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1. Choose a spokesperson

2. All students in the group are to work on all of the following questions/sections included in the Padlet

3. When we come back to the whole class, the spokesperson will feedback findings

4. You can use diagrams/images other visual resources to explain each respiratory condition.

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Pulmonary embolism is  blockage in one of the pulmonary arteries in your lungs. Most often, pulmonary embolism is caused by blood clots that travel to the lungs from deep veins in the legs or, rarely, from veins in other parts of the body.
Risk factors for PE include conditions and disorders that promote blood clotting as a result of venous stasis (immobilization, heart failure), hypercoagulability (inherited coagulation disorders, malignancy, hormone replacement
https://radiopaedia.org/articles/pulmonary-embolism

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Pulmonary embolism (PE) refers to embolic occlusion of the pulmonary arterial system. The majority of cases result from thrombotic occlusion, and therefore the condition is frequently termed pulmonary thromboembolism which is what this article mainly covers.

Non-thrombotic pulmonary emboli sources include ³⁰:

Classification of a pulmonary embolism may be based upon:

the presence or absence of hemodynamic compromise

temporal pattern of occurrence

the presence or absence of symptoms

the vessel which is occluded

The patient may report a history of recent immobilization or surgery, active malignancy, hormone usage, or a previous episode of thromboembolism. The physical exam may reveal suggestive features such as:

clinical signs of deep venous thrombosis (DVT)

asymmetric pitting lower extremity edema

prominent superficial collateral vessels

tenderness to palpation along the deep venous system

tachycardia

dyspnea

pleuritic chest pain

hemoptysis

Clinical decision rules, in conjunction with physician gestalt and estimated pretest probability of disease, may serve as a supplement in risk stratification:

sinus tachycardia: the most common abnormality

right heart strain pattern

incomplete or complete right bundle branch block

prominent R wave in lead V1

right axis deviation

T-wave inversion in the right precordial leads +/- the inferior leads is seen in up to 34% of patients and is associated with high pulmonary artery pressures ²⁵
simultaneous T-wave inversion in lead III and V₁ has been repeatedly shown to have strong sensitivity (90%), specificity (97%), positive predictive value (92%), negative predictive value (96%) and overall predictive accuracy of 95% 25,26

SIQIIITIII pattern: this refers to a deep S wave in lead I, Q wave and T wave inversion in lead III; this sign is seen as classical of PE but is, in fact, poor in terms of both sensitivity and specificity as a sign of PE

D-dimer (ELISA) is commonly used as a screening test in patients with a low and moderate probability clinical assessment, on these patients:

normal D-dimer has almost 100% negative predictive value (virtually excludes PE): no further testing is required

raised D-dimer is seen with PE but has many other causes and is, therefore, non-specific: it indicates the need for further testing if pulmonary embolism is suspected ⁴

In patients with a high probability clinical assessment, a D-dimer test is not helpful because a negative D-dimer result does not exclude pulmonary embolism in more than 15%. Patients are treated with anticoagulants while awaiting the outcome of diagnostic tests ⁴.

Depends to some extent on whether it is acute or chronic. Overall, there is a predilection for the lower lobes.

Chest radiography is neither sensitive nor specific for a pulmonary embolism. It is used to assess for differential diagnostic possibilities such as pneumonia and pneumothorax rather than for the direct diagnosis of PE.

Described chest radiographic signs include:

Sensitivity and specificity of chest x-ray signs ¹:

vascular redistribution

sensitivity: ~10%

specificity: ~87%

positive predictive value: ~21%

negative predictive value: ~74%

CT pulmonary angiography (CTPA) will show filling defects within the pulmonary vasculature with acute pulmonary emboli. When the artery is viewed in its axial plane the central filling defect from the thrombus is surrounded by a thin rim of contrast, which has been called the Polo Mint sign.

