AJR:188, May 2007 1255

AJR 2007; 188:12551261

0361803X/07/18851255

American Roentgen Ray Society

WittramCT Pulmonary Angiography

C h e s t I m ag i n g Pe r s p e c t i ve

How I Do It: CT Pulmonary Angiography

Conrad Wittram1

Wittram C

Keywords: chest, CT arteriography, CT technique, embolism

DOI:10.2214/AJR.06.1104

Received August 18, 2006; accepted after revision November 8, 2006.

1Department of Thoracic Radiology, Massachusetts General Hospital, Founders 202, 55 Fruit St., Boston, MA 02114. Address correspondence to C. Wittram.

CMEThis article is available for CME credit. See www.arrs.org for more information.

OBJECTIVE. The purpose of this article is to describe the techniques to improve motion ar-tifacts, vascular enhancement, flow artifacts, body habitus image noise, vascular opacification inparenchymal lung disease, streak artifacts, and the indeterminate CT pulmonary angiogram. Inaddition, this article will illustrate the diagnostic criteria of acute and chronic pulmonary emboli.

CONCLUSION. Pulmonary embolism is the third most common acute cardiovasculardisease, after myocardial infarction and stroke, and it leads to thousands of deaths each yearbecause it often goes undetected. For the more than 25 years that the direct signs of pulmonaryembolism have been available to the radiologist on CT, this noninvasive technique has produceda paradigm shift that has raised the standard of care for patients with this disease.

ulmonary embolism is the thirdmost common acute cardiovascu-lar disease, after myocardial in-farction and stroke, and results in

an estimated 200,000300,000 hospitaliza-tions and 37,00044,000 deaths per year in theUnited States [1]. In 1980, Godwin et al. [2]were among the first to describe pulmonaryembolism on contrast-enhanced CT. In 1990,the Prospective Investigation of PulmonaryEmbolism Diagnosis (PIOPED) study resultswere published [3]. This large multicenter trialcompared ventilationperfusion (V/Q) scintig-raphy with pulmonary angiography and estab-lished the diagnostic characteristics of pulmo-nary embolism on V/Q scintigraphy. Thesensitivity of V/Q scintigraphy was found to be98%, with a specificity of 10% [3]. The poten-tial of the noninvasive technique, CT pulmo-nary angiography (CTPA), has now been real-ized at most institutions; it has become the testof choice and thus the de facto standard of care[4]. Recent studies have shown the sensitivityof thin-slice MDCTPA to be 90100% and thespecificity to be 8994% for the detection ofpulmonary emboli to the level of the subseg-mental arteries, using pulmonary angiographyas the gold standard [5, 6].

A much larger multicenter study has been re-cently published: The PIOPED II study, whichused a composite gold standard, showed thatCTPA has a sensitivity of 83% and specificityof 96% for the detection of pulmonary embo-lism and that combined CTPA and CT venog-

raphy have a sensitivity of 90% and specificityof 95% for the detection of venous thromboem-bolic disease [7]. The PIOPED II study foundthat patients with a low or intermediate clinicalprobability of pulmonary embolism and normalresults on CTPA had a high negative predictivevalue for PE (96% for patients with a low prob-ability and 89% for patients with an intermedi-ate probability); however, the negative predic-tive value was 60% in patients with a highprobability before CTPA. The positive predic-tive value of abnormal findings on CTPA washigh (9296%) in patients with an intermediateor high clinical probability but much lower(58%) in patients with a low likelihood of pul-monary embolism. Therefore, additional test-ing is recommended when the clinical probabil-ity is inconsistent with the imaging results [7].

