Hemodynamic Disorders
Learning Objectives
By the end of this page you should be able to:
- Distinguish transudate from exudate and explain the four mechanisms that cause edema
- Differentiate active hyperemia from passive congestion, and describe chronic passive congestion in the lung and liver
- Classify hemorrhage by site and explain how it differs from hemostasis failure
- State Virchow's triad and explain how each arm predisposes to thrombosis
- Trace the fate of a thrombus (resolution, organization, recanalization, embolization)
- Classify emboli by origin (thromboembolism, fat, air, amniotic fluid) and predict where each lodges
- Explain why some infarcts are red and others are white, using organ vascular anatomy
- Classify shock into its four types and describe the three stages of shock progression
Quick Answer
Hemodynamic disorders are disturbances in how blood and fluid move through the vasculature and tissues. The core lesions are edema (fluid escaping into tissue), hyperemia/congestion (excess blood in a vascular bed), hemorrhage (blood escaping the vessel entirely), thrombosis (inappropriate clot formation inside an intact vessel, driven by Virchow's triad), embolism (a traveling mass that lodges downstream), infarction (tissue death from loss of blood supply), and shock (systemic circulatory failure that starves the whole body of perfusion). They matter because together they explain the mechanism behind most cardiovascular, obstetric, surgical, and critical-care emergencies you will see in the wards — a DVT, a heart attack, a stroke, or a septic patient in the ICU is a hemodynamic disorder in action.
Overview
Every cell in the body depends on a continuous, adequately pressured supply of blood. Hemodynamics is simply the physics of that supply — how fluid stays inside vessels, how it is supposed to move, and what happens when either goes wrong. Pathologists group the ways this system fails into a small number of named lesions, and the beauty of this chapter is that they are not isolated topics: they form a causal chain. A clot forms in a vein because of Virchow's triad (thrombosis) → part of it breaks off and travels (embolism) → it lodges in the pulmonary artery and cuts off blood supply to a portion of lung (infarction) → if the process is massive it can drop blood pressure so far that oxygen delivery to the whole body collapses (shock). Understanding one lesion well makes the next four easier, because they are stages of the same underlying story: blood in the wrong place, in the wrong amount, or not moving at all.
Edema
Definition. Edema is the accumulation of excess fluid in the interstitial tissue spaces or body cavities (when in a cavity it's called an effusion — pleural, pericardial, peritoneal/ascites).
The physiology behind it — Starling forces. Fluid movement across capillary walls depends on a balance:
- Hydrostatic pressure pushes fluid out of the capillary.
- Plasma oncotic pressure (mainly from albumin) pulls fluid back in.
Edema develops when this balance is disturbed, or when the lymphatics that normally drain excess interstitial fluid fail.
Four mechanisms, four classic causes — this is the single most tested list in this section:
| Mechanism | Why it happens | Classic example |
|---|---|---|
| Increased hydrostatic pressure | Venous outflow obstruction or pump failure raises upstream pressure | Right heart failure (peripheral edema), left heart failure (pulmonary edema), DVT (leg edema) |
| Reduced plasma oncotic pressure | Not enough albumin in blood to hold water in | Nephrotic syndrome (albumin lost in urine), liver cirrhosis (reduced albumin synthesis), protein malnutrition |
| Lymphatic obstruction | Fluid drained by lymphatics can't get back to circulation | Post-mastectomy lymphedema, filariasis (elephantiasis), tumor infiltration of lymph nodes |
| Sodium and water retention | Kidney retains salt/water, expanding plasma volume, which then leaks out | Acute glomerulonephritis, heart failure (secondary RAAS activation) |
Transudate vs exudate — the exam favorite. An edema fluid's protein content tells you the mechanism:
- Transudate: low protein (<3 g/dL), low specific gravity (<1.012), few cells. Caused by a hemodynamic imbalance (mechanisms 1, 2, 4 above) — the vessel wall itself is fine, fluid is just being pushed or pulled through it abnormally.
