Acute Pulmonary Embolism PE – Updated On 17/3/2021

 Definition : A thrombus usually formed in the systemic veins or rarely in right heart
(<10%) that dislodge & embolize into the pulmonary arterial system.
- 10% of PE are fatal ..!
- PE is the third most frequent acute cardiovascular syndrome behind myocardial infarction
and stroke.
- VTE (PE + DVT) is almost eight times higher in individuals aged ≥ 80 years than in the fifth
decade of life.
- Most common origin of emboli is Pelvic & abdominal veins.
 Causes AND Pathophysiology :
Virchow's triad :
A. Sluggish blood flow "stasis"
B. Local vessel wall injury
C. Hypercoagulability state
1. DVT ….. Most common !
2. Septic emboli (endocarditis affecting Tricuspid or pulmonary valves )
3. Tumor
4. Fat following fracture of lung bones ( femur )
5. Air following Pneumothorax
6. Amniotic fluid following labour
7. Foreign material during IV drug use
8. As a part of another disease like DIC.

Thromboxane A2
Serotonin
NOTES :
- Right ventricular (RV) failure is considered the primary cause of death in severe PE.
- The finding of massive inflammatory cells in the RV myocardia of patients who died within
48 h of acute PE may be explained by high levels of Epinephrine released as a result of the
PE-induced ‘Myocarditis’ → Explain the secondary hemodynamic destabilization that
sometimes occurs 24-48 h after acute PE, although early recurrence of PE may be an
alternative explanation in some cases.
- The association between elevated bio-markers of myocardial injury and an adverse early
outcome indicate that RV ischemia is of pathophysiological significance in the acute phase
of PE.
- In view of the above pathophysiological considerations :
 Acute RV failure : Defined as a rapidly progressive syndrome with systemic
congestion resulting from impaired RV filling and/or reduced RV flow out-put
- It is a critical determinant of clinical severity and outcome in acute PE.
- Clinical symptoms, and signs of overt RV failure and hemodynamic instability →
indicate a high risk of early mortality.
 High-risk PE is defined by Hemodynamic instability that encompasses the forms of
Cardiac arrest, Obstructive shock and persistent hypotension .

 Classifications of PE
 Based On Time of Symptoms Onset
- Acute → Symptoms appear Immediately after obstruction.
- Subacute → Symptoms appear Days-weeks after obstruction.
- Chronic → Symptoms appear Months-Years after obstruction
 Anatomical-based
- Saddle PE "Most-dangerous"
- Lobar PE
- Segmental PE
- Sub-segmental PE
 Symptomatic Vs. Asymptomatic PE
 Haemodynamically Stable Vs. Unstable (Table Above)
 Provoked Vs. Unprovoked PE
 Predisposing factors :

ESC-2019 Predisposing factors for VTE

NOTES :
 Contraceptive use (especially COCs ) is the most frequent VTE risk factor in women of
reproductive age.
 Third-generation COCs, containing Progestogens such as Desogestrel or Gestodene,
are associated with a higher VTE risk than the second-generation COCs, which
contain Progestogens such as Levonorgestrel or Norgestrel.
 Hormone-releasing intrauterine devices and some progesterone-only pills POPs are
not associated with a significant increase in VTE risk.
 Infection is a common trigger for VTE.
 Patients with VTE have an increased risk of subsequent myocardial infarction and
stroke, or peripheral arterial embolization.

 Presentations of Acute Pulmonary Embolism :

