Disorders of Circulation Flashcards
Hyperemia
Arteriolar dilatation and increased blood flow
Caused by sympathetic neurogenic discharge or chemical mediators (ACTIVE)
Tissues appear “redder” Ex: sites of inflammation, exercising skeletal muscle
Congestion
Impaired outflow of VENOUS blood from a tissue (passive process)
Tissues have abnormal “red-blue” color
Hemostasis
Series of regulated processes that;
- maintain blood in a fluid clot-free state in normal vessels
- rapidly form a localized hemostatic plug at the site of vascular injury
Hemorrhage - Mechanisms
Vessel is disrupted by:
- mechanical force (trauma)
- pathologic process (congestion, inflammation, neoplastic erosion of vessel)
Causes of Edema
Increased Hydrostatic Pressure
Systemic: Heart failure
Local: Impaired venous return post DVT
Causes of Edema
Decreased colloid osmotic pressure
Due to reduced plasma albumin
- Decreased synthesis (liver disease, malnutrition)
- Increased loss (nephrotic syndrome: glomular apparatus malfunctioning and excessively spilling proteins into urine)
Causes of Edema
Lymphatic obstruction
Neoplasm
Causes of Edema
Increased vascular permeability
Inflammation
Causes of Edema
Renal failure
Sodium Retention
Pathways leading to systemic edema
Thrombosis
Formation of blood clot (thrombus) within intact vessel
Pathologic process
Mechanisms of Thrombosis
Endothelial injury: inflammation; advanced atherosclerosis
Altered blood flow: turbulence (atherosclerotic vessel narrowing) vs stasis (a.fib, bed rest)
Hypercoagulable state: presidposition to easy clot formation - inherited (protein C deficiency) and aquired (woman who smokes and uses oral contraceptives; disseminated cancer)
Virchow’s triad in thrombosis
Endothelial injury
Abnormal blood flow
Hypercoagulability
Embolism
Intravascular substance (solid, liquid, gas) which is carried by blood from point of origin to distant site.
Types of Emboli
- Fragments of thrombi (thromboembolism)
- Atherosclerotic
- Amniotic fluid
- Air (gas)
- Fat
Infarct
Area of ischemic necrosis caused by occlusion of vascular supply to affected tissue
(pattern of necrosis will be most likely be coagulative, in brain is liquifactive)
White infarct
Arterial occlusions
Solid organ with end-arterial circulation: heart, liver spleen, kidney
Red infarct
Venous occlusions (ie ovarian torsion)
Tissues with dual circulations (lung, small intestine)
Loose tissues (lung)
When flow is re-established after infarction (s/p angioplasty of arterial obstruction)
Factors that influence infarct development
Nature of vascular supply
Rate of development of occlusion
Vulnerability of tissue to hypoxia
Oxygen content of blood
Shock
Characterized by systemic hypoperfusion of tissues with resultant;
- impaired tissue perfusion
- cellular hypoxia
Cardiogenic shock
Low cardiac output due to myocardial pump failure
- MI
- Ventricular repture
- Arrhythmia
- Cardiac tamponade
Hypovolemic shock
Low cardiac output due to loss of blood or plasma volume
- Hemorrhage
- Fluid loss (vomiting, diarrhea, burns, trauma)
Septic shock
Arteriolar vasodilation and venous blood pooling that stems from systemic immune response to microbial infection
