Last edited: 10/28/2021

1. PULMONARY EMBOLISM
Pulmonary Embolism Medical Editor: Maxine Abigale R. Bunao

OUTLINE I) INTRODUCTION

I) INTRODUCTION ● Pulmonary Embolism

II) CAUSES o Blood clot that develops within the pulmonary
III) PATHOPHYSIOLOGY artery circulation
IV) COURSE Table 1. General pathophysiology.
V) CLINICAL MANIFESTATIONS Location Events
VI) COMPLICATIONS
Pulmonary Embolus dislodged within the vessel
VII) DIAGNOSTICS
artery ↓
VIII) TREATMENT
Obstructs blood flow distal to the occlusion
IX) APPENDIX
↓
X) REVIEW QUESTIONS
Lung dysfunction  ↓ gas exchange
XI) REFRENCES

II) CAUSES

Figure 1. Causes of pulmonary embolism.

(3) Venous drainage:
(A) DEEP VEIN THROMBOSIS o IVC
Most common cause o internal iliac vein
o external iliac vein
(1) Location: o femoral vein  deep femoral vein
deep vein in the lower extremity o popliteal vein bifurcates:
 anterior tibial vein
(2) Pathophysiology:  posterior tibial vein
 peroneal / fibular vein
Table 2. Pathophysiology. These are deep veins
Location Events When clots form within these vessels,
Vessel wall Situated within the vessel wall
↓
Breaks off a small part of the
embolus
↓
Factors or causes that ↑ risk of clots forming within these
vessels (VIRCHOW’S TRIAD)
IVC Circulates
a. Stasis
↓
Stuck in the pulmonary artery  b. Hyper-coagulable condition
Pulmonary embolus c. Endothelial damage

RECALL:
Deep veins to take note of for: Mechanism:
o To know which veins are most commonly affected o Normal: Blood has a laminar flow within a vessel
especially when checking the reports (i.e., ultrasound) o Deranged:
Blood is stagnant in a particular area
↓
Platelets stick to the endothelial wall
↓
↑ aggregation of platelets

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(4) VIRCHOW’S TRIAD
Table 3. Virchow's triad: 3 things which increased risk of forming blood clots.
Factors Mechanism
Stasis Normal Muscular milking activity:
(↑blood flow staying
in a particular area)

↓ Ambulation:
o Post-operative (bed rest)
o Immobilized due to fracture
o Paralysis post cerebrovascular accident
o Airplane / long car rides (≥ 8 hours)
Varicose veins
o Leaky or incompetent valves
o ↑ Backflow of blood to the proximal area  stagnate
Compression of vessel
o Stasis is proximal to the compression
o Pregnancy: uterus compresses iliac vein
o May-Thurner’s Syndrome: Right iliac artery squeezes the iliac vein against lumbar vertebrae
 ↓ blood flow going up
Obesity
o ↑ Adipose / centrally located abdominal tissue

Hyper-coagulable ↑ Procoagulant Enzymes (Factor V, VII, X, XII, Thrombin) = ↑ Blood clots

condition ↑ Factor in V Leiden: ↑ thrombus formation
Prothrombin gene mutation: ↑ prothrombin activator system = ↑ thrombin

↓ Anticoagulant Enzymes = ↓ function or production = ↑ Blood clots

Protein C/S Deficiency
Antithrombin III Deficiency

Acquired Causes
↑ Estrogen activity = ↑ Procoagulant activity
o Pregnancy
o OCP (with Estrogen) intake
Malignancies = ↑ Procoagulant activity
o Lung Carcinoma
o Pancreatic Carcinoma
Nephrotic syndrome

Antiphospholipid syndrome (Acquired/genetic)

o Associated with Systemic Lupus Erythematosus
o Genetic:

Heparin induced Thrombocytopenia

o Pulmonary Embolism treated with Heparin but developed more clots

Endothelial Surgery (C-section, orthopedic, etc.)

damage Smoking: Nicotine causes direct cytotoxic injury to the endothelial cells
Obesity via:
o Compression  stasis
o Cytokine release  hypercoagulability
o IL-6 & CRP release  endothelial damage  ↑ procoagulant enzyme activity
Vascular catheter = ↑ clots within the vicinity of insertion

