Chapter 3 Nursingg PDF

Chapter 3: HEMODYNAMIC DISORDERS HYPEREMIA Definition: increased blood flow to an organ or tissue due active dilatation of its arterioles. Types: - Physiological: in muscular exercise - Pathological: in acute inflammation...

Chapter 3: HEMODYNAMIC DISORDERS HYPEREMIA Definition: increased blood flow to an organ or tissue due active dilatation of its arterioles. Types: - Physiological: in muscular exercise - Pathological: in acute inflammation CONGESTION Definition: Increased venous flow and stasis of blood in an organ due to obstruction of its venous outflow. Types: - Localized: Acute and Chronic STRANGULATED HERNIA - Generalized: Acute and Chronic Acute localized venous congestion - Results from sudden obstruction of venous outflow - Example: strangulated hernia, volvulous, intussusception Fig. (3-1): Strangulated hernea Chronic local venous congestion - Results from gradual obstruction of venous outflow of an organ or tissue. - Ex: * Liver cirrhosis --> portal hypertension. * Pregnancy --> compression on iliac veins --> leg edema. Acute generalized venous congestion - Acute increased venous pressure in all viscera - Ex: Acute heart failure Chronic generalized venous congestion Definition: Stagnation of venous blood in all organs and tissues. Causes: - Cardiac: - Mitral stenosis, pulmonary stenosis Fig. (3-2): Chronic venous - Pulmonary: lung fibrosis congestion liver Effects: 1- General effects: Hypoxia cyanosis and edema 2- Congestion of organs: as lung, liver, spleen and kidney 1  EMBOLISM Definition: Intravascular insoluble solid, fluid or gaseous mass circulating in the blood. Types: - Detached thrombi. - Fat: as in bone fractures fat of BM pass to circulation - Air: Caisson disease. Injury to the lung or neck veins. - Amniotic fluid: during labor. - Others: Tumor cells, parasitic ova, foreign body. FAT EMBOLISM Definition: Obstruction of arterioles and capillaries by fat globules circulating in blood. Causes: 1- Fractured long bone (fatty marrow). 2- Extensive trauma to the fatty tissue. 3- Severe fatty change of the liver. 4- Acute pancreatitis (enzymatic fat necrosis). Effects: Depend upon the size and quantity of fat globules. 1- Pulmonary and systemic embolism 2- Toxic effects of fatty acids on vascular endothelium. AIR EMBOLISM (gas embolism) Definition: Obstruction of the vascular flow by large amount of air or gas (50- 100 C.C). Causes: 1- Air enters uterine blood vessels in cases of criminal abortion or after obstructed labor. 2- Air enters large neck veins, in stab wound injuries. 3- Air enters pleural sac in cases of pneumothorax. 4- Air enters the tubal blood vessels in cases of uterine tube insufflation. Effects: - Small amount of air: Harmless. - Large amount of air: Impair heart action and may lead to death. 2  AMNIOTIC FLUID EMBOLISM Definition: Introduction of amniotic fluid and its contents into maternal circulation through utero-placental site. It is a rare condition (1:50000-80000 labor). Pathogenesis: 1- Strong uterine contractions leading to tear of fetal membranes or placental vein. 2- Amniotic fluid debris (Meconium, Lanugo hair, fetal squamous cells, mucin and fat ) causing mechanical obstruction of maternal pulmonary circulation. 3- Amniotic PGF2 causing reflex maternal pulmonary vaso- constriction. 