Hemodynamic disorders part (I)

Hemodynamic disorders part (I)

I. Microspecimens:

№ 10. Chronic hepatic congestion (nutmeg liver). (H-E. stain).

Indications:
1. Dilated and congested centrilobular vein.
2. Dilated and congested sinusoidal capillaries.
3. Atrophied hepatocytes in the center of lobule.
4. Unchanged hepatocytes and sinusoidal capillaries at the periphery of the lobule.

In the center of the hepatic lobules the trabecular structure is erased, there are hemorrhages ("blood
lakes") around central veins, veins are dilated and congested, the adjacent portions of the sinusoidal
capillaries are dilated, filled with erythrocytes, most of the hepatocytes are destroyed (necrosed),
preserved hepatocytes are atrophied, macrophages with hemosiderin granules are observed. In
peripheral areas, the hepatic tracts have usual appearance, the sinusoids are not congested, in some
hepatocytes there are lipidic degeneration (micro-macrovesicular steatosis).

The selective congestion of the central areas of the lobules is due to the peculiarities of the blood
circulation and angioarchitectonics of the liver and it is explained by the fact that the venous stasis
mainly comprises the hepatic veins and collecting veins but at the level of lobules - central veins and
adjacent portions of the sinusoidal capillaries. However, the stasis does not extend to the periphery of
the lobules due to the higher speed and pressure of blood in the peripheral areas of the sinusoids where
arterioles enter from hepatic artery system. Therefore, the center of the liver lobule is congested, and the
periphery - no.
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№ 10. Chronic hepatic congestion (nutmeg liver). (H-E. stain).

№ 9. Chronic pulmonary congestion. (H-E. stain).
Indications:
1. Clusters of sideroblasts and siderophages in the lumen and walls of the alveoli.
2. Dilated and congested vessels in interalveolar septa.
3. Sclerosed and thickened interalveolar septa.

The interalveolar septa are thickened, sclerosed, the veins and septal capillaries are dilated and
congested. Agglomerations of phagocytic cells (alveolar macrophages) loaded with hemosiderin
granules of brown color (sideroblasts and siderophages) are observed in the alveoli; part of the alveoli
contains eosinophilic edema fluid, erythrocytes or remnants of disintegrated red bloodcell.

Macroscopically the lungs in chronic congestion are enlarged in volume and mass, they have a dense
consistency and brown color on section. The increased consistency is due to the excessive proliferation
of connective tissue in the alveolar walls, and coloring - due to accumulation of hemosiderinic
pigment. The lesions are more pronounced in the postero-inferior areas of the lungs.

Chronic venous congestion of the lungs is encountering in left heart failure, mitral stenosis and
chronic ischemic heart disease (because of this it is also called "cardiac lung"). In the sputum of
patients with heart failure, macrophages with hemosiderin granules in the cytoplasm can be found and
they are called "heart failure cells". The presence of hemosiderinic pigment gives to sputum a rusty hue.
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№ 9. Chronic pulmonary congestion. (H-E. stain).
№ 1. Pulmonary hemorrhagic infarction. (H-E. stain).
Indications:
1. Infarction area:
a. necrotized interalveolar septa;
b. hemolyzed erythrocytes in alveolar lumen.
2. Adjacent lung tissue with venous stasis and edema.

With naked eye in microspecimen a non-aerated area is observed, at the small objective in this area
the alveoli are filled with extravasated erythrocytes, most of the them are hemolysed of eosinophilic
color, in some alveoli groups of siderophages are observed, the alveolar septa are necrotic, cells are
without nuclei (karyolysis) of intensely eosinophilic color. Adjacent lung tissue is with signs of chronic
venous congestion.

The hemorrhagic character of the infarction is determined by two factors: 1) double circulation of
the lung tissue: from the pulmonary artery (small circulation) and the bronchial artery (large
circulation); between these arteries there are multiple anastomoses, which are not functional under
physiological conditions; the obstruction of the pulmonary artery is followed by the reflex opening of
the anastomoses and penetration under pressure of the blood from the bronchial artery into the
ischemic area, which leads to rupture of the capillary and venules walls of the interalveolar septa and
the blood flow into the alveoli; 2) venous stasis, because it favors the retrograde circulation of blood in
veins and flooding of the ischemic area (it is most frequently encountered in left heart failure, especially
in mitral stenosis).
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№ 1. Pulmonary hemorrhagic infarction. (H-E. stain).

