Hemodynamic Disorders Overview

HEMODYNAMIC DISORDERS

• Hyperemia: Increased blood flow to an organ or tissue due to active dilation of arterioles. This can be physiological (exercise) or pathological (inflammation).

• Congestion: Increased venous flow and blood stasis in an organ due to venous outflow obstruction. This can be localized (e.g., strangulated hernia) or generalized (e.g., heart failure).

  • Acute localized venous congestion: Results from sudden obstruction of venous outflow (e.g., volvulus, intussusception).
  • Chronic localized venous congestion: Results from gradual obstruction (e.g., liver cirrhosis, pregnancy).
  • Acute generalized venous congestion: Increased venous pressure throughout the viscera (e.g., acute heart failure).
  • Chronic generalized venous congestion: Stagnation of venous blood in all organs and tissues due to various causes (e.g., cardiac issues, lung fibrosis). Results in hypoxia, cyanosis, and edema, as well as organ congestion (lungs, liver, spleen, kidneys).

EMBOLISM

• Definition: Intravascular insoluble solid, fluid, or gaseous mass circulating in the blood.

  • Types: Detached thrombi, fat (bone fractures), air (Caisson disease, lung/neck vein injury), amniotic fluid (labor), tumor cells, parasitic ova, foreign body.

• Fat embolism: Obstruction of arterioles and capillaries by fat globules, often caused by fractured long bones, extensive tissue trauma, or severe liver fatty change.

  • Effects: Depend on the size and quantity of fat globules. Can lead to pulmonary and systemic embolism and toxic effects of fatty acids on vascular endothelium.

• Air embolism: Obstruction of vascular flow by a large amount of air or gas (50-100 cc).

  • Causes: Air entering uterine blood vessels (abortion, obstructed labor), large neck veins (stab wounds), pleural sac (pneumothorax), uterine tube insufflation.
  • Effects: Small amounts are harmless; large amounts can impair heart action and be fatal.

AMNIOTIC FLUID EMBOLISM

• Definition: Introduction of amniotic fluid and its contents into maternal circulation through the utero-placental site.
• Pathogenesis: Often related to strong uterine contractions causing fetal membrane tears or placental vein rupture. Amniotic fluid components (meconium, lanugo, cells, mucin, fat) can mechanically obstruct maternal pulmonary circulation.
• Clinical features: Sudden respiratory distress, dyspnea, deep cyanosis, cardiogenic shock, convulsions, and sudden maternal death.

THROMBOSIS

• Definition: Formation of an insoluble mass of blood elements within the circulatory system during life.
• Predisposing factors: Inflammation of the vascular wall, changes in blood composition (thrombocytosis, polycythemia, dehydration, burns), and changes in blood stream (aneurysm).
• Mechanism of thrombus formation: Endothelial injury, hypercoagulability, and abnormal blood flow interact to form a thrombus.

ISCHEMIA

• Definition: Inadequate blood supply to an organ or tissue.
  • Types: Generalized (e.g., congestive heart failure) or localized (e.g., cardiac or renal ischemia).
  • Effects: Can lead to hypertension, chronic renal failure, angina pectoris, myocardial infarction, fainting, and cerebrovascular stroke.
  • Types: Acute (sudden complete arterial occlusion, e.g., embolism) or chronic (gradual incomplete occlusion, e.g., atherosclerosis).

INFARCTION

• Definition: Localized area of ischemic necrosis in an organ or tissue due to sudden cutting of its blood supply.
• Causes: Sudden arterial occlusion
• Gross picture: Wedge-shaped triangular area, apex at the site of occlusion.
• Microscopic: Only tissue framework remains after healing.
• Fate: Small infarcts resolve via macrophage fibrosis; large infarcts form fibrous capsules and may cause dystrophic calcification.

HEMORRHAGE

• Definition: Extravasation of blood outside the circulation.
  • Causes: Physiologic (menstruation) and Pathologic (trauma, spontaneous rupture, vasculitis, tumors, hemorrhagic blood diseases, vitamin deficiencies).
  • Mechanisms: Immediate blood pressure drop, local vasoconstriction (platelets, serotonin, thromboxane A2), clot plug formation, and healing.
  • Types: External (e.g., epistaxis), internal (e.g., hemothorax), interstitial (e.g., petechiae, ecchymosis, hematoma).
  • Effects: Local (clotting, organization, hemostasis); systemic (loss of blood volume, anemia, shock if acute and severe).

EDEMA

• Definition: Accumulation of fluid in interstitial tissue.
• Types: Generalized (e.g., cardiac, renal, nutritional, hepatic, allergic, inflammatory, lymphatic); or localised (e.g., inflammatory, lymphatic).
• Classification: Pitting (soft) edema (fluids displace on pressure); non-pitting (hard) edema (edema can't be displaced as it's part of the structure).

SHOCK

• Definition: Widespread hypoperfusion of tissues due to inadequate circulatory volume.
• Types: Primary (vasovagal), secondary (cardiogenic, hypovolemic, septic, anaphylactic).
• Nervous shock: Emotional stress, recovery typically occurs.
• Cardiogenic shock: Heart's inability to pump blood.
• Hypovolemic shock: Marked drop in blood pressure due to severe blood loss.
• Septic shock: Bacterial infection with endotoxin release.
• Anaphylactic shock: Allergic reaction to antigen (e.g., medication).

COMPENSATORY MECHANISMS IN SHOCK

• Vasoconstriction of skin and visceral blood vessels: Dilates cerebral & coronary vessels to maintain blood flow to vital organs.
• Hypoxia: Stimulation of respiratory center to promote hyperventilation.

CLINICAL STAGES OF SHOCK

• Compensatory stage: Compensatory mechanisms control blood pressure, recovery occurs.
• Decompensated stage: Failure of compensatory mechanisms, marked drop in blood pressure and ischemia. With appropriate interventions, this stage is potentially reversible.
• Irreversible stage: All therapeutic efforts fail to control the condition leading to death.