7: It’s Not CTEPH, but It Is Chronic Thromboembolic Disease (CTED)


Figure 7.1

Chest radiograph at time of evaluation for thromboendarterectomy



Lung scintigraphy (Fig. 7.2) demonstrated large right upper lobe and lingular perfusion defects, with a smaller unmatched defect in the anterior right lower lobe.

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Figure 7.2

Lung scintigraphy demonstrating unmatched perfusion defects in both lungs


Results of the right heart catheterization showed pulmonary hemodynamics at rest of right atrial mean of 6 mmHg, PA pressure 31/13 mmHg (20 mean), PAOP 10 mmHg, thermodilution cardiac output of 7.2 L/min (cardiac index 3.17 L/min/m2) and calculated PVR 112 dyn s/cm5. Exertion of his upper extremities resulted in a PA pressure of 46/12 mmHg (28 mean), a pulmonary capillary wedge pressure of 12 mmHg, and a thermodilution cardiac output 13.6 L/min (cardiac index 5.99 L/min/m2); calculated PVR was 94 dyn s/cm5.


Pulmonary angiography revealed evidence for chronic thromboembolic disease at the lobar level of a right upper lobe vessel and lingula (Fig. 7.3).

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Figure 7.3

Digital subtraction pulmonary arteriogram: “pouch defect” proximal right upper lobe (open arrow), and occluded lingula (closed arrow)


Though there was radiographic evidence for operable chronic thromboembolic disease, in the absence of significant exercise limitation and with essentially normal pulmonary hemodynamics at rest and during modest exertion, it was assessed that the risk of a surgical thromboendarterectomy was unwarranted and unlikely to result in a noticeable clinical benefit. However, to provide a more complete physiologic evaluation at higher levels of exercise, a cardiopulmonary exercise test (CPET) was requested.


The patient exercised up to 271 W for a total exercise time of 11 min 1 s and was reported stopping because of dyspnea (3 out of 10) At rest, minute ventilation (VE) at rest was 13.5 L/min, maximum voluntary ventilation was 194 L/min, and resting oxygen saturation was 99% (pulse oximetry). The patient’s physiological dead space proportion (VD/VT) at rest, estimated from the transcutaneous PCO2 (PtcCO2) and exhaled PCO2 (PexCO2), was 0.31. Anaerobic threshold, based on the rates of change in VE/VO2, VE/VCO2 and R was reached at a VO2 of 1.692 L/min (16.6 mL/kg/min), 59% of predicted peak VO2. At the point of AT, the VE/VCO2 ratio was 28, the RQ was 0.95 and the heart rate was 139 BPM (81% of the predicted max). At peak exercise, VO2 (3.505 L/min, 34.4 mL/kg/min) was 123% of the predicted peak (2.856 L/min). The RQ was 1.15. The anaerobic reserve (peak-AT VO2) was 1.81, which was 63% of the predicted peak VO2. VE peak (100.8 L/min) reached 52% of the MVV measured just prior to exercise (194 L/min). The oxygen saturation during peak exercise was 92%, physiological VD/VT was 0.27, heart rate (179 BPM) was 104% of the predicted maximum heart rate and the BP was 144 mmHg/90 mmHg. The O2 pulse at peak exercise was 19.6 mL/beat mL/beat (438% of the O2 pulse at rest and 109% of the predicted maximum of 17.9 mL/beat). The O2 pulse increased continuously throughout the point when the patient reached anaerobic threshold and continued to increase even after the VO2 exceeded the predicted peak VO2. Summary of the CPET results:



  • This was a maximal exercise test.



  • The patient reached >100% of maximal predicted oxygen consumption, consistent with supra-normal aerobic exercise capacity.



  • Normal cardiac response to exercise, with no evidence of impairment of heart rate or stroke volume reserve.



  • There was no evidence of a ventilatory limitation.



  • There was modest oxygen desaturation (nadir 92%), however, the SpO2 did not fall below 95% until a VO2 was twofold the value at the onset of anaerobic threshold and >100% of the maximal predicted VO2.



  • The absence of significant ventilatory inefficiency at peak workload as well as the absolute fall in the VE/VCO2 throughout exercise is consistent with relatively normal pulmonary vascular recruitment with exertion.

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Oct 30, 2020 | Posted by in Uncategorized | Comments Off on 7: It’s Not CTEPH, but It Is Chronic Thromboembolic Disease (CTED)

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