Hemodynamic Disorders

Hemodynamic Disorders

1. Hemodynamic Disorders Dr. Hadi Munib Oral and maxillofacial surgery resident

2. Outline Hyperemia and Congestion Edema Hemorrhage Hemostasis and Thrombosis Embolism Infarction Shock References

3. Introduction The health of cells and tissues depends on the circulation of blood, which delivers oxygen and nutrients and removes wastes generated by cellular metabolism. Often disturbed by Pathologic processes Hemostasis is the process of blood clotting that prevents excessive bleeding after blood-vessel damage. Inadequate hemostasis may result in hemorrhage Which can compromise regional tissue perfusion and if massive and rapid, may lead to hypotension, shock, and death

4. Hyperemia and Congestion Both refer to an increase in blood volume within a tissue, but have different mechanisms. Hyperemia is an active process resulting from arteriolar dilation and increased blood inflow [inflammation or in exercising skeletal muscle]. More reddish than normal tissues Congestion is a passive process resulting from impaired outflow of venous blood from a tissue. It can occur systemically, as in cardiac failure, or locally as a consequence of an isolated venous obstruction Cyanosis; Blue-Red colour due to accumulation of deoxygenated Blood

5. Liver Hemorrhage Necrosis

6. Edema Approximately 60% of lean body weight is water. Two thirds of which is intracellular. Most of the remaining water is found in extracellular compartments in the form of interstitial fluid. Only 5% of the body’s water is in blood plasma. Edema is an accumulation of interstitial fluid within tissues. Effusion: Extravascular fluid can also collect in body cavities. Hydrothorax; Effusions in the pleural cavity Hydropericardium ; effusions in the pericardial cavity Hydroperitoneum - Ascites; effusions in the peritoneal cavity

7. Edema Anasarca is severe, generalized colloid typically is a protein-poor transudate; by contrast, because of increased vascular permeability, inflammatory edema fluid is a protein-rich exudate with a high specific gravity.

8. Increased Hydrostatic Pressure

9. Reduced Plasma Osmotic Pressure

10. Hemorrhage Defined as the extravasation of blood from vessels Most often the result of damage to blood vessels or defective clot formation. Trauma, atherosclerosis, or inflammatory or neoplastic erosion of a vessel wall also may lead to hemorrhage. The risk of hemorrhage (often after a seemingly insignificant injury) is increased in a wide variety of clinical disorders collectively called hemorrhagic diatheses Hematoma; External Hemorrhage within tissues which ranges in significance from trivial (e.g., a bruise) to fatal. Hemothorax , Hemopericardium , Hemoperitoneum , or hemarthrosis (in joints)

11. Hemorrhage Petechiae are minute (1 to 2 mm in diameter) hemorrhages into skin, mucous membranes, or serosal surfaces [Platelet Defective function, Thrombocytopenia, Vitamin C Deficiency] Purpura are slightly larger (3 to 5 mm) hemorrhages [Petechiae causes, as well as trauma, vascular inflammation (vasculitis), and increased vascular fragility] Ecchymosis are larger (1 to 2 cm) subcutaneous hematomas (colloquially called bruises). [Enzymatic conversion of hemoglobin (red - blue color) to bilirubin (blue-green color) and eventually hemosiderin (golden-brown)] Amount of Blood lost [<20% blood volume loss]

12. Hemostasis vs. Thrombosis Normal hemostasis comprises a series of regulated processes that culminate in the formation of a blood clot that limits bleeding from an injured vessel. The pathologic counterpart of hemostasis is thrombosis, the formation of blood clot (thrombus) within non-traumatized, intact vessels.

13. Normal Hemostasis A precisely orchestrated process involving platelets, clotting factors, and endothelium that occurs at the site of vascular injury. Culminates in the formation of a blood clot, which serves to prevent or limit the extent of bleeding. Primary Hemostasis; vWF and Platelets  Primary Hemostatic Plug Secondary Hemostasis; Clotting Factors Tertiary Hemostasis; Clot Resorption Endothelial cells are central regulators of hemostasis; the balance between the anti- thrombic and prothrombotic activities of endothelium determines whether thrombus formation, propagation, or dissolution occurs.

14. Thrombosis The primary abnormalities that lead to intravascular thrombosis are Endothelial injury Stasis or turbulent blood flow; chaotic blood flow contributes to arterial and cardiac thrombosis by causing endothelial injury or Dysfunction Hypercoagulability of the blood “Virchow triad”

15. Hypercoagulability Abnormally high tendency of the blood to clot, and is typically caused by alterations in coagulation factors. Primary (inherited) hypercoagulability is most often caused by mutations in the factor V and prothrombin genes: Approximately 2% to 15% of whites carry a specific factor V mutation (Leiden mutation) Among those with recurrent deep venous thrombosis (DVT), the frequency of this mutation approaches 60%.

16. Embolism An embolus is a detached intravascular solid, liquid, or gaseous mass that is carried by the blood to a distant site, where it causes tissue dysfunction or infarction. Thromboembolism; The vast majority of emboli derive from a dislodged thrombus The primary consequence of systemic embolization is ischemic necrosis ( infarction ) of downstream tissues Whereas embolization in the pulmonary circulation leads to hypoxia, hypotension, and right-sided heart failure.

