HEMODYNAMIC DISORDERS

EMBOLISM
 is a detached intravascular solid, liquid, or gaseous
mass, carried by blood to a site distant from its point
of origin
 Types of emboli
- Thrombo-emboli
- Fat and bone marrow
- Gas (air, nitrogen)
- Athero-emboli
- Tumor fragments
- Foreign body (bullet)
Pulmonary Thrombo-Embolism

 In most instances, deep leg vein thrombi are the

source, depending on the size of the embolus, it;
 - may occlude main pulmonary artery
 - may impact across the bifurcation (saddle embolus)
 - may pass into the smaller arterioles
 - may enter the systemic circulation (para-doxical
embolism)
 Clinical consequences of pulmonary embolism
- most pulmonary emboli are silent
- sudden death (acute corpulmonale)
- obstruction of medium-size arteries> pulmonary
hemorrhage
- obstruction of small end-arterioles> infarction
- multiple emboli over time> chronic corpulmonale
Systemic Thrombo-Embolism

 Sources;

 - Intra-cardiac mural thrombi

 - Aortic aneurysm
 - Thrombi on ulcerated atherosclerotic plaques
 - Fragmentation of vegetation
 - Paradoxical emboli
 -15% are of unknown origin
 Main sites involved in embolism:

- Lower extremities (75%)

- Brain (10%)
- Intestines
- Kidneys
- Spleen
- Upper extremities
Fat Embolism

 May result from

- Fractures of long bones
- Soft tissue trauma and burns

 Clinical features
 - Pulmonary insufficiency
 - Neurologic symptoms
 - Anemia
 - Thrombocytopenia
 - Symptoms appear within 1 to 3 days
Fat Embolism
 Pathogenesis of fat embolism
- Mechanical obstruction
- Biochemical injury (release of fatty acids from fat
globules)

 Visualization of fat globules in tissue sections require:

- Frozen sections
- Fat stains (Sudan black, Oil-red-O)
Gas Embolism

 Air may enter the circulation during

 - Obstetric procedures
 - Chest wall injury
 More than100 cc is required to have a clinical effect
 The bubbles produce physical obstruction to
vessels>infarction
SHOCK
 Shock is pathological state of life-threatening hypoperfusion
of vital organs and cellular hypoxia, due diminished cardiac
output or reduced effective circulating blood volume

 ie: resulting in:

- Hypotension
- Impaired tissue perfusion
- Cellular hypoxia

 Initially, cellular injury is reversible; if shock is

sustained>cell death.
Stages of shock
 I. Stage of Compensation (initial nonprogressive stage )
 Decreased cardiac output cause reflex sympathetic
stimulation, which increases the heart rate (tachycardia) and
causes peripheral vasoconstriction that maintains blood
pressure in vital organs (brain and myocardium).

 Vasoconstriction in renal arterioles decreases the pressure

and rate of glomerular filtration, with resulting decreased
urine output (oliguria).
Stages of shock
 II. Stage of Impaired Tissue Perfusion (progressive stage )
 Prolonged excessive vasoconstriction, impairs tissue perfusion and
oxygenation.

 Impaired tissue perfusion;

 Promotes anaerobic glycolysis, leading to production of lactic acid and
lactic acidosis.
 Produces cell necrosis, which is most apparent in the kidney; causing
acute renal tubular necrosis and acute renal failure.
 In the lung, hypoxia causes acute alveolar damage with intra-alveolar
edema, hemorrhage, and formation of hyaline fibrin membranes (shock
lung, or adult respiratory distress syndrome [ARDS]
 In the liver, anoxic necrosis of the central region of hepatic lobules may
occur.
 Ischemic necrosis of the intestine is important because it is frequently
associated with hemorrhage or release of bacterial endotoxins that
further aggravate the shock state.
Stages of shock
 III. Stage of Decompensation
 As shock progresses, decompensation occurs.

 Widespread vasodilation and stasis result and lead to a

progressive fall in blood pressure to a critical level.
 Cerebral hypoxia causes brain dysfunction (loss of
consciousness).
 Myocardial hypoxia leads to further diminution of cardiac
output, and death may occur rapidly.
 Morphological changes in shock
 Changes are those of hypoxic injury,
 Most particularly involved organs, (brain, heart, lungs, kidneys,
adrenals, gastro-intestinal tract)
 Clinical features:

 - In hypovolemic and cardiogenic shock, the patient

presents with:
. Hypotension
. Weak rapid pulse
. Cool, clammy, and cyanotic skin

 -In septic shock, the skin initially is warm and flushed

 Prognosis

-Varies with the cause of shock and its duration;

 The best is in young with hypovolemic shock

 The worst is in an old with cardiogenic shock and that

with septic shock
Thank you