Hemodynamics Flashcards
Hyperemia
Locally increased blood flow as a result of active arteriolar dilation; leads to increased blood flow causing erythema
Congestion
Locally increased blood flow as a result of passive venous insufficiency; may be systemic (2/2 right sided heart failure) or local (2/2 venous obstruction)
Leads to edema and hypoxia due to accumulation of deoxygenated hemoglobin; tissue appears bluish/dusky
Virchow’s Triad
Describes the 3 key elements involved in thrombosis
- Endothelial injury - causes endothelial dysfunction, disrupting the normal balance of pro- and anti-coagulatory effects
- Stasis or turbulent blood flow - turbulent blood flow injures endothelial cells, causing pro-coagulatory activation; stasis brings platelets into contact with endothelial cells
- Hypercoagulability of blood - any alteration of the coagulation pathways that predisposes to thrombosis; may be primary (genetic) or secondary (acquired)
Cardiogenic Shock
Systemic hypotension resulting from low cardiac output; low cardiac output can result from pump failure (infarction, arrhythmias, tamponade) or from outflow obstruction (pulmonary embolism)
Hypovolemic Shock
Systemic hypotension resulting from loss of blood or plasma volume; often 2/2 hemorrhage, fluid loss from severe burns, etc.
Septic Shock
Systemic hypotension resulting from widespread vasodilation and peripheral pooling of blood 2/2 a systemic immune response to infection
Neurogenic Shock
Systemic hypotension resulting from loss of vascular tone and pooling of blood in the peripheral circulation; often 2/2 spinal cord injury
Anaphylactic Shock
Systemic hypotension resulting from systemic vasodilation and increased vascular permeability following an IgE-mediated hypersensitivity reaction
Stages of Shock
- Nonprogressive stage - reflex compensatory mechanisms (tachycardia, peripheral vasoconstriction, renal conservation of fluid) are activated and perfusion of vital organs is maintained
- Progressive Stage - tissue hypoperfusion, widespread hypoxia, metabolic acidosis
- Irreversible - Onset of cellular and tissue injury incompatible with survival
Disseminated Intravascular Coagulation
Characterized by the onset (sudden or insidious) of widespread fibrin thrombi in the microcirculation causing diffuse circulatory insufficiency to the vital organs; platelet and coagulation protein consumption occurs at the same time as fibrinolytic activation, causing risk for bleeding emergency
Classes of Edema
May be transudate or exudate
Local (2/2 local increase in hydrostatic pressure) or systemic (2/2 right ventricle failure causing pooling of blood in venous circulation)
Causes include decreased plasma colloid pressure (2/2 reduced synthesis of albumin in the liver), salt retention (2/2 decreased renal function), or lymphatic obstruction
Classification of hemorrhages
Petechiae - 1-2mm hemorrhages into skin, often 2/2 locally increased intravascular pressure & low platelet counts
Purpura - > 3mm hemorrhages
Ecchymoses - > 1-2cm hemorrhages
Infarct
An area of ischemic necrosis caused by occlusion of the arterial supply or venous drainage; usually 2/2 thrombotic arterial occlusions
Thrombosis
Pathological clotting within intact vessels, usually caused by Virchow’s triad of primary abnormalities
Arterial or venous
Embolus
Any detached, intravascular solid, liquid, or gas that is carried by the blood to a site distant from its point of origin; usually represent some part of a dislodged thrombus
May be venous - i.e. from the deep veins of the legs, leading to pulmonary embolism
May be arterial - leading to reduced perfusion of the brain, retina, spleen, kidney, intestine, and lower leg
