HEMODYNAMICS (Dr



HEMODYNAMICS (Dr. Lena)

general factors (hydrostatic pressure, osmotic pressure)

local factors (venous drainage/pressure, lymph obstruction, low tissue tension)

EDEMA

obsruction decrease blood flow

thrombus infarct shock

embolism

escape of blood increase blood flow

hemorrhage hyperemia congestion

(active) (passive)

EDEMA

← increase of extracellular fluid (Interstitial spaces & serous cavities) exceeding the rate of drainage via the lymphatics

← " transudate" - non-inflammatory fluid

← "exudate" - inflammatory fluid

accumulation in body cavities

▪ hemothorax (pleural effusion)

▪ hydroperitoneum (ascites)

▪ anasarica (dropsy) - generalized edema transudate

▪ hydropericardium

▪ synovial effusion

causes of edema

A. increase hydrostatic pressure (esp. in venular end)

e.g. congestive heart failure (generalized)

pedal edema with blockage of femoral vein (localized)

postural edema - common among elders

B. decrease oncotic pressure (protein ( 2.5 g/dL - albumin)

e.g. liver disease as cirrhosis

renal disease as nephritic syndrome

nutritional disease as kwashiorkor

protein - losing gastroenteropathy

C. obstruction of lymph flow

e.g. lymphedema in a Ca of breast (surgery)

Moroy's disease (congenital anomaly)

- absence of lymph vessels affecting the extremities

D. increase osmotic pressure of tissue fluid (due to Na & H2O retention)

e.g. secondary to conditions with renal perfusion (renin-angiotensin mechanism)

increase intake with diminished renal function

E. low tissue tension (usually in the eyelids)

- nephrotic syndrome

F. increase of capillary permeability

(infection, poisoning, anaphylactic reaction, anoxia, burns & trauma)

conditions that cause edema

I. generalized edema

A. congestive heart failure (CHF)

- usually dependent edema

1. backward failure (passive congestion)

2. forward failure

- ( CO - ( aldosterase - ( enzyme & renal disturbance - Na & H2O retention

B. nephrotic syndrome (proteinuria, hypoproteinemia, edema, increased cholesterol)

- edema in loose CT

C. liver cirrhosis

- due to: hypoproteinemia

( hydrostatic pressure in portal vein ( ( pressure sinusoids & lymphatic vessels ( transudation of fluid

← expansion of vascular bed ( hypoxia ( Na retention

D. starvation - because of diminished protein intake

E. Na retention

II. localized edema

A. impaired venous drainage (varicosities, phlebothrombosis)

B. increased vascular permeability

C. lymphatic obstruction

edematous

← tense

← swollenly large

← frothy fluid

← liver - bloody fluid

← granular sites - eosinophilic between cells & interstitium

EDEMA

1. lower leg - "mabug-at maglakat"

2. brain - ( intracellular pressure leading to herniation then death

3. lungs - "rals" - sound of ratlle snake

- severe - rattle death

4. allergy - anaphylactic shock

- laryngeal edema

pericardial effusion

- if it occurs gradually (not fatal)

- sudden (no chance to adjust & death occurs

HYPEREMIA (congestion)

- local incrase in blood to an organ (opening of inactive capillaries)

types of hyperemia

1. active

▪ local increase in the arterial blood supply (red color)

▪ due to stimulation of vasodilator nerve, paralysis of vasoconstriction

e.g. blushing, 1( burns, inflammation, fever

2. passive (venous congestion)

▪ accumulation of blood in veins due to mechanical obstruction (blue-rd color)

▪ chronic type usually

▪ types: a.) hypostatic congestion - due to gravitation of blood

b.) local congestion - any form of congestion

c.) systemic congestion - R & L heart failure

LVF - lungs (are first congested)

RVF - other organs are congested except lungs

general morphologic changes

1. ( size, weight of organ

2. dusky red color

3. bloody & wet section

4. microscopic: dilated blood vessel

fibrosis (chronic)

congested vessels (pressure of cells)

specific morphologic changes

1. acute - bluish discoloration

2. chronic - edema, atrophy, necrosis & hemorrhages

e.g. lungs

acute congestion edema

fibrosis chronic congestion

enlarged capillaries

heart failure cells rupture

release of hemosiderin pigment by RBC

hepatocyes - take up hemosiderin cells (laden macrophages)

brown induration of the lung = pigmentation + fibrosis

LIVER

heart failure, IVC, or hepatic vein obstruction

(

central vein congestion

(

hemorrhane, atrophy, fatty change, necrosis

(centrolobular, hemorrhagic necrosis)

(

mottling or nutmeg appearance (nutmeg liver)

(

fibrosis

(

cardiac cirrhosis

SPLEEN

congestive splenomegaly

(

sinusoidal congestion

(

hemorrhages

(

fibrosis

(

siderofibrotic nodules

HEMORRHAGE

← escape pf blood from cardiovascular system (rupture of vessel or heart)

