Concise Notes on Hemodynamic Disorders

Hemodynamic Disorders

Objectives

  • Edema: Definition, types, pathogenesis, morphology.
  • Hyperemia and congestion: Definition, pathogenesis, morphology.
  • Hemorrhage: Definition, clinical presentation. Types of brain hemorrhage.
  • Thrombosis: Definition, pathogenesis, gross and microscopic morphology.
  • Differences between venous and arterial thrombus.
  • Differences between antemortem and postmortem thrombus.
  • Fate of thrombus.
  • Embolism: Definition, pathogenesis, gross and microscopic morphology.
  • Infarct: Definition. Classification. Gross and microscopic morphology.

Cardiovascular Diseases

  • Leading cause of death worldwide (17.9 million lives each year).
  • Include: coronary heart disease, cerebrovascular disease, and rheumatic heart disease.
  • Major causes of death: coronary heart disease and stroke.
  • One-third of these deaths occur prematurely in people under the age of 70.

Disorders of Hemodynamics

  • Edema, congestion, and shock.
  • Hemostasis: Hemorrhage and thrombosis
  • Embolism

Body Water Composition

  • Water content varies by organ and individual characteristics (age, sex).
  • Kidneys regulate water balance (2.0-2.5 liters/day output).

Starling Forces

  • Hydrostatic pressure: Pushes fluid out of capillaries.
  • Plasma colloid osmotic pressure: Pulls fluid into capillaries.
  • Lymphatics: Collect excess interstitial fluid and return it to circulation.

Edema

  • Definition: Accumulation of interstitial fluid within tissues or body cavities.

Causes of Edema

  1. Increased hydrostatic pressure:
    • Impaired venous return (e.g., congestive heart failure, constrictive pericarditis).
    • Arteriolar dilation.
  2. Reduced plasma osmotic pressure (hypoproteinemia):
    • Protein-losing glomerulopathies, liver cirrhosis, malnutrition.
  3. Sodium retention:
    • Excessive salt intake, increased tubular reabsorption.
  4. Lymphatic obstruction:
    • Inflammatory, neoplastic, postsurgical, radiation therapy.
  5. Inflammation:
    • Acute, chronic; angiogenesis.

Pathophysiology of Edema

  • Heart failure: Increased capillary hydrostatic pressure.
  • Malnutrition/Hepatic synthesis/Nephrotic syndrome: Decreased plasma albumin.
  • Renal failure: Sodium and water retention; increased blood volume.
  • Lymphatic obstruction: Impaired fluid drainage.

Edema Types

  • Local edema: Result of vascular effects of inflammation.
  • Generalized edema: Affects visceral organs and skin (heart failure, nephrotic syndrome).
  • Anasarca: Extreme generalized edema.

Edema in Body Cavities

  • Hydropericardium: Pericardial effusion.
  • Hydroperitoneum (ascites): Peritoneal effusion.
  • Hydrothorax: Pleural effusion.

Gross Morphology of Edema

  • Subcutaneous edema: Diffuse, accumulates in dependent areas (legs, sacrum).
  • Pitting edema: Finger pressure leaves a depression.
  • Pulmonary edema: Heavy lungs with frothy, blood-tinged fluid.
  • Brain edema: Softer consistency, larger size, flattened gyri, slit-like ventricles.

Brain Edema

  • Can be localized or generalized.
  • Gross Morphology:
    • Softer consistency
    • Larger size
    • Heavier weight
    • Flattened gyri
    • Narrowed sulci
    • Slit-like ventricles

Microscopic Morphology of Brain Edema

  • Dilation of perivascular and cellular spaces.
  • Vacuolated appearance of gray matter.

Brain Herniations

  • Displacement of brain tissue due to increased intracranial pressure.
  • Causes:
    • Space-occupying lesions (tumors, hematomas, abscesses).
    • Cerebral edema (trauma, stroke, encephalitis).
    • Hydrocephalus.

