HF may occur in conditions where the heart is producing a normal cardiac output, but the metabolic needs of the tissues are increased, such as in hyperthyroidism or anemia, and so cardiac output fails to meet their needs. Thus, it may occur in conditions where the strength of the heart muscle appears normal.
However, most conditions that result in heart failure occur as a result of a markedly weakened left ventricle or right ventricle or both.
CHF occurs when the volume of blood presented to the heart is in excess of the heart's capacity to move it along. Consequently, fluid builds up behind the heart. If the inability to move the volume of blood forward is due to a left heart problem, then pulmonary venous congestion develops and later pulmonary edema. Subsequently this can lead to pleural effusion and abdominal effusion. If the abnormality lies in the right heart or the pulmonary arteries, wherein they limit the ability to move blood forward, then congestion occurs behind the right heart (causing pleural effusion and/or ascites).
Many but not all cases of heart failure also have congestive heart failure. Therefore, it is frequently useful to look for evidence of congestion to suggest the presence of heart failure.
MVO2 is increased when:
MVO2 is decreased when the opposite conditions occur.
The concept afterload is explained later.
Therefore, any situation that increases the myocardial oxygen consumption must also cause an increase in cardiac output and coronary flow (myocardial oxygen supply) or else demand for O2 will outstrip supply and anaerobic conditions will prevail. This anaerobic state results in less efficient cardiac performance (reduced contractility) and dysrhythmias which can result in a further reduction in cardiac output with further reductions in coronary flow (myocardial O2 supply). A vicious cycle occurs.
Therefore, preload is equal to venous return plus the residual volume left in the cardiac chamber after the last contraction.
Frank Starling Curves
The Frank Starling Curve shows that an increase in preload (end-diastolic volume) increases stroke volume. The Pressure-Volume Curve shows that as volume (preload) increases pressure in that chamber increases. As the pressure in the chamber rises so too does the intravascular pressure (hydrostatic pressure) of the vessels that feed into this chamber. As preload increases and so pressure continues to rise, a point will be reached at which the ventricular end-diastolic pressure is sufficiently elevated to force the intravascular fluid, in the vessels behind that chamber, to weep out into the interstitium that is adjacent to these vessels. If this occurs in the lungs, pulmonary edema results. The vertical line (in the figures) refers to a hypothetical point, such that preload levels to the right of the vertical line promote the extravasation of fluid out of the capillaries into the interstitium (pulmonary edema if we are referring to left ventricular preload). Note also, however, that as preload falls (moving to the left along the curves) the forces that promote pulmonary edema are abolished.
An increase in preload also increases afterload as the volume of the chamber increases (the concept afterload will be discussed later).
The figure on the left shows two left ventricular function curves. Note how an increase in preload causes a marked increase in stroke volume for the normal heart but only a modest increase in stroke volume for the failing left ventricle. Conversely, reductions in preload cause a marked fall in stroke volume for the normal heart but only a modest reduction in stroke volume for the failing heart. Therefore, a marked reduction in preload in the heart failure setting will result in a resolution of pulmonary edema with only a modest reduction in stroke volume (but then these patients can't afford a marked reduction in SV).
a) Excessive left ventricular preload may show
b) Excessive right ventricular preload may show
Afterload is affected mainly by:
Afterload is increased by:
Afterload is decreased by the opposite changes.
An increase in afterload also increases myocardial oxygen consumption. A reduction in afterload has the opposite effect.
The ability to improve cardiac output by reducing afterload represents one of the major advances in cardiovascular therapeutics in the last 25 years.
Therefore, if we can infer a fall in cardiac output on physical examination, we can expect a rise in arterial resistance and therefore afterload. And so, a fall in cardiac output (and resultant rise in afterload) is inferred by the following possible findings on physical examination: (these all indicate reduced CO)
Unfortunately, to directly measure a fall in cardiac output usually requires pulmonary artery catheterization, which is not commonly performed in small animals. Therefore, we are continually looking for indirect evidence of a change in cardiac output.
An increase in contractility results in:
As contractility falls one can anticipate the opposite effects.
As contractility increases the Frank-Starling function curve shifts upward and to the left. The opposite occurs with a reduction in contractility.
The best diagnostic aid to detect a change in contractility is the echocardiogram (cardiac ultrasound examination).
Increases in HR cause an increase in cardiac output. This becomes self limiting because when HR is excessive cardiac output falls due to:
If a normal heart is forced to beat at 250 bpm, it will be in heart failure in 3-4 weeks and the patient dies in 4-5 weeks.
Reduced distensibility of right ventricle or right atrium - may show evidence of right heart congestion:
Comments: Note how this looks like elevated preload in the adjacent upstream chamber. In fact, reduced distensibility causes a form of elevated preload in the adjacent upstream chamber.
Pulse deficits (the absence of a peripheral arterial pulse induced by the heart beat) may be detected if the cardiac rhythm is irregular. Pulses of greatly variable intensity may also be noted.
The electrocardiogram is the best diagnostic aid to identify and verify these abnormalities. For intermittent arrhythmias, a Holter recording may be required.
a) Increase in sympathetic tone - resulting in:
ACE = angiotensin converting enzyme
ADH = antidiuretic hormone
b) Redistribute cardiac output to coronary and cerebral vascular beds and away from:
c) Increased thirst - causing fluid overload (increasing preload).
d) Increased arginine vasopressin (ADH) resulting in:
Comments: The net effect of these compensatory measures usually has deleterious effects on cardiac performance chronically.
Comment: These factors support arterial blood pressure but increase afterload, which further aggravates the failing heart.
Comment: We are only just beginning to recognize the presence of vasodilator mechanisms in the setting of heart failure. Some of these endogenous protective mechanisms become blunted in heart failure thus rendering them relatively ineffective (such as atrial natriuretic factor). In general, the vasodilator mechanisms are overwhelmed by the vasoconstrictor mechanisms in heart failure. This promotes the relentless progression of heart failure.