A limitation of the PIOPED II study wasthat the composite gold standard was not 100%accurate for the diagnosis of venous throm-boembolic disease; it therefore follows that theperformance of CT was likely better than theresults indicate. In the PIOPED II study,among 824 patients with a reference diagnosisand a completed CT study, CTPA was incon-clusive in 51 because of poor image quality [7].A recent study that evaluated the causes of in-determinate CTPA findings found an indeter-minate rate of 6.6% [8]. The most commoncause was motion artifacts in 74% of the cases;other reasons included poor enhancement(40%), patient habitus (7%), parenchymal dis-ease (12%), and streak artifacts (7%) [8]. The

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purpose of this article is to describe the tech-niques used to improve the quality of CT pul-monary angiography and to illustrate the diag-nostic criteria of acute and chronic pulmonaryemboli. Indirect CT venography will not bedealt with in detail in this article.

CT TechniqueAt the moment, at our institution, Light-

speed (GE Healthcare) 16- and 64-MDCTscanners are used to acquire the images of thethorax in a caudalcranial direction. The cau-dalcranial direction is used because most em-boli are located in the lower lobes and, if thepatient breathes during image acquisition,there is more excursion of the lower lobes com-pared with the upper lobes. For IV access, theantecubital vein and an 18- or 20-gauge cathe-ter is preferred. The CT parameters are given inTables 1 and 2. Images are viewed on a PACSmonitor using IMPAX version 4.1 (AGFA) be-cause there is improved accuracy in viewingchest CT cases on a workstation comparedwith hard-copy film [9, 10]. The images aredisplayed with three different gray scales forinterpretation of lung window (window width,1,500 H; window level, 600 H), mediastinalwindow (window width, 350 H; window level,40 H), and pulmonary embolismspecific

(window width, 700 H; window level, 100 H)settings because pulmonary embolism can bemissed when a case with very bright contrast isviewed only on mediastinal window settings[11]. The pulmonary embolismspecific set-tings also help to differentiate between a sharpmargined embolus and an ill-defined artifact.However, modified window settings can alsoincrease the conspicuity of artifacts caused byimage noise and flow.

Multiplanar reformation images through thelongitudinal axis of a vessel can be used toovercome some of the difficulties encounteredwith axial-orientated images of obliquely oraxially orientated arteries [12]. Also, reformat-ted images can help to differentiate betweensome patient, technical, anatomic, and patho-logic factors that mimic pulmonary embolismand true pulmonary embolism [11].

Contrast-enhanced helical CT of the veinsof the lower extremities is performed usingthe same contrast bolus as used for chest CT.Images of the iliac, femoral, and poplitealveins are obtained 3 minutes after the onset ofthe initial contrast injection [13].

How to Reduce Motion ArtifactsRespiratory motion artifacts are the most

common cause of an indeterminate CTPA and

TABLE 1: 16-MDCT Pulmonary Angiography Protocol

Parameter Normal-Sized Patient Large Patient (> 250 lb [113 kg])

Detector width/reconstruction (mm) 1.25/1.25 2.5/1.2.5

Table speed/rotation (mm) 13.75 6.88

Pitch 1.375:1 0.562:1

Peak kilovoltage 140 140

Milliamperes 380 380

Rotation time (s) 0.5 1.0

Algorithm Standard Standard

Scanning field of view Large Large

Display field of view Rib to rib Rib to rib

TABLE 2: 64-MDCT Pulmonary Angiography Protocol

Parameter Normal-Sized Patient Large Patient (> 250 lb [113 kg])