Emboli may be occlusive or non-occlusive, the latter is seen with a thin stream of contrast adjacent to the embolus. Typically the embolus makes an acute angle with the vessel, in contrast to chronic emboli. The affected vessel may also enlarge ⁹.

Acute pulmonary thromboemboli can rarely be detected on non-contrast chest CT as intraluminal hyperdensities ¹².

Dual-energy CT holds much promise for the diagnosis and prognosis of PE (see cases 33 and 34). Z effective and iodine maps provide lung perfusion assessment. The use of low monoenergetic reconstructions (low monoE) allows 'iodine boosting' of the pulmonary arteries which are useful during suboptimal contrast opacification thereby preventing the need to repeat undiagnostic scans.

In contrast to acute pulmonary embolism, chronic thromboemboli are often complete occlusions or non-occlusive filling defects in the periphery of the affected vessel which form obtuse angles with the vessel wall ⁹. The thrombus may be calcified.

Features noted with chronic pulmonary emboli include:

webs or bands, intimal irregularities ³

abrupt narrowing or complete obstruction of the pulmonary arteries ³

"pouching defects" which are defined as chronic thromboembolism organized in a concave shape that "points" toward the vessel lumen ³

Indirect signs include ⁷:

Point-of-care ultrasonography is currently not recommended for a haemodynamically stable patient with suspected pulmonary embolism. In the presence of hemodynamic compromise, echocardiography may be of value to assess for the presence of severe right ventricular dysfunction;

if absent, another cardiopulmonary derangement is likely responsible

if unequivocally present, it can establish the need for emergent treatment

Echocardiographic features which may be suggestive include:

Of note, transesophageal echocardiography has a reported sensitivity of 80.5% and a specificity of 97.2% for ruling in acute pulmonary embolism after the detection of right ventricular overload on transthoracic echocardiography ²⁴.

Again not recommended as part of first-line work up.

Cumulative damage from repeated embolic insults is a common cause of chronic thromboembolic pulmonary hypertension, which demonstrates a variable degree of the aforementioned signs, but with significantly higher right ventricular pressures, right ventricular hypertrophy and diastolic dysfunction, and a higher degree of tricuspid regurgitation.

It is difficult to obtain technically adequate images for pulmonary embolism patients using MRI. Magnetic resonance pulmonary angiography (MRPA) should be considered only at centers that routinely perform it well and only for patients for whom standard tests are contraindicated. Technically-adequate magnetic resonance angiography has a sensitivity of 78% and a specificity of 99% ¹³.

A ventilation/perfusion (V/Q) scan will show ventilation-perfusion mismatches. A high probability scan is defined as showing two or more unmatched segmental perfusion defects according to the PIOPED criteria.

Providing cardiopulmonary support is the initial treatment. Anticoagulation is provided in patients without risk of active bleeding. If the emboli are large or there is a large clot burden, thrombolysis is an option. In some cases, embolectomy or placement of vena cava filters is required.

The right ventricular failure due to pressure overload is considered the primary cause of death in severe PE ¹⁴.

acute emboli

acute or chronic emboli
right ventricular dysfunction

CT features suggestive of right ventricular dysfunction include ⁸:

abnormal position of the interventricular septum

inferior vena cava contrast reflux

RVD (right ventricular diameter): LVD (left ventricular diameter) ratio >1 on reconstructed four-chamber views
RVD:LVD ratio >1 on standard axial views is not considered to be a good predictor of right ventricular dysfunction ⁸

termed submassive PE when right ventricular dysfunction demonstrated on imaging (CT or echo) but without clinical hemodynamic compromise ¹⁹

subacute-to-chronic emboli

chronic emboli

Several studies report around 80% emboli resolving at around 30 days 20,21. According to one study, residual pulmonary obstruction at 6 months after the first episode of pulmonary embolism was shown to be an independent predictor of recurrent venous thromboembolism and/or chronic thromboembolic pulmonary hypertension ²⁸.

