Pulmonary Embolism and Infarction

Slide 1 · Pulmonary Embolism

and Infarction

Pathogenesis • Morphology • Clinicopathologic correlation

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Learning objectives

Distinguish pulmonary thromboembolism from primary thrombosis and nonthrombotic emboli.

Explain why some emboli cause silent obstruction, whereas others cause shock or infarction.

Identify characteristic gross and microscopic findings of hemorrhagic pulmonary infarction.

Integrate clinical findings, diagnostic tests, and mechanisms of recurrent embolic disease.

Slide 3 · Pulmonary embolism: Central concept

Leg deep-vein thrombus

Inferior vena cava

Right heart

Pulmonary arteries

Embolus lodges at arterial narrowing

Schematic: Thrombus detachment → transport → pulmonary obstruction

A detached intravascular mass lodges within the pulmonary arterial circulation.

Most clinically important pulmonary arterial occlusions arise from venous thrombi.

Consequences depend on obstructed vascular territory and cardiopulmonary reserve.

Slide 4 · Thrombus, embolus, and infarct are distinct

Thrombosis

Embolization

Arterial blockage

Possible infarction

Thrombus: Intravascular clot formed at its site of attachment.

Embolus: Detached mass transported to a distant vascular territory.

Infarct: Ischemic tissue necrosis; It does not follow every pulmonary embolus.

Slide 5 · Why the deep veins matter

Leg deep-vein thrombus

Inferior vena cava

Right heart

Pulmonary arteries

Embolus lodges at arterial narrowing

Schematic: Thrombus detachment → transport → pulmonary obstruction

Leg deep venous thrombosis is the principal source of pulmonary thromboemboli.

Thrombus fragments move through the vena cava and right heart into pulmonary arteries.

Risk factors for pulmonary embolism largely overlap those for deep venous thrombosis.

Slide 6 · Proximal deep venous thrombosis

Popliteal, femoral, and iliac venous thrombi are particularly important embolic sources.

Thrombi may propagate in the direction of venous blood flow.

Proximal venous thrombi may fragment even when local leg symptoms are absent.

Slide 7 · The Virchow triad explains susceptibility

Abnormal flow / stasis

Endothelial injury

Hypercoagulability

Convergent mechanisms promoting venous thrombus formation

Abnormal flow, vascular injury, and hypercoagulability contribute to thrombus formation.

Clinical risk states often act through more than one mechanism.

Slide 8 · Immobility: Venous stasis

Immobility

Reduced venous flow

DVT

Pulmonary embolus

Loss of the leg-muscle pump reduces venous return.

Bed rest and prolonged immobilization favor lower-limb venous thrombosis.

Hip fracture combines immobility with major tissue injury.

Slide 9 · Trauma and surgery: Multiple mechanisms

Vessel injury and tissue damage can favor coagulation.

Postoperative immobility adds venous stasis.

Trauma, fractures, severe burns, and major surgery are important precipitating contexts.

Slide 10 · Inherited hypercoagulability

Factor V Leiden is an inherited risk factor named in the pulmonary embolism section.

Inherited antithrombin and other anticoagulant-pathway defects are discussed in Chapter 4.

A hereditary predisposition may interact with acquired triggers.

Slide 11 · Acquired hypercoagulability

Cancer, pregnancy, oral contraceptive use, and obesity are relevant examples.

Recent surgery and tissue injury can alter the coagulation balance.

Cardiac failure contributes through impaired venous return and reduced reserve.

Slide 12 · Malignancy-associated thrombosis

Disseminated cancer is strongly associated with venous thromboembolic disease.

Tumor-associated inflammation and procoagulant products contribute to thrombosis.

An unprovoked pulmonary embolus may occur in patients with an underlying malignancy.

Slide 13 · Pregnancy and the postpartum period

Hormonal changes and increased coagulation potential increase thrombosis risk.

Reduced return from lower-limb veins contributes to venous stasis.

