Showing papers on "Pulmonary artery published in 1979"
TL;DR: The aberrant artery in intralobar sequestration originated in 74% of all cases from the thoracic aorta, and in 14·8% there was more than one anomalous artery, and the mean diameter of the aberrant arteries was 6·3-6·6 mm.
Abstract: We present an analysis of 400 intralobar and 133 extralobar sequestrations, six cases presenting intra- and extralobar sequestration simultaneously, five sequestrations of one whole lung, and two bilateral intralobar sequestrations. This anomaly comprises 0·15-6·4% of all congenital pulmonary malformations. Usually the posterior basal segment is affected. The aberrant artery in intralobar sequestration originated in 74% of all cases from the thoracic aorta, and in 14·8% there was more than one anomalous artery. The mean diameter of the aberrant arteries was 6·3-6·6 mm. Usually arteries with predominantly elastic fibres were found. Arteriosclerotic changes were common, even in children. The venous return of the intralobar sequestration is, in 95·7% of all cases, via the pulmonary veins. In 13·7% of all cases other congenital malformations were observed. Symptoms arose within the first decade of life in 37·2% Bronchography and retrograde arteriography are the mainstay of diagnosis. Sequestrations are not supplied by a bronchial artery. Treatment of choice is operation as early as possible. Altogether seven operative deaths were reported, five of which were due to haemorrhage during operation. Of the 133 extralobar sequestrations, 77·4% were located between diaphragm and lower lobe. The arterial supply was provided by branches of the aorta. Some cases were supplied with venous blood by branches of the pulmonary artery. In six cases secondary changes, such as tuberculosis or carcinoma were found. In 60% of all the patients symptoms occurred within the first decade of life. Preoperative diagnosis was correct in only six cases. There were four postoperative deaths.
636 citations
TL;DR: In 55 Sprague-Dawley rats exposed to hypobaric hypoxia and 23 weight-matched controls kept in room air, pulmonary and systemic artery pressures were measured daily for 2 wk via indwelling catheters and three structural features were quantified microscopically.
Abstract: In 55 Sprague-Dawley rats (mean wt, 277 +/- 6.2 g) exposed to hypobaric hypoxia (air at 380 mmHg), and 23 weight-matched controls kept in room air, pulmonary and systemic artery pressures were measured daily for 2 wk via indwelling catheters. After each day of exposure, 1 or 2 hypoxic rats, to a total of 20, and 5 control rats were killed during the experiment. In these rats, the pulmonary arterial tree was injected post mortem with barium-gelatin and inflated with formaldehyde solution, and three structural features were quantified microscopically: 1) abnormal extension of muscle into peripheral arteries where it is not normally present (EMPA); 2) increased wall thickness of the normally muscular arteries, expressed as a percentage of external diameter (%WT); and 3) reduction in artery number expressed as an increase in the ratio of alveoli to arteries (A/a). Mean pulmonary artery pressure (Ppa) rose significantly after day 3 of hypoxic exposure (P less than 0.05) and had doubled by day 14; the mean systemic artery pressure (Psa) of hypoxic rats and Ppa and Psa of control rats were unchanged. The level of Ppa correlated with the degree of structural changes; for EMPA, r = 0.84; for %WT, r = 0.64; and for A/a, r = 0.73 (P less than 0.001 in all.
487 citations
TL;DR: A 2-year-old boy in whom this anomaly was associated with mitral regurgitation caused by papillary muscle dysfunction was successfully treated by this new surgical method, and the deformed mitral valve was concomitantly replaced by a Hancock porcine xenograft.
325 citations
TL;DR: The study of 116 pulmonary artery catheterizations concludes that although significant complications may result from pulmonary arterial catheterization and monitoring of critically ill patients, the incidence is low.
251 citations
TL;DR: It is postulate that in some COPD patients these initially transient events may lead to sustained pulmonary hypertension and cor pulmonale and nocturnal oxygen therapy may be indicated in more patients than previously suspected and may prevent the development of cor pulMonale.
