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Slide 2 New ones

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Slide 4 Note down areas that they had problems. If not covered in current session or planned sessions then will come back to at the end

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Slide 6 Q: Slide question A: hyperinflation, flattening of hemidiaphragms, inc retrosternal airspace, bulla, attenuated vessels, etc.Clarify that COPD requires pulmonary function testing and is not a radiological diagnosis. COPD does not = emphysemaQ: How sensitive do you think CXR is for COPD & Emphysema? A: Talk about poor sensitivity of radiographs,

Slide 7 What do you see? (Flattening diaphragms, increased retrosternal space) How do you judge flattening of hemidiaphragms? What is normal?

Slide 8 Show comparison normal on right with COPD on left

Slide 9 Show comparison normal on right with COPD on left. Discuss height of hemidiaphragms (<3cm normal)

Slide 10 What do they see here? What is going on. Large bulla in emphysema

Slide 11 Bullae, blebs, enlarged airspaces etc. Subpleural, parasepta.Q: Where do we typically see the most severe changes? A: apices typically except in a1 antitrypsin deficiency

Slide 12 Two different examples patients with emphysema. What do they see? How does this look different from normal lung? Which has the most severe changes?Q: What can CT be used for in patients with emphysema A: assessing severity/change, infection included infected bulla, small ptx. Severity air trapping. Screening for lung ca,

Slide 13 What might be going on in this patient? What is unusual about about the distribution of the bulla in this patient?Basal Infected bulla in alpha 1 antitripsin deficiency.

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Slide 15 TWO categories: 1. Aortic dissection and 2. TAI-traumatic aortic injury. Both of these may be catastrophically complicated by extravasation through the compromised aortic wall (i.e, rupture). Is it suggested by this slide that we need to introduce a third category (rupture)? Or, is it better to have just the dichotomy of Aortic dissection and TAI???***

Make sure that students understand the difference between aortic dissection and traumatic aortic injury/aortic rupture (terminology and etiology– commonly confused by students)

Slide 16 Q: Slide question 1? A: Marfans, hypertensives, smokers, aortic stenosis, Ehlers danlos and other connective tissue disorders,Q: Slide question 2? A: Hypertension, chest pain radiating to back, different BP in arms, often very non-specific

Slide 17 Q: Slide question? A: CT (only if +C), Mri (with or without gad) if stable, TEE.Q: What might affect your choice of exam? A: Patient’s ability to tolerate iodinated contrast for CTAQ: What patient factors (hemodynamic stability, renal function, contrast allergy etc).Q: What about doing a catheter angiogram? A: Little role for conventional angio currently outside of during therapy, because angio only shows the inside of the lumen. The real question is about the wall of the aorta when considering dissection.

Slide 18 Normal study, have them indicated what they would be looking forFlap, extravasation, periaortic changes, difference in contrast between the channels. Imaging down thro the illiacs. Finding where the vessels arise from etc.

Slide 19 What do we see? Why is the blood denser in one lumen than the other? What do the terms ‘false’ and true’ lumen mean? Show how these may extend down into the pelvisAsk them about what organs might be affected depending on what vessels are involved (kidneys, brain, gut)

Slide 20 True and False lumina clearly seen with some active arterial enhancement in the descending aortic false lumen

Slide 21 What do they see? What might you be concerned about here? (Celiac and renal arteries involved but currently good perfusion)

Slide 22 Ruptured dissection. What is different in this case? See if they can spot the blood outside the lumen.

Slide 23 What might this patient have? Note dilated aorta – have them point it out. Marfans patient.

Slide 24 DeBakey versus Stanford.type I : involves ascending and descending aorta = Stanford Atype II : involves ascending aorta only = Stanford Atype III : involves descending aorta only = Stanford BDraw on image. Don’t need them to know details, just concept.What is the significance of the classifications? – affects medical versus surgical management

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Slide 26 Get them to discuss cardiogenic and non-cardiogenic causes (neurogenic, ARDS, drowning, fluid overload etc)

Slide 27 History, Heart size, effusions, septal lines (much more specific for cardiogenic) peripheral location opacities in ARDs, asymmetry etc.Discuss the non-specificity of these findings often

Slide 28 Confirm that they know how to measure CTR correctly and the significance of the <0.5 normal ratioWhat would be a normal CTR on a AP chest XR? (<0.6). Why is this larger (magnification)

Slide 29 Confirm that they know how to measure CTR correctly

Slide 30 AP projectionObesity/pericardial fat padsLarge breastsLow inspirationPectusPericardial effusions