Detector width/reconstruction (mm) 0.625/1.25 0.625/1.25/2.5

Table speed/rotation (mm) 55 55

Pitch 1.375:1 1.375:1

Peak kilovoltage 140 140

Milliamperes 380 380

Rotation time (s) 0.5 1.0

Algorithm Standard Standard

Scanning field of view Large Large

Display field of view Rib to rib Rib to rib

can be a cause of misdiagnosis of pulmonaryembolism. They are best seen on lung windowsettings that show composite images of vessels[11]. A rapid change in position of vessels oncontiguous images also confirms motion artifact.A low-density abnormality that simulates pul-monary embolism may result from partial vol-uming of vessel and lung [11]. Motion artifactrenders the diagnosis of pulmonary embolism atthe affected anatomic level indeterminate. Thefrequency of examinations devoid of motion ar-tifacts is significantly higher for MDCT, whichhas a shorter breath-hold than single-detector CT[14, 15]. At the moment, the breath-hold re-quired for 16-MDCT is approximately 10 sec-onds, and for 64-MDCT, less than 3 seconds. Indyspneic patients, oxygen supplementation canhelp the patient provide the desired period of ap-nea. The implementation of higher order MDCTscanners should lower the indeterminate CTPArate due to respiratory motion.

Pulmonary Artery EnhancementTheory

An increase in the attenuation of blood onCT may be obtained with intravascular con-trast material containing the atoms of iodine orgadolinium. Previous work has defined the at-tenuation values of acute and chronic pulmo-nary emboli [16]. Combining these values withexperimental work by Meaney et al. [17], it ispossible to calculate the minimum amount ofIV attenuation required to perceive pulmonaryemboli on CT. Meaney et al. showed that thedetection of a low-contrast abnormality is notaccurate when the SD of the mean of the abnor-mality exceeds the difference in the means ofthe lesion and the surrounding region [17]. Foracute pulmonary emboli, the mean attenuationvalue is 33 H (SD, 15 H) [16].

Because it is important to detect all pulmo-nary emboli, we should calculate the highestpossible attenuation of an acute pulmonary em-bolism to be the mean plus 3 SDs; this would in-clude 99.75% of all acute emboli, which equatesto 78 H. According to Meaney et al. [17], weneed attenuation in the artery of at least one moreSD; the final figure therefore equals 93 H. Themean attenuation and SD values for chronic pul-monary embolism are 87 and 31 H, respectively.Therefore, the highest possible attenuation valueof chronic pulmonary emboli with 3 SDs is cal-culated to be 180 H. The minimum attenuationof adjacent opacified blood to identify this outly-ing chronic thrombus is 211 H. The theoreticminimum attenuations of blood required to seeall acute and chronic pulmonary venous throm-boemboli are 93 and 211 H, respectively.

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TABLE 3: Empirical Timing Delay for CT Pulmonary Angiography After IV Administration of 370 mg I/mL

Injection

Timing Delay (s)

16-MDCT 64-MDCT

Normal-SizePatient

Large Patient(> 250 lb [113 kg])

Normal-SizePatient

Large Patient(> 250 lb [113 kg])

Amount injected (mL) 110 130 110 130

Rate of injection (mL/s)

4 22 30 26 31

3.5 26 34 30 35

3 32 40 36 42

2.5 39 49 43 51

2 50 61 53 63

To detect abnormalities with low differ-ences in CT contrast, and to improve pulmo-nary embolism conspicuity, it is necessary toadjust the display window widths and levels[1719]. Also, the decision of the reviewer tointerpret a study as adequate or indeterminatewill be affected by the interplay of factors thatinclude the size of the suspected embolism,the anatomic level of the vessel being evalu-ated, and the amount of image noise.

Timing of BolusSeveral techniques are available for con-

trast delivery on CT studies. A high injectionrate with a uniphase injection bolus of 4 mL/sof contrast material is preferred [20]; this al-lows a high intensity of contrast enhancementin the pulmonary arterial system. The injec-tion duration has an important influence inoptimizing contrast delivery in CT.

Injection of contrast material can be consid-ered in two components: first pass and recircu-lation. The first-pass effect is optimized by theuse of contrast material with 370 mg I/mL. Asthe injection duration increases, the recircula-tion of contrast material causes a cumulative ef-fect on enhancement over time [21], so that anincrease in time increases the enhancement ofthe pulmonary arteries during the injection.This enhancement advantage is most optimallyused with the empiric delay technique, whereasbolus tracking starts the CT scan earlier on therise of the enhancement curve and results inworse pulmonary artery enhancement. Al-though no published data as yet can validatethis statement, preliminary work appears tosupport this observation [22, 23]. One could ar-gue that when the triggering threshold for bolustracking is increased, CT would start later onthe rise of the enhancement curve. However, incases with poor function of the right side of the

heart, the enhancement threshold might neverbe reached; this leaves the technologist uncer-tain as to when to start image acquisition.

