Systemic to Pulmonary Bronchial Blood Flow in Mitral Stenosis*

Systemic to Pulmonary Bronchial Blood Flow in Mitral Stenosis· Piergiuseppe Agostoni, M.D., F.C.C.R; Marco Agrifoglio, M.D.; Vincenzo Arena, M.D.; Elisabetta Doria, M.D.; Andrea Sala, M.D.; and Giuseppe Susini, M. D.

We measured systemic to pulmonary bronchial blood 80w [Qbr(s-p)] during total cardiopulmonary bypass in 15 patients with mitral stenosis and elevated pulmonary venous pressure (group A, mean pulmonary wedge pressure 22.2*5.4 mm Bg, mean ± SD) and in 15 patients with coronary artery diseases and DOrmai pulmonary venous pressure (group B). Qbr(s-p) is the volume of blood accumulating in the left side of the heart in the absence of pulmonary and coronary BoWs. This blood was vented through a cannula introduced into the left atrium and measured. Qbr(s-p) was 76.3 ± 13.9 mllmiP (2.18 ± 0.37 percent of extracorporeal circulation pump 80w) and 22.3±2.1 (0.63±0.15) in group A ~ B, respectively

(p
Bronchial blood How to the lung is approximately 1 percent ofcardiac output. 1 Because the bronchial blood for the greatest part is drained into the pulmonary circulation, an acu~e increase of pulmonary venous pressure may lead to a significant reduction of bronchial blood Ho~ and even to the appearance of a reverse How from the pulmonary to the systemic circulation.2-4 It is unknown whether chronic elevation of pulmonary venous pressure inHu~nces bronchial blood Ho~ Most chronic lung diseases increase the bronchial circulation, i~cluding pulmonary tuberculosis,I,5 chronic bronchitis, 1 lung fibrosis, 6 and chronic pulmonary artery obstruction. I,7 In such circumstances, the increase of bronchial blood How is associated with the formation of new vessels. 6,8 Pulmonary venous pressure is often chronically elevated in patients with mitral stenosis referred for mitral valve replacement. In humans systemic to pulmonary bronchial blood How [Qbr(s-p)], ie, the portion of bronchial blood How that drains into the pulmonary circulation, can only be measured during total cardiopulmonary bypass when pulmonary and coronary Hows are absent. 9 ,lo In such condition, Qbr(s-p) is the blood returning to the left side of the heart. In this stud~ we measured the Qbr(s-p) in patients with mitral stenosis and elevated pulmonary

venous pressQre while undergoing mitral valve replacement. For comparison, we measured Qbr(s-p) in patients with coronary artery diseases with normal pulmonary venous pressure while undergoing coronary artery surger~

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*From the Istituto di Cardiol~, Istituto di Ricerche Cardiovascolari CCG. Sisini," Centro di Studio ~r Ie Ricerche Cardiovascolari del CNR, UniversitA di Milano, anCl Cattedra di Cardiochirurgia, UniversitA di Milano, Unitl di Anestesia e Rianimazione, Fondazione ccl. Monzino," Milan, Ital~ Manuscript received June 18; revision accepted August 27.

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(Cheat 1991; 99:64!-4S)

=

Qbr(s-p) systemic to pulmonary bronchial blood Bow; ZF zeroBow .

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MATERIAL AND METHODS

Thirty patients participated in the study. None had asthma, congenital cardiac malformations, or had had previous heart surgery. Fifteen patients (group A) had mitral stenosis due to rheumatic heart disease and elevated pulmonary venous pressure at preoperative evaluation (mean pulmonary artery wedge pressure <12 mm

Table I-Group A: Mitral StenoBia* Patient/Age, yr/Sex lI53IF 2/74/F 3'55IF 4/49/F 5167/F 61401F 71601F

8I5OIF

9/72/F 10168IF 111WF 12/55/F 13160/F 14/64/F 15168IF Mean±SD60±9

*s = smoker;

Smoldng S NS NS NS ES NS NS NS NS NS NS S NS S ES

Ppa, mmHg

Ppavv, mmHg

CO, mVmin

33 36 29 24 30 30 33 52 28 30 22 45

22 24 26 18 18 ~ 20 36 19 20 13 23 28 22 20 22±5

3,300 2,850 4,880 2,850 4,050 3,980 2,980 3,070 2,950 3,010 4,120 4,115 3,180 3,340 4,060 3,520 ± 625

40

28 29 33±8

NS::;: nonsmoker; ES = exsmoker smoking at least 5 years before); Ppa = mean pressure; Ppaw = mean pulmonary artery CO::;: cardiac output. Hemodynamic data from eterization.

