PCM1 · FTCM · Lecture 33 · Hemodynamic Disorders 4
Thrombus, Embolism & Infarction
This is a revision reference. It covers the material from the pre‑reading and the class, and works through all ten clinical cases with their answers.
The opening case
The three questions from the pre-reading, with the reasoning from class.
Maria Santos, 52
On the third day after a right total hip replacement, she becomes acutely short of breath with sharp right-sided pleuritic chest pain during her first physiotherapy session. Pain from the surgery had kept her in bed for the previous two days, and her right calf has been swollen and painful since the previous evening. She has chronic heart failure. Her temperature is 99.3°F, pulse 118/min, respiratory rate 24/min, blood pressure 118/74 mmHg, and SpO₂ is 88% on room air. On examination, the jugular venous pressure is elevated and the chest is clear. Her right calf is swollen, warm, and tender.
1. What connects her surgery to this collapse?
Surgery and days of immobility tipped Virchow's triad toward clotting, mainly through venous stasis, and a deep vein thrombosis formed in her calf. A fragment detached, traveled through the IVC to the right heart, and lodged in a pulmonary artery branch: a pulmonary embolism.
2. Why did she infarct when most medium PEs do not?
The lung has a dual blood supply (pulmonary and bronchial arteries), so a medium embolus usually does not cause infarction. Her background heart failure raised pulmonary venous pressure and compromised the bronchial collateral supply, removing that protection, so the territory infarcted.
3. What does the infarct look like, and why?
A red (hemorrhagic), wedge-shaped infarct with its base at the pleural surface. The lung's loose tissue and residual bronchial supply let blood seep into the necrotic zone, so the infarct fills with blood rather than staying pale.
Thrombus
Definition. A thrombus is a solid mass of blood components (platelets, fibrin, and trapped red cells) formed within the living circulation. It differs from a postmortem clot in that it is adherent to the vessel wall and shows Lines of Zahn: alternating pale (platelet and fibrin) and dark (red cell) laminae deposited as blood flows over the growing mass.
Virchow's triad
Three factors promote thrombosis, and usually one dominates in a given patient.
| Component | Mechanism | Clinical example |
|---|---|---|
| Endothelial injury | Damage to the vessel lining exposes subendothelial collagen and tissue factor, activating platelets and the coagulation cascade at the site. | Surgical incision; atherosclerotic plaque; vasculitis |
| Stasis | When normal smooth flow is lost, platelets reach the wall, clotting factors are not washed away, and the body's natural inhibitors arrive more slowly. | Immobility after surgery; atrial fibrillation; aneurysm |
| Hypercoagulability | An altered balance of clotting factors makes the blood more likely to clot on its own. | Post-operative state; malignancy; inherited thrombophilia |
MariaAt 48 hours of bed rest after hip surgery, stasis is the principal driver: immobility removes the calf-muscle pump, slows venous return, and lets blood pool in the deep leg veins. Endothelial injury and a post-operative hypercoagulable state contribute, but stasis dominates.
Thrombus versus postmortem clot
| Feature | Postmortem clot | Thrombus (antemortem) |
|---|---|---|
| Platelets | Not involved | Central; initiate thrombus formation |
| Location | Inside postmortem vessels, or outside the body (hematoma, test tube) | Only inside a living vessel |
| Color | Red | Venous: red. Arterial: pale (platelet-rich) |
| Consistency | Gelatinous; slides freely | Firm and friable; adherent |
| Attachment | Not attached to the vessel wall | Firmly adherent at the point of formation |
| Microscopy | No Lines of Zahn; uniform fibrin mesh | Lines of Zahn: alternating pale (platelet + fibrin) and dark (RBC) laminae |
Fate of a thrombus
Once formed, a thrombus can follow one of four paths.
- Resolution. Plasmin dissolves the thrombus (fibrinolysis) and flow is fully restored. Most likely with small, recent thrombi, leaving no residual damage.
- Organization and recanalization. Fibroblasts and endothelial cells invade the thrombus, replacing it with connective tissue. New channels form through it (recanalization), partially restoring flow, and the thrombus is incorporated into the vessel wall.
- Propagation. Further platelet aggregation and fibrin deposition extend the thrombus along the direction of flow. This increases occlusion and, because a larger thrombus means a larger potential embolus, raises embolic risk.
