Understanding Congestive Cardiac Failure [Archives:2000/44/Health]

Dr. Rana Jaffer, Cardiologist  
The heart and lungs work together to pump oxygen to body tissues. Blood is pumped by heart which extracts oxygen from air in lungs. Without oxygen, cells of body stop functioning. In heart failure, the heart does not pump strongly enough and symptoms result at rest with activity. Arteries are vessels carrying blood away from heart, while veins carry blood towards heart and their valves prevent blood from flowing backward. Heart failure is a pathophysoiologic state which results from abnormality of cardiac function. In this case the heart is unable to maintain an output sufficient for metabolic needs of tissues. The main causes of Congestive Cardiac Failure (CCF) are either decreased myocardial capacity to contract or an inability to fill cardiac chambers with blood. Sometimes, the chambers are unable to expand during diastole as in case of left ventricular hypertrophy, myocardial fibrosis, amyloid deposit and constrictive pericarditis. Dynamics of Circulation in Cardiac Failure In Myocardial Infarction, hearts pumping ability decreases; thus there is decrease in cardiac output of jamming of blood in veins. Compensation for acute cardiac failure by sympathetic reflexes: The best known of these is baroreceptor reflex which is activated by decreased art. Pressure. It is probable that chemoreceptor reflex, CNS ischemic response and even responses that originate in damaged heart also contributed to nervous response. But whatever the responses, the sympathetic are strongly stimulated within few seconds, and parasympathetic are inhibited at some time. Strong sympathetic stimulation effects heart and vasculature. If all the ventricular vasculature is diffusely damaged but still functioning, sympathetic stimulation strengthens damaged muscle.
If part of muscle is non-functional, part of it is normal and is stimulated by sympathetic system, in this way compensating for non-functioning muscle. Thus the heart becomes stronger by one way or another by stimulation of sympathetic impulses. Sympathetic stimulation increases tendency for venous return because it increases tone of blood vessels of circulation in veins raising mean systemic filling pressure to 12 to 14 mm Hg, almost 100% above normal. Thus damaged heart become primed with more blood than usual and right atrial pressure rises which causes heart to pump large quantities of blood. Therefore, a person who has a sudden moderate heart attack can experience cardiac pain. Shortly, after this, by aid of sympathetic reflex compensations cardiac output returns to level adequate to sustain the person who remain quiet, although pain might be present.

Fluid Retention Helps to Compensate Cardiac Output
After acute heart attack, there is:
– Retention of fluids by kidney &
– Progressive recovery of heart over period of several weeks and months.

Renal Retention of Fluid and Increase in Blood Volume
Low cardiac output causes atria, disturbances in urine output which persists till the cardiac output returns to normal.
There are benefits of fluid retention in cardiac failure: it
– Increases mean system filling pressure which increases pressure gradient for causing flow of blood towards heart.
– Distends veins which reduce venous resistance and thus allows increased ease of flow of blood to heart.

Excessive retention of fluid in cardiac failure may result into:
– Overstretching and weakening of heart, filtration of fluid into lungs to cause pulmonary edema and development of edema in all tissues of the body.

Recovery of myocardium after Myocardial Infarction
There is development of new collateral blood supply in the infected area causing muscles functioning again. The recovery depends on severity of damage.
Heart recovers within 5-7 weeks. As the hearts function becomes normal, kidneys become normal and sympathetic function becomes normal.

Dynamics of Severe De compensated Heart Failure
There is no compensation, the cardiac output cannot rise to high enough value to bring return of normal renal function. Fluid is retained causing edema. Heart fails to pump enough blood to cause kidneys to excrete daily necessary amount of fluid.
Sometimes, due to decompensation, cardiac output is greatly decreased, effecting all the body tissues resulting in cardiogenic shock.