№ 5. Renal infarction. (H-E. stain).
Indications:
1. Infarction area: a. necrosed glomerulus;
b. necrosed tubule.
2. Demarcation zone: a. congested vessels;
b. hemorrhages.
3. Adjacent renal tissue: a. unchanged glomerulus;
b. unchanged tubule.

In microspecimen a zone of necrosis is determined, in which the glomeruli and tubes of

eosinophilic color have been preserved, but without nuclei (karyolysis), at the periphery of this area are
hyperemic vessels, haemorrhages, and neutrophilic infiltration (inflammation of the demarcation ), the
adjacent renal tissue has normal structure.

Macroscopically, the renal infarction has yellowish-white color and triangular shape with the tip
pointing towards the hilum and the base towards the capsule, on the surface of the capsule may be
fibrin deposits. Clinically it is manifested by hematuria.

The most common causes are thromboembolism or thrombosis of renal artery. It is encountering in
atherosclerosis of the aorta and renal arteries, rheumatic and infective endocarditis, hypertension,
myocardial infarction with intracardiac thrombosis. The most common consequence is organization
(cicatrization).
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№ 5. Renal infarction. (H-E. stain).

II. Macrospecimens:

№ 71. Chronic hepatic congestion (nutmeg liver).

The liver is enlarged in size and mass, has an extended, smooth capsule, increased consistency, rounded anterior
margin, with mottled appearance on section, similar to the nutmeg core due to the alternation of small, dark red spotty
foci of central areas of lobules with others of brown color (usual color of the hepatic parenchyma) or slightly yellow
due to the hepatocyte steatosis - of the peripheral areas of the lobes (the dimensions of the hepatic lobule are ~ 2 × 0.7
mm).

It can be seen in right heart failure or global heart failure ("cardiac liver"). Examples: pulmonary hypertension (in
pulmonary emphysema, bronchiectasis, diffuse pneumofibrosis, secondary pulmonary tuberculosis, etc.) and
pulmonary artery stenosis. An analogous pattern develops in hepatic vein thrombosis (Budd-Chiarisyndrome).

№ 141. Ischemic infarction of the spleen.

The infarct area is well delimited, it has white-yellowish color, dense consistency (coagulative necrosis) and conical
shape with the tip towards the spleen hilum and the base towards the capsule, on the capsule are fibrin deposits.

The most common cause is thrombosis or thromboembolism of the spleen artery. It is found in rheumatic or
infective endocarditis, leukemias, ischemic heart disease, atherosclerosis etc.

The conical shape and white color are determined by the magistral type of vascularization of the spleen with poor
collateral circulation, which excludes the possibility of the blood entering in ischemic area throughcollaterals.
The most frequent consequence is organization (cicatrization) of the infarction with spleendeformation.
№ 71. Chronic hepatic congestion (nutmeg liver).
№ 141. Ischemic infarction of the spleen.
№ 38. Pulmonary hemorrhagic infarction.

The infarct area has dense consistency, red-dark color, conical shape with the tip towards the hilum and the base
towards the pleura. It is compact, non-aerated, filled with blood. Fibrinous deposits are observed on the pleura.

The cause of pulmonary infarction is obstruction of a branch of the pulmonary artery by thrombosis or embolism
(with starting point from the peripheral venous system, especially from the veins of the lower limbs).

Clinically, the pulmonary infarction is manifested by hemoptysis (the presence of blood in the sputum) and pleural
friction rub at auscultation.
The common consequence of pulmonary infarction is organization (scarring). Possible complications: post-
infarction pneumonia, pulmonary abscess, pleural empyema, pneumothorax, pulmonarygangrene.

№ 9. Myocardial infarction.

In the wall of the left ventricle on section there is an area of yellow-white color of irregular shape, surrounded by
hemorrhages (white ischemic infarction with hemorrhagic rim), the consistency of the infarction zone is decreased
(myomalacia).

