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(Circulation. 1996;94:2485-2491.)
© 1996 American Heart Association, Inc.
Articles |
Hemodynamic Effects of Nonionic Contrast Bolus Injection and Oxygen Inhalation During Pulmonary Angiography in Patients With Chronic Major-Vessel Thromboembolic Pulmonary Hypertension
the Department of Radiology and the Department of Cardiovascular Surgery (E.M.), University Hospital, Johannes Gutenberg-University of Mainz, Germany.
Correspondence to Dr Michael B. Pitton, Klinik fur Radiologie, Universitatskliniken, Langenbeckstraße 1, 55101 Mainz, Germany.
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Abstract |
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Background Pulmonary angiography is the gold standard for the diagnosis of chronic thromboembolic pulmonary hypertension; however, major complications have been reported. This study evaluates the hemodynamic effects of direct pulmonary nonionic contrast bolus injection and oxygen inhalation in patients with chronic thromboembolic pulmonary hypertension.
Methods and Results In 33 patients, hemodynamic parameters were measured after oxygen inhalation and during bolus injection of nonionic contrast medium in a control group (group 1, n=11), in a group of patients with moderately severe pulmonary hypertension (group 2, n=9), and in a group with severe pulmonary hypertension (group 3, n=13). Oxygen inhalation significantly improved oxygen supply. Pulmonary artery pressure and heart rate were reduced, but pulmonary vascular resistance and total pulmonary resistance were not significantly affected. One hundred ninety-eight angiograms were performed selectively on both pulmonary arteries in the posterior-anterior, oblique, and lateral views. Before contrast bolus injection, RAP and PAP significantly increased because of initial inspiration. Contrast bolus injection caused only a minor pressure increase (
PA systolic, 2.3±1.4, 2.5±1.8, and 5.0±5.2 mm Hg, groups 1, 2, and 3, respectively) without significance between the groups. After the angiography, pulmonary artery pressure was moderately increased, predominantly in group 3, but pulmonary vascular resistance was not significantly changed. Systemic vascular resistance was decreased. Cardiac index increased in groups 1 and 2 but was unchanged in group 3. Systemic pressure therefore decreased in group 3.
Conclusions We concluded that bolus injection of nonionic contrast medium causes no major hemodynamic effects even in patients with severe chronic thromboembolic pulmonary hypertension. Oxygen contributes to safety during the procedure.
Key Words: cardiovascular diseases • pulmonary heart disease • hypertension, pulmonary • contrast media • hemodynamics
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Introduction |
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Because chronic major-vessel thromboembolic pulmonary hypertension is curable by pulmonary thrombendarterectomy,1 2 3 the diagnostic procedure becomes more important. Pulmonary angiography is still the gold standard to establish the diagnosis preoperatively because its characteristic abnormalities such as webs and bands, pouchlike endings of arteries, irregularities of the arterial wall, and unusual stenotic lesions are best seen angiographically.1 4 5 In our institution, experience with more than 200 patients indicates that pulmonary angiography can be safely performed even in patients with severe chronic thromboembolic pulmonary hypertension. However, major hemodynamic complications during angiocardiography have been reported in pulmonary hypertension,1 4 5 6 7 8 9 10 11 12 13 and experimental studies demonstrate that relevant changes in hemodynamic parameters may occur during contrast bolus injection.12 14 15 16 17 With respect to safety, some authors follow a rigorous protocol with only a single contrast bolus injection into both main pulmonary arteries and recommend oxygen administration during the procedure.13 However, multiplanar imaging is necessary for exactly localizing thrombi in segmental arteries. This study was performed to evaluate the hemodynamic effects of repetitive pulmonary bolus injections of nonionic contrast medium and oxygen administration to verify the safety of our angiography protocol in this high-risk patient group.
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Methods |
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In 33 consecutive patients (22 men and 11 women, 51±14 years of age), hemodynamic parameters were measured before, simultaneously to, and after pulmonary angiography. Thirty-one patients with history of pulmonary embolism (21 diagnostic procedures and 10 after thrombendarterectomy) and 2 patients without thromboembolic disease were included. In 1 patient with mediastinal mass, tumor invasion into the pulmonary artery was excluded angiographically, and a clinically suspected pulmonary embolism was excluded in another patient.