- Embolization. A fragment breaks off and travels until it lodges where the vessel narrows, causing ischemia or infarction at a distant site. The most dangerous fate. A venous thrombus embolizes to the pulmonary circulation; a left-heart thrombus to any end artery.
MariaHer thrombus embolized. A fragment detached from the proximal leg DVT, traveled via the IVC to the right heart, and lodged in a pulmonary artery branch.
Arterial versus venous thrombosis
| Feature | Arterial thrombus | Venous thrombus |
|---|---|---|
| Dominant force | Endothelial injury (e.g. atherosclerosis) | Stasis |
| Color | Pale (platelet-rich) | Red (RBC-rich) |
| Shape | Eccentric; does not fill the lumen | Cylindrical cast of the vessel |
| Limb appearance | Pale and cold (ischemia) | Warm and red (congestion) |
| Limb signs | Pulseless, painful, cold | Swelling, pitting edema, tenderness, warmth |
| Embolizes to | End arteries: brain, bowel, lower limbs | Pulmonary circulation |
Clinical note · Trousseau's syndromeRecurrent, unexplained, migratory thrombophlebitis with no obvious precipitant should prompt screening for occult malignancy, particularly pancreatic adenocarcinoma, which releases procoagulant substances and produces a chronic hypercoagulable state.
Embolism
Definition. An embolus is a detached intravascular solid, liquid, or gaseous mass carried by the blood to a distant site, where it causes tissue dysfunction or infarction. About 99% are dislodged thrombus fragments (thromboembolism); the rest are fat, air, nitrogen, bone marrow, tumor cells, amniotic fluid, atherosclerotic debris, or foreign body.
Classification of emboli
| Type | Key context / trigger |
|---|---|
| Thromboembolism | 99% of all emboli; a dislodged thrombus, usually from a DVT or a cardiac mural thrombus |
| Fat | Trauma to bone, subcutaneous tissue, or burns; marrow sinusoids rupture and release fat globules |
| Air / gas | Neck wounds, central-line placement; >150 mL can be fatal via right ventricular outflow obstruction |
| Nitrogen (caisson disease) | Rapid decompression in divers; N₂ bubbles out of solution, causing the bends, the chokes, and bone necrosis |
| Amniotic fluid | Labor and delivery; fetal squames and hair enter maternal pulmonary vessels; frequently fatal from DIC |
| Tumor cells | Hematogenous spread; the mechanism of distant metastasis |
| Atherosclerotic debris | Ulcerated plaque ruptures; cholesterol crystals and debris embolize distally |
| Bone marrow | Severe trauma or CPR; hematopoietic cells and fat enter the pulmonary vasculature |
| Infective | Septic emboli from infective endocarditis or other infected thrombi |
| Foreign body | Iatrogenic (catheter fragments, pacemaker leads) or injected material |
Pulmonary thromboembolism
Most pulmonary emboli arise from the deep leg veins and are clinically silent. PE is a major contributor to in-hospital death, often striking on a patient's first mobilization. The consequence depends on how much of the pulmonary vasculature is obstructed.
| Massive | Major | Minor | |
|---|---|---|---|
| Vessels occluded | ≥60% of the pulmonary vasculature; saddle embolus at the main bifurcation | Multiple medium-sized branches | Small peripheral branches |
| Consequence | Sudden death from obstructive shock; no time for an infarct to develop | Dyspnea and pleuritic pain; infarction in about 10%, where bronchial collateral supply is compromised (e.g. heart failure) | Usually asymptomatic; the clot is lysed |
Recurrent minor emboli are the exception to the benign picture: organized thrombi become incorporated into the vessel walls over time and produce pulmonary hypertension.
Systemic thromboembolism
Arterial emboli travel the systemic circulation and block end arteries, infarcting the tissue downstream. Most originate in the heart.
| Pulmonary | Systemic (arterial) | |
|---|---|---|
| Origin | Deep leg veins (95%) | Heart: mural thrombus (80%); aortic atherosclerotic plaque |
| Destination | Pulmonary arteries | Lower extremities (75%), brain (10%), bowel, kidney |
| Consequence | Hypoxia, hypotension, right-heart strain; infarction only if collateral supply fails | End-artery occlusion → infarction of the supplied tissue |
Paradoxical embolismA venous embolus normally cannot reach the arterial side. With a septal defect (ASD, VSD, or patent foramen ovale), a right-to-left shunt lets it cross into the systemic circulation, bypassing the lungs, so a clot that began on the venous side can produce an arterial infarct.