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 (B) AIR EMBOLUS “BENDS” IV) COURSE
When someone is scuba diving:
● IVC
o they descend deeper into the surface
o ↑ pressure
Rising up back too fast:
o can bring with it nitrogen
o Due to pressure change and solubility changes within
the gases  forms air bubbles  BENDS which form V) CLINICAL MANIFESTATIONS
in the pulmonary circulation Table 4. Mechanism and its clinical manifestations.
(C) FAT EMBOLUS Mechanism Clinical Manifestation
Clot within a deep vein Swelling of lower extremity
Seen in long bone fractures
↓
RECALL: Extravasation of plasma Edema
Within the center of the medullary cavity, it is filled with fat proximal to the clot
Fat globules escape into the pulmonary circulation Blood localized in the Redness
(D) PREGNANCY: AMNIOTIC EMBOLUS area
Swelling ↑ compartment Pain
Premature birth: syndrome
o Opening of the amniotic that leaks into the circulation
o Proteins inside the amniotic are amniogenic  clots ↑ Respiratory rate, depth
(Tachypnea)
 emboli
↑ Intercostal muscle use
Associated with premature complications Clot in pulmonary Dyspnea (shortness of breath)
circulation  Hypoxemia Hemoptysis
(E) BACTERIAL OR SEPTIC EMBOLUS Pleuritic chest pain (upon
IV drug abusers have an increased risk of carrying inhalation)
bacteria which can lead to Infective Endocarditis Respiratory alkalosis
Pathophysiology
o Organisms: RECALL:
 S. aureus spp.
(+) Homan’s sign  suspect of DVT
o Straight from the skin directly into the blood
o Asymmetric swelling, pain, and redness of lower
o S. aureus tend to stay within the tricuspid valve and
extremity 
form vegetations there o Pain upon dorsiflexion of the foot
o The vegetations can break off  RV  pulmonary
circulation  lodged off in pulmonary artery
VI) COMPLICATIONS
III) PATHOPHYSIOLOGY
● When embolus breaks off and gets stuck in pulmonary
● Ties the risk factors and causes with the clinical circulation  forms complications
manifestation ● Problem
● DVT is the most common cause o Stuck within the pulmonary circulation
o Clot within the pulmonary artery
o Clot at the center where it bifurcates  saddle
embolism
● Mechanism of clot in the pulmonary circulation
o Alveoli PO2 = 100mmHg
o Pulmonary capillary blood PaO2 = 100mmHg
o Normally, gradient makes it easier for oxygen to move
from alveoli into the arterial circulation

Table 5. Complications.
Location Mechanism
Clot V Q
Venous circulation (+) ↑/N ↓ Perfusion =
Pick up O2 + drops it ↓ blood =
off  exit as ↓ O2 or Hypoxemia
oxygenated blood

RECALL:
Normal Ventilation + Abnormal perfusion:
o ↑V/↓Q ratio = ↑ratio or alveolar-arterial gradient
o Alveolar O2 > very little arterial O2

Figure 2. Pathophysiology.