(patient who quit pulmonary artery wedge pressure; preoperative cath-

Bronchial Blood Flow in Mitral Stenosis (Agostonl et aI)

Table 2-Group B: Coronary Artery Diseases· Patient!Age, yr/Sex lI55IM 2/701F 3I58/F 415l/M 51641M 6141/M 7/58/F 8/52/F 9/701M lonOlF 1l/64/M 1~

13161/F 14164IF 1517O/M Mean±SD 6O±8

Smoking S NS NS NS ES NS NS NS NS NS NS S NS S ES

Ppa, mmHg 12 11 8 13 19 16 15 15 18 20 19 19 12 15 13 15±3

mmHg

8

8 9 4 10 10 4 5 7±2

during Total Cardiopulmonary ByptUUl·

CO, mVmin

ppa~

9 7 5 9 10 6 5

Table 3-Hemodynamic Parameters and Temperatures

7,630 4,570 3,180 6,510 5,160 8,180 6,525 6,035 4,920 5,310 7,010 4,850 4,400 5,010 6,810 5,740± 1,350

B~ mm Hg P airways, cm H 20 CO, mVmin T esophagous, °C T rectum, °C

90 (mllrrin)

72±17 2.0±2.1 3510±445 27.8± 1.1 30.5± 1.5

70± 12 2.2±2.3

Data are reported as mean ± SD. Differences between data from group A and B were assessed by unpaired t test.

6

• •• ••• • •

br(s-p)

3 (..CO)

FIGURE; 1. Systemic to pulmonary bronchial blood 80w [Qbr(s-p») in group A (mitral stenosis and elevated pulmonary venous pressure) and in group B (coronary artery disease and normal venous pressure). Left panel: Qbr(s-p) i~ reported as absolute 80w (mVmin). Right panel: Qbr(s-p) is reported as a percentage of cardiac output (percent CO = percent extracorporeal circulation pump flow). Asterisk = p
•

•

•

• •

I

~

• 50

27.1 ± 1.1 29.6± 1.9

Statistical Analysis

~

70

2480 ± 632

left atrium was open to atmosphere, left atrial pressure was atmospheric. In group B (coronary artery surgery), the left atrial cannula was introduced into the right superior pulmonary vein and advanced into the lowermost portion of the left atrium. In ~roup B, a second small cannula (8 F) was introduced a~ain into the ri~ht superior pulmonary vein and advanced into the left atrium. This cannula was open to atmosphere so that left atrial pressure was atmospheric. In both groups a roller pump propelled bronchial blood from the left atrial cannula to a calibrated cylinder. The calibrated cylinder was connected throu~ a stopcock to the cardiotomy reservoir. Cardioplegic solution (1,000 ml) was used to cool and to arrest the heart. During total cardiopulmonary hypass, the lungs were kept inflated by a constant Row of ~ (2 to 8 Umin, 50 percent O~h 50 percent air) with an airway pressure rangin~ between 2 and 5 cm H 20. Inspired gases were fully humidified with inspired gas temperature of 24°C. We <:ontinuously rec..'orded alveolar and systemic blood pressures, extracorporeal circulation pump flow (cardiac output), and esophageal and rectal temperahlres. Qbr(s-p) was collected continuously during total cardiopulmonary bypass. However, during the first 10 minutes, Qhr(s-p) measurements were discarded because both the cardioplegic solution was mixed into the left atrium with Qbr(s-p) and the patient's hody temperature was unstable. Durinf,t the patient's rewarminf,t, Qbr(s-p) measurements were interrupted when either rectal or esophageal temperature increased from the lowest achieved by 2°C.

Hg, Table 1). Fifteen patients (group B) had coronary artery disease with normal pulmonary venous pressure and were matched with group A for age and smoking habit (Table 2). Patients were studied while undergoing mitral valve replacement (group A) and coronary artery surgery (group B). Group A patients were enrolled in the study consecutively; group B patients were selected from a population of 211 subjects who underwent coronary artery surgery at our Institute between January 8, 1990, and May 31, 1990. All patients provided written informed consent to both the surgical intervention and the experimental procedure. The study was approved by the local ethics committee. Total cardiopulmonary bypass was achieved using a standard technique. A two-stage venous cannula (William Harvey extracorporeal cannula, 34 to 46 F Bard) was introduced into the inferior vena cava and advanced into the right atrium. Blood Rowed from the venous cannula to an Ot-heat exchanger (Oxy 41, Sorin), to the cardiopulmonary bypass pump (HLI0, Cambro), and to the aortic cannula (21-24 F). Both aorta (proximally to the aortic cannula) and pulmonary artery were clamped. Bronchial blood arriving into the left atrium was vented through 18 F cannula. In group A (mitral valve replacement), the left atrium was open and the cannula was positioned into the lowermost portion of the left atrium. Since the br(s-p)

Group B

*Data are mean±SD. BP=mean blood pressure; P=pressure; CO = cardiac output (extracorporeal circulation pump Row); T = temperature.