← hemorrhage by diapedesis

- extravasation of RBC due to passage of cells thru the apparently unruptured

capillary walls

types of hemorrhage

1. origin - capillary, venous, arterial, cardiac

2. visibility - external, internal

3. how it is infected

a. traumatic (mechanism in nature)

b. spontaneous (aneurotic)

4. size

a. petechiae - capillary

b. purpura - confluence of petechiae (~1 cm)

c. echymoses - blotchy

d. hematoma - larger, deeper (tumor-like sweeling of the organ)

5. location

a. epistaxis - nose

b. hemoptysis - cough, cough-out blood (frothy & bloody red)

c. hematemesis - vomit blood (from stomach)

d. melena - decomposed

- from upper portion of GIT

hematochizia

- red fresh blood in stool

- lower GIT

e. hemothorax, hemocardium, hemoperitoneum

f. hemarthrosis

g. menorrhagia - profuse menstruation bleeding

h. metrorrhagia - uterine hemorrhage in between menstruation

etiology

1. localized vascular change

mechanical injury: pathological process

2. generalized disorder

a. coagulation or wood disorder (hematophilia, leukemia)

b. vascular abnormality (Vit. C deficiency, hypertension)

clinical significance depends on:

← amount of blood loss

← rate of escape

← site of hemorrhage

THROMBOSIS

thrombus

- mass made up of blood constituents within vessels/heart during life in a non-interrupted cardiovascular system

thrombus formation

1. platelet adherens to inner vessel wall

2. accumulation of leukocytes

3. platelket liberation of thromboplastin

4. fibrin formation & progression into a thrombus

composition of a thrombus

1. platelets

2. WBC Lines of Zahns

3. fibrin

4. RBC

THROMBUS BLOOD CLOT

1. interactions of blood vessel wall, blood elements 1. coagulation system/sequence (loosely attached)

& coagulants (firmly attached)

2. in intravascular location/heart 2. in intravascular areas (hematoma)

3. in living individual 3. in post-mortem - current jelly (red fruit)

- chicken fat (yellowish)

4. made up of fibrin (rapidly moving arterial vessel) 4. mostly blood elements (RBC)

- with lines of Zahn - no lines of Zahn

etiology of thrombosis

1. change in the endothelium

2. change in blood flow

3. change in blood constituents

factors affecting normal homeostasis

1. vascular wall - endothelium

- subendothelial CT (has thrombotic sustances)

- muscular wall

2. platelets

3. soluble coagulation protein

ANTITHROMBOTIC PROTHROMBOTIC

Inhibition of platelet aggregation Stimulation of Platelet Aggregation & Adhesion

- prostacyclin (PGI2) - von Willebrand's factor

- NO - Platelet-activating factor (PAF)

- ADPase

Anticoagulant-Binding &

Inhibition of Thrombin Procoagulation Factors

- Anti-thrombin III acceleration by - Tissue factor

heparin like molecules - Binding factors Ixa, Xa

- Thrombomodulin activator of - Factor V

protein C/S

- (2-macroglobulin

Fibrinolysis Inhibition Fibrinolysis

- Tissue plasminogen activator (t-PA) - t-PA inhibitor

conditions causing injury to endothelium (fibrillar collagen exposed)

1. atherosclerosis

2. inflammation

3. mechanical, temperature, chemical, radiation

4. endogenous (( cholesterol)

5. immunologic (transport & immune rxn deposition)

changes in blood flow = stasis, eddying or turbulence

normal flow (axial)

effects of turbulence

1. disruption of laminar flow

2. prevent dilution & hepatic clearance of the activated coagulation factors

3. retards the inflow of inhibitors of clotting factors ( build up of thrombus

4. damaged endothelium; ( release of PGI2 & plasminogen activators

conditions ( stasis/turbulence

1. aneurysm (abnormal dilatation of vessel)

2. cardiac dilatation

3. varicosities

4. hyperviscosity ( polycythemia, macroglobulinemia, SS disease

5. giant cavernous hemangioma (Kasabach-Merritt syndrome)

changes in blood constituent

a. altered number/character of platelets ( increase in number + adhesioness

b. ( number of RBC

c. ( thromboplastin

d. ( coagulation factors & fibrinogen

e. ( inhibitors (AT IV, fibrinolysis, protein C)

Hypercoagulable States

I. primary (genetic)

- deficiency states in:

