Week 3: Hemodynamics

Question 1

What is hemodynamics?

Answer 1

Study of blood flow, including physical factors that govern blood flow

Question 2

What is laminar flow?

Answer 2

Fluid particles following smooth paths in layers, with each layer moving past the adjacent layers without mixing

Concentric layers (like a target) movind in parallel down the length of the blood vessel

Question 3

What physical elements of fluid flow might cause a change in the fluid balance in a blood vessel?

Answer 3

Changes in hydrostatic or plasma colloid (oncotic) pressure

Question 4

What are common forms of edema?

Answer 4

Pleural effusion (lung cavity)

Pericardial effusion (heart cavity)

Ascites (abdominal cavity)

Anasarca (generalized edema)

Question 5

What are common etiologies of edema?

Answer 5

Increased hydrostatic pressure (impaired venous outflow, arteriolar dilation)

Reduced plasma osmotic pressure (excessive loss or reduced synthesis of albumin)

Increased vascular permeability

Sodium retention

Lymphatic obstruction

Question 6

What are the gross, microscopic and clinical signs of edema?

Answer 6

Gross: heavier, appears swollen

Microscopic: increased clear/pink fluid with tissue and occasional cells

Clinical: signs/symptoms vary with organ and extent, general increase in fluid in the area

Question 7

What are the terms for a change in bloodflow through capillaries, and what is occuring in these cases?

Answer 7

Hyperemia (erythema) occurs when there is increased flow, as in exercise and/or inflammation–vessels are dilated and well-perfused with oxygenated blood

Congestion (cyanosis/hypoxia) occurs when there is a blockage of flow on the proximal end of the capillaries, preventing oxygenated blood from moving into tissues, and creating a buildup of blood in the proximal arterioles

Question 8

What has occurred in this tissue?

Answer 8

Infarction and necrosis have occurred in one area of tissue (white) due to congestion, which has caused hyperemia in the remainder of the organ (kidney). This presents as increased blood volume due to arteriolar dilation, giving the tissue a reddish appearance.

Question 9

What has occurred in this tissue?

Answer 9

Congestion in the liver, a passive process of increased bloodflow as a result (usually) of impaired outflow

Question 10

What is hemostasis?

Answer 10

The maintenance of blood in a fluid state, and the formation of clots at sites of vascular injury

Question 11

What can occur in abnormal hemostasis?

Answer 11

Hemorrhagic disorders

Thrombotic disorders

Question 12

What occurs in a hemorrhagic disorder?

Answer 12

Hemostatic mechanisms are insufficient to prevent blood loss

Question 13

What occurs in thrombotic disorders?

Answer 13

Blood clots form abnormally within intact blood vessels

Question 14

What occurs in normal hemostasis? What are the major blood elements involved?

Answer 14

It is the process that results in a blood clot and prevents excessive blood loss

Endothelium, platelets, and coagulation proteins (fibrin) working together

Question 15

What is involved in primary and secondary coagulation? What occurs in fibrinolysis?

Answer 15

Primary: aggregation of platelets and the formation of a platelet plug

Secondary: cascade and final formation of fibrin meshwork and stabilization of clot via factors released from the endothelium

Fibrinolysis: moderates clot size, limits clotting to the site of injury and ultimately leads to clot resorption

Question 16

What are the four major steps in hemostatic injury repair, and what generally occurs in each of them?

Answer 16

1) Vasoconstriction by release of endothelin, ECM pulles together
2) Primary homeostasis occurs by platelet adhesion, shape change, granular release/recruitment of other platelets, and formation of the hemostatic plug
3) Secondary homeostasis occurs by addition of tissue factors, phosopholipid complex expression, thrombin activation, and fibrin polymerization
4) Release of t-PA and thrombomodulin mediates and decreases thrombus size, helps clear vessel

Question 17

What are the major factors that are released during wound healing that assist in the process of hemostasis?

Answer 17

Primary hemostasis - von Willebrand factor

Secondary hemostasis - tissue factor

Question 18

What are the major elements of platelet plug formation, and what kinds of receptors are involved?

Answer 18

Disruption of the endothelium leads to exposure of activating factors on the damaged vessel wall (i.e. vWF in the collagen matrix)

Platelets adhere, change shape, release their contents and then aggregate to form a clot

Question 19

What are the two major pathways of the coagulation cascade? What are their major characteristics?

Answer 19

Intrinsic pathway - requires exposing Factor XII to a thrombogenic surface

Extrinsic pathway - requires the addition of an exogenous trigger

Question 20

What are the major factors of the extrinsic pathway? How can we analyze the efficacy of this pathway from a lab standpoint?

Answer 20

Factors I, II, V, VII and X

Lab testing for extrinsic coagulation abnormalities can be done with PT (Prothrombin Time)

Question 21

What are the major factors of the intrinsic pathway? What test can be done to assess the efficacy of this pathway?

Answer 21

Factors I-XIII EXCEPT VII and XIII

The efficacy of the intrinsic pathway can be assessed with aPTT (activated Partial Thromboplastin Time)

Question 22

Which factor is unique to the extrinsic pathway?

Answer 22

Factor VII

Question 23

Deficiencies of which factors typically leads to moderate/severe bleeding?

Answer 23

Factors V, VII, VIII, IX and X

(5, 7, 8, 9, 10)

Question 24

What is the main role of thrombin in the coagulation cascade?

Answer 24

It cleaves fibrinogen to fibrin

Activates Factor XIII (stabilizing clot)

Induces platelet aggregation

Activates leukocytes

Question 25

What factors can limit coagulation?

Answer 25

Dilution

Decreased exposure to phospholipid surfaces (platelets)

Anti-thrombotic properties of adjacent endothelium

Production of plasmin (fibrinolysis)

Question 26

What is the general sequence of the fibrinolysis cascade?

