Pulmonary Arteriovenous Shunting Research Articles

Immobility, hypoxemia, and pulmonary arteriovenous shunting.

Physiologic and pathologic effects of a systematic regimen of movement were compared with immobility in anesthetized, over-hydrated dogs. Immobile animals suffered early loss of oxygenating capability of the dependent lung that developed extensive atelectasis, hemorrhage, and pulmonary edema. A regimen of movement to alternate lateral positions every 30 minutes preserved oxygenating ability of both lungs, while hourly changes restored lost function and minimized the extent of pathologic findings in random zones of the lungs. Active regimens of movement were observed to prevent or relieve the arteriovenous shunting in patients. Pathophysiology was exaggerated in the dependent lung and reduced by change to the alternate position. Immobility, a critical factor in the genesis of hypoxemia, must be replaced by planned, systematic antigravity changes in position to maintain optimal lung mechanics and airway resistance and to prevent wasted work of the heart.

Pulmonary anatomic arteriovenous shunting caused by epinephrine.

Pulmonary anatomic arteriovenous (A-V) shunting was measured with technetium Tc 99m human albumin microspheres in 44 anesthetized dogs. In untreated dogs, after a 15- to 30-minute observation period following the first microsphere injection, no significant changes in heart rate, arterial pressure, cardiac output, or the pH occurred, but there was a small increase in arterial oxygen pressure and a small decrease in arterial carbon dioxide pressure. These were attributed to preanesthetic excitement or reactions to the anesthetic itself. The second microsphere injection showed no significant change in pulmonary shunting. Infusions of epinephrine hydrochloride at the rate of 2μg/kg/min and 4μg/kg/min showed significant increases in the pulmonary shunting to 320% and 573% of control values, respectively, during the same time intervals. Epinephrine in amounts that can be produced endogenously under conditions of stress may cause the opening of anatomic pulmonary A-V shunts.

Angiographic demonstration of arteriovenous shunts in pulmonary metastatic choriocarcinoma.

Arteriovenous shunting through uterine choriocarcinoma has been well demonstrated angiographically, but, despite physiologic evidence for similar communications through metastatic nodules in the lungs, angiographic documentation has not been reported. Two cases of respiratory distress, persistent arterial oxygen desaturation, and angiographic evidence of pulmonary arteriovenous shunting in metastatic pulmonary nodules are presented. Since even the most advanced form of this disease need not have a poor prognosis, an aggressive angiographic approach may differentiate it from pulmonary embolism causing similar symptoms and findings.

Respiratory support with a paracorporeal membrane oxygenator

The General Electric-Peirce Lung was used in the arteriovenous configuration as a paracorporeal respiratory assist device in dogs rendered cyanotic by left pneumonectomy and creation of a pulmonary arteriovenous shunt. The blood leaving the membrane lung was fully saturated and the extracorporeal oxygen exchange ranged from 5–20 ml/min depending on extra-corporeal flow, hematocrit and inflow saturotion. These experiments demonstrated that a paracorporeal lung can be used effectively with an AV fistula to treat chronic respiratory insufficiency in animals. Some of the experimental difficulties and the approaches to improving the results have been discussed.

Pulmonary arteriovenous shunting due to epinephrine.

Pulmonary arteriovenous shunting due to epinephrine.

Nomogram for estimating pulmonary arteriovenous shunt during ventilation with room air

Nomogram for estimating pulmonary arteriovenous shunt during ventilation with room air

Xenon-133 measurement of regional ventilation.

A clinically applicable method for quantitating regional ventilation and expressing both pulmonary ventilation and perfusion by 3-dimensional images is described. Studies on dogs intubated with Carlens tubes established the relationship between the slope of 133Xe disappearance from the lungs with regional ventilation. Three clinical cases illustrate a means of assessing pulmonary arteriovenous shunting, the value of quantitative pulmonary function measurements in chronic inflammatory lung disease and chronic pulmonary embolization. The data obtained required detector variability and dead-timeloss corrections by the 360/75 computer to be considered valid.

Effects of experimental recurrent microembolization on pulmonary function and distribution of labeled macroaggregates of sulfur

The effects of repeated microembolization using polystyrene beads were studied in twelve dogs. Hemodynamic changes included transient pulmonary hypertension with return to control values associated with increased cardiac output. In five long-term survivors the lack of development of persistent pulmonary hypertension correlated with evidence of increased arteriovenous shunting. Measurements of alveolar-arterial oxygen gradient showed an increase of 94 per cent mean at seven to eight weeks after initiation of embolization. Increased uptake of radioisotope by the liver was observed when lung scintiphotography was performed with technetium 99m macroaggregates of sulfur colloid. Passage of these 10 to 50 μ particles into the systemic circulation provided further evidence of increased pulmonary arteriovenous shunting and correlated quantitatively with changes in the A-aO 2 gradient. These changes were not observed in seven control dogs. Lung scintiphotography also showed decreased peripheral perfusion and focal perfusion defects. The most pronounced ventilatory change was an increase in ventilatory dead space of 55 per cent at the three to four week restudy period and V D subsequently remained significantly elevated. V T increased proportionately with the increase in V n so that the V D V T ratio did not change. These radioisotope studies combined with determinations of A-aO 2 gradient and ventilatory dead space are important diagnostic tools in documenting and quantitating recurrent or chronic pulmonary microembolization.

