Schemating drawing showing the location of different types of ASD, the view is into an opened right atrium. HV: right ventricle; VCS: superior caval vein; VCI: inferior caval vein; 1: upper sinus venosus defect; 2: lower sinus venosus defect; 3: secundum defect; 4: defect involving coronary sinus; 5; primum defect.Ultrasound picture of the heart, seen in a subcostal view. The apex towards the right, atria to the left. ASD secundum seen as a discuntinuation of the white band of the atrial septum. Enlarged right atrium below, enlarged pulmonary veins seen entering left atrium above. (Echocardiogram: Wikipedia editor Kjetil Lenes (Ekko) )
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Atrial septal defect

Atrial septal defects (ASD) are a group of congenital heart diseases that involve the interatrial septum of the heart. The inter-atrial septum is the tissue that separates the right and left atria from each other. Without this septum, or if there is a defect in this septum, it is possible for blood to travel from the left side of the heart to the right side of the heart, or the other way around, resulting in mixing of arterial and venous blood. more...

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Since the right side of the heart contains venous blood with a low oxygen content, and the left side of the heart contains arterial blood with a high oxygen content, it is beneficial to prevent any communication between the two sides of the heart and prevent the blood from the two sides of the heart from mixing with each other.

During development of the fetus, the inter-atrial septum develops to eventually separate the left and right atria. The foramen ovale remains open during fetal development to allow blood from the venous system to bypass the lungs and go to the systemic circulation. This is because prior to birth, the oxygenation of the blood is via the placenta and not the lungs. A layer of tissue begins to cover the foramen ovale during fetal development, and will close it completely soon after birth. After birth, the pressure in the pulmonary circulation drops, and the foramen ovale closes. In approximately 30% of adults the foramen ovale does not seal over. In this case, elevation of pressure in the pulmonary circulation (ie: pulmonary hypertension due to various causes, or transiently during a cough) can cause opening of the foramen ovale. This is known as a patent foramen ovale (PFO).

Pathophysiology

In normal individuals, the chambers of the left side of the heart make up a higher pressure system than the chambers of the right side of the heart. This is because the left ventricle has to produce enough pressure to eject blood to the entire body, while the right ventricle has to produce enough pressure to eject blood to only the lungs.

In the event of an atrial septal defect, blood will flow from the left atrium to the right atrium. This is called a left-to-right shunt. This extra blood will cause a volume overload of both the right atrium and the right ventricle.

Any process that increases the pressure in the left ventricle can cause worsening of the left-to-right shunt. This includes hypertension, which increases the pressure that the left ventricle has to generate in order to open the aortic valve during ventricular systole, and coronary artery disease which increases the stiffness of the left ventricle, thereby increasing the filling pressure of the left ventricle during ventricular diastole.

The right ventricle will have to push out more blood than the left ventricle due to the left-to-right shunt. This constant overload of the right side of the heart will cause an overload of the entire pulmonary vasculature. Eventually the pulmonary vasculature will develop pulmonary hypertension to try to divert the extra blood volume away from the lungs.

The pulmonary hypertension will cause the right ventricle to face increased afterload in addition to the increased preload that the shunted blood from the left atrium to the right atrium caused. The right ventricle will be forced to generate higher pressures to try to overcome the pulmonary hypertension. This may lead to right ventricular failure (dilatation and decreased systolic function of the right ventricle) or elevations of the right sided pressures to levels greater than the left sided pressures.

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Partial Pressure of Oxygen Is Lower in the Left Upper Pulmonary Vein Than in the Right in Adults With Atrial Septal Defect - )
From CHEST, 3/1/99 by Kanji Iga

Difference in [PO.sub.2] Between the Right and Left Pulmonary Veins

Background: The right-to-left shunt at the atrial level is responsible for arterial hypoxemia in patients with atrial septal defect.

