Hemodynamic Disorder and cardiovascular diseases. 台北醫學大學病理學科 林永和

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Hemodynamic Disorder and cardiovascular diseases 台北醫學大學病理學科 林永和 kevinyhl@tmu.edu.tw

(A) Hemodynamic Disorder Edema hyperemia or congestion hemorrhage thrombosis embolism infarction shock

Edema an excess of fluid in the interstitial spaces and/or body cavity 1. localized pitting edema :acute inflammation, allergy, venous obstruction, lymphatic edema 2 tissue or organ periorbital area, pulmonary edema, brain edema; ascites, hydrothorax (pleural effusion), pericardial effusion 3 generalized -- anasarca: heart, kidney, starvation transudate, exudate( more cell and protein)

Inducing reasons of edema A) increased hydrostatic pressure (blood vessel) 1).venous return pressure increase 2) arterial dilation EX: deep vein thrombosis, congestive heart failure (backward heart failure) B) decreased oncotic pressure (plasma) 1). Hypoproteinemia. 2). Hypoalbuminemia EX: nephrotic syndrome, cirrhosis C) obstruction of the interstitial fluid drainage (lymphedema) EX: tumor, surgery, radiation, filariasis D) increased tissue hydration (sodium retention) EX: hyperaldosteronism E) inflammation: congestion, vascular permeability increase

clinical signs of edema variable dependent on causes, rate, severity EX: lung and brain edema

Hyperemia 1. active (artery, capillary) arterial and capillary dilatation inflammation 2. passive (congestion), vein return obstruction a) acute local abrupt vein return obstruction, thrombosis, organ torsion systemic acute heart failure, asphyxia b) chronic ischemia cell degeneration or death local long term, progressive vein obstruction systemic chronic heart failure

Hemorrhage extravasation of blood *acute or chronic; *short term or long term; *external or internal 1. types of hemorrhage a) petechia: 1-2 mm mucosa, skin vascular pressure increase, platelet decrease b) purpura: 3mm skin trauma, vasculitis, increase in vascular fragility c) ecchymosis: 1cm skin trauma

hemorrhage Causes : trauma, vasculitis, tumor, hypertension, aneurysm rupture, hemorrhagic diathesis Clinical terms: hemoptysis ( 喀血 ) melena ( 瀝青性便血 ) hematemesis ( 吐血 ) hematochezia ( 便血 ) hematuria ( 血尿 ) metrorrhagia ( 陰道出血 ) menorrhagia ( 經血過多 ) hematoma ( 血腫血塊 )

Thrombosis clotting, is transformation of the fluid blood into a solid aggregate encompassing blood cells and fibrin. 1) Pathogenesis: endothelial cell injury platelet aggregation and deposition hemostatic plug formation vascular statis 2) Factors of intravascular coagulation: a) coagulation proteins b) platelets c) endothelial cells 3) Virchow s triad: three predisposing conditions for formation of pathologic thrombi a) endothelial cell injury b) hemodynamic change c) hypercoagulability of the blood

Thrombosis 4) Types a) arterial thrombosis heart, large artery multiple organs infarct b) venous thrombosis vascular stasis leg vein local congestion edema, lung infarct 5) Fate of the thrombi: a) Small thrombi lysis b) Large thrombi :1) narrowing, occlusion 2) organization recanalization 3) emboli ischemic infarction *clinical symptoms of thrombosis: 1) size 2) extent 3) rapid a) heart, cerebral artery death b) pulmonary Emboli high mortality (often not recognized clinically)

Disseminated intravascular coagulation (DIC) pathogenesis: activation and aggregation of intravascular fibrin protein consumption of platelet and coagulation factor resulting in hemorrhagic change reason: infection, amniotic fluid, malignant tumor, or unknown cause clinical signs: 1) diffuse microthrombosis formation ischemia of brain, lung, heart, kidney 2) consumption of platelet and coagulation factor hemorrhage * injury of red blood cell when pass through the fibrin thrombosis lysis microangiopathic anemia

