Mkgrady8 Gpmdc 2 Hemodynamics

alter the balance of protein, water, and electrolytes within the vasculature and tissues by= altering endothelial function, increasing vascular pressure, or decreasing plasma protein content; resulting EDEMA, depending on location and severity, has minimal to profound effects

blood clotting to prevent excessive bleeding= HEMOSTASIS; too little blood clotting= HEMORRHAGE; too much hemorrhage= hypotension, SHOCK, and death

inappropriate clotting= THROMBOSIS; migration of clots= EMBOLISM; leads to obstruction of blood vessels --> ischemic cell death or INFARCTION; leads to 3 major causes of morbidity and mortality= myocardial infarction, pulmonary embolism, and cerebrovascular accident (aka stoke)

active process; arteriolar dilation; increased blood flow; tissue becomes red= ERYTHEMA; due to inflammation or maybe exercise where you're trying to cool the blood

passive process; diminished outflow of venous blood and pooling of blood in the tissue; systemic or local; tissue becomes blue-red= CYANOSIS

pulmonary= blood engorged capillaries, alveolar septal edema, intra alveolar hemorrhage; hepatic= central vein and sinusoids distended, reversible fatty change may occur

pulmonary= septa thickened and fibrotic, macrophages containing hemosiderin (heart failure cells); hepatic= central lobules red brown ('nutmeg liver') and slightly depressed from cell loss, focal hemorrhages and necrosis, hemosiderin laden macrophages

severe generalized edema and accumulation in body cavities; NEED TO KNOW THIS

capillary hydrostatic and osmotic forces are normally balanced so there is little net movement of fluid into the interstitium; however increased hydrostatic pressure or diminished plasma osmotic pressure leads to extravascular fluid accumulation (edema); tissue lymphatics drain much of the excess fluid back to the circulation by way of the thoracic duct however if the capacity for lymphatic drainage is exceeded tissue edema results

heart failure increases cap hydrostatic pressure which causes edema; heart failure decreases renal blood flow (hypoperfusion of kidneys) --> activation of the renin-angiotensin system --> retention of Na and H2O (renal failure can also cause this) --> increased blood volume --> edema; malnutrition, decreased hepatic synthesis of albumin, nephrotic syndrome (leaky glomerular caps) --> decreased plasma albumin --> decreased plasma osmotic pressure --> edema

impaired venous return (ex. congestive heart failure, venous obstruction or compression) or arteriolar dilation (ex. heat); this leads to edema

lungs= dependent distribution of edema at the bottom of the lung (gravity), frothy blood tinged fluid air, edema, and extravasated blood; local clinical manifestations like= pitting edema in feet (cardiac failure), periorbital edema (renal disease where they are loosing protein in the urine so lower osmotic pressure? in blood and edema (NOT FAILURE))

inflammation, neoplasm, surgery, radiation

elephantiasis; often one sided

focal (infarct, abscess, neoplasm), generalized (encephalitis), trauma may result in either form of edema; features= narrowed sulci, distended, flattened gyri

annoying to rapidly fatal; can be indicator of disease (e.g. cardiac, or renal failure); can impair wound healing; can impair clearance of infection; can interfere with normal ventilatory function resulting in death; can cause herniation of brain or compression of brainstem vascular supply resulting in death

it's an extravasation of blood= can be external, within a tissue (any accumulation is a hematoma HEMOthorax, HEMarthrosis, etc), risk is increased in hemorrhagic diatheses; patterns of hemorrhage can be recognized in tissue (petechiae, purpura, ecchymoses (bruises); clinical significance= depends on volume and rate of bleeding, site of hemorrhage

1-2mm red dots; on skin, mucous membranes, serosal surfaces; causes= locally increased intravascular pressure, low platelet counts, defective platelet function, loss of vascular wall support