4- DIC with decrease clotting factors and hypo-fibrinogenemia. Clinical features: a) Sudden respiratory distress and dyspnea. b) Deep cyanosis. c) Cardiogenic shock. d) Convulsions and coma. e) Sudden maternal death. THROMBOSIS Definition: Formation of insoluble mass of blood elements within the circulatory system during life. Predisposing factors: 1- Inflammation of the vascular wall 2- Changes in the blood composition. Thrombocytosis. Polycythemia. Dehydration and burns 3- Changes in blood stream, Fig. (3-3): Pathogenesis of e.g. aneurysm thrombosis (Virchow's triad). Mechanism of thrombus formation: - Endothelial injury --> roughness of endothelium with release of tissue factor and platelet activation factor (PAF). - Platelet adhesion with release of vasoconstrictor substances which increase platelet aggregation. - Formation of fibrin network entangling other blood elements --> Thrombus formation 3 Types of thrombi: - According to color: 1- Pale thrombus: mainly formed of platelets as rheumatic vegetations 2- Red thrombus: Formed of fibrin network entangling platelets and blood cells. 3- Mixed thrombus: Containing red and pale areas - According to the site of formation: 1- Cardiac: Vegetations of rheumatic fever and infective endocarditis 2- Arterial: Coronary and cerebral arteries 3- Venous: Leg veins in prolonged recumbency Fig. (3-4): Arterial thrombus 4- Capillary: as arthus reaction Table (3-1): Differences between thrombus and clot: THROMBUS CLOT Occurs only during life Occurs during life and after death Attached to the vascular wall Not attached Friable Elastic Fate and effects of thrombi: 1- Resolution: The thrombus activates the fibrinolytic system with consequent release of plasmin which may dissolves the thrombus. 2- Organization: The thrombus becomes organized. Neutrophils and macrophages appear and phagocytose fibrin and cell debris. 3- Recanalization: Occasionally the thrombus is invaded by new capillaries which dilate and allow passage of blood through the thrombus (canalization) 4- Propagation: The thrombus may enlarge in size and propagates towards the heart. 5- Detachment: Septic or aseptic emboli emboli. 6- Incorporation: The thrombus is covered by endothelial cells and incorporated in the vascular wall. 7- Dystrophic calcification (Phlebolith). 4  ISCHEMIA Definition: inadequate blood supply to an organ or tissue. Types: - Generalized: in conditions of decreased cardiac output as CHF. - Localized : as cardiac and renal ischemia. Effects: - Renal ischemia --> hypertension, chronic renal failure. - Coronary ischemia --> Angina pectoris, myocardial infarction. - Cerebral ischemia --> fainting attacks, cerebrovascular stroke. Types of ischemia: 1- Acute ischemia: due to sudden complete arterial occlusion as embolism, surgical ligature, ergot poisoning and torsion. The effect depends on the state of collateral circulation. 2- Chronic ischemia: due to gradual incomplete arterial occlusion as in atherosclerosis. INFARCTION Definition: Localized area of ischemic necrosis in an organ or tissue resulting from sudden cutting of its blood supply. Cause: sudden arterial occlusion. Gross picrure: - Wedge-shaped triangular area, the apex of which at the site Fig. (3-5): Infarction Kidney of arterial occlusion - After healing , the infarct is replaced by depressed scar Microscopic: only tissue framework with no structural details Fate of the infarcts: 1- Small infarcts: The necrotic tissue is removed by macrophages and replaced by fibrosis. The surface of infarct area becomes depressed. 2- Large infarcts: The necrotic tissue becomes surrounded by fibrous capsule and may show dystrophic calcification. 5  HEMORRHAGE Definition: Extravasation of blood outside the circulation ( heart and blood vessels) Causes: 1- Physiologic: Menstruation 2- Pathologic: local and general causes. Local: - Trauma: surgical or accidental. - Spontaneous rupture e.g. aneurysm. - Vasculitis. - Tumors. General: Hemorrhagic blood diseases, vit. C and vit. K deficiency. Mechanisms of natural arrest of hemorrhage: 1- Immediate fall of blood pressure (due to blood loss). 2- Local vasoconstriction (from platelet serotonine and thromboxane A2). 3- Clot plug (from clotting of blood). 