Types of Brain Herniations

  • Subfalcine herniation: Cingulate gyrus under the falx cerebri.
  • Transtentorial (uncal) herniation: Temporal lobe uncus through the tentorium.
  • Tonsillar herniation: Cerebellar tonsils through the foramen magnum.

Microscopy of Edema

  • Clearing and separation of extracellular matrix elements.

Hyperemia and Congestion

  • Hyperemia: Active process; arteriolar dilation & increased blood inflow (e.g., exercise).
  • Congestion: Passive process; impaired venous outflow (e.g., cardiac failure, venous obstruction).

Gross Morphology of Hyperemia/Congestion

  • Wet cut surfaces oozing blood.

Microscopic Morphology of Hyperemia/Congestion

  • Acute pulmonary congestion: Blood-engorged alveolar capillaries, alveolar edema.
  • Chronic pulmonary congestion: Thickened septa, hemosiderin-laden macrophages ("heart failure cells").
  • Chronic passive congestion of the liver: "Nutmeg liver"; centrilobular necrosis & hemorrhage.

Hemorrhage

  • Extravasation of blood from vessels due to damage or defective clot formation.

Clinical Consequences of Hemorrhage

  • External hemorrhage or hematoma (localized collection of blood).
  • Body cavity effusions: hemothorax, hemopericardium, hemoperitoneum.
  • Petechiae: Minute hemorrhages (1-2 mm).
  • Purpura: Slightly larger hemorrhages (3-5 mm).
  • Ecchymoses: Larger subcutaneous hematomas (1-2 cm).

Clinical Significance of Hemorrhage

  • Depends on volume, speed, and localization.

Types of Brain Hemorrhage

  • Epidural hematoma: Between skull and dura mater.
  • Subdural hematoma: Under the dura mater.
  • Subarachnoid hemorrhage: Between pial and arachnoid membranes.
  • Intracerebral hemorrhage: Within brain tissue.

Thrombosis

  • Formation of a clotted mass of blood within the cardiovascular system in a living organism.
  • Consequence of inappropriate activation of normal hemostasis.

Pathogenesis of Thrombosis (Virchow's Triad)

  1. Endothelial injury
  2. Abnormal blood flow (stasis or turbulence)
  3. Hypercoagulability

Endothelium

  • Inner lining of blood vessels, controls blood fluidity, platelet aggregation, and vascular tone.
  • Regulates immunology, inflammation, and angiogenesis.

Endothelial Injury

  • Physical damage leading to subendothelial ECM exposure, platelet aggregation and tissue factor release.

Endothelial Cell Dysfunction

  • Altered balance of thrombotic and antithrombotic activity.
  • Causes: Hypercholesterolemia, homocystinemia, toxins, bacterial endotoxins, radiation damage.

Abnormal Blood Flow

  • Turbulence or stasis leading to endothelial dysfunction.
  • Causes countercurrents and local stasis pockets of blood.

Effects of Turbulence and Stasis

  • Endothelial cell activation, enhanced procoagulant activity, changes in gene expression.
  • Platelet and leukocyte interaction with endothelium.
  • Reduced washout of clotting factors and impeded inflow of inhibitors.

Clinical Settings of Abnormal Blood Flow

  • Ulcerated atherosclerotic plaques: Turbulence.
  • Aneurysms: Stasis.
  • Acute myocardial infarction: Ventricular remodeling causes aneurysms and stasis.
  • Mitral valve stenosis: Atrial dilation with stasis.
  • Hyperviscosity syndromes: Increased resistance to blood flow and stasis.

Hypercoagulability

  • Abnormally high tendency of blood to clot.

Causes

  • Genetic mutations.
  • Acquired conditions: prolonged bed rest, myocardial infarction, cancer.

Hypercoagulable States: Primary (Genetic)

  • Common: Factor V Leiden mutation, prothrombin mutation.
  • Rare: Antithrombin III, protein C, or protein S deficiency.

Hypercoagulable States: Secondary (Acquired)

  • High Risk: Prolonged bed rest, myocardial infarction, cancer, antiphospholipid antibody syndrome.
  • Lower Risk: Cardiomyopathy, nephrotic syndrome, hyperestrogenic states, smoking.

