hemodynamic disorders
-edema -hyperemia-hemorrhage-thrombosis-embolism-infarction
Edema
(swelling) extravasation of water i.e movement of water across the vascular wall into the interstitial space due to abnormalities of vascular permeability
Hyperemia
increased volume of blood in a particular tissue
Hemorrhage
extravasation of blood due to rupture of vessel or diseased vascular wall
Thrombosis
blood clotting at inappropriate sites, i.e within the vascular lumen
Embolism
migration of blood clots which are carried by the blood to a distant site obstructing blood flow
Infarction
development of necrosis in an area distal to the obstruction of an end-artery
Ions or molecules representing each compartment
-Sodium (na+) is the major extracellular cation-Potassium (K+) is the major intracellular cation-Glucose limited to extracellular fluid
types of edema fluid
-transudate-exudate-lymphedema-myxedema
transudate
Protein poor fluid (<3g/dL)Produces dependent pitting edema and body cavity effusion
exudate
Protein rich (>3g/dL)Produces no pitting edema
lymphedema
-Protein rich-Results from obstacles along the lymphatic pathway-Produces massive swelling of extremities but no pitting edema
myxedema
-Accumulation of glycosaminoglycans in the dermis-Produces swelling of the skin but no pitting edema
Pathophysiology of edema
Normal formation and retention of interstitial fluid depends on filtration and reabsorbed of plasma fluids at the level of the capillaries
Edema caused by increased hydrostatic pressure
Increases in vascular hydrostatic pressure result in greater filtration of fluid into the interstitial spaceexamples:-Deep venous thrombosis in lower extremities-Pulmonary edema in left sided heart failure-Peripheral pitting edema in right sided heart failure-Portal hypertension in liver cirrhosis producing ascite
Edema caused by decreased plasma oncotic pressure
-reduced plasma osmotic pressure leads to a net movement of fluid into the interstitial tissues and a resultant plasma volume contraction-Malnutrition with decreased protein intake → kwashiorkor-cirrhosis with decreased synthesis of albumin-nephrotic syndrome with increased loss of protein in urine -protein losing enteropathies
Edema caused by lymphatic obstruction
-Excess interstitial fluid is removed by lymphatics → obstruction of lymphatics-Lymphedema following radical mastectomy for breast cancer due to removal of axillary lymph nodes and lymphatics-Filariasis caused by the nematode W. bancrofti-Lymphogranuloma venereum, venereal disease caused by chlamydia trachomatis
Acute inflammatory edema
-Produces swelling and can be recognized by the cardinal signs of acute inflammation-Inflammatory edema is an exudate-The pitting phenomenon is absent-The mechanism of inflammatory edema is the increased microvascular permeability
Local edema
-Inflammatory edema-Venous obstruction (like a DVT)-Lymphatic obstruction
Generalized edema
-cardiogenic edema-nephrogenic edema-edema associated with liver cirrhosis
cardiogenic edema can be
backward failure or forward failure
Backward failure
-Failure of the left side due to an infarct of the left ventricle causes pulmonary edema-Failure of the right side causes generalized edema in subcutaneous tissues in the "dependent" parts of the body and in body cavities
Forward failure
Congestive heart failure is associated with reduced cardiac output and therefore, with reduced renal perfusion
Nephrogenic edema
-By a glomerular mechanism: during the inflammatory diseases of the glomeruli (glomerulonephritis) glomeruli become leaky and losing albumin and changing oncotic pressure gradient-By secreting renin: this causes adrenals to secrete more aldosterone which increases the reabsorption of sodium. The retained sodium produces edema by expanding the blood volume-By failing to secrete sodium and water: in acute renal failure, the daily volume of urine production decreases to a minimum. As fluid intake continues, the blood volume expands
Edema associated with liver cirrhosis
-During liver cirrhosis the fluid weeps from the cirrhotic liver surface and accumulates in the peritoneal cavity (ascites). Ascites is a combination of local and generalized factors-The roots of the portal vein are strangled. There is a backup of portal blood flow due to an obstacle in the liver (backward mechanism)-Insufficient albumin is produced by the liverAldosterone is inadequately inactivated by the liver cells which normally conjugate it
hyperemia congestion
-A passive process-Accumulation of venous stagnant blood resulting from impaired outflow from a tissue-Can be systemically or local-Congested organs enlarge due to overfilling with blood
Chronic liver congestion
-Aka nutmeg liver-The effects of chronic congestion on the structure and function of the liver-From heart failure (global or right sided)-Decompensated right ventricle causes transmission of elevated central venous pressure directly to the liver via the inferior vena cava and hepatic veinsExamples:>Edema in the lower extremities and dependent regions>Elevated jugular venous pressure with distention of neck veins>Enlarged and firm liver>Lab findings: modest elevation in AST, ALT, alkaline phosphatase, and total bilirubin as well as mild decreases in albumin
