Acute minor pulmonary embolism

If an embolus obstructs less than 50% of the pulmonary circulation, it often produces no symptoms. For example, about 40% of patients with DVT who have no symptoms of pulmonary embolism have evidence of the condition on lung scans. If symptoms do develop the most common is dyspnoea, possibly upon minor exertion. Sometimes, the first abnormality the patient notes results from pulmonary infarction, which occurs in obstruction of medium sized pulmonary artery branches. Sharp pleuritic pain develops, and there may be associated haemoptysis. Pulmonary infarction occurs in only about 10% of patients without pre-existing cardiopulmonary disease. If, however, there is already compromise of the oxygenation of the embolised area—either because the airways are abnormal or pulmonary venous outflow is impaired as a result of pre-existing left heart disease—then the incidence of infarction rises to 30%.

If there are any physical signs, they are those of pulmonary infarction. The patient is distressed with rapid and shallow breathing because of the pleuritic pain, but is not cyanosed because the disturbance of gas transfer is only slight. Signs of pulmonary infarction may be found in the lungs: a mixture of consolidation and effusion, possibly with a pleural rub. Fever is common and sometimes differentiation from infective pleurisy is difficult. The fever and pain often produce a sinus tachycardia. Pulmonary artery mean pressure rarely exceeds 25 mm Hg. As minor pulmonary embolism does not compromise the right ventricle, cardiac output is well maintained, hypotension does not occur, and the venous pressure and heart sounds are normal. A common misapprehension is that there is often a loud pulmonary component of the second heart sound; this is not the case because the right heart pressures are normal or only slightly elevated.

Acute massive pulmonary embolism

When more than 50% of the pulmonary circulation is suddenly obstructed, the pathophysiology and clinical signs become dominated by the severe derangement of cardiac and pulmonary function. Obstruction of the pulmonary artery and mediator induced vasoconstriction cause a substantial increase in right ventricular afterload and, if the cardiac output is to be maintained, consequent elevation of pulmonary artery systolic pressure and an increase in right ventricular work. If this work cannot be sustained, acute right heart failure occurs. The thin walled right ventricle is designed to work against the normally low pulmonary vascular resistance; it performs poorly against a sudden obstruction. As a result, it dilates, and a moderate rise in the right ventricular and pulmonary artery systolic pressure occurs which rarely exceeds 55 mm Hg because the ventricle, lacking time to develop compensatory hypertrophy, is unable to generate a higher pressure. The right ventricular end diastolic pressure and right atrial pressure rise to about 15–20 mm Hg as the ventricle fails. Right ventricular dilatation leads to tricuspid regurgitation and may compromise the filling of the left ventricle. Cardiac output falls and the patient becomes hypotensive. This may occur so rapidly that syncope is either the presenting feature or easily induced by a relatively minor cardiovascular stress. If the degree of obstruction is sufficient, death occurs almost immediately. The fall in aortic pressure and the rise in right ventricular pressure may cause ischaemia of the right ventricle through a critical reduction of right coronary perfusion. Electromechanical dissociation is the most frequent cause of final cardiac arrest.

Arterial hypoxaemia correlates roughly with the extent of embolism if there is no prior cardiopulmonary disease. Massive pulmonary embolism without hypoxaemia is so rare that if the arterial oxygen tension (Pao ₂) is normal an alternative diagnosis should be considered. Hypoxaemia decreases tissue oxygen delivery and can impede circulatory adaptation through its vasodilating effects.

The main causes of hypoxaemia in pulmonary embolism seem to be as follows:

(1)

Ventilation–perfusion mismatch. Unembolised areas of the lung are relatively overperfused, so that the ventilation in these areas may be insufficient to oxygenate fully the extra blood flow.

(2)

Shunting occurs through areas of collapse and infarction that are not ventilated but retain some blood flow. This may become more important a few days after the initial episode. In patients with a patent foramen ovale, raised right atrial pressure may open the foramen and cause right-to-left shunting at the atrial level. This should be considered if the degree of hypoxaemia is more profound than would be expected from other clinical features, if it cannot be corrected by oxygen administration and if it is accompanied by hypercapnia.

(3)

Low mixed venous oxygen saturation caused by the reduced cardiac output causes hypoxaemia because there is insufficient time for the extremely desaturated blood to become fully saturated as it passes through the alveolar capillaries in the overperfused areas of the lung.

