Home Random Page


CATEGORIES:

BiologyChemistryConstructionCultureEcologyEconomyElectronicsFinanceGeographyHistoryInformaticsLawMathematicsMechanicsMedicineOtherPedagogyPhilosophyPhysicsPolicyPsychologySociologySportTourism






Theoretical part of the lesson

Hemodynamic disorders are characterized by disturbed perfusion that results in organ and cellular injury.

Hemorrhage (i.e., bleeding) is a discharge of blood from the vascular compartment to the exterior of the body or into nonvascular body spaces. The most common and obvious cause is trauma—usually accidental, but often by the surgeon's scalpel. An artery may be ruptured in ways other than laceration. For instance, severe atherosclerosis may so weaken the wall of the abdominal aorta that it balloons to form an aneurysm, which then ruptures and bleeds into the retroperitoneal space. By analogically, an aneurysm may complicate a congenitally weak cerebral artery (berry aneurysm) and lead to subarachnoid hemorrhage.

Certain infections (e.g., pulmonary tuber­culosis) erode blood vessels; a similar vascular injury is caused by invasive tumors. Hemorrhage also results from damage at the level of tile capillaries. For instance, the rupture of capillaries by blunt trauma is evidenced by the appearance of a bruise. Increased venous pressure also causes extravasation of blood from capillaries in the lung. Vitamin Ñ deficiency is associated with capillary fragility and bleeding, owing to a defect in the supporting structures. It is important to recognize that the capillary barrier by itself is not suffi­cient to contain the blood within the intravascular space. The minor trauma imposed on small vessels and capil­laries by normal movement requires an intact coagulation system to prevent hemorrhage. Thus, a severe decrease in the number of platelets (thrombocytopenia) or a defi­ciency of a coagulation factor (e.g., factor VIII in hemo­philia) is associated with spontaneous hemorrhages un­related to any apparent trauma.

A person may exsanguinate into an internal cavity, as in the case of gastrointestinal hemorrhage from a peptic ulcer (arterial hemorrhage) or esophageal varices (venous hemorrhage). In such cases large amounts of fresh blood fill the entire gastrointestinal tract. Bleeding into a serous cavity can result in the accumulation of a large amount of blood, even to the point of exsanguination.

A few def­initions are in order:

Hemothorax: Hemorrhage into the pleural cavity

Hemopericardium: Hemorrhage into the pericardial space

Hemoperitoneum: Bleeding into the peritoneal cavity

Hemarthrosis: Bleeding into a joint space

Hematoma: Hemorrhage into the soft tissues. Such collections of blood can be merely painful, as in a muscle bruise, or fatal, if located in the brain.

Purpura: Diffuse superficial hemorrhages in the skin, up to 1 cm in diameter

Ecchymosis: A larger superficial hemorrhage. Follow­ing a bruise or in association with a coagulation defect, an initially purple discoloration of the skin turns green and then yellow before resolving. This sequence reflects the progressive oxidation of bilirubin released from the hemoglobin of degraded erythrocytes. A good example of an ecchymosis is a "black eye."

Petechia: A pinpoint hemorrhage, usually in the skin or conjunctiva. This lesion represents the rupture of a capillary or arteriole and occurs in conjunction with coagulopathies or vasculitis, the latter is classically as­sociated with infections of the heart valves (bacterial endocarditis).



Hyperemia is defined as an excess amount of blood in an organ. It may be caused either by an increased supply of blood from the arterial system (active hyperemia) or by an impediment to the exit of blood through venous path­ways (passive hyperemia or congestion).

Active hyperemia is an augmented supply of blood to an organ, usually as a physiologic response to an increased functional demand, as in the case of the heart and skeletal muscle during exercise. Neurogenic and hormonal influ­ences play a role in active hyperemia, exemplified at both extremes of the female reproductive span—namely, in the form of the blushing bride and the menopausal flush. Al­though these examples do not appear to promote any use­ful function, hyperemia of the skin in febrile states serves to dissipate heat. The increased blood supply is brought about by arteriolar dilatation and recruitment of inactive or latent capillaries.

The most striking active hyperemia occurs in associ­ation with inflammation. Vasoactive materials released by inflammatory cells cause dilatation of blood vessels; in the skin this results in the classic "tumor, rubor, and calor" of inflammation. In pneumonia the alveolar capillar­ies are engorged with erythrocytes as a hyperemic re­sponse to inflammation. Since inflammation can also damage endothelial cells and increase capillary perme­ability, the hyperemia of inflammation is often accom­panied by edema and local extravasation of erythrocytes.

