Congestive Heart Failure

For an Anatomy & Physiology class I am taking, my professor assigned a research paper for extra credit. The topic was restrained to any of the wide variety of diseases or conditions that the human body can suffer from. I decided to chose CHF, since it happens to be something I know a little bit about. She was surprised when she asked where my references were, and I said I didn't use any. Sure, at some point, I read this information somewhere, but I couldn't remember where if I tried. Guess I skipped the research part of this research paper. Anyhow, I figured I would share it. I have posted on CHF before and covered most of this, but a refresher never hurt anyone and this is much more basic.

Congestive Heart Failure

Congestive heart failure, or CHF, is a condition that afflicts millions of Americans. Over five hundred thousand new diagnoses are made every year. CHF is a condition that is entirely caused by the body’s homeostatic compensatory mechanisms. CHF arises from the condition simply termed, heart failure.

Heart failure is manifested by the heart’s inability to provide adequate perfusion to the body. This occurs due to other conditions or diseases such as chronic hypertension or a previous myocardial infarction. Clinical findings may include a decreased blood pressure, dizziness, or signs of hypoxia.

The body senses this decrease in cardiac output and attempts to maintain homeostasis. Baroreceptors detect inadequate pressure and norepinephrine is released by the adrenal gland. This causes profound vasoconstricion, as well as an increase in inotropy, chronotropy, and dromotropy. This just means that the heart is beating faster and harder due to the catecholamine release. The kidneys also lend a hand by releasing Angiotensin Converting Enzyme, or ACE. ACE converts angiotensin I into angiotensin II, which is yet another vasoconstrictor. The body will also act to increase volume by inhibiting fluid release. The heart itself produces a peptide called Brain or B-type Natriuretic Peptide (BNP).

All of these compensatory mechanisms acting together cause the cardiovascular system to go into overdrive. Too much vasoconstriction and cardiac force cause increased afterload. Afterload is the pressure in which the heart is pumping against. This is also known as arterial pressure and an increase results in an increase in palpable blood pressure. Since the heart can’t pump blood out efficiently against the increased after load, blood backs up. It first backs into the atria from the left ventricle. It then backs up into the pulmonary vein and then the lungs. This is where we get the congestion of congestive heart failure.

Pulmonary congestion is also known as pulmonary edema, and may be a lethal condition. Chest X-rays and BNP levels are used to diagnose CHF patients. Due to the increase in workload, the myocardium of the heart hypertrophies and shows up as an enlarged heart on a chest X-ray. Chronic CHF patients are treated with oral diuretics, and antihypertensives such as beta blockers and ACE inhibitors. The beta-blockers decrease the rate of contraction and ACE inhibitors block the Angiotensin Converting Enzyme.

Emergency treatment may include bronchodilators, nitrates to decrease preload and afterload, and continuous positive airway pressure, also known as CPAP. CPAP provides a continuous flow of air that keeps the alveoli open while forcing the fluid back out of the lungs via pulmonary capillaries, and back into the cardiovascular system. Nitates and CPAP have shown to drastically improve the outcome of emergency CHF patients with marked hypoxia.