Lecture 7 Hemodynamic Disorders II - University of Al-Ameed, 2024-2025 PDF

University of Al-Ameed College of Medicine Department of pathology and forensic medicine 3rd year / 2024-2025 Lecture 7 Hemodynamic disorders II Professor Dr. Rahem M. R. Hemodynamic disorders include: 1. Hyperemia and congestion 2. Edema 3. Th...

University of Al-Ameed College of Medicine Department of pathology and forensic medicine 3rd year / 2024-2025 Lecture 7 Hemodynamic disorders II Professor Dr. Rahem M. R. Hemodynamic disorders include: 1. Hyperemia and congestion 2. Edema 3. Thrombosis 4. Hemorrhage 5. Embolism 6. Infarction 7. Shock Hemorrhage  Hemorrhage: the extravasation of blood from vessels. The risk of hemorrhage is increased in a wide variety of clinical disorders collectively called hemorrhagic diatheses or bleeding disorders. Bleeding disorders caused by inherited or acquired defects in: o Blood vessel o Platelets o Coagulation factors o Other causes  Examples of bleeding manifestations Petechiae Ecchymosis Hematoma Hemarthrosis Conjunctival Gum bleeding Epistaxis hemorrhage Any simple bleeding may be a presentation to dangerous disorder.  The clinical significance of any particular hemorrhage depends on 1. Volume of blood that is lost 2. Rate of bleeding 3. Site of hemorrhage (brain) 4. Chronic or recurrent external blood loss (e.g., due to peptic ulcer or menstrual bleeding) EMBOLISM EMBOLISM An embolus is a detached intravascular solid, liquid, or gaseous mass that is carried by the blood from its point of origin to a distant site, where it often causes tissue dysfunction or infarction. The vast majority of emboli derive from a dislodged thrombus. I. Pulmonary Thromboembolism II. Systemic Thromboembolism Less commonly, emboli are composed of: 1. Fat droplets. 2. Amniotic fluid. 3. Bubbles of air or nitrogen. 4. Atherosclerotic debris (cholesterol emboli). 5. Bits of bone marrow. 6. Tumor fragments. I. Pulmonary Thromboembolism Pulmonary emboli originate from (deep vein thrombosis) DVT in more than 95% of cases. The thrombi within deep leg veins proximal to the popliteal fossa. Embolization from lower leg thrombi is uncommon. Fragmented thrombi from DVTs are carried through progressively larger channels, pass through the right side of the heart then arresting in the pulmonary vasculature.  The clinical and pathologic features of PE: Depending on site and size of emboli 1. Most pulmonary emboli (60%–80%) are small and clinically silent. 2. A large embolus can cause sudden death. 3. Embolic obstruction of medium-sized arteries can cause pulmonary hemorrhage. 4. Embolism to small end-arteriolar pulmonary branches usually causes infarction. 5. Multiple emboli occurring through time can cause pulmonary hypertension and right ventricular failure (cor pulmonale). II. Systemic Thromboembolism Most systemic emboli arise from intracardiac mural thrombi. Mostly associated with left ventricular infarcts. The remainder originate from: 1. Aortic aneurysms. 2. Atherosclerotic plaques. 3. Valvular vegetations. 4. Venous system (paradoxical emboli). Common arteriolar embolization sites in the lower extremities (75%). Can be to central nervous system, Intestines, kidneys, and spleen.  The consequences of embolization depend on: 1. The caliber of the occluded vessel. 2. The collateral supply. 3. The affected tissue’s vulnerability to anoxia. Arterial emboli often lodge in end arteries and cause infarction. Venous emboli lodge primarily in the lung. Arterial emboli can travel anywhere. III. Fat Embolism Microscopic fat globules release into the circulation due to: 1. Long bone and pelvis fractures and severe skeletal injuries. 2. Soft tissue injury and burn Main clinical findings: Respiratory insufficiency (Fat micro-emboli occlude pulmonary BV). Cerebral symptoms (Fat micro-emboli occlude cerebral BV). A diffuse petechial rash (Thrombocytopenia and endothelial injury). Because lipids are dissolved by the solvents used during tissue processing, microscopic demonstration of fat micro globules requires specialized techniques (frozen sections and fat stains). Fat and bone marrow embolus The embolus is composed of hematopoietic marrow and marrow fat cells (clear spaces) attached to a thrombus. III. Amniotic Fluid Embolism It is an uncommon. May occur at labor or immediate postpartum period with high mortality rate. The underlying cause is the entry of amniotic fluid into the maternal circulation via tears in the placental membranes and/or uterine vein rupture. The morbidity and mortality in such cases results from biochemical activation of substances in the amniotic fluid to: 1. The coagulation system. 