Passive hyperemia, or congestion, refers to the engorge­ment of an organ with venous blood. Acute passive congestion is clinically a consequence of acute failure of the left ventricle. The resulting venous engorgement of the lung leads to the accumulation of a transudate in the alveoli, a condition termed pulmonary edema.

A generalized increase in venous pressure, typically from chronic heart failure, results in slower blood flow, and a consequent increase in the volume of blood in many organs, including the liver, spleen, and kidneys. In the past, heart failure from rheumatic mitral stenosis was a common cause of generalized venous congestion, but with the decline in the prevalence of rheumatic fever and the advent of surgical valve replacement, such cases are unusual. Congestive heart failure secondary to coronary artery disease and right-sided failure because of pulmo­nary disease are now more common causes.

Passive congestion may also be confined to a limb or an organ as a result of more localized obstruction to the venous drainage. Examples include thrombophlebitis of the leg veins, with resulting edema of the lower extremity, and thrombosis of the hepatic veins (Budd-Chiari syn­drome), with secondary chronic passive congestion of the liver.

Shockis a condition of profound hemodynamic and metabolic disturbance characterized by failure of the circulatory system to maintain adequate perfusion of vi­tal organs. In this often catastrophic circumstance, tissue perfusion and oxygen delivery fall below the levels re­quired to meet normal demands. The term “shock” encom­passes all the reactions that occur in response to such dis­turbances. In the course of uncompensated shock, a rapid circulatory collapse leads to impaired cellular metabolism and death. However, in many cases, compensatory mech­anisms sustain the patient, at least for a while. When these adaptations fail, shock becomes irreversible. Shock is not synonymous with low blood pressure, although hypotension is commonly a part of the shock syndrome. Hypotension is actually a late sign in shock and indicates a failure of compensation. At the same time that peripheral blood flow falls below critical levels, ex­treme vasoconstriction can maintain arterial blood pres­sure. This distinction between shock and hypotension is important clinically because the rapid restoration of sys­temic blood flow is the primary goal in treating shock. When blood pressure alone is raised with vasopressive drugs, systemic blood flow may actually be diminished.

Pathogenesis. Decreased perfusion in shock is generally the result of a decreased cardiac output, resulting either from the in­ability of the heart to pump the normal venous return or from a decreased volume of blood secondary to a de­creased venous return. These two mechanisms, which lead to a decreased cardiac output, define the two major types of shock: cardiogenic and hypovolemic shock.

Cardiogenic shock is usually caused by myocardial infarction, myocarditis, or pericardial tamponade. In these conditions depressed systolic cardiac function (ejec-tion fraction less than 20%) is responsible for the de­creased cardiac output.

Hypovolemic shock is secondary to a pronounced decrease in blood volume, caused by the loss of fluid from the vascular compartment. Hemorrhage, diarrhea, exces­sive urine formation, and perspiration are the major mechanisms of external fluid loss. Internal fluid loss usu­ally results from an increase in the permeability of the microvasculature caused by endotoxemia, burns, trauma, or anaphylaxis. In the case of burns or trauma, direct damage to the microcirculation increases vascular perme- ability. Immunologic mechanisms, coupled to the activa­tion of complement and the release of anaphylotoxins, enhance vascular permeability in anaphylaxis.

In both hypovolemic and cardiogenic shock, a decreased cardiac output and resultant decreased tissue per­fusion comprise the essential pathogenetic mechanisms in the progression from reversible to irreversible shock. Anoxic injury is the common cellular consequence of the ini­tial decrease in tissue perfusion. A vicious circle of decreasing tissue perfusion and further cell injury is perpetuated by several mechanisms:

Injury to endothelial cells, secondary to the anoxia caused by decreased tissue perfusion, increases vascular permeability.

The increased exudation of fluid from the circulation reduces blood volume, venous return, cardiac output, thereby aggravating anoxic cell injury.

Decreased perfusion of the kidneys and skeletal muscles results in metabolic acidosis, which in turn further decreases cardiac output and tissue perfusion.

Decreased perfusion of the heart injures the myocardial cells and decreases their ability to pump blood, further reducing cardiac output and tissue perfusion

Hypovolemic shock is caused by a pronounced decrease in blood volume, which reduces venous return to the heart and consequently decreases cardiac output.

Practical part.


Date: 2016-03-03; view: 802


<== previous page | next page ==>
TASKS FOR SELF-CONTROL | Practical and theoretical parts
doclecture.net - lectures - 2014-2024 year. Copyright infringement or personal data (0.009 sec.)