Although pulmonary embolism impairs the elimination of CO₂, hypercapnia is rare because compensatory hyperventilation eliminates CO₂ in all but the most extensive embolism. In cases with a sufficient degree of vascular obstruction to produce hypercapnia, the haemodynamic sequelae of acute right ventricular failure usually prove fatal.

The clinical features of acute massive pulmonary embolism can be explained in terms of these pathophysiological changes (table 3). The patient becomes acutely distressed, severely short of breath, and may be syncopal because of the combination of hypoxaemia and low cardiac output. The combination of hypotension, hypoxaemia, and increased cardiac work may cause anginal chest pain. The physical signs are those of reduced cardiac output—that is, pronounced sinus tachycardia, hypotension, and a cool periphery, sometimes with confusion. The patient is obviously dyspnoeic (but not orthopnoeic), cyanosed both centrally and peripherally, and has signs of acute right heart strain: a raised venous pressure, which is often difficult to appreciate because of the respiratory distress; a gallop rhythm at lower sternum; and a widely split second heart sound due to delayed right ventricular ejection, which is difficult to detect because of the accompanying tachycardia. The pulmonary component of the second heart sound is usually not loud because the pulmonary artery pressure is only moderately raised.

Subacute massive pulmonary embolism

This is caused by multiple small or moderately sized emboli that accumulate over several weeks. Because the obstruction occurs slowly, there is time for the right ventricle to adapt and for some hypertrophy to develop; consequently, the right ventricular systolic pressure is higher than in acute pulmonary embolism. The rises in the right ventricular end diastolic and right atrial pressures are of a lesser extent than in acute massive pulmonary embolism since there is time for adaptation to occur and the degree of right ventricular failure is less for a given degree of pulmonary artery obstruction. The main symptoms are increasing dyspnoea and falling exercise tolerance. There is often an associated dry cough. The breathlessness is usually out of proportion to all other findings, and there may be central cyanosis. The blood pressure and pulse rate are usually normal because the cardiac output is well maintained. Commonly, the venous pressure is raised and a third heart sound is audible at the lower sternum which may be accentuated by inspiration. The pulmonary component of the second heart sound is sometimes loud. There may also be intermittent symptoms and signs of pulmonary infarction that occurred during the build up of the obstruction. In advanced cases, cardiac output falls and frank right heart failure develops. A further pulmonary embolus may change the picture to that resembling acute massive pulmonary embolism.

Estimating pretest clinical likelihood of venous thromboembolism

Until the 1970s, the diagnosis or exclusion of pulmonary embolism was made on clinical grounds alone. In the UPET (urokinase pulmonary embolism trial) study, several clinical findings, previously considered valuable in the diagnosis of pulmonary embolism, were not present in many patients with the condition, and less than one third of the 2200 patients with suspected pulmonary embolism actually had the disease after objective testing.1 These results led clinicians to virtually abandon clinical examination and diagnose pulmonary embolism solely based on the results of objective tests. A number of recent studies, however, have suggested that combining the individual components of clinical assessment, risk factors for venous thromboembolism, and simple investigations reliably categorises the likelihood of pulmonary embolism as low, moderate, or high in an individual patient.3-6

By adopting a thorough stratification system the clinician can more appropriately select further investigations to prove or exclude pulmonary embolism. Establishing the pretest clinical likelihood of pulmonary embolism is especially helpful in interpreting the scintigraphy. Clinical likelihood of pulmonary embolism is determined after consideration of risk factors (the most common being immobilisation, a history of previous venous thromboembolism, lower limb fractures, and recent surgery), presentation, and basic investigations (ECG and plain chest radiograph). Although the characteristics of these clinical estimates have not been extensively validated, those generally accepted are given in table4.

Nearly all patients with pulmonary embolism will have one or more of the following clinical features—dyspnoea of sudden onset, tachypnoea (> 20 breaths/minute), or chest pain (pleuritic or substernal)2; if the clinician remembers these three features, the possibility of pulmonary embolism will rarely be overlooked. When these clinical features are associated with ECG signs of right ventricular strain and/or radiologic signs of plump hilum, pulmonary infarction or oligaemia, the likelihood of pulmonary embolism is high, and it is further strengthened in the presence of risk factors for venous thromboembolism and arterial hypoxaemia with hypocapnia.4 On the contrary, the absence of all these three clinical features virtually excludes the diagnosis of pulmonary embolism.