Thrombi Morphology

  • Focally attached to vascular surface.
  • Arterial thrombi grow retrograde; venous thrombi extend in blood flow direction.
  • Lines of Zahn: Laminations of pale platelet/fibrin layers alternating with darker red cell layers.
  • Mural thrombi: Occur in heart chambers or aorta.

Arterial vs. Venous Thrombi

  • Arterial: Mainly platelets & fibrin; caused by endothelial injury.
  • Venous: Mainly red blood cells & fibrin; caused by stasis & hypercoagulability.

Microscopic Morphology of Thrombi

  • Lines of Zahn with layers of fibrin, red blood cells, leukocytes, and platelets.

Postmortem Clot

  • Not attached to vessel wall, gelatinous consistency, no lines of Zahn.

Antemortem vs. Postmortem Thrombus

  • Antemortem: Firm, attached to vessel wall, lines of Zahn.
  • Postmortem: Gelatinous, not attached, no lines of Zahn.

Fate of Thrombus

  • Resolution: Thrombus may be removed by fibrinolytic activity.
  • Propagation: Thrombus enlarges.
  • Thromboembolism: Thrombus detaches and travels elsewhere.
  • Organization: Ingrowth of cells into thrombus to produce scar tissue, and recanalization, which is the re-establishment of a blood flow channel.

Embolism

  • A detached intravascular solid, liquid, or gaseous mass carried by blood to a distant site causing dysfunction or infarction.

Types of Emboli

  • Thromboemboli (most common).
  • Fat droplets.
  • Air or nitrogen bubbles.
  • Atherosclerotic debris (cholesterol emboli).
  • Tumor fragments.
  • Bone marrow.
  • Amniotic fluid.

Pulmonary Thromboembolism

  • Originate from deep venous thromboses (usually from deep leg veins proximal to the popliteal fossa).

Clinical Significance of Pulmonary Embolus

  • Small: Clinically silent.
  • Medium: Pulmonary hemorrhage.
  • Large: Sudden death.
  • Multiple: Pulmonary hypertension and right ventricular failure (cor pulmonale).
  • Saddle embolus: Straddles the arterial bifurcation, blocking both arterial branches to the lungs.

Fat Embolism

  • Fat emboli in the bloodstream, often after long bone fractures.

Fat Embolism Syndrome

  • Multisystem dysfunction; complication of skeletal trauma/orthopedic surgery.

Pathogenesis of Fat Embolism Syndrome

  • Mechanical obstruction and biochemical injury (free fatty acids damage pneumocytes; toxic endothelial injury).

Amniotic Fluid Embolism

  • Amniotic fluid enters maternal circulation during labor/postpartum.

Air Embolism

  • Air or gas bubbles block blood vessels.
  • Causes: Neurosurgery, obstetric/laparoscopic procedures, chest wall injury, scuba diving, rapid ascent in unpressurized aircraft.

Infarction

  • Area of ischemic necrosis caused by occlusion of vascular supply.

Causes of Infarction

  • Major: Arterial thrombosis and embolism.
  • Minor: Vasospasm, atheroma expansion, extrinsic compression.

Factors Affecting Infarct Formation

  • Anatomy of vascular supply.
  • Rate of occlusion.
  • Tissue vulnerability to hypoxia.

Infarct Classification

  • Based on color and presence/absence of microbial infection.
    • Red (hemorrhagic).
    • White (anemic).
    • Bland.
    • Septic.

White Infarcts

  • Arterial occlusions in solid organs (heart, kidneys, spleen).
  • Wedge-shaped with occluded vessel at apex.

Red Infarcts

  • Occur in venous occlusions, loose tissues, dual circulations, congested tissues, or after flow reestablishment.

Septic Infarct

  • Infected cardiac valve vegetations embolize; microbes seed necrotic tissue.
  • Evolution: Abscess, healing by organization and fibrosis.