Haemostasis and Haemodynamic Disturbances II PDF

By: Dr. Maha Maha Tingari Maha Tingari     Is the formation of a solid or a semi-solid mass from the constituents of blood within the vascular system during life. Not from blood embolism Outside vascular system clotting or haemostasis After death clotting Maha Tingari Virchow’s triad:  Altered...

By: Dr. Maha Maha Tingari Maha Tingari     Is the formation of a solid or a semi-solid mass from the constituents of blood within the vascular system during life. Not from blood embolism Outside vascular system clotting or haemostasis After death clotting Maha Tingari Virchow’s triad:  Altered endothelium  Altered blood flow  Increased coagulability Maha Tingari Maha Tingari Maha Tingari Either:  Physical injury exposure of sub-endothelial collagen Release of tissue factor Loss of anticoagulant effect of normal endothelium  OR dysfunction tipping of pro-/anti-thrombotic balance Maha Tingari     Hypertension. DM. Atherosclerosis. vasculitis. Maha Tingari Either:  Stasis activation of coagulation cascade  OR turbulence endothelial dysfunction blood cells get contact with endothelium Maha Tingari Either: (for sake of simplification)  Increased coagulation factor activity , OR  Decreased natural anticoagulants activity Maha Tingari        Surgery Trauma Burns Postpartum Immobility Factor V mutation Mutation in prothrombin gene Maha Tingari    Antithrombin III deficiency Protein C deficiency Protein S deficiency Maha Tingari Pale thrombus: forms in rapidly flowing blood (e.g. arterial). Grayish and firm composed of a tangled mesh of platelets, fibrin  Red thrombus: forms in slowly flowing blood (e.g. venous). Dark and gelatinous , they contain more enmeshed erythrocytes  Mixed thrombus  Maha Tingari Maha Tingari     Venous (most common) Arterial (more serious) Cardiac (e.g. in narrow mitral valve, thrombus may form in the atrium) Capillary (e.g. during acute inflammation) Maha Tingari    Propagation Detachment and embolisation Removal Maha Tingari Removal is either by:  Shrinkage  Lysis by plasmin  Organization and recanalization  Endothelialization Maha Tingari Maha Tingari Maha Tingari   According to site, size, rate, ect In DVT (as example) swelling.  Pain  Skin: shiny, red, hot,..  Ulceration  Maha Tingari Maha Tingari   Embolism Is the transference of abnormal material by the blood stream and its impaction in a vessel distant to the site of injury. Embolus is the impacted material Maha Tingari   Emboli coming from the venous side impact in the lung Emboli coming from the arterial side impact in peripheral vascular beds (brain, kidney, spleen, …) Maha Tingari      Thromboembolism Fat embolism Amniotic fluid embolism Air embolism Septic emboli Maha Tingari Either:  Pulmonary Source :97% in DVT. Effects:  Large , rapid Small , slow sudden death. pulmonary hypertension (PHT) Systemic The commonest source of systemic thromboembolism is the left side of the heart  Maha Tingari Presence of fat globules in blood. Causes:  Trauma to fat containing tissue ( long bone fracture or operation, ( fatty tissue) liver grossly infiltrated with fat,..)  Total parentral nutrition  Acute pancreatitis Maha Tingari Consequences:  Thrombocytopenia  DIC  death Maha Tingari Complication of delivery and abortion  Humeral factors in fetal tissues causes DIC and pulmonary vasoconstriction owing to release of thrombogenic substances  Maha Tingari  Air bubbles (100- 50 ml). Example: IV lines. Large vein trauma neck wounds, decompression  Air causes mechanical obstruction to the right side of the heart Maha Tingari    Example: from infected heart valves (vegetations) Transmits the infection to impaction site Can lead to mycotic aneurysm Maha Tingari Maha Tingari    Ischaemia is deficient supply of blood Infarction is tissue death due to reduction or loss of blood supply Such tissue is termed an infarct Maha Tingari     Anatomy of vascular supply Tissue metabolic rate and type of metabolism Rate of development of occlusion Oxygen content of the blood Maha Tingari    End arteries VS anastomoses Dual blood supply Collaterals Maha Tingari   Highly active tissues can not withstand ischaemia for long Tissues that are able to metabolize anaerobically better withstand ischaemia Maha Tingari  Gradual occlusion leads to development of collaterals Maha Tingari   Is the blood fully oxygenated ? Is the Hb molecule ready to deliver oxygen? Maha Tingari   Infarction can be due to venous or arterial occlusion Can be due to hypotension in a person with diseased arteries Maha Tingari     Myocardial infarction Splenic infarction Cerebral infarction Intestinal infarction Maha Tingari Maha Tingari     Shock is a state of reduced tissue perfusion Shock is defined as a state of systemic tissue hypoperfusion due to reduced cardiac output and/or reduced effective circulating blood volume Before going into further discussion, we need to revise some physiological aspects of blood flow and blood pressure regulation. shock gives rise to systemic hypotension, impaired tissue perfusion, and cellular hypoxia. Maha Tingari     The paroreceptor reflex (at Aortic arch and carotid bifurcation) Osmoreceptor mechanisms (in the hypothalamus) Renin angiotensin aldosterone system Autoregulation in some organs: Brain Heart kidneys Maha Tingari    Cardiogenic shock Hypovolaemic shock Distributive shock Maha Tingari Examples:  Severe myocardial infarction  Ventricular rupture  Arrhythmia  Cardiac tamponade  Massive pulmonary embolism Maha Tingari Haemorrhage  Severe dehydration: Vomiting Diarrhoea Extensive burns  Maha Tingari    Septic shock Neurogenic shock Anaphylactic shock Maha Tingari    Nonprogressive stage Progressive stage Irreversible stage Maha Tingari BP is maintained during this stage:  Neurohumeral mechanisms: Sympathetic nervous system ADH release Renin Angiotensin Aldosterone system Catecholamines Maha Tingari  Failure of regulatory mechanisms to control BP and tissue perfusion Maha Tingari   Widespread tissue injury Death Maha Tingari         LPS engages upon its specific receptors Release of massive amounts of inflammatory cytokines Systemic vasodilatation and hypotension Diminished myocardial contractility Widespread endothelial injury and activation Widespread tissue and lung injury (ARDS) Activation of coagulation system and DIC MOF and death Maha Tingari Maha Tingari Please.. Fill the table below with one of the following: decreased (↓), (↑) or no change. Type SVR COP Intravascular fluid volume Cardiogenic ↑ ↓ Normal or ↑ Hypovolaemic ↑ ↑ or ↓ ↓ Distributive ↓ ↑ or ↓ Normal or ↑ Maha Tingari Maha Tingari