2. The innate immune system. Onset is characterized by sudden severe dyspnea, cyanosis, and hypotensive shock, followed by seizures and coma. Amniotic fluid embolism Two small pulmonary arterioles are packed with laminated swirls of fetal squamous cells. The surrounding lung is edematous and congested. IV. 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. A sufficient air can enter the pulmonary circulation during: 1. Obstetric procedures. 2. Laparoscopic procedures. 3. A chest wall injury 4. Decompression sickness: Is caused by sudden changes in atmospheric pressure. INFARCTION INFARCTION An infarct: is an area of ischemic necrosis caused by occlusion of the vascular supply to the affected tissue. Examples of infarction: 1. Infarction primarily affecting the heart and the brain is a common and extremely important cause of clinical illness. 2. Pulmonary infarction is a common clinical complication. 3. Bowel infarction often is fatal. 4. Ischemic necrosis of distal extremities (gangrene) causes substantial morbidity in the diabetic population. Causes of infarction: Arterial obstruction in the vast majority of cases like: 1. Arterial thrombosis or arterial embolism. 2. Less common vasospasm. 3. Expansion of an atheroma secondary to intraplaque hemorrhage. 4. Extrinsic compression of a vessel, such as by tumor. 5. Dissecting aortic aneurysm 6. Edema within a confined space. uncommon causes of tissue infarction include: 1. Vessel twisting (e.g., in testicular torsion or bowel volvulus) 2. Traumatic vascular rupture 3. Entrapment in a hernia sac. Infarcts caused by venous thrombosis usually occur only in organs with a single efferent vein (e.g., testis or ovary). Morphology of infarction: Infarcts are classified based on: 1. Color (reflecting the amount of hemorrhage) A. Red (hemorrhagic) B. White (anemic) 2. The presence or absence of microbial infection. A. Septic B. Bland Red infarcts occur: 1. As a result of venous occlusions (ovarian torsion). 2. In loose tissues (e.g., lung) where blood can collect in infarcted zones. 3. In tissues with dual circulations such as lung and small intestine, where partial, or adequate perfusion by collateral arterial supplies is typical. 4. In previously congested tissues (as a consequence of sluggish venous outflow). 5. When flow is re-established after infarction has occurred (e.g., after angioplasty of an arterial obstruction). Lung Brain Gut Liver Ovary Testis Lung Intestine Brain Testis White infarcts occur: 1. As a result of arterial occlusions 2. In solid organs 3. In organ with end-arterial circulations (e.g., heart, spleen, and kidney). 4. Where tissue density limits the seepage of blood from adjoining patent vascular beds. ▪ Infarcts tend to be wedge shaped. ▪ With the occluded vessel at the apex. ▪ The organ periphery forming the base. ▪ Lateral margins may be irregular, reflecting flow from adjacent vessels. Kidney Heart Spleen Spleen Kidney Heart  The margins of acute infarcts typically are indistinct and slightly hemorrhagic. With time, the edges become better defined by a narrow rim of hyperemia attributable to inflammation. Infarcts resulting from arterial occlusions in organs without a dual circulation typically become progressively paler and more sharply defined with time. By comparison, hemorrhagic infarcts are the rule in the lung and other spongy organs. The main histologic finding associated with infarcts is ischemic coagulative necrosis.  