Slide 31 Discuss: arrhythmias, acute MI, ruptured papillary muscle/septum post MI etc

Slide 32 Discuss and draw on images:(cardiomegaly)Distension and blurring of upper lobe pulmonary veins

Size > lower lobe vessel same distance from hilumPeribronchial cuffing/indistinct hilar “fuzziness”

Bronchitis, interstitial fibrosisKerley B (A and C) lines

Slide 33 Elderly patient with multiple cardiac issues, in acute pulmonary edema left, and after CABG, mitral valve replacement and pacemaker inserted right. Show intersitital markings, vascular haziness, peribronchial thickening

Slide 34 17 year old with post viral cardiomyopathy, acute (left) and baseline (right). Nice Kerly Bs, ‘shaggy’ heart

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Slide 36 Normal left, thickened on right

Slide 37 Alveolar opacities, air bronchograms, bat wing patters, pleural effusions.Draw on image

Slide 38 Explain ‘lag effect’ of effusion (I draw a graph of waxing and waning LA pressures with the effusions lagging behind)

Slide 39 Explain ‘lag effect’ of effusion (I draw a graph of waxing and waning LA pressures with the effusions lagging behind)

Slide 40 Describe the image. Typical batwing. Acute MI

Slide 41 Baseline 41year old man with dialysis dependent end stage renal disease who got shortness of breath from pulmonary edema. An image from a month before his acute onset of shortness of breath is the initial image Next image is 2 hours after admissionNote the cardiomegaly

Slide 42 Same patient to show progression of edema

Slide 43 What is different about this image? Note the assymetry (ruptured papillary muscle, severe pulmonary edema)

Slide 44 9 yr old. s/p ATV accident with terminal hypoxic brain damage. What could this be due to? Neurogenic pulmonary edema.

Slide 45 Compare and contrast prior cases with patient with ARDS. How is the distribution different? Peripheral rather than central

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Slide 47 Discuss use of D-dimer in low risk patients, when might you do a lower extremity Doppler, CT pulmonary angiogram, VQ. Conventional PA angiogramD-dimer not helpful in ‘sick’ patientsWELL’s criteria?Likelihood of PE, lower extremity symptoms, contraindications to CT (renal failure, allergy) etcConventional PA probably only for treatment, occasional for indeterinatem CT, or with CO2 if contrast cannot be given (larger emboli)VQ: contrast allergy, renal failure

Slide 48 Get them to think about what we want to see – do we want to see the PAs, aorta, liver etc?.Maybe extend this slightly to discuss why we need a good large bore IV to do CTAs and CTPAs and why we can’t always optimally scan for all things at once.More the concept of that we time boluses and scanning for different indicationsOmit if time issues

Slide 49 Have them identify the PAs, draw on image if possible .Understand concept of ‘filling defects’ –Flowing blood white, clots is black . . Lack distal perfusion, signs infarct etcGood study >95% accuracyDepends on study quality (bolus, respiration, body habitus) as to what size PEs we can see ,

Slide 50 Two different patients with PEs. See if they can see them.

Slide 51 Two further examples

Slide 52 What do you think happened here? RUL pulmonary infarct. Small occlusive RUL emboliHampton’s Hump

Slide 53 Have them trace out the ‘saddle embolus’ to understand the termWhat do you see here that might suggest that the patient is at cardiovascular risk from her PE?Signs RV strain – show vent dilatation, deviation of septum to left, triscupid valve plane larger than mitral

Slide 54 Contrast allergies, renal failure. Rarely inadequate IV accessDiscuss that they are reported as probabilities. Pioped (modified) criteria . Need to know the significance of the probabilities

Slide 55 <1%, 1-5%, 6-20%, 21-80%, >80%. Talk about how an pretest high risk patient still is at significant risk of PE even with a low prob VQ scan.

Slide 56 Normal study shown. If wanted, discuss how we obtain the ventilation and perfusion images (Tc99m DPTA/MAA).Talk about matched and mismatched segments.Not important that they know the criteria, just that there are specific criteria that are used to standardize interpretations.Explain that CXR is needed for interpretation

Slide 57 What do you see here? Normal CXR. High prob VQSee if they can find the multiple mismatches.

Slide 58 What looks different here?Abnormal ventilation ++in patient with COPD. Just to illustrate why COPD/emphysema patients can be a problem for VQ scans. Low prob by modified Pioped

(omit if time constraints)