At this point, the student understands the ways in which normal and abnormal cells accumulate a variety of products.
In this section, lesions related to circulatory disturbances are considered. Most lesions that develop in the body are influenced directly or indirectly by the blood and/or blood vessels. Those circulatory disturbances common to many types of lesions include hemorrhage, hyperemia, congestion, ischemia, thrombosis, embolism, infarction, edema, shock and disseminated intravascular coagulation.
Once this section is completed, each student should be able to perform the following tasks.
The student should attempt to define, spell and use the following terms prior to and after embarking on a study of circulatory disturbances.
The terms hyperemia and congestion refer to an increased volume of blood in an affected tissue or part. Hyperemia (also called "active hyperemia") occurs when arterial and arteriolar dilatation produces and increased flow of blood into capillary beds (inactive capillaries are opened). Congestion (also referred to as passive congestion or venous congestion) results from impaired venous drainage. Remember, in both hyperemia and congestion, blood is retained within the vascular system; whereas in hemorrhage, blood is found outside of the vascular system.
Occurs when too much arterial blood is brought to an organ or tissue by dilated arterioles and capillaries. The arteriolar dilatation is brought about by sympathetic neurogenic mechanisms or by the release of vasoactive substances. In most instances, active hyperemia occurs subsequent to an inflammatory reaction (it is the first stage of inflammation). Other situations characterized by active hyperemia include:
Microscopically, the capillaries are dilated and filled with blood. Grossly, the involved organ/part takes on the bright red color of arterial blood (depending on the original color). Clinically, the organ/part is warmer than normal.
(Congestion) occurs when the flow of blood leaving an organ or part is impeded (impaired venous drainage). Microscopically, congestion is similar to hyperemia (capillaries and veins are dilated and filled with blood). Grossly, the involved tissues appear bluish-red because of the poorly oxygenated venous blood.
Localized Passive Congestion is usually caused by pressure placed on veins leaving an organ or part (via bandage, rubber band, torsion, etc.). Oftentimes, the compression on vessels is such that blood still gets in through thick-walled, muscular arteries but pressure on thinner-walled veins restrict the outflow and venous blood accumulates.
Generalized Passive Congestion is associated with impediment of blood flow in the central circulation (heart, lungs, major vessels, etc.). It may be acute or chronic. Acute generalized passive congestion is usually associated with a failing heart. Chronic generalized passive congestion is most obviously manifested in the lungs, liver and spleen.
Chronic Generalized Passive Congestion of the Lungs is encountered in all forms of cardiac decompensation that occurs subsequent to reduced left ventricular output (left-sided heart failure). An accumulation of blood and increased hydrostatic pressure occurs in the lungs. Some of the distended lung capillaries may rupture or hemorrhage per diapedesis may occur. Eventually, the breakdown and phagocytosis of erythrocyte debris leads to the appearance of hemosiderin-laden macrophages (heart-failure cells) in the alveolar spaces. In time, the alveolar walls become fibrotic. Thus, the fibrosis and hemosiderin pigmentation constitute the basis for the designation "brown induration of the lung."
Chronic Passive Congestion of the Liver results from right-sided heart failure (rarely from obstruction of the posterior vena cava).
Hemorrhage refers to 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 or the erythrocytes may pass through an intact vascular wall by a process called diapedesis. The various etiologic agents that play a role in the development of hemorrhage are discussed in your textbook (pages 100-101). The following are some of the terms used to denote hemorrhage.
The significance of hemorrhage depends on:
About 30% of the total blood volume is the maximum which can be lost and the animal still recover. If more is lost, death is likely to occur subsequent to hypovolemic shock. However, the amount of blood which can be lost depends upon the rapidity with which it leaves the vascular system. For example, when the rate of hemorrhage is slow (stomach worm infections), fluid can be added to the blood rapid enough to maintain near normal blood pressure; thus, the loss of large amounts may have little clinical significance. Also, the site of hemorrhage will influence its effect on the host. A hemorrhage which would be trivial in the subcutaneous tissues may cause death when located in the brain stem.
Repeated or chronic external hemorrhages (i.e., when blood is shed from the skin, G.I. tract, etc.) represent losses not only of blood volume but also of valuable iron. Usually, the small but repeated volume losses are rapidly corrected by movement of water from the interstitial spaces into the vascular compartment, but the chronic losses or iron may lead to iron deficiency anemia. In contrast, when erythrocytes are retained, as occurs with hemorrhages into the body cavities, joints or tissues, the iron can be recaptured for synthesis of hemoglobin.