Objectives: This study investigated the mechanism of arterial hypoxemia in patients with atrial septal defect by measuring the [PO.sub.2] in both the right and left upper pulmonary veins. Subjects and method: We prospectively measured the [PO.sub.2] in the femoral artery and the right and left upper pulmonary veins during cardiac catheterization in 13 adults (median age, 53 years) and 7 children (median age, 7 years) with secundum atrial septal defect. The adults and children were studied consecutively. Contrast echocardiography was performed to evaluate right-to-left shunt in all adults.

Results: Among the children, there were no patients showing arterial hypoxemia, and there was no difference in the [PO.sub.2] ([+ or -] SD) between the right and left upper pulmonary veins (right, 100 [+ or -] 3.8 mm Hg vs left, 100 [+ or -] 7.8 mm Hg; p = 0.92). However, arterial hypoxemia was present in 11 of the 13 adult patients, although contrast echocardiography showed more than a moderate degree of right-to-left shunt in only four adults. The [PO.sub.2] was lower in the left upper pulmonary vein than it was in the right upper pulmonary vein in all adult patients (right, 91.6 [+ or -] 13.8 mm Hg vs left, 73.0 [+ or -] 11.5 mm Hg; p [is less than] 0.0001).

Conclusion: The [PO.sub.2] was lower in the left upper pulmonary vein than it was in the right upper pulmonary vein in adults with atrial septal defect. Care must be taken in measuring pulmonary blood flow if the [PO.sub.2] in the left upper pulmonary vein is low enough to influence oxygen content. The decreased [PO.sub.2] in the left upper pulmonary vein may contribute to arterial hypoxemia in addition to right-to-left shunt at the atrial level in adults with atrial septal defect.

(CHEST 1999; 115:679-683)

Key words: atrial septal defect; intracardiac shunt; [PO.sub.2]; pulmonary vein

Abbreviations: ASD = atrial septal defect; VC = vital capacity; V/Q = ventilation/perfusion ratio

Right-to-left shunt at the atrial level is responsible for decreased saturation of arterial blood in patients with patent foramen ovale and increased venous pressure[1,2] or in patients with large atrial septal defect (ASD) and severe tricuspid regurgitation.[3] In either situation, there is an assumption that saturation of the right and left pulmonary veins is equally high if arterial hypoxemia is caused only by this reverse shunt. To our knowledge, there has been no report of a comparison between the right and left pulmonary veins regarding [PO.sub.2].

In the present study, we investigated whether [PO.sub.2] is equal in the right and left upper pulmonary veins in both adults and children with ASD in order to look for a cause of arterial hypoxemia that is other than the right-to-left shunt.

MATERIALS AND METHODS

Subjects consisted of 13 adults (median age, 53 years; range, 40 to 78 years) and 7 children (median age, 7 years; range, 5 to 13 years) with secundum ASD. The adults and children were studied consecutively. Using an NIH catheter, cardiac catheterization was performed from the femoral approach in all patients. The catheters were easily advanced into the right and left upper pulmonary veins through the ASD. These upper pulmonary veins were identified as right or left when the catheter was superior to the cardiac silhouette and rightward and leftward, respectively. Blood was drawn from both the right and left upper pulmonary veins as well as from other cardiac chambers before the injection of contrast medium: 5 mL of blood in adults and 2 mL in children. Because an NIH catheter has six side holes about 2 cm proximal to the closed end, we were very careful about keeping the sampling position in the pulmonary veins at a distance from the cardiac silhouette such that it would not be contaminated by blood from the left atrium. If the hemoglobin concentration of any blood sample differed [is greater than] 0.3 g/dL from other blood samples, it was discarded as a sampling error. [PO.sub.2] and [PCO.sub.2] were measured (Chiron 288 blood gas system; Chiron Diagnostics Corp; Medfield, MA), and the oxygen content was then calculated mathematically.

