Haemodynamic Disorders
Pathology · General Pathology · lean revision notes
Haemodynamic Disorders
Haemodynamic disorders are derangements of fluid balance, blood flow, and vessel integrity. They form the backbone of cardiovascular pathology and are among the highest-yield, most consistently repeated areas in NEET PG—Virchow's triad, embolism types, and shock stages are near-guaranteed one-liners.
This cluster covers oedema, hyperaemia/congestion, haemorrhage, haemostasis, thrombosis, embolism, infarction, and shock. The unifying theme is the Starling forces, endothelial integrity, and the balance between procoagulant and anticoagulant pathways.
1. Oedema
Oedema is the accumulation of excess interstitial fluid within tissues or body cavities. Fluid movement across capillaries is governed by Starling forces: hydrostatic pressure pushes fluid out, oncotic (colloid osmotic) pressure pulls it in.
Pathophysiologic categories
| Mechanism | Example | Fluid type |
|---|---|---|
| ↑ Hydrostatic pressure | CHF, venous obstruction, DVT, cirrhosis (portal HTN) | Transudate |
| ↓ Plasma oncotic pressure | Nephrotic syndrome, cirrhosis, protein-losing enteropathy, kwashiorkor | Transudate |
| ↑ Vascular permeability | Inflammation, burns, anaphylaxis | Exudate |
| Lymphatic obstruction | Filariasis, post-mastectomy, malignancy | Lymphoedema |
| Sodium/water retention | Renal failure, hyperaldosteronism | Transudate |
High-yield: Transudate is a protein-poor, cell-poor ultrafiltrate (specific gravity < 1.012, protein < 2.5 g/dL); exudate is protein-rich (SG > 1.020) and arises from increased vascular permeability in inflammation. Light's criteria distinguish exudate in pleural effusions.
Light's criteria (exudate if ANY one is met)
- Pleural fluid protein / serum protein > 0.5
- Pleural fluid LDH / serum LDH > 0.6
- Pleural fluid LDH > two-thirds of upper limit of normal serum LDH
Clinical patterns
- Pitting oedema: subcutaneous, gravity-dependent (sacrum in bedridden, ankles when standing)—cardiac/renal/hepatic.
- Periorbital oedema: classically nephrotic syndrome and renal disease (loose periorbital connective tissue), also angioedema, trichinellosis.
- Anasarca: severe generalised oedema.
- Pulmonary oedema: heavy, wet lungs; "heart failure cells" = haemosiderin-laden macrophages in alveoli.
- Cerebral oedema: flattened gyri, narrowed sulci → risk of herniation.
High-yield: Brown induration of the lung = chronic pulmonary congestion (left heart failure) with heart-failure cells. Nutmeg liver = chronic passive hepatic congestion (right heart failure).
2. Hyperaemia and Congestion
Both denote increased blood volume in a tissue, but the mechanism differs sharply.
| Feature | Hyperaemia | Congestion |
|---|---|---|
| Process | Active | Passive |
| Cause | Arteriolar dilatation (↑ inflow) | Impaired venous outflow |
| Blood type | Oxygenated | Deoxygenated |
| Colour | Red (erythema) | Blue-red (cyanosis) |
| Examples | Exercise, inflammation, blushing | CHF, DVT, portal HTN |
High-yield: Nutmeg liver = chronic passive congestion. Centrilobular (zone 3, around central vein) congestion and necrosis with peripheral fatty change gives the mottled "nutmeg" cut surface. Severe chronic cases → cardiac cirrhosis (more fibrosis than true cirrhosis).
3. Haemorrhage
Extravasation of blood due to vessel rupture.
- Petechiae (1–2 mm): platelet defects, thrombocytopenia, ↑ intravascular pressure.
- Purpura (3–5 mm): same causes plus vasculitis, trauma.
- Ecchymoses (1–2 cm): "bruises"; RBCs degrade → haemoglobin (red-blue) → bilirubin (blue-green) → haemosiderin (golden-brown).
- Haematoma: accumulation within tissue.
- Cavity bleeds: haemothorax, haemopericardium, haemoperitoneum, haemarthrosis.
Clinical impact depends on volume, rate, and location. A trivial volume in the brain (e.g. brainstem) can be fatal; chronic external loss → iron-deficiency anaemia.
4. Haemostasis (foundation for thrombosis)
Normal haemostasis is a tightly regulated sequence triggered by vascular injury.