- Look for : Sudden onset of Unexplained SOB, Clear lungs on examination plus Normal
Chest X-ray. (Commonest Presentation)
- Other clinical findings "Non-Specific"
 Tachypnea (Most common sign), tachycardia, cough.
 Syncope, Pre-syncope (17%) → Unstable Pt.
 Unilateral leg pain from DVT .
 Pleuritic chest pain+ hemoptysis (Only if lung infarction)
 low-grade Fever "Common"
 Hypotension in extremely severe emboli.
 Hemodynamic Instability "Rare"
 Asymptomatic
 Crackles, wheezing, Loud P2, elevated JVP.
 Normal SpO2 in 30%
NOTES :
- Dyspnea may be acute-severe in central PE, and often mild–transient in Peripheral PE.
- In patients with pre-existing heart failure or pulmonary disease, worsening dyspnea may
be the only symptom indicative of PE.
- In central PE, chest pain may have a typical angina character, possibly reflecting RV
ischemia, and requiring differential diagnosis from an acute coronary syndrome or aortic
dissection.
- 40% of patients with PE have no predisposing factors.
- Hypoxemia is frequent, but ≤ 40% of patients have normal SaO2.
 Clinical presentation depend on number, size & distribution of emboli :
Acute massive PE Acute small/medium Chronic PE
PE
Pathophysiology Acute RV outflow Terminal/segmental Multiple recurrent
obstruction → ↓COP + pulmonary vessels Occlusion of pulmonary
Acute Rt side HF occlusion → infarction microvasculature
+/- effusion Rt side HF
Symptoms Faintness or collapse Pleuritic chest pain Exertional Dyspnea
Crushing Central pain Restricted breathing Late : P. HTN
Severe dyspnea Hemoptysis 30% Terminal : Rt HF
Signs Major circulatory Tachycardia RV heave, loud P2 +
collapse : Tachypnea Signs of Rt side HF
- Tachycardia Pleural rub
- Hypotension, Crackles
- Pale , sweaty Effusion( blood-stained )
- ↑JVP, gallop rhythm Low-grade fever
- Loud S2 Normal CVS Ex
- Severe cyanosis
- ↓Urinary output
- No abnormal chest
signs
CXR Usually normal Pleuropulmonary Enlarged pulmonary
Maybe subtle oligaemia opacities artery trunk
Pleural effusion Cardiomegaly
Linear shadows Prominent RV
Raised hemidiaphragm
ECG S1Q3T3 Sinus tachycardia RV hypertrophy & strain
Anterior T inversion
RBBB
ABG Markedly abnormal May normal or Exertional ↓PaO2
↓PaO2 ↓PaCo2 ↓PaO2 or ↓PaCo2
Metabolic acidosis
D.D MI Pneumonia Other causes of P. HTN
Pericardial tamponade Pneumothorax
Aortic dissection Musculoskeletal pain
 Integrated Approach for diagnosis of PE :
A. STEP 1 : For a patient to enter a PE testing regimen, he/she should have at least one
physiological manifestation of PE.
 Absence of a known sign or symptom Or Positive PERC rule → Does Not
mandate testing for PE or DVT.
B. STEP 2 : Determine Clinical Pre-Test Probability in Stable Patient.
- Widely used scoring systems → Avoiding overuse of diagnostic tests for PE.
1. Modified Well's criteria "Most Practically Used "
2. Revised Geneva Score
3. Pisa model "Most Recent"
4. Pulmonary embolism Rule-Out Criteria PERC rule
" It is necessary to determine the level of risk and adjust management decisions
accordingly" High-Risk PE requires an emergency diagnostic (upon suspicion) and
therapeutic (upon confirmation or if the level of suspicion is sufficiently high) strategy.

Modified Well's Criteria :

- Clinical Probability
- High Probability : >6
- Moderate Probability : 2-6
- Low Probability : <2

The Revised Geneva Score

PERC-Rule

 Regardless of the score used, the

proportion of patients with confirmed
PE can be expected to be :
- 10% in the low-probability
- 30% in the moderate-probability
- 65% in the high-probability
C. STEP 3 : Follow the Diagnostic algorithm for patients with suspected pulmonary
embolism without hemodynamic instability.

NOTE :
 The best next step for a patient with suspected PE and Positive D-dimer is CTPA.
 Contrast-enhanced CT Pulmonary Angiography CTPA ( Spiral CT scan )
- First line diagnostic test . Negative CT almost exclude PE

- Replaced By V/Q scan if Pregnant, Renal insufficiency Or Prior adverse reaction

to Contrast material.
  Plasma D-dimer : Elevated but not specific.
- High Negative Predictive value → Low levels with low clinical probability rule-
out PE.
- Low positive predictive value of elevated D-dimer → Testing with D-dimer is
not useful for confirmation of PE.
- Age-adjusted cut-off = Age × 10 mg/L ( for patients aged >50 years)