The fate of an area of hemorrhage depends upon the amount of blood that has escaped from the vascular system. If the hemorrhage is relatively small, the fluid portion of the blood is absorbed, the leukocytes move back into the vascular system and the erythrocytes are phagocytized. In a larger hemorrhage, there is disintegration and breakdown of erythrocytes with the formation of hematoidin and hemosiderin. Cholesterol may also be seen in the tissues. The escaped blood also clots with the formation of fibrin and this fibrin and the remaining leukocytes may eventually be phagocytized. In still larger areas of hemorrhage, fibroblasts and new capillaries may proliferate into the area of clotted blood. This process is known as organization of the area of hemorrhage.
Sludged blood refers to the conglutination or sticking together of erythrocytes within blood vessels and should be distinguished from simple rouleaux formation in which erythrocytes merely stack one on top of another. In the formation of sludged blood, large masses of erythrocytes adhere to each other and may settle to the lower portion of large vessels or even block smaller vessels. The etiologic mechanism is uncertain, but for some reason the erythrocytes lose their ability to repel each other and conglutinate. This condition has been studied extensively in man by microscopic examination of vessels in the conjuctiva during life and has also been reported in swine infected with hog cholera virus. It is postulated that sludged blood flows more slowly, may give rise to blood clots within the vessel and may cause hypoxia of the tissues involved.
Ischemia refers to local anemia or a deficiency of arterial blood to a portion of an organ or part. The chief causes of ischemia are
However, ischemia may be caused by vasoconstriction as observed in ergot poisoning. The effects of ischemia are dependent on the organ involved, the size of the vessel, the degree of occlusion and the degree of collateral circulation. If ischemia occurs in an "end artery," as in the kidneys, the result is likely to be acute necrosis of tissue supplied by the vessel. If the obstruction to blood flow is gradual, atrophy may occur.
Thrombosis refers to the formation of a clot from elements of the circulating blood within the vascular system during life. This clot is known as a thrombus (plural, thrombi). The development of a clot is life-saving when a large vessel ruptures or is severed. However, when a thrombus develops within the vascular system, it may be life-threatening because:
The ischemic necrosis created by a thrombus (embolus) is referred to as an infarct (thrombosis and embolism are so closely interrelated as to give rise to the term thromboembolism). To a considerable extent, thrombosis is the consequence of inappropriate activation of the processes of normal hemostasis. Therefore, the student should review normal hemostasis as outlined in the textbook (pages 115-118) before considering the pathogenesis of thrombosis.
"Normal Hemostasis" is influenced by components of the blood vessel wall, platelets and the clotting sequence. The integrity of the blood vessel wall is crucial in normal hemostasis as well as in thrombosis. The lining endothelium provides a nonreactive interface between the underlying reactive element of the vessel wall and the fluid blood. In addition, the endothelial cells serve to protect against thrombi formation by:
Platelets are assigned a central role in normal hemostasis and thrombosis. They adhere to sites of endothelial injury, aggregate to form platelet masses, release granules rich in a variety of secretory products and synthesize several types of prostaglandins. In normal hemostasis, platelets adhere to the severed margins of a vessel within seconds to a few minutes. The most important stimulus to such adherence is the exposure of collagen fibrils. Once adhered, platelets release two types of granules:
The release of platelet granules is triggered by a number of substances, including collagen fibrils, thrombin, plasmin, trypsin, endotoxin and antigen-antibody complexes. It is believed that these stimuli to platelet activation inhibit membrane-bound adenyl cyclase (decreased amounts of cyclic AMP are found in aggregated platelets). Within aggregated platelets, there is increased concentration of calcium (this cation is a potent stimulus to platelet activation). In addition, platelet factor 3, which participates in the intrinsic pathway of the clotting sequence, becomes activated. Initially, the platelet aggregation forms a temporary hemostatic plug which is friable and easily dislocated in rapidly flowing bloodstreams (however, at this time, the clotting sequence leads to the formation of thrombin which is the most powerful platelet aggregator yet identified). In summary, platelets:
The coagulation system plays a major role in normal hemostasis. Maintenance of normal fluidity of blood involves the interplay between procoagulants and anticoagulants. When the procoagulants dominate and clotting is triggered inappropriately in the intact cardiovascular system, thrombi result. Concurrent with the formation of the platelet plug, the coagulation system is activated (the clotting factors involved are listed on page 105 of your textbook). The critical events in blood clotting are the conversion of prothrombin to thrombin and the subsequent conversion of soluble fibrinogen into the stable fibrin polymer (the sequence of interactions among the clotting factors is present on pages 108-118 of your textbook). Remember, clotting may be initiated by the intrinsic pathway when blood is exposed to a negatively charged surface, such as collagen. The extrinsic pathway initiates clotting when injury exposes the blood to factors derived from injured cells and tissues. Thus, the evolution of a thrombus begins with the adherence of platelets at sites of vascular injury followed by the build-up, first of a temporary aggregation of platelets, and then the formation of a more permanent platelet mass which in turn leads to the standard clotting sequence, possibly involving both the intrinsic and extrinsic pathways.
