Lecture 3: Hemodynamics Flashcards
Artery or vein
artery
Artery or vein
vein
What is edema
Abnormal accumulation of fluid in the interstitium and body cavities
What are the 4 causes of edema
- Increased microvascular permeability
- Increased vascular hydrostatic pressure
- Decreased intravascular oncotic pressure
- Decreased lymphatic drainage
What are some causes of increase microvascular permeability
Inflammation, neovascularization, anaphylaxis, toxin, clotting abnormalities
What are some causes for increased vascular hydrostatic pressure
Portal hypertension, pulmonary hypertension, localized venous obstruction
What are some causes of decreased intravascular osmotic pressure
Hypoalbumemia, excessive albumin loss
What are some causes for decreased lymphatic drainage
Lymphatic obstruction or compression, lymphatic aphasia or hypoplasia, interstitial lymphangiectasia, lymphangitis, spirotrichosis
What are 2 major causes of non-inflammatory edema and transudate
- Hepatic disease- hypoalbumemia, portal hypertension—> increase hydrostatic pressure
- Heart failure- LHF- pulmonary edema, RHF- ascites—> increase hydrostatic presure
How does the body attempt to compensate for hepatic failure and heart failure resulting in decreased CO
Activate RAAS system—> increase Na+ and H20 retention, AII activates anti-diuretic hormone- retain water
Ends up increasing hydrostatic pressure
What is hyperemia and what are some reasons why
Ateriolar dilation (erythema in skin) due to inflammation, physical activity, increase BF to GI after meal, physiological mechanism of dissipate heat
What is congestion (BF and perfusion) and some reasons why
Impaired/decreased outflow due to CHF, local venous obstruction, displacement of organ
What is hemostasis
Physiological response to vascular damage and stop bleeding- normal to prevent blood loss
What is thrombosis
Inappropriate activation of hemostatic processes in blood vessels, occurs without trauma
What is Virchow’s Triad
3 factors that contribute to hemostasis and thrombosis
1. Endothelial injury
2. Alterations in blood flow
3. Blood hypercoaguability
What are the steps in the hemostatic process
- Primary hemostasis- vasoconstriction and platelet aggregation to form platelet plug at site of damage- uses von willebrand factor to help adhere platelets to endothelium
- Secondary hemostasis- coagulation to form a mesh work of fibrin- uses tissue factor because once activated upon endothelial injury activates extrinsic coagulation pathway
- Fibrinolysis
- Tissue/vascular repair
Describe the intrinsic and extrinsic coagulation pathway
Intrinsic: Factor XII—> Factor XI—> Factor IX—> Factor VIII— Factor X—> Factor II (thrombin)—> Factor I (fibrin)—> clot
Extrinsic: Factor III (tissue factor)—>factor VII—> Factor X—> Factor II (thrombin)—Factor I (fibrin)—> clot
What are the vitamin K dependent coagulation factors
Factor II, VII, IX, X
What is the purpose of fibrinolysis
Prevents blood clots forming pathogenic condition
What is the purpose of plasmin
Digest fibrin clots and releases fibrin degradation products and inhibits additional fibrin formation
What do FDP’s do
Inhibit thrombin and interfere with fibrin polymerization and coat platelet membranes to inhibit platelet agggregation
What is the most clinically significant and most potent coagulation inhibitor
Antithrombin III
What produces Anti-thrombin III
Hepatocytes and endothelium
What is hemorrhage
Extravasated blood caused by abnormal function or integrity of one or more of the major factors of Virchows triad
What are the 3 descriptive terms to describe hemorrhage
- Petechiae
- Ecchymosis
- Suffusive
What is petechia hemorrhage
1-2mm, pinpoint, associated with minimal vascular a damage
What is ecchmosis hemorrhage
2-3cm in diameter, more extensive vascular damage
What is suffusive hemorrhage
Larger, continuous areas of tissue, paintbrush
What type of hemorrhage
Suffusive hemorrhage
What type of hemorrhage
Petechia
What type of hemorrhage
petechia and ecchymosis
What type of hemorrhage
Ecchymosis
What is the pathogensis of hemopericardium causing cardiac tamponade
- Right auricular hemangiosarcoma ruptured—> compression on heart—> decreased diastolic filling—> decreased CO—> death
What % of blood needs to be lost to die from exsanguination
40%
What is thrombosis
Aggregate of platelets, fibrin and other blood elements in injured blood vessel
What is physiological thrombus
Part of normal hemostasis
What is persistent inappropriate thrombus
Forms on the wall of injured blood or lymphatic vessel or heart (mural thrombosis) or free in a vessel human (thromboembolism)
What is mural thrombosis
Thrombosis in the wall of blood vessel, lymphatic vessel, or heart
What is thromboembolism thrombus
Forms free in the vessel lumen
What are the major determinants of thrombosis
Virchows triad, specifically endothelial damage which results in increase production of pro-coagulant substances and decreases anticoagulants
How are small thrombi resolved
Thrombolysis and blood vessel returns to normal structure and function
How are large thrombi resolved
Removal or thrombotic debris by phagocytes with subsequent granulation tissue formation and fibrosis with regrowth of endothelium over sure to incorporate the affected area into vessel wall
How are large mural or occlusive thrombi resolved
Invasion and growth of endothelial lined blood channels through fibrotic area—> recanalization
Causes permanent vascular narrowing- leading to more turbulent flow
What does this show
thrombus resolution- recanalization
Fibrous tissue surrounding, but multiple smaller areas of blood flow
What does an acute infarct look like
Red, swollen and slightly raised due to hemorrhage
What does a subacute infarct look like
Pale, necrotic, swelling, still surrounded by hyperemia areas
What does a chronic infarct look like
Paleo, shrunken, firm, fibrosis
Identify the different types of infarcts
Red: acute infarct
Yellow: subacute infarct
Green: chronic infarct
What is the pathogensis of DIC
- Activation of intravascular coagulation
- Platelet consumption (decrease platelets), coagulation factor consumption (increase PT and aPTT, increase D-Dimer)—> impaired coagulation and bleeding
Endothelial damage—> microvascular thrombosis—> multi organ ischemia or failure
Summary: initially overactive coagulation system—> exhaust coagulation system—> excessive bleeding—> death