Transthoracic electrical impedance s a guide to intravascular overload.

Electrical impedance methods have been used to document the accumulation of fluid in living tissues. Change in transthoracic electrical impedance was studied in dogs during deliberate overinfusion with albumin in normal saline solution. Fall in transthoracic impedance was regularly observed with acute intravascular volume overload. Change in transthoracic impedance was accompanied by elevated cardiac output, fall in peripheral resistance and peripheral and pulmonary arteriovenous shunting. Pulmonary interstitial edema occurred in all animals. Impedance changes occur as the result of increased conductivity due to decreased intrapulmonary aeration (atelectasis) or to increased intrathoracic fluid volume. Relative changes in electrical impedance appear to be as sensitive as central venous pressure in the detection of intrathoracic volume changes.

Veno-arterial shunting in experimental pulmonary embolism

Cardiac output and pulmonary arteriovenous shunts were studied in two groups of sheep after pulmonary emboli. Hydrogensaline with a downstream platinum electrode was used as a dilution technique to measure cardiac output and transpulmonary shunting. The first group of sheep were given small clots and the second group one large clot. The recorded shunt was greater in these second group. The cardiac output fell after clot administration and the output/shunt ratio once established remained constant over 1 hour of study. In the animal given the largest clot compatible with survival the majority of the output traversed shunts, suggesting that this mechanism may avert right ventricular failure after massive pulmonary embolus.

Effect of intravenous alprenolol on ventilatory function and blood gas values in established obstructive airways disease

Intravenous administration of the beta-adrenergic blocking drug, alprenolol, to a group of patients with severe obstructive disease of the airways caused no deterioration of symptoms and a clinically insignificant fall in FEV1 in the majority. A minor reduction in PaO2 occurred which suggests that alprenolol may cause local hypoventilation and/or pulmonary arteriovenous shunting. The presence of obstructive disease of the airways does not seem to pose an absolute contraindication to the use of alprenolol, although caution must be exercised in its use in such patients.

Respiratory function in pulmonary thromboembolic disease

This is a correlative study of the clinical, electrocardiographic and respiratory function data in twenty-one subjects with respiratory symptoms and abnormal pulmonary perfusion scans as a result of pulmonary thromboembolic disease; sixteen subjects had subsequent functional studies and the duration of observation was up to three years. Two causal factors in the production of arterial hypoxaemia were recognized: ventilation-perfusion ratio nonhomogeneity and pulmonary arteriovenous shunting. Ventilation-perfusion ratio nonhomogeneity was the most important factor. In more than half of the patients reversible regional pulmonary vasoconstriction was demonstrated by a rise in the V D:V T ratio on breathing oxygen. The range of the steady state pulmonary diffusion capacity (D LCO) and the fractional carbon monoxide (CO) uptake was wide, but in the absence of other cardiovascular or respiratory diseases a reduction in the D LCO and fractional carbon monoxide uptake was unusual. The D LCO in pulmonary thromboembolic disease was usually normal, but there were unreal high and negative values. The vital capacity was reduced in about half of the patients, but the clinical and spirometric evidence of airways obstruction was infrequent.

Anomalous pulmonary venous drainage associated with mitral valve disease

Four cases of mitral stenosis associated with anomalous pulmonary venous return are described. In two of these cases there was severe mitral regurgitation as well. A pulmonary arteriovenous shunt was also found in one of these. A review of the records of patients admitted for cardiac catheterization revealed that in 0.42 per cent of the cases of mitral valve disease and 5.7 per cent of the cases of anomalous pulmonary venous drainage, both conditions were associated. The clinical, roentgenologic, electrocardiographic, and vectorcardiographic findings were predominantly characterized by the mitral valve disease. In every case, the diagnosis was established at cardiac catheterization. Hemodynamic studies were performed. These indicated that the circulatory consequences of the mitral valve disease were only little influenced by the anomalous pulmonary venous return.

Hypoxic hyperventilation and acute respiratory failure in the severely stressed patient: massive pulmonary arteriovenous shunts?

Hypoxic hyperventilation and acute respiratory failure in the severely stressed patient: massive pulmonary arteriovenous shunts?

