Brit. Heart J., 1968, 30, 654.

Site of Pulmonary Resistance in Cor Pulmonalein Chronic Bronchitis

F. HERLES, V. JEZEK, AND S. DAUM

From Second Medical Clinic, Charles University, Prague, Czechoslovakia

The pathogenesis of pulmonary hypertension inchronic bronchitis is still obscure, though the rela-tion of pulmonary artery pressure and tension ofalveolar gases has been recognized since the classi-cal experiment of von Euler and Liljestrand (1946).Our interest in the site of resistance was aroused

by the increased pulmonary.artery wedge pressurein cor pulmonale without overt pathological changesin the left heart. Most of these patients weremiddle-aged or older men and ischaemic heartdisease was suspected. However, the coincidenceof ischaemic heart disease with cor pulmonale wasfound to be less frequent than would correspondto their separate incidence in the general popula-tion (Kralova et al., 1965).Pulmonary artery wedge pressure is virtually an

artefact and the result of interplay of several fac-tors (Herles, 1966). Analysing a large group ofpatients with chronic obstructive bronchitis, em-physema, and cor pulmonale, we have attempted toelucidate the origin of increases in pulmonaryartery wedge pressure as well as the site of resis-tance modifying the pressure gradient in the pul-monary circulation.

SUBJECTS AND METHODS

Our subjects comprised a group of 121 patients withchronic bronchitis and pulmonary emphysema. Nopatients with other forms of pneumopathy or withvascular forms of cor pulmonale were included in theseries.

Catheterization of the right heart and the pulmonaryartery was carried out in all patients in the morning,after food, in the supine position. Blood pressure wastaken by the Hellige tensometer with the zero level10 cm. above the catheterization table and recorded bythe Multiscriptor Hellige. Another catheter was placedin the femoral artery. During the investigation, thepatient breathed atmospheric air through the Metabo-graph (Fleisch). After reaching the steady state, blood

Received November 24, 1967.654

for gas analysis was taken from the femoral and pul-monary artery under strict anaerobic conditions.The 02 and CO2 content of the blood was determined

by the method of Van Slyke and Neill (1924), the bloodpH by the pH meter (Godart and Cambridge). Theblood CO2 tension was calculated from the CO2 contentand pH.

Cardiac output was determained from oxygen consump-tion and the arterio-venous oxygen difference using theFick's formula. Total pulmonary resistance and arteri-olar resistance were expressed in arbitrary Wood'sunits calculated according to the following formulae.

TPR = -PAP (mPAP-mPAWP)The work of the right ventricle, expressed in kg.m.f,

min./m.2 BSA, was computed from the formulaCI x 1-055x 13-6(nmPAP-mRAP)

Wr=ooIr ~~~1000where mRAP is mean pressure in the right atrium,mPAP is mean pressure in the pulmonary artery,mPAWP is mean pressure in the wedged pulmonaryartery, CO is cardiac output in 1./min., CI is cardiacindex, TPR is total pulmonary resistance, PAR is pul-monary arteriolar resistance, and Wr is work of theright ventricle.

Extra-arteriolar or post-arteriolar (EAPR) pulmonaryresistance was calculated from the difference betweentotal resistance and arterial resistance. In calculatingtotal pulmonary resistance, the left atrial pressure wasnot deducted, since it had not been ascertained and thededuction of an arbitrary value of 5 mm.Hg does notincrease the comparability of the figures. Extra-arteriolar resistance includes both the resistances of pul-monary venules and the "resistance" of the left sideof the heart.

Pressures at rest in the right atrium exceeding 5 mm.Hg, in the pulmonary artery exceeding 20 mm.Hg, andin the wedged pulmonary artery reaching or exceeding12 mm.Hg, were considered to be increased.To follow separately the influence of pulmonary

hypertension and of heart failure, the group of92 patientswith cor pulmonale was subdivided into 3 groups: (1)45 patients who at the time of examination and for two

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Site of Pulmonary Resistance in Cor Pulmonale in Chronic BronchitisTABLE I

HAEMODYNAMIC AND RESPIRATORY FINDINGS IN CHRONIC BRONCHITIS WITHOUTPULMONARY HYPERTENSION (CONTROLS)

Case No.