Thrombosis is influenced by three major factors:
Endothelial injury plays a dominant role in the formation of thrombi in arteries and in the heart. Once the endothelium is damaged, subendothelial collagen may be exposed and tissue thromboplastic, etc., is released and the sequence of platelet adherence and activation of the clotting sequence follows.
Alterations in Normal Flow as encountered with stasis and turbulence of blood contributes to the development of arterial and cardiac thrombi and are probably requisite for venous thrombosis. In the normal flowing bloodstream, the larger particles, such as erythrocytes and leukocytes, occupy the central or more rapidly moving axial stream. The smaller platelets are carried in the more slowly moving laminar stream outside the central column. The periphery of the bloodstream adjacent to the endothelial layer moves more slowly and is free of all formed blood elements. If stasis or turbulence occurs, this laminar flow is disrupted and platelets are brought in contact with the endothelium. Evidence suggests that stasis and turbulence assume the greatest degree of importance in the formation of venous thrombi.
Alterations in blood that induce hypercoagulability have been proposed to explain the increased incidence of thrombosis encountered in certain clinical states (following surgical procedures, parturition, accidental trauma, etc.) Hyper-coagulability has been defined as "an altered state of circulating blood that requires a smaller quantity of clot-promoting substances to induce intravascular coagulation than is required to produce comparable thrombosis in a normal host." Increased numbers of platelets, increased platelet stickiness, elevated levels of fibrinogen, increased generation of thrombin, etc., have been identified as causing hypercoagulability in various clinical conditions.
Grossly, thrombi are friable, a mixture of red and gray in irregular layers, dull, and attached to the endothelium. Arterial thrombi formed in a rapidly flowing bloodstream are usually dry, friable gray masses composed of almost regularly arranged layers of platelets and fibrin, irregularly mixed with small amounts of darker red coagulated blood. The resulting laminations are known as the "lines of Zahn." Arterial thrombi are referred to as white or conglutination thrombi. Venous thrombi, formed in a slow-moving bloodstream, appear as an intravascular clot that closely resembles the clotting of blood in a test tube. Such thrombi are red, gelatinous, and they are referred to as stasis or red coagulation thrombi. The following terms are used to describe thrombi:
Microscopically, thrombi are eosinophilic masses in which leukocytes and erythrocytes may be seen. Fibrin is usually obvious, but it is seldom possible to identify platelets.
The significance, effects and outcome of thrombi should be reviewed in your textbook. If an animal survives the immediate ischemic effects of a newly developed thrombus, one of several pathways may be followed. The thrombus may
A thrombus must not be confused with postmortem clotting of blood within the vascular system. The two types of postmortem clots are:
Red or Current Jelly Clots occur when the components of the blood are evenly distributed throughout the clot. This type develops when there is rapid clotting of blood.
Yellow or Chicken Fat Clots result from a settling and separation of erythrocytes from the fluid phase of the blood. Such clots occur when postmortem clotting is delayed.
The following table gives the characteristic features of a thrombus and a postmortem clot.
Disseminated intravascular coagulation (DIC) refers to widespread microthrombi formation in capillaries, arterioles and venules. The thrombi are composed largely of fibrin and aggregated platelets. The disorder may be a complication of a diverse group of clinical diseases in which there is activation of the intrinsic pathway of blood clotting. During the widespread intravascular coagulation, fibrin is deposited throughout the vascular tree resulting in microthrombi. Although the fibrinolytic system is activated, it cannot effectively deal with the large deposits of fibrin. As a result, there is rapid consumption and eventually a deficiency of clotting factors, including fibrinogen, platelets, prothrombin and factor V, VII, and X (a deficiency of fibrinogen, platelets and prothrombin is required for the diagnosis of DIC). Therefore, animals with DIC have bleeding tendencies on hemorrhagic diathesis. Also the widespread occlusion of the microcirculation may induce signs of shock, acute respiratory distress, central nervous system depression, heart failure or renal failure. Remember, affected tissues may not necessarily disclose the microthrombi because of prompt activation of the fibrinolytic system.