Non-thrombotic emboli
Three non-thrombotic emboli come up repeatedly: fat, air, and amniotic fluid.
Fat embolism
Trigger: long-bone fracture, soft-tissue trauma, or burns. Mechanism: two injuries act together. Mechanically, fat globules from ruptured marrow sinusoids enlarge in the circulation and platelets adhere to them, obstructing pulmonary and systemic capillaries. Biochemically, free fatty acids released from the circulating lipid are directly toxic to endothelium, triggering DIC and diffuse capillary damage. Clinical: the triad of pulmonary insufficiency, neurological symptoms, and a petechial rash, with anemia and thrombocytopenia, appearing 1 to 3 days after the injury. Signature: fat globules in sputum or urine.
Air embolism
Trigger: neck wounds or central-line placement, where venous pressure is below atmospheric. Mechanism: air drawn into a vein collects as a frothy lock in the right ventricle and obstructs its outflow. About 150 mL can be fatal. Clinical: sudden obstructive shock. Management: place the patient in the left lateral decubitus position, so the air rises to the right-ventricular apex and clears the outflow tract.
Amniotic fluid embolism
Trigger: sudden collapse during or just after labor. Mechanism: fetal squames, hair, and debris enter the maternal pulmonary vessels. Clinical: dyspnea, then DIC and diffuse alveolar damage. Epidemiology: about 1 in 50,000 deliveries; usually fatal.
Infarction
Definition. An infarct is an area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage of a tissue. Most infarcts heal by organization to a fibrous scar; the exception is the brain, where liquefactive necrosis leaves a cystic cavity instead.
Red and white infarcts
Whether an infarct is red or white depends on whether blood can re-enter the dead tissue.
- Red (hemorrhagic). Blood re-enters the dead zone. This happens in soft organs with loose tissue spaces (lung), in tissues with a dual blood supply where anastomosing vessels bleed in (lung, small intestine), in venous infarcts where congestion precedes infarction, and after reperfusion of an arterial occlusion.
- White (anemic). Little blood enters. Solid organs with dense parenchyma (kidney, spleen, heart) prevent blood seeping back, and arterial occlusion is the usual mechanism. The territory becomes pale, firm, and dry.
Morphology
Most infarcts are wedge-shaped, with the occluded vessel at the apex and the organ surface at the base, because an end artery supplies a roughly triangular territory. The appearance evolves after the infarct forms.
| Stage | Gross appearance |
|---|---|
| Early | Congested, with ill-defined margins. Wedge-shaped: occluded vessel at the apex, organ periphery at the base. |
| Intermediate | Margins sharpen; a well-defined rim of hyperemia forms at the border with viable tissue. |
| Late | Brown discoloration from hemosiderin as red cells are cleared, then a contracting fibrous scar. |
Microscopy: ischemic coagulative necrosis throughout the wedge. Cell outlines are preserved as ghosts but nuclei are lost. This pattern is common to most infarcts regardless of organ.
Septic infarctWhen the occluding embolus is infected (e.g. from infective endocarditis), the infarct undergoes abscess formation rather than simple coagulative necrosis.
Factors that determine whether infarction occurs
Whether an occlusion causes an infarct depends on four factors.
- Nature of the blood supply. A dual supply protects: lung (pulmonary + bronchial), liver (portal + hepatic artery), brain (circle of Willis), hand (ulnar + radial). Collateral circulation does the same; coronary anastomoses can enlarge and protect against gradual narrowing.
- Rate of occlusion. Sudden occlusion infarcts. Slow occlusion gives time for collateral vessels to open and may prevent it.
- Tissue vulnerability to hypoxia. Neurons are the most vulnerable (irreversible injury within minutes); skeletal muscle and bone tolerate ischemia far longer.
- Oxygen-carrying capacity of the blood. With less oxygen in the blood (anemia or hypoxemia), even a partial blockage can cause an infarct.
Healing and evolution
| Stage | Cellular events |
|---|---|
| Acute | Cell death. Polymorphs, then macrophages, are recruited to clear the necrotic debris. |
| Subacute | Granulation tissue grows in from the viable margin, with lymphocytes and plasma cells. |
| Repair | A fibrous scar replaces the granulation tissue and contracts over time. In the brain, microglia clear the liquefied tissue, leaving a glial scar and a cystic space rather than fibrous tissue. |
Other clinical examples
Covered further in NCRS, and included here as examples of the principles above.