D. Step 4 : IF hemodynamically Unstable → Follow the Diagnostic algorithm for patients

with suspected high-risk pulmonary embolism presenting with hemodynamic instability.
E. STEP 5 : Further Investigations could be done.
 CBC : Polymorphonulcear leukocytosis in infarction.
 ESR : High in infarction.
 LDH : elevated in infarction.
 ECG Findings :
1. Normal, RAD
2. Sinus tachycardia 40-44% → Most common
3. Complete or incomplete RBBB 18%
4. Right Ventricle strain pattern (ST depression with T-wave inversion in Right
Precordial leads V1-V4 PLUS inferior leads) → Most Specific
5. Right atrial enlargement 9%
6. S1Q3T3 20% (McGinn-White pattern)- neither sensitive nor specific for PE →
Most classic
7. Non-specific ST-T waves changes (Anterior T wave inversion V1-V4)
8. Massive PE: Right atrial enlargement + P Pulmonale in lead II
9. QR pattern in Lead V1
10.Atrial Fibrillation Or MAT
- The Occurrence of AF without obvious causes associated or not with new
onset Dyspnea should suggest PE particularly in patients at risk of VTE.
- 2nd most common arrhythmia after sinus tachycardia
11.ST-elevation in Right Precordial leads, aVR and Lead II
 ABG
- Hypoxia & respiratory alkalosis ( High PH & Low PaO2 )
- Metabolic acidosis in Massive PE(Cardiogenic shock)
 Troponin I, T→ When elevated reflecting Right heart strain.
 Chest X-ray
1. Normal
2. Atelectasis "Most common"
3. Pleural-based Wedge shaped opacity (Hampton's hump)
4. Focal oligaemia in one lobe ( Wastermark sign)
5. Pleural effusion
6. Dilatation of right descending pulmonary artery (Knuckle/Palla's sign)
7. Fleischner sign
- Chest X-ray may be useful for excluding other causes of dyspnea or chest pain.
-
 ECHO :
Shows contracting left Ventricle with Dilated RV in massive PE and a colt may be
seen.
Echo is not mandatory as part of routine diagnostic workup in hemodynamically
stable patients with suspected PE
Absence of Echo signs of RV overload or dysfunction practically excludes PE as the
cause of haemodynamic instability
Echo may be of further help in the differential diagnosis of the cause of shock, by
detecting pericardial tamponade, acute valvular dysfunction, severe global or
regional LV dysfunction, aortic dissection, or hypovolaemia.
Most specific echo findings (60/60 sign, McConnell sign, or right-heart thrombi),
justify emergency reperfusion treatment for PE in a patient with high clinical
probability and no other obvious causes for RV pressure overload
Mobile right-heart thrombi essentially confirm the diagnosis of PE
  Planar Ventilation/perfusion (V/Q) scan (lung scintigraphy)
- Established diagnostic test for suspected PE
- In acute PE, ventilation is expected to be normal in hypoperfused segments
(mismatched)
- Lower-radiation and contrast medium-sparing procedure.
- Indications :
1. Pregnant women
2. History of contrast medium-induced anaphylaxis
3. Severe renal failure

 Doppler U/S (Compression Ultrasonography CUS )

- For DVT ( Especially Pelvic or iliofemoral clots)
- CUS shows a DVT in 30-50% of patients with PE

 Other Investigations : PT, INR, BNP, Lactate, Creatinine, Cyatatin C, Electrolyte

 Important Recommendations for PE diagnosis :

 Assessment Of Pulmonary Embolism Severity And The Risk Of Early Death

 2 types of Risk stratification :
A. For patients with hemodynamic instability → Symptoms and Signs
B. For patients without hemodynamic instability → requires the assessment of
two sets of prognostic criteria :
1. Clinical, imaging, and laboratory indicators of PE severity, mostly related
to the presence of RV dysfunction
2. Presence of comorbidity and any other aggravating conditions that may
adversely affect early prognosis
  Clinical parameters of pulmonary embolism severity
- Tachycardia, low systolic BP, respiratory insufficiency (tachypnoea
and/or low SaO2), and syncope
 Imaging of right ventricular size and function : ECHO, CTPA
 Laboratory biomarkers
1. Markers of myocardial injury→ Troponin I, T
2. Markers of right ventricular dysfunction → B-type natriuretic peptide (BNP)
and N-terminal (NT)-proBNP
3. Other laboratory biomarkers
- Lactate, Serum Creatinine, GFR, Cystatin C, Hyponatremia, Vasopressin
 Integration of aggravating conditions and comorbidity into risk assessment of acute
pulmonary embolism → Pulmonary Embolism Severity Index (PESI)

