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Transcript
Consequences of ischemia: metabolic changes: ATP depletion, lokal acidosis, increased inflow of calcium to the cells impaired contractility (decrease of stroke volume): impaired relaxation (diastolic dysfunction) impaired electrical events (arrhytmias, ECG) morphological changes (myocytes, necrosis, fibrotisation, steatosis etc.) clinical symptoms (pain, arrhytmia, heart failure) Postischemic changes * ischemia duration * reperfusion Stunned myocardium perfused but not functioning reversible continuous dysfunction of myocardium after reperfusion without apparent changes Hibernating myocardium chronically hypoperfused and functionally impaired situation with continuously decreased blood flow accompanied by impaired contractility adaptation of cells to decreased energy delivery Ischemic preconditioning increased resistence of myocardium against damage due to ischemia caused by preceding ischemia and reperfusion Secondary hypertension • Is due to some other cause (endocrine, kidney disease, medication • Up to 12% of hypertensive patients • Endocrine: – Primary hyperaldosteronism (Conn’s syndrome) – Secondary hyperaldosteronism – Cushing syndrome – Pheochromocytoma – Acromegaly – Estrogen therapy – Pregnancy • Renal disease – Stenosis of renal artery (unilateral = increased activity RAAS; bilateral = RAAS and decreased filtration) – Renal parenchymal disease • Other – Coarctation of aorta Cardiac output and blood pressure depend on: • Characteristics of the heart: • Contractility • Frequency • Characteristics (diameter) of the vessels • Tone of arteriols influences mainly resistence • Tone of veins (or less mid-size arteries) influences the volume of vascular bed. Volume of the bed is connected to pressure and vascular tone (compliance) • Volume of circulating blood Kidney-fluid mechanism of pressure control Heart and vessels are regulated by mechanisms that are of a proportional controller type. Kidney fluid regulator is a integral (I) controller type. (its long term sensitivity/gain is infinity) = kidneys excrete more fluid until the pressure is set exactly on the equilibrium (reference) value Increased peripheral resistance is common in hypertensive individuals, but it is not the main cause 1. hyperkinetic 2. postcapillary 3. precapillary restrictive – loss of pulmonary tissue obstructive – thromboembolism active-vasoconstrictive – hypoxia 4. pulmonary arterial hypertension Hypoxic pulmonary hypertension -many lung diseases, mainly chronic obstructive disease, alveolar hypoventilation, severe obesity, lung fibrosis -high altitude -syndrome of sleep apnoe mainly obstructive (relaxation of muscles…) apnoe over 10 sec, often even several dozens dozens or hundreds of such episodes during the night decreased ventilation and oxygen saturation Shock = Sudden, life threatening disorder of overall tissue perfusion and circulatory system failure Adequate perfusion is necessary for proper functioning of tissues and indeed, survival of whole organism Tissue perfusion depends on perfusion pressure Hypovolemic shock Clinical picture is determined partly by hypovolemia (decrease of systolic pressure, oliguria / anuria...), partly by compensation mechanisms (tachycardia, increased periferal resistence, redistribution of blood...) • Increased peripheral vessel resistence (cold sweaty acral parts, so called cold hypotension from hypovolemia) x peripheral=distribution shock • Decreased central venous pressure • Mortality about 20% Cardiogenic shock = Critical decrease of cardiac output, due to decrease of contractility of heart as a whole (i.e. failure of cardiac pump) Mechanisms: Necrosis / large part of heart muscle is lost (most frequently extensive anterior MI), supposed loss of >40% myocardium or less in already altered myocardium (repeated MI, chronic heart failure, cardiotoxic substances / medicaments, metabolic faktors) malignant tachy / brady-arrhythmia (ventricular fibrilation x extreme bradycardia), MV = SV x f Wall, papillary muscle or chordae tendineae rupture Obstructive shock Most common