1011121314151617181920212223242526272829

Total: AverageSigma

mRAP mPAP mPAWP(mm.Hg) (mm.Hg) (mm.Hg)

4-63 02-01-0

1-01-01-52-01-23 01-00.05 05-40 3

4-84-70.04-82-02-02-01-51-44 04-80.0

181718161112151315161416141211815171517161315171416131612

2-0 14-51-3 2-7

8-55 08-07-0306-07-05-2906-96-53-7305-0407-46-2908-63-66-911-36-3705-02-110-08-91-96-32-4

Cardiacindex

(l./min./m.2)

2-82-75-63-73-6203-32-33.54-140304-63-64-22-13-42-63.45-54-32-93-63-82-85-82-23-12-5

3-581-4

TotalPuim.resist.(units)

3-33-71-62-41-83-82-62-82-32-22-12-91-72-21-32-11-73-32-51 82-32-3.2-52-42-61-63-32 72-9

2-480-8

PAR EAPR(units) (units)

1-82-60 91-41-31-91-41-70-91-31-12-21-31-50-80-51-01-31-11-41-30 31-31-41-71-30 71-42-4

1-340-5

1-51-10 71-00-51-91-21-11-4091-00 70-40-70-51-60-72-01-40-41-02-01-21-0090 32-61-30 5

1 140-6

WI(kp.m./min./

M.2)

0-640541-29079

0-320-660400-640-890-640-650-920-840330-25

0440501-360-580450-640-820-511-130-290-51043

0-64034

Sa02(%)

929897

8286

88

87908787877690909187778886888483.91898190

87-86-3

P2C02(mm.Hg)

44

4238393725354235413727373338394047393939

37-65.9

months before examination had not had any clinicalsigns of right heart failure and whose right atrial pres-sure was normal. (2) 29 patients with clinical signs ofright heart failure at the time of eamintion. Oncatheterization the pressure in the right atrium wasraised. (3) 18 patients who on admission to the depart-ment also had signs of failure of the right heart, but whohad already been treated and whose clinical conditionwas improved.A separate group of 29 patients with chronic obstruc-

tive bronchitis without pulmonary hypertension wasused as controls.The data ofthe individual groups and their differences

were evaluated by the Student t test. Correlationcoefficients were calculated according to Pearson andSpearman.

RESULTS AND THEIR ANALYSISChronic Obstructive Bronchitis Without Pulmonary

Hypertension (Controls). (Table I). In chronicbronchitis without hypertension in the pulmonaryartery (mean pulmonary artery pressure averaging14-5 mm.Hg) the pressure in the right atrium wasa1ways nornal and so was the pulmonary arterywedge pressure. Blood flow, calculated resistance,and the work of the right ventricle were also withinnormal limits. There was a moderately severehypoxaemia, normal or slightly decreased C02

tension, and a normal pH. These patients wereconsidered controls for comparison with chroniccor pulmonale.

Cor Pulmonale Without Heart Failure (Compen-sated) (Table II). The mean pressure in the rightatrium was higher than in the previous group, butstill within normal range. The difference was notstatistically significant (t=1*016, p>010). Themean pressure in the pulmonary artery was in-

creased, and the pressure in the wedged pulmonaryartery did not differ significantly from that in con-trols (p > 0 1O), though in some cases it was foundto be higher.The cardiac output and. cardiac index remained

the same as in simple chronic bronchitis. Totaland arteriolar resistance were signifcantly in-creased (p<001), but the extra-arteriolar resist-ance remained the same as in the previous group

on the average. Neither was the arterial oxygensaturation significantly decreased (p > 010) nor

was the difference in the arterial pH significant.However, the increase in CO2 tension in the arterialblood was statistically significant (p < 0-05).

