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HEMODYNAMIC DISORDERS

Volume Disturbances:
1. EDEMA = Increase of interstitial fluid
- exudate = high protein edema in inflammatory edemas. >1016 specific gravity.
- transudate = low protein edema in most other edemas eg: cardiac or renal. <1016
- Increased HSP eg: hyperemia, valve/heart insuficiency. increased HSP can cause
heart failure, and decreased OP causes kidney failure.
- Increased Permeability eg: histamine, NO
- Decreased OP eg: cirrhosis, renal failure, malnutrition
- Decreased lymph drainage eg: lymphadenitis and LN dissection

- Hydrothorax / pleural effusion

- Hydropericardium
- Ascites / Hydroperitonium
- Hydrocele = Testi edema
- Anasarca = general body edema (transudate accumulates in subcutaneous fat)

- Pulmonary edema - from LHF, usually effects lower lobes (conjestion—>interstitial

edema—>alveolar edema)

- subcutaneous edema - of lower leg due to RHF/ gravity. Loose CT edema of face/
eyes due to renal failure
- renal edema- from renal failure, proteinurea decreases OP, increase HSP from Na/
H20 retention

- Cerebral edema - lethal because brain swells within skull, cerebellar hernia through
foramen magnum compresses medulla = no respiratory centre

2. HYPEREMIA = increased blood volume in microcirculation

- Arterial Hyperaemia / Active Hyperemia
- Increased arterial blood flow causing artery dilation
- Mostly physiological (exercise, starvation, blush, increased RBCs/blood flow)
- Some pathological (inflammation = local hyperemia)
- macroscopic symptom = erythema

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- Venous Hyperemia / Passive Hyperemia / Congestion
- Decreased venous blood flow causing vein dilation (congestion is chronic or acute)
- Always pathological ( Tumor compression, collateral blood flow development and
thrombosis cause local congestion. Left/right heart failure and lung diseases cause
systemic congestion.)

- macroscopic symptom = cyanosis, enlarged and firm

- Spleen and kidneys (and most organs) - Because of more venous blood, organs
swell and turn blue. Prolonged dilation of venules walls causes then to thicken and
scar, so organs are firm.
- Lungs - Brown
- Outcomes of congestion: edema, stasis, hemorrhage, thrombosis, induration or
atrophy

LEFT SIDED HEART FAILURE

• Acute LHF = Pulmonary edema (can be lethal, large heavy lungs, with more pink
transudate than white air spaces

• Chronic LHF = More blood in lungs/ swollen pulmonary veins -> increase HSP ->
alveolar haemorrhage ( RBCs forced out of vessels) -> RBC hemolysis -> releases
hemosidermin (which is phagocytised by macrophages) -> Hemosidermosis
Pulmonis (Brown lung)

RIGHT SIDED HEART FAILURE

• Right ventricle and vena cava dilation

• Causes Liver cyanosis (enlargement and increased venous blood and tender)

• Acute = if remove injuring stimuli, only get cyanosis

• Chronic = if don't remove injuring stimuli, cyanosis turns into NUTMEG LIVER
(macro= red and yellow dots on surface. micro= centrilobular hemorrhagic necrosis
and fibrosis):

• Straight nutmeg liver = hypoxia causes cell injury and fatty degeneration of cells
around central vein and middle of sinusoid.

• Reverse / Prolonged nutmeg liver = peripheral cells also damaged and have fatty
degeneration. Causes fibrosis and Cardiac Cirrhosis because all the hepatocytes
dies.

• Spleen = congestive splenomegaly and cyanosis

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3. HEMORRHAGE = bleeding out of vessels
- Per rhexin = ruptured vessel wall (by trauma/ aneurysm/ varices/ surgery)
- Per diabrosin = pathological change/corrosion of vessel wall (by inflammation/ tumor
necrosis/ TB/ ulcer)

- Per diapedesin = small haemorrhage where vessel wall stays intact and increases
permeability, more typical in capillaries, multiple small spots of blood. (by hypoxia,
infections)
- thrombocytopenia and lack of coagulation factors can also causes hemorrhages.
- Types according to origin: cardiac, arterial (aneurysm), venous (oes varices),
capillary

- External hemorhages:
• epistaxisis - nose bleed
• hematemesis - vomiting blood
• hematourea - blood in urine
• melena - dark faeces from upper GI hemorrhage
• Hemoptysis - coughing up blood/ lung hemorrhage
• metrorrhagia - blood from uterus
• menorrhagia - severe/ long menstruation
• hemotochezia - blood in stool from lower GI hemorrhage

- Internal hemorrhages:
• petechia - small mucosal/ serosal/ mini puncture haemorrhage (usually on skin or
conjunctiva). blood spots <2mm
• purpura - blood accumulates in tissue between cells. blood spots 3-5mm
• ecchymoses / bruise - blood accumulates in skin or mucus membrane (bruise turns
purple to green to yellow, because bilirubin from lysed RBCs is oxidised). >5mm
• hematoma - blood accumulates in soft tissue (very visible)
• hemothorax -blood in pleural cavity
• hemascos/hemoperitonium - blood in peritoneal cavity
• hemoperricardium - blood in pericardium cavity
• hemarthrosis - blood in joints cavity