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 Table 7. Saddle embolus pathophysiology.
Table 6. Complications, compensations, and its clinical Condition Compensation Clinical
manifestations. Manifestation
Condition Compensation Clinical • Baroreceptors in ↑ SNS:
Manifestation carotid and aortic
• Activates peripheral ↑ Respiratory sinus sense BP ↑ Reflexive HR/
chemoreceptors ↓ BP changes
rate (systemic Tachycardia
located in aortic bodies (Tachypnea) • Send to CN IX
and carotid bodies hypo- and X  medulla
and depth tension) ↑ Contractility
• CN IX (glosso-
Hypoxemia pharyngeal) CN X Dyspnea ↑ Vasoconstriction
 (vagus) sense changes (shortness of of PVR  ↑ BP
↓ O2 from the breath)
saturation chemoreceptors
• Send out to brainstem
VII) DIAGNOSTICS
and activate breathing
centers in the medulla Table 8. Diagnostic tests.
• Push ↑ blood into the ↑ HR Test Rationale
alveoli  ↑ CO  ↑ O2 • Helps identify underlying etiology (i.e., HIT
CBC
with ↓ RBC and ↓ platelets)
• ↑ O2 uptake Respiratory
Hypocapnia alkalosis • Best given to patients with ↓ renal function
due to ↑ = ↑ CO2 exhaled out
• Giving contrast to a person with renal
Respiratory BMP
• ↓ CO2 in the blood dysfunction (severe ↓ GFR)  contrast
rate induced nephropathy
= ↑ pH
• Early stages of PE: ↑ RR to breathe off CO2
• Release: ADP, Worsens
 Respiratory Alkalosis
Thromboxane A2, dyspnea ABG
• Later stages of PE: ↑ fatigued muscles from
5-HT
breathing  Respiratory Acidosis
• (+) bronchial smooth
muscle  • Gives idea about the activity of fibrinolysis
bronchoconstriction and inflammation in general
o Plasmin breaks off fibrin within clots
• (+) pulmonary Stress on the
o Recall: Fibrinogen  Fibrin
vasoconstriction due heart
o Fibrin degradation products  D-dimers
to inefficiency of D-Dimer o End product: ↑ plasmin to dissolve the
↑ Platelets ventilating a clogged
stick clot = ↑ D-dimers as products
vessel (with clot)
together • Clamps clogged vessel ● >500 = potential clot
 shunts blood to a o DVT
near, effective alveoli o PE
• Sequela: stress on the
Approach to patient with suspicion of PE
heart + ↓ O2 supply to
the lungs  Infarction Hemoptysis Table 9. Wells' Criteria.
of the lungs  (Cough bloody WELLS’ CRITERIA
ruptured alveolar sputum) High score = ↑ suspicion of PE
capillary membrane  Low score = ↓ suspicion of PE
blood leaks into it <4 ≥4
(1) Saddle Embolus or Proximal Pulmonary Artery PE unlikely PE likely
Embolus Low pre-test High pre-test probability
probability ↓
● Restricts blood flow moving through the vessel ↓
o ↓ diameter = ↑resistance to blood flow, SVR Check D-Dimer CT Pulmonary Angiogram
(definitive diagnostic test)
o ↑ afterload, ↑ BP in the pulmonary system
<500 (±) Contrast: lights up vessels; sees
● Sequela: ↓ filling defect and clot
PE ≥500  ↓
o RV has to overcome ↑ BP in the pulmonary system /
excluded ↓ Normal Indeterminate (+) Clot
pump against the high pressure
May do ↓ ↓ ↓
o ↑ RV dilation  RV dysfunction  another PE Pulmonary Treat
test excluded Angiogram PE
 ↓ RV SV and CO into LA
OR
• ↓ preload in the LV LE venous
ultrasound
• ↓ SV and CO
● Contraindications to CT Pulmonary Angiogram:
• ↓ systemic BP (Hypotension) o Contrast allergies
 Blood backs up into RA o Severe CKD, ↓ eGFR, ↑ risk for contrast-induced
• Reaches the SVC nephropathy
• ↑ Jugular venous distention o Alternative: V/Q Scan
 Deviates interventricular septum towards LV ● Pulmonary angiogram
lumen o Course of catheter with contrast:
 RA  RV  pulmonary circulation
• Obstructed LV = ↓LV afterload = hypotension
● Lower Extremity venous ultrasound
o (+) DVT  possible to find a PE

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 (A) ECG
(1) Electrocardiogram (ECG)

Figure 3. ECG and associated abnormalities with PE.

● Most common finding if with PE:
o Sinus Tachycardia
● S1Q3T3 Pattern:
o Lead I: deep S wave  S1 component
o Lead III:
 deep Q wave
 inverted T wave
 RAD:
• Left thumb – Lead I  down
• Right thumb – Lead aVF  up
o V1, V2, V3:
 rsr' pattern  Right bundle branch block

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 (B) IMAGING (2) CT Pulmonary Angiogram

(1) Chest X-Ray

Figure 4. Chest X-Ray findings. (+) Westermar's sign. (+)

Hampton's hump.

High suspicion of PE:

o Normal Chest X-Ray BUT in exams there are classic
findings:

(a) Westermar’s Sign Figure 6. CTPA findings in PE.