Empiric scanning delay also has the advan-tage of reducing operator error and motion arti-facts by removing the added complexity of whento start the study based on a threshold value. Tocomprehensively evaluate for venous throm-boembolic disease, patients need to receive alarge contrast material bolus to evaluate thelower-limb veins [7]. Using an empiric scanningdelay on 16- and 64-MDCT scanners, one aimsto be midscan at the peak of pulmonary arteryenhancement; therefore, the start of the scanningis calculated to equal the injection time minushalf the scanning time. If the size of the IV accesscatheter does not allow 4 mL/s, then the delayneeds to increase, as illustrated in Table 3.

If an indeterminate scan occurs with stan-dard delay due to poor enhancement, there isno extravasation of contrast material, and thetiming is appropriate, then poor venous flowdue to stenosis or obstruction may be a factor[8], in which case a different venous accesssite may be necessary. A repeat CTPA afterhydration of the patient is recommended.

Flow ArtifactsA transient interruption of contrast material

consists of a portion of the pulmonary arterythat shows relatively poor enhancement be-tween areas of higher attenuation both proxi-mally and distally [24, 25] (Fig. 1). Comparingpatients with this artifact with age- and sex-matched controls, Wittram and Yoo [25]showed that the artifact results from an increasein flow of unopacified blood from the inferiorvena cava. What can be done to avoid this flowphenomenon? A review of the literature showsthat the transient interruption of contrast artifactwas seen in 3% of the study population in that

study [25], whereas in the study by Gosselin etal. [24], it was present in 37% of the studygroup. An interesting major difference betweenthe studies, and a possible explanation of thedifference in frequency, is that the patients inthe study by Wittram and Yoo were instructedto take a breath in and hold it before imageacquisition. The patients in the study by Gosse-lin et al. were instructed to have five respiratorycycles of hyperventilation followed by a com-mand of full inspiration 2 seconds before initialimages were obtained [24]. The hyperventila-tion before inspiration and the breath-hold islikely the exacerbating factor of this artifact.Both studies used the same injection rate, butGosselin et al. used single-detector CT whereasWittram and Yoo used MDCT. However, thenumber of detectors should not affect the ap-pearance of this artifact.

The solution to transient interruption of con-trast flow of the pulmonary arteries is to reducethe volume of unopacified blood entering theright atrium from the inferior vena cava. Pres-canning hyperventilation is likely the cause;with the implementation of faster scanners,prescan hyperventilation should be dropped.Because the venous return from the inferiorvena cava to the right atrium is exaggerated with

Fig. 1Transient interruption of flow of contrast material in 59-year-old woman. Coronal oblique reformatted image through right posterior basal segmental artery from CT pulmonary angiography shows segment of poor opacification (arrow) between areas of higher attenuation both proximally and distally. Interface between low- and high-attenuation areas is ill-defined.

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A B

Fig. 2Localized increase in vascular resistance in 69-year-old woman with breast cancer who has right-sided talc pleurodesis.A, Staging CT was performed with injection of 65 mL of Isovue 370 (iopamidol, Bristol-Myers Squibb) at rate of 1.5 mL/s using scan delay of 35 seconds. Right lower lobe shows volume loss and consolidation. Note good opacification of left lower lobe pulmonary arteries (arrowheads). However, also note poor opacification of right lower lobe pulmonary arteries (arrows), indicating localized increase in vascular resistance in right lower lobe arteries.B, CT pulmonary angiogram 3 days after A using 110 mL of Isovue 370 at 4 mL/s and 22-second scanning delay. Note good opacification of right lower lobe pulmonary arteries (arrows). This image illustrates that peripheral vascular resistance can be overcome with large volume of contrast material injected rapidly and by acquiring images at very end of injection.

heightened respiratory movements [26], we ver-bally instruct our patients not to perform an ex-aggerated inspiration and the CT technologistprompts the patient to hold your breath beforeimage acquisition. Further study is required toassess the possible benefits of these maneuvers.