chronic pulmonary congestion
-Left sided heart failure due to>Chronic myocardial infarct>Stenosis of the mitral valve>Both cause a persistent backing up of blood in the lungs-Transudate escapes into the connective tissue spaces and alveoli (pulmonary edema)-The alveolar walls respond to chronic interstitial edema by developing a diffuse interstitial fibrosis-There may be several hemosiderin-laden macrophages in each alveolus "heart failure cells"-These cells will eventually be coughed out and give a rusty colored sputum
hemorrhage
can be internal or external
internal hemorrhages
-hematoma-hemothroax-hemopericardium-hemoperitoneum-hemarthrosis
Hematoma
-accumulation of blood within soft tissues-Rupture of aortic aneurysm leads to massive retroperitoneal hematoma
Hemothorax
-hemorrhage into pleural cavity
Hemopericardium
-hemorrhage into pericardial cavity
Hemoperitoneum
-hemorrhage into peritoneal cavity
Hemarthrosis
-hemorrhage into synovial cavity
Hemorrhages into skin and mucosae
-petechiae-purpura-ecchymoses
Petechiae
-pinpoint hemorrhages smaller than 1 mm-may become confluent and become purpura or ecchymosis
Purpura
-hemorrhages measuring 1 mm to 1 cm in diameter
Ecchymoses
-hemorrhages larger than 1 cm
Hemorrhages from body cavities
Hematuria Hematemesis Melena Hematochesia Epistaxis Hemoptysis MenorrhagiaMetrorrhagia
Hematuria
appearance of blood in the urine. It is a sign of kidney or urinary tract disease
Hematemesis
vomiting blood. Sign of esophageal or gastric
Melena
-coffee-ground material in the stool. Is a sign of upper GI bleeding. -Such blood is partially digested by the HCl of the gastric juice and transformed into a black pigment called hematein
Hematochesia
-bleeding through the rectum. -Caused by diseases of large intestines
Epistaxis
-bleeding from nose
Hemoptysis
bleeding from lungs
Menorrhagia
heavy menstrual bleeding
Metrorrhagia
hemorrhage from uterus that occurs at any time and is not related to menstrual bleeding
Thrombus
-a solid intravascular mass attached to the vessel wall -Is formed during life -is formed from constituents of the blood and contains platelets, fibrin, and entrapped cellular elements
Postmortem thrombus clots
-jelly like and moist-Surface is smooth and glistening-Not attached to the vessel wall-Endothelium is not damaged
Red thrombi
-Venous thrombi-Contain more erythrocytes-Formed slowly
White thrombi
-Arterial thrombi are gray-white-Composed of tangled mesh of platelets and fibrin-Contain less erythrocytes
Mixed thrombi
-lines of Zahn-Formed in the heart or aorta-Grossly apparent lamination-White layers are alternated with red layers
terms used to describe thrombi
Mural thrombi Occluding thrombi Valvular thrombi Canalized thrombi Saddle thrombus Septic thrombi
Mural thrombi
attached to part of the wall of the blood vessel and merely restricts the lumen (almost occluding)
Occluding thrombi
they fill the lumen completely
Valvular thrombi
attached to the heart valves and are also termed "vegetations
Canalized thrombi
occur when new blood channels from in an organized thrombus
Saddle thrombus
straddle the bifurcation of blood vessels (most of pulmonary arteries)
Septic thrombi
those that contain bacteria
pathogenesis of thrombosis involves principally three factors
(virchow triad)-endothelial cell injury-alterations in blood flowhypercoagulability
Endothelial cell injury
-After trauma, endothelial cells die and sloughed off, exposing subendothelial collagen-Thrombosis is triggered when circulating platelets contact the exposed collagen and undergo aggregationExamples>Athersclerotic plaques when they break open>Hypertension>Vascular trauma or surgery>Infectious vasculitis>Immune responses (graft)
Alterations in blood flow
-Sluggish blood flow-Turbulence and stasis
Hypercoagulability
-Any alteration of the coagulation pathways that predispose to thrombosis (thrombotic diathesis)-Can be inherited or acquired-Inherited causes:>Mutations in factor V gene or prothrombin gene>Homocystinuria
acquired causes of hypercoagulability
-Prolonged bed rest-Oral contraceptive use-Pregnancy (hyperestrogenic state)-Disseminated cancer-Heparin-induced thrombocytopenia syndrome-Antiphospholipid antibody syndrome
Many fates of thrombus
-Growth: mural to occluding-Propagation: increase in size and extend-Dissolution: dissolved-Embolization: thrombus breaks off and becomes an embolus-Organization: thrombus invaded by cellular elements and becomes firmly attached to vein wall-Fibrosis: end stage of organization-Recanalization: end stage of organization: new blood vessels grown within thrombus, run across the occluded segment of the vessel and restore blood flow
Venous thrombi