Electrocardiography

ECG changes are usually non-specific. In minor pulmonary embolism there is no haemodynamic stress and thus the only finding is sinus tachycardia. In acute or subacute massive pulmonary embolism, evidence of right heart strain may be seen (rightward shift of the QRS axis, transient right bundle branch block, T wave inversion in leads V1-3, P pulmonale), but the classic S_IQ_IIIT_III pattern occurs in only a few cases.2 The main value of ECG is in excluding other potential diagnoses, such as myocardial infarction or pericarditis.

Chest radiography

Chest radiograph findings are also non-specific but may be helpful. A normal film is compatible with all types of acute pulmonary embolism; in fact, a normal film in a patient with severe acute dyspnoea without wheezing is very suspicious of pulmonary embolism. The lung fields may show evidence of pulmonary infarction: peripheral opacities, sometimes wedge shaped or semicircular, arranged along the pleural surface (so called Hampton's hump). Atelectasis, small pleural effusions, and raised diaphragm have low specificity for pulmonary embolism. In massive pulmonary embolism a plump pulmonary artery shadow may be seen when the pulmonary artery pressure is elevated. It may be possible to detect areas of oligaemia in the parts of the lung affected by emboli (Westermark sign), but this is difficult on the type of film usually available in the acute situation. The radiograph is especially valuable in excluding other conditions mimicking pulmonary embolism (pneumothorax, pneumonia, left heart failure, tumour, rib fracture, massive pleural effusion, lobar collapse), but pulmonary embolism may coexist with other cardiopulmonary processes. The radiograph is also necessary for the proper interpretation of the lung scan.

Echocardiography

Transthoracic echocardiography rarely enables direct visualisation of the pulmonary embolus but may reveal thrombus floating in the right atrium or ventricle. With transoesophageal echocardiography, it is possible to visualise massive emboli in the central pulmonary arteries. In the presence of thrombi in right heart chambers, pulmonary angiography is not necessary and, indeed, is contraindicated because of risk of thrombus dislodgement.

In massive pulmonary embolism the right ventricle is dilated and hypokinetic, with abnormal motion of the interventricular septum. The inferior vena cava does not collapse during inspiration. Unfortunately, the finding of right ventricular dysfunction is non-specific and certain conditions commonly confused with pulmonary embolism (such as chronic obstructive pulmonary disease (COPD) exacerbations or cardiomyopathy) are also associated with abnormal right ventricular function. There is some evidence that regional right ventricular dysfunction (akinesia of the mid-free wall with apical sparing) may be more common in acute pulmonary embolism. The Doppler technique allows the pulmonary artery pressure to be estimated and together with contrast echocardiography it is useful in diagnosing patent foramen ovale which may indicate impending paradoxical embolism.

Although direct echocardiographic visualisation of intraluminal thrombi in patients with suspected pulmonary embolism is not frequent, and even when echocardiography provides only indirect signs compatible with haemodynamic consequences of massive pulmonary embolism, it is helpful in excluding or suggesting alternative causes for haemodynamic instability (aortic dissection, ventricular septal rupture, cardiac tamponade, etc). In an unstable hypotensive patient requiring immediate treatment, such information is of great importance. However, because the right ventricle may show no dysfunction even in patients with massive pulmonary embolism, echocardiography should be considered an ancillary rather than a principal diagnostic test for the diagnosis of pulmonary embolism.

Arterial blood gases

The characteristic changes are a reduced Pao ₂, and a Paco ₂ that is normal or reduced because of hyperventilation. The Pao ₂ is almost never normal in the patient with massive pulmonary embolism but can be normal in minor pulmonary embolism, mainly due to hyperventilation. In such cases the widening of the alveolo-arterial Po ₂ gradient (AaPo ₂ > 20 mm Hg) may be more sensitive than Pao ₂ alone. Both hypoxaemia and a wide AaPo ₂ may obviously be due to many other causes. Blood gases, therefore, may heighten the suspicion of pulmonary embolism and contribute to the clinical assessment, but they are of insufficient discriminant value to permit proof or exclusion of pulmonary embolism.2

