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The lungs of eight newborn infants who had died from pulmonary atresia were studied by quantitative morphometric techniques. It was established for the first time that the abnormal pattern of blood flow through the heart and great vessels in a fetus with pulmonary atresia is associated with impaired lung development as shown by arteries that are too few, too small, and with an abnormally thin muscle coat, although the distribution of muscle along the arterial pathway is normal. Differences between the cases in the degree of impairment of lung development could be detected and related to the degree of reduction in pressure and flow before birth in the individual case. Although blood flow through the pulmonary circulation is small before birth lung development seems sensitive to any further reduction.
Quantitative morphometric techniques have been applied to the injected and inflated lung and to the heart in 9 infants with total anomalous pulmonary venous return dying with obstruction to pulmonary venous return. In 5 (mean age at death 55 days) pge 20 days) to an infradiaphragmatic site. Structural changes were present in the pulmonary circulation in all patients, even in the youngest, an 8-day-old child. In both types of total anomalous pulmonary venous return increased arterial muscularity was severe, as shown by increase in wall thickness and by extension of muscle into smaller and more peripheral arteries than normal; these changes tended to increase with age. Where the pulmonary venous blood drained to a supradiaphragmatic site, the severity of arterial medial hypertrophy correlated inversely with the magnitude of the pulmonary: systemic flow ratio, increasing as the pulmonary blood flow fell. Vein wall thickness was increased and in all but the youngest child the veins were 'arterialised'. At the lung periphery the arteries and alveoli appeared to have multiplied normally. Arterial size varied according to whether pulmonary venous blood drained above or below the diaphragm; the diameter of pre- and intra-acinar arteries was increased only in cases where the pulmonary venous return drained to a supradiaphragmatic site, being normal when it drained to an infradiaphragmatic site. In the heart the left ventricle was of normal size in all but one case. Dilation and severe hypertrophy of the right ventricle and septum were present only in cases of drainage to a supradiaphragmatic site. In the older patients with the latter anomaly dilation of the pulmonary arteries and right ventricle suggested that a large left-to-right shunt had preceded the onset of obstruction to pulmonary venous return and that the more severe right ventricular and septal hypertrophy in these cases might be the result of a longer duration of pulmonary hypertension. In contrast, in total anomalous pulmonary venous return to an infradiaphragmatic site it appears that obstruction to pulmonary venous return develops soon after birth and prevents a large increase in pulmonary blood flow, and thus neither the pulmonary arteries nor the right ventricle become dilated. In infants with total anomalous pulmonary venous return and obstruction to pulmonary venous return, it is striking how rapidly the pulmonary circulation develops new muscle.
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BACKGROUND: A high incidence of pulmonary arteriovenous malformations (PAVMs) has been reported in patients who have polysplenia and congenital heart disease after superior cavopulmonary anastomosis. Interruption of hepatic venous return to the pulmonary circulation is believed to potentiate the development of PAVMs. Surgical inclusion of hepatic flow in the pulmonary circulation may result in their resolution. METHODS: We reviewed 3 patients with congenital heart disease and polysplenia in whom PAVMs developed and who had subsequent hepatic vein inclusion in the pulmonary circulation. RESULTS: Patients underwent superior cavopulmonary connection at a median age of 8 months. The PAVMs were diagnosed at a median duration of 8 months after operation (arterial saturation <75% in room air). Hepatic venous flow was included in the pulmonary circulation at operation. Resolution of PAVMs occurred at a median duration of 7 months after operation (arterial saturation >90% in room air). CONCLUSIONS: Surgical inclusion of hepatic venous blood in the pulmonary circulation results in the resolution of PAVMs. Electively associating the hepatic veins with the pulmonary vasculature may prevent the development of PAVMs in patients who are at risk.