Cerebral infarction
Embolism is a leading cause, mostly from cardiac mural thrombi (after myocardial infarction or in atrial fibrillation), though emboli can also arise from carotid atherosclerotic plaques. Thrombotic occlusions occur on plaques at the carotid, the origin of the middle cerebral artery, and either end of the basilar artery. The tissue undergoes liquefactive necrosis, evolving from the red neuron (shrunken, eosinophilic, pyknotic; the earliest sign of irreversible injury) through neutrophil then macrophage infiltration to a glial scar around a cystic cavity.
Myocardial infarction
The heart is supplied by end arteries with no effective collateral, so a coronary occlusion produces a white (anemic) infarct with coagulative necrosis. Cause: coronary atherosclerosis with superimposed thrombosis. Site: the left anterior descending is the most common vessel. Clinical: severe chest pain with elevated serum cardiac enzymes.
The ten clinical vignettes
The ten cases from the session, with every option explained.
Case 1 · Thrombus versus postmortem clot
A 32-year-old man comes to the physician because of a 3-day history of persistent pain over his right lower leg. He was involved in a motor vehicle accident 2 weeks ago and sustained a fracture of his right femur. Physical examination shows a swollen, tender right lower leg. Doppler ultrasound shows a thrombus in the popliteal vein. Which feature is most likely associated with this thrombus?
AIncorrect
Platelets not involved. Platelets are central to an antemortem thrombus and initiate its formation. A clot with no platelet involvement is a postmortem clot.
BIncorrect
No lines of Zahn. A true thrombus shows lines of Zahn (alternating platelet-fibrin and red-cell laminae). Their absence describes a postmortem clot.
CCorrect
Attached to vessel wall. An antemortem thrombus is firmly adherent to the vessel wall at its point of formation, so it does not slide free when the vessel is opened.
DIncorrect
Gelatinous consistency. Gelatinous, free-sliding material is a postmortem clot. A thrombus is firm and friable.
EIncorrect
Can occur outside the vessel. A thrombus forms only inside a living vessel. Material that can form outside a vessel (test tube, hematoma) is a clot.
Case 2 · Pulmonary embolism: origin
A 60-year-old man has just got off a direct flight from New York to Tokyo. He develops sudden chest pain and shortness of breath, collapses after a few steps, and dies. He has no history of ischemic heart disease. Autopsy shows a thrombus in the left branch of the pulmonary artery. Which is most likely associated with this condition?
AIncorrect
Uniformly pale thrombus. A pale, platelet-rich thrombus is arterial. A pulmonary embolus comes from the venous side and is red.
BIncorrect
Ruptured atherosclerotic plaque. Plaque rupture drives arterial events such as myocardial infarction or stroke, not a venous embolus lodging in the pulmonary artery.
CCorrect
Left lower extremity venous thrombus. Pulmonary emboli almost always arise from the deep veins of the lower limb. Long-haul immobility (stasis) is the precipitant here.
DIncorrect
Thrombus from the carotid artery. A carotid thrombus embolizes forward into the brain through the systemic arterial circulation, not into the pulmonary artery.
EIncorrect
Left ventricular mural thrombus. A left ventricular thrombus embolizes into the systemic arteries. To reach the pulmonary artery, an embolus must originate on the venous or right-heart side.
Case 3 · Massive embolus: lung morphology
The same traveller. Autopsy now shows a large thrombus occluding the bifurcation of the pulmonary trunk. Which additional morphological feature in the lung is most likely present?
AIncorrect
Red infarct. A red infarct takes time to develop. A massive saddle embolus kills by obstructive shock before any infarct can form.
BIncorrect
White infarct. The lung does not form white infarcts (it has a dual supply and loose tissue), and there is no time for an infarct of any kind.
CCorrect
Normal lung parenchyma. Instantaneous death from acute right-heart failure leaves no time for an infarct, so the parenchyma is morphologically normal.
DIncorrect
Liquefactive necrosis. Liquefactive necrosis is characteristic of the brain and abscesses, not a pulmonary infarct.
EIncorrect
Coagulative necrosis. Coagulative necrosis is the pattern of an established infarct, which has not had time to form.
Case 4 · Pulmonary infarction: pathogenesis
A 60-year-old man with a 1-year history of congestive heart failure develops pleuritic chest pain. EKG is normal and cardiac enzymes are not elevated. CT angiogram shows reduced flow in a branch of the pulmonary artery, consistent with pulmonary embolism causing pulmonary infarction. What is the most likely pathogenesis of the infarction?