4- Healing by organization. Types of hemorrhage: - External: loss of blood outside the body. Ex: Epistaxis, hemoptysis, hematemasis, melena, hematuria, metrorrhagia. - Internal: loss of blood in body cavities Ex: Hemothorax, Hemopericardium , Hemoperitonium, Hematocele, Hemoarthrosis. - Interstitial: loss of blood in the interstitial tissue * Small spots as in purpura (petichae). * Moderate amount (ecchymosis). * Large collection (hematoma). Effects of hemorrhage: 1- Local effect: Clotting and organization leads to hemostasis. 2- Systemic effect: - Loss of small amount --> No effect. - Repeated loss of small amounts --> Hypochromic microcytic anemia - Sudden severe loss, more than 20-30% --> Shock. - Acute loss of more than 33% of blood volume is fatal. 6  EDEMA Definition: accumulation of fluid in the interstitial tissue. Types of edema: 1- Generalised: * Cardiac: CHF. * Renal: Glomerulonephritis, nephritic syndrome. * Nutritional: Kwashiorkor. * Hepatic: Hepatic cell failure. * Allergic: Urticaria. 2- Localized: * Inflammatory edema * Lymphatic edema: - Filariasis. - Surgical removal of lymph nodes. Edema is also classified into: A- Pitting (soft) edema: The accumulated fluid is free in tissue spaces and can be displaced by pressure which creates a temporary skin depression or a pit as in cardiac, renal and nutritional edema. B- Non-Pitting (hard) edema: Edema which doesn't pit under pressure. The edema fluid is excess and united with tissues and not displaced by pressure as in lymphatic edema. Fig. (3-6): Pitting edema of the foot. 7  SHOCK Definition: widespread hypoperfusion of tissues due to inadequate circulatory volume Types: 1- Primary (vasovagal or nervous) shock: 2- Secondary shock: Cardiogeneic, Hypovolemic, Septic, Anaphylactic NERVOUS SHOCK: - Following emotional stress and mediated by nervous mechanisms. - Recovery is the rule except in rare cases. CARDIOGENIC SHOCK: The heart fails to pump blood to organs and tissues. - Causes: * Acute heart failure * Myocardial infarction * Myocarditis * Rupture of valve cusps * Cardiac tamponade * Arrhythmias HYPOVOLEMIC SHOCK: Shock results from marked fall in blood pressure. - Causes: * Loss of blood in severe hemorrhage. * Loss of plasma as in severe burns. * Loss of fluids as in dehydration. SEPTIC SHOCK: - Caused by bacterial infection by gram negative organisms due to release of endotoxins. - Endotoxins promote disseminated intravascular coagulation (DIC). ANAPHYLACTIC SHOCK: - It is a form of type I hypersensitivity mediated by IgE. - Exposure to small amount of antigen as penicillin stimulate formation of IgE which is fixed to mast cells. - On re-exposure to large amount of the same antigen, antigen- antibody reaction occurs at the surface of mast cells which degranulate and release vasodilator and bronchoconstrictor substances --> fall of blood pressure --> shock. 8 COMPENSATORY MECHANISMS IN SHOCK - Vasoconstriction of skin and visceral blood vessels while cerebral and coronary vessels are dilated to maintain cardiac and cerebral circulation. - Hypoxia --> stimulation of respiratory center--> hyperventilation. - Renal ischemia --> stimulation of rennin- angiotensin system --> vasoconstriction. Also release of aldosterone and ADH --> sodium and water retention to increase blood volume. CLINICAL STAGES OF SHOCK: 1- Compensatory stage: Compensatory mechanisms control blood pressure and recovery occurs. 2- Decompensated stage: * Failure of compensatory mechanisms --> marked fall in blood pressure, hypoxia --> more renal, cerebral and cardiac ischemia --> shock. * With correction of blood pressure and metabolic acidosis as well as control of infection in septic shock, the condition is reversible. 3- Irreversible stage: All therapeutic efforts fail to control the condition --> death. 9