 Prognostic assessment strategy

 Emergency Treatment of Acute Pulmonary embolism PE (Non-Pregnant)

1. ABC Approach (Including Vital signs)
2. 2 Wide-bore cannula → + Blood taken for CBC, Electrolytes and Urea
3. Oxygen High concentration 60–100% continuous
- Indicated in patients with SaO2 <90%
- To keep SaO2 >94%
4. IV fluids : 1 L of N/S.
- Hypervolemia can be harmful if RV strain is present. No excessive IV fluids should be
given.
- Treatment of right ventricular failure (Massive PE) in acute high-risk pulmonary
embolism → ICU

→ Used If Systolic BP <70mmHg

→Used if systolic BP 90-70mmHg

- Signs and Markers of RV strain :

 ECG : inversion of T waves in leads V- V4, QR pattern in V1, S1Q3T3 pattern,
incomplete or complete RBBB
 ↑ BNP, Troponins
 ECHO features of RVF
5. Analgesia : 5-10mg IV Morphine Or NSAIDs iF hypotensive
6. Anticoagulation :
- Initially : Subcutaneous Low molecular weight heparin or IV unfractionated heparin
- Then : warfarin .

- Indications :
 low probability of PE with diagnostic study is expected to be delayed >24hours
 Intermediate Or high Probability
- Duration : Acute phase (5-10days), Maintenance (at least 3months), Long-term P.
- Choice of Anticoagulation :
A. Stable → LMWH
B. Unstable, Renal insufficiency, Severe obesity → UFH
 7. Systemic Fibrinolytic/thrombolysis therapy
- Streptokinase 250000 units IV infusion over 30 minutes then Streptokinase 100000
units IV hourly for up to 12-72. Or
- Accelerated regimen: 1.5 million IU over 2 h
- Faster improvement In PAP, PVR, RV dilatation on Echo.
- The greatest benefit is observed when treatment is initiated within 48 h of
symptom onset
- UFH may be administered during continuous infusion of alteplase, but should
be discontinued during infusion of streptokinase or urokinase.
- Indications :
 Haemodynamically Unstable patient and shock state ( Massive PE with
Cardiogenic shock)
 Persistent Hypoxia despite high O2 concentration
 Presence of RV dysfunction and dilation by ECHO
 Presence of thrombus in the main pulmonary vessel
 Persistent hypotension or shock when SBP <90 mmHg
 Haemodynamically stable with - RV dysfunction OR - extensive clot burden
 Persistent profound bradycardia or shock
 Patient with DVT

8. No role for diuretics nor vasodilators.

9. Percutaneous catheter-directed treatment OR Surgical embolectom

Note : Starting heparin based on strong clinical suspicion is a good practice if no CI.
 Recommendations for acute-phase treatment of high-risk PE

 Recommendations for acute-phase treatment of intermediate-low-risk PE

 Recommendations for the regimen and duration of anticoagulation after pulmonary
embolism in patients without cancer

 Anti-Thrombotic therapy Dosing

 Clinical Tips AND Recommendations regarding PE During Pregnancy
 Avoiding PE overdiagnosis in pregnancy is as important as not missing a PE diagnosis
 LMWH is the treatment of choice for PE during pregnancy
 LMWH does not cross the placenta, and consequently does not confer a risk of fetal
hemorrhage or teratogenicity
 Fondaparinux may be considered if there is an allergy or adverse response to LMWH
 In women receiving therapeutic LMWH, strong consideration should be given to
planned delivery to avoid the risk of spontaneous labour while fully anticoagulated

 Differential Diagnosis Of Acute PE

 Complications Of Acute PE
1. Post thrombotic syndrome
2. Pulmonary HTN

References

 Davidson 23rd Edition

 Kumar 10th edition
 2019 ESC Guidelines for the diagnosis and management of acute PE
 Tintinalli’s Emergency medicine 10th edition
 Rosen's Emergency medicine 9th Edition
 Oxford EM 5th edition

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