After informed consent was obtained, the procedure was performed by use of a femoral approach when thrombosis was excluded phlebographically or by color Doppler. Otherwise, a transcubital approach was used. A 7F pigtail catheter was selectively placed in the main right and left pulmonary arteries. Hemodynamic parameters were measured with a 7.5F Swan-Ganz catheter simultaneously introduced in the pulmonary artery through the right cubital vein.
Digital subtraction angiography was performed in deep inspiration (the cine technique, 25 images per second, Integris V3000, Philips), and three different projections were obtained in the posterior-anterior, 30° anterior oblique, and lateral orientations, respectively. The contrast bolus consisted of 25.3±2.4 mL of the nonionic contrast medium iopamidol (Solutrast 300, Byk Gulden) and a flow rate of 12.7±1.5 mL/s. The total contrast amount was 167.9±34.2 mL. Systemic BP, HR, RAP, PAP, PCWP, SO2, and cardiac output (thermodilution method) were measured at rest, after oxygen inhalation for 20 minutes (10 L of O2 per minute), and after pulmonary angiography. RAP and PAP were recorded continuously during angiography. CI, SVI, SVRI, PVRI, TPRI, LVSWI, and RVSWI were computed automatically (Sirecust 1260, Siemens).
Pulmonary hypertension was considered for PAP >30 mm Hg (systolic) or a mean pressure of 20 mm Hg and a pulmonary vascular resistance >130 dyne·s·cm-5.18 Systolic PAP between 30 and 60 mm Hg was defined as moderately severe pulmonary hypertension (group 2), and PAP >60 mm Hg (systolic) was defined as severe pulmonary hypertension (group 3). According to this definition, the control group (group 1) consisted of 11 patients (9 men and 2 women), 5 after an earlier pulmonary thrombendarterectomy with completely normalized hemodynamic parameters and 6 for initial diagnostic procedure. Group 2 included 9 patients with moderately severe pulmonary hypertension (5 men and 4 women), 4 for preoperative evaluation and 5 in whom the hemodynamic parameters had not yet completely normalized after pulmonary thrombendarterectomy. Group 3 consisted of 13 patients with severe chronic thromboembolic pulmonary hypertension (8 men and 5 women) before pulmonary thrombendarterectomy.
Statistical Analysis
ANOVA was performed by use of the Kruskal-Wallis test for assessment of differences between groups. The Friedman test was used to compare intraindividual changes of cardiovascular parameters during the procedure. Differences were considered significant if P<.05.
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Results |
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The patient groups were defined by their hemodynamic data corresponding to the definition mentioned above and are summarized in Table 1
. Systolic PAP and PVRI differed significantly between the groups (PAPsyst, 22.4 [group 1] versus 42.4 [group 2] versus 94.0 mm Hg [group 3], P<.001; PVRI, 205.4 [group 1] versus 434.3 [group 2] versus 1606.2 dynes·s·m2·cm-5 [group 3], P<.001). Compared with groups 1 and 2, CI was reduced in group 3 (2.4 L·min-1·m-2, P<.01) because of the slightly reduced SVI and consequently the increased SVRI (SVRI, 2848.9 dynes·s·m2·cm-5, P=NS). Compared with the control group, the RVSWI was doubled in group 2 and increased fourfold in group 3 (5.8, 11.3, and 21.9 g·m·m-2 per beat for groups 1, 2, and 3, respectively; P<.001). There were no significant differences in left ventricle filling pressure (ie, PCWPmean) and LVSWI, so all differences between groups were related to the thromboembolic disease and its right ventricle affection.