Vascular injury → reflex vasoconstriction (endothelin) → primary haemostasis (platelet plug, vWF + GpIb adhesion, ADP/TXA2 aggregation via GpIIb/IIIa) → secondary haemostasis (coagulation cascade → fibrin) → clot stabilisation & retraction → fibrinolysis (plasmin)
Endothelial balance
| Antithrombotic | Prothrombotic |
|---|---|
| Prostacyclin (PGI2), NO, ADPase | vWF |
| Thrombomodulin → protein C activation | Tissue factor |
| Heparin-like molecules (antithrombin III) | PAI (plasminogen activator inhibitor) |
| Tissue plasminogen activator (t-PA) |
High-yield: Protein C (with cofactor protein S) inactivates factors Va and VIIIa. Factor V Leiden is resistant to protein C cleavage → most common inherited hypercoagulable state (heterozygous ~5% of Caucasians).
5. Thrombosis
Thrombosis is the pathologic formation of a clot (thrombus) within an intact vascular system during life. The three predisposing factors are Virchow's triad.
Virchow's triad (THE classic NEET PG one-liner)
- Endothelial injury — the dominant factor in cardiac and arterial thrombi (MI, atherosclerosis, vasculitis, hypertension, hyperhomocysteinaemia, smoking).
- Abnormal blood flow (stasis or turbulence) — dominant in venous thrombi and cardiac chambers (atrial fibrillation, aneurysms, immobility, hyperviscosity, polycythaemia, sickle cell).
- Hypercoagulability — inherited or acquired.
Mnemonic: "SHE" — Stasis, Hypercoagulability, Endothelial injury.
Hypercoagulable (thrombophilic) states
| Inherited | Acquired |
|---|---|
| Factor V Leiden (commonest) | Antiphospholipid antibody syndrome |
| Prothrombin G20210A mutation | Heparin-induced thrombocytopenia (HIT) |
| Antithrombin III deficiency | Malignancy (Trousseau syndrome) |
| Protein C / Protein S deficiency | Nephrotic syndrome, OCPs, pregnancy |
| Hyperhomocysteinaemia (MTHFR) | Prolonged immobilisation |
High-yield: HIT is caused by IgG antibodies against platelet factor 4–heparin complex, paradoxically causing thrombosis despite thrombocytopenia (5–14 days after unfractionated heparin). Trousseau syndrome = migratory thrombophlebitis with visceral malignancy (classically pancreatic carcinoma).
Lines of Zahn
Alternating pale (platelet/fibrin) and dark (RBC) laminations seen in thrombi formed in flowing blood (ante-mortem). They help distinguish a true thrombus from a post-mortem clot.
| Feature | Antemortem thrombus | Post-mortem clot |
|---|---|---|
| Lines of Zahn | Present | Absent |
| Attachment to wall | Firmly attached | Not attached |
| Consistency | Dry, friable | Gelatinous |
| Appearance | Laminated | "Chicken fat" (yellow) over "currant jelly" (red) |
Fate of a thrombus
Propagation → Embolisation → Dissolution (fibrinolysis) → Organisation & Recanalisation
- Organisation: ingrowth of endothelium, smooth muscle, fibroblasts.
- Recanalisation: new channels re-establish flow.
High-yield: Arterial thrombi are usually occlusive and retrograde (grow against flow toward heart) and tend to be pale/white (platelet-rich). Venous (red/stasis) thrombi are propagating in the direction of flow and are occlusive, RBC-rich.
6. Embolism
An embolus is a detached intravascular solid, liquid, or gaseous mass carried to a distant site. 99% are dislodged thrombi (thromboembolism).
Pulmonary thromboembolism (PTE)
- Source: ≥ 95% from deep leg veins (popliteal, femoral, iliac).
- Saddle embolus lodges at the pulmonary artery bifurcation → sudden death.
- Small emboli → may be silent; with poor cardiopulmonary reserve → infarction.
- Recurrent emboli → pulmonary hypertension and right heart strain.
- Investigation of choice: CT pulmonary angiography (CTPA). D-dimer is a sensitive screening tool (high negative predictive value).
Systemic (arterial) embolism
- 80% arise from intracardiac mural thrombi (post-MI left ventricle, AF left atrium).
- Common targets: lower limbs (75%) and brain (10%).
Special embolism types
| Type | Source / setting | Key feature |
|---|---|---|
| Fat embolism | Long-bone/pelvic fractures, severe burns | Triad: dyspnoea, neuro symptoms, petechial rash; 1–3 days post-injury |
| Air embolism | Chest wall injury, surgery, diving (decompression), obstetric | > 100 mL needed; "the bends" / caisson disease |
| Amniotic fluid embolism | Labour/immediate postpartum | Sudden dyspnoea, shock, DIC; fetal squames in maternal pulmonary vessels; high mortality |
| Tumour embolism | Metastatic spread | — |
| Septic embolism | Infective endocarditis | Mycotic aneurysm |
| Atheroembolism | Ruptured plaque | Cholesterol clefts |
High-yield: Caisson disease (decompression sickness) = chronic gas embolism; nitrogen bubbles in bone → ischaemic necrosis of femoral/humeral heads (dysbaric osteonecrosis). Amniotic fluid embolism is the classic obstetric cause of DIC.