189 citations
TL;DR: The morphological features of a series of 37 specimens of pulmonary atresia with intact ventricular septum were reviewed and if these anatomical findings are representative for the condition as a whole, they provide a good explanation for its disastrous prognosis.
Abstract: The morphological features of a series of 37 specimens of pulmonary atresia with intact ventricular septum were reviewed with particular emphasis on features which might influence the results of pulmonary valvotomy. The degree of right heart hypoplasia was quantified by measuring right and left heart dimensions and comparing them with 20 normal infant hearts. Right ventricular cavity size was usually smaller than normal but constituted a spectrum ranging from tiny to a dilated ventricle larger than normal. There was a positive correlation between triscuspid annular size and right ventricular size but no correlation between the size of the pulmonary artery and the right ventricle. Successful pulmonary valvotomy with subsequent adequate right ventricular function would have been precluded by a tiny right ventricular cavity or infundibular atresia in 14 specimens and by severe tricuspid stenosis or regurgitation in an additional 4. Severe right or left ventricular endocardial fibroelastosis may have adversely affected ventricular function in several others. Ten specimens displayed convex bulging of the left ventricular septal surface. If these these anatomical findings are representative for the condition as a whole, they provide a good explanation for its disastrous prognosis.
131 citations
TL;DR: A patient with symptomatic primary pulmonary artery hypertension underwent therapeutic trials with parenteral and oral phentolamine and continues to enjoy symptomatic improvement with a marked increase in exercise tolerance.
Abstract: A patient with symptomatic primary pulmonary artery hypertension underwent therapeutic trials with parenteral and oral phentolamine. Before drug therapy, he manifested marked increases in ...
126 citations
TL;DR: It is concluded that the lungs play a significant role in the inactivation of circulating norepinephrine in man and this metabolic function of the lungs appears to be lost in pulmonary hypertension.
Abstract: We directly measured the net pulmonary extraction of circulating norepinephrine, epinephrine and dopamine in control patients and patients with primary or secondary pulmonary hypertension. Mixed pulmonary artery norepinephrine, epinephrine and dopamine were 314 +/- 13 pg/ml, 102 +/- 9 pg/ml, 51 +/- 5 pg/ml, respectively, for the control group; values were similar in patients with pulmonary hypertension. The pulmonary extraction of norepinephrine was 25.4 +/- 2.6% (clearance 266 +/- 62 ng/min) in control patients; epinephrine and dopamine were not extracted. There was no net extraction or production of any of the three catecholamines by the lungs in any of the patients with pulmonary hypertension. We conclude that the lungs play a significant role in the inactivation of circulating norepinephrine in man. This metabolic function of the lungs appear to be lost in pulmonary hypertension.
121 citations
TL;DR: Tolazoline proved to be very effective in the treatment of two patients with pulmonary vasoconstriction secondary to hypoxia, and postoperative monitoring of pulmonary artery and RV pressures in infants with large ventricular septal defects is essential when unexplained complications are encountered.
Abstract: In this paper we discuss two infants and one child who experienced a previously unreported complication after complete correction of a large, unrestrictive ventricular septal defect. Two patients had documented pulmonary hypertensive crises and severe right-heart failure secondary to hypoxia and pulmonary vasoconstriction. These crises were associated with significantly increased right ventricular (RV) peak systolic and end-diastolic pressures and right-to-left shunting via a foramen ovale which, in turn, exaggerated the hypoxis. The crises were treated successfully with tolazoline in the second and third patients. RV pressure returned to normal values and have remained normal up to 12 months postoperatively in the second patient. Although the RV pressures decreased with tolazoline in the third patient, they never reached normal values. Postoperative monitoring of pulmonary artery and RV pressures in infants with large ventricular septal defects is essential when unexplained complications are encountered. Tolazoline proved to be very effective in the treatment of two patients with pulmonary vasoconstriction secondary to hypoxia.
105 citations
TL;DR: Echocardiographic abnormalities were noted in 37 (69 per cent) of 54 patients with progressive systemic sclerosis (PSS) as mentioned in this paper, and one of the patients also underwent right heart catheterization.
