T20: hemodynamics, edema, hemorrhage, hemostasis

hemodynamics

how blood flows through your vessels

hemodynamic factors

things that affect how well your blood flows

hemodynamic instability

means body can't get enough blood flow (aka shock)

hyperemia and congestion refer to

an increase in blood volume within a tissue

hyperemia

active process resulting from arteriolar vasodilation and increased blood inflow

where does hyperemia occur

sites of inflammation and in exercising skeletal muscle

describe hyperemic tissues

redder than normal bc engorged with oxygenated blood

congestion

passive process resulting from impaired outflow of venous blood from a tissue

congestion in liver and extremities is caused by

right heart failure

congestion in lungs is caused by

left heart failure

describe congested tissues

abnormal blue-red color (cyanosis) that stems from accumulation of deoxygenated hemoglobin

2/3 of body water is

intracellular

1/3 of body water is

extracellular

extracellular blood is composed of

interstitial fluid

blood plasma

edema

an accumulation of interstitial (extravascular) fluid within tissues

effusion

accumulation of extravascular fluid in body cavities

hydrothorax/pleural effusion

fluid in the pleural cavity

hydropericardium / pericardial effusion

fluid in pericardial cavity

hydroperitoneum/free fluid/ascites

fluid in peritoneal cavity

anasarca

severe, generalized edema marked by profound swelling of SQ tissues and accumulation of fluid in body cavities

pitting edema

edema that retains an imprint when touched, commonly associated with left-sided CHF, usually LE

why does edema accumulate

increase vascular hydrostatic pressure

decreased plasma osmotic pressure

lymphatic obstruction

inflammation

fluid movement between vascular and interstitial spaces is governed by what

vascular hydrostatic pressure

colloid osmotic pressure

hydrostatic pressure

the pressure within a blood vessel that tends to push water out of the vessel

osmotic pressure

the external pressure that must be applied to stop osmosis

the edema fluid that accumulates due to high hydrostatic pressure or low colloid osmotic pressure is a _______

protein-poor transudate

inflammatory edema fluid is a _______

protein-rich exudate

why is inflammatory edema a protein-rich exudate

because increased vascular permeability

causes of edema

increased hydrostatic pressure

impaired venous return

arteriolar dilation

reduced plasma osmotic pressure

lymphatic obstruction

sodium retention

inflammation

hemorrhage

the leakage of blood from vessels

hemorrhagic diatheses

bleeding disorders

4 types of hemorrhage

petechiae

purpura

eccymoses

hematoma

large bleeds into body cavities are described according to their _____

location

why do large hemorrhages occasionally result in jaundice

RBC and hemoglobin are broken down by macrophages

petechiae

minute hemorrhages into skin, mucous membranes, or serosal surfaces

causes of petechiae

low platelet counts

defective platelets

loss vascular wall-support

increased vascular pressure

(1-2mm diameter)

purpura

3-5mm hemorrhages and usually raised

causes of purpura

vascular inflammation

trauma

increased vascular fragility

same disorders that cause petechiae

petechiae (picture

purpura (picture

ecchymosis

1-2 cm SQ hematomas (bruises)

extravasated

let or forced out from the vessel into the surrounding area

cause of ecchymosis

trauma

early bruising appears

red-blue to blue-green

bruising eventually turns what color

golden-brown

ecchymosis (picture)

hematoma

hemorrhage that accumulates within a tissue

clinical impact of a hemorrhage depends on:

