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Upozornění: 1.Tento powerpoint není zdrojem vší moudrosti. 2.Je určen jako doplněk k přednášce, či semináři 3.Je určen spolu s přednáškou jako doplněk ostatních zdrojů. 4.Naprosto mylná je představa, že nabiflování zde uvedených bodů stačí ke zkoušce. 5.Z hlediska autorského práva k částem a obrázkům pocházejícím z jiných zdrojů vycházím z příkazu děkana, jehož součástí je právní informace, že je možné je takto použít Heart and work dW=F·ds Zdroje: Atlas patofyziologie (Silbernagl); Essentials of pathophysiology (Porth): web a další Cardiac reserve • The difference between resting and maximal cardiac output; non-athletes have a cardiac reserve about 4 times their normal cardiac output while trained athletes and our astronaut corps have cardiac reserves up to 7 times their normal cardiac output. Energy • • • • • • The heart can use a variety of substrates to oxidatively regenerate ATP depending upon availability. Several hours after a meal, the heart utilizes fatty acids (60-70%) and carbohydrates (~30%). Following a high carbohydrate meal, the heart can adapt itself to utilize carbohydrates (primarily glucose) almost exclusively. Lactate can be used in place of glucose, and becomes a very important substrate during exercise. The heart can also utilize amino acids and ketones instead of fatty acids. Ketone bodies (e.g., acetoacetate) are particularly important in diabetic acidosis. During ischemia and hypoxia, the coronary circulation is unable to deliver metabolic substrates to the heart to support aerobic metabolism. Under these conditions, the heart is able to utilize glycogen (a storage form of carbohydrate) as a substrate for anaerobic production of ATP and the formation of lactic acid. However, the amount of ATP that the heart is able to produce by this pathway is very small compared to the amount of ATP that can be produced via aerobic metabolism. Furthermore, the heart has a limited supply of glycogen, which is rapidly depleted under severely hypoxic conditions Energy • • • • • Oxygen Substrates = energy Energy = functions and surviving Energy - work Force and pressure dW=F·ds Pressure – force; distance - volume PV diagram (area) - work Possible consequences of MI depend on site, extent, and scarring of the infarct. In addition to various arrhythmias, among them acutely life-threatening ventricular fibrillation, there is a risk of a number of morphological/mechanical complications : • Tearing of the chordae tendineae resulting in acute mitral regurgitation; • Perforation of the interventricular septum with left-to-right shunting; • Fall in cardiac output that, together with • stiffened parts of the ventricular wall (akinesia) due to scarring, • will result in a high end-diastolic pressure. Still more harmful than a stiff infarct scar is • a stretchable infarct area, because it will bulge outward during systole (dyskinesia), which will therefore—at comparably large scar area—be more likely to reduce cardiac output to dangerous levels (cardiogenic shock) than a stiff scar will; • Finally, the ventricular wall at the site of the infarct can rupture to the outside so that acutely life-threatening pericardial tamponade occurs. Heart failure (HF) • due to reduced systolic ejection (systolic or forward failure), resulting from either an – increased volume load, – myocardial disease, – an increased pressure load, or – impaired diastolic filling of the heart, • HF in which diastolic filling is impaired (diastolic or backward failure), for example as a result of – greater ventricular wall stiffness. HF caused by volume load • In forward HF the stroke volume, and thus cardiac output, can no longer adequately meet the organism’s requirements. • In backward HF this can be counteracted only by increasing the diastolic filling pressure. • Usually HF only becomes manifest initially on severe physical work (whenmaximal O2 uptake and maximal cardiac utput is decreased, but otherwise without symptoms; – stage I of the NYHA [New York Heart Association] classification). – However, symptoms later develop progressively, at first only on ordinary physical activity, later even at rest (NYHA stages II–IV). • Aortic and mitral regurgitation, for example, are characterized by the regurgitant volume that is added to the effective stroke volume. The enddiastolic volume, and therefore the radius (r) of the left ventricle, are increased so that, according to Laplace’s law the wall tension (T), i.e., the force that has to be generated per myocardial cross-sectional area, must rise to achieve a normal, effective stroke volume. • As this succeeds only inadequately, stroke volume and thus CO (= heart rate · stroke volume) decrease and the blood pressure falls. Sympathetic stimulation occurs as a counterregulatory mechanism, resulting in increased heart rate and peripheral vasoconstriction. HF caused by volume load • If chronic volume load develops, the dilated ventricle reacts with hypertrophy to compensate, i.e., with an increased wall thickness (d). However, r remains elevated (eccentric hypertrophy), and this form of HF usually has a less favorable course than one with concentric hypertrophy . If the underlying condition (e.g., valvar defect) is not removed early, HF gets worse relatively rapidly because of the resulting myocardial remodeling . Stiffening of the ventricle, caused by the hypertrophy, is involved in this development. • Because of its steeper compliance (= lusitropic = relaxation) curve,it has a diminished enddiastolic volume and thus a small stroke volume (backward HF). A vicious circle arises, in that the dilated ventricular wall gives way even more (dilation with myocardial