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Compared with rest, mean oxygen saturation increased significantly during oxygen inhalation, and HR was reduced slightly (SO2mean, 1.3% [group 1, P<.01], 4.4% [group 2, P<.05], and 3.9% [group 3, P<.01]; HRmean, -4.0 [group 1, P<.01], -1.0 [group 2, P=NS], and -3.3 s-1 [group 3, P<.05]; see Table 2). PAP decreased slightly in all groups, predominantly in group 3 (PAPmean, -0.7 [group 1, P=NS], -1.5 [group 2, P<.05], and -2.3 mm Hg [group 3, P<.05], without statistical significance between groups. PVRI was not significantly affected; however, CI and RVSWI were reduced slightly in group 3 (CI, -0.2 L·min-1·m-2, P<.05; RVSWI, -1.6 g·m·m-2 per beat, P<.05). SVRI was moderately increased in all groups; however, PCWP (ie, left ventricle filling pressure) remained unchanged.
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During angiography, the pressure curves of the right atrium and the pulmonary artery were recorded continuously (Fig 1). Because angiography was performed in deep inspiration, the initial inspiratory breath hold before the bolus injection increased both the RAP and PAP, predominantly in group 3 (RAPmean, 3.5 [group 1, P<.05], 2.4 [group 2, P=NS], and 5.1 mm Hg [group 3, P<.01]; PAPsyst insp, 6.9 [group 1, P<.05], 6.6 [group 2, P<.05], and 7.4 mm Hg [group 3, P<.05]; see Table 3 and Figs 1 and 2). However, there was no significance between the groups. The maximal inspiratory pressure increase was 34 mm Hg in a patient with severe pulmonary hypertension with a systolic PAP of 104 mm Hg at rest. The contrast bolus itself caused only minor systolic pressure peaks, predominantly in group 3 (PAPsyst bolus, 2.3 [group 1, P<.05], 2.5 [group 2, P<.01], and 5.0 mm Hg [group 3, P<.01]); however, there was no significance between the groups. The maximal bolus-dependent pressure changes varied between -14 and 18 mm Hg in patients with severe pulmonary hypertension. These bolus-related systolic pressure peaks ascended slightly during repetitive bolus injections (Fig 3), and these increases were accompanied by slightly increasing inspiratory pressure levels in both RAP and PAP, representing the increasing right ventricle volume load. In contrast to groups 1 and 2, the mean diastolic pressures decreased slightly in group 3 during the first repetitive bolus injections; however, it finally increased. There was no strong correlation between the bolus-related pressure peaks and the corresponding pressure levels at rest (Fig 4).
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P<.01 vs rest. §P<.05, 
P<.01 vs inspiration.
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After contrast bolus injection (Table 4), the right ventricle filling pressure was moderately increased in groups 2 and 3. The PAP was significantly increased in all (PAPsyst, 4.8 [group 1, P<.01], 8.4 [group 2, P<.01], and 12.1 mm Hg [group 3, P<.01]), and there was statistical significance between the groups. In group 3, PVRI was increased slightly compared with rest; however, there was no significance between the groups. The systemic vascular resistance was moderately decreased in all groups. The PCWP was increased slightly in group 2 and remained unchanged in groups 1 and 3. CI increased significantly in groups 1 and 2. It remained unchanged in group 3; consequently, the systemic BP was reduced (BPmean, -3.2 mm Hg; P<.05). One patient with severe pulmonary hypertension and markedly reduced CI (PAPmean, 67 mm Hg; CI, 1.8 L·min-1·m-2) was hyperhydrated after angiography to maintain the reduced renal function; however, he developed right ventricle congestion 1 day later and was therefore immediately operated on.