Embolism refers to the 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. Inevitably, emboli lodge in vessels too small to permit their further passage resulting in partial or complete occlusion of the vessel. The majority of all emboli arise from thrombi (thromboembolism). These are pieces of thrombi which have been broken loose by the force of the bloodstream. Less common forms of emboli include fat emboli, gas emboli, bacterial emboli, tumor emboli and parasitic emboli (see your textbook).
Depending on their site of origin, emboli may come to rest anywhere within the cardiovascular system. (Unless otherwise qualified, the term "embolus" implies thromboembolism throughout this discussion).
7.13.1 PULMONARY EMBOLISM:
Pulmonary emboli usually originate from thrombi in veins or in the right heart. Dislodgement of venous thrombi, in part or whole, produces an embolus which flows with the venous drainage through progressively larger vessels to the right heart. Unless the embolus is very large, it passes through the spacious chambers and valve openings of the right heart and enters the pulmonary arterial circulation. Lodgement of emboli in major pulmonary vessels is commonly fatal, resulting in sudden death. When pulmonary emboli occlude smaller vessels, they usually cause lung hemorrhage or infarcts. However, in animals without cardiac or circulatory insufficiency, the bronchial circulation suffices to substain the vitality of lung tissue. Remember, pulmonary infarction results only when the bronchial circulation is inadequate to compensate, which is common in animals with impaired cardiovascular function.
7.13.2 SYSTEMIC EMBOLISM:
Systemic embolism refers to emboli which travel through the arterial circulation. Such emboli usually arise from thrombi within the left heart. In contrast to venous embolism, arterial emboli travel through vessels of progressively diminishing caliber. The myocardium, spleen, kidneys, brain and lower extremities are commonly the victims of arterial embolism.
Paradoxical embolism refers to emboli which enters the right side of the heart and pass through interatrial or interventricular septal defects to gain access to the arterial side of the circulation.
An infarct is a localized area of ischemic necrosis in an organ or tissue resulting from occlusion of either its arterial supply or venous drainage. The vascular occlusion is usually caused by thrombosis and/or embolism of the arterial blood supply. More rarely, external compression of vessels by expanding tumors, etc., may result in infarction.
Infarcts are classified on the basis of their color (red or pale infarcts) and on the presence or absence of bacterial contamination (septic or aseptic infarcts). Pale or anemic infarcts are encountered with arterial occlusion and in solid tissue. When a solid tissue is deprived of its arterial circulation, the infarct may be transiently hemorrhagic, but most become pale in a very short time. The reasons for the development of pale infarcts are as follows:
"The arterial circulation to an area is occluded. Vessels, particularly capillaries, as well as parenchymal cells are destroyed. At the moment of vascular occlusion, blood from anastomotic peripheral vessels flows into the focus of injury, producing the initial hemorrhagic appearance. If the affected tissue is solid, seepage of blood from the anastomotic vessels is minimal. Soon after the initial blood seepage, the erythrocytes are lysed and the released hemoglobin pigment either diffuses out or is converted to hemosiderin. Therefore, in solid organs, the arterial infarct will soon (24 to 48 hours) become pale or anemic. The heart and kidneys are representative of solid, compact organs which tend to have pale infarcts."
Red or Hemorrhagic Infarcts are encountered usually under the following circumstances:
Red or hemorrhagic infarcts develops in loose tissue subsequent to arterial obstruction in the following manner.
The arterial circulation to an area is obstructed. If the tissue is loose (lung, etc.), large amounts of blood collect in the spongy, loose tissue at the moment of vascular occlusion. This blood remains for long periods; thus, the arterial infarct remains red. The lungs and intestine are sites where red infarcts tend to occur.
Factors that influence the severity of damage resulting from infarction include the following:
A dual blood supply is received by the lungs and liver. In animals with normal cardiac and cardiovascular status, the bronchial circulation is capable of preventing ischemic necrosis of the lungs when a branch of the pulmonary artery is obstructed. Similarly, infarction is uncommon in the liver because the portal supply of blood may be adequate, even when the hepatic arterial supply is compromised. However, in the presence of cardiac failure, severe anemia, or reduced oxygenation of the blood, occlusion of one system may precipitate ischemic necrosis.