- Exudate: high protein, high specific gravity (>1.020), often cell-rich. Caused by increased vascular permeability from inflammation — the vessel wall itself is damaged/leaky.
Why it matters clinically. Where the edema appears tells you the failing organ before you order a single test: pitting ankle edema plus raised JVP points to right heart failure; periorbital puffiness with frothy urine points to nephrotic syndrome; a tense, distended abdomen with a low serum albumin points to cirrhotic ascites.
Hyperemia and Congestion
Both terms mean "increased blood volume in a tissue," but the mechanism is opposite, and the exam loves this contrast.
- Hyperemia is an active process: arteriolar dilation increases blood inflow (e.g., exercising muscle, an area of acute inflammation). The tissue is bright red because it's full of oxygenated blood.
- Congestion is a passive process: impaired venous outflow causes blood to back up (e.g., heart failure, local venous obstruction). The tissue is blue-red (cyanotic) because the blood is deoxygenated and stagnant.
Chronic passive congestion — the two organs you must know:
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Lung, in left heart failure. Chronically elevated pulmonary capillary pressure causes microhemorrhages; macrophages eat the extravasated red cells and turn the iron into hemosiderin, producing "heart failure cells" (hemosiderin-laden macrophages) seen in sputum/lung sections. Long-standing congestion also causes interstitial fibrosis — the lung becomes firm and brown, called brown induration.
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Liver, in right heart failure. Central veins and centrilobular sinusoids (zone 3, farthest from the oxygen-rich portal supply) become congested and dilated, while the periportal zone stays relatively normal or shows fatty change. On cut section this alternating pattern of red (congested) and pale/yellow (fatty) areas looks like the cut surface of a nutmeg — hence nutmeg liver. If congestion is prolonged and severe, centrilobular necrosis and fibrosis progress to cardiac cirrhosis.
Hemorrhage
Definition. Hemorrhage is extravasation of blood out of the vascular compartment, most often due to vessel wall damage (trauma, atherosclerotic rupture) but sometimes due to a bleeding tendency (coagulopathy) without obvious injury.
Named patterns by size/site — these are descriptive terms examiners like to test as picture questions:
- Petechiae: 1–2 mm pinpoint hemorrhages in skin/mucosa/serosa — classically from low platelets (thrombocytopenia) or platelet dysfunction.
- Purpura: slightly larger (>3 mm), seen in the same settings as petechiae plus vasculitis or trauma.
- Ecchymosis: a bruise (1–2 cm+), subcutaneous hematoma; the color changes over days (red-blue → blue-green → gold-brown) as hemoglobin is enzymatically degraded, first to biliverdin then to bilirubin/hemosiderin.
- Hematoma: a larger, enclosed collection of blood within a tissue, can be clinically significant if it compresses a structure (e.g., epidural hematoma compressing brain).
- Body-cavity hemorrhage gets its own names: hemothorax, hemopericardium, hemoperitoneum, hemarthrosis (into a joint, classic in hemophilia).
Clinical significance depends on volume and rate, not just presence: losing 20% of blood volume rapidly can cause hemorrhagic shock, while the same volume lost slowly (e.g., chronic GI bleed) may only cause iron-deficiency anemia because compensatory mechanisms have time to act.
Thrombosis
Definition. A thrombus is a solid mass formed from blood constituents (platelets, fibrin, trapped red/white cells) within an intact, living vessel or the heart — the key word is intact: thrombosis is clotting where it shouldn't happen, as opposed to normal hemostasis sealing an injured vessel.
Virchow's Triad
Every thrombus, arterial or venous, forms because of one or more of three abnormalities. This triad is essentially a guaranteed exam question.
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Endothelial injury — the single most important factor, and dominant in arterial/cardiac thrombosis. Damaged endothelium exposes subendothelial collagen and tissue factor, triggering platelet adhesion and the coagulation cascade. Causes: atherosclerotic plaque rupture, hypertension, turbulent flow, vasculitis, direct trauma, myocardial infarction (over the infarcted endocardium).