102 citations
TL;DR: Prediction of postrepair PRV/LV when transannular patching or an external conduit is planned allows identification of patients in whom right and left pulmonary arteries are too small for safe complete repair, and in them an initial palliative operation should be done to enlarge the arteries.
TL;DR: It is concluded that the rapid action of midazolam maleate and its modest effects on haemodynamic parameters, make it a safe and efficacious induction agent in patients with ischaemic heart disease.
Abstract: Midazolam maleate is a new water soluble benzodiazepine used for induction of anaesthesia. Ten patients with symptomatic ischaemic heart disease were premedicated intramuscularly with morphine 0.l mg · kg-1 and scopolamine 6–8 µg · kg-1, 60–90 minutes before induction. The heart rate, systolic/diastolic blood pressure, mean systolic blood pressure, mean pulmonary artery blood pressure, pulmonary artery occluded pressure, mean right atrial pressure, cardiac output (duplicate thermodilution) and arterial blood gas tensions were measured at four time periods: (1) after instrumentation while breathing room air, (2) after transfer to the operating room while breathing 100 percent oxygen by mask, (3) one to two minutes after intravenous midazolam maleate 0.2 mg · kg-1 and (4) four to five minutes after midazolam maleate. The cardiac index, stroke index, heart ratesystolic blood pressure product, systemic vascular resistance index, pulmonary vascular resistance index, left ventricular stroke work index and right ventricular stroke work index were calculated for each of the study time-periods from the measured parameters.
TL;DR: Indomethacin administration during pregnancy causes constriction of the fetal ductus arteriosus and fetal pulmonary arterial hypertension which, if severe, may cause rapid fetal death, and it is possible that this mechanism may be one cause of persistent pulmonary hypertension or tricuspid insufficiency or both in the newborn infant.
TL;DR: Twenty-five patients with proven patent ductus arteriosus were examined by pulsed Doppler echocardiography before invasive assessment and PDE correctly distinguished between patients with normal pressure and those with evidence of pulmonary hypertension; the ECG did not allow such differentiation.
Abstract: Twenty-five patients with proven patent ductus arteriosus were examined by pulsed Doppler echocardiography (PDE) before invasive assessment. Ten patients had normal pulmonary artery pressures, and by PDE, pandiastolic ductal flow. Fifteen patients had elevation of mean pulmonary artery pressure, and by PDE, all had abbreviations of diastolic ductal flow. PDE correctly distinguished between patients with normal pressure and those with evidence of pulmonary hypertension; the ECG did not allow such differentiation. Detection by PDE of pulmonary hypertension complicating patent ductus arteriosus appears to be clinically useful.
TL;DR: Three patients with anomalous origin of the right coronary artery from the pulmonary artery are presented together with a review of the 14 patients with this anomaly previously reported, finding no diagnostic electrocardiographic or chest roentgenographic changes.
TL;DR: Since capillary recruitment correlated with pulmonary artery pressure in each dog, but not with pulmonary vein pressure, it is concluded that arterial, not venous, constriction is the probable cause of this recruitment.
Abstract: Hypoxia has been shown to cause an increased number of pulmonary capillaries to be perfused. Changes in cardiac output and left atrial pressure have been previously ruled out as causes of this capillary recruitment. Increased pulmonary vein pressure and increased pulmonary artery pressure remain as two potential mechanisms. To differentiate between these two possible causes, we measured pulmonary artery and vein pressures with directly placed catheters and capillary recruitment with in vivo microscopy. During isocapnic hypoxia pulmonary artery pressure doubled, observed capillary recruitment increased fivefold, and pulmonary vein pressure remained constant. When the vasodilator prostaglandin E1 was infused during hypoxia, pulmonary artery pressure and capillary recruitment fell to control values and pulmonary vein pressure remained constant. Since capillary recruitment correlated with pulmonary artery pressure in each dog, but not with pulmonary vein pressure, we conclude that arterial, not venous, constriction is the probable cause of this recruitment.
