Hemodynamic Disorders PDF

EMBOLISM & INFARCTION  EMBOLISM  An embolus is an intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin.  The vast majority of emboli derive from a dislodged thrombus hence the term thromboembolism....

EMBOLISM & INFARCTION  EMBOLISM  An embolus is an intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin.  The vast majority of emboli derive from a dislodged thrombus hence the term thromboembolism.  Inevitably, emboli lodge in vessels too small to permit further passage, resulting in partial or complete vascular occlusion.  The primary consequence of systemic embolization is ischemic necrosis (infarction) of downstream tissues.  Pulmonary Thromboembolism  In greater than 95% of cases, venous emboli originate from thrombi within deep leg veins.  Fragmented thrombi from DVTs are carried through progressively larger channels and usually pass through the right side of the heart before arresting in the pulmonary vasculature.  Depending on size, a PE can occlude: 1. The main pulmonary artery. 2. Lodge at the bifurcation of the right and left pulmonary arteries (saddle embolus). 3. Pass into the smaller, branching arterioles.  The major clinical and pathologic features PE are: 1. Most pulmonary emboli (60% to 80%) are small and clinically silent. Undergo organization and become incorporated into the vascular wall. 2. A large embolus that blocks a major pulmonary artery can cause sudden death. 3. Embolic obstruction of medium-sized arteries and subsequent rupture of capillaries can cause pulmonary hemorrhage. 4. Embolism to small end-arteriolar pulmonary branches usually causes infarction.  Systemic Thromboembolism  (80%) of systemic emboli arise from intracardiac mural thrombi.  Two thirds are associated with left ventricular infarcts  25% with dilated left atria.  The remainder originate from aortic aneurysms, thrombi overlying ulcerated atherosclerotic plaques.  By contrast with venous emboli, which lodge primarily in the lung, common arteriolar embolization sites include :  Lower extremities (75%)  central nervous system (10%).  The consequences of embolization depend on the caliber of the occluded vessel, the collateral supply, and vulnerability of the affected tissue’s to anoxia.  Other types of emboli  Fat Embolism: Soft tissue crush injury or rupture of marrow vascular sinusoids (long bone fracture) releases microscopic fat globules into the circulation.  Fat embolism syndrome characterized by pulmonary insufficiency, neurologic symptoms, anemia, thrombocytopenia, and a diffuse petechial rash, which is fatal in 10% of cases.  Thepathogenesis of fat emboli syndrome involves both mechanical obstruction and biochemical injury.  Fat microemboli occlude pulmonary and cerebral microvasculature, both directly and by triggering platelet aggregation (mechanical).  This deleterious effect is exacerbated by fatty acid release from lipid globules, which causes local toxic endothelial injury (biochemical injury).  Platelet activation and granulocyte recruitment complete the vascular assault.  Amniotic Fluid Embolism: this is, grave complication of labor and the immediate postpartum period.  The mortality rate approaches 80%, making it the most common cause of maternal death in the developed world.  Onset is characterized by sudden severe dyspnea, cyanosis, and hypotensive shock, followed by seizures and coma.  The underlying cause is entry of amniotic fluid (and its contents) into the maternal circulation via tears in the placental membranes and/or uterine vein rupture.  Histologic analysis reveals squamous cells shed from fetal skin, fat from vernix caseosa, and mucin derived from the fetal respiratory or gastrointestinal tracts in the maternal pulmonary microcirculation  Air Embolism: Gas bubbles within the circulation can coalesce and obstruct vascular flow and cause distal ischemic injury.  Small venous gas emboli generally have no deleterious effects, some exceptions.  Sufficient air can enter the pulmonary circulation inadvertently during obstetric procedures or as a consequence of a chest wall injury to cause hypoxia, and very large venous emboli may arrest in the heart and cause death.  INFARCTION  An infarct is an area of ischemic necrosis caused by occlusion of the vascular supply to the affected tissue.  Arterial thrombosis or arterial embolism underlies the vast majority of infarctions.  Less common causes of arterial obstruction include: Vasospasm, expansion of an atheroma secondary to intraplaque hemorrhage, and extrinsic compression of a vessel, such as by tumor, a dissecting aortic aneurysm.  Other causes are vessel twisting (e.g., in testicular torsion or bowel volvulus) and entrapment in a hernia sac.  MORPHOLOGY  Infarcts are classified on the basis of their color (reflecting the amount of hemorrhage) 1. Infarcts may be either red (hemorrhagic) 2. White (anemic)  The presence or absence of microbial infection in to: 1. Septic infarct. 2. Bland infarct.  Red infarcts This occur in the following cases 1. Venous occlusions (such as in ovarian torsion). 2. In tissues with dual circulations such as lung and small intestine, where partial, inadequate perfusion by collateral arterial supplies is typical. 3. In previously congested tissues (as a consequence of sluggish venous outflow) 4. When flow is reestablished after infarction has occurred (e.g. after angioplasty of an arterial obstruction).  White infarcts  This type occur with arterial occlusions in solid organs with end- arterial circulations (e.g., heart, spleen, and kidney).  Infarcts tend to be wedge-shaped, with the occluded vessel at the apex and the organ periphery forming the base.  The main histologic finding associated with infarcts is ischemic coagulative necrosis.  An inflammatory response begins in the margins of infarcts within a few hours and usually is well defined within 1 to 2 days.  Eventually, inflammation is followed by either regeneration or repair by fibrous tissue and scar formation.  The brain is an exception to these generalizations: Ischemic tissue injury in the central nervous system results in liquefactive necrosis.  Septic infarctions occur when infected cardiac valve vegetations embolize, or when microbes seed necrotic tissue. In these cases the infarct is converted into an abscess.  Factors That Influence Infarct Development.  Degree of tissue infarction depend on the following factors: 1. Anatomy of the vascular supply: tissue of dual circulation like lung, liver and intestine are less vulnerable to infarction. 2. Rate of occlusion: Slowly developing occlusions are less likely to cause infarction because they allow time for the development of collateral blood supplies. 3. Tissue vulnerability to ischemia: Neurons undergo irreversible damage when deprived of their blood supply for only 3 to 4 minutes. Myocardial cells die after only 20 to 30 minutes. While, fibroblasts within myocardium remain viable after many hours of ischemia. Thank you