features akutní obstrukce: - Heart tamponade - Large pulmonary embolism - other (acute) block/compression of pulmonary circulation or inferior vena cava Peripheral = distributive shock = Alteration of circulation caused by a decreased peripheral resistance, lost venous tone and and/or movement of fluid to extracellular space 1. Anaphylactic shock 2. septic/ toxic shock 3. Neurogennic shock 4. Some endocrine based shocks Peripheral = distributive shock 1. Anaphylactic shock • Starting mechanism: Reaction of antigens with IgG (as opposed to atopy, where IgA is involved) • mediators of histiocytes, mast cells etc are released (histamine, serotonin, SRS-A...), • generalized vasodilation and an increased peripheral permeability (very fast development - seconds to minutes) Peripheral = distributive shock 2. septic/toxic shock Occurs in 25% Gram- bacteremias (Escher. coli, pseudomon...) and 5% Gram+ bacteremias (Staphyloc., Streptoc. betahemolyticus, pneumococci) Pathogenesis: Exaggerated defence reaction (SIRS): bacterial antigen (LPS) macrophage activation TNF, IL1 endotel NO vasodilation Develops during hours or days, 50 % mortality 6 Systemic inflammatory response syndrome (SIRS) Definition • Delocalized and dysregulated inflammation process of high intensity. It leads to disorders of microcirculation, organ perfusion and finally to secondary organ dysfunction. • This secondary dysfunction is not due to primary insult, but due to autoaggressive systemic inflammatory response of the organism to the primary insult. • This systemic inflammatory response syndrome (SIRS), leads without therapeutic intervention to multiple organ dysfunction syndrome (MODS) and death. 8 Pathophysiology of SIRS Insult • hypoxic-reperfusion damage • infection (endotoxin, other microbial toxins or microorganisms) • primary mediators -histamin, anaphylatoxins C3a, C5a • complexes antigen-antibody • thrombin a plasmin (DIC) Defensive reactions • First detected signs of defense after insult are local and generalized hemodynamic changes (vasodilatation, vasoconstriction). Regulation of hemodynamic changes • systemic sympathic-adrenal activation (changes in organ blood distribution of minute volume) • local microcirculatory changes - mediators produced by endothelial cells and other inflammatory systems (NO, PGI2 x endothelin-1, thromboxan A2) Endothelial cells reaction Endothelial stimulation • Key process in development of microcirculatory disorders • release of protective mediators (vasodilatatory and antithrombotic) • contraction of endothelial cells and P-selectin expression (adhesion of neutrophils) • aged endothelial cells desquamation, intracellular gaps, disturbances of endothelial surface • release of vasoconstrictive and prothrombotic mediators • Result of stimulation process - thrombogenic vascular intima with increased permeability. Reversibility • Fast stimulation of endothelium by primary mediators and development of acute inflammatory response is process not dependent on proteosynthesis. Endothelial cells are rapidly active, however, this activation without further stimulation disappears within few minutes. If insult persists (hours): Activation of other inflammation components • • • • • • • • • activation of mononuclear cells - release of TNF- and IL-1 adhesive receptors on mononuclear cells and tissue factor release endothelium activation: endothelial cells activated by cytokines - release of adhesive receptors, tissue factor expression endothelial cytoskeleton rebuilt to irreversible active state chemotaxis of neutrophils - activation (reactions worsening hypoxia) interstitial edema and microthrombotization edema compresses lymphatic and blood stream anaerobic metabolism of tissue cells (decrease of pH optimal for hydrolytic enzymes) hypoxia and organ dysfunction Reversibility • Activation of mononuclear cells and release of TNF- a IL-1 is inhibited by corticosteroids released after activation of hypothalamicadrenal stress reaction. Those acute microcirculatory disorders can be reversible, if the insult is eliminated and appropriate intensive care started. Tissue