|Congestive Heart Failure (CHF)|
CHF is one of the most common causes of dyspnea (difficulty breathing) in adults, particularly in hospitalized patients. CHF is a syndrome, not a specific disease - the diagnosis of CHF is a description of a clinical presentation, not a definitive explanation of the pathology occurring in a given patient. There are a number of subtypes, but the common problem is an inability of the heart to effectively pump fluids. The hallmark is "increased venous pressure."
When the left side of the heart fails, the heart is no longer able to effectively pump fluids away from the lungs, and this results in inefficient flow from the lungs to the rest of the body. When fluids build up in the lungs (from increased pulmonary venous pressure), respiration becomes labored and ineffective.
When the right side fails, fluids build up in the rest of the body (increased systemic venous pressure), which leads to generalized edema. Remember that the most common cause of right-sided failure is left-sided failure - in other words, damage to the left side of the heart reduces the heart's ability to clear fluid from the lungs, which increases the pressure against which the right side has to pump. Eventually, the right side gets worn out and it begins to "fail," as well.
Hallmark signs & symptoms include:
Be aware that none of these findings need be present - patients may have CHF but not have any signs or symptoms.
To confirm the diagnosis, cardiac function (particularly LV, or left ventricular) should be assessed. The most commonly accepted analysis of LV function rests in determination of "Ejection Fraction" (EF). This refers to the percentage of blood in its interior that the LV can expel during a contraction. For example, if the LV contains 100cc when fully dilated (at the end of diastole) and 60cc when fully contracted (at the end of systole), then 40cc have been expelled, resulting in an EF of 40%.
"Normal" EF is generally considered to be between 60 and 75%, although there is disagreement on these figures even among cardiologists. A common definition of systolic dysfunction, however, is EF <50%. Most patients with CHF will present with EF < 40%, although this is not a useful diagnostic criterion.
EF is typically calculated by either echocardiography (ultrasound of the heart) or coronary angiography (x-ray inspection of the coronary arteries while they are injected with radio-opaque dye). A more recent technique (practiced at FAHC but not elsewhere in the area) includes the "bubble study," in which CO2 bubbles are injected into the heart as an alternative contrast medium.
Additionally, anatomic causes need to be investigated - these include mitral or tricuspid regurgitation, aortic or pulmonic stenosis, aortic or mitral insufficiency, and AV shunts. Also, one must consider possible PE or obstructive lung disease.
The underlying pathology tends to be some form of cardiomyopathy - either from ischemic damage or from dilation. Both have the effect of reducing the contractile abilities of the heart. The syndrome can also be caused by ventricular pressure overload (which may or may not in turn lead to dilation), such as from systemic (or pulmonary) hypertension or from valvular stenosis. The single most common cause of CHF is ischemia.Treatment:
In treating CHF, one must first assess volume status. Is the patient edematous? Are there lung sounds consistent with pulmonary edema (coarse crackles, rhonchi)? Are mucous membranes moist? Is there skin tenting? Is blood pressure stable, and WNL for this patient? Is heart rate WNL? Some patients may be using a Swann-Gantz catheter, which enables measurement of pulmonary arterial "wedge" pressure - a measurement that acts as a surrogate for right atrial pressure, which can help in interpretation of volume status.
If there are signs of fluid retention, initial treatment should generally be with a diuretic, followed by either an ACE inhibitor or a beta-blocker (the latter for NYHA class II or III - see below).
Although there is strong evidence that diuretics should be used in patients with CHF & signs of fluid retention, beware that there are potential pitfalls. Patients with pulmonic stenosis, for example, may be edematous, which will lead you to try to reduce preload (venous pressure on the atria - generally synonymous with fluid volume) for symptomatic relief. These patients may be "preload-dependent," however - meaning that they require high filling pressures in order to overcome the resistance of their stenotic valve, and use of a diuretic may reduce the heart's ability to compensate, resulting in shock. These patients need a reduction in afterload (the pressure against which the heart pumps - generally synonymous with systemic pressure, although not in this example), in this case by repair or replacement of their valve.
If there are no signs of fluid retention, treatment should begin with an ACE inhibitor &/or digoxin. Additional treatments should include beta-blocker for NYHA Class II-III, or Spironolactone for NYHA Class III-IV.
For acute (and emergent) pulmonary edema:
|Class||Official Description||Brief Description|
|I||Patients with cardiac disease but without resulting limitations of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation, dyspnea, or anginal pain.||No Sx, tolerates strenuous exercise|
|II||Patients with cardiac disease resulting in slight limitation of physical activity. They are comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnea, or anginal pain.||Dyspnea on strenuous exertion|
|III||Patients with cardiac disease resulting in marked limitation of physical activity. They are comfortable at rest. Less than ordinary physical activity causes fatigue, palpitation, dyspnea, or anginal pain.||Dyspnea on routine, light exertion|
|IV||Patients with cardiac disease resulting in inability to carry on any physical activity without discomfort. Symptoms of cardiac insufficiency or of the anginal syndrome may be present even at rest. If any physical activity is undertaken, discomfort is increased.||Dyspnea at rest|