Using hand-agitated 5% dextrose in water from an antecubital vein, contrast echocardiography was done during normal breathing in all adults (Table 1). We used the transesophageal technique in 11 adult patients to confirm whether the right-to-left shunt was directed toward the left upper pulmonary vein. The degree of right-to-left shunt on contrast echocardiography was classified as follows: severe if the bubble was seen entirely in the left atrium; mild if the bubble was slightly in the left atrium; and moderate if in between. Ventilatory function tests were done in all adult patients except for one, and pulmonary ventilation by [sup.13]Xe gas and perfusion scan by [sup.99m]Tc macroaggregated albumin were done in 10 adult patients. Statistical analysis was done using Student's paired t test. None of the patients had a history of thoracotomy.

(*) M = male; F = female; Af = atrial fibrillation; SR = sinus rhythm; CTR = cardiothoracic ratio; R-Shunt = right-to-left shunt; - = none; 1+ = mild; 2+ = moderate; 3+ = severe; TR = tricuspid regurgitation; Qp = pulmonary flow using the right upper pulmonary vein as a reference chamber; Qs = systemic flow; PAR = pulmonary arterior resistance; Scinti = V/Q scan of the lung; m = V/Q mismatch; n = normal; (-) = not done; % VC = percent vital capacity; Rt PV = right pulmonary vein; Lt PV = left pulmonary vein; FA = femoral artery.

RESULTS

In the children, there was no arterial hypoxemia and no difference in [PO.sub.2] ([+ or -] SD) between the right and left upper pulmonary veins (right, 100 [+ or -] 3.8 mm Hg vs left, 100 [+ or -] 7.8 mm Hg; p = 0.92; Fig 1). In the adults, arterial hypoxemia was present in 11 patients, if arterial [PO.sub.2] [is greater than] 80 mm Hg is considered normal, and [PO.sub.2] ([+ or -] SD) was lower in the left upper pulmonary vein than in the right upper pulmonary vein (right, 91.6 [+ or -] 13.8 mm Hg vs left, 73.0 [+ or -] 11.5 mm Hg; p [is less than] 0.0001; Fig 2). The [PCO.sub.2] in the left upper pulmonary vein was statistically greater than that of the right upper pulmonary vein (right, 37.4 [+ or -] 5.4 mm Hg vs left, 39.4 [+ or -] 6.7 mm Hg; p = 0.03; Fig 3). The difference in oxygen content between the right and left upper pulmonary veins ranged from 2 to 34 mL/L, with the difference being [is greater than] 5 mL/L in 11 adult patients (Fig 4). The pulmonary blood flow in patient 1 was measured as 4.1 L/min when only the oxygen content of the right pulmonary upper vein was used, whereas it was measured as 8.3 L/min when the averages of both the fight and left upper pulmonary veins were used. Contrast echocardiography showed that the right-to-left shunt was mild in eight adult patients and that there was no shunt in one patient. During contrast transesophageal echocardiography, no bubble was seen in the left upper pulmonary veins of all 11 adult patients. In two adult patients who had severe reverse right-to-left shunt, acquired cyanosis was seen, and severe tricuspid regurgitation and atrial fibrillation were observed to be present (patients 1 and 4). The mean cardiothoracic ratio was 62%. Both the [FEV.sub.1]/FVC ratio and the percent vital capacity (VC) were normal in five adult patients, and either the [FEV.sub.1]/VC ratio or the percent VC was abnormal in seven adult patients (Fig 5). Five adult patients showed decreased perfusion in the left lung, and one adult patient showed decreased perfusion in the fight lung. A ventilation/perfusion (V/Q) mismatch was present in the left lung in four adult patients (patients 1, 2, 4, and 12) and in the fight lung in one adult patient (patient 3). There was one adult patient whose perfusion and ventilation were equally disturbed with no V/Q mismatch (patient 9).