Embolus and Embolism a detached intravascular solid, liquid or gaseous mass a procedure of an embolus is carried by blood to a distal site fixed in the vascular lumen Forms of emboli: a) Thromboemboli the most pattern 1) pulmonary thromboembolism venous embolism - deep vein of leg and pelvis - small emboli lung infarct, lung hemorrhage, silent (60-80%) - large emboli acute lung failure, sudden death EX: traveler syndrome 2) systemic thromboembolism arterial embolism intracardiac mural thrombi (80%), dilated left atrium, atherosclerotic plaque, valvular vegetation, unknown origin (10-15%) intestine, brain, spleen, kidney infarct

Forms of emboli b) Liquid emboli 1) fat emboli, 2) amniotic fluid 1) long bone fracture (90%), fat tissue injury, burn 2) rare (1/50000) but deathful complication (20-40%) of labor, can t to prevent the amniotic content (amniotic fluid, fetal skin, hair, feces) into the mother vascular circulation lung infarct, DIC, hemorrhage and shock c) Gaseous emboli (100cc volume) Chest wall injury, decompression sickness, caisson disease bone necrosis and organ infarct d) Solid particle emboli - cholesterol crystal, tumor cells, bone marrow, foreign material

Infarction and infarct A consequence of ischemic necrosis of distal tissue from an embolic event; an area of ischemic necrosis caused by occlusion of vessels 1) causes: thrombus or embolus ( the most), vascular spasm, compression, torsion, injury 2) Morphologic change: Gross: triangle or wedge-shape, pale or hemorrhagic Micro: coagulative necrosis, liquefactive necrosis, abscess (septic infarction) 3) type: a) white (anemic) infarct arterial occlusion heart, spleen kidney, brain, solid organs b) red or hemorrhagic infarct venous obstruction or two sets blood supply ovary, testis, intestine, lung, liver

The major factors that influence development of an infarct 1) nature of the vascular supply 2) rate of development of occlusion 3) vulnerability to hypoxia 4) oxygen content of blood

Shock (cardiovascular collapse) Definition: a state of systemic hypoperfusion of tissue with blood 1) Type of shock: a) cardiogenic shock --reduction in cardiac out myocardial injury, ventricular occlusion, external compression b) hypovolemic shock --reduction in the effective circulating blood volume hemorrhage, trauma, burn c) septic shock --loss of peripheral vascular tone endotoxic shock, Gram (-), systemic infection *neurogenic shock loss of sympathetic and vasomotor tone peripheral pooling of blood---pain, fear, spinal cord injury *anaphylactic shock allergy IgE release, systemic vasodilation and increased vascular permeability drug, nuts, insect bite

Symptoms and signs of shock a) Skin, pale and cold b) Kidney, decreased GFR, oliguria, anuria, metabolic acidosis c) Acidosis potentiates heart failure - causes vasodilatation, peripheral pooling of blood Left ventricular insufficiency raises the intrapulmonary venous pressure, pulmonary edema shock lung, ARDS respiratory acidosis Anoxia cytokines release, (IL-1, TNF), vasodilatation *anoxic endothelial cell lose their antithrombogenic properties revert into clot-forming cells, release clotting factors, combined with platelet, plasma clotting factors DIC

Stages of shock a) early or compensated shock: tachycardia, vasocontriction of peripheral arterioles, skin pale, * blood pressure is normal b) decompensated but reversible shock: tachypnea and shortness of breath (anoxia) acidosis, arterial dilatation, oligouria, confused * hypotension c) irreversible shock: circulatory collapse severe tissue and organ injury

Decreased blood pressure Compensations to main of heart and brain function 1) Stimulate sympathetic nervous system a. thirst b.anxiety, restlessness c. tachycardia d.vasoconstriction, pallor 2) Renin angiotensin aldosterone a. vasoconstriction b. retention of Na+, and water, oliguria 3) Increased ADH secretion a. retention of water

Direct Effects of Decreased Blood Pressure Lethargy, weakness Anaerobic metabolism- Metabolic acidosis Vasodilation and decreased cell function Slow blood flow in microcirculation Ischemia on organ Thrombus forms Decreased function Necrosis (eg., kidney) Decreased venous retum Further decrease in cardiac output Severe acidosis, CNS depression, Organ damage (eg., acute renal failure, lung damage) Decompensation

pathologic changes of shock brain ischemic neuropathy heart coagulation necrosis, subendocardial hemorrhage kidney acute tubular necrosis lung diffuse alveolar damage (shock lung) G-I system hemorrhagic gastroenteropathy Liver fatty change Adrenal hemorrhagic necrosis

