Hemodynamics Flashcards
EDEMA, HYPEREMIA AND HEMORRHAGE
symptoms (5)
-Tumor
-Rubor
-Calor
- Dolar
- Loss of function
Edema –
escape of fluid
Congestion –
Abnormal accumulation of blood
Infarction –
ischemic necrosis
Shock –
tissue injury secondary to systemic hypotension
Hemorrhage –
escape of whole blood
Thrombosis –
undesired clotting of blood
Embolism –
detached intravascular mass
Water accounts for –% of the lean body weight
60
Total body water is distributed between the
intracellular and extracellular compartments
Extracellular compartment
(2)
• Intravascular 5%
• Interstitial 15%
Hydrostatic Pressure
• Pressure exerted by volume of blood when confined
to a blood vessel
Osmotic (Oncotic) Pressure
(2)
• Proteins in blood vessels
• Albumin
Movement of Water Between the
Intravascular and Interstitial Spaces
Opposing effects of
vascular
hydrostatic pressure and
plasma colloid osmotic
pressure
Outflow at the arterial end
is nearly balanced by
inflow
at the venular end
Residual fluid left in the
interstitium is drained by
lymphatic vessels
— ml/min out
14
— ml/min in
12
— ml/min to
lymphatics
2
Increased hydrostatic pressure or decreased plasma osmotic pressure will cause
interstitial fluid to increase
If the capacity for lymphatic drainage is exceeded,
fluid accumulates (edema)
Edema -
swelling of tissues that result from excessive accumulation of fluid
Edema -
may be (3)
• May be highly localized as occurs in a small region of skin involved with an insect bite
• May be more regionalized, involving an entire limb or a specific organ, such as the lungs (e.g., pulmonary edema)
• May be generalized, involving the whole body
Hydrothorax
pleural effusion
Hydropericardium
pericardial effusion
Hydroperitoneum
ascites
Anasarca
generalized edema
Inflammatory causes of edema -
-inflammatory edema is caused by increased vascular permeability of a protein-rich exudate (exudate)
Non-inflammatory causes of edema -
edema caused by increased hydrostatic pressure or reduced oncotic pressure is usually protein-poor fluid (transudate)
Non-inflammatory causes of edema -
ex (4)
• Heart failure
• Renal failure
• Hepatic failure
• Malnutrition
Exudate –
high specific gravity – protein rich
• Inflammatory edema
Transudate –
low specific gravity – protein poor
• Volume or pressure overload
• Reduced plasma protein
Lymphangitis (2)
• Lymphatic spread of
bacterial infection
• Painful red streaks
and regional
lymphadenopathy
Lymphedema – (3)
a term used to describe an increase in
fluid in the interstitial space caused by an abnormality
in the lymphatic system
• Lymphatic fluid collects in tissues causing edema
• May be congenital or acquired
Acquired lymphedema
(2)
• Infection - filariasis
• Surgery, radiation therapy
Congenital Lymphedema - Aplasia
• Congenital malformation
of lymphatic system
Congenital Lymphedema - Aplasia
• Age 1 Week:
Lymphoscintigraphy exhibits
no migration of
radiopharmaceutical agent
from right foot to right
inguinal nodes
Congenital Lymphedema - Aplasia
• Diagnosis:
congenital aplasia
of the lymphatic system of
right leg
Congenital Lymphedema - Aplasia
Age 4.5 months:
debulked
Stewart-Treve Syndrome
(2)
• Angiosarcoma arising
from chronic
lymphedema
• Long-standing
lymphedema
secondary to surgical
lymph node dissection
and/or radiation
therapy
Anasarca in Renal Disease
(2)
• Severe
• Generalized edema
Edema Danger Zones (2)
• Lungs - Pulmonary edema
• Brain - Cerebral edema (central nervous system)
Cerebral Edema -
Cerebellar Tonsil Herniation (2)
• Increased intra-cranial pressure may result in herniation through the foramen magnum
• Compression of the medulla results in depression of the centers for respiration and cardiac rhythm control
Localized edema is usually caused by
(2)
• Increased vascular permeability (injury-inflammation)
• Obstruction of venous or lymphatic outflow
Generalized edema is generally caused by
decreased
plasma osmotic pressure
Increased hydrostatic pressure -
def