Early mobilization after delivery is one component of preventive care.

Slide 14 · Risk factors often cluster

Abnormal flow / stasis

Endothelial injury

Hypercoagulability

Convergent mechanisms promoting venous thrombus formation

A hospitalized patient may have immobility, heart failure, recent surgery, and cancer.

Each risk factor may affect stasis, vascular injury, or coagulation.

Thromboembolic risk should be viewed as cumulative rather than single-cause.

Slide 15 · Deep venous thrombosis may be silent

Local collateral venous channels can prevent marked symptoms despite DVT.

Chapter 4 reports that many deep venous thrombi are clinically unrecognized.

Pulmonary embolism can therefore be the first manifestation of venous thrombosis.

Slide 16 · Thromboembolism is the dominant subtype

Thromboembolus

Detached venous clot; Common

Nonthrombotic embolus

Fat, air, tumor or marrow; Uncommon

Primary pulmonary thrombus

Forms in situ; Uncommon in major vessels

Blood-clot emboli account for the overwhelming majority of large pulmonary artery occlusions.

Nonthrombotic emboli can comprise fat, air, bone marrow, or tumor material.

Different embolus composition should not be confused with a routine venous thrombus.

Slide 17 · Primary pulmonary arterial thrombosis

Large-vessel pulmonary thrombosis formed in situ is unusual.

The source associates it particularly with pulmonary hypertension and heart failure.

An arterial filling defect should not automatically be labeled an in-situ clot.

Slide 18 · Anatomy determines embolus lodging

Main pulmonary artery

Left branch

Right branch

Peripheral embolus

Schematic—not gross anatomy

A larger embolus can remain in a main pulmonary artery or lobar branch.

A smaller embolus may pass distally into segmental and peripheral branches.

The distal territory determines regional ischemic and hemorrhagic injury.

Slide 19 · Saddle pulmonary embolus

Main pulmonary artery

Left branch

Right branch

Embolus at bifurcation

Schematic—not gross anatomy

A saddle embolus lies across the bifurcation of the main pulmonary artery.

A large obstructive clot may severely compromise pulmonary blood flow.

Anatomic location alone does not measure physiologic severity.

Slide 20 · Peripheral arterial embolization

Main pulmonary artery

Left branch

Right branch

Peripheral embolus

Schematic—not gross anatomy

Distal emboli obstruct smaller vessels supplying limited pulmonary territories.

Peripheral embolization may produce focal hemorrhage or infarction.

The accompanying pleural response helps explain pleuritic symptoms.

Slide 21 · Emboli may be multiple

Large venous thrombus

Fragmentation

Several arterial occlusions

Cumulative vascular loss

A thrombus may fragment into several emboli.

Emboli can arrive together or occur as repeated episodes.

The aggregate obstruction can be more important than any single fragment.

Slide 22 · Four determinants of physiologic severity

Extent of pulmonary arterial blood-flow obstruction.

Size and location of affected vessels.

Number and timing of emboli.

Pre-existing cardiopulmonary functional reserve.

Slide 23 · Ventilation–perfusion mismatch

Ventilated alveolus

Occluded pulmonary artery

Gas present in alveolar space

No perfusion

Ventilation–perfusion mismatch (high local V/Q)

Air may reach alveoli despite interruption of pulmonary blood flow.

This generates ventilated but inadequately perfused lung units.

The resulting respiratory impairment contributes to dyspnea.

Slide 24 · The nonperfused alveolus

Ventilated alveolus

Occluded pulmonary artery

Gas present in alveolar space

No perfusion

Ventilation–perfusion mismatch (high local V/Q)

Pulmonary arterial obstruction interrupts local capillary inflow.

Alveolar ventilation alone cannot achieve normal oxygen transfer without perfusion.

This explains a major respiratory consequence of pulmonary embolism.

