Pulmonary Embolism

Slide 1 · Pulmonary Embolism

Thromboembolism, vascular obstruction, and pulmonary infarction

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Learning objectives

Trace venous thrombi to the pulmonary arterial circulation.

Relate embolic burden and cardiac reserve to respiratory and hemodynamic consequences.

Distinguish pulmonary hemorrhage from hemorrhagic infarction.

Interpret the main morphologic, clinical, diagnostic, and preventive principles.

Slide 3 · Pulmonary embolism: Core definition

Embolism = material traveling to and lodging in a vessel

A circulating embolus lodges in the pulmonary arterial tree and obstructs downstream perfusion.

Most clinically important pulmonary emboli are thromboemboli originating in the systemic venous circulation.

The consequences range from clinically silent obstruction to sudden cardiovascular collapse.

Slide 4 · Embolic obstruction is not the same as local thrombosis

Pulmonary thromboembolism

In situ pulmonary thrombosis

Clot formed elsewhere and migrated

Clot formed within pulmonary vasculature

Typical mechanism of major pulmonary artery occlusion

Rare in large pulmonary vessels

Commonly linked to venous DVT

Described with pulmonary hypertension and heart failure

Slide 5 · Why pulmonary embolism matters

It is a major cause of morbidity and death in immobilized or thrombosis-prone patients.

A single event may produce abrupt pulmonary perfusion failure.

A small embolus can be an early warning of subsequent larger emboli.

Prevention requires recognition of the underlying thrombotic predisposition.

Slide 6 · The usual source: Deep venous thrombosis

Leg deep veins

A thrombus forms in a low-flow venous compartment

Venous thrombus

A portion separates from the parent thrombus

Embolic fragment

The fragment is swept through the right heart

Pulmonary artery

Arterial lodging stops local perfusion

Slide 7 · Virchow triad explains thrombus formation

Stasis / abnormal flow

Reduced venous return

Endothelial injury or activation

Trauma, inflammation, vascular insults

Hypercoagulability

Inherited or acquired procoagulant tendency

Predisposition to venous thrombosis

Slide 8 · Stasis: Why immobility increases risk

Bed rest / restricted movement

Lower-extremity movement is reduced

Reduced calf-muscle pump

Normal venous blood propulsion declines

Venous stasis

Activated clotting factors persist locally

Deep-vein thrombosis

Thrombi can subsequently embolize

Slide 9 · Heart failure also promotes venous stasis

Hemodynamic setting

Impaired venous return favors thrombus formation.

Stasis is an important contributor to venous thrombosis.

Pathologic consequence

An embolic fragment enters the venous return.

Right-heart transit delivers it to pulmonary arteries.

Slide 10 · Surgery, trauma, and burns are multifactorial triggers

Altered flow and injury

Immobilization promotes venous stasis.

Injured tissue and vessels provide prothrombotic stimuli.

Coagulation balance

Procoagulants are released from injured tissue.

Reduced fibrinolytic activity can sustain thrombi.

Slide 11 · Inherited thrombophilia: Mechanisms

Inherited state

Biologic effect

Factor V Leiden

Reduced susceptibility of factor V to protein C inactivation

Prothrombin G20210A variant

Higher prothrombin synthesis / levels

Antithrombin deficiency

Loss of physiologic anticoagulant effect

Protein C or protein S deficiency

Impaired anticoagulant regulatory pathway

Slide 12 · Inherited and acquired risks can combine

Inherited predisposition

Examples: Factor V Leiden, prothrombin variant

Acquired trigger

Examples: Bed rest, pregnancy, surgery

Venous thrombus

Combined risk promotes thrombosis

Pulmonary embolus

Distal embolization creates PE

Slide 13 · Acquired prothrombotic states

Clinical setting

Prominent contributing process

Malignancy

Tumor-associated procoagulants and inflammation

Pregnancy / hormonal exposure

Systemic hypercoagulability; Altered venous return

Obesity

Acquired hypercoagulable predisposition

Major surgery / trauma

Stasis, tissue injury, and procoagulant activation

Slide 14 · Cancer-associated thromboembolism

Malignancy

Tumor-associated inflammation contributes

Procoagulant release

Tumor-derived tissue factor or mucin may act as procoagulants

Venous thrombosis

Thrombi may develop or recur

Pulmonary embolization

Fragments may travel to the lungs

Slide 15 · Pregnancy and postpartum thrombotic risk

Venous component

Reduced venous return from leg veins may contribute.