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Abnormal blood flow (stasis or turbulence) — dominant in venous thrombosis. Normal laminar flow keeps platelets and clotting factors away from the vessel wall and dilutes activated clotting factors. Stasis (immobilization, prolonged bed rest, long flights, atrial fibrillation with a stagnant atrium, an aneurysm sac) lets platelets settle onto endothelium and lets activated factors accumulate instead of being washed away. Turbulence similarly causes endothelial injury and counter-currents.
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Hypercoagulability — a shift in the balance of clotting favoring coagulation. Primary (genetic): Factor V Leiden (resistance to protein C, the most common inherited thrombophilia), prothrombin gene mutation, protein C/S or antithrombin III deficiency. Secondary (acquired): malignancy (Trousseau syndrome/migratory thrombophlebitis), pregnancy and oral contraceptives (estrogen raises clotting factor synthesis), prolonged immobilization, nephrotic syndrome (loss of antithrombin III in urine), and antiphospholipid antibody syndrome.
Fate of a Thrombus
A thrombus doesn't just sit there — it follows one of four paths, and knowing them explains later complications:
- Resolution: complete dissolution by fibrinolysis (best outcome, most likely if small and recent).
- Propagation: it accumulates more platelets/fibrin and grows, increasing the risk of vessel occlusion or embolization.
- Organization and recanalization: fibroblasts and endothelial cells grow into the thrombus over weeks; new capillary channels form through it, partially restoring flow (recanalization). This is how a chronic DVT is eventually incorporated into the vessel wall.
- Embolization: part or all of the thrombus breaks free and travels downstream — this is precisely how thrombosis becomes embolism.
Arterial vs venous thrombi — a quick contrast worth memorizing:
| Feature | Arterial thrombus | Venous thrombus |
|---|---|---|
| Dominant Virchow factor | Endothelial injury (atherosclerosis) | Stasis |
| Composition | Platelet-rich, "white," lines of Zahn prominent | Fibrin/RBC-rich, "red," propagates in direction of flow |
| Classic site | Coronary, cerebral, femoral arteries | Deep veins of the leg (DVT) |
| Main complication | Infarction downstream (MI, stroke, limb ischemia) | Pulmonary embolism |
Embolism
Definition. An embolus is any intravascular solid, liquid, or gas mass carried by blood to a site distant from its origin, where it lodges and obstructs flow. Over 95% of emboli are thromboemboli — fragments of a thrombus.
Types and where they lodge (this pairing is very examinable):
| Type of embolus | Source | Typical destination |
|---|---|---|
| Pulmonary thromboembolism | DVT of leg/pelvic veins | Pulmonary arteries; large ones lodge at the bifurcation ("saddle embolus") and can cause sudden death |
| Systemic thromboembolism | Left heart (mural thrombus after MI, atrial fibrillation), aortic aneurysm, valve vegetations | Lower limbs, brain, kidney, spleen, gut — wherever the artery leads |
| Fat embolism | Long bone fracture or orthopedic surgery (marrow fat released into torn venous sinusoids) | Lungs and brain; classic triad is respiratory distress, neurological symptoms/petechial rash, thrombocytopenia, 1-3 days after trauma |
| Air embolism | Chest wall/neck trauma, IV line mishap, laparoscopic surgery, decompression sickness (nitrogen bubbles, "the bends") | Needs >100 mL of air in the right heart to cause obstruction; produces a "mill-wheel" murmur |
| Amniotic fluid embolism | Amniotic fluid and fetal material entering maternal circulation during labor/delivery | Pulmonary vessels; causes sudden dyspnea, cyanosis, shock and disseminated intravascular coagulation (DIC) — high maternal mortality |
| Paradoxical embolism | A venous embolus crossing to the arterial side | Through a patent foramen ovale/atrial septal defect, causing a systemic (e.g., stroke) event from a venous source |
Consequence depends on collateral supply. An embolus lodging in an organ with a single (end-arterial) blood supply, like the spleen or kidney, reliably causes infarction. The same-sized embolus in the lung, which has a dual supply (pulmonary artery + bronchial arteries), may cause no infarct at all unless the patient already has compromised circulation (e.g., heart failure).