Slide 25 · Hemodynamic effect: Increased resistance

Large pulmonary embolus

Pulmonary vascular resistance ↑

Acute right ventricular load ↑

Reduced forward flow / impaired LV filling

Potential endpoint: Obstructive shock or acute cor pulmonale

Embolic obstruction reduces the cross-sectional area available for pulmonary blood flow.

Pulmonary vascular resistance increases.

The right ventricle must eject against an acutely greater load.

Slide 26 · Acute right ventricular failure

Large pulmonary embolus

Pulmonary vascular resistance ↑

Acute right ventricular load ↑

Reduced forward flow / impaired LV filling

Potential endpoint: Obstructive shock or acute cor pulmonale

A large obstruction can overwhelm right ventricular reserve.

Acute cor pulmonale denotes acute right-heart dysfunction due to pulmonary disease or vascular load.

Decreased cardiac output may culminate in obstructive shock.

Slide 27 · Mechanism of sudden collapse

Major obstruction

Low pulmonary flow

Poor LV filling

Pulseless collapse

Rapid hemodynamic failure may precede any pulmonary infarction

Extensive pulmonary arterial blockage may abruptly curtail forward blood flow.

A perfusing pulse can disappear even while organized electrical cardiac activity persists.

The source describes this clinical scenario as electromechanical dissociation.

Slide 28 · Cardiopulmonary reserve modifies injury

A similar embolic burden may be tolerated differently across patients.

Cardiac or pulmonary disease can magnify hemodynamic compromise.

Reduced systemic perfusion also favors parenchymal infarction.

Slide 29 · Why the lung resists infarction

Pulmonary artery

(low-pressure supply)

Bronchial artery

(systemic collateral supply)

Lung parenchyma

Failure of one arterial inflow does not always produce tissue death

Pulmonary parenchyma receives both pulmonary arterial and bronchial arterial inflow.

The bronchial circulation can sustain tissue when a pulmonary arterial branch is blocked.

Therefore pulmonary embolism can produce hemorrhage without necrosis.

Slide 30 · Pulmonary hemorrhage ≠ pulmonary infarction

Pulmonary embolus

Arterial occlusion

Hemorrhage

Blood extravasation; Tissue may survive

Infarction

Ischemic necrosis with hemorrhage

Hemorrhage indicates escape of blood into pulmonary tissue or airspaces.

An infarct requires ischemic necrosis of supporting structures.

Collateral perfusion helps explain why these may occur separately.

Slide 31 · When does infarction become likely?

Pulmonary artery

(low-pressure supply)

Bronchial artery

(systemic collateral supply)

Lung parenchyma

Failure of one arterial inflow does not always produce tissue death

Pre-existing cardiovascular compromise reduces the compensatory supply.

Heart and lung disease lower the ability to sustain the affected region.

Smaller peripheral occlusions can produce localized infarction.

Slide 32 · Gross pattern: Pleura-based wedge

Pleural base

Hilar apex →

Peripheral, pleura-based wedge (schematic)

The infarct classically extends to the pleura as a wedge.

The apex points toward the pulmonary hilum and may contain an occluded vessel.

The pleural surface may develop a fibrinous exudate.

Slide 33 · Distribution and multiplicity

The source describes a predilection for lower lobes.

Multiple infarcts may be present in a single patient.

Infarct size ranges from minute lesions to extensive lobar involvement.

Slide 34 · Early gross appearance

Pleural base

Hilar apex →

Peripheral, pleura-based wedge (schematic)

An acute pulmonary infarct is typically hemorrhagic.

It initially appears as a raised red-blue area.

The gross appearance reflects ischemic tissue damage accompanied by hemorrhage.

Slide 35 · Evolution from hemorrhage to scar

Raised red-blue

Red-cell breakdown

Red-brown pigment

Gray-white scar

The gross appearance evolves with clearance of erythrocytes and repair

Erythrocytes begin to lyse and color becomes paler.

Hemosiderin accumulation can produce a red-brown appearance.