An arterial blood supply with rich interarterial anastomoses is found in the small intestine. Here, blood is able to bypass focal areas of occlusion.
An arterial blood supply with so-called "end arteries" is found in the kidneys, for example. The major branches of the renal artery supply well-defined segments of the kidneys. Occlusion of one of the major branches, or of the main renal artery, is invariably followed by ischemic necrosis. However, if the occlusion occurs at the terminal ramification and involves subcapsular parenchyma, there may be sufficient blood flow from capsular vessels to prevent tissue damage.
Parallel arterial system is encountered in the forelimbs. Either the radial or the ulnar artery is sufficient to sustain the vitality of the tissues when one or the other is occluded.
Microscopically, all areas of infarction undergo coagulative necrosis and resorption as discussed in Section 3
The typical coagulative appearance may be modified by extensive hemorrhage in red infarcts and by bacterial suppuration in septic infarcts. Within a few days after an infarct is initiated, an inflammatory reaction becomes well-defined. Later, a reparative process begins.
Grossly, both red and pale infarcts tend to be wedged-shaped, with the apex of the wedge pointing toward the focus of vascular occlusion.
Edema refers to an abnormal accumulation of fluid (water) in the intercellular tissue spaces or body cavities. It may occur as a localized (e.g. obstruction of venous outflow from the leg), or it may be generalized in distribution (e.g., in chronic congestive heart failure). The following terms are used to describe edema:
Edematous fluid may be inflammatory or non-inflammatory. Inflammatory edema is referred to as an exudate and it is associated with an inflammatory reaction. Non-inflammatory edema is referred to as a transudate.
The term "edema" refers to non-inflammatory edema throughout this discussion, unless otherwise qualified.
Non-inflammatory edema (transudate) can be distinguished from an inflammatory edema (exudate) on the basis of the following features.
Before embarking on a study of the pathogenic mechanisms of edema, the normal control and relationships of tissue fluid must be clearly understood.
Under normal physiologic conditions, the main filtration force that expels fluid from the vessel is the hydrostatic pressure at the arterial end of the capillary minus the osmotic pressure of the blood. The main absorption force that draws fluid into the vessel is the osmotic pressure of the blood minus the hydrostatic pressure at the venous end of the capillary. In the normal animal, there is a continuous circulation of fluid from the arterial end of the capillary through the tissues and back into the venous end of the capillary.
Physiologically, blood enters the arterial end of a capillary with a hydrostatic pressure (blood pressure) of about 45 millimeters of mercury, which expels fluid and smaller dissolved molecules into the intercellular spaces. However, this hydrostatic pressure (expulsive force) is opposed by the osmotic pressure of blood exerted by such molecules as albumin and globulin. The osmotic pressure is about 30 mm of mercury. Therefore, at the arterial end of the capillary, hydrostatic pressure at 45 mm of mercury is overcoming the 30 mm osmotic pressure of the blood plasma, and fluid is forced into the intercellular spaces at the rate of 15 mm of mercury. As blood travels through capillaries, its hydrostatic pressure decreases rapidly to about 15 mm of mercury. Therefore, at the venous end of the capillary, hydrostatic pressure at 15 mm of mercury cannot overcome 30 mm osmotic pressure of the blood, and fluid flows from the intercellular spaces into the bloodstream at the rate of 15 mm of mercury. Since fluid enters tissues at about the same rate as it leaves, there is no accumulation of fluid in the intercellular spaces in the normal animal. However, edema occurs if there is any interference with this normal flow.
Occurs when there is a deficiency of blood proteins (hypoproteinemia). Thus, hypoproteinemia may result from decreased formation or excessive loss from the blood. Albumin is most important in maintaining osmotic pressure and it exerts four times the osmotic pressure of globulin. A low osmotic pressure in the blood increases the pressure differential at the arterial end of the capillary so that 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. Thus, there is an accumulation of fluid in intercellular spaces and/or body cavities.
A failure to form blood proteins results from malnutrition (starvation, emaciation) in which the "building blocks" for blood protein formation are not available. Severe or advanced liver diseases (cirrhosis, etc.) may lead to hypoproteinemia since this is the site in which blood proteins (albumin and globulin) are synthesized. The loss of plasma proteins from the blood occurs through the intestine and kidneys. 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.