Cardiac Hypertrophy
Pathophysiology and Progression to failure:
Increased workload results in cardiac hypertrophy which finally results into CCF. In CCF, the myocytes increase in size, which later increase the overall mass and size of the heart. Hypertrophy may result from several causes but the main one is hypertension.
Hypertensive people are more prone to develop left ventricular hypertrophy which leads to CCF.
In cardiac hypertrophy, there is a balance between adaptive changes and potentially deleterious structural alterations including decreased capillary to myocyte ratio, increased fibrous tissue and synthesis of abnormal proteins. 
On autopsy, patients with congestive cardiac heart are seen to have their hearts to increase in weight, increase in chamber dilatation and other microscopic changes of hypertrophy. CCF produces different effects in different tissues.
Under various pathologic stresses, left sided and right sided failure occur separately. Often both sides fail together.

Precipitating Causes
– Infection: Most of the pulmonary congestion leads to CCF.
– Anemia: it decreases oxygen supply & precipitates heart failure.
– Thyrotoxicosis: it increases cardiac output & leads to its failure.
– Arrhythmia
– Rheumatic fever
– Infective endocarditis
– Systemic Hypertension
– Myocardial Infraction
– Pulmonary embolism
– Marked obesity
– Diabetes mellitus
– Family history of heart failure

Classification of Heart Failure
Congestive Heart Failure
Fluid in lungs or body resulting from failure of heart as a pump.

Right Sided Heart Failure
Failure of right side of heart resulting in swelling of body especially the legs and abdomen

Left Sided Heart Failure
Failure of pumping action of left side of heart resulting in congestion of lungs.

Forward heart Failure
The inability of heart to pump blood forward at sufficient rate t meet oxygen needs of body at rest or during exercise.

Backward Heart Failure
The ability of heart to meet needs of body only if heart filling pressure are abnormally high.

Left Sided heart Failure
Causes: IHD – Hypertension – Aortic & Mitral Valvular Diseases – Myocardial Diseases.
The left ventricle dilates which in turn causes the left atrium to dilate. Atrial fibrillation & thrombosis are evident, too. Left-sided heart failure mostly affects kidneys, lungs and brain.

Lungs: There is pulmonary congestion and edema.
Changes in lung include:
– Perivascular transudate, particularly in interlobular septa
– Progressive edematous widening of alveolar septa
– Accumulation of edema fluid in alveolar spaces.

Chief Complaints
Dysponea: Use of respiratory muscles to inflate lungs, resulting in shortness of breath.
Orthonea: Dysponea in recumbent position which is relieved on lying down.
Paroxysmal nocturnal Dysponea: Attacks of dysponea occurring at night, leading to cough.
Cheyenne-Strokes Resp: Decreased sensitivity of respiratory center to arterial pulmonary carbon dioxide. There is hyperventilation with intervals of apnea.
Kidneys: Here there is reduction in renal perfusion whichresults into tubular necrosis.
Brain: Cerebral hypoxia results into encephalopathy

Right-Sided Heart Failure
It often results when pressure increases in pulmonary circulation.
Pure, right-heart failure occurs with cor plumonale. Right-sided failure results in right ventricle and atrium dilatation. The major organs affected are: liver, spleen, kidney, subcutaneous tissue and brain.

Liver: it increases in size & weight and it displays pattern of nutmeg liver, chronic passive congestion. This is composed of congested red centers of liver lobules surrounded by pale, fatty peripheral regions.
There is centrolobular necrosis along with sinusoid congestion, Rupture of sinusoids produces central hemorrhagic necrosis. Central areas with time become fibrotic creating cardiac sclerosis.

Kidneys: There is fluid retention, edema and pronounced arotemia.
Portal System of Drainage: There is increase in pressure of portal system leading to enlargement of spleen.

Microscopically, sinusoids dilate with areas of hemorrhage. Later sinusoids are fibrosed leading to congestive splenomegaly. There is also fluid accumulation in peritoneum forming ascites.
Subcutaneous Tissues: edema of dependent areas e.g. at the ankle is often seen. Generalized edema is called anasarca.
Pleural & Pericardial Cavities: Effusions are seen here
Brain: Venous congestion & hypoxia of CNS.
Most often, patients with CCF are seen to have cardiac manifestations of right and left side heart failures.

Living with Heart Failure
Healthy Life Style: a healthy, balanced diet with regular exercise.
Doctor visits: regular visits to doctor like a good patient.
Medical treatments: Regular intake of medicines.

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