23 heart failure_jh


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congestive heart failure

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23 heart failure_jh

  1. 1. PATHOPHYSIOLOGY OF HEART FAILURE Prof. J. HanacekTechnical co-operation: L. Šurinová
  2. 2. Notes to heart physiology• Essential functions of the heart • to cover metabolic needs of body tissue (oxygen, substrates) by adequate blood supply • to receive all blood comming back from the tissue to the heart• Essential conditions for fulfilling these functions • normal structure and functions of the heart • adequate filling of the heart by blood
  3. 3. Essential functions of the heart are secured by integration of electrical and mechanical functions of the heart Cardiac output (CO) = heart rate (HR) x stroke vol.(SV) - changes of the heart rate - changes of stroke volume• Control of HR:- autonomic nervous system- hormonal(humoral) control• Control of SV: - preload - contractility - afterload
  4. 4. Adaptive mechanisms of the heart to increased load• Frank - Starling mechanism• Ventricular hypertrophy – increased mass of contractile elements → ↑strength of contraction• Increased sympathetic adrenergic activity – increased HR, increased contractility• Incresed activity of R–A–A system
  5. 5. Causes leading to changes of number and size of cardiomyocytes
  6. 6. PreloadStretching the myocardial fibers during diastole by increasing end-diastolic volume → ↑ force of contraction during systole = Starling´s lawpreload = diastolic muscle sarcomere length leading to increased tension in muscle before its contraction (Fig.2,3)- venous return to the heart is important → end-diastolic volume is influenced- stretching of the sarcomere maximises the number of actin-myosin bridges responsible for development of force- optimal sarcomere length ∼ 2.2 µ m
  7. 7. Myocardial contractilityContractility of myocardium Changes in ability of myocardium to develop the force by contraction that occur independently on the changes in myocardial fibre length Mechanisms involved in changes of contractility • ↑ amount of created cross-bridges in the sarcomere by ↑ of [ Ca ++] i concentration - catecholamines → ↑[ Ca++] i→ ↑ contractility - inotropic drugs → ↑[ Ca++] i→ ↑ contractility↑ contractility → shifting the entire ventricular function curve upward and to the left↓ contractility → shiffting the entire ventricular function curve (hypoxia, acidosis) downward and to the right
  8. 8. The pressure – volume loop• It is the relation between ventricular volume and pressure• This loop provides a convenient framework for understanding the response of individual left ventricular contractions to alterations in preload, afterload, and contractility• It is composed of 4 phases: - filling of the ventricle - isovolumic contraction of ventricle - isotonic contraction of ventricle(ejection of blood) - isovolumic relaxation of ventricle
  9. 9. Pressure – volume loops recorded under different conditions
  10. 10. AfterloadIt is expressed as tension which must be developed in the wallof ventricles during systole to open the semilunar valves andeject blood to aorta/pulmunary arteryLaplace law: intraventricular pressure x radius of ventriclewall tension = -------------------------------------------------------- 2 x ventricular wall thickness↑ afterload: due to - elevation of arterial resistance - ↑ ventricular size - myocardial hypotrophy↓ afterload: due to - ↓ arterial resistance - myocardial hypertrophy - ↓ ventricular size
  11. 11. Heart failureDefinition It is the pathophysiological process in which the heart as a pump is unable to meet the metabolic requirements of the tissue for oxygen and substrates despite the venous return to heart is either normal or increased
  12. 12. Explanation of the terms• Myocardial failure = abnormalities reside in the myocardium and lead to inability of myocardium to fulfilling its function• Circulatory failure = any abnormality of the circulation responsible for the inadequacy in body tissue perfusion, e.g. decreased blood volume, changes of vascular tone, heart functiones disorders• Congestive heart failure = clinical syndrome which is developed due to accumulation of the blood in front of the left or right parts of the heart
  13. 13. General pathomechanisms involved in heart failure development Cardiac mechanical dysfunction can develop as a consequence in preload, contractility and afterload disordersDisorders of preload↑↑ preload → length of sarcomere is more than optimal → → ↓ strength of contraction↓↓ preload → length of sarcomere is well below the optimal → → ↓ strength of contraction
