6 hemodynamic disorders
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Hemodynamic
Disorders
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• Normal fluid homeostasis is maintained by vessel
wall integrity, intravascular pressure and osmolarity
within certain physiologic ranges.
• Changes in intravascular volume, pressure, or
protein content, or alterations in endothelial
function will affect the movement of water across
the vascular wall.
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1- Edema
Increased fluid in the interstitial tissue spaces.
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Patho-physiologic Causes of Edema
- Increased Hydrostatic Pressure: Impaired venous return
- Reduced plasma osmotic pressure (Hypo-proteinemia): Liver
cirrhosis, nephrotic syndrome
- Lymphatic Obstruction: Neoplastic, or postsurgical
- Sodium Retention: Excessive salt intake with renal insufficiency
- Inflammation : Acute inflammation, Chronic inflammation
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Types of edema
• Anasarca: Generalized edema
• Dependent edema: Prominent feature of congestive
heart failure, particularly of the right ventricle.
• Renal edema: Edema as a result of renal dysfunction or
nephrotic syndrome is generally more severe than
cardiac edema and affects all parts of the body equally.
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• Peri-orbital edema: is a characteristic finding in
severe renal disease.
• Pitting edema: finger pressure over substantially
edematous subcutaneous tissue displaces the interstitial
fluid and leaves a finger-shaped depression
• Pulmonary edema: most typically seen in the setting
of left ventricular failure
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Fetal Anasarca
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EDEMA
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Effusion
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2- Hyperemia and Congestion
• Both indicate a local increased volume of blood in
a particular tissue.
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Hyperemia versus congestion.
In both cases there is an increased volume and pressure of
blood in a given tissue with associated capillary dilatation
and a potential for fluid extravasation.
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In hyperemia, increased inflow
leads to engorgement with
oxygenated blood, resulting in
erythema.
In congestion, diminished
outflow leads to a capillary bed
swollen with deoxygenated
venous blood and resulting in
cyanosis.
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Hyperemia
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Varicose Veins
Congestion
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3- Hemorrhage
Extravasation of blood due to vessel rupture
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Types
• Hematoma: accumulation of blood within tissue.
• Petechiae: minute 1 to 2mm hemorrhages into skin,
mucous membranes, or serosal surfaces.
• Purpura: slightly larger (≥3 mm) hemorrhages.
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• Ecchymoses: larger (>1 to 2 cm) subcutaneous
hematomas (i.e., bruises)
• Hemothorax, hemopericardium, hemoperitoneum, or
hemarthrosis (in joints): Large accumulations of blood in
one of the body cavities
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Petechial hemorrhages of
the colonic mucosa
Intracerebral bleeding
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Subarachnoid Haemorrhage:
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Petechiae &Ecchymoses
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Conjunctival Petechiae
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Hemorrhage: Epidural hematoma
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Hemothorax
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4- Thrombosis
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Hemostasis and Thrombosis
Normal hemostasis result of a set of well-regulated
processes that accomplish two important functions:
(1) They maintain blood in a fluid, clot-free state in
normal vessels.
(2) They are aimed to induce a rapid and localized
hemostatic plug at a site of vascular injury.
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• Thrombosis: an inappropriate activation of
normal hemostatic processes, such as the
formation of a blood clot (thrombus) in
uninjured vasculature or thrombotic occlusion of
a vessel after relatively minor injury.
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Both hemostasis and thrombosis are regulated by
three general components:-
– the vascular wall
– platelets
– the coagulation factors.
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• Three primary causes for thrombus formation,
the so-called Virchow triad:
(1) Endothelial injury
(2) Stasis or slowing of blood flow
(3) Blood hyper-coagulability
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• Virchow triad in thrombosis. Endothelial integrity is the single most important
factor. Note that injury to endothelial cells can affect local blood flow and/or
coagulability; abnormal blood flow (stasis or turbulence) can, in turn, cause
endothelial injury. The elements of the triad may act independently or may
combine to cause thrombus formation.
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• Thrombi may develop anywhere in the
cardiovascular system, but stasis is a major factor
in the development of venous thrombi
• An area of attachment to the underlying vessel
or heart wall, frequently firmest at the point of
origin, is characteristic of all thromboses.
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• The propagating tail may not be well attached and,
particularly in veins, is prone to fragmentation,
creating an embolus.
• Mural thrombi - arterial thrombi that arise in heart
chambers or in the aortic lumen, that usually adhere
to the wall of the underlying structure
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• Mural thrombi. Thrombus in the left and right ventricular
apices, overlying a white fibrous scar.
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Thrombosis
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• Fate of the Thrombus.
1. Propagation.
2. Embolization.
3. Dissolution.
4. Organization and recanalization.
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• Potential outcomes of venous thrombosis.
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Laminated thrombus in a dilated abdominal aortic
aneurysm.
Mural thrombi.
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Lines of Zahn: alternating
layers of platelets and
fibrin in the thrombus
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5- Embolism
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• An embolus is a detached intravascular solid,
liquid, or gaseous mass that is carried by the
blood to a site distant from its point of origin.