Cor Pulnonale in Right Heart Failure (Decom-pensated) (Table III). The difference from thecontrols was most significant in this group. The

655

pH

7.33

7.377-417-437.397.447-417-357.407.407.407.407-387-417.397-427.397-367.397-377-35

7.3930-08

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656 Herles, Jelek, and Daum

TABLE IIHAEMODYNAMIC AND RESPIRATORY FINDINGS IN COR PULMONALE WITHOUT HEART FAILURE

Case. No. mRAP mPAP mPAWP Cardiac Total PAR EAPR Wr Sa°2 PICO2 pH(mm.Hg) (mm.Hg) (mm.Hg) index pulm. (units) (units) (kp.m./min./ (%) (mm.Hg)

(1./min./m.2) resist. m.2)(units)

1 4-8 30 7-5 3 0 4-6 3 9 0 7 1*11 87 44 7-372 3-8 32 15.0 4-4 4-8 2-6 2-2 1*81 89 45 7-333 0-8 20 2-7 5-8 1.9 1-6 0 3 1-36 98 59 7-284 4-1 24 3-5 4-6 3-2 2-9 0 3 1-13 85 55 7-355 1*8 26 4-6 3-6 5-0 4-1 0 9 1*12 88 47 7 406 3-6 25 7-3 3-3 4-5 3-3 1*2 1 00 87 52 7-367 0.0 21 0.0 4 0 3-2 3-2 0.0 1*21 74 62 7-298 1-5 41 12-4 2-7 8-0 5-6 2-4 1-60 87 - -

9 2-0 22 8-0 5-2 2-7 1-7 1-0 1-49 96 - -

10 2-0 23 7 0 2 5 6-1 4 2 1.9 0 76 98 - -

11 2 0 26 9 0 2-5 6 1 4 0 2-1 0-85 91 - -

12 1-0 27 9 0 4-3 3-8 2-5 1-3 1-55 85 - -

13 1.0 22 2-0 3 0 4-3 3*9 0 4 0-85 73 - -

14 2-0 32 2-0 3-8 5 0 4-7 0 3 1-62 85 - -

15 3-0 35 5-0 4-1 4-6 3 9 0 7 1*89 82 - -

16 2-0 24 2-0 2-0 7-1 6-5 0-6 0-62 81 - -

17 2-3 31 5 0 3-8 4-5 3-7 0-8 1-56 79 - -

18 1.0 23 7-0 2-8 5 0 3-5 1-5 0 90 94 - -

19 1-7 26 5 0 3-7 4-3 3-5 0-8 1-25 91 - _20 1-8 30 7 0 3-8 4-5 3-5 1-0 1-53 97 - -21 2-0 38 7 0 3-6 6-0 4 9 1 1 1-66 92 - _22 2-0 40 6-0 4 0 5-6 4-7 0 9 2-18 92 - _23 2-0 37 6-0 3-4 6-5 5-4 1.1 1-73 86 - _24 4-0 27 9 0 5 0 3-6 2-4 1-2 1-65 94 - _25 2-0 32 16-0 5 0 4 0 2-0 2-0 2-15 80 - _26 1-4 27 13-0 4-6 3-3 1-7 1-6 1-68 74 - _27 3 0 41 17-0 2-6 9-6 5-8 3-8 1-42 91 - _28 3.9 26 8-9 2-5 6-8 4-5 2-3 0 59 89 37 7-4129 1*2 21 5-7 2-4 5-3 3*9 1*4 0 50 88 30 7-3730 3-5 22 5-7 3-5 4-7 3-7 1.0 0-92 78 52 7-3631 5.0 19 8-0 2-1 5-3 3-1 2-2 0-42 97 40 7 3932 1-0 28 6-2 7-1 2-6 2-0 0-6 2-74 85 39 7-3933 3 0 19 2-3 5-7 1*8 1*6 0-2 1*32 92 31 7-4134 2-0 20 3 0 4-7 2-4 2-1 0 3 1*21 87 - -