*Abbreviations: see Table 1.

6

Group A

2

•

· I

•

•

• • .....

• ••••••• •• • * •••

30

10

A

B

••• I

---A--

A

*

B

CHEST I 99 131 MARCH, 1991

643

experimentally Qbr(s-p) stops at a lower pulmonary venous pressure. 4 The dotted lines represent possible Qbr(s-p)/pulmonary wedge pressure relationships in such a condition.

Qbr(s-p)

+80 mllmin

+40

DISCUSSION

-40 -80

o

20

Ppaw

40

mmHg

FIGURE 2. Systemic to pulmonary bronchial blood Row [Qbr(s-p)] vs mean pulmonary artery wedge pressure (Ppaw). This relationship was plotted to obtain an estimate of Qbr{s-p) during nonnal circulatory C<]ndition. Triangles = group A; circles = group B. Solid line = Qbr(s-p)/ppaw relationship with nonnal systemic blood pressure. Dashed line = Qbr(s-p)IPpaw relationship with low systemic blood pressure. Open symbols refer to data obtained during total ~ardiopulmonary bypass. Closed symbols indicate an estimate of Qbr(s-p) during nonnal circulatory conditions (Ppaw wer~ obtained during preoperative catheterization). ZF = zero Bow (or Qbr(s-p) = 33 mm "g.4 Asterisk = P
RESULTS

Measurements were done for an average period of 28± 15 minutes and of 32±25 in group A and B, respectivel~ Mean systemic blood and airways pressures, cardiac output, and esophageal and rectal temperatures, recorded during total cardiopulmonary bypass, are reported in Table 3. As absolute flow Qbr(s-p) was 76.3± 13.9 mVmin and 22.3±2.1 mV min in group A and B, respectively (P
In this study, Qbr(s-p) was measured in humans during total cardiopulmonary bypass.9-11 We observed that Qbr(s-p) was three times greater in patients with mitral stenosis and elevated pulmonary wedge pressure compared with patients with ischemic heart disease and normal wedge pressure. Several factors may influence Qbr(s-p) during total cardiopulmonary bypass, including body temperature,12 airways pressure,IO and inspired gas relative humidity. II Body temperature was by necessity unphysiologically lo~ However, care was taken to perform Qbr(s-p) measurements during stable thermal conditions, and no differences were appreciable in this regard between the two groups. The inspired gas relative humidity and airways pressure were not different in the two groups, and their effects on Qbr(s-p) were minimized by keeping airways pressure low and by fully humidifing the inspired gas. II The values for Qbr(s-p) were measured in patients with coronary artery disease and normal pulmonary artery wedge pressure (group B) are considerably less and less variable than those previously reported by Baile et al9 and by our laboratory.lo This presumably relates to patient selection. Indeed, different from previous studies, our patients were free from lung diseases9 and they were mainly nonsmokers. 9 •10 Furthermore, in the present study, we fully humidified inspired gas and it has been reported that humidification of inspired gas reduces Qbr(s-p).ll During total cardiopulmonary bypass, pulmonary vascular pressure was approximately atmospheric pressure and, therefore, lower than in normal condition. Because Qbr(s-p) is drained into the pulmonary circulation, Qbr(s-p) measurements might be significantly affected by the presence of a low pulmonary venous pressure. In group A, the difference between pulmonary venous pressure during normal perfusion conditions and during total cardiopulmonary bypass is significant. Therefore, the Qbr(s-p) we measured during total cardiopulmonary bypass is probably much higher than the Qbr(s-p) during normal pulmonary perfusion. Therefore, the How measurements from this study cannot be directly extended to physiologic condition. However, from these data we might predict the Qbr(s-p) under physiologic condition. It is known that, in the dog, an acute increase of pulmonary venous pressure stops Qbr(s-p) at about 33 mm Hg or at a lower value in case oflow systemic blood pressure, 4 and that the bronchial artery pressure/blood How relationship is approximately linear. 13 In Figure 2, we Bronchial Blood Flow in Mitral Stenosis (Agostonl et aJ)