Answer 26

Plasminogen is activated by:

Tissue plasminogen activator (endothelium)

Urokinase (endothelium)

Factor XII-dependent pathway

Plasminogen then generates plasmin

Question 27

What is the function of plasmin?

Answer 27

It breaks down fibrin and interferes with it’s polymerization

Fibrin split products are released (D-dimers)

Question 28

What are the pro- and anti-thrombotic properties of primary hemostasis?

Answer 28

Pro: von Willebrand factor

Anti: Prostacyclin, NO, ADP

Question 29

What are the pro- and anti-thrombotic elements of secondary homeostasis?

Answer 29

Pro: Tissue factor

Anti: Heparin-like molecules, thrombomodulin, tissue factor pathway inhibitor

Question 30

What are the pro- and anti-thrombotic elements of fibrinolysis?

Answer 30

Pro: Plasminogen activator inhibitor

Anti: Tissue type plasminogen activator

Question 31

What is hemorrhage?

Answer 31

Extravasation of blood outside the vessel

Question 32

What is thrombosis?

Answer 32

Formation of a thrombus. A thrombus is an abnormal aggregate or collection of platelets, fibrin, and other entrapped cellular elements within a vascular lumen

Question 33

What are petechiae? Why does it occur?

Answer 33

“Peh-teak-ee-ay” is a collection of small pinpoint hemorrhages in tissue.

Petechiae often occurs due to hypoxic capillary damage, or due to abnormalities in platelets

Question 34

What is stenosis?

Answer 34

Narrowing of a blood vessel

Question 35

What are the three major issues that can lead to thrombosis? What is this referred to as?

Answer 35

1: Endothelial injury

This is referred to as Virchow’s triad. We remember this by SHE

Stasis of bloodflow (venous side)

Hypercoagulability

Endothelial injury

Question 36

Where does abnormal bloodflow tend to occur and why? What is the etiology of hypercoagulability?

Answer 36

Abnormal bloodflow tends to occur on the arterial end of blood vessels (rather than the venous). This is called turbulance.

Hypercoagulability arises from the improper and/or unregulated coagulation of blood (can include hereditary abnormalities, inactivity, and smoking for example)

Question 37

What appears in arterial thrombosis?

Answer 37

Occlusive buildup and gray-white accumulation due to platelet accumulation

Question 38

What appears in venous thrombosis?

Answer 38

Reddish skin, edema–stasis is usually made of red blood cells

Question 39

What is mural thrombosis and where does it occur?

Answer 39

Thrombus that forms in the heart wall. That thrombus is subjected to high pressure, so all or part of it can break off and move to other locations, possibly causing a stroke in the brain for example.

Usually from hypocontractility and endocardial damage

Can lead to MI

Question 40

What are the outcomes of thrombosis?

Answer 40

Resolution (clearing)

Embolization (detachment and movement) to lungs

Organized and incorporated into endothelial wall

Organized and recanalized (reformation of smaller “tube” structures)

Question 41

What is an embolism?

Answer 41

A detached intravascular solid, liquid or gaseous mass that is carried by the blood to a site distant from the point of origin

Question 42

What is a thromboembolism?

Answer 42

The most common kind of embolism, usually pulmonary thromboembolism (lung embolism), brain/CNS (stroke)

The brain is a common source of thromboemboli with decreased valves or secondary to mural thrombi. The result is a systemic arterial embolism that may lodge in the brain, intestine, lower extremety or kidney.

Question 43

How do fat embolisms commonly occur?

Answer 43

Portions of marrow–normally containing fat–are released into bloodstream. Usually follows severe injury, like multiple bone fractures or burns (sometimes in ortho surgery, but rare)

Fat embolism syndrome: respiratory failure, mental confusion, DIC (disseminated intravascular coagulation) secondary to mechanical injury of fatty tissue, and from initiation of the coagulation cascade

Question 44

How can air embolisms occur?

Answer 44

Gas bubble formation that can obstruct vascular flow and lead to distal ischemic injury. May occur when divers ascend rapidly, decompressing and releasing gas bubbles into the blood

Question 45

How do amniotic fluid embolisms occur?

Answer 45

Amniotic fluid enters maternal circulation postnatally via tears in maternal veins. Amniotic fluid is highly thrombogenic (sometimes contain infant’s epithelial cells), and can cause obstruction.

Symptoms: mental confusion/agitation, shortness of breath. Onset is sudden and it is often fatal.

Question 46

What is an infarction?

Answer 46

An area of ischemic necrosis caused by occlusion of either the arterial supply or venous drainage in a particular tissue

White infarct: end-artery

Red: may occur in areas of previous congestion, dual circulation, venous infarction, and re-perfusion

Question 47

What is shock?

Answer 47

A state of diminished CO or reduced effective circulating blood volume, which impairs perfusion and leads to cellular hypoxia

Secondary to serious medical issues like trauma or sepsis

Creates circulatory collapse from systemic hypotension, hypoperfusion, impaired tissue oxygenation, cell hypoxia and metabolic disturbances

Question 48

What are the different stages of shock?

Answer 48

Non-progressive: compensatory mechanisms make it hard to recognize

Progressive: tissue hypoperfusion and worsening metabolic/circulatory imbalances

Irreversible: tissue damage is not reversible and the pt will not survive

Question 49

What is septic shock?

Answer 49

Clinical syndrome in response to infectious agents (usually bacteria). Causes vasodilation and pooling of peripheral blood. Inflammatory cells and thrombosis are occurring simultaneously.

Symptoms:

Hypovolemic/cardiogenic shock = weak, rapid pulse, tachypnea, cool, clammy, cyanotic skin

Septic shock = fever, tachycardia, tachypnea, confusion, warm skin initially, with failure skin becomes cool and clammy