35 5s0 21 5 0 4-7 2-4 1-8 0-6 1-08 77 - -

36 4 0 36 5 0 3-8 4-8 4-1 0 7 1*75 85 49 7-3537 6-0 19 110 5 0 2-3 1.0 1*3 0-93 76 43 7-3538 2-0 23 6-0 3-5 3-6 2-7 0 9 1 04 87 38 7-3839 9-2 28 14-0 3-2 5-2 2-6 2-6 0-86 89 32 7-3740 7 0 22 13-0 3-6 3-5 1*4 2-1 0-78 94 42 7-3541 0.0 47 3 0 4-2 5-5 5-2 0 3 2-80 82 - -

42 - 34 10-5 3 9 5 0 3-2 1-8 - 90 37 7-3543 - 21 3-2 3-1 4-1 3-5 0-6 - 85 37 7-3644 2-3 35 11*5 3-3 6-6 4-4 2-2 1*45 92 43 7-3645 - 23 5 0 3-4 4 0 3-1 0 9 - 87 44 7-38

Total: Average 2-7 27-7 7-2 3-81 4-61 3 40 1-21 1-31 86-9 43-6 7-362Sigma 2-1 4-1 4.9 1-55 1-3 1-3 0-8 0-51 8-1 6-2 005

mean pressure in the right atrium was significantly (p > 0 05). When compared with this group thereraised (p <0001) as compared with the two pre- was a significant decrease in the oxygen saturationvious groups, as was the mean pressure in the pul- (p < 0 05), a highly significant increase in CO2 ten-monary artery (p <0 01). The increase in the sion in the arterial blood (p < 0 01), and a significantpulmonary artery wedge pressure was highly signi- decrease in the pH (p < 0 05).ficant, the average value being almost twice thatof the preceding groups. This pressure was found Cor Pulmonale after Recovery From Failure (Re-to be increased in more than half of the decompen- compensated) (Table IV). Haemodynamic valuessated patients. The blood flow values were not and blood gas readings were within the range ofstatistically different from those of the preceding mean findings in cor pulmonale with and withoutgroups (p>0 10). However, the increase in the heart failure. Therefore, statistical differencesmean value of total, arteriolar, and extra-arteriolar among these groups were not significant, thoughpulmonary resistances was highly significant in some parameters, e.g. extra-arteriolar resistance,(p<001l, for EAPR p <0001). There was a work of the right ventricle, and oxygen saturationstatistically significant increase in the work of the of the arterial blood, this group resembled thatright ventricle (p < 0 01) as opposed to the control with heart failure.group, but when compared with the compensatedcor pulmonale group, the difference was not signifi- Interrelation Between Haemodynamic Values andcant because of the wide scatter of the results Blood Gases in Individual Groups of Patients. There

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TABLE III

657

HAEMODYNAMIC AND RESPIRATORY FINDINGS IN COR PULMONALE WITH HEART FAILURE

Case No. mRAP mPAP mPAWP Cardiac Total PAR EAPR Wr SaO2 PaCO2 pH(mm.Hg) (mm.Hg) (mm.Hg) index pulm. (units) (units) (kp.m./min./ (a) (mm.Hg)

(k/1mini/M.2) resist. rn.2)(units)