Is influenced mainly at the venous end of the capillary and it usually results from venous stasis (severe passive congestion that results in increased back pressure in the venous circulation). The increased hydrostatic pressure at the venous end of the capillary which pushed fluid out of the bloodstream counterbalances the osmotic pressure which pulls fluids into the bloodstream. Therefore, fluid fails to return to the vessel from the intercellular tissue. 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.
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).
Occurs 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.
In summary, decreased plasma osmotic pressure produces generalized edema, whereas increased hydrostatic pressure may induce either localized or generalized edema. Increased permeability of capillary endothelium and lymphatic obstruction almost always lead to localized edema.
Microscopically, when well-defined, edema appears as a granular, eosinophilic interstitial precipitate that separates the cellular and fibrillar elements of tissue (the pink-staining appearance is due primarily to the presence of albumin in the edematous fluid). In the absence of albuminous precipitate, edema is represented by empty spaces in the interstitial areas.
Grossly, edematous tissues are swollen, firm, doughy and pit on pressure. There is no redness and not sign of pain. If the edematous part is external, it is cool to the touch.
Edema of the brain and lungs is the most life-threatening form of abnormal fluid retention. In animals, edema is almost always parasitic, nutritional, cardiac or renal in origin. If the cause is removed, edematous fluid disappears quickly, leaving no permanent defect in the area. However, if edematous fluid persists, it acts as a tissue irritant.
Shock is a clinical term which refers to 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.
The clinical signs of shock are inconsistent and vary with the precipitating cause. However, animals with shock 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.
The causes of shock may be classified as hypovolemic, septic, cardiogenic and neurogenic.
7.16.1 HYPOVOLEMIC SHOCK:
Is due to loss of blood volume (hemorrhage, trauma, loss of fluids in burns, etc.) which directly induces inadequate perfusion of organs and tissues.
Remember, extensive blood loss is required before animals develop hypovolemic shock. The following sequence of changes is associated with hypovolemic shock (as well as other forms).
Severe blood loss occurs. The arterial blood pressure drops and venous return to the heart decreases. The heart rate may increase but stroke volume and cardiac output are decreased. Arterial vasoconstriction occurs rapidly with the drop in blood pressure and increased peripheral resistance is produced which shunts blood from the skin and viscera to the heart and brain. In the kidneys, vasoconstriction reduces perfusion and causes activation of the juxtaglomerular apparatus with the release of the enzyme renin into the plasma. Renin acts on an unidentified plasma protein substrate converting it to a polypeptide angiotensin I. Angiotensin I is converted to the potent vasoactive polypeptide angiotensin II by another converting enzyme. Also, the pituitary gland is stimulated to release the antidiuretic hormone (vasopressin) which acts to conserve water normally lost from the lower nephrons. Aldosterone secretion by the adrenal cortex is augmented which leads to increased resorption of salt and water by the renal tubules. All of the above mechanisms conserve fluid and support blood volume.
Remember, progressive deterioration of the circulatory system may occur despite the above compensatory mechanisms. The term "irreversible shock" implies the refractory state of circulatory failure with inability to clinically control the condition.
7.16.2 SEPTIC SHOCK:
Implies septicemia or an overwhelming infection with gram-negative (endotoxic shock) or gram-positive (exotoxic shock) organisms. In toxic and septicemic conditions, there is oftentimes peripheral dilatation of the capillary beds which subsequently lead to shock. When capillary beds are fully dilated (vasodilation), they have the capacity to accommodate nearly the total blood volume. If this occurred, blood pressure would drop to zero (normally, continual vasoconstriction of the terminal arterioles prevents this from happening).
7.16.3 CARDIOGENIC (CARDIAC) SHOCK:
Can be viewed as "pump failure." It occurs subsequent to the sudden decrease in cardiac output which accompanies sudden extensive damage to the heart. However, most animals succumb directly to the myocardial failure. In those animals that do not, shock may ensue because of the pooling of the blood.
7.16.4 NEUROGENIC SHOCK:
Implies 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).
The manifestations of shock involve many vital organs (depending on the severity and duration of the shock state). The sequence of changes at the cellular and subcellular levels are those described for hypoxic injury (refer to section 3 of this syllabus). In general, the brain and heart are highly susceptible to hypoxia generated by the shock state.
7.17 POST-INSTRUCTIONAL SELF-EXAMINATION
After completing this section, each student should be in a position to provide appropriate answers for the following questions.
Please complete the following statements: