Dr Eman MS Muhammad

1. HEART FAILUIRE Dr Eman MS Muhammad

2. The human heart is a remarkably efficient, durable, and reliable pump that propels more than 6000 liter of blood throughout the body daily during the individual lifetime. • Thereby, it provides the tissues with a steady supply of vital nutrients and facilitating the excretion of waste products. • The normal heart has great reserve power and this can be substantially ↑ by physical training. • During exercise there is a greater venous return with consequent ↑ in the diastolic filling and stretching of the muscle fiber. • According to Frank Starling’s law this leads to a more vigorous contraction and a great ↑ in the stroke volume.

3. The law states that the stroke volume of the heart increases in response to an increase in the volume of blood in the ventricles, before contraction (the end diastolic volume), when all other factors remain constant. • Cardiac dysfunction can be associated with devastating physiologic consequences. • The normal heart weight varies with body height and weight. • It averages 250-300gm in females and 300-350gm in males.

4. The expected thickness of the free wall of the RV is 0.3-0.5cm and that of the LV is 1.3-1.5cm. • Greater heart weight or ventricular thickness indicates cardiac hypertrophy. • Enlarged chamber size implies dilatation. • ↑ in cardiac weight and size is called cardiomegaly.Heart diseases is the predominant cause of disability and death in industrialized countries. • HF is a clinical syndrome and not a single diagnosis or pathological entity.

5. HEART FAILURE • Definition: • Cardiac failure OR heart failure (HF) refers to impairment of cardiac function that fails to maintain a circulation adequate for the metabolic needs of the body despite an adequate blood volume. • Consequently, there is inadequate tissue perfusion leading to a syndrome in which the most important features are fatigue, dyspnea, and edema.

6. These result from a complex interaction of many factors: • Impaired cardiac output “forward failure”,and ↑ central venous pressure (CVP) “backward failure”, impaired gas exchange in the lung, activation of neurohumoral mechanisms causing disturbances in salt and water balances, and changes in skeletal muscle function. • There is a spectrum of HF ranging from mild asymptomatic cardiac dysfunction, through severe failure and reduced exercise tolerance.

7. Compensatory mechanisms (ventricular hypertrophy, peripheral vasoconstriction, and salt and water retention) maintain tissue perfusion. • Finally compensatory mechanisms are exhausted and symptoms and signs of failure occur at rest. • Essentially failure is due to an abnormal ↑ in the work required by the myocardium, weakness or insufficiency of the myocardial contraction, or a combination of both. • HF is classified as acute HF and chronic HF. • The later is also subdivided into LSHF, RSHF, or both; congestive HF; CHF.

8. ACUTE HEART FAILURE • Causes: • Sudden occlusion of a large main coronary artery causes acute LSHF due to VF. • Massive pulmonary embolism causes acute RSHF. • Acute infections with marked toxemia as diphtheria causes toxic myocarditis and wide spread peripheral capillary dilatation. • Hemopericardium prevent the filling of the heart during diastole with decrease in the cardiac output (COP).

9. CHRONIC HEART FAILURE • Diseases which cause chronic HF affect primarily left or right side of the heart. • Causes of RSHF: • Heart diseases: • Increase in the work load leading to pulmonary hypertension due to: • Mitral stenosis. • Pulmonary stenosis or incompetence.

10. Tricuspedstenosis or incompetence. • Large ASD or VSD. • Constrictive pericarditis. • LSHF; it is the most common cause. • Pulmonary embolism. • Myocardial injury as in myocarditis, IHD, and cardiomyopathy.

11. Lung diseases: (Cor-pulmonale; it is RSHF due to lung causes) as in cases of: • Emphysema. • Pulmonary fibrosis caused by TB, bilharziasis, bronchiectasis, pneumoconiosis ... etc.

12. Causes of LSHF: • Increase workload in cases of: • Systemic hypertension. • Aortic stenosis or incompetence. • Mitral incompetence. • Congenital heart disease as coarctation of the aorta.

13. Myocardial injury: • IHD and healed cardiac infarcts. • Myocarditis. • Cardiomyopathy. • Adherent mediastino-pericarditis. • Increased COP: • Anemia. • Thyrotoxcosis.