damage The degree of reversibility of secondary MODS is influenced by: • necrotic tissue damage • changes of vessel wall caused by proinflammatory cytokines • during chronic process - proliferation of less valuable cells (fibroblasts) • apoptosis (induced during SIRS) 9 Diagnosis of SIRS Diagnostic criteria - a weak part of SIRS theory. • Official diagnostic criteria SIRS (Tab.) are not able to cover dynamics and degree of SIRS. Symptoms Assessed factors Body temperature >38oC or <36oC Pulse rate >90 /min Rate of breathing or PCO2 (arterial blood) Frequency of breathing >20 /min PaCO2 <32 mm Hg White blood count or I/T ratio >12 000/mm3 or <4 000/m3 >10% SIRS diagnosis Presence of SIRS indicated by presence of minimum 2 of described signs. (Bone et al., 1992). Aortic stenosis (ejection click) Pulmonary stenosis Mitral insufficiency/ septal defect Aortic insufficiency Mitral stenosis (opening snap) Mitral stenosis Patent ductus arteriosus Aortic stenosis Mitral stenosis Aortic insufficiency Mitral insufficiency Congenital Rheumatic Cusp abnormalities Endocarditis Rheumatic Calcific Rheumatic, endocarditis Infarction Degenerative Congenital Dilation Trauma Collagen-vascular disease Aneurysm, connective tissue disorder Degeneration Inflammation Rheumatic Arthritic diseases, syphylis Angina pectoris Dyspnea, hemoptysis, ortopnea Dyspnea, hemoptysis, ortopnea Syncope Palpitations Dyspnea Palpitations Congestive failure Neurological Hyperdynamic pulses Fatigue Shunt malformation Cyanosis depends on: -Underlying anatomical defect and - pressure conditions (blood flows from the area Of higher pressure to area of lower pressure). Pressure conditions can change if the marformation persists for a long time (shunt reversal) 1) Ventricular septal defect 2) Subpulmonary stenosis (obstruction) 3) Aorta on the VSD 4) Right ventricle hypertrophy Angina pectoris (AP) stable: fixed stenosis atherosclerotic plaque decreases coronary reserve, increased oxygen requirements of myocardium (tachycardia) ... subendocardial ischemia Other contributing factors: anemia, increased blood viscosity, diastolic hypotension, hypertrophy of myocardium vasospastic (Prinzmetal’s): spasmus of epicardial artery, transmural ischemic changes; in rest (frequently nocturnally), reperfusion may be accompanied by arrythmia Acute coronary syndromes unstable AP + acute MI Unstable AP: unstable stenosis rupture, thrombosis, spasmus, uncomplete obturation + shorter time of ischemia without necrosis Preload filling of the heart at the end of the diastole enddiastolic volume = EDV Frank-Starling mechanisms Volume in the ventricle corresponds to the pressure – enddiastolic pressure, EDP, filling pressure Factors influencing preload - Venous return total blood volume blood distribution (position of the body, intrathoracic pressure, venous tonus…) - atrial systole - size of ventricle cavity - intrapericardial pressure Low preload is the cause of the decreased CO in case of syncope and shock In heart failure the preload is not decreased but it is increased as one of the the compensatory mechanisms J.Kofránek intraventricular pressure EDP ventricle volume Endothelium Main functions: * regulated permeability * regulation of vasodilatation and vasoconstriction * vessel integrity Functional endothelium: VD: nitric oxide – NO, prostacyclin (PGI2) VC: endothelin, angiotensin II impedes platelets and leukocytes adhesion and aggregation anticoagulant – trombomoduline regulation of fibrinolysis: tPA + PAI-1 Endothelial function reflects a balance between factors such as nitric oxide (NO), which promotes vasodilatation and inhibits inflammation and vascular smooth muscle proliferation, and endothelial-derived contracting factors, which increase shear stress and promote the development of atherosclerosis. Current evidence suggests that endothelial status is not determined solely by individual risk factor such as lipids, hypertension, and smoking, but by an integrated index of all the atherogenic and atheroprotective factors present in an individual, including known and as yet unknown variables and genetic