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Discussion |
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Characterization of Patient Groups
The presented data compare the hemodynamic effects of direct pulmonary bolus injection of nonionic contrast medium and oxygen administration in patients with moderately severe (group 2) and severe (group 3) chronic thromboembolic pulmonary hypertension and a control group (group 1). According to Grossmann and Braunwald,18 definite pulmonary hypertension is present when systolic PAP and mean pressure exceed 30 and 20 mm Hg, respectively.19 To better differentiate between the influence of moderate and severe pulmonary hypertension, we defined group 2 with moderately severe pulmonary hypertension (ie, PAPsyst >30 and
60 mm Hg) and group 3 with severe pulmonary hypertension with systolic PAP >60 mm Hg. Besides two patients with completely normal angiograms, group 1 included five patients after thrombendarterectomy and four patients with histories of pulmonary embolism but normal pulmonary hemodynamics. Despite this heterogeneous history, all patients had completely normal pulmonary hemodynamics at rest and comprise the control group (1). Groups 2 and 3 were characterized by their elevated PAPs and PVRIs and markedly increased RVSWI. CI was significantly reduced in group 3, but mean systemic BP was maintained by the increased SVRI. This was related to the impaired right ventricle function in group 3, because the left ventricle filling pressure, ie, PCWPmean, and the LVSWI were not different. Different courses of hemodynamic parameters during the procedure were therefore related to the thromboembolic disease.
Oxygen Inhalation
Oxygen administration significantly increased oxygen saturation and reduced HR. PAP was reduced, predominantly in group 3. The maximal systolic pressure decrease was P=-8.5 mm Hg (-9%) in a patient with considerable pulmonary hypertension at rest (PAPsyst=98.5 mm Hg). According to others,15 SVRI and mean systemic BP were slightly increased.
Oxygen is known to reduce PAP and pulmonary vascular resistance.17 20 21 22 23 24 25 26 Several other drugs such as nitric oxide, acetylcholine,27 28 29 30 31 nifidipine, and prostacyclin PGI231 32 33 34 35 have been reported to lower pulmonary artery pressure in experimental studies and in different clinical conditions. However, oxygen is the most physiological agent, and its handling is simple. Moser et al1 therefore suggested that pulmonary angiography must be performed with oxygen administration during the procedure. Although the oxygen effect was only moderate, our clinical data support this recommendation. Histopathological examinations demonstrated that the small pulmonary arteries in chronic major-vessel thromboembolic pulmonary hypertension have hypertensive lesions, including plexogenic lesions, that could not be differentiated from primary pulmonary hypertension. Conversely, Moser and colleagues36 37 recently reported that patients with primary pulmonary hypertension may develop extensive central pulmonary thrombi. Patients with severe chronic thromboembolic pulmonary hypertension can therefore be expected to have fixed arteriolar walls without significant pulmonary vasodilation capacity. In our patients, PVRI varied extensively and was not significantly changed; however, mean PAP was slightly decreased. The extent of pressure release has to be related to the starting points and seems to be neglectable in the hypertensive groups. However, the maximal decrease of systolic PAP was 9%, indicating that there might be some preserved vasodilation capacity in selected patients. Further investigation is required to correlate the distribution pattern of angiographic findings (diffuse or more circumscribed) and the vasodilation capacity in those patients.
The control group included patients after pulmonary thrombendarterectomy and those with hemodynamically nonrelevant thromboembolism. Their pulmonary vessels might have had histopathological lesions to attenuate the physiological oxygen effect; however, the baseline parameters were completely normal. Our data suggest that oxygen only moderately affects pulmonary vasodilation even in physiological conditions. However, it improves the hemodynamic parameters in selected cases and at least significantly improves the oxygen supply in all groups. With respect to safety, in these high-risk patients, pulmonary angiography should be performed with the administration of oxygen during the procedure.
Hemodynamic Effects Caused by Contrast Bolus Injection
The simultaneous recording of RAP and PAP demonstrates the effects of direct pulmonary contrast bolus injection. However, because angiography was performed in inspiratory rest, the intrathoracic pressure level was elevated, and RAP and mean PAP were significantly increased. Compared with these new inspiratory starting points, the contrast bolus only slightly increased the PAP within the very first heart cycles. The maximal bolus-dependent pressure changes varied between -14 and 18 mm Hg in patients with considerable pulmonary hypertension; however, clinical problems were not observed. The bolus-related pressure peaks increased during the repetitive bolus injections, which was accompanied by increasing inspiratory pressure levels, indicating the reduced tolerance to short-term repetitive volume load in the hypertensive group (Fig 3
). However, a small bolus-related decrease of mean diastolic pressure was recognized in group 3 during the first repetitive bolus injections (Fig 3) and may represent an early decrease in pulmonary vascular resistance. This was superposed by the following bolus injections and might have weakened the pressure increase caused by successive bolus injections.