Peripheral fibrosis progresses toward a contracted scar.

Slide 36 · Fibrinous pleuritis

Peripheral infarct

Pleural irritation

Fibrinous exudate

Pleuritic symptoms

Pleura overlying an infarct can be coated by fibrinous inflammatory exudate.

This accounts for pleuritic pain and sometimes a friction rub.

Pleural inflammation is not an obligatory feature of every embolus.

Slide 37 · Microscopy: Ischemic necrosis

Ischemic alveolar-wall necrosis

Associated vascular and bronchiolar injury

Conceptual tissue-architecture schematic; Not a histologic section

Infarcted pulmonary tissue shows necrosis of alveolar walls.

Bronchioles and small vessels within the region also undergo ischemic necrosis.

Hemorrhage is a characteristic accompaniment of pulmonary infarction.

Slide 38 · What distinguishes necrosis from hemorrhage?

Hemorrhage

Extravasated erythrocytes

True infarct

Necrotic alveolar walls and vessels

Interpret together

Vascular blockage + tissue response

Blood in airspaces alone does not establish infarction.

Loss of viable alveolar-wall architecture indicates ischemic tissue death.

Assess vessel occlusion and the geographic relationship of tissue injury.

Slide 39 · Infected emboli and septic infarcts

Infected embolus

Occluded artery

Intense inflammation

Potential abscess

The presence of infection modifies the tissue response

An infected embolus can cause ischemic injury with marked neutrophilic inflammation.

Such a lesion is described as a septic infarct.

Some septic infarcts develop into pulmonary abscesses.

Slide 40 · Antemortem embolus versus postmortem clot

Antemortem thrombus

Postmortem clot

Lines of Zahn: Laminated layers

Gelatinous; “chicken-fat” / red layering

An antemortem thrombus can contain laminations known as lines of Zahn.

Postmortem clots are typically gelatinous and exhibit dependent red-cell settling.

Morphology helps distinguish a vital thrombotic event from a postmortem artifact.

Slide 41 · Clinical manifestations follow clot burden

Uncomplicated / small embolus

Often silent or transient symptoms

Infarction

Pleuritic pain, hemoptysis, focal necrosis

Large obstruction

Shock, acute RV failure, sudden death

Most small emboli are clinically silent or produce transient symptoms.

Intermediate embolic events may cause dyspnea, cough, or pleuritic pain.

Massive obstruction can produce shock, acute cor pulmonale, or sudden death.

Slide 42 · Small emboli: Clinically quiet events

Small emboli may produce no recognizable clinical syndrome.

Some cause transient chest pain or cough.

Even a minor embolus may herald a later, more serious episode.

Slide 43 · Symptomatic pulmonary embolism

Dyspnea is a leading presenting symptom.

Pleuritic chest pain and cough are frequent associated complaints.

Severity of symptoms does not by itself identify the anatomic size of the thrombus.

Slide 44 · Pleuritic pain: Mechanism

Distal vascular occlusion

Peripheral infarction

Pleuritis

Pain / friction rub

A peripheral infarct can inflame the adjacent pleura.

Pleuritic pain is typically accentuated by respiration.

A pleural friction rub may be audible when fibrinous pleuritis is present.

Slide 45 · Why hemoptysis may occur

Pleural base

Hilar apex →

Peripheral, pleura-based wedge (schematic)

Peripheral embolic injury often produces hemorrhage.

Hemorrhagic infarction may release blood into the airways.

Fever and hemoptysis support tissue injury but are not specific diagnostic tests.

Slide 46 · Leg symptoms and source identification

Calf or thigh swelling and pain can accompany pulmonary embolism.

Absence of these symptoms does not exclude a deep venous source.

Ultrasound can identify DVT when clinically indicated.

Slide 47 · Diagnostic logic: Suspicion to confirmation

Recognition

Estimation of probability

Appropriate testing

Action / prevention

Clinical and morphologic information answer different questions

Clinical risk and hemodynamic stability shape the testing pathway.