 Dark hyperlucent area

• tissue distal to the clot, has undergone
avascular necrosis

(b) Hampton’s Hump

 Wedge shaped opacification
• Due to pulmonary infarction

Symptoms:
 Dyspnea
 Tachypnea
 Tachycardia
 Hemoptysis

Figure 7. CTPA.
● Gold standard

Figure 5 Hampton's Hump [Wikimedia commons]
Orientation:
o Looking from the feet (inferior) towards the head
(superior)
o Right of the image: Right hemithorax
o Left of the image: Left hemithorax
o Heart points towards the left side
o Within the heart, bifurcation of the pulmonary trunk
(right and left) will be seen as WHITE
Evidence of pulmonary embolus:
o Right pulmonary artery: (+) dark clot
o Left pulmonary artery: (+) dark clot
o Bilateral emboli

Contraindications to CT Pulmonary Angiogram:

o Contrast allergies
o Severe CKD, ↓ eGFR, ↑ risk for contrast-induced
nephropathy
o Alternative: V/Q Scan

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 (3) V/Q Scan (4) Pulmonary Angiogram

Figure 9. Pulmonary angiogram findings in PE.

Figure 8. V/Q Scan findings in PE.

Mechanism:
o Uses an element called Technetium which lights up
in V/Q scan when inhaled

Perfusion Deficits:
o Manifest at the lower right lung and middle lower left lung
o Potential emboli occluding perfusion to the said
segments of the lung

Figure 10. Angiography.

● Invasive test but the most definitive diagnostic test
o Increased risk due to invasiveness

Mechanism:
o Uses contrast-filled catheter  fill up the pulmonary
arteries
o Black pulmonary arteries

Orientation:
o Left image shows filling defect at the lower portion of
the arteries (dependent segments)
o Possibly secondary to an emboli

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(5) Echocardiogram

Orientation:
o Lower part of the picture:
 Left upper: LV
 Left lower: LA
 Mitral valve
o Upper part of the picture:
 RA
 RV
o Right side of the picture:
 IVC – dark anechoic structure

Suspected pulmonary embolism:

o RA dilated with a dilated IVC
o RV dilated – dysfunctional, not contracting very well,
↓ hypokinesis
Figure 11. Echocardiogram.
 RV bigger size > LV
● May be done at ease, on bedside  LV squeezes well than RV

(6) Lower Venous Ultrasound

● Compressibility of veins
o Good sign that there’s no kind of thrombus blocking
the compressibility
● Abnormal compression:

Figure 13. Not compressed vs decreased compression (right

image) due to a possible clot within the femoral vein.
o Femoral vein (bigger, lower right of the image)
o Femoral artery (smaller, upper left the image)
Figure 12. Lower venous ultrasound. Normal findings.
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 VIII) TREATMENT

Figure 14 Treatment overview for PE

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 Table 10. Approach to treatment of PE. (2) Direct Oral Acting Anticoagulants (DOACs)
Hemodynamic Status
● Outpatient administered for 3-6 months
Hemodynamically Stable Hemodynamic Instability (↓ BP, ↑ ● Examples:
HR, ↓ O2, ↑ JVP, altered mental o X-A inhibitors
↓ status, or severe pleuritic chest  Rivaroxaban
pain)  Apixaban
Anti- IVC filter Tissue Embolectomy  Edoxaban
coagulation If (+) CI to Plasminogen If (+) CI o II-A inhibitors
anticoagulation Activator to TPA  Dabigatran
● Lesser monitoring, less drug interaction
Table 11. Grading of severity of PE. ● Risk:
Grading of Pathophysiology Treatment o Lesser risk of hemorrhage than Warfarin
severity of
PE
• Clot in the pulmonary • Anticoagulation
Sub- circulation • IVC Filter
massive • Hemodynamically stable
• (+) RV Dysfunction
• Clot in the pulmonary trunk • Thrombolytics,
Massive
• Hemodynamically unstable TPA
(Saddle)
• (+) RV Dysfunction • Embolectomy
(3) Warfarin
● Outpatient administered for 3-6 months
(A) ANTICOAGULATION
● Must bridge with Heparin before transitioning to Warfarin
● Does NOT break off the clot o Especially on the first 5 days
● Main mechanism is to PREVENT FURTHER o Warfarin is hypercoagulable  bridge with LMWH or
development of the clot and PROPAGATION of the clot UH
● Augments the coagulation cascade:
● Examples:
o ↓ hypercoagulable states o X-A inhibitors
o Prevents clot formation  Rivaroxaban
 Apixaban
(1) Heparin
 Edoxaban
o II-A inhibitors
 Dabigatran
● Lesser monitoring, less drug interaction
o MUST monitor INR
o ↑ Warfarin = ↑ INR is super therapeutic = ↑ bleeding