The initial pressure peaks mechanically induced by the abrupt pulmonary volume load were demonstrated by Lange et al38 for contrast media as well as for bolus injection of NaCl, blood, and mannitol without relevant differences. This volume effect usually is followed by a decrease in pulmonary vascular resistance during the next 15 to 30 seconds. These early changes in vascular resistance could not be detected with the thermodilution method. For that, on-line pulmonary blood flow measurement would have been necessary. On the other hand, calculations of vascular resistance immediately with the bolus injection may be incorrect when the bolus volume has not yet reached the left atrium, resulting in false high pressure differences between the pulmonary artery and left atrium. A normal pulmonary vasodilation capacity could not be expected because of the assumed hypertensive vascular lesions36 ; however, some early decrease in diastolic PAP may indicate some preserved dilatory capacity and might have contributed to the fact that clinically relevant pressure peaks were not observed.
After angiography, PAP was significantly increased in all groups, predominantly in groups 2 and 3 (Table 4). The right ventricular filling pressure, ie, mean RAP, was significantly increased and SVI was reduced in group 3, indicating impaired right ventricular function; however, CI was maintained by an increased HR. The reduced systemic vascular resistance caused by the vasodilation effect of the contrast medium was not compensated for by an increased CI; consequently, the systemic BP decreased in group 3. One right ventricle congestion was recognized 1 day after angiography in a patient who was hyperhydrated to maintain a markedly reduced renal function. As in all other patients, his hemodynamic parameters were changed only slightly during the procedure; therefore, his right ventricle congestion was most likely related to the volume administered after angiography rather than the contrast medium. Immediately after pulmonary thrombendarterectomy, he was well. In group 2, PAP also increased, but the increase in the right atrial pressure was less. In contrast to group 3, the stroke volume was increased; ie, the hemodynamic situation was well compensated. PVRI tended to increase from group 1 to 3 with large variances. It is not yet clear whether these variances reflect different thrombi distribution patterns or whether these variances could be related to different vasodilation capacities, reflecting the hypertensive lesions of the small pulmonary vessels mentioned above.36 A clinical study recently reported that only 13 of 35 patients with primary pulmonary hypertension responded to vasodilators like nitric oxide and prostacyclin; ie, a variant dilatory capacity of the small pulmonary vessels is common in this entity31 and might be assumed in the chronic thromboembolic disease.
In contrast to pulmonary hypertension secondary to diverse cardiac diseases, experimental thromboembolic pulmonary hypertension in dogs demonstrated that amidotrizoate bolus transitorily increased pulmonary vascular resistance.11 That was accompanied by an increased right ventricular end-diastolic pressure and a reduced pulmonary flow, indicating impaired right ventricle function,11 14 which is consistent with our clinical data. However, within 1 minute of bolus injection, the pulmonary and systemic vascular resistances decreased and the pulmonary blood flow increased, demonstrating the preserved vasodilation capacity in this canine model. Our measurements after angiography was finished might not have realized the very initial hemodynamic effects as discussed above. However, the reduction of systemic vascular resistance was well recognized, and postulating the same time course of these effects, it is most likely that there were indeed no relevant changes detected in pulmonary vascular resistance in this period.
Most clinical data concerning the tolerance of contrast media in pulmonary hypertension refer to pulmonary hypertension secondary to diverse cardiac or lung disease rather than to chronic thromboembolic pulmonary hypertension. However, Tajima et al39 recently reported the effects of iohexol on pulmonary artery pressure in seven patients with thromboembolic pulmonary hypertension. Corresponding to our data, the nonionic iohexol caused only slight effects on PAP, and the authors concluded that iohexol may be safe in these patients. Concerning the location of the bolus injection, the most impressive hemodynamic changes can be expected after direct pulmonary bolus injection compared with right ventricular or right atrial injection.38 The data presented give very detailed insight into hemodynamic alterations caused by direct pulmonary bolus injections of a nonionic contrast medium that to the best of our knowledge, have not yet been reported for this high-risk group. Despite repetitive bolus injections into both main pulmonary arteries and total contrast amounts much higher compared with amounts in the studies referred to above, hemodynamic problems were not observed.