14. Patho-physiological concepts: • The heart must not only expel enough blood during systole, it must also fill adequately during diastole. • HF most commonly results from impaired cardiac emptying; “systolic failure”. • Less commonly impaired filling leads to “diastolic failure”.

15. The simple concept apply equally to both the RV and the LV and their respective circulation. • Although the pressure in the pulmonary circulation is much lower, the flow within it must equal that in the systemic circulation. • Myocardial ischemia produces a combination of both diastolic and systolic dysfunction, since relaxation like contraction is an energy consuming process.

16. Systolic failure (inadequate emptying): • Impaired ventricular contraction: • The normal LV expels at least 50% of its contents during systole. • This is known as the left ventricular ejection fraction (LVEF). • It is the best measure of left ventricular function. • The weakened ventricular muscle can not achieve a normal LVEF.

17. The LV enlarges to accommodate the residual volume plus blood which arises from the atrium. • The LV enlarge to compensate for impaired contraction. • The wall tension is an important determinant of myocardial oxygen demand, and maintenance of stroke volume. • When the heart dilates this ↑ metabolic coast. • During exercise the COP can not rise appropriately → to tiredness and dyspnea.

18. Tiredness is due to under-perfusion of the exercising muscles. • Dyspnea is due to the combination of: • Increase in pressure and volume in the pulmonary circulation leading to ↓ compliance in the lungs. • Increase anaerobic metabolism with accumulation of lactate causing acidosis and stimulating the respiratory center.

19. Increased volume load: • Incompetence of heart valves leads to ↑ volume load on the appropriate ventricle. • In aortic or mitral incompetence, the LV has to accommodate not only the volume of blood returning from the lungs but also the regurgitated volume from the LA in case of mitral incompetence, and from the aorta in case of aortic incompetence. • This leads to dilatation accompanied by hypertrophy, followed by dilatation and HF. • Intracardiac shunts also ↑ volume load on the lower pressure chamber, i.e. RA and RV in ASD, and RV in VSD.

20. Pressure overload: • It is usually due to: • Increased pressure in the systemic or pulmonary circulation (systemic or pulmonary hypertension). • Stenosis in the aortic and pulmonary valves causes pressure overload in the LV and the RV respectively. • Myocardial hypertrophy ↑ the power of contraction and maintains the stoke volume for a time. • Ultimately fibrosis and dilatation occurs, leading to impaired contractility and HF.

21. Diastolic failure(inadequate filling): • Pericardial diseases: • Accumulation of fluid in the pericardium or the presence of pericardial thickening or calcification impedes filling of all cardiac chambers during their diastolic phases. • This causes ↑ pressure in both pulmonary and systemic venous systems. • Clinically it is first detected by distension of the jugular veins in the neck.

22. Stenosis of mitral or tricuspid valve: • It impairs filling of LV and RV respectively. • In mitral stenosis this caused ↑ pressure in the pulmonary circulation and later this causes RSHF due to ↑ load in the RV. • The peripheral venous pressure is ↑ leading to edema and heptomegaly.

23. Atrial arrhythmias: • Atrial fibrillation may precipitate HF because the tachycardia leaves less time for the heart to fill. • The final phase of ventricular filling due to normal atrial contraction is lost.

24. Decreased myocardial compliance: • This impairs ventricular filling. • This occurs in severe left ventricular hypertrophy. • This typically occurs in hypertrophic cardiomyopathy, and to a lesser extent in all cases of severe left ventricular hypertrophy. • Decreased compliance occurs also in amyloid infiltration.

25. Severe endocardial thickening: • This occurs in endomyocardial fibrosis, giving rise to diastolic dysfunction, by restricting ventricular contraction during diastole.

26. Manifestation of cardiac failure • In mild degree of cardiac failure the heart is no longer able to ↑ COP sufficiently to fulfill extreme metabolic demands, as in sternous physical exercise, but is still able to meet lesser demands. • With ↑ in severity the cardiac reserve is further diminished, leading to ↓ exercise tolerance. • In severe failure, the circulation is inadequate even at rest.

27. Failure may be acute or chronic depending on the causal factors. • Impaired myocardial efficiency or ↑ workload develop rapidly or slowly. • The causal factors affect predominantly either ventricle, giving rise to left or right ventricular failure, or both with consequent congestive HF.

