Page 257 - Feline Cardiology

264 Section G: Congestive Heart Failure

Normal Normal
Chronic myocardial failure End Patent ductus arteriosus
End Acute myocardial failure systole
systole
120 c 120 Ees d c’
Ees d d’ c
LV Pressure (mm Hg) 80 d’ c’ LV Pressure (mm Hg) 80

End
40
diastole End
b’ 40 diastole b’
25 b CHF
a a’ 25 b CHF
a a’
1.5 5 10 15 f
LV Volume (ml) 1.5 5 10 15
Figure 19.5. Left ventricular pressure volume curve of a normal LV Volume (ml)
cat and a cat with dilated cardiomyopathy. The pressure volume Figure 19.6. The pressure volume curve of a normal cat (blue
Congestive Heart Failure The slope of the end-systolic pressure volume relation line (Ees) to right shunt causes severe left ventricular volume overload (in-
curve of a normal cat (blue line) is contrasted with the pressure
line) is contrasted with the curve of a cat with a large left to
volume curve of a cat with acute myocardial failure (green line).
right shunting patent ductus arteriosus (red line). The large left
represents contractility, and it is decreased with myocardial fail-
creased end-diastolic volume, b′). There is secondary myocardial
ure, which initially shifts the pressure volume curve downward
failure, which decreases Ees and increases the end-systolic vol-
and to the right. Acute myocardial failure causes a decrease in
ume (d′). The stroke volume (a′ to b′) remains high due to the
systolic pressure (c′) and hypotension, as well as increased end-
marked volume overload and only mild myocardial failure. The
systolic volume (d′) since less blood is ejected out during systole.
Stroke volume is decreased (a′ to b′) and cardiac output falls,
steeper slope of the normal end-diastolic pressure volume rela-
leading to arterial hypotension. Due to chronic compensatory left ventricular pressure volume curve is shifted rightward, on the
tion (dashed line), leading to congestive heart failure.
mechanisms of heart failure, chronic myocardial failure (red line)
is illustrated by marked chamber enlargement (eccentric hyper-
trophy and increased end-diastolic volume), marked increase in
end-systolic volume, decreased Ees, and normalized stroke vol- reach the arterial circulation in its entirety. The reduced
ume. The left ventricular pressure volume curve is shifted right- cardiac output triggers RAAS to increase sodium and
ward, on the steeper slope of the normal end-diastolic pressure water reabsorption, which increases circulating blood
volume relation (dashed line); elevated end-diastolic pressures volume and ventricular preload (i.e., diastolic wall
are above threshold (grey line) and consistent with congestive stress). The left ventricular response to increased dia-
heart failure. stolic wall stress is to replicate sarcomeres end-to-end
and grow a larger left ventricular chamber. End-diastolic
volume greatly increases, and forward stroke volume
ventricular remodeling with progressive ventricular normalizes (Figure 19.6). Total stroke volume is very
enlargement. high, because systolic function is normal and the end-
systolic volume is normal. This creates a high ejection
Left ventricular volume overload and fraction, and wall motion appears hyperdynamic. Left
heart failure ventricular diastolic pressure increases secondary to the
Diseases that cause left ventricular volume overload volume overload, and pulmonary edema (±pleural effu-
include abnormalities of the mitral valve (mitral valve sion in cats) develops once the diastolic pressure exceeds
dysplasia, myxomatous degeneration, infective endocar- 25 mm Hg. Secondary myocardial failure may develop
ditis, or systolic anterior motion of the mitral valve), left when there is chronically increased wall stress from
to right shunting congenital heart diseases (e.g., patent severe volume overload of the left ventricle, especially in
ductus arteriosus or ventricular septal defect), or aortic animals with a patent ductus arteriosus or aortic insuf-
valve insufficiency. A quantity of total stroke volume is ficiency (Figure 19.6). Myocardial failure causes an
lost either backward into the left atrium (regurgitant increase in end-systolic volume, which normalizes the
volume), or in left to right shunting cardiac defects such previously high ejection fraction and decreases stroke
as a PDA it is lost into the pulmonary artery, which volume. Myocardial failure is evidenced as a rightward
decreases effective forward stroke volume. That is, the shift of the left ventricular pressure volume curve and
full volume of blood that leaves the ventricle does not flattening of the Ees slope of the left ventricular end-