Congestive Cardiac failure is a condition associated with heart disorders leading to impairment of the heart to supply sufficient blood to meet the body requirements. Cardiac Failure may be associated with the failure of the right or left ventricle or both. Cardiac failure, causes the blood to move through the heart and body at a slower rate, leading to increased pressure in the heart. As a result, the heart is unable to pump enough oxygen and nutrients to meet the body's requirements. The heart chambers thus respond by stretching in order to hold more blood to pump through the body or by becoming more stiff and thickened. Such mechanism helps to keep the blood moving for a short while, but the heart muscle walls tend to weaken with time and then are unable to pump with enough strength.
The direct result of the reduced contractility of the cardiac muscles especially those of the ventricles which cause a decrease in the cardiac output and increase in the blood volume of the heart.
This causes the kidneys to often respond by causing the body to retain fluid (water) and sodium as the systemic blood pressure and the renal blood flow both are reduced. Resulting into building up of fluid in the arms, legs, ankles, feet, lungs or other organs causing oedema which makes the body congested, hence the name Congestive cardiac failure.
There are many causes of congestive heart failure including:
Rarer causes of heart failure include:
- coronary artery disease leading to heart attacks and heart muscle weakness,
- primary heart muscle weakness from viral infections or toxins such as prolonged alcohol exposure,
- heart valve disease causing heart muscle weakness due to too much leaking of blood or heart muscle stiffness from a blocked valve, and
Major Causes include Ischemic heart, Hypertension, cardiomyopathy.
- Viral Myocarditis (an infection of the heart muscle).
- Infiltrations of the muscle such as amyloidosis.
- HIV cardiomyopathy (caused by Human Immunodeficiency Virus).
- Connective Tissue Diseases such as Systemic lupus erythematosus.
- Abuse of drugs such as alcohol.
- Pharmaceutical drugs such as chemotherapeutic agents.
Typical Symptoms include, breathlessness, orthopnea, coughing, ankle swelling and reduced exercise capacity.
Treatment of Congestive Cardiac Failure is focused on improving the symptoms and preventing the progression of the disease.
The Major and often neglected form of treatment is lifestyle improvement, which includes:
As the entire body suffers from congestion due to fluid accumulation and also that sodium leads to increased fluid accumulation in the body tissues, it is often recommended to restrict the sodium and fluid intake during the Cardiac failure.
It is recommended to do any activity which one can sustain for more than just a few minutes while your heart, lungs, and muscles work overtime. Such an exercise is known as aerobic exercise. Regular exercise, according to the patient's tolerance level, appears to provide significant benefits and should be used only when the patient is compensated and stable.
Pharmacological treatment involves the use of following category of medications:
These agents act by inhibiting the Angiotensin converting enzyme which is responsible for conversion of Angiotensin I (inactive) to Angiotensin II (active).
ACE Inhibitors improve symptoms, decrease mortality and reduce ventricular hypertrophy. Angiotensin II receptor antagonist therapy (also referred to as AT1-antagonists or angiotensin receptor blockers), particularly using candesartan, is an acceptable alternative if the patient is unable to tolerate ACEI therapy. ACEIs and ARBs decrease afterload by antagonizing the vasopressor effect of angiotensin, thereby decreasing the amount of work the heart must perform. It is also believed that angiotensin directly affects cardiac remodeling, and blocking its activity can thereby slow the deterioration of cardiac function.
Fluid retention is the major manifestation observed during Congestive Cardiac Failure. Removal of excess extracellular fluid with diuretics is one of the mainstays of therapy in patients with systolic or diastolic heart failure.
Following are the classes of Diuretics used for this purpose.
As the name suggests Loop Diuretics act on the ascending loop of Henle of the Kidney Nephron, where they act on the sodium, potassium and chlorine cotransporter thus inhibiting sodium and chlorine reabsorbtion. By inhibiting the sodium and chlorine reabsorbtion loop diuretics prevent the urine from getting consentrated and disrupt the generation of hypertonic renal medulla, which ultimately leads to increased urine production. Loop Diuretics also increase the renal blood flow by this mechanism. Thus this mechanism of diuresis leaves less urine to be reabsorbed and thus result in decreased blood volume. The combined effect of decreased blood volume and vasodilation lead to decrease blood pressure and ameliorate edema.
Potassium sparing diuretics are a class of diuretics which cause diuresis by not promoting the secreating of potassium in the urine. Potassium sparing Diuretics act be competing with aldosterone for intracellular cytoplasmic receptor sites, or by directly blocking sodium channels. Potassium sparing diuretics by acting as competitive antagonists prevent the production of certain mediator proteins. As these mediator proteins are not produced, and so stimulation of sodium-potassium exchange sites in the collection tubule does not occur. This prevents sodium re-absorption and potassium and hydrogen ion secretion.
Derived from Benzothiadiazine, Thiazide Diuretics inhibit sodium-chloride reabsorption from the distal convoluted tubules in the kidneys by blocking the thiazide-sensitive sodium-chloride cotransporter.
Thiazide diuretics by causing diuresis result in lowered blood pressure, fall in plasma volume and a reduction in cardiac output. However, after chronic use thiazides cause a reduction in blood pressure by lowering peripheral resistance and leading to vasodilation.