CONGESTIVE HEART FAILURE [Symptoms and Signs / Pathophysiology of CHF / Decompensation / Pathophysiology Basis of Treatment]

        Congestive heart failure (CHF),or heart failure is defined as an inability of the heart to pump blood at a rate appropriate for the metabolic requirements of the tissues;   

   Aetiology: Important causes include:

      *Hypertension: Due to high blood pressure, explusion of blood requires more forceful ventricular contraction during each systole. Over time, the left ventricle initially undergoes hypertrophy and later it dilates leading to heart failure.

      *Coronary artery disease: Myocardial infarction weakens the myocardium.

      *Valvular disease: Disorders of aortic or mitral valve cause extra burden on the heart. Initially heart undergoes hypertrophy and later dilatation. 

Symptoms and Signs

     *Exercise intolerance

     *Fatigue

     *Dyspnoea on effect

     *Cyanosis

     *Angle edema

     *Distended neck veins

     *Liver enlargement (hepatomegaly)

     *Spleen enlargement (splenomegaly)

     *Oedema feet

     *Ascites (fluid in peritoneal cavity, abdomen)



Pathophysiology of CHF 

    When the heart is unable to pump out sufficient amount of blood, a number of natural compensatory mechanisms are activated so as to improve the cardiac output and maintain normal perfusion of the vital organs. These mechanisms include:

     *Frank-starling mechanism

     *Increased adrenergic discharge

     *Regional redistribution of cardiac output 

     *Hormonal mechanisms

  As you have learnt in physiology lectures, cardiac output can be increased by an increase in end-diastolic volume (EDV) (Starling mechanism) as well as an increase in sympathetic discharge to the heart. Both of these mechanisms are utilized to bring the failing heart to produce normal cardiac output. The other two compensatory mechanisms help in these primary mechanisms are; 


1.Frank-starling mechanism: As shown in working at greater EDV (Y in failure), the heart can pump out normal amount of blood. EDV is increased by the fourth compensatory mechanism mentioned above.


2.Increased adrenergic discharge: In the failing heart, depressed cardiac output is sensed by high pressure baroreceptor located in the carotid sinus and aortic arch, leading to a reflex increase in adrenergic discharge improves the cardiac output by increasing the heart rate as well as stroke volume. In the blood vessels, it causes redistribution of cardiac output described next.

3.Redistribution of cardiac output: The redistribution of cardiac output serves as an important compensatory mechanism when cardiac output is reduced. Blood flow is redistributed so that thee delivery of oxygen to vital organs, such as the brain and myocardium, is maintained at normal or near-normal levels, while flow to less critical areas, such as the cutaneous and muscular beds and viscera, is reduced. Vasoconstriction medicated by the adrenergic nervous system is largely responsible for this redistribution.

4.Hormonal mechanism: Decreased cardiac output activates renin-angiotensin 2-mechanisms. Angiotensin 2 produces arteriolar constriction and increases thirst (increased water intake). It also increases aldosterone secretion, thereby producing salt and water retention in the kidney. As a result of both these factors, blood volume and thereby EDV is increased.


Decompensation

      As the cardiac function gradually deteriorates, the compensatory mechanisms discussed above cannot maintain normal cardiac output. Moreover, excessive increase in EDV increases left and right atrial pressures resulting in congestion in the lungs and in systemic veins. At this point, congestion heart failure is said to have set in.

Pathophysiological Basis of Treatment 

1. Strengthening the force of contraction of the heart: Digitalis

2. Reducing salt and water retention: Diuretics

3. Reducing sympathetic over-activity: Beta blockers