reported Qbr(s-p} vs pulmonary artery wedge pressure; the Qbr(s-p) measurements were obtained with pulmonary artery wedge pressure = 0 mm Hg. We drew a line connecting the data observed in group A and B with the Qbr(s-p} stop flow pressure (33 mm Hg); these plots should represent the Qbr(s-p}/pulmonary artery wedge pressure relationships in group A and B. Because we do know from the preoperative catheterization the pulmonary artery wedge pressure, it is possible to obtain an estimate of the Qbr(s-p} under normal circulatory conditions. It should be emphasized that we do not know for how long pulmonary venous pressure was elevated and that other factors, besides chronically elevated pulmonary venous pressure, might have generated the difference of Qbr(s-p) observed in group A and B. Indeed, it is possible that patients with mitral stenosis more frequently had lung inflammatory diseases, pulmonary fibrosis, alveolar hypoxia, pulmonary hypertension, or alterations of lung ventilation/perfusion relationship,14 all of which might alter Qbr(s-p}. Regardless of the mechanism(s} responsible for the elevated Qbr(s-p) measured in group A, it should be noted that systemic blood pressure, extracorporeal circulation pump Ho~ and airways pressure were similar in both groups. Therefore, the Qbr(s-p} differences observed between group A and B were related to differences in bronchovascular resistances. This implies the presence in group A of larger or more numerous Qbr(s-p) vessels. It has been shown in the dog that an acute increase of pulmonary venous pressure may generate a blood flow through the bronchial vessels from the pulmonary to the systemic circulation. 2-4 However, in normal dogs, the pulmonary to systemic blood flow is very small. 4 The relationship between Qbr(s-p} and pulmonary venous pressure cannot be studied in humans. However, our observations in patients with mitral stenosis and elevated pulmonary venous pressure suggest that the size or the number of the Qbr(s-p} vessels is functionally, if not anatomically, increased. Furthermore, when pulmonary venous pressure is elevated, a relevant flow between the pulmonary and the systemic circulation might occur. This pulmonary to systemic bronchial blood flow should be even greater when systemic blood pressure is reduced, because, in such condition, the Qbr(s-p} stop flow pressure is reduced4 and the Qbr(s-p}/pulmonary artery wedge pressure

relationship is shifted downward (Fig 2). Therefore, it is possible that in patients with mitral stenosis, such pulmonary to systemic communications might function as an additional, lower resistance, pathway for pulmonary venous return. During increases in pulmonary blood flow or in pulmonary vascular resistance, the Qbr(s-p} vessels could serve as a safety valve and prevent excess of pulmonary artery pressure. This safety valve might be particularly useful in patients with mitral stenosis in case of cardiogenic shock complicating pulmonary edema when systemic blood pressure is low and pulmonary vascular pressure is elevated. REFERENCES 1 Deffebach ME, Charan NB, Lakshminarayan S, Butler J. The bronchial circulation: smaIl, but a vital attribute of the lung. Am Rev Respir Dis 1987; 135:463-81 2 Auld PAM, Rudolph M, Golinko RJ. Factors affecting bronchial collateral blood 80w in the dog. Am J Physiol 1960; 198:116070 3 Goetz RH, Rohman M, State D. The hemodynamics of bronchopulmonary anastomoses. Surg Gynecol Obstet 1965; 120:51729 4 Agostoni PG, Deffebach ME, Kirk ~ Laksminarayan S, Butler J. Upstream pressure for systemic to pulmonary Row for the bronchial circulation in dogs. J Appl Physioll987; 63:485-91 5 Cudkowicz L. Cardiorespiratory studies in pulmonary tuberculosis. Can Med Assoc J 1965; 92:111-15 6 Muller KM, Bordt J. Der bronchial arterienkreislauf unter krankhaften verhaItnissen. Prax Pneumoll980; 34:324-31 7 Williams MH, Towbin EJ. Magnitude and time of development of the collateral circulation to the lung after occlusion of the left pulmonary artery. Circ Res 1955; 3:422-24. 8 Weibel ER. Early stage in the development of collateral circulation of the lung in the rat. Circ Res. 1960; 8:353-76 9 Baile EM, Ling H, Heyworth JR, Hogg JC, Pare PD. Bronchopulmonary anastomotic and non-coronary collateral blood Row in humans during total cardiopulmonary bypass. Chest 1985; 87:749-54 10 Agostoni PG, Arena ~ Biglioli ~ Doria E, Sala A, Susini G. Increase of alveolar pressure reduces systemic to pulmonary bronchial blood Row in humans. Chest 1989; 96:1981-85 11 Agostoni PC, Arena ~ Doria E, Susini G. Inspired gas relative humidity affects systemic to pulmonary bronchial blood Row in humans. Chest 1990; 97:1377-80 12 Agostoni PG, DeB"ebach E, Kirk ~ Brengelmann GL. Temperature dependence of intraparenchymal bronchial blood 80~ Respir Physioll987; 68:259-67 13 Mitzner ~ Wagner EW Pulmonary and bronchial vascular resistance. In: Scharf SM, Cassidy SS, eds. Heart-lung interactions in health and disease. New York: Dekker; 1989:45-76 14 McFadden R, Ingram RH. Relationship between diseases of the heart and lungs. In: Braunwald E, 00. Heart diseases. Philadelphia: WB Saunders Co, 1988:1870-82

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