Infarction
Definition. An infarct is a localized area of ischemic (coagulative, except in the brain) necrosis caused by occlusion of either the arterial supply or, less commonly, the venous drainage of a tissue.
Why some infarcts are red and others are white — this single concept explains an entire category of exam images:
| Red (hemorrhagic) infarct | White (anemic) infarct | |
|---|---|---|
| Organs | Loose, dual-supply organs: lung, intestine; also venous occlusion (testicular torsion) and reperfused tissue | Solid organs with end-arterial (single) supply: spleen, kidney, heart |
| Why the color | Blood re-enters the necrotic area from a collateral/dual supply or via loose tissue that allows back-bleeding | End-arterial supply means no blood can re-enter the dead zone |
| Shape | Often wedge-shaped with the apex at the occlusion, same as white infarcts | Classically wedge-shaped, apex pointing to the occluded vessel, base at the organ surface |
Special cases:
- Brain infarct undergoes liquefactive, not coagulative, necrosis because of the brain's high lipid content and lack of a sturdy stromal framework — it forms a cystic cavity, not a firm scar.
- Timing matters: an infarct needs roughly 12-24 hours to become grossly visible, and the histologic hallmark of an early (coagulative) infarct is preserved cell outlines with loss of the nucleus — "ghost cells."
- Septic infarct: if the occluding embolus was infected (e.g., from valve vegetations in infective endocarditis), the infarct becomes a walled abscess instead of healing by simple scarring.
Shock
Definition. Shock is a state of systemic hypoperfusion where blood flow is inadequate to meet the metabolic demands of tissues, leading to cellular hypoxia. Untreated, it progresses to irreversible multi-organ failure and death — this is the final common pathway many of the lesions above can lead to.
Classification by mechanism
| Type | Core problem | Cardiac output | Systemic vascular resistance | Classic cause |
|---|---|---|---|---|
| Hypovolemic | Not enough volume in the tank | Low | High (compensatory) | Severe hemorrhage, dehydration, burns |
| Cardiogenic | Pump can't push what's there | Low | High (compensatory) | Massive MI, arrhythmia, cardiomyopathy |
| Distributive (septic/anaphylactic/neurogenic) | Vessels inappropriately dilated | Normal or high | Low | Sepsis (endotoxin-mediated vasodilation), anaphylaxis (histamine), spinal cord injury (loss of sympathetic tone) |
| Obstructive | Physical blockage to flow | Low | High | Cardiac tamponade, tension pneumothorax, massive pulmonary embolism |
Distributive (especially septic) shock is the odd one out physiologically — the patient is often warm and flushed (warm shock) rather than cold and clammy, because the problem is vessels stuck open, not a failing pump or empty tank.
The three stages of shock — why "early shock" is reversible and "late shock" often isn't
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Non-progressive (compensated) stage. Baroreceptor reflexes, catecholamine release, and RAAS activation maintain perfusion to the heart and brain by shunting blood away from skin, muscle, and gut (hence cool clammy skin, tachycardia). Blood pressure may still be near-normal. Fully reversible if the cause is treated now.
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Progressive stage. Compensatory mechanisms begin to fail. Widespread tissue hypoxia forces cells into anaerobic metabolism, producing lactic acidosis, which further impairs myocardial contractility and vasomotor tone. Arterioles dilate and blood pools in the microcirculation (worsening the very hypoperfusion that started the cascade) — a vicious cycle. Clinically: hypotension, oliguria, confusion, metabolic acidosis.
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Irreversible stage. Cellular injury becomes so severe (lysosomal enzyme leakage, mitochondrial failure, worsening DIC) that even correcting the original hemodynamic problem cannot save the patient. Multi-organ failure (kidneys, lungs = "shock lung"/ARDS, gut, brain) follows and death is likely regardless of treatment.