Localized increase in vascular resistance canresult from lung consolidation or atelectasis[27]. The focal slow pulmonary artery flow canbe a cause of an indeterminate CTPA (Fig. 2)and can be a cause of misdiagnosis of pulmo-nary embolism [11]. Recognition of this phe-nomenon is important because the poorly opac-ified vessel may be normal or the poor contrastenhancement may obscure thrombus. A region-of-interest measurement may be helpful in thisdecision if the attenuation is greater than 78 H,which is the upper value of acute pulmonaryemboli [16]. Further imaging may be neces-sary, either repeating CTPA with an increaseddelay or pulmonary angiography. Although ourexperience is anecdotal, this is an uncommonartifact with empiric timing delay; it is likelydue to the wider temporal window of contrastinjection that occurs with empiric timing delaycompared with other techniques (Fig. 2).

Patient HabitusTwo major issues are related to imaging pul-

monary arteries of large patients: image noiseand the volume of IV contrast material. For pa-tients weighing more than 250 lb (113 kg), it isnecessary to increase the radiation dose to de-crease the amount of image noise. In addition,the protocol is modified to help decrease display

image noise and improve scan quality by in-creasing reconstruction width to 2.5 mm. How-ever, the reconstruction width will decrease thesensitivity of pulmonary embolism detection[28]. In larger patients, for optimal pulmonaryartery enhancement, the quantity of contrast ma-terial needs to be adapted to the patients size[29]; to simplify the protocol, 110 mL of 370 mgI/mL contrast material is used for patients weigh-ing 250 lb (113 kg) or less and 130 mL of 370 mgI/mL contrast material is used for those weight-ing more than 250 lb (113 kg) (Tables 1 and 2).

For pregnant patients, the volume of con-trast material should be reduced to 70 mL andthe timing adjusted accordingly (Table 4).The reason for this rationale is that the legsand pelvis are not imaged and that the quan-tity of iodine to the fetus is also reduced.

Parenchymal DiseaseConsolidation can cause a focal increase in

vascular resistance and focal poor vascularopacification [27]. However, the frequency ofthis artifact will be reduced with the use ofempiric timing delay (Fig. 2) because imageacquisition is performed at the end of the in-jection. As for reviewing vessels surroundedby consolidation, as with all radiology inter-pretation, it is important to be systematic andreview one vessel at a time and ignore theconsolidation or any other pathology thatmight distract the attention of the reviewer. Inthis manner, any case with adequate enhance-ment and no or minimal motion can be confi-dently interpreted.

Streak ArtifactsStreak artifact that obscures pulmonary ves-

sels because of metallic implants can make astudy indeterminate, a repeat CT will not im-prove this problem, and additional imagingwith V/Q scintigraphy or pulmonary angiogra-phy may be necessary. Streak artifact fromhigh-density contrast material in the superiorvena cava can obscure adjacent pulmonary ar-teries. The frequency of this artifact can be re-duced by using a saline bolus immediately af-ter the contrast material injection [30].

The Indeterminate CTPAThis article discusses the solutions to the

common causes of an indeterminate CTPA. Inpractice, if a diagnosis of pulmonary embolismcannot be confidently confirmed or refuted andthe study is indeterminate, it is recommendedthat the radiologist decide at which anatomiclevel the study is indeterminate; for example, ifthe radiologist can clear the vessels to the levelof the segmental arteries, and the subsegmentalarteries are indeterminate, the clinician mightnot require further imaging in cases with a lowclinical pretest probability for pulmonary embo-lism. However, some patients with indetermi-nate CTPA findings will need further imaging,with ultrasound scan of the legs after hydration,a repeat CTPA, V/Q scintigraphy (if the lungsare clear on CT), or pulmonary angiography.

