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Heart Failure
Outline
A. Background
a. C.O. = HR x SV
1. C.O. = cardiac output, amount of blood the heart pumps each minute, approx. = 5- 7 liters in an adult
2. HR = heart rate
3. SV = stroke volume, amount of blood pumped from the ventricle with each contractionb. ejection fraction = the percentage of blood emptied from the ventricle with each contraction. For example, the ventricle fills with140 ml of blood, 90 ml is pumped forward (50 ml remains in the ventricle), hence the ejection fraction is 90/140 = 63%
c. preload - volume of blood in ventricle at the end of diastole, also called left ventricular end diastolic pressure (LVEDP).
N.B. for all practical purposes the volume translates into a pressure, the greater the volume, the greater the pressure in the ventricle.d. afterload- the force the ventricle must develop to eject blood into the circulatory system
e. Starlings Law- as preload increases stroke volume increases because the heart muscle displays a greater contractility (up to a point). Beyond that point further increases in preload do not result in further increases in stroke volume, stroke volume may actually decrease.
B. Descriptions of Heart failure
1. high output failure vs low output failure
a. high output failure- uncommon, increased cardiac output but still inadequate to meet the metabolic demands of the tissue because of excessive increased metabolic demand. For example, as occurs in thyrotoxicosis.
b. low output failure - decreased cardiac output due to decreased pumping ability of heart
2. Systolic vs Diastolic failure a.systolic failure - impaired ejection of blood from heart during systole- due to decrease in contractility, low ejection fractions (< 45%), often result of CAD or MI
b. diastolic failure - impaired filling of the heart during diastole because of smaller ventricular chamber size. Causes - aging, mitral stenosis,increased ventricular wall size, elevated filling pressures, ejection fractions typically higher than 45%, often result of HTN
c. most people with heart disease have a combination of systolic and diastolic, in both cases, though, cardiac output decreased.
3. Right sided vs Left sided heart failure a. right sided failure- causes edema in peripheral tissues and visceral congestion, may result from pulmonary failure or progression of left sided failure
b. left sided heart failure- most common, causes pulmonary congestion
C. Congestive Heart Failure
1. general definition- inability of heart to pump an adequate supply of blood, i.e. inability to maintain an adequate cardiac output.
2. Three Categories (grouped by etiology)
a. Conditions that result in direct damage to heart (i.e. decreased contractility of fibers)
1. MI
2. myocarditis
3. CAD
4. ventricular aneurysm
b. Conditions that result in ventricular overload
1. increases in preload due to mitral or aortic regurgitation atrial or ventricular septal defects or hypervolemia
2. increases in afterload due to aortic or pulmonary valve stenosis, systemic hypertension pulmonary hypertension
c. Conditions that lead to constriction of ventricle
1. cardiac tamponade
2. constrictive cardiomyopathies
3. pericarditis
D. Compensatory Mechanisms (in an effort to maintain cardiac output)
1. increased SNS activity
2. activation of renin angiotensin system (see diagram in lecture on hypertension)
3. myocardial hypertrophy
4. release of atrial natriuretic peptide (ANP or atriopeptin) -released
from atrial cells in response to increased stretch and pressure. This
hormone produces rapid and transient natriuresis, diuresis and
moderate loss of potassium in urine.
Discussion
Symptoms of congestive heart failure are related to the two major pathophysiological events: decreased cardiac output and increased pressure in the left ventricle. The increased pressure in the ventricle is either because there is an increased filling pressure (diastolic dysfunction) or because there is an increased preload (systolic dysfunction) ( the heart can't pump the blood forward so it becomes congested in the ventricle- remember volume quickly translates into pressure). When pressure increases in the ventricle (congestion) it becomes harder for the lungs to return blood to the left side of the heart, so it backs up in the lungs, increasing volume and hence pressure in the lungs. When the pressure of blood in the capillaries of the lungs increases (increased hydrostatic pressure), plasma can be pushed out into the surrounding tissue causing pulmonary edema. The effect may be positional- because gravity can help to overcome the tendency for pressure to increase in the lungs by pulling down towards the heart when the person is standing- in other words gravity counteracts increased hydrostatic pressure. So when standing the person experiences no shortness of breath or dyspnea (consequence of pulmonary edema). However, when the person lies down, the effect of gravity to pull blood into the heart is negated, hydrostatic pressure is unopposed and edema results. The patient experiences positional dyspnea or orthopnea. As congestive heart failure progresses the congested lungs soon make it difficult for the right ventricle to pump blood into the lungs, so the right ventricle becomes congested. Gravity may affect distribution of fluids in other parts of the body Hence when the person is standing, dependent edema results, (in this case the ankles are below the heart) and so the veins in order to return blood to the heart have to overcome gravity by pumping against it. When they lie down or elevate their legs, the edema disappears (now gravity helps drain blood to the heart). When they lie down, fluid in the lower extremities returns to the circulation and may lead to increased urinary output, hence nocturia is a frequent symptom. The reduced cardiac output results in fatigue and weakness, possibly cyanosis .
Clinically
Digoxin, because of its positive inotropic effect, is a logical choice for treatment of CHF. (By improving contractility, you can enable the heart to pump more blood forward, relieving the congestion and increasing the cardiac output). Combine this with a diuretic and you would seem to have a winning combination. A diuretic basically interferes with the renin angiotensin system by inhibiting the kidneys re-absorption of sodium (again, remember, in a compensatory effort to increase cardiac output the body activated the renin angiotensin system but this, in a sense, backfires because by pulling more fluid into the intravascular compartment, it only increases preload and further aggravates the situation). Of course, if you use a diuretic such as Lasix in combination with digoxin, you create a potentially dangerous situation. Lasix causes the wasting of potassium, and the resultant hypokalemia can easily lead to dig toxicity. The preferred choice for treatment of CHF, according to newer protocols, is the use of an ACE inhibitor. An ACE inhibitor works by upsetting the renin angiotensin loop and by preventing the vasoconstriction associated with Angiotensin II. The resultant vasodilation can decrease afterload and thus make it easier for a diseased heart to pump blood forward, thus relieving the congestion and improving cardiac output.