Peripartum reduced mobility may add stasis.

Systemic component

Hormonal changes are associated with hypercoagulability.

Pregnancy and the postpartum period increase venous thrombotic risk.

Slide 16 · Orthopedic injury: A high-risk clinical context

Patient scenario: An adult remains largely immobile after a hip fracture.

Which mechanisms in Virchow triad increase the risk of subsequent PE?

Venous stasis from immobility

Tissue / vascular injury after trauma

Acquired procoagulant changes

Slide 17 · Central lines and right atrial thrombi

Indwelling central venous line

A potential local nidus

Right atrial thrombus

Thrombus forms near an intravascular device

Embolization

An attached mass can detach

Pulmonary circulation

Emboli enter the pulmonary arterial tree

Slide 18 · The embolus follows the right-heart circulation

Leg / pelvic deep vein

Fragment enters larger veins

Inferior vena cava

Returns to the right heart

Right atrium → right ventricle

Passes through cardiac inflow and outflow

Pulmonary arterial tree

Becomes impacted at a vessel branch

Slide 19 · Anatomical lodging determines embolic effects

Pulmonary arterial bifurcation

Proximal pulmonary arterial occlusion

Slide 20 · Saddle embolus: Obstruction at the bifurcation

Pulmonary arterial bifurcation

Saddle embolus lies across the bifurcation

Slide 21 · Small emboli lodge in peripheral branches

Pulmonary arterial bifurcation

Distal embolus occludes a peripheral branch

Slide 22 · Multiple emboli may be simultaneous or recurrent

Shower of emboli

Several fragments may detach from one large thrombus.

Obstruction occurs at multiple sites at once.

Serial embolization

Repeated episodes can occur over time.

Each event may reduce the effective vascular bed.

Slide 23 · Paradoxical embolism: Venous-to-systemic passage

Systemic venous thrombus

A venous thrombus detaches

Interatrial or interventricular defect

A right-to-left route allows bypass of lung filtering

Systemic arterial circulation

Embolus reaches the arterial system

Peripheral organ embolism

Destination depends on vascular distribution

Slide 24 · Not every pulmonary embolus is a blood clot

Embolic material

Context in the supplied source

Thrombus

Usual substrate of pulmonary embolism

Fat

Rare nonthrombotic pulmonary embolus

Air

Rare nonthrombotic pulmonary embolus

Tumor

Rare nonthrombotic pulmonary embolus

Slide 25 · Two parallel pathophysiologic consequences

Respiratory compromise

Ventilation continues in poorly perfused lung units.

Gas-exchange efficiency is reduced.

Hemodynamic compromise

Obstruction increases resistance to pulmonary blood flow.

Right ventricular function may fail acutely.

Slide 26 · Ventilated but nonperfused lung: The mismatch

Ventilated alveolus

Airflow

Embolus

Reduced flow beyond the clot

Arterial inflow

Ventilation persists without matching perfusion

Physiologic schematic — not a clinical imaging study

Slide 27 · Vascular obstruction raises right-heart afterload

Pulmonary arterial occlusion

Available perfused vascular bed falls

Increased vascular resistance

Blood must traverse fewer channels

Right-ventricular pressure load

The RV faces an acute outflow burden

Acute right-heart failure

Severe cases progress to shock

Slide 28 · What determines clinical severity?

Degree of arterial obstruction

Caliber of occluded vessels

Number of emboli

Pre-existing cardiac reserve

Slide 29 · Clinical spectrum: Small to catastrophic

Silent obstruction

Transient symptoms

Hemorrhage / infarction

Shock or sudden death

Outcome depends on embolic burden, vessel caliber, embolus number, and cardiac reserve

Slide 30 · Why many small emboli remain clinically silent

Small emboli may obstruct only a limited fraction of the pulmonary vascular bed.

The remaining perfused lung can maintain adequate function.

Thromboemboli may subsequently organize into the arterial wall.