1 14-4 66 20-2 6-2 5 9 4-1 1-8 4 59 72 40 7-432 6-8 38 11*2 3-6 7-5 4-7 2-8 1*58 90 58 7-313 9*6 42 9 0 3-6 7-4 5-8 1*6 1*65 84 39 7-334 11*8 48 15-6 4 0 6-8 4-6 2-2 2-07 70 43 7-385 9 0 40 210 4-7 4-7 2-2 2-5 2-08 89 57 7-256 10-0 51 15-0 4-1 8-5 6-0 2-5 2-41 63 - -7 12-0 24 18-0 2-3 6-1 1*5 4-6 0 40 76 - _8 8-0 29 15-0 1-7 9 7 4-7 5 0 0-51 - - _9 10-0 36 25-0 2-7 8-4 3-0 5.4 1*13 96 - _10 6-5 42 13-0 2-2 11*1 7-7 3-4 1 03 82 - _11 7 0 72 25-0 2-8 14-8 9 9 4.9 2-61 - - _12 15-0 59 17-0 2-6 11*7 8-3 3-4 1*64 77 - _13 8-0 41 15 0 2-8 10-2 6-4 3-8 1*33 54 - _14 10-0 42 14-0 1-8 16-5 11-0 5-5 0-84 - - -

15 6-0 42 7 0 4-1 5-3 4-4 0 9 2-12 98 - -

16 5 0 32 8-0 3-1 6-8 5-1 1-7 1-18 90 - -17 7-0 36 4 0 2-3 6-8 6-0 0-8 0-96 89 - -18 6-0 24 9 0 2-0 7-3 4.5 2-8 0-52 - - -

19 6 0 39 7 0 4-7 5-5 4-5 1.0 2-23 82 37 7-4720 26-8 70 21-0 3-4 13-1 9*1 4 0 2-09 49 57 7-2921 7 8 40 10-8 2-8 7-5 5-5 2-0 1*43 90 59 7-2922 10-2 27 15-8 4-7 3-3 1-4 1-9 1-14 85 53 7-3423 5-2 23 6-5 4-0 3-5 2-5 1.0 0-98 77 47 7-3724 9 5 40 8-0 2-9 6-8 5-4 1-4 1-25 71 - -25 8-5 49 17-0 6-5 4-2 2-8 1-4 3-73 60 - -

26 8-3 24 15-0 3-3 4 0 1*5 2-5 0 74 86 44 7-4127 2-5 24 7-2 3-6 3-7 2-6 1.1 1 09 79 52 7 3028 - 31 3-5 4-2 5-1 4-6 0 5 - 78 49 7-3729 - 54 4 0 3-4 9-8 9.1 0 7 - 63 67 7-28

Total: Average 9 4 40-8 13-0 3-42 7-65 5-21 2-44 1-60 78 0 51-1 7-335Sigma 4-6 13-5 5-8 0 95 3-3 2-5 1-5 0-96 13 0 7-3 0 050

was an indirect relation between the arterial oxy- wedge pressure or pressure in the right atrium, orgen saturation and the mean artery pressure between the arterial oxygen saturation and blood(r =0O220, p < 0 05). However, it was significant flow (p always > 0 10).only in the groups with heart failure and after There was no significant correlation between therecovery (r= 0O304 and 0 452, p <0 -01), whereas cardiac output and the cardiac index and the meanthis relation is not significant in controls and in right atrial pressure, the pulmonary artery or pul-compensated cor pulmonale. No correlation was monary artery wedge pressure, blood gases, andfound between the SaO2 and pulmonary artery pH. The relation between the mean pressure in

TABLE IVHAEMODYNAMIC AND RESPIRATORY FINDINGS IN COR PULMONALE RECOVERING FROM

HEART FAILURE

Case No. mRAP mPAP mPAWP Cardiac Total PAR EAPR Wr S02 PaC02 pH(mm.Hg) (mm.Hg) (mm.Hg) index puim. (units) (units) (kp.m./min./ (%) (mm.Hg)

(I./min./M.2) resist. in.2)(units)

1 6-1 24 5-2 5-5 2-2 1-6 0-6 1-43 85 - -

2 12-0 29 110 1*8 7-8 4-8 3 0 0-41 97 40 7-433 2-5 26 4 0 4-5 4 0 3-4 0-6 1-52 79 - -