Biochemistry

No blood test will diagnose venous thromboembolism. Although endogenous fibrinolysis is indicated by the sensitive assay of cross linked fibrin degradation products (D-dimers), this test has low specificity and is positive not only when there is venous thromboembolism but also in the presence of disseminated intravascular coagulation, malignancy, and after trauma or surgery. Although a negative test may be strong enough evidence that clotting has not occurred and that anticoagulants can be withheld, a positive test cannot confirm venous thromboembolism. The test could reduce the number of investigations in outpatients with suspected pulmonary embolism and a low pretest likelihood for venous thromboembolism, and may be useful as a screening test in an emergency unit when lung scintigraphy or computed tomography (CT) is not immediately available. However, if there is a high clinical suspicion of acute pulmonary embolism, diagnostic tests should proceed in spite of a normal D-dimer. In elderly or inpatients, D-dimer retains a high negative predictive value, but is normal in less than 10% of patients, and, hence, not very useful. Not all D-dimer testing methods have equal and sufficient sensitivity (the latex agglutination test is not reliable in excluding pulmonary embolism), but the rapid assays with a negative predictive value approaching 100% are comparable to the reliable but labour and time consuming ELISA (enzyme linked immunosorbent assay) tests.

Lung scintigraphy

A normal perfusion scan essentially excludes the diagnosis of a clinically relevant recent pulmonary embolism because occlusive pulmonary embolism of all types produces a defect of perfusion. Normal results are almost never associated with recurrent pulmonary embolism, even if anticoagulants are withheld. However, many conditions other than pulmonary embolism, such as tumours, consolidation, left heart failure, bullous lesions, lung fibrosis, and obstructive airways disease, can also produce perfusion defects. Addition of a ventilation scan increases the specificity of scintigraphy. Pulmonary embolism usually produces a defect of perfusion but not ventilation (“mismatch”) while most of the other conditions produce a ventilation defect in the same area as the perfusion defect (matched defects). Pulmonary embolism can also produce matched defects when infarction has occurred, but in this situation the chest radiograph nearly always shows shadowing in the area of scan defect.

The lung scan is an indirect method of diagnosis since it does not detect the embolus itself but only its consequence, the perfusion abnormality. The probability that perfusion defects are caused by pulmonary embolism can be assessed as high, intermediate or low depending on the type of scan abnormality (although there are significant variations in the interpretative patterns and diagnostic accuracy even between experienced readers using standard algorithms).3 ,7 If the scan is of a high probability type (basically multiple segmental or larger perfusion defects with a normal ventilation scan) there is a more than 85% chance that the patient has pulmonary embolism. However, the majority of patients with clinically suspected pulmonary embolism do not have high probability scans and instead have ones that suggest either low or intermediate probability (= non-diagnostic scans); in these patients the prevalence of pulmonary embolism is about 25%. Taking the clinical assessment into account improves diagnostic accuracy (when the clinical likelihood of pulmonary embolism and scan interpretation is concordant, the ability to diagnose or exclude pulmonary embolism is optimised (table 5)), but the diagnosis can still be made or excluded with accuracy in only about a third of patients. A low probability scan does not rule out pulmonary embolism, but in fact there is up to a 40% probability of pulmonary embolism when clinical likelihood is high.3

In theory the addition of ventilation scanning should improve the usefulness of perfusion imaging, but the PIOPED (prospective investigation of pulmonary embolism diagnosis) study showed such benefit to be marginal. Perfusion defects caused by pulmonary embolism are most often wedge shaped. In the PISA-PED (prospective investigation study of acute pulmonary embolism diagnosis) study, when only wedge-shaped defects were classified as suspect for pulmonary embolism, perfusion scintigraphy without the use of ventilation scans, combined with clinical assessment of pulmonary embolism likelihood (table 6), made it possible to confirm or exclude the condition in 76% of patients with abnormal scans, with an accuracy of 97%.4 ,8 Angiography was then required only in about one fourth of patients with abnormal scans. This suggests that where ventilation imaging is unavailable, perfusion scanning alone is acceptable. The simple PISA-PED criteria are likely to become an attractive alternative to the complex PIOPED criteria.

Although the lung scan is often an imprecise guide it is useful in clinical decision making: a normal scan or a low probability scan with low clinical likelihood of pulmonary embolism means that treatment for suspected pulmonary embolism can be withheld, and a high probability scan with a high clinical likelihood of pulmonary embolism means that treatment is mandatory. Objective tests for DVT and pulmonary angiography or CT must be used to decide on the treatment in patients between these extremes and in whom the clinical likelihood of pulmonary embolism and scan interpretation are discordant.

