Pujasari Hemodynamic Alteration Neo
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Transcript of Pujasari Hemodynamic Alteration Neo
Hemodynamic DisordersHemodynamic Disorders
Hening P. Syahrin
Basic Science and Fundamental of Nursing Group Faculty of Nursing Universitas Indonesia
2009
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Disturbances of Blood FlowDisturbances of Blood Flow� Hyperemia and congestion� Hemorrhage� Ischemia � Thrombosis � Postmortem clots � Disseminated intravascular coagulation � Embolism � Infarction � Edema � Shock
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Hyperemia and CongestionHyperemia and Congestion
Increased volume of blood in an affected tissue or part
� Hyperemia (active hyperemia):Arterial and arteriolar dilatation produces an increased flow of blood into capillary beds
� Congestion (passive congestion or venous congestion):Impaired venous drainage
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Active HyperemiaActive Hyperemia
Too much arterial blood is brought to an organ or tissue by dilated arterioles and capillaries– Sympathetic neurogenic mechanisms or– The release of vasoactive substances
– Inflammatory reaction– Heat applied locally to a part– Increased physiological activity
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Can the increased blood flow Can the increased blood flow (active hyperemia) in acute (active hyperemia) in acute inflammation be a defense inflammation be a defense mechanism of the body?mechanism of the body?
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Passive CongestionPassive Congestion
� Blood leaving an organ or part is impeded (impaired venous drainage)
� Grossly, the involved tissues appear bluish-red because of the poorly oxygenated venous blood
� Microscopically, congestion is similar to hyperemia (capillaries and veins are dilated and filled with blood)
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Types of Passive CongestionTypes of Passive Congestion
� Localized passive congestion
� Generalized passive congestion– Chronic generalized passive congestion of the
lungs: Reduced left ventricular output (left-sided heart failure).
– Chronic passive congestion of the liver: Right-sided heart failure (rarely from obstruction of the posterior vena cava).
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HemorrhageHemorrhage
The presence of erythrocytes outside the blood vessels– The vessel may be physically damaged so that
erythrocytes flow out through a break in the wall (hemorrhage by rhexis) or
– The erythrocytes may pass through an intact vascular wall by a process called diapedesis (hemorrhage by diapedesis)
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Naming HemorrhageNaming Hemorrhage--11
� Petechiae� Ecchymoses� Purpura� Agonal hemorrhages� Linear hemorrhages� Paint-brush hemorrhages� Hemothorax� Hemopericardium
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Naming HemorrhageNaming Hemorrhage--22� Epistaxis
� Hemoptysis
� Enterorrhagia
� Metorrhagia
� Hematuria
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The Significance of Hemorrhage The Significance of Hemorrhage Depends on:Depends on:
(1) The volume of blood loss
(2) The rate of blood loss, and
(3) The site of hemorrhage
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IschemiaIschemia
Local anemia or a deficiency of arterial blood to a portion of an organ or part. The chief causes of ischemia are:
(1) External pressure upon an artery
(2) Narrowing of the lumen of an artery
(3) A thrombus or embolus
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Effects of IschemiaEffects of Ischemia
� The organ involved
� The size of the vessel
� The degree of occlusion
� The degree of collateral circulation
� End artery (as in kidneys): Acute necrosis
� Gradual obstruction: Atrophy
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ThrombosisThrombosis� Formation of a clot from elements of the
circulating blood within the vascular system during life
� May decrease or obstruct vascular flow causing ischemic/hypoxic injury to cells, tissues and organs
� May become dislodged or fragmented to create emboli (an embolus is an intravascular mass carried in the bloodstream to some site remote from its origin)
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Factors Effective in Factors Effective in ThrombosisThrombosis
(1) Injury to vascular endothelium
(2) Alterations in normal blood flow
(3) Alterations in the blood (hypercoagulability)
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Arterial vs Venous ThrombusArterial vs Venous Thrombus� Grossly: Thrombi are friable, a mixture of red and
gray in irregular layers, dull, and attached to the endothelium
� Arterial thrombus: Dry, friable gray masses composed of almost regularly arranged layers of platelets and fibrin, irregularly mixed with small amounts of darker red coagulated blood
(White or conglutination thrombus)
� Venous thrombus:Red, gelatinous
(Stasis or red coagulation thrombus)
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Nomenclature of ThrombiNomenclature of Thrombi--II� Mural thrombi - are attached to the wall of the
heart or blood vessel
� Occluding thrombi - are attached to the entire circumference of the vessel
� Valvular thrombi - are attached to the heart valves
� Canalized thrombi - occur when new blood channels form in an organized thrombus
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Nomenclature of ThrombiNomenclature of Thrombi--IIII
� Saddle thrombi - straddle the bifurcation of blood vessels
� Septic thrombi - are those which contain bacteria
� Aseptic thrombi - are those that do not contain bacteria, etc.