The impaired pulmonary vasodilation capacity characterizes chronic thromboembolic pulmonary hypertension and primary pulmonary hypertension.36 The injected contrast medium increases the volume load and PAP. In severe thromboembolic pulmonary hypertension, the reduced pulmonary vasodilation capacity prevents an adequate increase of CI and results in a reduced systemic BP. Despite a marked increase in RAP, the stroke volume decreases significantly, demonstrating the exhausted right ventricular capacity. Patients with severe chronic thromboembolic pulmonary hypertension therefore have a reduced tolerance to abrupt volume load. However, in our group 3 patients, CI was maintained by the increased HR, and elevated PAP was compensated for during the procedure. In moderately severe thromboembolic pulmonary hypertension, the stroke volume is maintained to a certain extent by an increase in right ventricular filling pressures, ie, mean RAP, demonstrating the well-compensated hemodynamic status.
The vasodilation effect is related mainly to the osmolality of the contrast media used and is accompanied by an osmotic volume shift, resulting in increased circulatory volume.14 15 16 In his experimental work, DiDonato et al14 emphasized the relationship between osmolality and cardiovascular effects not only for contrast media but also for hypertonic glucose or mannitol solutions. Calcium binding effects are not relevant for nonionic contrast media. Experimental data demonstrated the hemodynamic effects in general to be significantly stronger for diatrizoat compared with ioxaglat and weakest for iopamidol. The duration of these effects was also related to the hyperosmolality and lasted up to 20 minutes for diatrizoat compared with 5 minutes for iopamidol.38 Schrader et al11 17 reported stronger alterations of RAP, PAP, pulmonary vascular resistance, pulmonary artery flow, CI, and right ventricular end-diastolic filling pressure for diatrizoate or amidotrizoate compared with iopamidol in patients with normal right ventricle function and in patients with pulmonary hypertension. Comparative studies with detailed data on the hemodynamic effects of ionic and nonionic contrast media are not available for patients with chronic thromboembolic disease, and a comparative study would be ethically irresponsible in terms of the data presented above. Analogous to the experimental and clinical data discussed, the moderate hemodynamic effects in our patients also depend on the nonionic character and the low osmolality of iopamidol. Regarding all these aspects, it is mandatory to only use nonionic contrast media in critical hemodynamic situations. Although we demonstrated slightly impaired right ventricle function after injection of large total contrast amounts in patients with severe chronic thromboembolic pulmonary hypertension, iopamidol is proposed to be safe even in these high-risk patients.
In conclusion, pulmonary bolus injection of iopamidol only moderately changes hemodynamic parameters even in patients with severe chronic thromboembolic pulmonary hypertension. Considerable contrast amounts were compensated for without hemodynamic complications; therefore, iopamidol seems to be safe in critical hemodynamic situations. Oxygen contributes to safety during the procedure.
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Selected Abbreviations and Acronyms |
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Received March 11, 1996; revision received June 11, 1996; accepted June 24, 1996.
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S. Ley, K.-F. Kreitner, I. Morgenstern, M. Thelen, and H.-U. Kauczor Bronchopulmonary Shunts in Patients with Chronic Thromboembolic Pulmonary Hypertension: Evaluation with Helical CT and MR Imaging Am. J. Roentgenol., November 1, 2002; 179(5): 1209 - 1215. [Abstract] [Full Text] [PDF]
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C J Emery, L Fang, E A Laude, and S K Morcos Effects of radiographic contrast media on pulmonary vascular resistance of normoxic and chronically hypoxic pulmonary hypertensive rats Br. J. Radiol., December 1, 2001; 74(888): 1109 - 1117. [Abstract] [Full Text] [PDF]
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