predisposition. Endothelial dysfunction: imbalance between vasoactive and procoagulant/fibrinolytic factors * vasoconstriction * inhibition of fibrinolysis * leucocyte adhesion (selectins…) * increased permeability * procoagulant activity * release of cytokins Pathogenesis of atherosclerosis Damage to the endothelium – shear stress, smoking, infection ?, hypertension... Macromolecules and cell penetration – LDL, monocytes Macromolecules and cell retention – LDL, monocytes-macrophages LDL modification: oxidation, glycation, aggregation LDL accumulation in the macrophages – foam cells Inflammation – production of reactive oxygen species, cytokines, growth factors, enzymes... N.Engl.J.Med., 2000 Fibrous changes – fibrous cap N.Engl.J.Med., 2000 Advanced lesion and thrombosis plaque stability – necrotic debris, inflammatory activitity neovascularisation + hemorrhage thinning of the fibrous cap calcifications ulcerations injury to the plaque, intraplaque bleeding... Nature, 2000 Sequelae of the necrosis • hemodynamic (disturbances of contractility, decrease of ejection fraction) – large necrosis or repeated infarction - heart failure, if about 40% of myocardium destroyed, cardiogenic shock can develop • electrical instability – arrhytmias, ventricular fibrillation, sudden death • remodelation of the ventricle – scarring, aneurysma (dyskinesis, thrombosis with embolism), dilatation – importance for prognosis • rupture of the wall, aneurysma (pericardial tamponade), septum, papillary muscle Intraventricular pressure insufficiency ..smaller stroke volume Stroke volume Stroke volume Stroke volume increased stroke volume Increase in preload Ventricular volume Minute cardiac output insufficiency increased stroke volume Lowering of “Starling curve” smaller stroke volume greater preload End-diastolic pressure Cardiomyopathy Definition: = chronic disorder of myocardium with abnormal ventricular both function and morphology weakening of the heart muscle or a change in heart muscle structure prolonged course, slow progression Pathogenesis: “universal” reaction of cardiac muscle on various noxa → inflammation, hypertrophy, degeneration, necrosis, fibrosis → accumulation of lipids, glycogen, amyloid Lipoid deposits in myocardium Cardiomyopathy Dilated CM Restrictive CM • • • • destruction of muscle fibers dilatation without hypertrophy Hypertrophic CM • • asymmetric hypertrophy obstruction of LV offtake subendocard. fibrosis arrhythmia Cardiomyopathy Secondary: infectious bacterial viral (coxsackie) ricketsia mycosis parasitic (Chagas dis.) toxic (alcohol, Co, narcotics, psychofarmacs, adriamycin, prokainamid) endocrine / metabolic (↓T4, ↑T4, ↑GH, uremia, ↓vit.B1, K, Mg) allergy, autoimmunity (immunocomplex., SLE, sarkoidosis…) Restrictive CM Characteristics: ♥ subendocardial fibrosis (event. eosinophil infiltration) ♥ frequent arrhythmia ♥ heart is normal in size or only slightly enlarged ♥ rare form amyloid deposits Constrictive pericarditis and cardiac tamponade • Cardiac tamponade manifests when pressure in pericardial cavity reaches values of diastolic pressure in RV and left atrial pressure Atrial fibrillation atrial activity: irregular f waves AV conduction is absolutely irregular The most common arrythmia Ventricular fibrilation (or flutter) Acute situation, hemodynamic arrest – 0 cardiac output, 0 pulsation, coma, resuscitation REENTRY main cause of tachyarrhytmias - two pathways proximally and distally connected - different conductivity (slow) - unidirectional conduction block of 1 pathway ischemia, fibrosis typically accessory pathways Atrial (supraventricular) extrasystole (SVES) spreading of impulse in the ventricles is normal, QRS complex is of normal shape/duration Ventricular extrasystole spreading of impulse in the ventricles is abnormal, QRS complex is different and longer Compensatory pauses in VES SA node cannot be discharged in SVES the impulse in SA node is discharged by retrograde conduction AV block 2rd degree AV block 3rd degree Preexcitation, WPW syndrome Bundle branch blocks (raménkové blokády) LBBB (left, levý) RBBB (right, pravý)