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We investigated the pulmonary vascular effects of E4021, a potent inhibitor of cGMP-specific phosphodiesterase, in control late-gestation fetal lambs, and in newborn lambs with persistent pulmonary hypertension (PPHN) after prenatal ligation of the ductus arteriosus. E4021 alone significantly relaxed fifth-generation pulmonary arteries isolated from control fetal lambs, an effect completely blocked after inhibition of nitric oxide synthase (NOS). In contrast, E4021 did not relax pulmonary arteries isolated from hypertensive lambs. Pretreatment with E4021 (10(-7) M) significantly enhanced relaxations to the NO donor S-nitrosyl-acetyl-penicilamine (SNAP) in arteries from both control and hypertensive lambs. In control, fully instrumented fetal lambs, infusions of E4021 (31 microgram/min) selectively dilated the pulmonary circulation, an effect again blocked after inhibition of NO synthase. Further studies were performed in newborn lambs with PPHN to study the vascular effects of E4021 alone, and in combination with inhaled NO. E4021 alone (1 to 100 microgram/kg/min) decreased pulmonary artery pressure (Ppa) in a dose-dependent fashion, and had minimal effect on systemic pressure. At the highest dose (100 microgram/kg/min), the dilation was selective for the pulmonary circulation. In subsequent protocols, E4021 (10 microgram/kg/min) significantly decreased Ppa and pulmonary vascular resistance (PVR), but these pulmonary vascular effects were not enhanced after NO inhalation at 0.5 or 5 ppm. We speculate that the lack of enhancement was due to the dramatic effects of E4021 alone. Potent, specific phosphodiesterase inhibitors such as E4021 may prove to be useful in the treatment of PPHN.
Although it is well known that the pulmonary circulation is altered in patients with pulmonary arterial or venous hypertension, the resultant hemodynamic behavior has not been systematically studied. We undertook to do so in a group of patients with pulmonary hypertension of diverse etiology. We measured pulmonary arterial (PAP) and occlusive wedge pressures and cardiac output at rest (i.e., standing) and during progressive upright treadmill exercise in 51 patients. Forty-two had chronic, stable, cardiac failure secondary to ischemic, myopathic or valvular heart disease and were grouped according to whether their mean PAP was less than (normotensive) or greater than (hypertensive) 19 mm Hg, and nine had pulmonary vascular disease of diverse etiology and were considered separately. In the majority of patients, we found that irrespective of whether the hypertension was arterial or venous in origin or etiology: the mean PAP-flow relationship was linear; pulmonary capillary wedge pressure was greater than or equal to the average closure pressure of the pulmonary vascular bed and could therefore be used as the downstream pressure in calculating pulmonary vascular resistance; and pulmonary vascular resistance declined with exercise. Notable exceptions to the third observation were patients with valvular heart disease or a resting pulmonary vascular resistance greater than 800 dyne-sec-cm-5.
PURPOSE OF REVIEW: Disorders of the pulmonary circulation might develop as a primary disease process of the pulmonary vascular bed or, more often, as the acute or chronic consequence of pulmonary or cardiac pathologies. For the anaesthesiologist and intensivist it is particularly interesting to gain insight into the regulation of the pulmonary circulation since pulmonary hypertension and concomitant right heart failure contribute to high perioperative mortality rates in patients at risk, especially after cardiac surgery. Therefore, modulation of the pulmonary circulation may be a life-saving therapy in patients suffering from acute or chronic pulmonary circulatory disorders. Furthermore, routinely performed intra-operative interventions such as the use of volatile anaesthetics or cardiopulmonary bypass systems may have relevant side effects on the pulmonary circulation. RECENT FINDINGS: This review focuses on new insights into the modulation of pulmonary circulation during general anaesthesia with volatile anaesthetics and anaesthesiological management during cardiopulmonary surgery. Recent publications in the field of cardiopulmonary bypass surgery, one-lung ventilation and heart and lung transplantation are discussed. Furthermore, the role of conventional and experimental therapeutic strategies to modulate pulmonary circulation in intensive care medicine is reviewed. SUMMARY: Despite the performance of a large number of clinical and experimental studies, the pathophysiology of pulmonary circulatory disorders is not completely understood. Therefore, any new therapy has to be carefully evaluated as a therapeutic option. Several formerly experimental therapeutic interventions such as inhaled vasodilators, however, appear to have found their way into clinical practice for selected indications.