Why this staging matters clinically: it's the entire justification for early, aggressive resuscitation ("golden hour") in trauma and sepsis protocols — the same insult treated in stage 1 is survivable, in stage 3 it usually is not.
Key Terms
| Term | Definition |
|---|---|
| Transudate | Low-protein, low-cell edema fluid from a purely hemodynamic (pressure/oncotic) imbalance |
| Exudate | High-protein, cell-rich edema fluid from increased vascular permeability due to inflammation |
| Hyperemia | Active, arteriolar-driven increase in blood volume in a tissue (bright red) |
| Congestion | Passive, venous-outflow-driven increase in blood volume in a tissue (blue-red) |
| Nutmeg liver | Gross appearance of chronic passive hepatic congestion — congested centrilobular areas alternating with paler periportal zones |
| Heart failure cells | Hemosiderin-laden alveolar macrophages, marker of chronic pulmonary congestion from left heart failure |
| Petechiae | Pinpoint (1-2 mm) hemorrhages, classically from thrombocytopenia |
| Virchow's triad | Endothelial injury, abnormal blood flow, and hypercoagulability — the three drivers of thrombosis |
| Lines of Zahn | Alternating pale (platelet/fibrin) and dark (RBC) bands seen in a thrombus formed in flowing blood, distinguishing it from a postmortem clot |
| Thromboembolism | An embolus derived from a fragmented or detached thrombus |
| Paradoxical embolism | A venous embolus that reaches the systemic arterial circulation via a right-to-left shunt (e.g., PFO) |
| Infarct | Localized area of ischemic necrosis due to vascular occlusion |
| Ghost cells | Necrotic cells with preserved outline but lost nuclear detail, an early histologic sign of coagulative (infarct) necrosis |
| Shock | Systemic hypoperfusion insufficient to meet tissue metabolic demand |
| Lactic acidosis | Metabolic acidosis from anaerobic glycolysis during tissue hypoxia; a hallmark of progressive shock |
Common Mistakes
Misconception 1: "A thrombus and a normal blood clot are the same thing." Why it's wrong: A postmortem or in-vitro clot forms in static, non-flowing blood and has no attachment to the vessel wall, with cells simply settling by gravity (a "chicken-fat" layer over a "currant-jelly" layer). Correct understanding: A thrombus forms in flowing blood inside a living, intact vessel, is attached to the wall at its point of origin, and characteristically shows lines of Zahn (alternating platelet-fibrin and RBC layers) — a feature true clots lack.
Misconception 2: "All infarcts look the same, so their color doesn't tell you anything useful." Why it's wrong: Students often try to memorize infarct color as a fixed organ fact without understanding why. Correct understanding: Color depends on blood supply architecture, not the organ's identity per se — solid organs with a single end-arterial supply (kidney, spleen, heart) infarct white because no blood can re-enter the dead zone, while loose/dual-supply tissues (lung, gut) or venous occlusions infarct red because blood re-enters the necrotic area. Recognizing the mechanism lets you predict the color even for an organ you haven't memorized.
Misconception 3: "Shock means low blood pressure." Why it's wrong: Hypotension is a late and sometimes absent sign; a young, healthy patient can maintain near-normal blood pressure well into progressive shock because of powerful compensatory vasoconstriction, then decompensate suddenly. Correct understanding: Shock is defined by inadequate tissue perfusion and cellular hypoxia (look for tachycardia, oliguria, altered mentation, rising lactate), not by a specific blood pressure number — waiting for hypotension to diagnose shock means you are diagnosing it late.