AIncorrect
Total occlusion of the pulmonary artery. Total occlusion of the main pulmonary artery causes massive PE and sudden death, not a localized infarct; and occlusion alone usually does not infarct because of the dual supply.
BCorrect
Compromised bronchial artery blood flow. The bronchial (collateral) supply normally protects the lung. A medium PE infarcts only when that collateral flow is compromised, as in left heart failure.
CIncorrect
Recurrent minor pulmonary emboli. Recurrent minor emboli organize and cause pulmonary hypertension, not an acute infarct. This is a single embolus.
DIncorrect
Partial occlusion of the pulmonary artery. Partial occlusion is usually tolerated because of the dual supply. The deciding factor is loss of the bronchial collateral, not the degree of pulmonary-artery occlusion.
EIncorrect
Increased pulmonary arterial pressure. Elevated pulmonary pressure is a consequence of obstruction, not the mechanism of tissue death. The infarct follows failure of bronchial collateral perfusion.
Case 5 · Systemic embolism: heart to brain
A 65-year-old man with untreated hypercholesterolemia presents with an ST-elevation myocardial infarction. While in hospital he suddenly develops left-sided loss of motor function and is diagnosed with a stroke. What is the most likely etiopathogenesis of the neurological event?
ACorrect
Embolism of thrombus from the left ventricle. A transmural MI produces a left ventricular mural thrombus, the most common source of systemic arterial emboli. It travels the arterial tree to the brain, causing the stroke.
BIncorrect
Impaired pulmonary venous return. Impaired pulmonary venous return does not embolize to the brain and is not an embolic mechanism for stroke.
CIncorrect
Embolism of fat globules to the brain. Fat embolism follows long-bone trauma. There is no fracture in this patient.
DIncorrect
Embolism of a deep vein thrombus. A venous thrombus embolizes to the lungs, not the brain, unless a right-to-left shunt is present (paradoxical embolism), which is not described.
EIncorrect
Embolism of thrombus from the right ventricle. A right ventricular thrombus embolizes to the pulmonary circulation. The brain is supplied by systemic arteries fed from the left heart.
Case 6 · Fat embolism
A 65-year-old man sustains a comminuted fracture of the right femur and has a central line placed. Two days later he develops dyspnea, tachycardia, and diffuse skin petechiae. Laboratory studies show anemia and thrombocytopenia. He becomes irritable and restless, lapses into coma, and dies. What is the most likely cause?
ACorrect
Fat embolism. A long-bone fracture followed at 1 to 3 days by the triad of pulmonary insufficiency, neurological signs, and petechiae, with anemia and thrombocytopenia, is classic fat embolism syndrome.
BIncorrect
Air embolism. Air embolism causes immediate obstructive shock when air enters the circulation, not a delayed petechial rash with anemia and thrombocytopenia. The central line is a distractor.
CIncorrect
Atherosclerotic plaque embolism. Cholesterol emboli occur in elderly patients with severe atherosclerosis, often after a vascular procedure, and cause distal ischemia, not this post-fracture triad.
DIncorrect
Thromboembolism. A bland pulmonary thromboembolus causes dyspnea but not the combination of petechial rash, neurological decline, anemia, and thrombocytopenia.
EIncorrect
Septic embolism. Septic emboli arise from infective endocarditis and seed infection or abscesses. There is no source of infection here.
Case 7 · Air embolism: pathogenesis
A 30-year-old man sustains fractures of the right clavicle and ribs. CT shows a comminuted clavicular fracture with laceration of the right subclavian vein, and distended neck veins are noted. His collapse is attributed to a massive air embolism. What is the most likely pathogenesis?
ACorrect
Right ventricular outflow obstruction. Air drawn into the lacerated subclavian vein collects as a frothy lock in the right heart and obstructs right ventricular outflow. The distended neck veins reflect that outflow obstruction.
BIncorrect
Increased pulmonary venous hydrostatic pressure. That mechanism causes cardiogenic pulmonary edema from left-heart failure, not the obstructive picture of air embolism.
CIncorrect
Increased alveolar capillary permeability. Increased permeability describes ARDS and non-cardiogenic edema, a different mechanism.