- Outcomes of hemorrhage:
• coagulation, brown cystic formation, organisation/incapsulated or complications
• chronic -> iron deficient anaemia

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• acute -> hypovolemic shock
• brain haemorrhage and hemorrhagic shock are life threatening
• rapid blood loss >33% is life threatening
• postmortem = pale, vein collapse and shrunken grey spleen

4. SHOCK = CV collapse with less blood flow and blood to tissue. Causing
hypotension, hypoxia and sometimes impaired metabolism and death
- primary/initial shock = sudden trauma, pain or emotions cause a few seconds of
shock by decreasing venous return to heart.

- secondary/ true shock = more severe

- 6 Types of true shock:
• Hypovolemic- blood loss or fluid loss(burns/vom/dia) causes low blood volume
• Cardiogenic- Heart/circulatory failure decreases CO but have normovolemia,
caused by outflow obstruction or filling(tamponade)/emptying(MI) deficiency.
• Septic- Bacteria exo/endotoxins
• Anaphylactic - type 1 immediate hypersensitivity
• Neurogenic - by drugs
• Hormone deficient - eg; thyrotoxic shock or adrenal insuficiency
- Pathogenesis 3 stages:
1. Non progressive compensated shock (reversible) - compensatory
mechanisms try to maintain blood flow to heart and brain. Via peripheral
vasoconstriction and kidney fluid conservation.

2. Progressive Decompensated shock - deteriorates and suffers from other stress

3. Decompensated shock (irreversible) - shocks too severe for compensatory

mechanisms to work. No recovery.
- Symptoms: Hypotension, fever, weak/irregular pulse and dyspnea. Can lead to
coma/death. renal dysfunction causes oliguria and diuresis.

- morphology: vessel spasms, incrrased vessel permeability, microthrombi,

hemorrhages, necrosis. Liquid blood when dead, Disseminated Intravascular
Coagulation syndrome, and hemorrhagic diathesis.
- Complications: kidney/ lung/ heart/ gi/ brain shock

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Obstructive Disturbances:
- STASIS = Stop of blood flow in microcirculation. Capillaries and veins fill with blood
and dilate. Short term is reversible, probonged can cause thrombi/edema/bleeding.
hypoxias Isolated vein spasm can cause leukostasis/ RBS accumulation (shock-
general leukostasis)
- Pre-stasis = RBC columns stick together
- sludge syndrome = type of stasis where RBCs, WBCs and platelets stick together,
this increases blood viscosity
- causes: venous hyperemia or ishemia, physical or chemical factors, infection, allergy,
autoimmunity
- microcirculation disturbances: microcirculation normally exchenge blood and tissue
• Inflow link -arteriole to pre capillary
• Intermediate link - capillary exchange
• Depot link - post capillaries to venule
• Drainage link - post capillaries to lymph
• Vascular change - vessel thickness/ shape/ permeability —> hypoxia
• Intravascular change - blood stasis, prestasis and sludge
• Extravascular change - edema, hemorrhage, lymphostasis

1. THROMBOSIS = blood clot in a vessel (or heart cavity) of living person.

- post mortem clot = when dead, not attached to walls, red, gelitanous, smooth
surfaces, No Zahn lines, removed as same shape as vessel
- thrombus = when alive, attached to wall, white granular surface, fibrous, Lines of Zahn
(only in flowing blood)
- same mechanism as haemostasis but always pathological:
1. endothelial disruption (by MI, hypertension, mitral stenosis…)
2. blood flow changes speed (slow and turbulent )
3. hyper coagulation by platelets and coag factors
- Mechanisms of formation:
• Platelet agglutination - to damaged endothelium
• RBC agglutination - occludes vessel
• Fibrinogen coagulation- fibrin clot stops blood getting to damaged area
• Plasma protein precipitation
- Thrombi structure:
• Formed from thrombocyte agglutination and fibrinogen accumulation. size/ shape
depends on vessel

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- Thromus Types:
• Red - Venous thrombi in stagnant blood. Consists of fibrin and RBCs. Usually
occlusive

• White - Arterial Thrombi in flowing blood. Consists of Fibrin, WBC and Platelets
cause Lines of Zahn. Usually mural.

• Mixed - red thrombi tail, white thrombi head and body has both thypes
• occlusive - complete obstruction of small vessels—> ishemia—>necrosis—>MI
• Mural/ parietal - adhered to large vessel wall/ heart cavities—> embolism
• Hyaline - Consists of plasma proteins and destroyed RBC/WBS. No fibrin

• Agonal - yellow fibrin, localised in RV apex and can extend to pulumonary artery.
Formed when dying slowly

ARTERIAL THROMBI VENOUS THROMBI

at turbulence / injury/ fast blood flow at stasis/ slow blood flow

commonly cerebral and coronary thromi commonly DVT and varicose vein thrombi
grow retrograde to heart extend with blood flow towards heart

usually mural usually occlusive

Platelets, fibrin, WBC—> Lines of Zahn can have lines of zahn if lots of RBC

white thrombi Red thrombi

- Clinical effects of thrombi:

• cardiac thrombi - sudden death
• arterial thrombi - ischemic necrosis, gangrene, coronary artery thrombi=MI
• venous thrombi - thromboembolism, edema, ulcers, DVT
• capillary thrombi - disseminated intravascular coagulation syndrome (DIC):
1. increase blood coagulation—> fibrin clot
2. hemmorhage coz coag factors used up in 1st stage
3. fibrinolysis activated to make hemmorhagic syndrome
worse.