(B) Disease of cardiovascular system 1) Acquired heart disease: Heart failure, Ischemical heart disease, Hypertensive heart disease, Cor pulmonale, Rheumatic heart disease, Infective endocarditis, Nonbacterial thrombotic endocarditis, Valvular heart disease, Myocardial disease, 2) Congenital heart disease, 3) Vascular diseases: Arteriosclerosis, Varicose vein

A) right-sided heart failure: Heart failure Cause: pulmonary artery occlusion, lung parenchyma disease, chronic inflammatory disease, lung tumor, chest wall deformity or exercise disturance Clinical signs: central venous pressure increase, hepatosplenomegaly, organ congestion, ascites, peripheral edema, nutmeg liver B) Left-sided Heart Failure: Causes: hypofunction of left ventricle, aortic or mitral valve pathologic change Clinical signs: lung edema, pleural effusion, cardiogenic asthma, hemoptysis, dyspnea

Ischemic heart disease 1) causes: coronary arterial occlusion or spasm, vasculitis, tumor, hypovolemic shock, ventricular fibrillation coronary artery blood flow decreased or interruption 2) clinical signs: angina pectoris, acute myocardial infarct, chronic ischemia heart disease, cardiogenic sudden death 3) gross and microscopic changes: myocardial necrosis, hemorrhage and fibrosis 4) complications: arrhythmia, left-sided heart failure, papillary muscle rupture, mural thrombus formation, heart rupture, ventricular aneurysm, pericarditis 5) death: arrhythmia, cardiogenic shock, thromboemboli

Hypertensive heart disease 1) definition : blood pressure >140/90mmHg 2) gross: left ventricle hypertrophy, dilatation, heart failure 3) side effects: pathological change in central nervous system and kidneys

Cor pulmonale 1) cause: pulmonary hypertension, pulmonary thromboemboli, chronic obstructive lung disease, lung tumor, chest wall deformity or exercise disturbance 2) gross: acute form right ventricle dilatation, right-sided heart failure chronic form right ventricle hypertrophy, right-sided heart failure

Rheumatic heart disease 1) acute rheumatic fever Group A beta, hemolytic streptococcus pharyngitis clinical signs: * myocarditis Aschoff s nodule (diagnostic characteristic), * migratory polyarthritis, * subcutaneous nodule, * erythema marginatum, * Sydenham s chores #ASLO (antistreptolysin O) antibody elevation, fever Endocardium vegetation, heart failure

Rheumatic heart disease 2) chronic rheumatic heart disease gross: valve deformity mitral & aortic valve atrophy, hypertrophy, fibrosis, calcification clinical signs: stenosis or insufficiency blood flow stasis, left ventricle dilatation, mural thrombus formation, atrial fibrillation, lung congestion, heart failure

Infective endocarditis a) acute: present in healthy heart *pathogen staphylococcus, pneumococcus sepsis bacterial vegetation infective emboili, pyemia abscess b) subacute: present in heart with congenital deformity or valvular abnormality *pathogen streptococcus viridans bacterial vegetation, anemia, multiple emboli, splenomegaly

Nonbacterial thrombotic endocarditis patient with chronic disease, or malignant tumor gross: small nonbacterial vegetation over the leaflets of mitral valve or tricuspid valve

valvular heart disease 1) mitral valve stenosis cause: congenital, rheumatic heart disease clinical signs: progressive left heart failure, heart murmurs, lung congestion and edema, pleural effusion 2) mitral valve insufficiency cause: congenital, rheumatic heart disease, myocardial infarct clinical signs: left ventricular hypertrophy, heart murmur

valvular heart disease 3) aortic valve stenosis cause: congenital, rheumatic heart disease, myocardial hypertrophy, calcification clinical signs: left ventricle hypertrophy, heart murmur 4) aortic valve: insufficiency cause: congenital, syphilic aortitis 5) pulmonary valve stenosis cause: congenital

