Principles Of Hemodynamics

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Blood clot

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A gelatinous or semisolid mass of coagulated blood.

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Cor pulmonale

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enlargement of the right ventricle of the heart due to disease of the lungs or of the pulmonary blood vessels

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D-dimer test

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test that detects the cross-linked fibrin degradation fragment, d-dimer. Elevations in this fragment are seen in primary and secondary fibrinolysis; during thrombolytic or defibrination therapy with tissue plasminogen activator; as a result of thrombotic disease, such as deep-vein thrombosis, pulmonary embolism or DIC; in vasoocclusive crisis of sickle cell anemia; in malignancies; and in surgery.

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ecchymosis

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A discoloration of the skin resulting from bleeding underneath, typically caused by bruising

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embolus

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A blood clot, air bubble, piece of fatty deposit, or other object that has been carried in the bloodstream to lodge in a vessel and cause an embolism

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epistaxis

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Bleeding from the nose

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fibrin

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An insoluble protein formed from fibrinogen during the clotting of blood. It forms a fibrous mesh that impedes the flow of blood

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fibrinogen

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A soluble protein present in blood plasma, from which fibrin is produced by the action of the enzyme thrombin

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fibrinolysis

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The enzymatic breakdown of the fibrin in blood clots

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hemarthrosis

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bleeding into joint spaces.

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hematemesis

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The vomiting of blood

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hemachezia

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passage of stools containing blood

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hematoma

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A solid swelling of clotted blood within the tissues

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hemoptysis

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The coughing up of blood

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infarction

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The obstruction of the blood supply to an organ or region of tissue, typically by a thrombus or embolus, causing local death of the tissue

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ischemia

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An inadequate blood supply to an organ or part of the body, esp. the heart muscles

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lines of zahn

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Lines of Zahn are a characteristic of thrombi[1] that appear when formed in the heart or aorta. They have visible and microscopic laminations produced by alternating pale layers of platelets mixed with fibrin and darker layer containing red blood cells. Their presence implies thrombosis at a site of rapid blood flow that happened before death. In veins or smaller arteries, where flow is not as constant, they are less apparent.

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melena

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Dark sticky feces containing partly digested blood

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paradoxic embolus

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A paradoxical embolism is a kind of stroke or other form of arterial thrombosis caused by embolism of a thrombus (blood clot) of venous origin through a lateral opening in the heart, such as a patent foramen ovale.[1]
The opening is typically an atrial septal defect, but can also be a ventricular septal defect.
Paradoxical embolisms represent two percent of arterial emboli.[2

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partial thromboplastin time

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A test that checks the clotting factors of the intrinsic pathway.

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petechia

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A small red or purple spot caused by bleeding into the skin

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plasmin

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An enzyme, formed in the blood in some circumstances, that destroys blood clots by attacking fibrin

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protien c

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Protein C, also known as autoprothrombin IIA and blood coagulation factor XIV,[1]:6822[3] is a zymogenic (inactive) protein, the activated form of which plays an important role in regulating blood clotting, inflammation, cell death and maintaining the permeability of blood vessel walls in humans and other animals.

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prothrombin time

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a test that measures the blood's clotting ability

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purpura

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A rash of purple spots on the skin caused by internal bleeding from small blood vessels

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recanalization

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The restoration of the lumen of a blood vessel following thrombotic occlusion by restoration of the channel or by the formation of new channels

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saddle embolus

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A saddle embolus or straddling embolism is a thrombus that straddles a dividing blood vessel.

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shock

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Inadequate perfusion and resultant hypoxia os the tissues

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thrombomodulin

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is an integral membrane protein expressed on the surface of endothelial cells

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thrombosis

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Local coagulation or clotting of the blood in a part of the circulatory system

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thrombus

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A blood clot formed in situ within the vascular system of the body and impeding blood flow

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Outline of intrinsic and extrinsic coagulation cascades

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Significance of anticoagulation

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Events that occur in thrombolysis

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Discuss the prominent role of thrombin in blood hemostasis

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Thrombin, an enzyme, catalyzes the conversion of fibrinogen into fibrin, an insoluble protein which creates a network of interlocking fibers that traps platelets and blood cells to form a fibrin plug.
In the presence of thrombin and heparin, antithrombin III has a negative feedback effect on thrombin by inactivating factors Xa, XIIa, XIa, and IXa.
Excess thrombin also reacts with undamaged endothelial cells to uncover a membrane receptor which binds and activates circulating Protein C. APC inhibits further thrombin production by inactivating Va and VIIIa.
Excess thrombin in the presence of fibronectin and fibrinogen acts on endothelial cells and monocytes trapped in the thrombus to induce release of urokinase and tissue plasminogen activator which converts circulating plasminogen to plasmin. Plasmin cleaves fibrinogen and fibrin into fibrin split products which further act to inhibit platelet aggregation, thrombin activity, and cross-linking of fibrin strands.