The absence of early symptoms does not eliminate the risk of another embolus.

Slide 31 · Massive obstruction can produce abrupt collapse

Extensive pulmonary obstruction

A substantial part of the vascular bed becomes unavailable

Marked fall in pulmonary blood flow

Right-heart output through the lungs declines

Acute right ventricular failure

Acute cor pulmonale may ensue

Circulatory collapse

Severe obstruction may be rapidly fatal

Slide 32 · Pulseless electrical activity in catastrophic PE

Electrical rhythm ≠ effective circulation

Electrical activity may remain visible on the ECG despite absence of a palpable pulse.

Severe vascular blockage prevents effective forward flow through the lungs.

This mechanism explains electromechanical dissociation during resuscitation in some fatal PE cases.

Slide 33 · Cardiovascular reserve modifies the outcome

Preserved reserve

Bronchial arterial flow may maintain lung tissue viability.

Hemorrhage may occur without infarction.

Compromised reserve

Pre-existing heart or lung disease reduces tolerance.

Pulmonary infarction is more likely.

Slide 34 · The lung has a dual arterial supply

Alveolar tissue viability

Pulmonary arterial inflow

Bronchial arterial inflow

May be blocked by PE

May preserve perfusion

Dual inflow helps explain why embolic hemorrhage may occur without infarction.

Schematic; Flow contributions not drawn to scale

Slide 35 · Hemorrhage does not necessarily mean infarction

Pulmonary hemorrhage

Blood may extravasate after embolic vascular injury.

Viable tissue can remain because bronchial perfusion persists.

Pulmonary infarction

Ischemic necrosis develops when compensatory perfusion fails.

The resulting infarct is characteristically hemorrhagic.

Slide 36 · Small distal branches can cause infarction

Distal arterial embolus

Occlusion occurs near the microvascular bed

Reduced local perfusion

The affected territory is perfusion-limited

Insufficient alternative flow

Reserve and bronchial supply determine survival

Hemorrhagic infarction

Alveolar wall necrosis accompanies hemorrhage

Slide 37 · Infarction is not the usual outcome of PE

Pulmonary infarction in approximately one tenth of embolic episodes.

Most emboli do not infarct lung tissue because of the dual arterial supply.

Pre-existing cardiopulmonary impairment makes infarction more likely.

Infarction therefore reflects both vascular obstruction and reduced collateral reserve.

Slide 38 · Gross distribution of pulmonary infarcts

Hilum

Pleural surface

Typical pleural-based infarct; Most occur in lower lobes

Schematic (not a specimen)

Slide 39 · The classic infarct is wedge-shaped

Hilar apex ← wedge → pleural base

The broad end reaches the pleural surface; The apex points toward the hilum.

An occluded vessel may be found near the apex.

The wedge shape reflects the downstream territory of an obstructed arterial branch.

Slide 40 · Early pulmonary infarction: Gross morphology

Infarcted lung

Raised, red-blue hemorrhagic area.

Often extends to the pleural surface.

Pleural reaction

Fibrinous exudate may cover the adjacent pleura.

The pleuritis helps explain pleuritic chest pain.

Slide 41 · The infarct changes appearance with time

Initial red-blue hemorrhage

Gross red-blue lesion

Erythrocyte breakdown

Red cells begin to lyse

Red-brown hemosiderin

Hemosiderin accumulates

Fibrous replacement / scar

Fibrosis and contraction develop

Temporal sequence — schematic; Not a photographed specimen

Slide 42 · Infarct healing ends in contraction and scarring

Necrotic lung region

Tissue is not recoverable in the infarcted territory

Marginal fibrous replacement

Repair advances inward from the margins

Gray-white peripheral zone

Fibrosis progressively replaces necrotic tissue

Contracted scar

The mature lesion contracts

Slide 43 · Microscopic hallmark: Ischemic parenchymal necrosis

Injured compartments

Alveolar walls undergo ischemic necrosis.

Bronchiolar and vascular walls may also be involved.

Associated changes

Hemorrhage fills or surrounds injured parenchyma.

The morphology reflects both ischemia and blood extravasation.