Planar scintigraphy is the standard technology in most institutions. With SPECT (single photon emission CT) technology, pictures can be reconstructed in any plane and the specificity of scintigraphy substantially improves because of the reduction in the frequency of non-diagnostic scans.9

Scanning should be performed within 24 hours of the onset of symptoms of pulmonary embolism, since some scans revert to normal quickly. A follow up scan at the time of discharge is helpful in establishing a new baseline for subsequent episodes of suspected pulmonary embolism. The only clinically important cause of a false positive study is prior pulmonary embolism that has not resolved, leaving a lung scan pattern that remains in the high probability category.

Computed tomography (CT, spiral or electron beam CT)

Contrast enhanced spiral or electron beam CT have emerged as valuable methods for diagnosing pulmonary embolism and, because of its availability, spiral CT is becoming the first choice method at many institutions. The technique is faster, less complex, and less operator dependent than conventional pulmonary angiography, and has about the same frequency of technically insufficient examinations (about 5%). The thorax can be scanned during a single breath hold. There is better interobserver agreement in the interpretation of CT than for scintigraphy. Another advantage of CT over scintigraphy is that by imaging the lung parenchyma and great vessels, an alternative diagnosis (for example, pulmonary mass, pneumonia, emphysema, pleural effusion, mediastinal adenopathy) can be made if pulmonary embolism is absent. This advantage of CT also pertains to pulmonary angiography, which images only the arteries. CT can also detect right ventricular dilatation, thus indicating severe, potentially fatal pulmonary embolism.

Criteria for a positive CT scan result include a partial filling defect (defined as intraluminal area of low attenuation surrounded by a contrast medium), a complete filling defect, and the “railway track sign” (masses seen floating in the lumen, allowing the flow of blood between the vessel wall and the embolus). The procedure has over 90% specificity and sensitivity in diagnosing pulmonary embolism in the main, lobar, and segmental pulmonary arteries. When CT is used to evaluate patients with a non-diagnostic lung scan, the sensitivity is lower.10 ,11

Although recent advances in CT technology enable better visualisation of subsegmental arteries, these small vessels remain difficult to evaluate. The clinical significance of isolated subsegmental emboli is unclear, and it is not current practice to ignore them. They may be of importance in patients with poor cardiopulmonary reserve, and their presence is an indicator for current DVT, which thus potentially heralds more severe emboli. One recent study showed, however, that patients with pulmonary embolism negative spiral CT do well without anticoagulation treatment.12 This should be especially true when these patients also have a leg venous study that is negative for thrombus.

Other reasons for falsely negative results may be inadequate visualisation of a portion of the lung, difficulty in evaluating non-vertically oriented arteries (particularly of the lingula and the middle lobe), and difficulty in opacifying the arteries in patients with superior vena caval obstruction or intracardiac or intrapulmonary shunts. These sources of falsely negative results are significant and one cannot therefore regard CT as a new “gold standard” to replace angiography. If clinical suspicion for pulmonary embolism is high and the CT is interpreted as negative or inconclusive, further investigation should be performed.

CT may also be falsely positive for pulmonary embolism. Enlarged hilar lymph nodes and volume averaged atelectatic lung or mediastinal fat may be misinterpreted as emboli. Perivascular oedema (such as occurs in congestive heart failure) may appear as an embolus. An insufficient delay from the administration of contrast to the initiation of the scan can lead to filling defects that can be misinterpreted as emboli.

Additional research is required to establish the place of CT in clinical practice. In particular, the sensitivity of CT for small clots should be carefully examined and the utility of testing strategies employing CT must be determined in outcome studies and compared with currently employed algorithms. Because of the small number of non-diagnostic results and a potentially greater out-of-hours availability, spiral CT may replace scintigraphy as the primary test in patients with suspected pulmonary embolism.

After performing lung CT (involving intravenous injection of contrast medium) to diagnose pulmonary embolism, sufficient opacification of the venous system remains to evaluate the veins of the legs, pelvis, and abdomen for DVT, without additional venepuncture or contrast medium. Such an examination is a continuous study, adding approximately five minutes to pulmonary scanning, with the added expense of only one sheet of film. The pelvic and abdominal images screen the iliac veins and vena cava for thrombosis, an important advantage over sonography, particularly when caval filter placement is considered. This potential for performing in a single study both venography and pulmonary CT angiography is promising. If the accuracy of venous imaging after lung scanning is confirmed in large studies, its use should be considered whenever CT pulmonary angiography is indicated.

