Page 256 - Feline Cardiology

Chapter 19: Congestive Heart Failure 263

End cardiomyopathy) or secondary. Idiopathic DCM is an
systole Normal inherent defect within the myocardium that leads to
120 c Diastolic dysfunction myocardial failure. Causative defects may occur within
d
various regions of the cardiomyocyte, including the con-
tractile sarcomeric proteins (affecting actin-myosin
LV Pressure (mm Hg) production), cytoskeleton (disrupting the intracellular
cross-bridge cycling), mitochondria (impairing energy
80
and intercellular scaffold and impairing force transmis-
sion), nuclear envelope, and transcriptional coactivator
40
End b’ proteins (Maron et al. 2006). Secondary causes of myo-
diastole cardial failure include nutritional causes (taurine or car-
25 CHF nitine deficiency), and diseases that lead to chronic
a’ b
a pressure or volume overload of the ventricle (e.g., severe
aortic stenosis or ventricular septal defect, respectively),
1.5 5
and end-stages of other cardiomyopathies (e.g., HCM).
LV Volume (ml)
In cats, the only recognized cause of primary myocardial
Figure 19.4. Left ventricular pressure volume curve of a nor- failure is idiopathic DCM.
mal cat and a cat with hypertrophic cardiomyopathy and diastolic Systolic myocardial failure is characterized by
dysfunction. reduced myocardial contractility, which decreases
The pressure volume curve of a normal cat begins at end-systole stroke volume and cardiac output. Myocardial failure
(a [blue curve]). The left ventricle is compliant, with low pressure Congestive Heart Failure
at end-diastole (b). Isovolumetric contraction is represented from causes the tangent (Ees) of the left ventricular end-
points b to c, systole occurs from c to d, and isovolumetric relax- systolic pressure-volume relation to flatten and
ation occurs from points d to a. The left ventricle of a cat with increases end-systolic volume (Figure 19.5). Initially,
HCM or other disease causing severe diastolic dysfunction is stiff, end-diastolic volume is normal and end-systolic
and the end-diastolic pressure volume relation is shifted upward volume is increased, decreasing stroke volume. Cardiac
and to the left (dashed line: a’ to b’) with a high end-diastolic output decreases, which leads to arterial hypotension
pressure. End-systolic volume is decreased due to reduction in and activates the sympathetic nervous system. Beta
left ventricular wall stress, and end-diastolic volume (b’) is de- receptor stimulation increases heart rate and contrac-
creased due to left ventricular concentric hypertrophy encroach- tility, which increases cardiac output for a short time.
ing on the chamber lumen. The grey line represents the threshold Sympathetic nervous system activation increases arte-
for congestive heart failure (CHF); if the end-diastolic pressure (b’) riolar vasoconstrictor mediators, which normalize
is above this threshold, CHF is likely.
blood pressure, at the expense of increased afterload on
the failing heart. After 24–72 hours of adrenergic acti-
isoform switches in sarcomeric proteins in cats with dia- vation, the cardiac beta receptors undergo down-
stolic heart failure. regulation and uncoupling, and contractility decreases.
Myocardial hypertrophy, fibrosis, and myocyte disar- A more sustained compensatory mechanism is needed
ray (all hallmark histopathologic abnormalities in to increase cardiac output. Theoretically, vasodilation
HCM) increase myocardial stiffness, which shifts the LV and afterload reduction would allow the failing heart to
end-diastolic pressure volume relationship upward (i.e., increase stroke volume and cardiac output, but the
increases the slope of the diastolic filling curve). For any top cardiovascular priority is to maintain normal
given diastolic volume, the diastolic pressure in a stiff blood pressure. Instead, chronic compensation in
ventricle is greater (Figure 19.4). Once left ventricular myocardial failure occurs by increasing circulating
diastolic pressure exceeds 25 mm Hg, left heart failure blood volume and preload through activation of RAAS.
develops. Left ventricular concentric hypertrophy In response to increased preload, the left ventricle
decreases systolic wall stress, which decreases end- develops eccentric hypertrophy, which markedly
systolic volume and shifts the left ventricular pressure increases end-diastolic volume and dramatically shifts
volume curve to the left (Figure 19.4). Left ventricular the left ventricular pressure volume curve to the right
end-diastolic diameter is also decreased due to the (Figure 19.5). Stroke volume and cardiac output
encroachment of the chamber by the thickened ven- increase to near normal at the expense of a marked
tricular wall (Figure 19.4). increase in diastolic wall stress. End-systolic volume
and end-systolic wall stress are increased due to the
Systolic heart failure myocardial failure and systemic arteriolar vasoconstric-
Myocardial failure is defined as a decrease in myocardial tion. The final result is progressive myocardial failure
contractility and is either primary (i.e., idiopathic dilated (progressive flattening of Ees slope) and pathologic