[Figures 1-5 ILLUSTRATION OMITTED]

DISCUSSION

Patients with ASD may become cyanotic with increasing age. This is caused by a reverse shunt through the defect, which is caused by progressive tricuspid regurgitation, which, in turn, is due to pulmonary hypertension. A jet originating from tricuspid regurgitation can cross the ASD, resulting in a right-to-left shunt.[3]

Performing contrast echocardiography by using hand-agitated 5% dextrose in water from peripheral veins, is the most sensitive method for looking for the reverse shunt. We performed contrast echocardiography under normal breathing so as not to enlarge the reverse shunt by straining. In the present study, although the degree of right-to-left shunt was more than moderate in only 4 of the 13 adult patients, arterial hypoxemia was present in 11 adult patients, if arterial [PO.sub.2] of more than 80 mm Hg is considered normal. Therefore, the degree of arterial hypoxemia seen in the adult group cannot be completely explained by this reverse shunt.

[PO.sub.2] was lower in the left upper pulmonary vein than in the right pulmonary vein in all of the adult patients, but there was no difference between the fight and left pulmonary veins in the children. Therefore, this difference is not congenital but acquired. It is not clear whether this is specific to adult ASD patients, because drawing blood from both pulmonary veins is possible only in the presence of ASD or patent foramen ovale. Hypoxemia in the left upper pulmonary vein significantly contributed to arterial hypoxemia in the adult group, because the difference in oxygen saturation between the fight and left upper pulmonary veins may derive from the right-to-left shunt being directed to the left upper pulmonary vein. However, because the transesophageal contrast echocardiography, which can visualize the left upper pulmonary vein easily and was performed in 11 of the 13 adult patients, did not show any bubble toward the left upper pulmonary vein during right-to-left shunting in any patient, this possibility is unlikely.

As patients with ASD age, the main pulmonary artery may enlarge and compress the left bronchus, which is progressing pulmonary vascular disease. Pulmonary vascular resistance was [is greater than] 4 Wood units in 5 of the 13 adult patients. In addition, the increase in heart volume of the left thoracic cavity may collapse that part of the lung, resulting in V/Q mismatch. V/Q mismatch was present in 5 of the 10 adult patients undergoing the pulmonary V/Q scan: in the left lung in four patients, and in the fight lung in one patient.

The result of ventilatory function tests in the present study showed that either [FEV.sub.1]/FVC or percentage of VC was abnormal in seven patients, reflecting the above speculation. Hypoxemia in the left upper pulmonary vein was present even in the remaining five patients with normal pulmonary function tests whose cardiothoracic ratio was rather small in comparison with that of patients with abnormal pulmonary function tests. Accordingly, the difference in [PO.sub.2] between the fight and left pulmonary veins cannot be completely explained by this mismatch.

During cardiopulmonary bypass, some blood returns to the left atrium while the aorta is cross-clamped.[4] An abundant network of collaterals has been observed between the bronchial vein and the pulmonary vein in normal lungs obtained at autopsy.[5] In patients with inflammatory pleuritis, neovascularization can develop from the internal thoracic artery and intercostal arteries and drain into pulmonary veins.[6] Pulmonary veins are also reported as a draining chamber for collaterals derived from portal hypertension.[7,8] Most of the collaterals reported so far were located in the left pulmonary vein.[9] In the present study, the pulmonary scintigram showed hypoperfusion of the left lung in 5 of the 10 adult patients undergoing pulmonary ventilation and the perfusion scan. This decreased pulmonary blood flow in the left lung may change bronchial circulation after an increase in pulmonary blood flow for a long period of time. The deoxygenated blood, after passing through the capillary phase from the bronchial artery or intercostal artery, might drain into the left pulmonary vein more often than into the fight vein.