• Emboli lodge in vessels too small to permit
further passage, resulting in partial or complete
vascular occlusion
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Pulmonary Thrombo-embolism
• 95% of venous emboli originate from deep
leg vein thrombi
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• Large embolus derived
from a lower extremity deep
venous thrombosis and now
impacted in a pulmonary
artery branch.
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Systemic Thromboembolism
• Emboli traveling within the arterial circulation.
• Most (80%) arise from intra-cardiac mural thrombi,
• Two thirds of which are associated with left ventricular
wall infarcts
• The major sites for arteriolar embolization are:
1. Lower extremities (75%)
2. Brain (10%)
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A- Fat Embolism
• Microscopic fat globules may be found in the
circulation after fractures of long bones (which
have fatty marrow) or, rarely, in the setting of soft
tissue trauma and burns.
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• Bone marrow embolus in the pulmonary circulation. The
cleared vacuoles represent marrow fat that is now
impacted in a distal vessel along with the cellular
hematopoietic precursors.
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Fat embolus in a glomerulus (kidney)
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B- Air Embolism
• Gas bubbles within the circulation can obstruct vascular flow.
• Enter the circulation during obstetric procedures or as a
consequence of chest wall injury.
• In excess of 100 cc is required to have a clinical effect
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C- Amniotic Fluid Embolism
• Underlying cause is the infusion of amniotic fluid or fetal
tissue into the maternal circulation via a tear in the placental
membranes or rupture of uterine veins.
• Characterized by sudden severe dyspnea, cyanosis, and
hypotensive shock, followed by seizures and coma.
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6- Infarction
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• An infarct is an area of ischemic necrosis caused by
occlusion of either the arterial supply or the venous
drainage in a particular tissue.
• Nearly 99% of all infarcts result from thrombotic or
embolic events, and almost all result from arterial
occlusion.
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• Infarcts are classified on the basis of their color
(reflecting the amount of hemorrhage) and the
presence or absence of microbial infection
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• Red (hemorrhagic) infarcts occur
(1) with venous occlusions (such as in ovarian torsion);
(2) in loose tissues (such as lung)
(3) in tissues with dual circulations (e.g., lung and small
intestine).
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• White (anemic) infarcts occur
1. with arterial occlusions in solid organs with end-
arterial circulation (such as heart, spleen, and kidney)
2. Solid tissues
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Examples of infarcts. (A) Hemorrhagic, roughly wedge-shaped
pulmonary infarct. (B) Sharply demarcated white infarct in
the spleen.
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• The dominant histologic characteristic of infarction is
ischemic coagulative necrosis
• most infarcts are ultimately replaced by scar tissue.
• The brain is an exception to these generalizations;
ischemic injury in the central nervous system results
in liquefactive necrosis
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• Remote kidney infarct,
now replaced by a large
fibrotic cortical scar.
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• Septic infarctions may develop when embolization
occurs by fragmentation of a bacterial vegetation
from a heart valve or when microbes seed an area
of necrotic tissue.
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7- Shock
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• Shock, or cardiovascular collapse, is the final
common pathway for a number of potentially
lethal clinical events, including severe hemorrhage,
extensive trauma or burns, large myocardial
infarction, massive pulmonary embolism, and
microbial sepsis.
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• gives rise to systemic hypo-perfusion caused by
reduction in:
1. cardiac output
2. the effective circulating blood volume.
• The end results are hypotension, followed by
impaired tissue perfusion and cellular hypoxia.
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Principal MechanismClinical ExamplesType of Shock
Failure of myocardial
pump owing to intrinsic
myocardial damage,
extrinsic pressure,
or obstruction to outflow
- Ventricular rupture
- Arrhythmia
- Cardiac tamponade
- Pulmonary embolism
- Myocardial infarction
Cardiogenic
Inadequate blood or plasma
volume
- Hemorrhage
- Fluid loss, e.g., vomiting,
diarrhea, burns, or traumaHypo-volemic
Peripheral vasodilation and
pooling of blood;
endothelial
activation/injury;
leukocyte-induced
damage; disseminated
intravascular coagulation;
activation of cytokine
cascades
- Overwhelming microbial infections
- Endotoxic shock
- Gram-positive septicemia
- Fungal sepsisSeptic
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Less commonly:
1. Neurogenic shock -in the setting of anesthetic
accident or spinal cord injury, owing to loss of
vascular tone and peripheral pooling of blood.
2. Anaphylactic shock, initiated by a generalized
IgE-mediated hypersensitivity response, is
associated with systemic vasodilatation and
increased vascular permeability
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Clinical Course
• The clinical manifestations depend on the precipitating
insult.
• In hypovolemic and cardiogenic shock, the patient
presents with hypotension; a weak, rapid pulse;
tachypnea; and cool, clammy, cyanotic skin.
• In septic shock, the skin may initially be warm and
flushed because of peripheral vasodilation.
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