TL;DR: The data suggest that the development of right ventricular hypertroph is characterized by a sustained compensatory response of the coronary circulation to the augmented work load and mass, and that is not associated with a proliferativeresponse of the vasculature supplying the enlarged ventricle.
Abstract: The effects of right ventricular hypertrophy on the overall and regional distribution of myocardial blood flow in the absence of an elevated coronary arterial driving pressure were evaluated in 18 concscious dogs subjected to a chronic pressure overload of the right ventricle induced by pulmonary artery constriction. The sustained pressure overload for duration of 4--6 wk or 4--5 mo resulted in significant increases in right ventricular mass (45 and 110%, respectively) and right ventricular fiber diameter (22 and 60%, respectively). Moreover, the presence of moderate and severe hypertrophy was associated with marked increases in transmural blood flow per gram to the right ventricle proportional to the observed increases in mass, i.e., of 36 and 109%, respectively, from a normal value of 0.67 +/- 0.04 ml/min per g, whereas left ventricular blood flow remained unaltered from a normal value of 1.00 +/- 0.06 ml/min per g. Despite the large increase in blood flow per gram to moderately and severely hypertrophied right ventricle, no significant changes in the ratio of capillary:muscle fiber number were observe. These data suggest that the development of right ventricular hypertroph is characterized by a sustained compensatory response of the coronary circulation to the augmented work load and mass, and that is not associated with a proliferative response of the vasculature supplying the enlarged ventricle.
TL;DR: The late appearance of sudden death in three Group A patients and no late deaths in Group B patients suggests that ligation and SVG, or its equivalent, may be the therapy of choice for patients with anomalous left coronary artery from the pulmonary artery.
TL;DR: It is suggested that unilateral lung hyperinflation reflexed depresses heart rate and blood pressure, which are partially compensated with time, and reflexly depresses stroke volume, which persists uncompensated until the lung is deflated.
Abstract: We have examined whether lung hyperinflation in the anesthetized dog reflexly depresses cardiac output, stroke volume, heart rate, and blood pressure and whether these changes persist for more than a minute. To eliminate any mechanical restriction to venous return and pulmonary blood flow during lung hyperinflation, a model was developed in which all pulmonary artery blood flow and all ventilation were directed to the right lung in dogs with widely open chest and the left lung was hyperinflated before and after left cervical vagotomy. Heart rate, stroke volume, and blood pressure decreased by 24, 20, and 27%, respectively, within 15 s of left lung inflation to 30 cm H(2)O. Heart rate increased to preinflation levels by 1 min, but stroke volume and blood pressure remained depressed during lung hyperinflation for at least 15 min. Upon deflation, stroke volume and blood pressure returned to control levels within 1 min. Division of the left vagosympathetic trunk at the neck interrupted all autonomic afferent and efferent nerves of the left lung, but left intact the right vagal sympathetic and parasympathetic afferent and efferent nerves of the heart. After left cervical vagotomy the transient fall in heart rate, stroke volume, and blood pressure during left lung hyperinflation was greatly reduced or eliminated. These results suggest that unilateral lung hyperinflation reflexly depresses heart rate and blood pressure, which are partially compensated with time, and reflexly depresses stroke volume, which persists uncompensated until the lung is deflated. These findings may explain the depressed cardiovascular function observed during regional lung overdistention especially when it occurs during positive pressure ventilation.
TL;DR: Results suggest that pulmonary receptors sensitive to capsaicin and accessible via the pulmonary circulation produce reflex bronchoconstriction, and one possible function of this vagal reflex is to assist fluid movement from microvasculature to peribronchial space by reducing peribronschial pressure.