Slide 44 · Septic emboli produce a different inflammatory pattern

Infected embolus

Embolic material contains infectious organisms

Focal pulmonary occlusion

Vascular occlusion creates local injury

Intense neutrophilic reaction

Infection amplifies inflammation

Septic infarct ± abscess

Some infarcts progress to an abscess

Slide 45 · An antemortem thrombus differs from a postmortem clot

Antemortem thrombus

Postmortem clot

Formed in flowing blood before death

Develops after circulation stops

May show lines of Zahn

Does not display genuine flow-related lines of Zahn

Can embolize and occlude arteries

Does not explain antemortem thromboembolism

Slide 46 · Most common symptomatic presentations

Dyspnea is a prominent symptom.

Pleuritic chest pain is common in symptomatic cases.

Cough may accompany pulmonary embolization.

Symptom intensity varies with the amount and location of obstruction.

Slide 47 · Look for clues to the deep-vein source

Leg symptoms

Calf or thigh swelling may be present.

Pain in the affected limb may accompany DVT.

Clinical interpretation

Leg findings support a thromboembolic source.

Absence of obvious limb symptoms does not rule out PE.

Slide 48 · Infarction adds fever, hemoptysis and pleuritis

Parenchymal injury

Hemorrhagic infarction can cause hemoptysis.

Fever may accompany tissue injury.

Pleural involvement

Pleuritic pain may reflect fibrinous pleuritis.

An audible pleural friction rub can occur.

Slide 49 · Large emboli may mimic myocardial infarction

Shared clinical features

PE-specific context

Severe chest pain

Recent immobility or thrombotic predisposition

Dyspnea

Possible accompanying leg DVT

Shock

Acute pulmonary vascular obstruction

Slide 50 · Diagnostic testing must reflect clinical likelihood

Clinical assessment

Evaluate symptoms, risk context, and stability

Low / moderate likelihood

The textbook frames D-dimer use in this group

D-dimer screening

A negative result may assist exclusion in this setting

Definitive vascular imaging

CT pulmonary angiography identifies occlusion

Slide 51 · D-dimer is a rule-out test in selected patients

Interpret a test in its pretest-probability context

D-dimer in hemodynamically stable patients at low-to-moderate clinical risk.

A normal result can help exclude PE when appropriately interpreted in that group.

D-dimer alone is not presented as an imaging substitute in patients with high clinical suspicion.

Slide 52 · CT pulmonary angiography identifies the obstruction

Anatomic question

Is contrast flow interrupted in a pulmonary artery?

Which central or branch vessels are affected?

Role

Usually provides definitive diagnosis.

Displays obstructed pulmonary arterial branches.

Slide 53 · Ventilation–perfusion imaging: An alternative

Ventilation study

Maps inspired-air distribution within the lungs.

Air entry may be relatively preserved in an embolized region.

Perfusion study

Assesses regional pulmonary blood flow.

A corresponding perfusion deficit may reveal mismatch.

Slide 54 · Duplex ultrasonography evaluates DVT

Suspected PE

Clinical syndrome prompts vascular assessment

Evaluate thrombotic source

DVT can coexist with pulmonary embolism

Venous duplex ultrasound

Ultrasonography examines deep venous flow and compressibility

Identify deep-vein thrombosis

Support for a venous source

Slide 55 · Chest radiography may be initially unrevealing

Uncomplicated PE

Chest radiograph may appear normal.

A normal radiograph does not exclude PE.

Pulmonary infarction

A peripheral wedge-shaped infiltrate may appear.

Visibility about 12–36 h after infarction.

Slide 56 · Clot resolution follows fibrinolysis and contraction

Acute embolic thrombus

Pulmonary arterial lumen becomes obstructed

Fibrinolysis

Enzymatic dissolution may occur

Thrombus contraction

The clot may shrink after the acute event

Restored or remodeled vessel

Some resolve; Others leave residual organized material

Slide 57 · Organized emboli can leave fibrous webs

Persistent embolus

Not all thrombus dissolves completely

Thrombus organization

Fibrous tissue replaces thrombotic material

Incorporation into arterial wall

Chronic remodeling changes the lumen

Bridging fibrous web

Thin residual webs may persist

Slide 58 · Recurrent emboli: Cumulative vascular injury

Repeated embolic episodes

Small events occur over time

Loss of perfused vascular bed

Functional cross-sectional area diminishes

Higher pulmonary resistance

Hemodynamic load increases

Right-ventricular strain

Chronic cor pulmonale can develop

Slide 59 · Chronic thromboembolic pulmonary hypertension

Recurrent obstruction → pulmonary hypertension → cor pulmonale

Persistent or recurrent thromboemboli narrow the effective pulmonary vascular bed.