D-dimer may help exclude disease in selected stable, lower-risk patients.

CT pulmonary angiography usually demonstrates intraluminal arterial obstruction.

Slide 48 · D-dimer: A contextual rule-out test

Hemodynamically stable

Low–moderate clinical probability

D-dimer used to exclude PE

Normal appropriately sensitive D-dimer

Positive test / unresolved suspicion

Use imaging / further assessment when not safely excluded

The source emphasizes its use in hemodynamically stable, low-to-moderate-risk patients.

A suitably normal result can make pulmonary embolism unlikely in that setting.

An elevated D-dimer is not specific proof of pulmonary embolism.

Slide 49 · CT pulmonary angiography

Main pulmonary artery

Left branch

Right branch

Embolus at bifurcation

Schematic—not gross anatomy

The source describes CT pulmonary angiography as the usual definitive test.

Imaging demonstrates filling defects or obstruction within pulmonary arteries.

Assessing location and extent complements the clinical hemodynamic assessment.

Slide 50 · Ventilation–perfusion imaging

Ventilated alveolus

Occluded pulmonary artery

Gas present in alveolar space

No perfusion

Ventilation–perfusion mismatch (high local V/Q)

Ventilation–perfusion scanning is an alternative diagnostic approach.

Its central logic compares ventilation and regional pulmonary perfusion.

The source notes that this is required only in a minority of diagnostic pathways.

Slide 51 · Duplex ultrasonography

Venous duplex ultrasound can identify a deep venous thrombus.

It investigates a potential source of thromboembolism.

A negative leg study alone should not be treated as proof that PE is absent.

Slide 52 · Chest radiography and pulmonary infarction

Pleural base

Hilar apex →

Peripheral, pleura-based wedge (schematic)

Plain chest radiography can be normal in pulmonary embolism.

An infarct may later appear as a peripheral, wedge-shaped infiltrate.

This radiographic finding is less direct than imaging the obstructed artery.

Slide 53 · Evolution of an embolus

Acute embolus

Contraction + fibrinolysis

Resolution

Persistent / recurrent obstruction

Pulmonary hypertension / cor pulmonale

After the acute event, emboli may contract and undergo fibrinolysis.

Complete resolution is possible, particularly in younger patients.

Persistent or repeated obstruction creates a different chronic vascular burden.

Slide 54 · Recurrent embolization

Predisposition persists

Recurrent DVT

Repeated PE

Cumulative obstruction

A previous embolus indicates increased vulnerability when a provoking condition persists.

Several small events can cumulatively reduce the pulmonary vascular bed.

Recurrence prevention is important even after a relatively mild episode.

Slide 55 · Chronic vascular sequelae

Acute embolus

Contraction + fibrinolysis

Resolution

Persistent / recurrent obstruction

Pulmonary hypertension / cor pulmonale

Persistent and recurrent emboli may increase pulmonary vascular resistance.

Chronic pulmonary hypertension can result.

Advanced disease may cause chronic right-sided heart failure (cor pulmonale).

Slide 56 · Primary prevention targets thrombosis

Abnormal flow / stasis

Endothelial injury

Hypercoagulability

Convergent mechanisms promoting venous thrombus formation

Early ambulation reduces venous stasis in relevant postoperative and postpartum settings.

Mechanical compression is an option in selected immobilized patients.

Anticoagulant prophylaxis can be used for individuals at increased thrombotic risk.

Slide 57 · Anticoagulation and supportive care

Anticoagulation is a central treatment component in the source.

Supportive measures address respiratory and hemodynamic compromise.

Anticoagulation primarily limits new clot propagation rather than immediately dissolving the embolus.

Slide 58 · Thrombolysis: Benefit and harm

Clinical problem

Severe obstructive physiology

Potential benefit

Rapid reduction of thrombus burden

Major hazard

Serious hemorrhagic complications

Thrombolytic treatment may be considered in severe complications, such as shock.