17. Pulmonary Thromboembolism Pulmonary emboli originate from deep venous thromboses Are responsible for the most common form of thromboembolic disease. The incidence 2 to 4 per 1000 hospitalized patients. Most pulmonary emboli (60%–80%) are small and clinically silent. A large embolus that blocks a major pulmonary artery can cause sudden death. Embolic obstruction of medium-sized arteries and subsequent rupture of downstream capillaries rendered anoxic can cause pulmonary hemorrhage. Embolism to small end-arteriolar pulmonary branches usually causes infarction. Multiple emboli occurring through time can cause pulmonary hypertension and right ventricular failure ( cor pulmonale ).

18. Systemic Thromboemboli (80%) arise from intra-cardiac mural thrombi; Two-thirds of these are associated with left ventricular infarcts 25% with dilated left atria The remainder originate from aortic aneurysms, thrombi overlying ulcerated atherosclerotic plaques, fragmented valvular vegetations or the venous system 10% to 15% of systemic emboli are of unknown origin. Arterial emboli can travel virtually anywhere; their final resting place understandably depends on their point of origin and the relative flow rates of blood to the downstream tissues.

19. Systemic Thromboembolism Common arteriolar embolization sites include the lower extremities (75%) and central nervous system (10%). Intestines, kidneys, and spleen are less common targets. The consequences of embolization depend on the caliber of the occluded vessel, the collateral supply, and the affected tissue’s vulnerability to anoxia. Arterial emboli often lodge in end arteries and cause infarction.

20. Infarction An infarct is an area of ischemic necrosis caused by occlusion of the vascular supply to the affected tissue. Infarction primarily affect the heart and the brain Roughly 40% of all deaths in the United States are a consequence of cardiovascular disease, with most of these deaths stemming from myocardial or cerebral infarction. Pulmonary infarction is a common clinical complication, bowel infarction often is fatal, and ischemic necrosis of distal extremities ( gangrene )

21. Infarction 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. Infarcts are classified based on their color (reflecting the amount of hemorrhage) and the presence or absence of microbial infection. May be either red (hemorrhagic) or white (anemic) and may be either septic or bland.

22. Three Types of Shock

23. Definition A state in which diminished cardiac output or reduced effective circulating blood volume impairs tissue perfusion and leads to cellular hypoxia. At the outset, the cellular injury is reversible. Prolonged shock eventually leads to irreversible tissue injury and is often fatal. Cardiogenic shock results from low cardiac output as a result of myocardial pump failure. Caused by myocardial damage (infarction), ventricular arrhythmias, extrinsic compression (cardiac tamponade) or outflow obstruction Hypovolemic shock results from low cardiac output due to loss of blood or plasma volume

24. Definition Septic shock is triggered by microbial infections and is associated with severe systemic inflammatory response syndrome (SIRS). SIRS may be triggered by a variety of insults, including burns, trauma, and/or pancreatitis. Massive outpouring of inflammatory mediators from innate and adaptive immune cells that produce arterial vasodilation, vascular leakage, and venous blood pooling.

25. Septic Shock Responsible for 2% of all hospital admissions in the United States. Of these, 50% require treatment in intensive care units. Incidence is rising due to growing ranks of immunocompromised hosts (because of chemotherapy, immunosuppression, advanced age, or HIV infection) The increasing prevalence of multi drug resistant organisms in the hospital setting. The mortality remains at a staggering 20% to 30%. Septic shock is most frequently triggered by gram positive bacterial infections, followed by gram-negative bacteria and fungi. An older synonym, “ endotoxic shock,” is no longer appropriate

26. Stages of Shock These stages have been documented most clearly in hypovolemic shock but are common to other forms as well: An initial non-progressive stage during which reflex compensatory mechanisms are activated and vital organ perfusion is maintained, A progressive stage characterized by tissue hypoperfusion and onset of worsening circulatory and metabolic derangement, including acidosis, An irreversible stage in which cellular and tissue injury is so severe that even if the hemodynamic defects are corrected, survival is not possible.

27. Clinical Features In hypovolemic and cardiogenic shock, patients exhibit hypotension, a weak rapid pulse, tachypnea, and cool, clammy, cyanotic skin. In septic shock, the skin may be warm and flushed owing to peripheral vasodilation. The primary threat to life is the underlying initiating event (e.g., myocardial infarction, severe hemorrhage, bacterial infection). The cardiac, cerebral, and pulmonary changes rapidly aggravate the situation. If patients survive the initial period, worsening renal function can provoke a phase dominated by progressive oliguria, acidosis, and electrolyte imbalances. Prognosis varies with the origin of shock and its duration. Thus, more than 90% of young, otherwise healthy patients with hypovolemic shock survive with appropriate management; by comparison, septic or cardiogenic shock is associated with substantially worse outcomes, even with state-of-the-art care.

28. References Chapter 4: Hemodynamic Disorders, Thromboembolism, and Shock

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