HEART FAILUIRE Dr Eman MS Muhammad HEART FAILURE

HEART FAILUIRE Dr Eman MS Muhammad

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.

ACUTE HEART FAILURE Causes: 1. Sudden occlusion of a large main coronary artery causes acute LSHF due to VF. 2. Massive pulmonary embolism causes acute RSHF. 3. Acute infections with marked toxemia as diphtheria causes toxic myocarditis and wide spread peripheral capillary dilatation. 4. Hemopericardium prevent the filling of the heart during diastole with decrease in the

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

c) Tricusped stenosis or incompetence. d) Large ASD or VSD. e) Constrictive pericarditis. f) LSHF; it is the most common cause. g) Pulmonary embolism. B. Myocardial injury as in myocarditis, IHD, and cardiomyopathy.

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

Causes of LSHF: A. Increase workload in cases of: 1. Systemic hypertension. 2. Aortic stenosis or incompetence. 3. Mitral incompetence. 4. Congenital heart disease as coarctation of the aorta.

B. Myocardial injury: 1. IHD and healed cardiac infarcts. 2. Myocarditis. 3. Cardiomyopathy. 4. Adherent mediastino-pericarditis. C. Increased COP: 1. Anemia. 2. Thyrotoxcosis.

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”.

I. Systolic failure (inadequate emptying): A. 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. The LV enlarges to accommodate the residual volume plus blood which arises from the atrium.

During exercise the COP can not rise appropriately → to tiredness and dyspnea. Tiredness is due to under-perfusion of the exercising muscles. Dyspnea is due to the combination of: a) Increase in pressure and volume in the pulmonary circulation leading to ↓ compliance in the lungs. b) Increase anaerobic metabolism with accumulation of lactate causing acidosis and stimulating the respiratory center.

B. 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.

C. Pressure overload: It is usually due to: A. Increased pressure in the systemic or pulmonary circulation (systemic or pulmonary hypertension). B. 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 stroke volume for a time.

II. Diastolic failure (inadequate filling): A. 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.

B. 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.

C. 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.

D. Decreased myocardial compliance: This impairs ventricular filling. This occurs in severe left ventricular hypertrophy, e. g. , hypertrophic cardiomyopathy. Decreased compliance occurs also in amyloid infiltration.

E. Severe endocardial thickening: This occurs in restrictive cardiomyopathy, giving rise to diastolic dysfunction, by restricting ventricular contraction during diastole.

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.

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.

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, beri and congestive cardiomyopathy. Congestive failure can also result from conditions which ↑ the work load of both ventricles, 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. The term high COP failure is applied.

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