Antithrobin III Protein C

Protein S Fibrinolysis defects

II. secondary (acquired)

a. high risk

prolonged bed rest or immobilization myocardial infarction

tissue damage (including surgery, cardiac failure

fractures, burns) cancer

acute leukemia myeloproliferative disorders

prosthetic cardiac valves disseminated intravascular coagulation

thrombotic thrombocytopenia homocystinuria

b. lower risk

atrial fibrillation cardiomyopathy

nephrotic syndrome late pregnancy/postdelivery

oral contraceptives hyperlipidemia

lupus anticoagulant sicke cell anemia

smoking thrombocytosis

types of thrombi

I. color:

red

white

mixed

II. age

Recent - reddish

old - whitish (paler red)

III. site

a. venous (red-blue)

phlebothrombosis - no inflammatory inflammation in the vein

thrombophlebitis - thrombus in front of an inflammation

b. arterial (red & dry)

conglutination, white thrombus

c. cardiac

d. capillary

fates of the thrombus

1. propagation

- thrombus may propagate & eventually cause obstruction of some critical vessel

2. infection

- septic thrombus if infected

3. contraction

4. absorption

- resolution of a thrombus brought by fibrinolysis

- beneficial to patient because it created good circulation

5. organization

- endothelial & smooth muscle cells & fibroblast invade thrombus

6. calcification

- phleboleaf - calcified vein thrombus

7. canalization

- organized thrombus

- blood vessel invade thrombus resulting to canalization

8. embolization

- thrombus ( thromboembolus

Hazards of Thrombosis

vegetation

- minute thrombi attached to myocardium of heart & valves

endocarditis

- small arranged in linear fashion

- have bacterial colonies & inflammation

mural thrombus

- attached to wall of heart & big vessels

- does not occlude

1. race

2. age

3. smoking

4. obesity

5. synergism (smoking & pills)

6. congestive heart failure

7. cancer (Trousseau's sign = migratory thrmbophlebitis

Phlegmasia Alba Dolens : "milk leg"

- ileofemoral venous thrombosis (3rd trimester ff. delivery)

(+) lymphatic obstruction

Homan's sign

- pain in the calf muscle with dorsiflexion of foot

EMBOLISM

- a condition characterized by transport of foreign body from one part of the circulatory system to another where it becomes impacted

Venous - thrombi to heart and lungs

Foreign bodies:

thrombus fat gas

amniotic fluid bacteria atherosclerotic debris

tumor bone marrow

Types of Embolism

1. thromboembolism

paradoxical embolism: from venous to arterial compartment

2. fat embolism

incidence: in 0.5% to 5% of trauma cases

mortality rate: 10-15%

may occur in: DM, fracture of bones, SS anemia, pancreatitis, burns

release FFA:

damages the endothelium

activates coagulation (due to release of peptides & vasoactive amines)

clinical significance:

pulmonary insufficiency (sudden onset)

mental deterioration (due to hypoxia)

thrombocytopenia (platelets adhere to fat)

fat globules in the urine

morphology:

1. lungs: (a) with pressure fat globules are released from blood vessels

(b) ARDS (adult respiratory distress syndrome)

signs: edema, hyaline membrane, atelectasis, & congestion

2. kidneys: fat in microvessels

3. brain changes ( edema, hemorrhage

3. gas embolism (bubbles of air or nitrogen)

in conditions like: delivery/abortion

performance of pneumothorax

chest trauma

decompression sickness (barotrauma)

acute: "bends"/chokes ( in lungs: hemorrhage, edema, atelectasis, emphysema & ARDS

in heart/brain: vascular obstruction

chronic: Caisson Disease (infarcts in skeletal system)

4. amniotic fluid embolism or infusion

incidence: 1 per 50,000 deliveries

mortality rate: 86%

associated with: tear of placental membrane, uterus & cervical vein rupture

predisposing factors:

a. advance age

b. multiparity

c. tumultuous labor

d. abortion

e. caesarian section

clinical manifestations: dyspnea ARDS convulsion ( coma & DIC

(usually pulmonary) cynosis shock

morpgologic findings:

contents of embolus

1. epithelial squames

2. lanugo hair

3. fat (cervix caseosa)

4. bile (mecronium)

5. mucin (from fetal respiratory tract)

5. atheromatous embolism

embolus contains: a. cholesterol crystals (cholesterol embolus)

b. hyaline debris

c. calcified sustances

types of embolism as to site

1. systemic embolism

sources: 1. heart (80-85%) - MI, RHD, cardiomyopathy

2. arterial - atherosclerosis, aneurysm

3. unknown (10-15%)

effect: infarction

sites of lodgement: 1. lower extremities (70-75%)

2. brain

3. viscera

4. upper extremities

treatment: anticoagulant Rx, embolectomy

2. pulmonary embolism

features:

pulmonary artery occlusion ( pulmonary hypertension

difficult to diagnose

source: leg thrombus (95%); iliac, femoral, popliteal

types of emboli: 1. saddle emboli (bifurcation)

2. multiple emboli

effects: depends upon the size, number, location (Px status degree) of obstruction

1. silent (resolution)

2. sudden death (acute COR pulmonale or CV collapse)