In the absolute majority of cases myocardial infarction occurs on the background of stenosing atherosclerosis of the
coronary arteries, the causes being thrombosis, angiospasm or thromboembolism. It is the main form of ischemic
heart disease. The clinical significance and effects of myocardial infarction depend on its location and extention.
The most frequent consequence is organization (cicatritation) of the necrosed area - macrofocal postinfarction
cardiosclerosis.
№ 38. Pulmonary hemorrhagic infarction.
№ 9. Myocardial infarction.
Arterial hyperemia (hyperemia)
& Venous hyperemia (congestion)
Both processes represent an
increase pressure and volume
of blood in an organ or tissue.

Arterial hyperemia (hyperemia): active process;

macroscopically manifested by red color, elevated
temperature.

Venous hyperemia (congestion): passive process;

macroscopically manifested by dark purple-red (cyanotic)
color, low temperature.
Arterial hyperemia.
Venous hyperemia (congestion).
Chronic liver congestion.
Hepatic blood circulation.
Chronic venous hyperemia (congestion)
of the lung
(brown induration of the lung).
Infarction.
 Acute myocardial infarction.
One-day-old infarct Up to 3 days duration

wavy fibers

Neutrophilic infiltrate

coagulative necrosis
>3 weeks
1 -2 weeks

Granulation tissue
Scar
Pulmonary infarction.
Renal infarction.
 EDEMA
“Increased Fluid in the Interstitial
Tissue Spaces”

Also Includes:
Hydrothorax, Hydropericardium
Hydroperitonium or Ascites and
Anasarca.
 EDEMA
 Increased interstitial fluid
volume
 Two major types
 Local - inflammation
 Generalised - anasarca -
Systemic causes.
 Pathophysiological Classification

 Inflammatory Edema
 Non-Inflammatory Edema
1. Increased Hydrostatic
Pressure
2. Reduced Plasma Osmotic
Pressure
3. Lymphatic Obstruction
4. Sodium Retention
Pathophysiological Classification
(Continued….)
 Increased Hydrostatic Pressure:
1. Impaired Venous Return: (e.g. CCF,
Constrictive Pericarditis, Liver
Cirrhosis, Venous Obstruction)
2. Arteriolar dilatation: (e.g. Exposure
to Heat, Neurohormonal
dysregulation)
 Pathophysiological
Classification(Continued….)

 Reduced Plasma Osmotic Pressure

1. Protein-Loosing Glomerulopathies
(Nephrotic Syndrome)
2. Liver Cirrhosis (Ascites)
3. Malnutrition
4. Protein-Loosing gastroenteropathies
 Pathophysiological
Classification(Continued….)

 Lymphatic Obstruction
1. Inflammatory
2. Neoplastic
3. Postsurgical
4. Postirradiation
Pathophysiological Classification
(Continued….)

 Sodium Retention
1. Excessive salt Intake with Renal
Insufficiency
2. Increased Tubular Reabsorption of
Na+
3. Renal Hypoperfusion
4. Incresed Renin-Angiotension-
Aldosterone Secretion
 EDEMA

increased fluid in the interstitial tissue spaces

 Fetal
Anasarca
Factors affecting fluid balance across capillary walls. Capillary
hydrostatic and osmotic forces are normally balanced so that there is
no net loss or gain of fluid across the capillary bed. However,
increased hydrostatic pressure or diminished plasma osmotic
pressure leads to a net accumulation of extravascular fluid (edema).
As the interstitial fluid pressure increases, tissue lymphatics remove
much of the excess volume, eventually returning it to the circulation
via the thoracic duct. If the ability of the lymphatics to drain tissue is
exceeded, persistent tissue edema results.
 TRANSUDATE EXUDATE

