Hemodynamic Tutorial

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Transcript Hemodynamic Tutorial

Hemodynamic Tutorial
Describe what you see?
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What are other causes of arterial
thrombosis?
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Vasculities.
Trauma
What is the thrombus made of?
Fibrin, platelets, and red cells.
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What causes arterial thrombosis? ...venous
thrombosis?
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Arterial thrombosis is caused by endothelial damage (eg,
atherosclerosis or vasculitis);
venous thrombosis is caused by stasis (sluggishness) of
blood flow.
Both types of vessels are affected in hypercoagulable
states such as antithrombin or protein C deficiency.
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What are the various fates of thrombi?
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Propagation, embolism, dissolution, and organization with
recanalization.
Which of these fates is clinically most significant in the
arterial circulation vs. the venous circulation?
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The most significant problem with arterial thrombi is propagation
leading to luminal obstruction, resulting in infarction of the tissue
supplied. Important examples include myocardial and cerebral
infarction. In contrast, the most significant problem with venous
thrombi is the possibility of potentially fatal embolization into the
pulmonary circulation.
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What is the difference between a postmortem clot
and a thrombus?
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Postmortem clots are not attached to endothelium;
they are gelatinous, rubbery, dark red at the ends and
yellowish elsewhere.
Thrombi are attached to endothelium and are traversed by
pale grey fibrin strands that can be seen on cut section;
they are more firm but fragile.
What do you see her
The well-defined pale area in the acute myocardial infarct represents
coagulative necrosis. It is surrounded by a red area of reactive
hyperemia. In contrast, the ill-defined pale area in the old myocardial
infarct represents a fibrous scar.
What is the organ?
What do you see here?
The congestion and accompanying sinusoidal dilatation are
maximum in and around central veins and decrease
progressively toward portal triads
The alveolar septa are prominent, due to marked
congestion of the capillaries. The alveolar lumens
contain pale-staining edema fluid.
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What is the pathogenesis of pulmonary edema?
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Left ventricular failure (eg, caused by a myocardial
infarct) causes pump failure, and secondarily there is
impaired flow of blood from the lung to the left atrium.
This causes increased hydrostatic pressure in pulmonary
alveolar capillaries and subsequent transudation of fluid
into alveoli.
Pulmonary edema in other cases may also result from
damage to alveolar capillaries (eg, in adult respiratory
distress syndrome).
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How does this type of edema differ from
that seen in acute inflammation?
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The fluid in pulmonary edema is a transudate (ie,
it is protein poor, has low specific gravity, and
does not contain inflammatory cells).
Edema in inflammation is an exudate.
What are the cells seen here?
What do you see here?
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Why are some infarcts red and others pale?
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Red infarcts result from hemorrhage into the
necrotic area. This is likely to occur in tissues that
have a loose texture and dual blood supply (eg,
lung); by contrast, pale infarcts occur in compact
tissues and those in which the collaterals do not
readily refill the necrotic area (eg, heart).
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What is the most common symptom of
pulmonary embolism?
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There are usually no symptoms. Most pulmonary
emboli (60-80%) are clinically silent because of
their small size and because of the dual blood
flow through the bronchial circulation. With time,
these emboli organize and are incorporated into
the vessel wall.
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How and when does pulmonary
thromboembolism cause sudden death?
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If more than 60% of the pulmonary circulation is
obstructed by emboli, the patient is at a high risk
of sudden death due to acute right heart failure
(cor pulmonale) or shock (cardiovascular
collapse).
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When does pulmonary thromboembolism
result in infarction?
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The possibility of developing pulmonary
infarction is higher in a previously diseased lung,
especially in the setting of sluggish bronchial
arterial flow or prior pulmonary congestion due to
left heart failure.