( 60% of pulmonary vasculature obstructed

3. pulmonary infarction

- small end arteries involved

4. pulmonary hemorrhage

- central involvement: with infarcts if with CHF & lunge disease

5. pulmonary hypertension

- with organized embolus

- pulmonary vascular sclerosis

- COR pulmonale

INFARCTION

- necrosis of tissue deprived of their blood supply thru obstruction

infarct - area of ischemic necrosis ( ( oxygenation

causes of infarction

1. thrombosis

2. embolism

3. atherosclerosis

4. venous obstruction

5. congenital vascular anomaly (stenosis)

types of infarcts

I. color

A. pale infarcts (anemic)

- arterial obstruction of solid organ without adequate collaterals

- "white collaterals"

B. hemorrhagic infarcts

- in ff. set-ups: venous acclusion

loose, soft tissues

previously congested tissue

tissue with double circulation

II. age

A. recent (elevated) - reddish

B. old (depressed) - replaced by scar or fibrosis, lighter

III. presence or absence of infection

A. bland infarct

B. septic infarct

caused by: 1. presence of organism prior to infaction

2. infected thrombus or clot (septic embolus)

3. bacteremic seeding of the margin of the infarct

morphology:

gross: wedge shape (no change if very early)

← 24 hours:

- color change

- elevated, demarcated surface

- with coagulation necrosis

- inflammatory change

( later stage:

- regeneration

- scar formation

- abscess ( cavity (septic infarct)

Factors that Detrmine the Severity of Infarction

1. general status of the blood & cardiovascular system

- anemia, hypoxemia, CHF, shock, blood loss, etc.

2. anatomic pattern of arterial supply

a. single arterial supply

intestines: with many anastomosis

kidneys: with few anastomosis

b. double arterial supply

lungs (bronchial & pulmonary artery)

liver (hepatic & portal artery)

c. parallel blood supply

brain (circle of willis)

forearm (radial & ulnar artery)

3. rate of development of infarction

4. vulnerability of the tissues to ischemia

very sensitive: ganglion cells, proximal convoluted tubular cells, & myocardial cells

more resistant: mesenchymal cells

SHOCK

- circulatory deficiency resulting from a disparity between the volume of blood & the volume capacity of the vascular system causing decreased tissue perfusion thus:

( O2, ( nutritional supply, ( removal of metabolites

Basic Characteristics

( circulating blood

( BP

Types of Shock

I. neurogenic (primary) shock

- characterized by ( volume capacity of the vascular bed due to vasodilatation (widened capillaries & venules of the visceral areas)

e.g. syncope

injury with severe pain

II. hypovolemic shock

- characterized by actual ( of blood flow

- causes: 1. direct loss of blood, plasma, fluid

2. generalized ( capillary permeability

III. cardiogenic shock

e.g. in acute MI

in cardiac tamponade

IV. septic shock

mechanisms:

1. peripheral vasodilatation ( pooling of blood (( perfusion) & cardiac dilatation

2. cellmembrane injury

3. endothelial cell injury

4. disseminated intravascular clotting

5. myocardial depression/multiple organ failure

Secondary Mediators in Causing Shock

1. catecholamines 8. histamines

2. kinin 9. complement (C3a & C5a)

3. prostaglandins 10. leukotrienes

4. interleukin 1, 6 & 8 11. interferons

5. endorphins 12. PAF

6. TNF - alpha 13. myocardial depression factor

7. nitric oxide

Bacterial Products

Lipid A

Peptidoglycans

membrane cell damage

endothelial cells platelets macrophages

activation of histamine PG, leukotriene complement activation

coagulation serotonin TNF, IL-1,6,8 C3a & C3b

DIC arterioles die inc. vascular permeability

venous congestion transudation

& diffuse toxic

cell injury

decreased effect effective cardiac volume

decreased CO decreased cell perfusion

SHOCK

Syndrome of ( BP

Septic Shock ( myocardial contractility

Morphological Changes in Shock

reversible irreversible

kidneys: ischemia brain: hypoxic encephalopathy

adrenals: lipid depletion heart: subendocardial hemorrhages/necrosis & "zonal lesions"

(zona reticularis) (hypercontractic myocytes)

GIT: hemorrhages liver: cenrilobular necrosis

liver: fatty changes lungs: "shock lungs" ( edema ( fibrosis

kidneys: ATN

cardiogenic/hypovolemic shock

s/s: pallor, ( BP, cool & clammy skin (cyanotic)

thready PR, ( CR, ( RR

septic shock

s/s: warm, pinkish skin (vasodilatation)

stages: 1. early compensated - BP near normal, increase HR ( with arteriolar constriction

2. progressive (decompensated) - ( BP, ( RR, oliguria & acidosis

3. irreversible stage - ischemic cell death (heart, kidneys, brain, etc.)

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