Cardiac Heart Failure mods t paul's.pptx

It is ppt about cardiac heart failure from dr abdo

1. Congestive Heart failure(CHF)

2. Objectives Types of heart failure Causes of lt side and rt side heart failure Clinical manifestation differences

3. Principles of Cardiac Dysfunction Cardiac dysfunction results from five principal mechanisms 1.Failure of the pump- Inadequately or weakly contracting muscle OR insufficiently relaxing muscle. 2.Obstruction of flow- Lesions preventing valve opening or lesions causing increased ventricular chamber pressure. 3.Regurgitant flow- Lesions which cause pumped blood to reflux backwards producing volume overload in the ventricles.

4. Principles of Cardiac Dysfunction Cardiac dysfunction results from five principal mechanisms 4.Disorders of cardiac conduction- These lead to non-uniform and inefficient muscular contractions. 5.Disorders of the continuity of the circulatory system- (e.g.- gun shot wound through the thoracic aorta). This permits blood to escape.

5. Heart Failure (Congestive Heart Failure, CHF) Definition Heart failure (HF) is a clinical syndrome that occurs in patients who, because of an inherited or acquired abnormality of cardiac structure and/or function, develop a constellation of clinical symptoms ( dyspnea and fatigue) and signs (edema and rales ) that lead to frequent hospitalizations, a poor quality of life, and a shortened life expectancy.

6. Heart failure (HF) is an end point of many cardiac diseases. Worldwide, about 20 million people are thought to suffer from HF

7. Most commonly CHF results from progressive deterioration of myocardial contractility (Systolic dysfunction). However, in 20-50% of the cases, CHF results in normally contracting hearts with inadequate relaxation (Diastolic dysfunction)

8. HF may be caused by valve failure (e.g., endocarditis) or can also occur in normal hearts suddenly burdened with an abnormal load (e.g., fluid or pressure overload).

9. In HF, the heart is unable to pump blood at a rate that meets the requirement of the metabolizing tissues, or can do so at elevated filling pressures. In a minority of cases, HF results due to increased demand of peripheral tissues for oxygen (high-output failure).

10. CHF is characterized by diminished cardiac output (forward failure) or damming back of blood in the venous system (backward failure). Almost always, forward failure is accompanied by backward failure. This results in ↑ ed end diastolic volume→ ↑ ed end diastolic pressure→ ↑ ed venous pressure.

11. Eventually, in CHF, every other organ is involved by some combination of forward and backward failure.

12. The cardiovascular system can adapt to reduced myocardial contractility or increased hemodynamic burden by a few different pathways. The most important are: Activation of neurohumoral systems 1.Norepinephrine → ↑ ed myocardial contractility and vascular resistance. 2.ANP → vasodilation, natriuresis , diuresis .

13. The cardiovascular system can adapt to reduced myocardial contractility or increased hemodynamic burden by a few different pathways. The most important are: Frank-Starling mechanism- Shorter sarcomeres have considerable overlapping of actin and myosin filaments, with consequent reduction of contractile force, whereas longer fibers increase contractility. i.e preload dilation helps to sustain cardiac performance by enhancing contractility

14. -Compensated heart failure- When the dilated ventricles are able to sustain the body’s requirement. - Decompensated heart failure- When an already compromised myocardium can no longer pump to meet requirements, even at rest.

15. The cardiovascular system can adapt to reduced myocardial contractility or increased hemodynamic burden by a few different pathways. The most important are: Myocardial structural changes including hypertrophy with or without dilation

16. Cardiac Hypertrophy: Pathophysiology and progression to failure Myocytes are considered to be terminally differentiated cells incapable of division Myocytes respond to mechanical load by hypertrophy The pattern of hypertrophy depends on the type of stimulus

17. Pressure overload (concentric) hypertrophy (e.g. in hypertension, valve stenosis ) There is ↑ ed left ventricular wall thickness There may be reduction of cavity diameter sarcomeres are deposited parallel to the long axis of the myocytes (↑ ed cell diameter but not cell length)

18. Volume overload (eccentric) hypertrophy (e.g. in valvular regurgitation) there is ↑ ed left ventricular wall thickness and dilation sarcomeres deposition causes both increase in cell length and diameter however, because of dilation, the wall thickness of a heart with both hypertrophy and dilation may be normal or even less.

19. Pathologic changes resulting in functional and structural abnormalities include - myocyte apoptosis, -cytoskeletal alterations and -altered ECM synthesis and remodelling. Heart failure can affect predominantly the left side or the right side, or both sides of the heart.

20. The most common causes of left-sided cardiac failure are: (1) IHD, (2) systemic hypertension, (3) mitral or aortic valve disease, and (4) primary diseases of the myocardium .

21. The most common cause of right-sided heart failure is left ventricular failure . Right-sided failure can also occur in the absence of left-sided heart failure in patients with - intrinsic diseases of the lung parenchyma and/or pulmonary vasculature ( cor pulmonale ) and - primary pulmonic or tricuspid valve disease.

22. The most common cause of right-sided heart failure is left ventricular failure . -it sometimes follows congenital heart diseases, i.e., in the setting of left-to-right shunts with chronic volume and pressure overloads.

23. Left-Sided Heart Failure The morphologic and clinical effects of left-sided CHF primarily result from -progressive damming of blood within the pulmonary circulation -the consequences of diminished peripheral blood pressure and flow.

24. Morphologic Changes The left ventricle is usually hypertrophied and dilated, sometimes massively (except in mitral valve obstruction and conditions that restrict ventricular size). Non-specific changes of myocardial hypertrophy and fibrosis are seen. Secondary left atrial enlargement → atrial fibrillation→high incidence of thromboembolic events. Pulmonary congestion and edema

25. Kidneys . -Persistent renal hypoperfusion → impaired nitrogenous waste excretion→ Prerenal azotemia Brain-hypoxic encephalopathy

26. Clinical Features Dyspnea (breathlessness) Cough due to fluid transudation into airspaces Orthopnea - dyspnea when patient is in recumbent position Paroxysmal nocturnal dyspnea

27. Clinical Features Enlarged heart (cardiomegaly), tachycardia, a third heart sound (S3), and fine rales at the lung bases. mitral regurgitation and a systolic murmur. atrial fibrillation, manifested by an "irregularly irregular" heartbeat.

28. Right-Sided Heart Failure In pure right-sided HF, pulmonary congestion is minimal whereas engorgement of the systemic venous system is pronounced

29. Morphology- congestion=>edema, chronic ischemia Liver. Spleen. Intestines Peritoneum Kidneys Brain Pleural and Pericardial spaces Subcutaneous tissues In many cases of chronic cardiac decompensation , patients present with a picture of biventricular CHF, encompassing the clinical syndromes of both LHF and RHF.

30. Objectives Types of heart failure Causes of lt side and rt side heart failure Clinical manifestation differences Complications

31. Reading assignments Vasculitides and tumors of the blood vessels and the heart We may arrange a make up class for ‘congenital heart diseases’, but still you need to read it!

32. Reference: Robinns & Cotran 7,or 8,or 9 th eds. Thank you for your time!