  14. 14. Important: failing ventricle requires higher end-diastolic volume to achieve the same improvement of CO that normal ventricle achieves with lower ventricular volumes Disorders of contractility In the most forms of heart failure the contractility of myocardium is decreased (ischemia, hypoxia, acidosis, inflammation, toxins, metabolic disorders... ) Disorders of afterload due to: • fluid retention in the body • ↑ arterial resistance • valvular heart diseases ( stenosis )
  15. 15. Characteristic features of systolic dysfunction(systolic failure)• ventricular dilatation• reducing ventricular contractility (either generalized or localized)• diminished ejection fraction (i.e., that fraction of end-diastolic blood volume ejected from the ventricle during each systolic contraction – les then 45%)• in failing hearts, the LV end-diastolic volume (or pressure) may increse as the stroke volume (or CO) decreases
  16. 16. Characteristic features of diastolic dysfunctions(diastolic failure)• ventricular cavity size is normal or small• myocardial contractility is normal or hyperdynamic• ejection fraction is normal (>50%) or supranormal• ventricle is usually hypertrophied• ventricle is filling slowly in early diastole (during the period of passive filling)• end-diastolic ventricular pressure is increased
  17. 17. Causes of heart pump failure A. MECHANICAL ABNORMALITIES1. Increased pressure load – central (aortic stenosis, aortic coarctation...) – peripheral (systemic hypertension)2. Increased volume load – valvular regurgitation – hypervolemia3. Obstruction to ventricular filling – valvular stenosis – pericardial restriction
  18. 18. B. MYOCARDIAL DAMAGE1. Primary a) cardiomyopathy b) myocarditis c) toxicity (e.g. alcohol) d) metabolic abnormalities (e.g. hyperthyreoidism)2. Secondary a) oxygen deprivation (e.g. coronary heart disease) b) inflammation (e.g. increased metabolic demands) c) chronic obstructive lung disease
  19. 19. C. ALTERED CARDIAC RHYTHM1. ventricular flutter and fibrilation2. extreme tachycardias3. extreme bradycardias
  20. 20. Pathomechanisms involved in heart failureA. Pathomechanisms involved in myocardial failure• Damage of cardiomyocytes → ↓ contractility, ↑ ↓ complianceConsequences: • defect in ATP production and utilisation • changes in contractile proteins • uncoupling of excitation – contraction process • ↓ number of cardiomyocytes • impairment of relaxation of cardiomyocytes with decrease compliance of myocardium • impaired of sympato-adrenal system (SAS) → ↓ number of β 1-adrenergic receptors on the surface of cardiomycytes
  21. 21. 2. Changes of neurohumoral control of the heart function• Physiology: • SNS → ↑ contractility ↑ HR ↑ activity of physiologic pacemakers Mechanism: • ↑ sympathetic activity →↑ cAMP → →↑[ Ca ++] i → ↑ contractility • ↑ sympathetic activity → ↓ influence of parasympathetic system on the heart• Pathophysiology: normal neurohumoral control is changed and creation of pathologic neurohumoral mechanisms are present
  22. 22. Chronic heart failure (CHF) is characterized by an imbalance ofneurohumoral adaptive mechanisms with a net results of excessivevasoconstriction and salt and water retention Catecholamines : - concentration in blood : - norepinephrin – 2-3x higher at the rest than in healthy subjects - circulating norepinephrin is increased much more during equal load in patients suffering from CHF than in healthy subject - ↓ number of beta 1 – adrenergic receptors → → ↓ sensitivity of cardiomyocytes to catecholamines → → ↓ contractility System rennin – angiotensin – aldosteron heart failure →↓ CO →↓ kidney perfusion → stim. Of RAA system
  23. 23. Important:Catecholamines and system RAA = compensatory mechanisms ↑ heart function and arterial BP The role of angiotensin II in development of heart failure • vasoconstriction ( in resistant vesels) • retention of Na →↑ blood volume • ↑ releasing of arginin – vasopresin peptide (AVP ) from neurohypophysis
  24. 24. • facilitation of norepinephrine releasing from sympathetic nerve endings• ↑ sensitivity of vessel wall to norepinephrine• mitogenic effect on smooth muscles in vessels and on cardiomyocytes → hypertrophy• constriction of vas efferens ( in glomerulus )• ↑ sensation of thirst• ↑ secretion of aldosteron from adrenal gland• mesangial conctraction → ↓ glomerular filtration rate
  25. 25. Pathophysiology of diastolic heart failure• systolic heart failure = failure of ejecting function of the heart• diastolic heart failure = failure of filling the ventricles, ↑ resistance to filling of ventricles Diastolic failure is a widely recognized clinical entity But, which of the cardiac cycle is real diastole ?