Abstract: To determine whether receptors stimulated by the injection of capsaicin into the pulmonary circulation cause reflex changes in airway size, six dogs were anesthetized with chloralose, paralyzed with succinylcholine, and mechanically ventilated (2 cm H2O PEEP). Intrapulmonary airways were outlined with tantalum dust, and diameters were determined by taking serial roentgenograms at end expiration. Capsaicin (20 micrograms/kg) injected into the right ventricle significantly decreased airway diameter (20%), heart rate, aortic pressure, and pulmonary artery pressure. In contrast, capsaicin injected into the left ventricle did not alter airway diameter or aortic pressure, although heart rate and pulmonary artery pressure decreased but to a lesser extent than after right ventricular injection. After vagotomy, capsaicin had no effect on airway diameter or heart rate but aortic pressure and pulmonary artery pressure increased slightly. Results suggest that pulmonary receptors sensitive to capsaicin and accessible via the pulmonary circulation produce reflex bronchoconstriction. One possible function of this vagal reflex is to assist fluid movement from microvasculature to peribronchial space by reducing peribronchial pressure.
TL;DR: It is suggested that absent main pulmonary artery may exist with both infundibular pulmonary atresia and persistent truncus arteriosus, and total surgical repair should be associated with ligation of the SCA to avoid residual left-to-right shunt.
Abstract: A histologic study was performed on 22 specimens of pulmonary atresia with ventricular septal defect to 1) ascertain the existence of the main pulmonary artery; 2) distinguish the ductus arteriosus from the systemic collateral arteries (SCA); 3) establish the nutritive or functional nature of collateral circulation; and 4) evaluate the morphology of the distal pulmonary bed. Three cases had absent main pulmonary artery, one with and two without signs of infundibular septation. We suggest that absent main pulmonary artery may exist with both infundibular pulmonary atresia and persistent truncus arteriosus. SCAs have been found to have similar histological features as systemic muscular arteries of the same size--their medial muscular layer merges gradually into an elastic one at different depth inside the lungs. Injection of contrast material allowed us to demonstrate that these vessels are functional, since they inosculate into efficient pulmonary arteries ending in the respiratory units. When the distal pulmonary vascular bed is perfused by large SCAs, proliferative lesions like those found in large left-to-right shunts may occur. Early in infancy, banding of large, nonstenotic SCAs could protect the distal pulmonary vasculature. Moreover, total surgical repair should be associated with ligation of the SCA to avoid residual left-to-right shunt, if the pulmonary arteries can carry the full pulmonary blood flow.
TL;DR: Calculations using Alfieri and colleagues’ equation indicate that the enlargement of right pulmonary artery and left pulmonary artery was sufficient to predict significantly lower right ventricular peak pressure after intracardiac repair than would have been measured after the initial catheterization.
TL;DR: The cardiorespiratory effects of etomidate were measured in two groups of six patients with aortic or mitral valve disease and no patient complained of pain during injection, nor did myoclonic movements occur.
Abstract: The cardiorespiratory effects of etomidate were measured in two groups of six patients with aortic or mitral valve disease. The induction of anaesthesia with etomidate 0.3 mg kg−1 was followed by a second dose 10 min later. After the first dose, a 19% decrease in systemic arterial pressure was associated with a decrease in systemic vascular resistance and left ventricular heart work. Cardiac index, pulmonary artery pressure and wedge pressure all decreased slightly. Central venous pressure and heart rate did not change. A slight increase in respiratory frequency failed to prevent an increase in PaCO2. Changes after the second dose were similar. The two groups of patients did not differ significantly in their response to etomidate. No patient complained of pain during injection, nor did myoclonic movements occur.
TL;DR: To assess prevailing guidelines for the oximetric detection of intracardiac left-to-right shunts, the variability of right heart oxygen saturation step-ups in catheterisations in children with aortic and pulmonary stenosis is examined.
