Hemodynamics Flashcards
How is the body’s 60% water allocated?
15% interstitial, 40% in the cell, 5% in vasculature
Osmolality
Concentration of particles in a solution. In plasma, mostly sodium.
Two things that osmosis requires?
Driving force and semi permeable membrane. This allows the movement of fluid.
How do small polar molecules move from vascular spaces into the interstitium?
Intercellular clefts between endothelium. However, these molecules can’t traverse the lipid bilayer.
How does osmolarity of intravascular, interstitial and intracellular spaces compare? How about concentration of small ions?
Osmolarity is the same across all three spaces. Concentration of small polar molecules is the same between vascular and interstitial space, but not in cells.
Outward Hydrostatic Pressure
The outward force exerted by moving blood on capillary walls.
What is absorption?
The inward hydrostatic pressure and the inward oncotic pressure.
Oncotic pressure
A type of osmotic pressure created by proteins.
Inward oncotic pressure
Proteins in the vasculature generate an inward oncotic pressure. Water wants to move in. Opposed by outward oncotic pressure, created by proteins in interstitium.
Net Filtration Pressure
(Pc + πi) - (πc + Pi). If negative, absorption is favored.
Starling’s Equation
Fluid movement (Jz) = Kf (hydraulic conductance) *(Pc + πi) - (πc + Pi)
Role of lymphatics in hemodynamics
Return excess filtered fluid and proteins to circulation.
Hypoalbuminemia
πc is too low, so net movement of water is out of vasculature. Usually due to loss of proteins in urine.
Difference in clinical presentation for left vs right sided heart failure?
Right sided? Peripheral edema. Left sided? Pulmonary edema.
What happens if Kf is increased?
Sepsis and inflammation occurs
What happens if lymphatic drainage is blocked?
Edema due to increased πi.
Edema
Too much interstitial fluid, not to be confused with hydropic change, which is increased intracellular fluid.
Effusion
Edema in a body cavity
Anasarca
Generalized edema
Transudates
Accumulations of mostly salt water. Low protein content, low specific gravity (<1.012). Result when hydrostatic pressure is higher than inward oncotic pressure, lymphatic obstruction, or excess body fluid due to sodium retention (renal failure).
Transudate Histology
Filled cavities with a uniform pink, very acellular.
Exudates
Protein rich accumulations with a higher specific gravity. Result from increased vascular permeability. Most commonly seen with inflammation.
Thrombosis
Transformation of flowing blood to a semisolid containing platelets, fibrin, and other cellular elements, within the vascular system of a living organism.
Extrinsic pathway of blood coagulation
Tissue Factor sits in extravascular space. Vessel ruptured, TF contacts plasma, binds factor VII, that complex activates factor X, which converts prothrombin into thrombin. Thrombin converts fibrinogen to fibrin. TF can also activate IX to amplify clotting via intrinsic pathway.
Fibrinolysis
Cutting of fibrin clot to prevent overclotting. Controlled by plasmin.
Role of platelets in thrombosis
When platelets aggregate, they release calcium, ADP, and Thromboxine A. This promotes fibrin, which weaves platelets together.
Role of endothelial cells in thrombosis
In their resting state, endothelial cells are anti-thrombotic. Have heparin like molecules where antithrombin can bind, thrombomodulin, PGI and NO2.
Virchow’s Triad
Endothelial Injury (arterial), Alteration in Flow, Hypercoagulable Blood.
Causes of thrombosis.
Primary Vs Secondary Hypercoagulable Blood
Primary is defect in clotting factors, like increased factor 5. Secondary are things like oral contraceptives etc.
Lines of Zahn
Alternating layers of fibrin/platelets and red cells. Indicative of thrombus in flowing blood.
Clot
Clot is a solidified mass outside the vascular system, or in blood vessels in a dead person. Chicken fat (plasma) and currant jelly (RBCs).
What can thrombi do?
Propagate (grow towards heart in veins, away from heart in arteries), lyse, organize (scar), recanalize, become infected, embolize.
Embolus
Anything that travels through vessels that is not liquid blood.
Thromboemboli
Most common in deep veins of legs, can also be arterial
Paradoxical embolus
Embolus forms in venous circulation, passes through PFO and ends up in systemic circulation.
Other emboli
Atheroemboli, air, fat (from marrow)
Infarction
Area of irreversible tissue necrosis due to ischemia.
White Infarct
Spleen, Kidney, Heart. Caused by arterial insufficiency, single blood supply, tissue not reperfused.
Red Infarct
Testicle, Lungs, Intestines, Liver. Caused by venous insufficiency, or in tissues with dual blood supply.
Infarct histology
Coagulative Necrosis. Thick, bright pink, no nuclei.
Disseminated Intravascular Coagulation
Excessive secondary activation of coagulation where thrombi form in microvasculature, which depletes clotting factors. However, this causes bleeding elsewhere. Micro-infarction of organs occurs, hemmorhage, and shock! Also show schistocytes!!!!
Shock
Circulatory collapse. Global hypotension and hypoperfusion. This causes acidosis and multi-system organ failure.
3 Major causes of Shock
Cardiogenic (MI, arrythmia), hypovolemic (hemmorhage), Septic (infection).
Septic Shock
Secondary to infection (most commonly bacteria). Bacterial products cause vasodilation and increased vascular permeability. Associated with proinflammatory cytokines like IL-1 and TNF
Nonprogressive (compensated) shock
Blood pressure maintained, no urine output, tachycardia, vasoconstriction. Cold and clammy with rapid heart beat. Recovery possible.
Progressive (decompensated) shock
Hypotension, tissue hypoperfusion and hypoxia, renal insufficiency
Irreversible shock
BP down, pH down, organs die, death occurs
Histology of shock in liver
Centrilobular necrosis of the liver so it kind of looks like cirrhosis without the rigidity of the nodules.