Increased pulmonary vascular resistance may result in pulmonary hypertension.

Long-standing pressure overload can progress to right-ventricular failure.

Slide 60 · Preventing venous thrombosis prevents PE

Preventive strategy

Mechanistic purpose

Early postoperative / postpartum ambulation

Limit venous stasis

Mechanical compression in appropriate patients

Improve venous return

Anticoagulation when clinically indicated

Reduce thrombus formation and extension

Slide 61 · Anticoagulation and supportive care

Anticoagulation

Central element of PE treatment.

Targets the underlying thromboembolic process.

Supportive measures

Address the consequences of respiratory compromise.

Support hemodynamics when cardiac output is impaired.

Slide 62 · Thrombolysis: Potential benefit and bleeding risk

Potential role

Important limitation

Considered in severe complications such as shock

Can cause serious bleeding

Targets obstructing thrombus more rapidly

Decision requires careful clinical risk assessment

Slide 63 · Inferior vena cava filter: Selected use

High recurrence risk

Further embolic events remain a concern

Anticoagulation contraindicated

Anticoagulant therapy cannot be used

IVC filter placed

A mechanical barrier is deployed in the vena cava

Venous clot capture

May intercept clots before reaching the lungs

Slide 64 · Case: Dyspnea after prolonged immobilization

A patient is bedridden after surgery and suddenly develops dyspnea with a painful swollen calf.

What source and pathway best explain the pulmonary findings?

Deep-vein thrombosis in an immobilized leg

Fragment transit via vena cava and right heart

Obstruction of pulmonary arterial branches

Slide 65 · Case: Hemorrhage versus true infarction

Two patients have peripheral pulmonary arterial emboli. One has preserved cardiac function; The other has severe pre-existing cardiac disease.

Why may only the second patient develop infarction?

Bronchial circulation can preserve tissue perfusion

Cardiopulmonary compromise reduces compensatory reserve

Vascular hemorrhage does not itself prove necrosis

Slide 66 · Case: Abrupt shock and absent pulses

A high-risk patient develops sudden severe dyspnea, hypotension, and pulseless electrical activity.

What pathophysiology links a large embolus to collapse?

Major pulmonary outflow obstruction

Abruptly increased right-ventricular afterload

Failure of effective forward pulmonary blood flow

Slide 67 · Compare three major outcomes of pulmonary emboli

Outcome

Typical mechanism

Major implication

Clinically silent

Limited perfusion loss / preserved reserve

Risk of later embolization may persist

Hemorrhagic infarction

Distal occlusion plus insufficient collateral perfusion

Wedge-shaped pleural lesion

Acute cor pulmonale / collapse

Extensive pulmonary vascular obstruction

Acute right-heart failure

Slide 68 · Integrating source, mechanism and morphology

Predisposing state

Stasis, endothelial injury, or hypercoagulability

Deep-vein thrombosis

Embolization is the key intermediate

Pulmonary arterial obstruction

Location and burden determine perfusion loss

Anatomic / clinical consequence

Silent PE, infarction, or acute RV failure

Slide 69 · Core principles to retain

Most pulmonary thromboemboli begin as thrombi in systemic deep veins.

Perfusion loss and increased pulmonary vascular resistance account for major consequences.

Dual circulation limits infarction; Compromised reserve increases its likelihood.

Recurrent or unresolved emboli may culminate in pulmonary hypertension and right-heart failure.

Slide 70 · Primary references

Robbins, Cotran & Kumar. Pathologic Basis of Disease. 11th edition (2026).

Pulmonary Embolism — Hemodynamic Disorders, Thromboembolic Disease, and Shock.

Pulmonary Embolism and Infarction — The Lung.

The clinical and morphologic content of this lecture is grounded in these textbook sections.