4 6-5 32 6-5 2-5 7-2 5-7 1-5 0 93 93 - -

5 2-3 49 5-0 2-4 11*5 10-3 1*2 1*62 71 - -6 2-0 47 6-0 2-9 8-9 7-8 1 1 1-90 82 - -7 13-8 40 6-6 2-6 8-0 6-7 1-3 1.19 85 - -8 3 0 27 8-0 3-1 5-1 3-6 1-5 1-08 90 - -9 9 0 30 7 0 2-3 7-8 6-0 1-8 0-68 83 - -10 1-0 23 18-0 3-9 4-3 0 9 3-4 1-23 84 - -11 4-0 32 15-0 5-1 3-3 1*8 1*5 2-05 65 - -12 1-0 42 14-0 4-2 5-6 3-7 1-9 2-53 84 - -13 5 0 31 10-8 2-7 7-0 4-6 2-4 1.01 92 35 7-4314 0.0 39 4 0 7-7 3-1 2-9 0-2 4-44 60 48 7-3615 2-0 37 11*5 3-1 6-7 4-6 2- 1 1*53 72 50 7-3716 4-0 42 19.0 4-0 6-8 3-7 3-1 2-18 87 38 7.3917 5 0 29 110 4-2 4-2 2-6 1*6 1*45 81 63 7 3918 8-9 24 11-2 3-5 3-8 2-1 1-7 0-76 88 41 7-35

Total: Average 4*6 33*5 9*6 3*68 6*10 4*40 1 70 1*60 81-8 45 1 7*388Sigma 3-9 8-8 5-1 1-2 2-5 2 7 0-8 0-58 9 0 5.9 0-076

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TABLE VHAEMODYNAMIC AND BLOOD GASES IN PATIENTS WITH NORMAL AND RAISED PULMONARY

WEDGE PRESSURE

All patients Heart failure

Normal (65 cases) High (27 cases) Normal (13 cases) High (16 cases)

Average Sigma Average Sigma Average Sigma Average Sigma

mRAP (mm.Hg) 3-9 5-6 7 9 3 9 6-5 4-6 11-0 3 0mPAP (mm.Hg) 29-8 8-1 40-1 16-8 35-8 7-2 45 0 15-4mPAWP (mm.Hg) 6-3 5-1 16-6 10-1 7-3 4-1 17-7 6-1Cardiac index (l./min./

M.2) 3-7 1-4 3-7 1-4 3-4 1-5 3-5 1-3Total pulm. resist.

(units) 5-24 3-34 7-31 2-7 6-39 3-6 8-69 3 79PAR (units) 4-11 2-38 4 30 2-49 5 0 2-75 5-26 3-14EAPR (units) 1-13 0-51 3-01 1-53 1-39 0 50 3-43 1-26Wr (kp.m./min./m.2) 1-36 0-89 1-73 1-01 1-36 0-91 1-77 1-04SaO2(%) 85-8 6 1 78-4 12-9 82-6 5-7 73-7 13 1PaCO2 (mm.Hg) 46-2 7-3 45-1 8-1 51-0 6-6 49-0 11-3pH 7-373 0 077 7-352 0-092 7*340 0*086 7 350 0*101

the pulmonary artery and in the wedged catheterwas on the borderline of statistical significance(r= 0-216, p = 005). The coefficients of correla-tion in the clinical groups varied a great deal butwere homogeneous. Extra-arterial resistanceshowed no significant correlation either with thetotal or with the arteriolar pulmonary resistances.Surprisingly, no relation was found betweenarterial CO2 tension or blood pH and any haemo-dynamic values.

Patients with Increased Pulmonary Artery WedgePressure. In controls with normal pulmonarypressure, the pulmonary artery wedge pressure

15

ECL

crEE

10

5-

0

00

* S

* .