Myocardial disease: myocarditis Inflammation with myocardial necrosis (not induce by ischemia) a) cause: virus, bacterial, parasite, fungus, drug, alcohol, radiation b) clinical signs: abrupt or progressive heart failure c) gross or micro changes: cardiomegaly, myocardial necrosis d) complication: acute heart failure, arrhythmia, death

cardiomyopathy unknown cause, (not by coronary artery disease, hypertension, valvular disease) a) dilated cardiomyopathy cause: unknown, may be associated with myocarditis or mutation of gene of myocardial contraction protein clinical signs: progressive heart failure gross: heart enlarged and weight, dilatation of the four chambers, mitral and tricuspid insufficiency micro: cardial cell hypertrophy, hyperchromatic nucleus, interstitial fibrosis

cardiomyopathy b) hypertrophic cardiomyopathy cause unknown: but 25% associated with abnormal gene in cardial contractile protein clinical signs: progressive heart failure gross and micro changes: ventricle and septum hypertrophy, cardial cell hypertrophy and disarrayed distribution

cardiomyopathy 3) restrictive cardiomyopathy ventricular space decrease cause unknown amyloidosis, glycogen storage disease, hemochromatosis, endocardial fibrosis, endocardial fibroelastosis

Congenital heart disease a) cyanotic 1) tetralogy of Fallot (TOF) 2) transition of great vessel (TFA) 3) truncus arteriosus

Tetralogy of Fallot Complex congenital defect of heart and major vessel Cyanosis in newborn, 10% of CHD Four typical lesions a) valvular stenosis (narrowing) of the pulmonary artery b) ventricular septal defect c) dextroposition of the aorta d) hypertrophy of the right ventricle Blue baby Treat: surgical correction

Congenital heart disease b) non-cyanotic 1) ventricular septal defect (VSD) the most 2) patent ductus arteriosus (PDA) 3) atrial septal defect (ASD) 4) coarctation of aorta 5) pulmonary stenosis (PA) 6) aortic stenosis (AS)

Septal defects: 30~40% a) Atrial foramen ovale b) Ventricle 1) foramen ovale (upper part) 2) muscular septa (lower part) VSD the most common CHD - L to R shunt - R ventricular hypertrophy - pulmonary hypertension - R to L shunt, cyanosis *easy detection by heart murmurs *defect small one, close spontaneous large one, surgery

vascular disease Arteriosclerosis 1) arteriolosclerosis muscular wall thickened, fibrinoid degeneration benign or malignant hypertension hypertensive heart disease, hemorrhagic stroke, hypertensive renopathy

2) atherosclerosis a) high risk factors: hyperlipiemia, hypertension, diabetes mellitus (DM), smoking factors can not be changed: age, sex, hereditary factors can be changed: 1) lipid metabolism-related factors diet, hyperlipidemia, obesity, D.M. 2) hypertension 3) clotting factors 4) cigarette smoking 5) behavior

2) atherosclerosis b) muscular wall thick, lipid aggregation, fibrosis, calcification, hemorrhage, ulceration, thrombus formation, lumen narrowing, chronic ischemia c) aorta, coronary artery, cerebral artery, femoral artery, popliteal artery, radial artery d) complications: thromboemboli formation, aneurysm, myocardial infarct, ischemic stroke, peripheral infarct and necrosis

Arteritis 1) infective arteritis 2) syphilitic arteritis ascending aorta 3) thromboangiitis obliterans 4) giant cell arteritis

Aneurysm abnormal vascular dilatation due to vascular wall destruction cause: atherosclerosis, trauma, inflammation, vascular degeneration, congenital gross change: compression, thrombus formation, hemorrhage type: atherosclerostic aneurysm, aortic dissection, mycotic aneurysm

diseases of vein 1) varicose vein cause: intraluminal pressure increase, extraluminal supporting decrease, vascular wall weakness common site: lower leg, esophagus, anus, umbilicus area complications: ulceration, hemorrhage, pigment deposition, abscess, fistula, thromboemboli formation 2) thrombophlebitis thrombotic occlusion of vein