Comparison and Connections
| Concept | Vs. | Key distinguishing point |
|---|---|---|
| Edema | Effusion | Edema is fluid in interstitial tissue; effusion is fluid in a body cavity (pleural, peritoneal, pericardial) — same Starling mechanisms, different location |
| Transudate | Exudate | Transudate = low protein, hemodynamic cause; exudate = high protein, inflammatory/permeability cause |
| Hyperemia | Congestion | Hyperemia is active (arteriolar, red); congestion is passive (venous, blue-red) |
| Thrombus | Embolus | A thrombus is a stationary clot in an intact vessel; once part of it detaches and travels, it becomes an embolus |
| Arterial thrombosis | Venous thrombosis | Arterial: endothelial injury-driven, platelet-rich, causes infarction downstream; venous: stasis-driven, fibrin/RBC-rich, causes pulmonary embolism |
| Red infarct | White infarct | Red: dual/loose blood supply or venous occlusion; white: solid organ with single end-arterial supply |
| Hypovolemic shock | Distributive shock | Hypovolemic: low volume, high SVR, cold/clammy patient; distributive: normal/high volume, low SVR, warm/flushed patient (classically septic) |
| Cardiogenic shock | Obstructive shock | Cardiogenic: the heart muscle itself fails to pump; obstructive: the heart is fine but something mechanically blocks flow (tamponade, tension pneumothorax, massive PE) |
Practice Questions
Recall
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What are the four mechanisms that cause edema? Answer guidance: increased hydrostatic pressure, reduced plasma oncotic pressure, lymphatic obstruction, sodium/water retention.
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Name the three components of Virchow's triad. Answer guidance: endothelial injury, abnormal blood flow (stasis/turbulence), hypercoagulability.
Understanding
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Explain why chronic left heart failure produces "heart failure cells" in the lung, and why chronic right heart failure produces a "nutmeg" appearance in the liver. Answer guidance: In left heart failure, raised pulmonary capillary pressure causes microhemorrhage; macrophages phagocytose the RBCs and store iron as hemosiderin. In right heart failure, raised central venous pressure congests the centrilobular (zone 3) hepatic sinusoids first because they are farthest from the oxygen-rich portal inflow, creating the alternating congested/pale pattern.
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Why does a fat embolism classically present 1-3 days after a long bone fracture rather than immediately? Answer guidance: marrow fat is released into torn venous sinusoids at the time of fracture, but the classic triad (respiratory distress, neurologic changes, petechial rash) develops after a latent period as fat globules mechanically obstruct pulmonary/cerebral capillaries and free fatty acids released from the fat cause local toxic endothelial injury — a delayed inflammatory/biochemical process, not just simple blockage.
Application
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A 68-year-old man with atrial fibrillation suddenly develops a cold, pulseless left leg. What is the likely source of the embolus and why does AF predispose to it? Answer guidance: A systemic thromboembolism, most likely originating as a mural thrombus in the fibrillating, poorly contracting left atrium/atrial appendage — AF causes blood stasis in the atrium (Virchow's triad, stasis arm), promoting thrombus formation that can embolize to a limb artery.
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A patient with a femur fracture is found to have petechiae over the chest and axilla, confusion, and low platelets two days post-injury. What is the diagnosis and mechanism? Answer guidance: Fat embolism syndrome — marrow fat entered the venous circulation at the fracture site and embolized to lungs and brain (respiratory distress, neuro symptoms), consuming platelets and damaging capillaries to produce petechiae/thrombocytopenia.
Analysis
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Compare and explain why a splenic infarct is typically white while an intestinal infarct from the same-sized embolus is typically red. Answer guidance: The spleen has an end-arterial (single) blood supply, so once the artery is occluded no blood can re-enter the necrotic zone, producing a pale white infarct. The intestine has a looser, richly anastomosing dual supply (and loose connective tissue), allowing blood to seep back into the dead area from collateral vessels, producing a red, hemorrhagic infarct.
