Understanding the Heart and Heart Failure
The human heart consists of left and right halves, which behave as two parallel “pumps” with distinct roles in circulation. Both the left and right side of the heart contain two chambers: a smaller atrium, at the top, receives blood into the heart and transfers it to a larger, more muscular ventricle, which is situated at the bottom and pumps blood from the heart into circulation (Marieb 2010).
The right atrium receives low-oxygen blood from vessels throughout the body (systemic circulation), and the right ventricle then pumps it to the lungs to become oxygenated. The left atrium of the heart receives high-oxygen blood from vessels of the lungs (pulmonary circulation), and the left ventricle then pumps it into systemic circulation. Thus, the two sides of the heart work in parallel to collect oxygen-poor blood from peripheral tissues, send it to the lungs for gas exchange (to pick up oxygen and remove carbon dioxide), and redistribute the newly oxygenated blood to tissues and organs to meet metabolic demands (Marieb 2010).
As the heart begins to fail, compensatory mechanisms throughout the body are initiated to ensure that adequate oxygen is delivered to tissues. During compensated heart failure, signals from the brain and kidneys result in fluid retention (to increase blood pressure in an attempt to better distribute oxygenated blood), increased heart rate and contractile force, dilatation (expansion) of the ventricle to hold more blood, and growth of new heart muscle to increase the force of ejection. Increases in blood volume and ventricular filling pressures cause blood to “back up” in systemic or pulmonary circulation and leak fluid into peripheral tissues, causing edema (swelling) in the lungs, abdomen, and extremities. This is termed “congestive” heart failure (Goldman 2013). Since not all patients have fluid accumulation at the time of initial evaluation, the term “heart failure” is preferred over the older term “congestive heart failure” (Hunt 2005; Hunt 2009).
As heart failure progresses, compensatory reactions are increased to keep up with tissue oxygen demands. However, the compensatory mechanisms of the heart are not without their limits; the heart is restricted in how much it can expand to hold more blood or increase its contractile force and rate, and the kidneys can only retain so much water before fluid begins to infiltrate other organs and tissues. Once the limits of compensation are reached, the cardiovascular system is no longer able to satisfy tissue oxygen demands. This is called decompensated heart failure and requires aggressive medical intervention or death will occur (Goldman 2013).
Left-Sided vs. Right-Sided Heart Failure
Heart failure is manifested differently depending on which part(s) of the heart are affected. The heart must generate a substantial amount of force to pump blood into the systemic circulation. This is accomplished by the left ventricle, which is the largest and most muscular of the four heart chambers. In left-sided heart failure, the ability of the left ventricle to push oxygenated blood into circulation is compromised. Left-sided heart failure can be further characterized as systolic failure (where the ventricle cannot contract normally and lacks the force to adequately eject blood) or diastolic failure/diastolic dysfunction (where the ventricle is unable to relax and fill properly). Left-sided heart failure can result in a decrease in oxygen delivery to the tissues and may cause fluid to back up in the lungs (pulmonary edema). Conditions that can lead to left-sided heart failure include valvular diseases (eg, mitral valve regurgitation or aortic insufficiency), structural defects in the heart muscle, anemia, hyperthyroidism, high blood pressure, and aortic stenosis (ie, narrowing of the aorta, the large artery that carries blood from the left ventricle for distribution throughout systemic circulation) (Marieb 2010; Foley 2012).
Right-sided heart failure usually occurs as a result of left-sided failure. When the left ventricle fails, increased fluid pressure backs up through the pulmonary circulation and increases the resistance against which the right ventricle must pump. As the right side of the heart fails, blood backs up in the body's veins. Increased venous pressure can cause fluid to leak out of veins and collect in peripheral tissues, the liver (causing enlargement or hepatomegaly), or abdomen (ascites). Conditions that specifically affect right-heart filling include valvular diseases (eg, tricuspid valve regurgitation or pulmonary valve insufficiency) and structural defects in the heart muscle (eg, atrial septal defects or patent foramen ovale) (Marieb 2010).