- Thrombi Outcomes: Dissolution, organisation, recanalisation, vascularisation,

petrification, thromboembolism, septic autolysis, propogation.

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2. EMBOLISM = Embolus moves through vessels and can lodge somewhere
Types:
- Autograde embolism - with normal blood flow
- Retrograde embolism - moves opposite blood flow
- paradoxical embolism = need connection between venous and arterial systems. `Eg:
congenital septal defect allows thrombus to pass from right to left heart
- thromboembolism = thrombus moves:
• arterial embolism - causes ischemic infarction anywhere - systemic
thrombimbolism -from heart thrombus, aortic aneurisms, valve problems

• venous embolism = pulmonary embolism - pulmonary artery branch occlusion

from thrombus from peripheral vessels or right atrium. Caused by stasis (heart
failure/vein insuficiency), injury, age, immobilisation…
- DVT —> vena cava —> right side of heart —> pulmonary artery —> lodged in
different places of pulmonary tree depending on size —> pulmonary oedema—>
pulmonary hypertension to counteract permeability edema—> Cor Pulmonale
(RHF) coz RV overworks
- consequences: ………..
- fat embosslism - after long bone fracture, bone marrow fats enter vessels. also from
burns and soft tissue damage. causes pulmonary insufficiency and anaemia and
thrombocytopenia.
- air embolism- from surgery, venous air embolism - air can enter VC and move to
brain. arterial air embolism - marble skin because of cutaneous artry occlusion, also
brain, eye, lingual artery occlusions.
- Amnyotic embolism - amnyotic fluid enters uterine veins and goes to fetus right heart
- Gas embolism - Cassian/decompression sickness - divers at high pressure = easily
dissolved nitrogen in blood, turns back to gas bubbles when coming back up too
quickly. Causes joint pain, dyspnea, coma, cerebral problems, death.
- atherioembolism - atherosclerotic plaques dislodge, causing hypertension, ischemis,
atropy, necrosis, infarction, gangrene.

3. ISCHEMIA = loss of blood supply to tissue, usually by thrombi or atherosclerosis,

pathological or physiological. Ischemia causes hypoxia.

Absolute ishemia = Complete vessel obstruction, no blood to tissue = necrosis

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Relative Ischemia = Chronic, usually effects lower limbs (eg; femoral stenosis),
atherosclerotic plaque restricts blood flow. when exercising- cant get enough blood to
tissue so cause pain
- Types: Reflex, Obstructive, compressive or because of redistribution.
- acute - edema
- chronic- infarction/atrophy/sclerosis

4. INFARCTION = area of ischemic necrosis caused by vessel obstruction/

narrowing by thrombi, spasms, hemmorage, inflamed vessel…
- types:
• ischemic (white) -arterial occlusion in solid tissues (spleen)
• Hemorrhagic (red) - venous occlusion in congested/double circ tissue (lungs)
• white with red halo- in kidneys and heart
• Types according to age: recent vs fresh, old vs healed
• Types according to propagation: total, subtotal (part of organ) and microinfarction

- Pathogenesis:
1. Local hyperemia
2. edema and hemorrhage
3. cloudy swelling and degeneration
4. necrosis and RBC lysis
5. hemosiderin released
6. granulation tissue growth

- Clinical:
• Anemic infarction - artery occlusion in solid organs—> coagulative necrosis
• Renal Infarction - renal artery occludes—> renal parenchyma coagulative necrosis
• Myocardial Infarction - coronory artery thrombus —> cardiomyocyte coag nec
• Sleen Infarction - splenic artery occludes —> coag nec and inflamation
• Pulmonary Infarction
• Cerebral infarction

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- Hemorrhagic infarctions: caused by vein occlusion, loose tissue, double circulation
and chronic congestion
• Hemorrhagic infarction of the lung - because of lungs double circulation (nutrient
and functional circulations) can overcome congestions resistance. So needs both
chronic venous congestion/ lungs brown induration(from LHF) and thromboembolism
of branch of pulmonary artery to cause occlusion and ischemic necrosis. Because of
blood pumping force of double circulation, alveoli capillaries rupture so it becomes
hemorrhagic.
• Liver hemorrhagic infarction - portal vein embolism
• Bowel hemorrhagic infarction - mesenteric vein embolism. Double circulation of
mesenteric vessels causes haemorrhage.
• Brain hemorrhagic Infarction - cerebral artery embolism causes anemic infarction,
then artery increases pressure to cause nleeding.