CH 6

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1/3

Accumulation of excessive body fluid in interstitial space or serous body cavity

Imbalance of fluid exchange between plasma and interstitial space

1. Increased venous pressure
2. Increased permeability of the vessel wall
3. Decreased oncotic pressure of plasma resulting from low albumin concentration
4. Obstruction of lymphatics

1. Inflammatory
2. Hydrostatic
3. Decreased oncotic
4. Lymphedema
5. Hypervolemic

Lead to increased vessel permeability
(Fluid escapes between endothelial cell gaps and into interstitial space)

Arterial pressure leads to increased pressure
(Venous stagnation most common cause of hydrostatic edema)

Increased retention of Na and H2O in kidney; leads to increased renin (RAS activation)

Increase protein and fluid leakage, cell inflammation

1. Increase hydrostatic pressure in blood vessels
2. Decreased oncotic pressure
3. Lymphatic obstruction
4. Na retention

Capillaries

Increased protein loss, decreased protein synthesis, hypoproteinemia

Lymphatic obstruction

1. Capillary hydrostatic and osmotic forces normally balanced
2. Increased hydrostatic pressure or decreased plasma osmotic pressure causes accumulation
3. Tissue lymphatics remove excess, if already at capacity, edema results

Hypervolemic and hydrostatic

RAS activated (increase of Na retention and H2O -> increased edema

Venous stagnation (typically in heart failure)

Increased pressure in pulmonary veins, congested pulmonary edema and pleural effusion

Venous congestion in lower extremities
(Pitting edema, ascites)

Inadequate perfusion of tissues
inability to generate adequate cardiac output to perfuse

Inability to pump oxygenated blood out of left side of heart to rest of body

Ventricle cant pump or fill with or eject blood; heart cant pump which affects lungs the most

Nephrotic syndrome, liver disease

Heart failure, mitral stenosis

Infections, aspiration, drugs, radiation

Increased capillary hydrostatic pressure and decreased blood flow

Decreased plasma albumin

Organ malfunction

Dilation of arterials

(congestion)
increase venous backpressure, stagnation of blood

hydrostatic edema

cyanosis

increased venous pressure leads to leakage of RBC into alveoli and alveolar edema

cardiac, aortic, arterial, capillary, and venous

passage of blood outside cardiovascular system

trauma, MI softening of muscle, ventricular rupture

trauma, aneurysm

wounds, damage to arterial wall, pulsating flow of blood

petechiae

slow, free-flowing, possible hypovolemia, internal

shock (>1000 mL blood loss) or death (>1500 mL blood loss)

blood loss, hypovolemic shock, exsanguination, death

internal hemorrhage fills body cavities, compression of tissues

stroke, death

slow blood loss, iron deficiency, anemia

pathologic intravascular thrombosis; promote activation of coagulation, or when there is stasis of blood flow

clotting and anticlotting factors remain in balance

end products of coagulation sequence, normally activated to prevent blood loss from disrupted vessels

activated in intact blood vessels leading to intravascular thrombosis

predisposing factors that lead to thrombosis

1. endothelial injury: vessel wall injury
2. alteration of blood flow (stasis)
3. hypercoagulability of blood

increased blood viscosity, immobility, mechanical blockage

increased procoagulants, platelet activity
decreased anticoagulants, fibrinolysis

alters local blood flow and affects coagulability

1. coagulation factors
2. platelets
3. endothelial cells

switch to procoagulation to bind platelets, adhesion, and stimulate release of von Willebrand factor

activates F8 and platelet adhesion
increases coagulation

allows them to bind coagulation proteins and promote thrombus formation

IL-1 and TNF124 which activates endothelial cells

lose their negative charge and antithrombogenic properties

factors that promote coagulation

1. disturbs normal flow of blood causing turbulence, platelets exposed and discharge granules
2. things that slow blood flow, promotes sedimentation of blood cells and formation of blood eddies

promotes coagulation and also damages the endothelial cells

platelets, coagulation proteins, endothelial cells

1. endothelial cell defect covered with fibrin and platelets
2. fibrin forma mesh that anchors blood cells to thrombus
3. full formed thrombus has layers of fibrin and blood cells

neutralize anti-coagulation factors and secrete procoagulation factor

stasis can lead to endothelial injury or hypercoagulability
hypercoagulability leads to endothelial injury

Overlying myocardial infarct

Endocarditis

Atherosclerosis, aneurysms

Varicose veins

Disseminated intramuscular coagulation (DIC)

Attached to the mural endocardium of the heart

Attached to arterial wall and typically cover ulcerated at hero as in atherosclerotic aorta or coronary arteries

Thrombi

Usually found I n dilated veins (varicose veins)

Small blood vessels in peripheral portion of circulation

Original lumen is delineated by internal elastic lamina and is totally filled with organized thrombus

Fibrin and platelet

Conglutination

Layers of Zahn (?)

1. Occlusion of lumen
2. Occlusion of vascular lumen
3. Narrow lumen of vessel
4. Lysis of thrombus
5. Organization of thrombis
6. Recanalization
7. Embolization

Infarct, ischemia

Hypoxia

Reperfusion

Reestablished blood flow

Detached thromboemboli carried by blood causing infarcts

Thrombotic occlusions of cardiac and cerebral arteries are major causes of death

Small thrombi

Attached, ingrowth granulation tissue (organization)

Stimulates in growth of inflammatory cells and vessels

Freely moveable, intramuscular mass that is carried from one anatomical site to another

All emboli can occlude blood vessels interrupting blood supply to an organ

Pulmonary embolism

Veins of lower extremities

Carried by venous blood to vena cava through r. Atrium and ventricle to pulmonary artery

Vessel bulging outward

Extravasating of blood leading to hematoma in extra vascular connective tissue

Suddenly onset of insufficiency of blood supply leading to ischemic necrosis

Sudden onset insufficiency of blood resulting in ischemic necrosis

Caused by thrombi or emboli
could be arterial or venous depending on site of vascular occlusion

Arterial occlusion preventing entry of blood

Venous obstruction of intestines and testes

Anatomic site
type of cells forming tissue
circulatory status of organisms
extent of necrosis
etc

Shock is profound circulatory failure leading to hypoperfusion of vital organs

1. Cardiogenic shock
2. Hypervolemic shock
3. Hypotensive shock

Pump failure of heart
decreased contractibility

Any major loss of fluid from circulation

Hemorrhage
surgery
trauma
burns
vomiting
diarrhea

Loss of peripheral vascular tone
dilation of blood vessels, pooling of blood in vessels

1. Early (reversible)
2. Cerebral arteries dilation
3. Compensatory vasoconstriction

Arterial networks can compensate to some extent

Cerebral arteries dilate when blood pressure is reduced, to keep normal rate of blood flow

Vasoconstriction to increase peripheral vascular resistance to maintain effective BP

Heart failure

Alterations in smooth muscle tone

Hypersensitivity, histamine

Infection

Insufficient intravascular fluid

Decreased BP, cardiac output, and urinary output; increased respiratory rate

Oxygenation! ; remove underlying cause
supportive therapy