0

0

0

.00

&

0 5 10 15 20 25mPAWP (mm.Hg)

FIG.-Relation between the mean right atrial pressure andthe mean pulmonary arterial wedge pressure. This relation

was highly significant (r = 0-506; p < 0-01).

was also normal. Raised pulmonary artery wedgepressure was rare in cor pulmonale before failure(16%) and after recovery from failure (22%), butin cor pulmonale with heart failure this pressurewas raised in 55 per cent of cases. Patients withincreased pulmonary artery wedge pressure differedin several respects from other patients with corpulmonale. (1) They had a higher pressure in thepulmonary artery (p < 0 05). (2) Total pulmonaryresistance was higher since the average blood flowwas the same in the group with normal as well aswith raised pulmonary wedge pressure. As thearteriolar resistance did not differ in the two groups,the extra-arterial component was at fault (TableV). (3) The right atrial pressure was higher andthere was a highly significant correlation betweenthe pulmonary artery wedge pressure and the pres-

sure in the right atrium (Figure). (4) In patientswith increased pulmonary artery wedge pressure,the arterial oxygen saturation was significantlylower than in patients with normal wedge pressure(Table VI).The difference between patients with increased

and normal pulmonary artery wedge pressure incor pulmonale was even more significant if onlypatients with heart failure were taken into con-

sideration.

TABLE VIHYPERTENSION AND ARTERIAL OXYGEN

SATURATION

SaO2 (%) No. of Per cent of casescases with raised pulm.

artery wedgepressure

91-100 20 15-081-90 41 24-471-80 19 26-3<71 8 750

658

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DISCUSSION

The comparison ofrespiratory and haemodynamicdata in our patients shows the well-known relationbetween hypoxaemia and increases of pressure inthe pulmonary artery; however, an indirect relationbetween S02 and mPAP could be ascertainedonly in patients with low mean 02 saturation, i.e.in the group manifesting heart failure or recoveringfrom failure (recompensated cor pulmonale).

In progressive cor pulmonale, a highly significantdifference in the tension of arterial CO2 was found

between the cases ofcompensated cor pulmonale andthose with heart failure. There was, however, nostatistically significant correlation of mPAP withPaCO2 or with pH of the arterial blood. It ispossible that the relation between PaCO2 andmPAP in our patients is closer than would followfrom the figures we obtained. In our series only6 patients had PaCO2 higher than 55 mm.Hg andonly 2 were higher than 60 mm.Hg. In acutehypercapnic acidosis produced by breathing CO2mixtures, the relation of ZPaCO2 to AmPAP wassignificant (Herles, Jezek, and Boudik, 1966).

Increased pulmonary artery wedge pressure mcor pulmonale has been recorded by many authorsbut has not received due attention. It was as-cribed usually to complicating- failure of the leftheart, i.e. to the simultaneous presence of ischaemicheart disease. However, in most instances theincrease in wedge pressure cannot be explained inthis way (Herles, Daum, and Bedn&it, 1960), sincein such cases at necropsy no changes in the leftside of the heart and no signs of pulmonary con-gestion have been found. We assume that pul-monary artery wedge pressure belongs to the re-arrangement of pulmonary circulation in certainstages of chronic cor pulmonale.A number of factors contribute to the pulmonary

artery wedge pressure: (1) pressure in the leftatrium; (2) vasoconstriction, or increased capillary,or venular resistance elicited in other ways; (3) in-creased blood flow through bronchopulmonaryanastomoses, both arterial and venous.

The possibility of increases in pressure in theleft atrium in uncomplicated cor pulmonale cannotbe denied. It need not be a consequence of in-sufficiency of the left ventricle, but it might be a

result of a diminished compliance of the leftventricle in the presence of hypertrophy of theright ventricle, if the blood flow to the left sideof the heart is increased. In some cases of cor

pulmonale in chronic bronchitis we did find in-creased pressure in the left atrium (Jeiek, 1967).Nevertheless, this cannot be the only factor ofincreased post-arterial resistance and of increase in

pressure in the wedged pulmonary artery, sincewe were able to find differences in pressure atdifferent sites in the lung which could not be ex-plained by hydrostatic influences (Herles andJeiek, 1967). The experimental work of vonEuler and Liljestrand (1946), Nisell (1948), andothers suggested that the post-arteriolar resistancemight be increased by constriction of the pulmonaryvenules. The high incidence of advanced venulo-sclerosis in chronic cor pulmonale suggests thatthe site of increased vascular resistance might alsobe sought there.