>3mm red dots; same locations as petechiae; causes= same as petechiae or secondary to trauma, vascular inflammation, increased vascular fragility

aka bruises >1-2 cm; they are subcutaneous; due to trauma, coloration due to enzymatic degradation of hemoglobin in tissue by macrophages (degradation of RBC releases hemoglobin which is RED BLUE, enzymatic conversion of hemoglobin forms bilirubin which is BLUE GREEN, enzymatic conversion of bilirubin forms hemosiderin which is GOLD BROWN)

normal hemostatis is a consequence of tightly regulated processes= maintain blood in fluid state in normal vessels, yet premit rapid formation of a hemostatic clot at the site of vascular injury; VASCULAR WALL, PLATELETS, COAGULATION CASCADE = components of hemostatis (details will be covered in the next lecture)

ANTITHROMBOTIC AND PROTHEOMBOTIC functions

in the normal vascular endothelium there are anti platelet functions, anti coagulant functions, and fibrinolytic functions

intact endothelium= inhibits platelet adhesion; NO and prostacyclin (PG12)= inhibit platelet adhesion, vasodilators, inhibit platelet aggregation; adenosine diphosphatase= degrades ADP, inhibits platelet aggregation

heparin like molecules= enhance antithrombin III activity; thrombomodulin= binds thrombin so that it activates protein C; protein C= inactivates factor 5a and 8a; tissue factor pathway inhibitor (TFPI)= inhibits tissue factor-factor 7a complex and factor 10a

tissue type plasminogen activator (t-PA)= cleaves plasminogen to plasmin; plasmin= cleaves fibrin, degrades clots

injured vascular endothelium has primary hemostasis and secondary hemostasis

local neurohumoral factors at injury site cause= platelet adhesion, platelet activation, platelet aggregation; FORMATION OF PRIMARY HEMOSTATIC PLUG

synthesis of tissue factor= initiation of clotting cascade, thrombin activation, fibrin polymerization; FORMATION OF SECONDARY HEMOSTATIC PLUG

pathologic counterpart of hemostasis; the formation of a clot within a vessel; components of thrombosis= VASCULAR WALL, PLATELETS, COAGULATION CASCADE; virchow's triad= endothelial injury, hypercoagulability, and abnormal blood flow (either stasis or turbulence) cause thrombosis

myocardial infarction; ulcerated plaques in atherosclerosis; inflammatory (vasculitis) or traumatic vascular injury; dysfunctional endothelial cells that produce more procoagulant factors than anticoagulant factors (hypertension, turbulant blood flow, bacterial endotoxins, toxins from cig smoke, radiation injuries, metabolic abnormalities)

turbulence contributes to arterial and cardiac thrombosis (forms countercurrents and local pockets of stasis); stasis contributes to venous thrombosis (sickle cell anemia, hyperviscosity (e.g. polycythemia)); stasis or turbulence= brings platelets into contact with endothelium, prevents dilution of activated clotting factors, retards inflow of clotting factor inhibitors permitting buildup of thrombi, promotes endothelial cell activation leading to local thrombosis, leukocyte adhesion, and so on

hypercoagulability

>1% of pop; MUTATION IN FACTOR V GENE (FACTOR V LEIDEN); MUTATION IN PROTHROMBIN GENE; deficiencies in antithrombin III, protein C, or protein S

lower risk; cardiomyopathy, nephrotic syndrome; hyperestrogenic states, oral contraceptive use; sickle cell anemia; smoking

prolonged bed rest or immobilization; myocardial infarction or atrial fibrillation; tissue injury, cancer, prosthetic valves; DISSEMINATED INTRAVASCULAR COAGULATION; HEPARIN INDUCED THROMBOCYTOPENIA (HIT)(NEED TO KNOW THIS ONE (WILL BE DISCUSSED IN NEXT LECTURE) (HEPARIN CAUSES THE CELLS TO CLOT); ANTIPHOSPHOLIPID ANTIBODY SYNDROME (LUPUS ANTICOAGULANT) (YOU CHECK THEIR BLOOD AND IT LOOKS LIKE IT TAKE STHEM FOREVER TO CLOT BUT REALLY THERE IS LONGER CLOTTING OUTSIDE OF THE BODY AND TOO FAST CLOTTING IN THE BODY)(THIS IS THE OTHER ONE THAT YOU REALLY NEED TO KNOW)