Magnetic resonance imaging

Magnetic resonance imaging (MRI) offers both morphological and functional information on lung perfusion and right heart function, but its image quality still needs improvement to be comparable with CT. MRI has several attractive advantages, including the avoidance of nephrotoxic iodinated contrast and ionising radiation, and excellent sensitivity and specificity for DVT, together with the potential for performing lung perfusion imaging. This technique may ultimately allow simultaneous and accurate detection of both DVT and pulmonary embolism. Additional data are needed, however. A disadvantage of MRI compared to CT is the long time (15–30 minutes) needed to perform the examination, which is not suitable for clinically unstable patients. Improvements in MRI angiographic techniques will inevitably produce better results in the future.

Pulmonary angiography

Catheter pulmonary angiography remains the “gold standard” and the only technique that can diagnose or exclude pulmonary embolism with relative certainty. It should be considered, first, if cardiovascular collapse or hypotension are present and, second, when other investigations are inconclusive. However, angiography has disadvantages of limited availability and a small (< 0.3%) but definite risk of mortality.7 ,13 This risk gets higher the more seriously ill the patient is, particularly when there is significant pulmonary hypertension. Relative contraindications include pregnancy, significant bleeding risk, renal insufficiency, and known right heart thrombus. The presence of a left bundle branch block is an indication for a temporary pacemaker during the procedure. The safety of the procedure is enhanced by monitoring (ECG, pulse oximeter, automated blood pressure device), ready oxygen availability, and by reducing the amount of contrast material given at lower pressure.

Injection of low osmolar non-ionic contrast through a pigtail catheter into the main pulmonary artery, with radiographs of the whole chest in two projections taken in rapid succession using an automatic film changer, is sufficient to delineate the emboli in most cases. Where prior scintigraphy is non-diagnostic, angiography can be first confined to the more abnormal side. When the embolus is small, selective injections into subdivisions of the arteries, oblique views and cineangiography, which can separate superimposed vessels as they move apart due to the pulsation of the arteries, improves diagnostic accuracy. The digital subtraction technique makes the examination easier and faster (because of the cinematic review and work station manipulation) and results in comparable image quality and improved interobserver agreement compared with conventional cut-film angiography. An embolus appears as an abrupt vessel cutoff or a convex filling defect often with contrast leaking beyond its edges and the sides of the vessel containing it. The overall perfusion of the affected region is reduced.

The assumption that life threatening pulmonary embolism is not missed by pulmonary angiography seems to hold true. However, although false positives are difficult to prove and probably scarce, false negative examinations can occur despite important intravascular embolus. Non-diagnostic pulmonary angiography can also occur.

Pulmonary angiography can be performed by the femoral, brachial, subclavian or internal jugular approaches. The femoral venous approach is useless in patients who have had an inferior caval interruptive procedure. Disadvantages of the femoral approach relate to the possibility of dislodging iliofemoral or caval thrombus and a high risk of bleeding from a fresh femoral venous puncture site during thrombolytic treatment. This risk can be reduced by leaving the catheter in the vein for mechanical haemostasis during the thrombolysis. The main difficulty with catheterisation from the brachial approach relates to the possibility of catheter induced venous spasm with inability to advance the catheter into the central veins; this may be particularly problematic in patients with excessive circulating catecholamines caused by shock or vasopressor administration. In fully anticoagulated patients the internal jugular and, especially, the subclavian approach are contraindicated.

The changes in the right heart pressures that occur in pulmonary embolism are summarised in table 3. It is important to measure the pressures and oxygen saturations before angiography so that the haemodynamic situation, including cardiac output and any intracardiac shunting, can be assessed. This facilitates determination of the patient's underlying cardiopulmonary reserve, identification of any haemodynamic derangements that might require specific treatment to increase the safety of angiography, and more careful selection of the contrast agent and dose to maximise diagnostic information while minimising the risk of hypotension, myocardial depression or a further increase in ventricular filling pressures. Occasionally if the diagnosis of pulmonary embolism before catheterisation is wrong the haemodynamic data may suggest the correct diagnosis and lead to appropriate treatment.