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Arterial thrombi

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are more frequently found in areas of atherosclerotic damage to the vessel wall, in the heart, over areas of previous myocardial infarction. Cardiac and aortic thrombi tend to be firmly attached to the underlying vessel wall and are generally nonocclusive while thrombi in smaller arteries may be occlusive. As they develop they tend to develop alternating layers of fibrin (lines of Zahn) and aggregated platelets which grossly give the thrombus a grey laminated appearance.

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Venous thrombosis

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Usually form in areas of blood stasis and most clinically significant venous thrombi form in deep leg veins. They are also found in periprostatic, periovarian and periuterine pelvic venous plexi as well as other venous structures. Since most are the result of sluggish blood flow they ten to be occlusive and there is less tendency to develop lines of Zahn. RBCs remain trapped within the developing thrombus and this produces a dark red-blue appearance.

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Capillary thrombi

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Usually due to local endothelial damage they generally consist of platelets and fibrin and are not grossly visible.

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Sequelae

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Neutrophils and monocytes trapped in a thrombus will degrade and phagocytize fibrin and cell debris. Lysosomal enzymes from neutrophils and platelets will digest the coagulum and lead to softening. Fibroblasts and endothelial cells from the underlying vascular wall infiltrate the thrombus and a combination of fibrinolytic activity and endothelial proliferation may reestablish vascular flow through an occlusive thrombus. Presence of a thrombus predisposes to continued coagulation and propagation or enlargement of itself. A thrombus may fragment or become completely detached from its place of origin to tumble through the circulation as a thrombo embolus.

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Pale infarcts

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In those tissues that have a single blood supply without significant anastomoses, occlusion of an artery will result in coagulation necrosis of the tissue supplied by that artery. Since blood perfusion of the tissue is interrupted, the tissue becomes pale.

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Hemorrhage infarcts

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Tissues that have a single blood supply with rich anastomoses or that have a dual blood supply are somewhat protected against abrupt hypoxia. If necrosis does occur, that blood source may bleed into the necrotic tissue creating a red, hemorrhagic, infarct.

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Discuss disseminated intravascular coagulation (DIC) in terms of etiology, signs and symptoms and clinical significance.

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It is a coagulation abnormality involving the coagulation factors and platelets. The primary mechanism is activation of intrinsic and or extrinsic coagulation pathways in the micro circulation. Numerous fibrin thrombi are formed consuming platelets, fibrinogen, and coagulation factors and secondarily activating the fibrinolytic system. The microthrombi may lead to microinfarcts of the affected tissue, acute tubular necrosis of the kidneys, and hemolytic anemia while the consumption of clotting factors and activation of the fibrinolytic system may lead to a hemorrhage diathesis. Acute DIC patients are more prone to hemorrhage problems while those with a more chronic DIC tend to have more problems with thrombosis. Shock is a frequent complication and treatment must be based on the individual patient.

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Embolization

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Embolization refers to the process in which a free-floating mass is carried through the vascular system to a point distant to its site of origin or entry.

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Arterial emboli

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80-85% arise from mural thrombi in the left ventricle or left arterial appendage of the heart but valve vegetations, aortic mural thrombi, fragments of atherosclerotic plaque may also embolize. Depending on the size of the embolus and location of impaction, it may or may not cause infarction. Major sites of impaction include lower extremities, brain, kidney, and spleen. Although rare, if a right – to left shunt is present in the heart, a venous embolus can gain access into the systemic circulation (paradoxical embolus)