1. volume blood lost

2. rate of bleeding

3. location of bleed

4. health of individual

hemostasis

process initiated by a traumatic vascular injury that leads to the formation of a blood clot

pathogenic counterpart of hemostasis

thrombosis

thrombosis

formation of a clot (thrombus) within vessels that is inappropriate

thrombus

blood clot

thrombus is formed of

platelets, fibrin, +/- RBC

when does a thrombus occur

when procoagulant component of hemostasis escapes the regulatory factors and fibrinolysis (when disruption of factors that contsitute Virchow's triad)

virchow triad

the primary abnormalities that lead to intravascular thrombosis

components of virchow's triad

endothelial injury

stasis/turbulent blood flow

hypercoagulability

how does abnormal blood flow lead to arterial/cardiac thrombosis

-by causing endothelial injury/dysfunction

-by forming countercurrents and local pockets of stasis

hypercoagulability

an abnormally high tendency of the blood to clot

hypercoagulability is an important risk factor for

venous thrombosis (occasionally contributes to arterial or intercardiac thrombosis)

what is hypercoagulability caused by

alterations in coagulation factors

arterial thrombosis commonly present as

myocardial infarction or stroke

venous thrombosis commonly present as

DVT in smaller veins of legs/arms

embolize

when venous thrombi can detach and travel elsewhere

what happens to thrombi?

propagation

organization

recanalization

dissolution

embolization

primary complication of thrombi

occlusion of BV > leading to ischemia

embolus

detached intravascular solid/liquid/gaseous mass that is carried by the blood from its point of origin to a distant site (where it often causes tissue dysfunction or infarction)

the vast majority of emboli derive from _____

dislodged thrombi (blood clot)

fat emboli

emboli composed of fat droplets

air emboli

bubbles of air/nitrogen

cholesterol emboli

atherosclerotic debris

primary consequence of systemic embolization (arterial)

ischemic necrosis (infarction) of downstream tissues

primary consequence of pulmonary embolization (venous)

hypoxia, hypotension, R sided heart failure

infarct

area of ischemic necrosis (dead cells) caused by occlusion of vascular supply of affected tissue

effects of vascular occlusion are influenced by

- anatomy of vascular supply

- rate of occlusion

- tissue vulnerability to hypoxia

most important factor in determining whether occlusion of an individual BV causes damage

presence or absence of an alternative blood supply

organs that can withstand infarction due to dual blood supply

lungs, liver

organs that cannot withstand infarction due to end-arterial circulations

kidneys, spleen

why are slow developing occlusions less likely to cause infarction

because they allow time for the development of collateral blood supplies

neurons and hypoxia

die after 3-4 minutes of ischemia

mycardial cells and hypoxia

die after 20-30 minutes of ischemia

thromboembolism underlies 3 major causes of morbidity and death:

mycardial infarction

pulmonary embolism

stroke

primary hemostasis

formation of platelet plug

steps of hemostasis

1. vasoconstriction

2. primary hemostasis

3. secondary hemostasis

4. clot stabilization

what happens in arteriolar vasoconstriction

injured endothelial cells release endothelin > vessels contract

steps of primary hemostasis

1. platelet adhesion

2. shape change

3. granule release

4. recruitment

5. aggregation

platelet adhesion

platelets bind to von willebrand's factor (released by endothelial cells) on collagen

how do platelets bind to vWf

GP1b receptor on platelets binds to vWf on collagen

platelet shape change

platelets change from small and round to flat, spiky protrusions that increase SA

granule release and recruitment

platelets release granules (vWf, serotonin, ADP, thromboxane A2) to attract more platelets

aggregation

aggregation of platelets at site of injury to form a platelet plug

secondary hemostasis

deposition of fibrin

tissue factor (factor 3)

membrane-bound procoagulant glycoprotein normally expressed by subendothelial cells in vessel wall (ie smooth muscle cells and fibroblasts)

extrinsic and intrinsic pathways lead to activation of _______ at the ______ pathway

factor Xa

common pathway

activation of factor Xa leads to what?

formation of fibrin mesh

tissue factor binds and activates factor 7 that lead to

thrombin generation

functions of thrombin

-activates platelets

-activates 5a (commmon) and 8 (intrinsic)

-cleaves fibrinogen > fibrin

-cleaves stabilizing factor (8a)

prothrombin

factor 2

thrombin

factor 2a

fibrin

factor 1a

fibrinogen

factor 1