Direct Signs of Acute and Chronic Embolism

Both acute and chronic pulmonary emboliare identified as intraluminal filling defects thatshow a sharp interface with IV contrast mate-rial. The diagnostic criteria for acute pulmo-nary embolism include, first, complete arterialocclusion with failure to opacify the entire lu-men; the artery may be enlarged in comparisonwith pulmonary arteries of the same order ofbranching [3133] (Fig. 3); second, a central

TABLE 4: Empirical Timing Delay for CT Pulmonary Angiography for Pregnant Patients After IV Administration of 70 mL of 370 mg I/mL

Rate of Injection (mL/s)

Timing Delay (s)

16-MDCT 64-MDCT

4 12 16

3.5 15 18

3 18 21

2.5 23 26

2 30 33

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Fig. 3Acute pulmonary embolism in 27-year-old woman. CT pulmonary angiogram shows thrombus (arrow) that expands diameter of right posterior basal subsegmental artery compared with pulmonary arteries of same order of branching (arrowheads).

A

B

Fig. 4Acute pulmonary embolism in 27-year-old woman.A, Centrally located thrombus, in right posterior basal segmental artery, has well-defined margins and is completely surrounded by contrast material (arrow). Acute emboli are also noted in right lateral basal segmental and left posterior basal subsegmental arteries.B, Curved reformatted image of posterior basal segmental artery of right lower lobe shows that central arterial filling defect (seen in A) cannot occur in isolation without embolism draping over vessel branch point or touching vessel wall at some point. Axial image of thrombus (A) was acquired at level of arrow.

arterial filling defect surrounded by IV contrastmaterial [31] (Fig. 4); and third, a peripheral in-traluminal filling defect that makes an acute an-gle with the arterial wall [32, 33] (Fig. 5).

The diagnostic criteria for chronic pulmo-nary embolism include complete occlusion ofa vessel that is permanently smaller than pul-monary arteries of the same order of branch-ing [32, 33] (Fig. 6), a peripheral eccentricfilling defect that makes an obtuse angle withthe vessel wall [32, 33] (Fig. 7), contrast ma-terial flowing through apparently thick-walled arteries that are smaller due to recanal-ization [32, 33] (Fig. 8), a band or web in acontrast-filled artery [32, 33] (Fig. 9), and anintraluminal filling defect with an acute pul-monary embolism morphology that has beenpresent for more than 3 months [16].

Fig. 5Acute pulmonary embolism in 28-year-old woman. Eccentrically located embolism (arrow) forms acute angle with vessel wall. Emboli are also noted in right lower lobar and left anteromedial basal segmental arteries.

Indirect Signs of Acute and ChronicPulmonary Embolism

These signs include nonuniform arterialperfusion for both acute and chronic pulmo-nary embolism; this radiologic sign is diffi-cult to identify in cases of acute pulmonaryembolism but manifests as mosaic attenuationin cases of chronic pulmonary embolism. Amosaic pattern of lung attenuation is identi-fied on the lung window settings.

The three major causes of mosaic lung atten-uation are airways disease, chronic pulmonaryembolism (in which the abnormal region is moreradiolucent), and interstitial lung disease (inwhich the abnormal lung is more opaque).Oligemia, or a decrease in the flow rate due toacute pulmonary embolism, is often identifiedon angiography [34, 35]. In my experience, thisfinding is more often seen on angiography thanon CT; this discrepancy is thought to be relatedto the larger temporal window of IV contrast ma-terial for CT as compared with angiography. Oc-casionally, a large acute central pulmonary embo-lism can cause oligemia and a reversible decreasein vessel diameter; this CT equivalent of the Wes-termark sign has been previously illustrated [36].

