in 6% of patients. No significant differences in pulmonary function tests were noted between the patients with and without echocardiographic evidence of pulmonary hypertension. However, patients with pulmonary hypertension had significantly lower DLCO values. Conclusions The authors detected pulmonary hypertension by using Doppler echocardiography in a significant proportion of patients with VA shunts. It is therefore recommended that practitioners perform regular echocardiography and pulmonary function tests, including single-breath DLCO in these patients to screen for pulmonary hypertension to prevent hazardous late cardiopulmonary complications.

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VENTILATION-PERFUSION RELATIONSHIPS IN CHILDREN WITH HEART DISEASE AND DIMINISHED PULMONARY BLOOD FLOW

PEDIATRICS ◽

10.1542/peds.42.5.778 ◽

1968 ◽

Vol 42 (5) ◽

pp. 778-785

Author(s):

Martin H. Lees ◽

Richard H. Burnell ◽

Clarence L. Morgan ◽

Benjamin B. Ross

Keyword(s):

Blood Flow ◽

Heart Disease ◽

Pulmonary Artery ◽

Pulmonary Function ◽

Pulmonary Artery Pressure ◽

Pulmonary Blood Flow ◽

Alveolar Ventilation ◽

Uneven Distribution ◽

Artery Pressure ◽

Major Abnormality

Pulmonary function of infants and children with diminished pulmonary blood flow was studied by measurement of alveolar ventilation and alveolar-arterial gas tension differences of O2, CO2, and N2. The increased ventilation of these subjects was found to be effective in CO2 elimination (arterial CO2 tension, 31 mm Hg), but there was evidence of considerable unevenness of distribution of ventilation/perfusion ratios (VAQ). A measure of the degree of VA/Q unevenness was obtained by use of the urine-alveolar nitrogen tension difference. It is likely, under the prevailing conditions of hyperventilation and hypoperfusion, that maldistribution of perfusion is the major abnormality. Uneven distribution of perfusion is most probably due to the effects of gravity enhanced by low pulmonary artery pressure and blood flow—an exaggenation of the normal physiologic relative overperfusion of the lower-most parts of the lung.

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Inflammation and Congenital Heart Disease Associated Pulmonary Hypertension

The Heart Surgery Forum ◽

10.1532/hsf.1228 ◽

2015 ◽

Vol 18 (1) ◽

pp. 038 ◽

Cited By ~ 2

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

Background: 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. Methods: 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. Results: 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 < .001, P < .001, and P = .004) and mean pulmonary artery pressure (P < .001, P < .001, and P = .001), whereas preoperative mean pulmonary artery pressure was found to be independently correlated with intensive care unit stay (P < .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). Conclusion: 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.

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