ex (2)
impaired venous return
• Congestive heart failure
• Venous obstruction or compression
Decreased plasma osmotic pressure (hypoproteinemia)
(3)
• Protein-losing glomerulopathies (nephrotic syndrome)
• Liver cirrhosis (ascites)
• Protein malnutrition
Lymphatic obstruction
(4)
• Inflammatory
• Neoplastic
• Postsurgical
• Postirradiation
Sodium retention
(4)
• Excessive salt intake with renal insufficiency
• Increased tubular reabsorption of sodium
- Renal hypoperfusion
- Increased renin-angiotensin-aldosterone secretion
Inflammation
increased permeability
Hyperemia
An active process in which
arteriolar dilation leads to
increased blood flow
• Sites of inflammation
• Skeletal muscle during
exercise
Hyperemia
Affected tissues turn red
(erythema) because of
engorgement of vessels with
oxygenatged blood
Congestion –
Deep Venous Thrombosis
(3)
• A passive process resulting from
reduced outflow of blood from a tissue
(stasis)
• May be systemic (heart failure) or
local (isolated venous obstruction)
• Congested tissues take on a dusky,
reddish-blue color (cyanosis) due to
red cell stasis and accumulation of
deoxygenated hemoglobin
Nutmeg Liver
Chronic Passive Congestion of Liver
Superior Vena Cava Syndrome
Compression of
superior vena cava
by neoplasm
obstructing venous
return
Hemorrhage –
extravasation of blood into the extravascular space
Capillary bleeding
oozing
Venous hemorrhage
seeping
Arterial hemorrhage
pulsating
Severe hemorrhage
rupture of a large vessel secondary to injury
Severe hemorrhage
ex (3)
Trauma, atherosclerosis, erosion of a vessel wall (inflammation or neoplasia)
Hemorrhagic diathesis –
increased tendency to hemorrhage occurs in a
variety of clinical disorders collectively called hemorrhagic diatheses
Hemothorax
thoracic cavity
Hemopericardium
pericardial cavity - cardiac
tamponade
Hemoperitoneum
peritoneal cavity
Hemarthrosis
joints
Petechiae
pinpoint hemorrhages
Purpura
petechiae become
confluent
Ecchymosis
purpurae become
confluent
Hematoma
cavity
Hemoglobin
red-blue
Biliverdin
yellow-green
Bilirubin
green-brown
Hemosiderin
golden yellow
Site of hemorrhage
• Subcutaneous tissues vs brain
Volume and rate of hemorrhage
• Rapid loss of up to —% of blood
volume, or slow losses of larger
amounts may have little impact on
healthy adults
• Greater losses may cause
20
hemorrhagic (hypovolemic) shock
Immune Thrombocytopenic Purpura (ITP) (2)
• Autoimmune disease–
antiplatelet
autoantibodies produce
thrombocytopenia
• Treatment with
steroids, splenectomy
Hemostasis –
a physiologic process that maintains blood in a fluid state in normal vessels, yet also permits the rapid formation of a hemostatic clot at the site of a vascular injury
Thrombosis –
pathologic counterpart of hemostasis that involves blood clot
Hemostasis and Thrombosis
Both involve three components
• Vascular wall (endothelium)
• Platelets
• Coagulation cascade
von Willebrand Disease (5)
Most common hereditary bleeding disorder
• Group of bleeding disorders
• Quantitative or qualitative abnormality of
the von Willebrand factor (vWF)
• vWFis required for normal platelet
adhesion
• vWF is the carrier protein for factor VIII
vWF has functions in both
primary and secondary hemostasis
Primary hemostasis – vWF:
(2)
• Attaches to platelets via a receptor for glycoprotein Ib on the platelet surface
• Acts as a bridge between the platelets and damaged subendothelium at the site of vascular injury
Secondary hemostasis – vWF:
(2)
• Protects factor VIII from degradation
• Delivers factor VIII to the site of injury
von Willebrand Disease (2)
• Normal platelet count with increased bleeding time
• Compound defect involving platelet function and coagulation pathway
Factors Favoring Thrombosis (Virchow’s Triad)
• Endothelial injury
• Stasis or turbulent blood flow
• Hypercoagulability of the blood
• Balance between antithrombotic and prothrombotic properties of endothelium determines
whether thrombus formation, propagation or dissolution occurs