Nonuniform arterial perfusion due to acutepulmonary embolism can uncommonly mani-fest as a mosaic pattern of attenuation on CT.Additional indirect signs seen in chronic pul-monary embolism include poststenotic dilata-tion, tortuous vessels, enlargement of the mainpulmonary artery, and enlargement of the bron-chial arteries [36]. For a long time we have beenat a stage at which the direct radiologic signs, asshown on CT angiography, are required tomake a diagnosis of acute or chronic pulmo-nary thromboembolic disease. Because the in-direct signs have a differential diagnosis, theyare helpful only as indicators of the sites of thedirect radiologic signs of pulmonary embolism.

Severity of Acute Pulmonary Embolism

After the initial embolic event, the patientmay be at risk for circulatory collapse second-ary to right heart failure, and a subsequent em-bolism may be fatal. It has been suggested thatthe early detection of acute right ventricularfailure allows the implementation of the mostappropriate therapeutic strategy [37]. Rightventricular strain or failure is optimally moni-tored on echocardiography. However, somemorphologic abnormalities that indicate rightventricular failure can be quantified by CTPA.The most robust CT sign is right ventricular di-lation (in which the greatest right ventricleshort-axis measurement is wider than the max-

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Fig. 6Chronic pulmonary embolism in 37-year-old woman. Curved coronal reformatted CT image viewed on lung window setting shows pouch defect (arrow) of anterior basal segmental artery of right lower lobe. Contracted or obliterated artery (arrowheads) is shown peripheral to site of chronic obstruction.

Fig. 7Chronic pulmonary embolism in 60-year-old man. Axial CT image obtained at level of right lower lobe pulmonary artery shows broad-based, smoothly margined, eccentric filling defect (arrow) that forms obtuse angle with vessel wall.

Fig. 8Chronic pulmonary embolism in 65-year-old man. Curved coronal reformatted CT image viewed on maximum intensity projection shows abrupt vessel narrowing that affects posterior basal segmental artery of right lower lobe. Note abrupt convergence of contrast material, leading to thin column of more distal IV contrast material (arrow). In addition, organized thrombus is identified surrounding column of contrast material (arrowheads).

A B

Fig. 9Chronic pulmonary embolism in 54-year-old man. Axial CT image of right lower lobe pulmonary artery shows band or web (arrow) surrounded by contrast material. Subcarinal and right hilar lymphadenopathy is also noted, which is associated with chronic pulmonary embolism.

Fig. 10Acute right ventricle dilatation in 33-year-old woman with large acute pulmonary embolism clot burden.A, Maximum short-axis diameter (black rule) of right ventricle measures 5.2 cm.B, At more cephalad level, maximum short-axis diameter (black rule) of left ventricle measures 3.2 cm. CT pulmonary angiography right ventricletoleft ventricle ratio equals 1.6.

imum left ventricle short-axis measurement)[38] (Fig. 10). The greater the right ventri-cletoleft ventricle short-axis ratio in acutepulmonary embolism, the greater the risk of

death [39]. A ratio of 1.0 is associated with a5% chance of death; 1.3, 10%; 1.7, 20%; 1.9,30%; 2.1, 40%; and a ratio of 2.3 is associatedwith a 50% chance of death [39].

ConclusionFor more than 25 years, the direct signs of pul-

monary embolism have been available to the ra-diologist on CT, and this noninvasive technique

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has produced a paradigm shift that has raised thestandard of care for patients with this disease.This article outlines the approaches necessary toimprove the quality of CT pulmonary angiogra-phy and summarizes the diagnostic criteria foracute and chronic pulmonary emboli.

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F O R Y O U R I N F O R M A T I O N

This article is available for CME credit. See www.arrs.org for more information.

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