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Pathophysiology: Heart Failure

Heart failure (HF) is an abnormal clinical syndrome involving impaired cardiac pumping and/or
filling. HF, formerly called congestive HF, is the terminology preferred today since not all
patients will have pulmonary congestion or volume overload.

HF is associated with numerous
types of cardiovascular diseases, particularly long-standing hypertension, coronary artery
disease (CAD), and myocardial infarction (MI). CAD and advancing age are the primary risk
factors for HF. Other factors, such as family history and genetics, hypertension, diabetes,
sedentary lifestyle, cigarette smoking, obesity, and high serum cholesterol, can also contribute
to the development of HF. Hypertension is a major contributing factor, increasing the risk of HF
approximately threefold. The risk of HF increases progressively with the severity of
hypertension. Diabetes predisposes an individual to HF regardless of the presence of
concomitant CAD or hypertension. HF may be caused by any interference with the normal
mechanisms regulating cardiac output (CO). CO depends on (1) preload, (2) afterload, (3)
myocardial contractility, and (4) heart rate (HR). Any alteration in these factors can lead to
decreased ventricular function and the resultant manifestations of HF.
HF is usually manifested by biventricular failure, although one ventricle may precede the other
in dysfunction. Normally the pumping actions of the left and right sides of the heart are
synchronized, producing a continuous flow of blood. However, as a result of pathologic
conditions, one side may fail while the other side continues to function normally for a period of
time. Because of the prolonged strain, both sides of the heart will eventually fail, resulting in
biventricular failure. The most common form of HF is left-sided failure. Left-sided failure results
from left ventricular dysfunction, which prevents normal blood flow and causes blood to back
up into the left atrium and into the pulmonary veins. The increased pulmonary pressure causes
fluid extravasation from the pulmonary capillary bed into the interstitium and then the alveoli,
which manifests as pulmonary congestion and edema. In heart failure, baroreceptor and
osmotic stimuli lead to vasopressin release from the hypothalamus, causing reabsorption of
water in the renal collecting duct. Although these neurohormonal pathways initially are
compensatory and beneficial, eventually they are harmful, and neurohormonal modulation is
the basis for modern medical treatment of heart failure. Heart failure is a process, not a
disease. The heart doesn't "fail" in the sense of ceasing to beat (as occurs during cardiac arrest).
Rather, it weakens, usually over the course of months or years, and as it weakens it works
harder and harder in order to maintain homeostasis. Eventually, the heart reaches such a
compromised state, that it is unable to pump out all the blood that enters its chambers. As a
result, fluids tend to build up in the lungs and tissues, causing congestion. This is why heart
failure is also sometimes referred to as "congestive heart failure." Thus, pulmonary edema
causes fluid buildup within the alveoli in the lungs preventing adequate exchange of oxygen and
carbon dioxide, leading to various signs and symptoms: SOB, dyspnea, orthopnea, wheezing
and coughing, edema, fatigue, headaches, anorexia, pain, irritability, and altered mental status.

*Yellow denotes conditions consistent with my patient.