The use of intravenous digital subtraction angiography (DSA) avoids the need for pulmonary artery catheterisation but has been disappointing because opacification of the pulmonary vessels is poor. Although intravenous DSA may be adequate for showing large proximal arterial occlusions, resolution is usually inadequate to identify an embolus in the segmental vessels and beyond. Thus minor pulmonary embolism cannot be excluded on the basis of a normal DSA with peripheral contrast application.13

Search for deep venous thrombosis

DVT cannot be reliably diagnosed on the basis of the history and physical examination. Patients with lower extremity DVT often do not exhibit pain, tenderness, erythema, warmth, or swelling. When present, however, these findings merit further evaluation. Impedance plethysmography, compression ultrasonography with venous imaging (colour duplex ultrasound), and MRI are established non-invasive methods for diagnosing DVT. While contrast venography remains the gold standard, it is rarely performed because it is invasive and difficult to carry out in the acutely ill patient. Venography is no longer appropriate as the initial diagnostic test for the evaluation of symptoms that suggest acute DVT; it should be performed whenever non-invasive testing is non-diagnostic or impossible to perform. While plethysmography and ultrasound are reliable for the diagnosis of symptomatic proximal DVT, they are much less reliable for recognising asymptomatic DVT. They are also not able to detect floating thrombus in the vena cava. Plethysmography also has other limitations and is inferior to the latest ultrasound techniques; it is now used in only a few institutions.

Although all the above methods for detecting thrombus in the deep veins do not establish the diagnosis of pulmonary embolism, the confirmation of DVT is of major importance in management decisions. The logic of leg vein imaging is that many patients with pulmonary embolism have residual proximal clot even in the absence of clinical evidence of DVT, itself an indication for treatment even if there is no direct proof of pulmonary embolism. If there is no thrombosis in the proximal leg or pelvic veins the chance of a further significant pulmonary embolism is low; therefore, even if a small pulmonary embolism has occurred already, anticoagulation can be omitted. This approach needs caution if the patient has inadequate cardiorespiratory reserve, is likely to remain immobile, or if there could be an embolic source elsewhere (for example, right atrium or vena cava).14

Failure to identify thrombosis of the calf veins rarely has serious sequelae, and the investigation can be repeated if there is persisting clinical concern. In patients with documented isolated calf vein thrombosis, repeated impedance plethysmography or compression ultrasonography can be used to separate the 20% of patients who develop proximal extension (and require treatment) from the remaining 80% of patients who do not and in whom the risks of anticoagulant treatment may outweigh the benefits (for example, in patients at high risk of bleeding).14

Basic tests

Basic tests include the ECG and plain chest radiograph. These must be performed in all patients both to support clinical suspicion of pulmonary embolism and, in particular, to exclude alternative diagnoses. As ECG and chest radiographic abnormalities in pulmonary embolism may be non-specific, absent, transient, or delayed, they cannot be used to confirm the diagnosis. Normal blood gases do not rule out pulmonary embolism; findings of hypoxaemia or hypocapnia may increase the physician's level of suspicion, but they are not specific for pulmonary embolism. More specific investigations are always required, but choosing which road to follow from the myriad of possibilities of imaging examinations can be confusing.

Various combinations of tests have resulted in several elaborate algorithms which, however, are seldom followed in clinical routine. Algorithms that inevitably result in large numbers of patients being referred for angiography are unhelpful. The availability of and familiarity with certain technology may influence the diagnostic approach. The specific clinical scenario also impacts on the diagnostic procedure that is chosen. There is no single algorithm to be recommended for all situations; rather, the investigations should be chosen according to the haemodynamic state of the patient (suspicion of massive versus minor pulmonary embolism), the onset of symptoms (in versus out of hospital), the presence or absence of other cardiopulmonary diseases, and the availability of specific tests.15 ,16

Haemodynamic instability

In critically ill patients suspected of having a massive pulmonary embolism, particularly those with cardiovascular collapse, echocardiography can be rapidly performed at the bedside to exclude other diseases or, occasionally, to establish the diagnosis by finding clots in the central pulmonary arteries or the right heart. By visualisation of thrombi further investigations are not necessary. When evidence of right heart strain without clots is present on echo, spiral CT or pulmonary angiography should follow, depending on faster availability.

In patients with life threatening instability where emergency treatment is necessary and CT or cardiac catheterisation is unavailable, intravenous DSA may be adequate for showing large proximal arterial occlusions. Image quality can be improved by delivering the contrast to the pulmonary artery via a flow directed, balloon tipped catheter. The floating catheter may also be useful in showing the characteristic haemodynamic changes with massive pulmonary embolism and suggesting an alternative diagnosis.

Haemodynamically stable patients

The principal challenge in stable patients is to develop a logical sequence of investigations that allow early, cost effective diagnosis and are associated with the most favourable markers of outcome. Depending on timely availability of tests and patient presentation, several approaches are possible.