Normally, endothelial cells exhibit (3) properties
antiplatelet, anticoagulant and antifibrinolytic
Endothelial cells may be activated by (5)
trauma,
infectious agents,
hemodynamic forces,
plasma mediators and
cytokines
After activation, endothelial cells acquire
procoagulant activities
• Mural thrombi
• Occur in heart chambers or aortic lumen
• Arterial thrombi
(3)
• Frequently occlusive
• Coronary, cerebral, femoral arteries, most commonly
• Superimposed on ruptured, ulcerated atherosclerotic plaque
• Venous thrombi
(2)
• Usually occlusive – thrombus forms a long cast of the lumen
• Veins of lower extremities
• Vegetations –
thrombi on heart valves
Thrombi are focally
attached to the
underlying
vascular surface
Thrombi propagate from
the point of attachment in
the direction of blood flow
The propagating portion
of a thrombus is often
poorly attached and is
prone to
fragmentation
and embolization
Arterial or cardiac thrombi
(2)
• Begin at sites of turbulence or endothelial injury
• Propagate away from the heart
Venous thrombi
(2)
• Occur at site of stasis
• Propagate toward the heart
Lines of Zahn (4)
• Thrombi often have groosly and microscopically apparent laminations called lines of Zahn
• Pale platelet and fibrin deposits alternating with darker red cell-rich layers
• Laminations signify that a thrombus has formed in flowing blood
• Their presence can therefore distinguish antemortem thrombosis from the bland, non-laminated clots that occur postmortem
Fate of a Thrombus (4)
Dissolution
Propagation
Embolization
Organization and recannalization
• Dissolution –
fibrinolysis (plasmin)
• Propagation –
accumulate additional platelets and fibrin
• Embolization –
dislodge and travel to other sites in the vasculature
• Organization and recannalization
(2)
• Ingrowth of endothelial cells, smooth muscle cells and fibroblasts
• Capillary channels eventually form that re-establish the continuity of the original lumen to a variable degree
Clinical Consequences of Thrombi (2)
• Obstruct veins and arteries
• Embolize downstream
Venous thrombi (phlebothrombosis)
(2)
• Congestion and edema in vascular beds distal to the obstruction
• Embolize to lungs and cause death
Arterial thrombi
(2)
• Thrombotic occlusions at critical sites (stroke, myocardial infarct)
• Embolize and cause downstream infarctions
Most venous thrombi occur in
superficial or deep veins of lower extremity
Superficial venous thrombi
(2)
• Cause local congestion, swelling, pain and tenderness
• Rarely embolize
Deep venous thrombi (DVT)
(3)
• Cause local pain and edema – rapidly offset by collateral channels
• More often embolize to lungs
• Half are asymptomatic, recognized in retrospect after embolization
15
Risk Factors for Venous Thrombi (7)
• Hypercoagulable states
• Endothelial injury
• Bedrest, immobilization
• Congestive heart failure
• Trauma, surgery, burns
• Thrombotic diathesis of pregnancy
Neoplasia
Risk Factors for Arterial
and Cardiac Thrombi (3)
• Cardiac and aortic mural thrombi may embolize
peripherally and cause infarcts of brain, kidney and spleen
• Major cause of arterial thrombi is atherosclerosis
• Predisposition to cardiac thrombi associated with
• Myocardial infarct
• Rheumatic heart disease
• Atrial fibrillation
Disseminated Intravascular
Coagulation (DIC)
• Formation of widespread fibrin thrombi in the microcirculation
• Thrombi not grossly visible – can be seen microscopically
• May cause diffuse circulatory insufficiency, especially in brain,
heart, lungs and kidneys
• Widespread microvascular thrombosis results in platelet and
coagulation protein consumption (consumptive coagulopathy)
• Fibrinolytic mechanisms are activated
• The initially thrombotic disorder may evolve into a bleeding
disorder
• Not a primary disease but a potential complication of any
condition associated with widespread activation of thrombin
• Obstetric complication
• Advanced malignancy
Embolus
A detached intravascular solid, liquid or gaseous