  26. 26. Definition of diastolic heart failureIt is pathophysiological process characterized by symptoms andsigns of congestive heart failure, which is caused by increasedfilling resistance of ventricles and increased intraventriculardiastolic pressurePrimary diastolic heart failure - no signs and symptoms of systolic dysfunction is present - ! up to 40% of patients suffering from heart failure! Secondary diastolic heart failure - diastolic dysfunction is the consequence of primary systolic dysfunction
  27. 27. Main causes and pathomechanisms of diastolic heart failure1. structural disorders →↑passive chamber stiffness • intramyocardial – e.g. myocardial fibrosis, amyloidosis, hypertrophy, myocardial ischemia... b) extramyocardial – e.g. constrictive pericarditis2. functional disorders → ↓ relaxation of chambers e. g. myocardial ischemia, advanced hypertrophy of ventricles, failing myocardium, asynchrony in heart functions
  28. 28. Causes and mechanism participating on impaired ventricular relaxationa) physiological changes in chamber relaxation due to: – prolonged ventricular contraction Relaxation of ventricles is not impaired !b) pathological changes in chamber relaxation due to: Impaired relaxation process • delayed relaxation (retarded) • incomplete (slowed) relaxation
  29. 29. • Consequences of impaired ventricular relaxation - filling of ventricles is more dependent on diastasis and on the systole of atrias than in healthy subjectsSymptoms and signs: • exercise intolerance = early sign of diastolic failure • ↓ coronary blood flow during diastole• Causes and mechanisms involved in development of ventricular stiffness• ventricular compliance = passive property of ventricle Source of compliance: cardiomyocytes and other heart tissue to stretching
  30. 30. ↓ Ventricular compliance is caused by structural abnormalities localized in myocardium and in extramyocardial tissuea) Intramyocardial causes : myocardial fibrosis, hypertrophy of ventricular wall,restrictive cardiomyopathyb. Extramyocardial causes : constrictive pericarditis The role of myocardial remodelling in genesis of heart failure • adaptive remodelling of the heart • pathologic remodelling of the heart
  31. 31. Main causes and mechanisms involved in pathological remodelation of the heart1.Increased amount and size of myocytes = hypertrophy Due to: - ↑ volume and/or pressure load (excentric, concentric hypertrophy) - hormonal stimulation of cardiomyocytes by norepinephrine, angiotenzine II2. Increased % of non-myocytic cells in myocardium and their influence on structure and function of heart a. endothelial cells – endothelins : mitogenic ability → → stimulation growth of smooth muscle cells of vessels, fibroblasts b. fibroblasts - ↑ production of kolagens
  32. 32. Symptoms and signs of heart failure• forward failure: symptoms result from inability of the heart to pump enough blood to the periphery (from left heart), or to the lungs (from the right heart)a) forward failure of left heart:- muscle weakness, fatigue, dyspepsia, oliguria.... • general mechanism: tissue hypoperfusionb) forward failure of right heart: - hypoperfusion of the lungs → disorders of gas exchange - decreased blood supply to the left heart
  33. 33. 2. backward failure: – symptoms result from inability of the heart to accept the blood comming from periphery and from lungs• backward failure of left heart: – increased pulmonary capillary pressure → dyspnoea and tachypnoea, pulmonary edema (cardiac asthma) → → arterial hypoxemia and hypercapnia....b. backward failure of right heart: – increased pressure in systemic venous system → → peripheral edemas, hepatomegaly, ascites →↑nocturnal diuresis....