Conjective Heart Failure occurs when the cardiac output cannot meet the metabolic needs of the bodies tissues. It can be caused by myocardial infarction, aortic and mitrial sternosis, aortic regurgitation, myocarditis and systemic hypertension. A whole myriad of symptoms from coughing with sputum, peripheral edema, systemic congestion, hepatomegaly, splenomegaly, mental confusion, tissure hypoxia, metabolic acidosis, dyspnea, orthopnea, tachypenea and cyanosis. To fully understand how and why we can the above mentioned symptoms, we need to understand the physiology of the heart.

Normal heart performance is related to the Cardiac Output which, is the product of heart rate multiplied by stroke volume (CO=HRXSV). Now heart rate can either increase or decrease. HR and SV will be adjusted and increased when we need more blood flow to an active tissue or in other words when the tissue is not receiving enough O2. In a failing heart we are unable to meet the O2 needs of the tissue. Therefore we continually adapt by making the heart work more to satisfy this discrepancy which further progresses heart failure. Now, asking “why is the heart failing to supply CO?” There are only two reasons. First, the heart may not fill properly leading to a reduced ventricular volume (EDV). Causes, could be failed venous return, inadequate blood volume, or a decreased ventricular size (hypertrophy). Either way, since EDV is one of the components of SV, a reduced EDV = reduced SV. This etiology is called Diastolic heart failure (diastolic being resting heart and during rest the heart should be filling but it isn’t). Second, the heart my not be able to contract forcefully enough and thus more blood is left in the ventricle following ventricular systole meaning that the ESV has increased and this being the second component of SV, an increased ESV is a reduced SV. This etiology of CHF is referred to as Systolic failure (failure to contract (systole) forcefully enough to eject the blood). Conditions that result in Systolic failures are failed blood supply to the myocardium (CAD) or a necrotic myocardium (MI) or a degenerative infectious disease (Myocarditis), or valve defects that allow the misdirection of blood or back flow. Therefore, CHF is either the result of a condition that reduces EDV or increases ESV and is referred to as Diastolic or Systolic Failure respectively.

Forward and Backward Effects

When the heart fails, two important considerations need be examined as they explain the manifestations of and a proper diagnosis for CHF. These considerations are called the Forward and Backward effects and they are specific as to which side of the heart is failing. If considering what each side of the heart is attempting to accomplish but can not because it is failing explains the forward effects and a progression of CHF. Conversely, since blood is continuously circulated, a failure to positively move blood will cause the system to back up thus, causing the backward effects and manifestations of CHF. Therefore by knowing where the blood in the ventricles was received from, we now can trace the backward movement and determine the congestion in the appropriate system. Now, examine the heart as it pertains to either right or left side. The example below attempts to relate the above considerations into a logical, systematic order using right heart failure as the disorder.

Right Side Failure Case Study

The right side of the heart pumps blood to the pulmonary system. Using a disorder that causes the lung to become congested (COPD), we have an increased pressure in the pulmonary circuit that the right heart must overcome to properly circulate the blood. The early adaptation to working against a high afterload is for the myocardium to enlarge (hypertophy). In other words, since the lung is backed up with blood, the right ventricle has to work harder to pump blood to the lungs. Hypertrophy is an innate response that reduces the size of the ventricle so it could pump harder and redueced volume also reduced the demand. Thus the EDV is reduced leading to a reduction in SV. If this pulmonary pressure (afterload) continues to rise and the right heart continues to reduce the SV, eventually the heart will not be able to make the adaptation necessary to meet the tissue’s O2 demands and thus CHF is apparent.

To examine the forward effects, determine what has been lost by not circulating the blood. The right side has decreased SV which, causes a decrease in left ventricular filling (EDV) which results in a decreased left heart stroke volume causing less oxygenated blood to reach the tissues. The body attempts to adapt and adequately supply the body’s oxygen needs through compensatory mechanisms (adjusting HR and Blood return to heart), which adds further stress on the heart and eventually the Left heart fails (condition known as biventricular failure). Additionally, bodily tissues become hypoxic.

Backward effects for Right heart failure are due to blood backing up in the system as the left heart continuously pumps more blood toward the lungs, and eventually the right heart can’t handle the load against it from the backflow from the lungs (preload, which is also increased as a compensatory mechanism). Therefore blood back-flows causing venous pressure to rise. At the capillary where fluid is returned to the venules, the pressure difference between interstitial and vascular forces now is decreased and excess fluid remains in the tissues resulting in systemic edema. This loss of blood volume can again be a stimulus for more compensatory mechanisms leading to a further stimulus to overwork the heart. Eventually, compensatory mechanisms fail and the patient enters shock and death or the heart enters cardiac arrest and all function is lost resulting in patient death.

Basically, the Right Side Heart failure always progresses to systemic edema due to the backward effects and this manifestation is a diagnostic tool. Next, the progression of the disease is the development of biventricular failure from over working the heart through activation of compensatory mechanisms. Therefore, the treatment of CHF is to reduce the compensatory mechanisms and prolong the life of the heart. In End stage or complete failure the only treatment is heart transplant.