(B) IVC FILTER

● Indication:
o Contraindicated to anticoagulation
o Anticoagulation failed
● Mechanism:
o Allow solute, plasma particles to pass through IVC
Table 12. UH vs LMWH. filter (like a sieve) via IVC
Unfractioned Heparin Low Molecular o Course: RA  RV  pulmonary circulation
Weight Heparin o Sieve blocks clot coming from i.e. DVT which
Indication Hospitalized patients Outpatients propagates into the pulmonary circulation
Administration Drip or infusion (titrate per Given SQ injection
partial thromboplastin time or as a bridge for a
PTT) couple of days 
UH for long term
↑ PTT = ↑ heparin = lower usage
dosage
Monitoring Need PTT No need for PTT
Risk No anti-Xa activity
Caution for CKD:
Heparin induced
must renally dose
thrombocytopenia
this med or use
another one

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 (C) THROMBOLYSIS (E) SUPPORTIVE CARE
● Indication: If hemodynamically unstable
● Mechanism:
o Breaks off and busts off the clot
o Stimulates enzyme plasminogen  plasmin (breaks
down fibrin into D-dimers)
(1) Tissue Plasminogen Activator (TPA)
● Alteplase
o Mostly given
o 50-100 mg

Table 13. Supportive care.

Test Corrects Notes
(D) EMBOLECTOMY Preload  SV • Caution:
 CO  BP  Overloading the
● Indication:
IV Fluids effective arterial right side of the
o Hemodynamically unstable
blood volume heart
o Contraindication to thrombolysis (TPA)
o Cerebral Hemorrhage
Hypotension • Next in line if IV
● Mechanism: Vasopressors
fluids don’t work
o Catheter driven suction/aspiration of the clot
Hypoxemia • Forms: Non-
o Course:
Oxygen rebreather,
 SVC  RA  RV  pulmonary trunk support Nasal cannula,
 Sucks up some of the clot intubation
● Saddle Embolism
o Dangerous because they straddle between the actual (F) VTE PROPHYLAXIS
pulmonary trunk as it bifurcates (1) Subcutaneous LMWH: 5000U twice a day
o No blood going into both pulmonary circulations
o Reduce risk of forming clots
o Significant effects on:
 RV (2) Ambulating: ↓ stasis
 Hypoxemia

(3) Compression stockings

o Pneumatic compression device inflates and squeeze
down to induce “contractions”

IX) APPENDIX

Table 14. Abbreviations.

BP Blood pressure
CI Contraindications
CKD Chronic Kidney disease
CO Cardiac output
DOAC Direct oral acting anticoagulants
DVT Deep vein thrombus
INR International Normalized Ratio
IVC Inferior vena cava
LMWH Low molecular weight heparin
RA Right atrium
RV Right ventricle
TPA Tissue plasminogen activator
UH Unfractioned heparin
VTE Venous thromboembolism

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 X) REVIEW QUESTIONS

1) Patient Greg, 40/M, was recently diagnosed with a

DVT. What is the initial treatment for deep venous
thromboembolism?
a) Aspirin
b) Enoxaparin
c) Heparin
d) Warfarin
2) 32/F post NSD had a sudden onset of unilateral,
progressive, and painful swelling of the lower
extremity. Which of the following is the root cause?
a) Pulmonary embolism
b) Mitral valve regurgitation
c) Atrial fibrillation
d) None of the above
3) Intermediate complication of supracondylar fracture:
a) Osteomyelitis
b) Malunion
c) Fat embolism
d) Volkmann
4) A 30/M presents at the ER with severe leg pain with
suspicion of deep vein thrombosis. Which is NOT
part of the management for this patient?
a) Anticoagulation with heparin
b) Duplex scan of the lower extremity
c) Pain management
d) Revascularization procedure
5) A 24/F supermarket cashier came in due to bilateral
leg pains and intermittent pitting edema. PE showed
varicosities in the greater saphenous vein
distribution. Short of doing surgery, what can afford
the most relief of her symptoms?
a) Recommend medical grade stockings
b) Start on oral Diosmin/Hesperidia
c) Start on oral Furosemide
d) Therapeutic rehabilitation exercises

CHECK YOUR ANSWERS

XI) REFRENCES
● https://commons.wikimedia.org/wiki/File:Hampton_hump_bei_sc
hwerer_Lungenembolie_-_Roe_Thorax.jpg
●

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