Pulmonary Vasoconstriction Due to Nonocclusive Distention of Large Pulmonary Arteries in the Dog

The pulmonary vascular changes caused by distention of the pulmonary artery with the lumen fixed were compared to those produced by occlusive arterial distention. In 13 urethane-anesthetized dogs, nonocclusive distention was produced by distention of a corrugated rubber cuff around a hollow metal cylinder affixed to the end of a cardiac catheter. In 10 other dogs, occlusive distention was produced by inflation of a standard balloon catheter. Pressures were measured in large and small pulmonary veins and in the left and right atria with transseptal techniques, and in the pulmonary and femoral arteries. Simultaneously, pulmonary blood volume and flow were measured with dyedilution techniques. Pulmonary arteriovenous shunting was studied with the hydrogen-electrode technique. Nonocclusive distention of a pulmonary artery greatly increased pulmonary arterial and venous pressure and decreased pulmonary blood volume without changing left atrial pressure or cardiac output. Pulmonary vascular resistances increased, and pulmonary arteriovenous shunting was detected. Occlusive distention of one pulmonary artery caused smaller increases in pressure in the pulmonary artery and vein of the unobstructed lung. Vascular resistances in the unobstructed lung decreased, while blood volume and flow in that lung doubled. Pulmonary arterial distention leads to active constriction of the pulmonary arteries and veins, but these responses may be obscured by the passive responses to increasing blood flow and volume.

Cyanosis with hepatic cirrhosis. A case with pulmonary arteriovenous shunting.

A case is reported of cirrhosis of the liver associated with cyanosis and finger clubbing in a man of 31 years. The chest radiograph showed diffuse nodular shadows in both lower zones. Pulmonary function tests gave an arterial oxygen saturation of 91% at rest, falling to 68% on exercise; the single breath diffusing capacity for carbon monoxide was reduced to 55% of the predicted value and there was an estimated right-to-left shunt of 23%. Post-mortem injection of the lungs with Micropaque-gelatin suspension showed numerous pleural spider naevi, denser over the lower lobes, arteriovenous communications in the infrahilar regions, including leashes of dilated vessels in pleural adhesions on the diaphragm and diffuse arterial vasodilatation in the lungs; although the injection mass could be traced into the pulmonary veins in only a few regions of the lung, the dilated arterioles and spiders were possible additional channels through which blood might be shunted from the alveolar surfaces. The very low arterial oxygen saturation on exercise was probably caused by a shunt greater than the 23% estimated at rest, but the low diffusing capacity may have been partly responsible. The cause of the low diffusing capacity remains uncertain.

The krypton-85 method in the detection of pulmonary arterio-venous shunts.

Two cases of pulmonary arteriovenous fistulae were studied by the krypton-85 test and by angiocardiograhv. The relative merits of the two methods are discussed. © 1967 S. Karger AG, Basel.

Alveolar-arterial oxygen tension gradients in cirrhosis of the liver: Further evidence of existing pulmonary arteriovenous shunting

Alveolar-arterial oxygen tension gradients in cirrhosis of the liver: Further evidence of existing pulmonary arteriovenous shunting

CARDIO-RESPIRATORY ASPECTS OF TROPHOBLASTIC TUMOURS

In a group of 60 patients with trophoblastio tumours, 52 had pulmonary metastases and these caused serious symptoms in 12 patients. Six patients presented with cardio-respiratory symptoms, and four of these had no symptoms of a gynaecological nature. Three main forms of pulmonary metastases have been distinguished. The commonest metastasis is the easily recognized discrete mass. This is normally asymptomatic, but confluent growth may progress to a fatal respiratory acidosis. Miliary metastitio involvement of the lungs is the least common form, and may be associated with hyperventilation and tachycardia. Tumour emboli of sufficient size, number, or growth potential to occlude the pulmonary arteries cause pleuritio pain, dyspnoea, hyperventilation, signs of pulmonary hypertension, and large pulmonary arterio-venous shunts. Gross functional disturbances may be corrected by specific chemotherapy.

OSLER'S DISEASE WITH A DISSECTING ANEURYSM OF THE AORTA.

HEREDITARY hemorrhagic telangiectasia (Osler's disease) is a well recognized disease entity. It is manifested by (1) a hereditary tendency toward the disease, (2) the presence of typically distributed telangiectasia, and (3) the tendency of telangiectatic areas to bleed.1-2Various associations with the disease have been described, ie, the occurrence of pulmonary arteriovenous shunts,3aneurysms of the splenic 4 and hepatic arteries,2and hemangiomas of the liver.5Muggia reported a patient with this disease and an aortic arch aneurysm.6It has been emphasized by Bean2and Muggia6that greater awareness of the association of this disease with aneurysms of large vessels might prove rewarding with respect to prognosis and therapeutic considerations in these patients. The following report deals with the presence of a dissection of the aorta in a patient with the disease. Such an occurrence has not been previously reported Report of a Case A 60-year-old white man