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Venous emboli

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3rd most common cause of death. The pathologic change and the clinical manifestations of pulmonary emboli are dependent on the size of the vessels in which the embolis impacts and also on the pre existent cardiovascular status of the lung. Small emboli lodge in peripheral pulmonary vessels causing local congestion, edema, and hemorrhage but may produce no clinical symptoms.
Recurrent showers of small emboli will result in progressive reduction of the perfusable pulmonary vascular bed and give rise to pulmonary hypertension. This may be manifested by dyspnea on exertion, anginal pain, syncope, and venous distention of the neck veins.
Occlusion of medium-size pulmonary arteries may produce a sudden onset of dyspnea, hyperventilation and tachycardia, anxiety, syncope and anterior chest pain.
Massive embolization, particularly of the saddle type, may induce the immediate catastrophic syndrome of acute cor pul monale and sudden death. If not immediately fatal, they may result in shock with central chest pain, severe dyspnea, cyanosis, tachycardia and diaphoresis. Most clinically significant emboli are the larger ones that originate from thrombi in the femoral/iliac veins and not the deep calf veins.

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List predisposing factors that may lead to pulmonary emboli

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Surgery, immobility/immobilization, congestive heart failure, pregnancy, obesity, muscular weakness, cancer and use of oral contraceptive or exogenous estrogens.

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Describe the morphologic changes in the lung and the clinical signs and symptoms which may occur as result of pulmonary emboli

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Morphologically – Grossly, the lesions will vary in size from those barely visible to wedge-shaped involvement of a large part of an entire lobe. Classically, they abut on the visceral pleura with the apex of the wedge shaped infarct pointing toward the hilus. Majority of infarcts are within the lower lobes, and more frequently seen on the right.
Clinically - When symptomatic, a clinical triad indicative of pulmonary infarction includes dyspnea, hemoptysis, and pleuritic chest pain. A low grade fever and leukocytosis may be additional findings. Radiologically, a wedge-shaped consolidation along a pleural surface is classic although not frequently seen. Elevation of the diaphragm may occur.

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Discuss the fat emboli syndrome in terms of etiology, clinical manifestations, and clinical outcomes.

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These most frequently occur after long-bone trauma when marrow fat is exposed to the venous circulation. Fat emboli larger that 20µ are filtered in the lung while smaller aggregates may pass through the lung and lodge in the brain and/or kidneys. This may give rise, 1-3 days after trauma, to a clinical syndrome of progressive respiratory distress, CNS impairment and possible renal dysfunction that is related to the mechanical and chemical effects of fat in the circulation.

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List five potential etiologies of shock.

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1. Hypovolemic – Acute loss of blood or fluid from the circulation may be due to hemorrhage, burns, vomiting, diarrhea, “third-spacing”.
2. Cardiogenic – Inability of the heart to maintain adequate output may be due to myocardial infarcts, cardiac tamponade, and pulmonary emboli.
3. Vascular neurogenic – The inability to maintain peripheral vascular muscle tone with subsequent peripheral pooling of blood may be due to CNS injury, drugs.
4. Vascular septic – Severe gram-negative bacterial infections may produce endotoxins that cause peripheral vascular pooling. The ensuing shock may also be complicated by direct toxic damage to the vessels and by disseminated intravascular coagulation.
5. Vascular anaphylactic – Hypersensitivity reactions may lead to widespread vasodilatation and increased capillary permeability with fluid loss from the vasculature. Both can lead to hypovolemia and hypoferfusion of vital organs.

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Discuss the underlying hemodynamic events that occur in patients in shock.

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1. Decreased cardiac output which is reflected by a compensatory tachycardia.
2. Reduction in blood volume from peripheral pooling, this leads to hypotension and a weak, thready pulse. This also activates the reninangiotensin-aldosterone system to retain sodium and water. This produces oliguria.
3. In hypovolemic and cardiogenic shock, peripheral vasoconstriction leads to cool, clammy skin. In septic shock, the peripheral vasodilatation and increased vascular permeability leads to warm, moist skin. Increased levels of reduced hemoglobin in the peripheral tissues may cause cyanosis.

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Describe the potential morphologic changes of tissue that occur in patients in shock.

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1. Renal tubular epithelial necrosis (acute tubular necrosis).
2. Centrilobular hepatic necrosis.
3. Focal mucosal necrosis of the GI Tract (ischemic enteritis).
4. Adult respiratory distress syndrome (shock lung).
5. Neural ischemia in the brain.