Consider:

pulmonary artery sarcoma

pulmonary artery vasculitis e.g. Takayasu arteritis

misidentification of pulmonary veins for arteries

arterial bifurcations (or branch points) can mimic PE but usually easily distinguished on multiplanar assessment

artifact may cause pseudo-filling defects and can be caused by:

chronic emboli may be mistaken for acute emboli

thromboembolic emboli may be mistaken for other embolized material

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Pulmonary embolism | Radiology Reference Article | Radiopaedia.org

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Pulmonary embolism (PE) refers to embolic occlusion of the pulmonary arterial system. The majority of cases result from thrombotic occlusion, and therefore the condition is frequently termed pulmonary thromboembolism which is what this article mainly covers.

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Neither
(but is it either? Doesn't this refer to lung conditions, and PE isn't a lung condition but a perfusion issue? Like you get obstructive shock but that's not obstructive lung disease)

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How does the condition effect lung compliance and/or airway resistance?

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How does the condition effect lung compliance and/or airway resistance?

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PE's themselves should not affect lung compliance or airway resistance as it is purely a perfusion issue (that is, the lungs still ventilate in the same manner as normal but the reduced blood flow causes decreased perfusion). This in and of itself creates dead space, as there are ventilated areas with little to no perfusion, however this is not a defect of the lungs but of the perfusion mechanism.

In some forms of decompensated PEs, you can see elements of both due to complications such as APO

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Explain the role of V/Q mismatch in this condition.

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Explain the role of V/Q mismatch in this condition.

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The VQ mismatch occurs due to redistribution of blood from occluded pulmonary arteries to the nonoccluded vessels.
Increased Dead Space.
This will cause a raised V/Q due to underperfusion in the presence of normal ventilation.

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What type of respiratory failure would this condition lead to?

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What type of respiratory failure would this condition lead to?

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T1RF can lead to T2RF once compensating

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Initially - low PaO2, Low/Normal CO2, Respiratory alkalosis most often.
initially - CO2 is low/normal. then once compensating, can remain normal or can rise to compensate for lactic acidosis.
Lactate Rise which can cause metabolic acidosis due to anaerobic respiration.

(low co2 = alkalosis, high = acidosis)

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What are the typical clinical manifestations/ patient assessment data? (relate these to pathophysiology concepts already described)

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What are the typical clinical manifestations/ patient assessment data? (relate these to pathophysiology concepts already described)

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Increased pulmonary artery pressure, can lead to right ventricular dilation and increase afterload. Decrease in surfactant production, the overall affect is atelectasis. Which further contributes to hypoxemia.  Increased JVP
Pulmonary oedema, hypoxic vasoconstriction , dysrhythmias , decreased cardiac output, shock
https://litfl.com/ecg-changes-in-pulmonary-embolism/

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A review of the ECG features of pulmonary embolism with specific ECG examples

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ECG changes in Pulmonary Embolism

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How is oxygenation and ventilation affected? Eg. consider O2 content, O2 delivery, alveolar ventilation 

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How is oxygenation and ventilation affected? Eg. consider O2 content, O2 delivery, alveolar ventilation 

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Reduced pulmonary perfusion leads to hypoxia as less haemaglobin is being oxygenated, as dead space is formed. The dead space will result in an increase in CO2 due to less gas exchange. Decrease in SPO2 due to less O2 being carried on Hb.
An elevated A-a gradient: because the partial pressure of O2 is higher in the alveoli than in arterial blood.

Patients experience SOB and compensate by hyperventilating to get rid of excess CO2. Therefore, administering supplemental O2 to maintain SPO2 >94%  is ideal treatment.

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OPTIONAL: Important vocabulary (include list of key vocabulary referenced; if you do not know the term(s), look up and add a definition for the word(s))

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OPTIONAL: Important vocabulary (include list of key vocabulary referenced; if you do not know the term(s), look up and add a definition for the word(s))