DIncorrect
Decreased sympathetic outflow. Reduced sympathetic outflow produces neurogenic, vasodilatory shock, not the obstructive shock of an air lock.
EIncorrect
Dilation and vascular pooling of blood. Pooling is the mechanism of distributive shock. Here the problem is mechanical obstruction of RV outflow, which raises venous pressure, the opposite of pooling.
Case 8 · Amniotic fluid embolism
A 22-year-old woman at 38 weeks gestation, recovering from a tibial fracture, goes into labor and delivers. One hour later she develops dyspnea and chest pain, bleeds from her intravenous sites, and shows prolonged bleeding time, PT, and PTT. She decompensates and dies. Autopsy of the pulmonary vessels is most likely to show which of the following?
AIncorrect
Thromboembolus. A thromboembolus would not explain the DIC (bleeding from line sites, prolonged BT, PT, and PTT) that dominates this peripartum collapse.
BCorrect
Fetal squames. Peripartum collapse with DIC is amniotic fluid embolism. The maternal pulmonary vessels contain fetal squames, hair, and meconium.
CIncorrect
Fat globules. Fat embolism follows a fracture and presents 1 to 3 days later with petechiae. The tibial fracture is a distractor; the timing and DIC point to amniotic fluid. Fat also dissolves in routine processing and needs frozen section.
DIncorrect
Gas bubbles. Air embolism follows air entry through a vascular injury and causes immediate obstructive shock, not peripartum DIC.
EIncorrect
Bone marrow cells. Bone-marrow emboli follow severe trauma or CPR and show hematopoietic cells with marrow fat; they do not explain the obstetric DIC picture.
Case 9 · White infarct: myocardium
A 65-year-old man dies of an acute myocardial infarction. Autopsy shows a pale area of myocardial tissue overlying the territory of the left anterior descending artery. What is the most likely cause of this morphological change?
AIncorrect
Collateral blood supply. Collateral supply protects against infarction and would limit a pale infarct rather than cause it. The heart's lack of effective collateral is precisely why it infarcts.
BCorrect
Arterial occlusion. A pale (white, anemic) infarct in a solid, end-arterial organ such as the myocardium results from arterial occlusion, here of the LAD.
CIncorrect
Reperfusion. Reperfusion lets blood back into the dead zone and makes the infarct red, not pale.
DIncorrect
Venous congestion. Venous congestion produces red, hemorrhagic infarcts, not a pale myocardial infarct.
EIncorrect
Increased vessel permeability. Increased permeability causes edema, not the coagulative necrosis of a pale infarct.
Case 10 · Red infarct: lung
A 60-year-old man with congestive heart failure has a pulmonary embolism. Which morphological change in the lung is most likely associated with his condition?
AIncorrect
Pale area of coagulative necrosis. A pale, coagulative (white) infarct is the pattern of solid end-arterial organs such as the heart or kidney, not the loose, dual-supplied lung.
BCorrect
Hemorrhage into infarcted lung parenchyma. With the bronchial collateral compromised by heart failure, the medium PE infarcts, and blood from anastomosing bronchial vessels seeps into the necrotic wedge: a red (hemorrhagic) infarct.
CIncorrect
No morphological change. That applies to a massive embolus causing death before an infarct forms. Here the patient survives long enough to infarct.
DIncorrect
Liquefactive necrosis. Liquefactive necrosis is characteristic of the brain, not a pulmonary infarct.
EIncorrect
Hemorrhage without infarction. There is true tissue death here, not merely hemorrhage into otherwise viable lung.
Learning objectives
3043Distinguish a postmortem clot from a thrombus on gross and microscopic features.
3044Identify the four outcomes of a thrombus: resolution, organization and recanalization, propagation, and embolization.
3045For venous or arterial thrombosis, identify the site, predisposing factors, and clinical correlations.
3046Define embolism and distinguish the types: thrombus, fat, air, bone marrow, tumor, amniotic fluid, atherosclerotic, and others.
3047Distinguish the effects of minor, major, and massive pulmonary thromboemboli.
3048Explain how cardiovascular and respiratory status and collateral circulation determine the outcome of a pulmonary embolus.
3049Delineate the pathway for paradoxical embolism.
3050Define infarction and identify its main causes.
3051Distinguish arterial and venous, and red and white, infarcts by location, morphology, and pathogenesis.
3052Identify the factors that determine whether infarction occurs.
3053Work through vignettes of obstructive thrombosis and embolism in the lung, brain, and heart.