-example : deep venous thrombosis (in deep veins of LE)-From: activation of coagulation in areas of sluggish blood flow and venous stasis-Causes local venous congestion-Predispose for development of varicose veins-Danger of pulmonary thromboembolism (PE!! Anytime pt has chest pain w or w/o SOB)-Do not miss a PE!-Use anticoagulants heparin and warfarin to prevent formation of venous thrombi
Arterial thrombi
-Majority of arterial thrombi overlie atherosclerotic plaques-Cardiac mural thrombi arise in the setting of myocardial infarction related to dyskinetic contraction of the myocardium-Obstructs arterial lumen which results in acute infarction of the area supplied by the occluded vessel
emboli
-solid, liquid, or gaseous objects carried out by blood that are large enough to become impacted in the downstream lumen-Almost all emboli represent some part of a dislodged thrombus-Rare forms of emboli>Droplets of fat>Bubbles of air or other gases>Amniotic fluid>Foreign bodies>Parasites>Fragments of bone marrow
two types of embolism
-Emboli arising from the peripheral veins end in the lungs (pulmonary thromboembolism)-Emboli airising in arterial blood (left heart, aorta and branches) end up in arteries anywhere in the body (systemic thromboembolism)
Pulmonary embolism
-blockage of the pulmonary artery-When a thrombus becomes dislodged from site of formation and embolizes to the arterial blood supply of one of the lungs or both lungs-About 95% of all thromboemboli arise from the deep veins of the thigh from the popliteal vein-Depending on size of embolus, it may occlude the main pulmonary artery, it may impact across the bifurcation (saddle embolus) or pass out into small branching arteries-Causes sudden death due to occlusion of the main pulmonary artery or saddle embolus occluding the major pulmonary branches
Paradoxical embolism
-Rule breaking, emboli arise in the systemic veins but instead of ending in the lungs, they embolize the systemic arteries-They bypass the lungs in 2 ways>Large emboli pass through a ventricular septal defect or a patent foramen ovale (i.e a right to left passage in the heart)>Small emboli pass through arteriovenous anastomoses in the pulmonary circulation. Normal lungs contain arteriovenous shunts that are 20-40 times the diameter of the capillaries
systemic thromboembolism
-Emboli airising in arterial blood (left heart, aorta and branches) end up in arteries anywhere in the body -80% of cases of thrombi from the left side of the heart-20% of cases of thrombi from aorta-Usually in LE, brain, small bowel, spleen kidneys, upper extremities
fat embolism
-Fat tissue passes into bloodstream and lodges within a blood vessel-Complication of trauma-Can also arise from with parenteral lipid infusion, pancreatitis, burns and childbirth-Almost every fracture is accompanied by some degree of fat embolism-Clinically only 1% of pts with a single fracture develop pulmonary and systemic symptoms-Usually characterized by cardiorespiratory insufficiency, neurologic symptoms, anemia, and thrombocytopenia-Reddish brown non palpable petechiae develop on upper anterior of body
Gas embolism
-Gas bubbles within the circulation that obstruct vascular flow and cause distal ischemic injury-Iatrogenic gas embolism can complicate>IV catheter>Extracorporeal bypass pump>Carotid artery endarterectomy>Obstetric procedures-Trauma of neck and chest>Subatmospheric pressure can draw air through the tear in the traumatized veins-Decompression sickness>Scuba and deep sea diving, workers in underwater occupations
Amniotic fluid embolism
-Mixture of amniotic fluid, debris, and procoagulants that have gotten into the maternal circulation via a tear in the placental membranes-Maternal mortality is 60 to 80%-Pts become acutely dyspneic with cyanosis, hypotension and shock, and neurological manifestations such as loss of consciousness and seizures-Pts die within first minutes or hours-On autopsy blood vessels in the lung show evidence of fetal epithelial squamous cells obstructing about 80% of the pulmonary capillaries
infarction
-Area of ischemic necrosis-No blood flow, no nutrients, no waste removal, no oxygen-Mass of tissue that dies of inadequate blood flow-Nearly 99% of all infarcts result from thrombotic or thromboembolic events-The infarct shape corresponds to that of the arterial tree supplying it and is therefore approximately conical or that of wedge, the base being toward the periphery of the organ-Size depends on occluded artery-Color is white or yellowish unless hemorrhage is added to the necrosis-The infarction of the bowel develops in a segment of bowel involving the entire circumference-The infarction of myocardium is not conical in shape either, involving the subendocardial layer or the whole thickness of left ventricle wall
White infarcts
-(ischemic, anemic, pale infarcts)-Occur in organs with end arterial circulation-End arterial circulation is a circulation in which there are no anastomoses connecting the terminal arteries to each other-Examples: heart, spleen, kidney, brain, retina
Red infarcts
-hemorrhagic-Occurs in tissues with dual blood supply (like the lungs)-Pulmonary infarcts are most frequent in pts with heart disease