Abstract: To assess prevailing guidelines for the oximetric detection of intracardiac left-to-right shunts, we examined the variability of right heart oxygen saturation step-ups in 1121 catheterisations in children with aortic and pulmonary stenosis, who were studied as part of the joint study of the natural history of congenital heart defects. It is estimated that in the absence of intracardiac shunting, a step-up of more than 5i9 per cent between the superior vena cava and the pulmonary artery, 3-5 per cent between the right atrium and the pulmonary artery, and 3-6 per cent between the right ventricle and pulmonary artery, occurs 5 per cent of the time. By extrapolation from a 'normal' distribution, a step-up of 8 7 per cent between the superior vena cava and pulmonary artery, 5-6 per cent between the right atrium and pulmonary artery, and 5-2 per cent between the right ventricle and the pulmonary artery would occur 1 per cent of the time in the absence of intracardiac shunting. Assuming a normal haemoglobin concentration of 15 g/dl, the 1 per cent false positive rate corresponds to a step-up of 1'7 volumes per cent from the superior vena cava to the pulmonary artery, 141 volumes per cent from the right atrium to the pulmonary artery, and 1 0 volumes per cent from the right ventricle to the pulmonary artery. These data provide guidelines for the detection ofabnormal shunts, but other independent methods such as indicator dilution or angiography should be employed in borderline situations.
TL;DR: The outcome suggests caution in the use of this drug in such patients with primary pulmonary hypertension, and a 39-year-old woman with severe pulmonary hypertension with no apparent cause is recommended.
Abstract: Sir, After reading the report by Wang et al. in the British Heart Journal (1978, 40, 572-574), we attempted a trial of diazoxide in a patient with primary pulmonary hypertension. The outcome suggests caution in the use of this drug in such patients. A 39-year-old woman with severe pulmonary hypertension with no apparent cause had previously undergone unsuccessful trials of oxygen, nitroprusside, isoprenaline, and tolazoline during cardiac catheterisation. In August 1978 diazoxide was injected into the main pulmonary artery, and haemodynamic measurements were taken 5 minutes after each dose using the procedure described by Wang et al. (1978). The results are given in the Table.
Journal Article•
TL;DR: Experimental studies demonstrate that triglyceride elevations are capable of adversely affecting pulmonary gas exchange and mechanics, and add support to the concept that the respiratory insufficiency that is seen in acute pancreatitis could be mediated through triglyceride Elevations.
Abstract: Respiratory failure is a frequent complication of acute pancreatitis. Two clinical studies of this association have demonstrated a high incidence of concomitant hypertriglyceridemia. Experimental studies were carried out using an ex vivo, isolated, perfused, ventilated, canine pulmonary lobe to evaluate the effects of triglyceride elevations on pulmonary mechanics and gas exchange. Control lobes perfused for a four hour period remained stable. When 5g and 10g of triglyceride were added to the perfusate, the lobes became grossly edematous and hemorrhagic. Intrapulmonary shunting developed (23 and 46%), weight gain occurred (130 and 189g), effective compliance decreased, and the pressure-volume deflation curves became abnormal. Free fatty acid (FFA) levels increased markedly during the perfusion periods. When small quantities of FFA were infused directly into the pulmonary artery, similar changes, but less severe, occurred. These studies demonstrate that triglyceride elevations are capable of adversely affecting pulmonary gas exchange and mechanics. Such changes probably occur secondary to FFA release. These data thus add support to the concept that the respiratory insufficiency that is seen in acute pancreatitis could be mediated through triglyceride elevations.
TL;DR: Excerpt To the editor: The paper "Fatal Pulmonary Hemorrhage After Use of the Flow-Directed Balloon-Tipped Catheter" by Pape and associates in the March issue (1) serves to highlight the single fatal event following use of the flow-directed balloon-tipped catheter.
Abstract: Excerpt To the editor: The paper "Fatal Pulmonary Hemorrhage After Use of the Flow-Directed Balloon-Tipped Catheter" by Pape and associates in the March issue (1) serves to highlight the single mos
TL;DR: Postoperative catheterizations in eight patients showed no significant gradients in six and severe pulmonary venous obstruction in two (late deaths); more late postoperative results are required, including postoperativeCatheterization and electrophysiological studies, before the relative merits of the Senning versus the Mustard operation can be assessed.
TL;DR: RAP is the most important factor influencing conduit flow, and the absence of a valve, ventricular rhythm, and tachycardia did not significantly alter flow in this acute experimental model.