OBJECTIVE: To identify the types of pulmonary vascular blood supply in tetralogy of Fallot with pulmonary atresia by use of hemodynamic study. METHODS: Fifty-six patients with tetralogy of Fallot and pulmonary atresia, and ages ranging from 20 days to 4 years, underwent cineangiocardiographic study with contrast medium injections in the following vascular structures: 1) wedged pulmonary vein; 2) aortopulmonary collaterals; 3) thoracic aorta; and 4) ductus arteriosus or systemic-pulmonary shunt. RESULTS: In the 56 patients studied, pulmonary blood was supplied as follows: in 15, by aortopulmonary collaterals; in 36, only by the ductus arteriosus; and in 5, by the ductus arteriosus and aortopulmonary collaterals. The patients were classified into 6 types depending on the type of pulmonary vascular perfusion and the presence or absence of vascular structures that compose the pulmonary circulation in tetralogy of Fallot with pulmonary atresia. CONCLUSION: This type of approach enables the obtainment of information necessary for the correct clinicosurgical management of patients, due to the great complexity and extreme variability of the pulmonary blood supply in tetralogy of Fallot with pulmonary atresia.
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In vivo haemodynamic responses to human urotensin-II were determined in two models of pulmonary hypertension: rabbits with left ventricular dysfunction following coronary artery ligation and the hypoxic rat. Effects were also examined in the presence of the nitric oxide synthase inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME). Human urotensin-II increased pulmonary arterial pressure to a greater extent in ligated rabbits than their controls and L-NAME increased pulmonary pressure without significantly affecting these responses to human urotensin-II. Human urotensin-II raised right ventricular pressure slightly in control rats but not in hypoxic rats. Human urotensin-II did not constrict control rat isolated small pulmonary arteries and only induced a small constriction of these vessels in hypoxic rats. In conclusion, exogenous human urotensin-II exerts pulmonary pressor responses in vivo in rabbits and also induced small pulmonary pressor responses in control rats. Pulmonary pressor responses to urotensin-II were increased by pulmonary hypertension in rabbits but not in rats.
To determine the safety of the ultrasound contrast agent Albunex, its influence on right and left heart haemodynamics in patients with pulmonary artery hypertension or left heart failure was assessed after intravenous injection. Patients with a left ventricular ejection fraction smaller than 40% or a systolic pulmonary artery pressure greater than 40 mmHg received 0.08 and 0.22 ml.kg-1 Albunex and 10 ml albumin in random order during right heart catheterization and transthoracic echocardiography. Right atrial, systolic and diastolic pulmonary artery and capillary wedge pressures were measured at 3 min and 5 min and cardiac output at 5 min after the intravenous injection of Albunex and control. The mean differences of pre- and postinjection values and their confidence intervals were tabulated and significance was anticipated if the confidence interval did not include 0. Significant changes to pre-injection values could be observed in diastolic pulmonary artery pressure 5 min after the injection of albumin and 0.08 ml.kg-1 Albunex, and in right atrial pressure 5 min after the injection of 0.22 ml.kg-1 Albunex only. Since intermediate opacification of the left ventricle was seen in only four patients with 0.22 ml.kg-1 Albunex, in the patients studied higher doses of Albunex and their safety need to be assessed.
To assess the effects of endothelin 1 (ET) on the pulmonary and systemic vascular beds simultaneously, we examined the hemodynamic responses to ET in awake calves implanted with a Jarvik total artificial heart (TAH), a device that maintains constant cardiac output (CO). During basal conditions, successive incremental intravenous (i.v.) injections of 1, 3, and 10 micrograms ET caused a dose-dependent decrease in pulmonary arterial pressure (PAP), (from 24 +/- 3 to 15 +/- 1 mm Hg, p less than 0.05) while having no effect on systemic arterial (SAP), left atrial (LAP), and right atrial (RAP) pressures. Administration of 30 micrograms ET i.v. also decreased PAP, had no effect on LAP and RAP, but increased SAP from 100 +/- 6 to 118 +/- 4 mm Hg (p less than 0.05). The decrease in PAP was rapid, occurring within seconds and lasting 10 min, whereas the increase in SAP occurred after 2-5 min and was prolonged for greater than or equal to 20 min. As compared with injection in the right atrium, administration of 30 micrograms ET into the left atrium reduced PAP to a similar extent, but induced a greater increase in SAP (+32.5 +/- 4 vs +17.5 +/- 2 mm Hg, p less than 0.05). ET also dose-dependently reversed the acute pulmonary vasoconstriction induced by inhalation of an hypoxic gas mixture. In all cases, pulmonary vasodilation occurred without evidence of short-term tolerance. The results demonstrate that ET is a potent in vivo pulmonary vasodilator. In calves, the predominant hemodynamic response to ET is pulmonary vasodilation, with systemic vasoconstriction apparent only at higher concentrations of the peptide.