The difference in [PO.sub.2] between the right and left upper pulmonary veins caused the difference in the calculation of oxygen content to range from 3 to 34 mL. This difference in oxygen content was sometimes severe enough to influence the measurement of pulmonary blood flow but was often insignificant because the relationship between [PO.sub.2] and saturation is not linear but sigmoid. When the shunt ratio is measured using oximetry in patients with ASD, blood drawn from either pulmonary vein is used as a reference.[10] This is based on the assumption that the oxygen contents in the right and left pulmonary veins are equal. In the first patient who had severely disturbed pulmonary function, presumably due to increased heart volume and combined pulmonary vascular disease, the calculated pulmonary blood flow was two times greater when the average of the fight and left upper pulmonary veins was used as a reference than when only the fight upper pulmonary vein was used. The use of average oxygen contents is also based on the assumption that both the fight and left pulmonary flows are equal, which was not proved to be correct.

Care must be taken in measuring an intracardiac shunt in patients with ASD if only the fight upper pulmonary vein is used as a reference. In addition to right-to-left shunt at the atrial level, decreased [PO.sub.2] in the left upper pulmonary vein may contribute to decreased arterial [PO.sub.2].

Study Limitations

We did not offer a very clear explanation as to the cause of this difference; we simply described the phenomenon. Even during thoracic surgery, it is impossible to take blood samples from both pulmonary veins simultaneously when the fraction of inspired oxygen is 20% of the blood. Further study is necessary but can be done only in the presence of an ASD or patent foramen ovale.

ACKNOWLEDGMENT: We acknowledge the helpful advice and comment of Professor Peter Harris, formerly of the Royal Brompton and National Heart Hospital, London, England.

REFERENCES

[1] Remy-Jardin M, Remy J, Wallaert B. Right-to-left shunting through a patent foramen ovale without pulmonary hypertension. Chest 1990; 97:1250-1252

[2] Dear WE, Chen P, Barasch E. Sixty-eight-year-old woman with intermittent hypoxemia. Circulation 1995; 91:2284-2289

[3] Kai H, Koyanagi S, Hirooka Y, et al. Right-to-left shunt across atrial septal defect related to tricuspid regurgitation: assessment by transesophageal Doppler echocardiography. Am Heart J 1994; 127:578-584

[4] Baile EM, Ling H, Heyworth JR, et al. Bronchopulmonary anastomotic and noncoronary collateral blood flow in humans during cardiopulmonary bypass. Chest 1985; 87:749-754

[5] Murata K, Itoh H, Todo G, et al. Bronchial venous plexus and its communication with pulmonary circulation. Invest Radiol 1986; 21:24-30

[6] Chino M, Kawaguchi T, Sakai T, et al. Intercostal-to-pulmonary arterial anastomosis, complicated by high-output heart failure: case report. Angiology 1991; 42:256-260

[7] Sano A, Kuroda Y, Moriyasu F, et al. Porto-pulmonary venous anastomosis in portal hypertension demonstrated by percutaneous transhepatic cine-portography. Radiology 1982; 144: 479-484

[8] Sano A, Nishizawa S, Sasai K, et al. Contrast echocardiography in detection of portopulmonary venous anastomosis. Am J Roentgenol 1984; 142:137-140

[9] Sano A, Nishizawa S, Sasai K, et al. Demonstration of porto-pulmonary venous anastomosis by cine-portography and contrast echocardiography [in Japanese]. Nihonrinshougazouigakuzasshi 1983; 2:402-412

[10] Grossman W, Baim DS. Cardiac catheterization, angiography, and intervention. 4th ed. Philadelphia, PA: Lea & Febiger, 1991; 166

(*) From the Department of Cardiology (Drs. Iga, Izumi, Kitaguchi, Himura, Gen, and Konishi), and the Department of Pediatrics (Dr. Matsumura), Tenri Hospital, Tenri City, Japan.

Manuscript received June 6, 1998; revision accepted October 13, 1998.

Correspondence to: Takashi Konishi MD, Department of Cardiology, Tenri Hospital, 200 Mishimacho, Tenri City, 632-8552 Japan; e-mail: igakan@kcn.ne.jp

COPYRIGHT 1999 American College of Chest Physicians
COPYRIGHT 2000 Gale Group

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