Paradoxical embolism
A venous embolus enters the systemic circulation through a patent foramen ovale or septal defect, bypassing the lung filter—causes systemic/cerebral events from a venous source.
7. Infarction
An infarct is an area of ischaemic necrosis caused by occlusion of arterial supply or venous drainage. About 99% result from thrombotic/embolic arterial occlusion.
Red vs white infarcts
| Feature | Red (haemorrhagic) infarct | White (pale/anaemic) infarct |
|---|---|---|
| Organs | Lung, intestine, testis, ovary, brain (venous) | Heart, spleen, kidney |
| Vasculature | Dual/loose, with reperfusion | Single, end-arterial; solid tissue |
| Mechanism | Venous occlusion OR reflow into necrotic tissue | Arterial occlusion in dense tissue |
| Shape | — | Wedge-shaped, apex toward occlusion |
Mnemonic for red infarcts: organs with dual blood supply or loose tissue bleed in. Lung (bronchial + pulmonary), liver (hepatic artery + portal vein), intestine (anastomosing mesenteric arcades).
Type of necrosis
- Most organs → coagulative necrosis.
- Brain → liquefactive necrosis (the key exception).
Factors influencing infarct development
- Nature of vascular supply (dual supply protects: lung, liver, hand).
- Rate of occlusion (slow → collaterals develop).
- Tissue vulnerability to hypoxia — neurons (3–4 min) > myocardium (20–30 min) > fibroblasts (hours).
- Oxygen content of blood (anaemia, hypoxaemia worsen).
High-yield: Watershed/border-zone infarcts occur between two arterial territories during hypotension—e.g. splenic flexure of colon (SMA/IMA junction), cerebral cortex between ACA/MCA/PCA.
8. Shock
Shock is a state of systemic hypoperfusion due to reduced cardiac output or reduced effective circulating blood volume, leading to cellular hypoxia, anaerobic metabolism, and ultimately multi-organ failure.
Classification
| Type | Mechanism | Examples | CO | SVR | PCWP |
|---|---|---|---|---|---|
| Cardiogenic | Pump failure | MI, arrhythmia, tamponade, PE | ↓ | ↑ | ↑ |
| Hypovolaemic | ↓ blood/plasma volume | Haemorrhage, burns, vomiting | ↓ | ↑ | ↓ |
| Distributive – Septic | Vasodilatation, pooling | Gram-negative/positive sepsis | ↑/↓ | ↓ | ↓/N |
| Distributive – Anaphylactic | IgE-mediated vasodilatation | Drugs, stings, foods | ↓ | ↓ | ↓ |
| Distributive – Neurogenic | Loss of vascular tone | Spinal cord injury, anaesthesia | ↓ | ↓ | ↓ |
| Obstructive | Mechanical outflow block | Massive PE, tamponade, tension pneumothorax | ↓ | ↑ | variable |
High-yield: Septic shock is the only major type that is classically "warm" (vasodilated, bounding pulses, ↓ SVR) in early stages. The others are "cold" (vasoconstricted). Neurogenic shock → hypotension with bradycardia (loss of sympathetic tone), distinguishing it from hypovolaemic (tachycardia).
Pathogenesis of septic shock
Most often gram-negative LPS (endotoxin) → massive cytokine release (TNF, IL-1) → endothelial activation → vasodilatation, ↑ permeability, DIC, and metabolic derangement → multiorgan dysfunction.
Stages of shock
- Non-progressive (compensated): baroreceptor reflexes, catecholamines, RAAS, ADH maintain perfusion to vital organs.
- Progressive: tissue hypoperfusion, lactic acidosis (anaerobic glycolysis), blunted vasomotor response, blood pooling.
- Irreversible: widespread cell injury, lysosomal leakage, NO myocardial depression, gut ischaemia with bacterial translocation → death despite correction.
Organ-specific changes in shock
- Kidney: acute tubular necrosis → oliguria (most clinically important).
- Lungs: diffuse alveolar damage → ARDS ("shock lung") — rare in pure cardiogenic shock.
- Adrenals: cortical lipid depletion; Waterhouse–Friderichsen syndrome (bilateral haemorrhagic necrosis) in meningococcaemia.