An inflammatory response begins to develop along the margins of infarcts within a few hours and usually is well defined within 1-2 days. Eventually, inflammation is followed by repair, beginning in the preserved margins. Most infarcts, however, are ultimately replaced by scar. The brain is an exception; ischemic tissue injury in the central nervous system results in liquefactive necrosis. Septic infarct is occur when: 1. Infected cardiac valve vegetations embolize, or when 2. Microbes seed necrotic tissue. In these cases the infarct is converted into an abscess, with a greater inflammatory response and healing by organization and fibrosis. Factors That Influence Infarct Development The effects of vascular occlusion range from inconsequential to tissue necrosis leading to organ dysfunction and sometimes death. The range of outcomes is influenced by the following three variables: 1. Anatomy of the vascular supply: The presence or absence of an alternative blood supply is the most important factor. (lung: pulmonary & bronchial arteries) (liver: hepatic a. & portal v.) and (hands & forearm: ulnar & radial aa) all are resistant to infarction. By contrast, the kidney and the spleen both have end-arterial circulations, and arterial obstruction generally leads to infarction in these tissues. 2. Rate of occlusion: Slowly developing occlusions are less likely to cause infarction because they allow time for the development of collateral blood supplies. For example, small inter-arteriolar anastomoses, interconnect the three major coronary arteries. If one coronary artery is slowly occluded (e.g., by atherosclerotic plaque), flow in this collateral circulation may increase sufficiently to prevent infarction—even if the original artery becomes completely occluded. 3. Tissue vulnerability to hypoxia: Neurons undergo irreversible damage when deprived of their blood supply for only 3-4 minutes. Myocardial cells, although hardier than neurons, still die after only 20 to 30 minutes of ischemia. By contrast, fibroblasts within myocardium remain viable after many hours of ischemia SHOCK SHOCK: is an acute circulatory failure resulting in inadequate organ perfusion and cellular hypoxia. At the outset, the cellular injury is reversible. Prolonged shock eventually leads to irreversible tissue injury and is often fatal. Three major types of shock are: I. Cardiogenic shock: Results from low cardiac output as a result of myocardial pump failure. Clinical examples: Infarction, arrhythmias, cardiac tamponade, pulmonary embolism. II. Hypovolemic shock: Results from in adequate blood or plasma volume. Clinical examples: hemorrhage, vomiting, diarrhea, burn, trauma. III. Septic shock: Result from sever microbial infection which release some products that lead to different pathophysiological changes with end results of multiorgan failure. is triggered by microbial infections (Gram +ve, Gram –ve and fungi) and is associated with severe systemic inflammatory response syndrome (SIRS). These cardiovascular abnormalities result in tissue hypoperfusion, cellular hypoxia, and metabolic derangements.  Pathogenesis of Septic Shock M.O. infection Release of microbs derive products Factor 12 procoagulant Endothelial Complement Neutrophils and monocytes activation activation activation activation Release of mediators: C3a TNF, IL-1 Microvascular thrombus Fever C3b C-reactive protein DIC C5a Procalcitonin Prostaglandins Platelet-activating factor (PAF) ROS: Reactive O2 species nitric oxide (NO) Vasodilatation Multiorgan failure Increase vascular permeability and edema Decrease tissue perfusion Hypotension Other types of shock are: IV. Neurogenic shock : Less commonly. Shock can result from a loss of vascular tone associated with: 1. anesthesia or 2. secondary to a spinal cord injury. V. Anaphylactic shock: Results from systemic vasodilation and increased vascular permeability. Triggered by an immunoglobulin E–mediated hypersensitivity reaction. Clinical course In hypovolemic and cardiogenic shock, the patient presents with: 1. hypotension 2. a weak, rapid pulse 3. tachypnea 4. cool, clammy, cyanotic skin. In septic shock, however, the skin may be warm and flushed as a result of peripheral vasodilation. Stages of Shock: I. Compensatory stage: During which reflex compensatory mechanisms are activated and vital organ perfusion is maintained. II. Progressive stage: Characterized by tissue hypoperfusion Onset of worsening circulatory and metabolic derangement, including acidosis. III. Irreversible stage: In which cellular and tissue injury is so severe that even if the hemodynamic defects are corrected, survival is not possible. Good Luck