28. Acute heart failure • Occurs when the causal factors develop rapidly or suddenly. • Examples include MI, massive pulmonary embolism, arrhythmias, myocarditis, RF, and rupture of valve cusp. • In severe acute failure the COP ↓ drastically and there is peripheral vasoconstriction due to ↑ sympathetic activity.

29. The term “cardiogenic shock”is then appropriate. • The full picture of cardiogenic shock develops only in a small proportion of cases, but when it does the prognosis is poor.

30. Cardiogenic shock: An acute severe reduction in the COP caused by cardiac catastrophe such as MI, and less commonly rupture of a valve cusp or any cause of tamponade with hemopericardium. • The essential feature is “pump failure”. • Both the CVP and the ventricular end-diastolic pressure (VEDP) are raised. • The homodynamic changes which develop are similar to those of hypovolemic shock, and are triggered by ↓ in blood pressure and ↓ tissue perfusion. • The mortality rate approaches 80%.

31. Chronic heart failure • Chronic HF occurs when the causal factors develop slowly. • The commonest causes are IHD, chronic valvular dysfunction, and diseases of the lungs with pulmonary hypertension. • Chronic HF usually develops insidiously, but acute HF may progress to chronic HF.

32. In chronic failure the COP is diminished and hypoxia results. • Although two thirds of cases die from progressive failure, the other third die suddenly, probably from arrhythmias. • As with acute HF the clinical and pathological changes depend on the nature of the causal factors, and whether they affect mainly the LV, RV or both ventricles.

33. Left-sided heart failure • Common causes of HF affect the LV more than the RV, however left ventricular failure (LVF), usually leads to right ventricular failure (RVF); the right heart failed behind the left. • In the later stages, the picture is that of chronic congestive HF; CHF. • As LVF develops, the LV can no longer expel all the blood it receives during diastole, causing dilatation which further impairs contraction.

34. Dilatation results in stretching of the mitral ring with consequent mitral valve incompetence, leading to lung congestion, pulmonary edema, and further reduction of left ventricular output. • The main clinical feature of LSHF are dyspnea and cough due to pulmonary congestion and failure. • During early stage of LVF, the LV fails to meat ↑ circulatory demands, so that dyspnea and cough are precipitated by physical activity. • As failure ↑, exercise tolerance ↓ until pulmonary congestion is present even at rest.

35. Acute exacerbations of LVF commonly occur at night (paroxysmal nocturnal dyspnea). • Such attacks result from ↑ venous return in the recumbent position and from ↑ blood volume following resorption of fluid from the extravascular spaces. • Pulmonary congestion and edema of LVF are most pronounced when there is severe imbalance between the functional capacities of the LV and RV.

36. Right-sided heart failure • It occurs most often as a consequence of pulmonary hypertension, and the commonest cause of this is LSHF. • When the LV fails, pulmonary arteriolar vasoconstriction with ↑ in the pulmonary arteriolar pressure in response to ↑ pressure in the LA and pulmonary veins. • The mechanisms of this are not fully understood.

37. The most acute RSHF occurs with massive pulmonary embolism, which is fatal in few minutes, but multiple large emboli can cause acute RVF, and multiple embolism over along period causes chronic RVF. • When the RV fails, it becomes dilated and unable to eject all the blood which enters during diastole. • Stretching of the tricuspid ring results in incompetence. • The right atrium dilates and there is an ↑ in CVP which gives rise to systemic venous congestion and peripheral cardiac edema.

38. Congestive (biventricular) failure • It develops usually in cases of LVF, although both ventricles may fail simultaneously as a result of diffuse or extensive myocardial damage. • This occurs in cases of extensive infarction, severe myocarditis, beriberi and congestive cardiomyopathy. • Congestive failure can also result from conditions which ↑ the work load of both ventricles.

39. For example, lesions of mitral and aortic valves. • It also occurs in cases of persistent raised cardiac output such as thyrotoxicosis, anemia, and congenital abnormalities with left to right shunts. • In latter states, failure is associated with the usual ↓ in COP, but fail is relative to the previous abnormally high output. • So, even in failure the absolute output may be normal or even increased. • The term high COP failure is applied

40. Thank you