The intended effect is accelerated dissolution of obstructing thrombus.

Major bleeding is a potentially serious adverse consequence.

Slide 59 · Inferior vena cava filter: Restricted role

Leg / pelvic venous thrombus

Inferior vena cava

Right heart → lung

Filter intercepts embolizing thrombi; Does not treat the DVT itself

A filter may intercept embolizing thrombi before they reach the pulmonary arteries.

The text discusses its use when recurrent PE risk persists but anticoagulation is contraindicated.

The device does not correct the underlying hypercoagulability or clear established emboli.

Slide 60 · Three pathophysiologic patterns

Uncomplicated / small embolus

Often silent or transient symptoms

Infarction

Pleuritic pain, hemoptysis, focal necrosis

Large obstruction

Shock, acute RV failure, sudden death

Silent PE: Small embolic obstruction without major symptoms.

Hemorrhagic infarction: Distal embolus plus insufficient collateral perfusion.

Circulatory collapse: Extensive obstruction with acute RV failure or low pulmonary flow.

Slide 61 · Clinicopathologic case: Sudden collapse

Large pulmonary embolus

Pulmonary vascular resistance ↑

Acute right ventricular load ↑

Reduced forward flow / impaired LV filling

Potential endpoint: Obstructive shock or acute cor pulmonale

A postoperative immobilized patient suddenly develops severe dyspnea and shock.

Examination reveals profound circulatory failure without a preceding focal lung syndrome.

Question: Which pathophysiologic consequence is most likely dominant?

Slide 62 · Case resolution: Massive vascular obstruction

Obstructive embolus

RV load ↑

Forward flow ↓

Shock

Acute obstruction sharply increases pulmonary vascular resistance.

Right-heart output and systemic circulation may fail within minutes.

The fatal process may occur without time for morphologically evident infarction.

Slide 63 · Clinicopathologic case: Pleuritic pain

Pleural base

Hilar apex →

Peripheral, pleura-based wedge (schematic)

A patient with cardiac dysfunction develops pleuritic chest pain and hemoptysis.

A peripheral pleura-based wedge-shaped pulmonary lesion is identified.

Question: Why is tissue necrosis more likely in this patient?

Slide 64 · Case resolution: Failed collateral protection

Pulmonary artery

(low-pressure supply)

Bronchial artery

(systemic collateral supply)

Lung parenchyma

Failure of one arterial inflow does not always produce tissue death

The pulmonary arterial branch is blocked by an embolus.

Compromised cardiovascular function limits compensatory bronchial perfusion.

Ischemic necrosis with hemorrhage explains the pleura-based wedge lesion.

Slide 65 · Morphology checklist for an infarct

Identify a peripheral hemorrhagic wedge with its apex toward the hilum.

Assess a vessel near the apex for occluding thromboembolic material.

Confirm ischemic necrosis of alveolar walls, bronchioles, or small vessels.

Note overlying fibrinous pleuritis and evolution toward fibrosis when present.

Slide 66 · High-yield clinicopathologic synthesis

Uncomplicated / small embolus

Often silent or transient symptoms

Infarction

Pleuritic pain, hemoptysis, focal necrosis

Large obstruction

Shock, acute RV failure, sudden death

The primary source of thromboemboli is venous thrombosis.

Obstruction produces both ventilation–perfusion mismatch and increased vascular resistance.

Dual pulmonary/bronchial supply explains why infarction is not inevitable.

Bleeding, necrosis, acute right-heart failure, and chronic pulmonary hypertension reflect distinct outcomes.

Slide 67 · References and image provenance

Robbins, Cotran & Kumar. Pathologic Basis of Disease. 11th edition (2026). Chapter 15: The Lung, pp. 639–640.

Background: Chapter 4, Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 112–115.

All displayed vascular and tissue diagrams are original, editable PowerPoint schematics; no clinical images are presented as specimens.