arterial and cardiac thrombi are sites of injury or turbulence= mural thrombus forms in aorta or cardiac chamber; venous thrombi= sites of stasis; focal attachment to vascular surface and propagate toward the heart= arterial (retrograde from point of attachment), venous (in direction of blood flow), propagating may break off and migrate through blood as EMBOLUS

thrombus in the left and right ventricular apices overlying white fibrous scar

lines of Zahn= platelet and fibrin deposits alternating with RBC rich layers; forms ONLY in flowing blood SO ONLY IN SOMEONE WHO IS STILL ALIVE (distinguishes premortem from postmortem clots)

propagation= enlarges, increasing odds of vascular occlusion or embolization; embolization= all or part of clot dislodges and is transported through vasculature; dissolution= newly formed clot may be dissolved by activation of fibrinolytic factors, does not work with older thrombi; organization and recanalization= ingrowth of endothelial cells, smooth muscle cells, and fibroblasts, formation of capillary channels

superficial veins of the leg= varicosities in saphenous system, rarely embolize, painful local congestion and edema; deep veins of the leg (DVT)= larger leg veins at or above the knee joint (popliteal, femoral, iliac), congestion and edema but often channelized, frequently embolize, 50% have no symptoms until embolized to lungs

0.2-0.4% of hospitalized pts; 200,000 deaths/yr; 95% from deep leg vein thrombi; most are trapped in lungs= most of these are small and clinically silent (60-80%), large embolus blocking a major pulmonary artery causes sudden death, embolism to medium sized arteries with subsequent rupture of caps leads to pulmonary hemorrhage

emboli in arterial circulation= 80% from intracardiac mural thrombi, some are paradoxical emboli (venous emboli that cross from right to left heart and into circulation); may travel anywhere= 65% lower extremities, 10% brain

fat embolism= long bone fracture or crushing trauma; gas embolism= air in circulation or 'the bends'; amniotic fluid embolism= trauma, placenta abruptio

area of ischemic necrosis caused by occlusion of vascular supply to tissue; myocardial infarction, cerebral infarction, pulmonary infarction (common clinical complication), bowel infarction (often fatal), ischemic necrosis of distal extremities (gangrene)(morbidity in diabetic pop)

99% from thrombotic or embolic events (majority from arterial occlusion); classified by color and presence (septic) or absence (bland) or infection; red infarct= venous occlusions, spongy tissue, where blood can reach tissue; white infarct= arterial occlusions in solid organs with end arterial circulation (heart, spleen, kidney) and in dense tissue where circulation is limited

severe hemorrhage, extensive trauma or burns, large myocardial infarction, massive pulmonary embolism, microbial sepsis; characteristics= HYPOPERFUSION OF TISSUES due to reduced cardiac output or reduced effective circulating blood volume; consequences= impaired tissue perfusion, cellular hypoxia

cardiogenic, hypovolemic, septic, anaphylactic (systemic histamine activation), neurogenic (spinal cord injury or anesthesia)

initially reversible but continued hypoperfusion leads to permanent tissue injuries; culminated in multiple organ dysfunction syndrome (MODS)= lung, kidney, heart, liver and ultimately death; presentation= tachycardia, oliguria, hypotension, weak pulses, mental status chages, cool extremities; stages= compensation, decompensation, and irreversible damage; compensation= reflex maintenance of vital organ perfusion; decompensation= metabolic acidosis, renal insufficiency, still reversible

kidney= acute tubular necrosis; intestines= mucosal ischemic necrosis, patchy hemorrhages, sepsis; brain= necrosis; liver= centilobular necrosis; adrenal= waterhouse-friderichsen syndrome with acute hemorrhagic infarction and adrenal insufficiency; lung= acute respiratory distress syndrome

d nephrotic syndrome (no symptoms of hepatitis)

b laminations (lines of Zahn) (alive=blood flow=these lines in clots) HIGH YIELD

b hypovolemic; low hemoglobin suggests bleeding (wouldn't get this with cardiogenic); c no indication of a spine injury

aka hydroperitoneum; blood build up in the peritoneum