Increased hydrostatic
Etiology Inflammation
pressure

Specific gravity (g/mL) <1.015 >1.015

Total protein (g/dL) <3.0 >3.0

Fluid/serum protein
<0.5 >0.5
ratio

Fluid/serum LDH ratio <0.6 >0.6

Fluid/serum glucose
>1.0 <1.0
ratio
Cells (leukocytes) No Yes
 Shock
:
 “Depressed vital functions due to decreased
circulating blood volume”
 Types:
 Hypovolaemic - true/vasovagal
 Cardiogenic – Heart failure, MI.
 Obstructive – Pulm embolism.
 Anaphylactic – vasodilation due to allergy.
 Septic – capillary damage by infection.
 Shock Features:
 Hypotension
 Tachycardia
 Cold clammy skin
 Rapid shallow respiration.
 Drowsiness, confusion, irritability
 Multi organ failure.
 HYPERMIA AND
CONGESTION

“Both indicates a local

increased volume of blood in a
particular tissue. ”
HYPERMIA AND CONGESTION
HYPEREMIA CONGESTION

1 An active process A passive process

2 Increased blood flow Impaired blood flow

(vasodilatation)
3 During exercise & in Venous obstruction &
inflammation cardiac failure

4 Oxygenated blood (Redder) Deoxygenated blood

(Cyanosed)
 Hyperemia versus
congestion.
In both cases there is an increased volume and pressure of blood in a
given tissue with associated capillary dilation and a potential for
fluid extravasation.
 Hyperemia versus
congestion.
In hyperemia, increased inflow leads to
engorgement with oxygenated blood, resulting in
erythema.
Hyperem
ia
 Hyperemia versus
congestion.
In congestion, diminished outflow leads to a capillary bed swollen
with deoxygenated venous blood and resulting in cyanosis.
 Liver with chronic passive congestion
and hemorrhagic necrosis.
 A, Central areas are red and slightly depressed compared
with the surrounding tan viable parenchyma, forming the
so-called "nutmeg liver" pattern.
 B, Centrilobular necrosis with degenerating hepatocytes,
hemorrhage, and sparse acute inflammation.
 Ischemia
 •Greek ischein“to restrain” + haima“blood”
 •Ischemia occurs when the blood supply to a
tissue is inadequate to meet the tissue’s
metabolic demands
 •Ischemia has 3 principal biochemical
components:
 –Hypoxia (including anoxia)
 –Insufficiency of metabolic substrates
 –Accumulation of metabolic waste
 •Therefore, ischemia is a greater insult to
the cells and tissues than hypoxia alone
Causes of Ischemia:
Decreased Supply

•Vascular insufficiency:
–Atherosclerosis
–Thrombosis
–Embolism
–Torsion
–Compression

•Hypotension:
–Shock
–Hemorrhage
Causes of Ischemia:
Increased Demand

• Increased tissue mass

(hypertrophy)
• Increased workload (tachycardia,
exercise)
• Increased tissue “stress” (cardiac
dilatation)
Effect of Ischemia
Depends on Cell Type
• “Parenchymal” cells are more susceptible
than “stromal” cells
•Different parenchymalcells have different
thresholds for ischemia:
–Neurons: 3-4 min
–Cardiac muscle, hepatocytes, renal tubular
cells, gastrointestinal epithelium: 20-80 min
–Fibroblasts, epidermis, skeletal muscle:
hours
Effect of Ischemia Depends
on Microvascular Anatomy

 •Subendocardial hypoxia in the heart

 •Watershed infarcts in the brain
 •Ischemia due to countercurrent
exchange in the intestinal villi
 •Resistance in dual perfusion organs
 Infarctio
n
Latin infarctus, pp. of infarcire“to
stuff”
• An infarct is an area of tissue/organ
necrosis caused by ischemia
• Infarctions often result from sudden
reduction of arterial (or occasionally
venous) flow by thrombosis or
embolism
•Infarctions can also result from
progressive atherosclerosis, spasms,
torsions, or extrinsic compression of
the vessels
 Morphology of
Infarcts
 •Infarcts can be anemic (white) or
hemorrhagic (red)
 •White infarcts occur with arterial occlusion
of solid organs
 •Red infarcts occur with venous occlusion or
with arterial occlusions in organs with
double or collateral circulation
 •White infarcts can become hemorrhagic
with reperfusion
Renal Infarction
Renal
Infarction
Remote kidney
infarct, now
replaced by a
large fibrotic
cortical scar.
A, Hemorrhagic,
roughly wedge-
shaped
pulmonary
infarct.
B, Sharply
demarcated
white infarct in
the spleen.