In considering the genesis of increased pressurein the wedged pulmonary artery, the broncho-pulmonary collaterals deserve special attention.Pathologists (Hayek, 1951; Cudkowicz and Arn-strong, 1953; Bednia and Dobias, 1965; Liebow,1953, 1954) have shown that arterial bronchopul-monary anastomoses are common in emphysema.In chronic bronchitis with emphysema all branchesof the pulmonary artery can easily be filled up fromthe bronchial arteries, in contradistinction to thenormal lung or to other lung diseases (Dobias,1965). On wedging the catheter into the pulmon-ary artery, the circulation in the terminal part ofthe pulmonary branches can be maintained by thebronchial arteries. In cases of increased systemicvenous pressure, such as in right ventricular failurein cor pulmonale, bronchial veins may carry syste-mic blood into pulmonary veins (Liebow, 1953,1954).

Significant correlation between the raised pres-sure in the right atrium and in the wedged pul-monary artery in progressive cor pulmonale withheart failure supports this concept. If the venulesconstrict or their extensibility is curtailed, thewedge pressure may increase. When explainingthe enlargement of the left ventricle in some casesof emphysema, increased blood flow from broncho-pulmonary anastomoses into the left heart andleft-to-right circulatory shunt bypassing the rightheart have been assumed in the past (Kountz,Alexander, and Prinzmetal, 1936) and morerecently (Fluck, Chandrasekar, and Gardner, 1966).The increased filling of the left heart may raise theend-diastolic pressure in the left ventricle as wellas the pulmonary artery wedge pressure.

Statistical and clinical studies to date do notexplain the mechanism of increase of pressure inthe pulmonary artery in chronic cor pulmonale.Our findings, however, show that the site of pul-monary resistance in cor pulmonale in chronicbronchitis must be sought also in the post-arteriolarsector of the pulmonary circulation. Conspicuoushypoxaemia and respiratory acidosis, which ac-company heart failure and which do not completely

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recede with clinical recovery, may bring about thischange in post-arteriolar resistance. The signifi-cant changes in acute respiratory acidosis evokedin men by inhalation of air mixture with CO2(Fishman, Fritts, and Cournand, 1960; Herles et al.,1966) as well as the animal experiments with acutenon-respiratory acidosis (Bergofsky et al., 1961;Harvey et al., 1951) support this.

SUMMARY

In examining the haemodynamics of chronicbronchitis, we frequently came across cases withthe post-arteriolar type of pulmonary hypertension,i.e. with pulmonary artery wedge pressure of 12mm.Hg or higher, where no overt clinical changesin the function or anatomy of the left heart werefound. In the effort to assess the incidence ofraised pulmonary artery wedge pressure in corpulmonale and to elucidate its origin, we analysedhaemodynamic and respiratory data in 121 patientswith chronic obstructive bronchitis. The patientswithout pulmonary hypertension were comparedwith those with cor pulmonale, i.e. with those whosepulmonary artery mean pressure exceeded 20mm.Hg. In uncomplicated chronic bronchitis thepulmonary artery wedge pressure was never raised.In cor pulmonale it was found to be higher in 20per cent before and after recovery from failure,and it was raised in more than half of the patientswith heart failure. A significant relation was foundbetween the pulmonary artery wedge pressure andthe pulmonary artery pressure, the pressure in theright atrium, and hypoxaemia. Pulmonary hyper-tension with high pulmonary artery wedge pressureseems to form a particular haemodynamic type ofprogressive cor pulmonale in chronic bronchitis.It is assumed that increased post-arteriolar resist-ance plays a major part in the development ofpulmonary hypertension in chronic obstructivebronchitis.

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