restructuring) and r rises steeply. • This decompensation is characterized by a life-threatening fall in stroke volume despite an enormously elevated enddiastolic volume. HF caused by myocardial disease. • In coronary heart disease (ischemia) and after myocardial infarction the load on the uninvolved myocardium increases, i.e., forward HF develops due to diminished contractility. This is reflected by a shift of the contractility (C) curve of the ventricular work diagram. The endsystolic volume and, to a lesser extent, the EDV also rises, while stroke volume falls. • Hypertrophy of the remaining myocardium, a stiff myocardial scar as well as the diminished effect of ATP on actin–myosin separation in the ischemic myocardium will lead to additional backward HF. • Finally, a compliant infarct scar may bulge outward during systole (dyskinesia) , resulting in additional volume load (regurgitant volume). Cardio-myopathies can also lead to HF, volume load being prominent in the dilated form, backward HF in the hypertrophic and restrictive forms. HF due to pressure load • The wall tension (T) of the left ventricle also rises in hypertension or aortic stenosis, because an increased left ventricular pressure (PLV) is required (Laplace’s law). Forward HF with diminished contractility develops. An analogous situation exists regarding the right ventricle in pulmonary hypertension. Compensatory hypertrophy will also develop when there is an increased pressure load, but it will be “concentric” , because in this case the ventricular volume is not enlarged and may in some circumstances actually be decreased. However, even in concentric hypertrophy the enddiastolic volume will be reduced and thus also the stroke volume (backward HF). When there is a high pressure load, myocardial remodeling (see below), and unfavorable capillary blood supply (relative coronary ischemia), a “critical heart weight” of ca. 500 g may be attained, at which the myocardial structure gives way, causing decompensation. Left Heart Failure Symptoms • Dyspnea – on exertion – at rest • Orthopnea – redistribution of peripheral edema fluid – graded by number of pillows needed • Paroxysmal Nocturnal Dyspnea (PND) Right Sided Heart Failure • Etiology – left heart failure – cor pulmonale • Symptoms and signs – Liver and spleen • passive congestion (nutmeg liver) • congestive spleenomegaly • ascites – Kidneys – Pleura/Pericardium • pleural and pericardial effusions • transudates – Peripheral tissues • • • Oxygen demand rises as a consequence of increased cardiac work (= pressure times volume; orange area). The diastolic pressure (important for coronary perfusion), is reduced and simultaneously the wall tension of the left ventricle is relatively high — both causes of a lowered transmural coronary artery pressure and hence underperfusion which, in the presence of the simultaneously increased oxygen demand, damages the left ventricle by hypoxia. Left ventricular failure and angina pectoris or myocardial infarction are the result. Finally, decompensation occurs and the situation deteriorates relatively rapidly (vicious circle): as a consequence of the left ventricular failure the endsystolic volume rises, while at the same time total stroke volume decreases at the expense of effective endsystolic volume (red area), so that blood pressure falls (left heart failure) and the myocardial condition deteriorates further. Because of the high ESV, both the diastolic PLV and the PLA rise. This can cause pulmonary edema and pulmonary hypertension , especially when dilation of the left ventricle has resulted in functional mitral regurgitation. LEFT Heart Failure Dyspnea Orthopnea PND (Paroxysmal Nocturnal Dyspnea) Blood tinged sputum Cyanosis Elevated pulmonary “WEDGE” pressure (PCWP) (nl = 2-15 mm Hg) RIGHT Heart Failure FATIGUE “Dependent” edema JVD Hepatomegaly (congestion) ASCITES, PLEURAL EFFUSION GI Cyanosis Increased peripheral venous pressure (CVP) (nl = 2-6 mm Hg) Congestive Heart Failure • heart valve disease caused by past rheumatic fever or other infections • infections of the heart valves and/or heart muscle (i.e., endocarditis) • cardiac arrhythmias (irregular heartbeats) • cardiomyopathy, or another primary disease of the heart muscle • chronic lung disease • anemia • high blood pressure (hypertension) • hemorrhage (excessive bleeding) Congestive Heart Failure Dilated Cardiomyopathy Dilated Cardiomyopathy • Dilated cardiomyopathy involves enlargement of the heart muscle and is the most common type of cardiomyopathy. The heart muscle is weakened and cannot pump blood efficiently. Decreased heart function affects the lungs, liver, and other body systems. Cor Pulmonale Hypertrophic Cardiomyopathy Definition: Stimulus: WHO: left and/or right ventricular hypertrophy, usually asymmetric and involves the interventricular septum. • • • • Unknown Disorder of intracellular calcium metabolism Neural crest disorder Papillary muscle malpositioned and misoriented Genetic abnormality: Pathophysiology of HCM • Autosomal dominant. • Mutations in genes for cardiac sarcomeric proteins. • Polymorphism of ACE gene. • ß-myosin heavy chain gene on chromosome 14. • • • • • • Left ventricular outflow tract gradient • ↑ with decreased preload, decreased afterload, or increased contractility. • Venturi effect: anterior mitral valve leaflets & chordae sucked into outflow tract → ↑ obstruction, eccentric jet of MR in mid-late systole. Maneuvers that ↓ end-diastolic volume (↓ venous return & afterload, ↑ contractility) • Vasodilators • Inotropes • Dehydration • Valsalva • Amyl nitrite • Exercise → ↑ HCM murmur Dynamic LV outflow tract obstruction Diastolic dysfunction Myocardial ischemia Mitral regurgitation Arrhythmias