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A trauma patient's blood pressure is 118/76 with a heart rate of 128 and cool, clammy skin, and urine output has dropped. A colleague says "vitals are basically normal, this isn't shock yet." Evaluate this claim. Answer guidance: The claim is wrong — blood pressure is a poor and late marker of shock. Tachycardia, cool/clammy skin, and oliguria all indicate compensatory vasoconstriction is already occurring (non-progressive/compensated stage of shock) to protect perfusion of the brain and heart at the expense of skin, muscle, and kidney. Waiting for hypotension to call it "shock" delays resuscitation until the patient may already be moving into the progressive stage.
FAQ
1. Is edema always a sign of disease? Not always — mild dependent edema after long standing or sitting (e.g., swollen ankles after a long flight) reflects normal hydrostatic pressure effects and resolves with elevation. Pathological edema is persistent, generalized, or associated with an underlying disease (heart, kidney, liver, lymphatic).
2. What's the actual difference between an embolus and a thrombus once it's traveling? None — once a thrombus (or fragment of one) detaches and enters the bloodstream, it is by definition now called an embolus. "Thromboembolism" is simply naming the embolus by its origin.
3. Why do doctors care so much about distinguishing red from white infarcts? Because the color reflects the underlying vascular anatomy and mechanism, which changes management — for example, anticoagulation is generally more cautious in hemorrhagic (red) infarcts (like a hemorrhagic stroke transformation) because of bleeding risk, whereas it's central to treating an ischemic (white-infarct-prone) arterial event.
4. Can someone be in shock with a completely normal blood pressure? Yes, especially early ("compensated") shock — powerful sympathetic compensation can maintain blood pressure while tissues are already underperfused. This is exactly why clinicians track heart rate, mental status, urine output, and lactate rather than blood pressure alone.
5. Why is pregnancy considered a hypercoagulable state? Estrogen increases hepatic synthesis of several clotting factors, and the gravid uterus causes venous stasis in the pelvis and legs — this combination satisfies two arms of Virchow's triad simultaneously, which is why pregnancy and the postpartum period carry a markedly higher risk of DVT and pulmonary embolism.
Quick Revision
- Edema = fluid in interstitium; four causes: ↑hydrostatic pressure, ↓oncotic pressure, lymphatic obstruction, Na/water retention.
- Transudate = low protein, hemodynamic cause; exudate = high protein, inflammatory/permeability cause.
- Hyperemia = active/arteriolar/red; congestion = passive/venous/blue.
- Chronic lung congestion → heart failure cells (hemosiderin-laden macrophages), brown induration.
- Chronic liver congestion → nutmeg liver → can progress to cardiac cirrhosis.
- Virchow's triad: endothelial injury, stasis/turbulence, hypercoagulability — memorize both arterial (injury-dominant) and venous (stasis-dominant) patterns.
- Thrombus fates: resolution, propagation, organization/recanalization, embolization.
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95% of emboli are thromboemboli; know fat, air, and amniotic fluid embolism as the classic "special" types.
- White infarct = solid organ, end-arterial supply (spleen, kidney, heart); red infarct = dual/loose supply or venous occlusion (lung, gut).
- Shock types: hypovolemic and cardiogenic (both ↑SVR, cold), distributive (↓SVR, warm — septic/anaphylactic/neurogenic), obstructive (mechanical block).
- Shock stages: non-progressive (compensated, reversible) → progressive (lactic acidosis, vicious cycle) → irreversible (multi-organ failure).
- Blood pressure is a late sign of shock — tachycardia, oliguria, and confusion appear first.
Related Topics
Prerequisites
- Basic cardiovascular physiology (Starling forces, cardiac output, vascular resistance)
- Normal hemostasis (platelet plug formation, coagulation cascade)
Related Topics
- Inflammation (exudate formation shares mechanisms with acute inflammation)
- Cardiovascular Pathology (atherosclerosis is the leading cause of endothelial injury and arterial thrombosis)
- Coagulation Disorders (DIC, hemophilia, thrombophilias covered in more depth)
Next Topics
- Cell Injury and Necrosis (to deepen understanding of infarct histology and cell death patterns)
- Cardiovascular Pathology (ischemic heart disease builds directly on thrombosis and infarction concepts here)