mass that is carried by the blood to a site distant
from its point of origin
Embolus
Lodge in vessels…
too small to permit further
passage and cause partial or complete occlusion
Embolus
Major consequence is
ischemic necrosis (infarction) of
the downstream tissue
Thromboembolus –
almost all emboli represent
some detached part of a thrombus
Venous emboli –
tend to lodge in one vascular bed (lung)
• Arterial emboli –
can travel to a wide variety of sites
Arterial emboli
Point of arrest depends on (2)
source and relative amount of blood flow
Arterial emboli
Major sites are
Major sites are lower extremities and brain
Arterial emboli
Consequences depend on
vulnerability of tissue to ischemia, caliber of occluded vessel and collateral blood supply
Paradoxical Embolus
An embolus that originates on the right
side venous circulation and lodges in
the left side systemic arterial
circulation
• Thromboemboli –
most emboli are thromboembolic in origin
• Fat -
bone fractures
• Bone marrow -
bone fractures
• Air -
• Nitrogen bubbles –
decompression sickness in divers caisson disease
• Atherosclerotic debris (cholesterol emboli) -
• Tumor fragments -
• Amniotic fluid –
obstetric complication
• Foreign bodies –
catheters, etc.
• Infarct -
an area of ischemic necrosis caused by occlusion the
vasculature
• Most infarcts occur from
thrombotic or embolic arterial
occlusions
• Venous thrombosis may cause
infarction, but usually just
congestion
• Atherosclerotic vascular disease causes
40% of all deaths in the
United States – mostly myocardial infarction or cerebral
infarction
Ischemia
(2)
• Restriction in blood supply, usually due to factors in
the blood vessels
• Oxygen, glucose and other blood-borne materials
• Infarct
(2)
• Complete loss of blood supply, resulting in necrosis
• An area of ischemic necrosis
• Hypoxia
(2)
• More general term denoting a shortage of oxygen
• Usually a result of lack of oxygen in the air being
breathed
Factors that Influence Development of an Infarct
(4)
Nature of the vascular supply – single vs double
Rate of occlusion development
Vulnerability of individual tissue to hypoxia
Amount of oxygen in the blood – anemia or cyanosis
Nature of the vascular supply – single vs double
(3)
• Lungs – dual pulmonary artery and bronchial artery
blood supply
• Liver – dual hepatic artery and portal vein circulation
• Kidney and spleen circulations are end-arterial
Rate of occlusion development
• Slowly-developing occlusions provide time to develop
alternate perfusion pathways – collateral circulation
Vulnerability of individual tissue to hypoxia
• Neurons –
• Cardiac myocytes –
• Fibroblasts -
3 to 4 minutes
20 to 30 minutes
hours
Insufficient blood supply is the most common cause of
gangrene
types of gangrene
• Ischemic gangrene (dry gangrene)
• Infectious gangrene (wet gangrene)
gangrene
Often associated with
peripheral vascular disease secondary to diabetes and long-term smoking
Thrombophlebitis -
Phlebothrombosis (2)
• Superficial veins
• Deep leg veins – high risk
of pulmonary embolus
Trousseau Syndrome (4)
• Migratory thrombophlebitis
• Paraneoplastic syndrome
• Hypercoagulability
• Adenocarcinoma
• Pancreas
• Colon
• Lung
Shock
Systemic hypotension due to either reduced
cardiac output or to reduced effective
circulating blood volume
shock leads to
impaired tissue perfusion and
cellular hypoxia
shock
Initially — cellular injury
reversible
Prolonged shock leads to
irreversible cellular
injury
Cardiogenic shock –
low cardiac output due to pump
failure
Causes of Shock (4)
• Myocardial infarct
• Ventricular arrythmias
• Extrinsic compression (cardiac tamponade)
• Outflow obstruction (pulmonary embolism)
Hypovolemic shock –
def
ex (2)
low cardiac output due to loss of
blood or plasma volume
• Massive hemorrhage
• Fluid loss from severe burns
Septic shock –
vasodilation and peripheral pooling of blood
as part of a systemic immune reaction to a bacterial or
fungal infection