- GIT: haemorrhagic enteropathy.
- Heart: subendocardial/contraction band necrosis.
- Brain: ischaemic encephalopathy.
High-yield: Waterhouse–Friderichsen syndrome = fulminant meningococcaemia → DIC, hypotension, and bilateral adrenal haemorrhage. Classic NEET PG association.
9. Disseminated Intravascular Coagulation (DIC)
A consumptive coagulopathy—widespread microthrombi consume platelets and clotting factors, paradoxically causing simultaneous thrombosis and haemorrhage.
- Triggers: sepsis, obstetric complications (amniotic fluid embolism, abruption, retained products), malignancy (APML, mucinous adenocarcinoma), massive trauma/burns, snake bite.
- Labs: ↓ platelets, ↑ PT/aPTT, ↓ fibrinogen, ↑ D-dimer/FDPs, schistocytes on smear (microangiopathic haemolytic anaemia).
High-yield: Acute promyelocytic leukaemia (APML, t(15;17)) is the classic malignancy precipitating DIC; treat with all-trans retinoic acid (ATRA).
Key Differentials
- Transudate vs exudate — Light's criteria; transudate = systemic (CHF, cirrhosis, nephrosis), exudate = local (infection, malignancy, PE).
- Thrombus vs post-mortem clot — lines of Zahn, attachment, friability.
- Red vs white infarct — organ and vascular architecture.
- Septic (warm) vs hypovolaemic/cardiogenic (cold) shock — SVR and skin findings.
- Neurogenic shock (bradycardia) vs hypovolaemic shock (tachycardia).
- DVT vs cellulitis vs ruptured Baker's cyst for a swollen calf.
Recently asked / exam angle
- Virchow's triad components and which factor dominates arterial vs venous thrombosis (endothelial injury vs stasis) — repeated annually.
- Most common source of pulmonary embolism → deep veins of the lower limb (popliteal/femoral/iliac).
- Fat embolism triad and time course (24–72 h post long-bone fracture); petechial rash.
- Amniotic fluid embolism → DIC; squamous cells in maternal pulmonary vasculature.
- Red vs white infarct organs — "Lung, GIT, testis = red; heart, spleen, kidney = white."
- Lines of Zahn — antemortem thrombus marker.
- Brain undergoes liquefactive necrosis in infarction (the exception to coagulative).
- HIT — anti-PF4 antibody, thrombocytopenia + thrombosis.
- Waterhouse–Friderichsen — meningococcaemia + bilateral adrenal haemorrhage.
- Light's criteria for exudative effusion.
- Septic shock haemodynamics: ↑ CO, ↓ SVR ("warm shock").
- Nutmeg liver = chronic passive venous congestion (right heart failure).
- Factor V Leiden = commonest inherited hypercoagulable state, resistant to protein C.
Rapid revision
- Transudate = SG < 1.012, protein < 2.5 g/dL, systemic cause; exudate = inflammatory, protein-rich, Light's criteria positive.
- Periorbital oedema → think nephrotic syndrome; brown induration → chronic lung congestion; nutmeg liver → chronic hepatic congestion.
- Hyperaemia = active arteriolar inflow (red, oxygenated); congestion = passive impaired outflow (blue, deoxygenated).
- Virchow's triad = endothelial injury + abnormal flow (stasis/turbulence) + hypercoagulability.
- Lines of Zahn distinguish an antemortem thrombus from a post-mortem chicken-fat clot.
- Factor V Leiden = commonest inherited thrombophilia; resistant to protein C; protein C/S inactivate factors Va and VIIIa.
- HIT = IgG vs heparin–PF4 complex, 5–14 days after unfractionated heparin, thrombosis despite low platelets.
- ≥ 95% of pulmonary emboli arise from lower-limb deep veins; saddle embolus → sudden death; CTPA is the investigation of choice.
- Fat embolism = long-bone fracture + dyspnoea + neuro signs + petechiae at 24–72 h; amniotic fluid embolism → DIC.
- Red infarcts: lung, intestine, testis, ovary (dual supply / loose tissue); white infarcts: heart, spleen, kidney (end-arterial, solid).
- Brain infarct → liquefactive necrosis; all other organs → coagulative necrosis; watershed zones infarct in hypotension.
- Septic shock = warm, ↑ CO, ↓ SVR; neurogenic shock = hypotension + bradycardia; Waterhouse–Friderichsen = meningococcaemia + bilateral adrenal haemorrhage; DIC labs = ↓ platelets, ↑ PT/aPTT, ↓ fibrinogen, ↑ D-dimer.