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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