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The Thrombus may The Thrombus may ……
(1) increase in size and, by its enlargement, eventually cause obstruction of some critical vessel
(2) give rise to emboli
(3) be removed by fibrinolytic action or
(4) become organized
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Disseminated Intravascular Disseminated Intravascular Coagulation (DIC)Coagulation (DIC)
� Widespread microthrombi formation in capillaries, arterioles and venules
� Composed largely of fibrin and aggregated platelets
� A complication of a diverse group of clinical diseases in which there is activation of the intrinsic pathway of blood clotting
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EmbolismEmbolism
� Process of a foreign body moving through the circulatory system and becoming lodged in a vessel causing obstruction
� An embolus (plural, emboli) is a detached intravascular solid, liquid or gaseous mass that is carried by the blood to a site distant from its point of origin
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InfarctionInfarction
� A localized area of ischemic necrosis in an organ or tissue resulting from occlusion of either its arterial supply or venous drainage
� Usually caused by thrombosis and/or embolism of the arterial blood supply
� More rarely, external compression of vessels by expanding tumors, etc.
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EdemaEdema
� Abnormal accumulation of fluid (water) in the intercellular tissue spaces or body cavities
� Localized (e.g. obstruction of venous outflow from the leg)
� Generalized in distribution (e.g. in chronic congestive heart failure)
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NomenclatureNomenclature� Anasarca: Generalized edema in which fluid in
subcutaneous tissues is especially prominent
� Ascites: Collection of edematous fluid in the peritoneal cavity
� Hydrothorax: Collection of edematous fluid in the thoracic cavity
� Hydropericardiumor Pericardial Effusion: Collection of edematous fluid in the pericardial sac
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TransudateTransudate--ExudateExudate
� Inflammatory edema is referred to as an exudateand it is associated with an inflammatory reaction
� Non-inflammatory edema is referred to as a transudate
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Edema is caused by Edema is caused by ……
(1) Decreased plasma osmotic pressure
(2) Increased hydrostatic pressure
(3) Increased permeability of vascular endothelium
(4) Lymphatic obstruction
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Decreased Plasma Osmotic Decreased Plasma Osmotic PressurePressure
� Deficiency of blood proteins(hypoproteinemia)
� Decreased formation or excessive loss
� Albumin
� More fluid is pushed into the intercellular spaces. Also, the force available to pull fluid into the bloodstream at the venous end of the capillary is reduced
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Decreased Plasma Osmotic Decreased Plasma Osmotic PressurePressure--II
� Malnutrition (starvation, emaciation)
� Severe or advanced liver diseases (cirrhosis, etc.)
� The loss of plasma proteins (intestine and kidneys)
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Decreased Plasma Osmotic Decreased Plasma Osmotic PressurePressure--IIII
� In the intestine, blood protein loss is usually the result of hemorrhage over a long period of time (stomach worms in sheep and cattle, slowly bleeding stomach ulcers in pigs and dogs, etc.)
� In the kidneys, renal amyloidosis is the only frequently encountered condition in animals in which large volumes of blood protein are lost through the urine
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Increased Hydrostatic Increased Hydrostatic PressurePressure
� Venous stasis
� Subsequent to venous stasis, the capillaries become more permeable to large molecules (albumin and globulin), since they are deprived of their normal supply of oxygen and other nutrients
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Increased Permeability of Increased Permeability of Capillary EndotheliumCapillary Endothelium
Occurs subsequent to venous stasis(resulting in increased hydrostatic pressure),as well as from direct damage, as in inflammation. Increased vascular permeability is the most important mechanism in the formation of inflammatory edema (exudate)
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Lymphatic ObstructionLymphatic ObstructionOccurs when any lesion impedes normal lymphatic drainage by pressure or obstruction. Under normal conditions, the lymphatics constantly drain small amounts of fluid from the intercellular spaces. Thus, in the absence of lymphatic drainage from a area, fluid accumulates
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ShockShock
� Peripheral circulatory failure with pooling of the blood in the terminal circulatory beds (small capillaries)
� The fundamental disturbance is that blood volume is too small to fill the vascular system, resulting in a fall of blood pressure and cell damage due to anoxia
� Hypovolemic, septic, cardiogenic and neurogenic
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Clinical Signs of ShockClinical Signs of Shock� Inconsistent and vary with the precipitating
cause� Animals are usually inactive and unresponsive
to external stimuli� Muscle weakness is prominent and there is
pallor and coolness of the skin� Body temperature is subnormal and the heart
rate is increased in most types of shock (but it may be slow and irregular). Depression of renal function and urine production often occur
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ShockShock� Hypovolemic shock: Due to loss of blood
volume (hemorrhage, trauma, loss of fluids in burns, etc.)
� Septic shock: Septicemia or an overwhelming infection with gram-negative (endotoxic shock) or gram-positive (exotoxic shock)organisms. Peripheral dilatation of the capillary beds which subsequently lead to shock
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ShockShock� Cardiogenic (Cardiac) shock: “Pump
failure." Subsequent to the sudden decrease in cardiac output
� Neurogenic shock: A shock state mediated by the nervous system which induces peripheral dilatation (dilatation of the capillary bed). It occurs in animals with severe fright, pain and trauma (without hemorrhage)
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