Hemodynamic 3

Study Notes

Fat Embolism:
- Occurs in 90% of individuals with severe skeletal injuries (long bone fracture) but less than 10% show clinical findings.
- Fat microemboli occlude pulmonary and cerebral microvasculature.
Fat Embolism Syndrome:
- Pulmonary insufficiency
- Neurological symptoms
- Anemia
- Thrombocytopenia
- Diffuse petechial rash
- Fatal in 10% of cases
- Signs and symptoms appear 1 to 3 days after injury
- Sudden onset of tachypnea, dyspnea, tachycardia, irritability, and restlessness, which can progress to delirium or coma.

Gas bubbles within the circulation can coalesce and obstruct vascular flow, causing distal ischemic injury.
Air may enter the circulation during obstetric procedures, chest wall injuries, or due to decompression sickness.
Decompression sickness occurs in individuals exposed to sudden changes in atmospheric pressure.
Deep-sea divers and underwater construction workers are at risk.
- Breathing air at high pressure (e.g., during a scuba dive) increases gas amounts (particularly nitrogen) dissolved in blood and tissues.
- If the diver ascends too rapidly (depressurizes), nitrogen bubbles form, causing gas emboli, which can induce focal ischemia in tissues such as the brain and heart.
- Rapid formation of gas bubbles in skeletal muscles and joints leads to the painful condition called "the bends."
- In the lungs, gas bubbles cause edema and hemorrhaging, leading to respiratory distress ("the chokes").
Treatment for decompression sickness involves a compression chamber to increase barometric pressure forcing gas bubbles back into solution.

Ischemic necrosis caused by occlusion of the vascular supply to affected tissue.
Examples include myocardial, cerebral, pulmonary, and bowel infarction, and ischemic necrosis of distal extremities (gangrene), especially in diabetics.
Causes:
- Arterial thrombosis or arterial embolism (most common)
- Less common causes include vasospasm, expansion of an atheroma, extrinsic compression of a vessel (by tumor), venous thrombosis (only in organs with a single efferent vein, e.g., testis, ovary).
Types of infarcts:
- Red (hemorrhagic): In venous occlusions (e.g., ovarian torsion); loose tissues (e.g., lung); tissues with dual circulations (e.g., lung, small intestine); previously congested tissues (sluggish venous outflow); when flow is re-established after infarction.
- White (anemic): In arterial occlusions in solid organs with end-arterial circulations (e.g., heart, spleen, kidney); ischemic coagulative necrosis; in the central nervous system, liquefactive necrosis.
- White infarcts are often wedge-shaped with the occluded vessel at the apex and organ periphery forming the base.
Most infarcts are replaced by scar tissue.

Characterized by systemic hypoperfusion of tissues.
Causes:
- Diminished cardiac output
- Reduced effective circulating blood volume.
Consequences: Impaired tissue perfusion, cellular hypoxia (organ failure).

Cardiogenic shock: Low cardiac output due to myocardial pump failure.
- Can be caused by myocardial damage (infarction), ventricular arrhythmias, extrinsic compression (cardiac tamponade), or outflow obstruction (e.g., pulmonary embolism).
Hypovolemic shock: Low cardiac output due to loss of blood or plasma volume (e.g., hemorrhage, severe burns).
Septic shock: Arterial vasodilation and venous blood pooling due to systemic immune response to microbial infection (commonly gram-positive bacteria).