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Pathophysiology of Heart Failure
Barret J. Bulmer, DVM, MS, DACVIM (Cardiology)

Tufts Veterinary Emergency Treatment & Specialties, Walpole, MA, USA

Heart failure represents a potential sequela of nearly all to propel blood from the right and left heart to the
congenital and acquired cardiac diseases in dogs and pulmonary and systemic circulations, respectively.
cats. Without an appropriate understanding of the Impaired mechanical function may occur with disor-
pathophysiologic alterations that produce heart failure, ders of the myocardium, cardiac valves, or pericardium.
and the knowledge of which therapies can successfully Effective filling and emptying, along with an appropri-
mitigate their consequences, veterinarians will be unable ate increase or decrease in the rate of contraction,
to treat this life‐impairing and often life‐threatening further rely on coordinated activity driven by pace-
condition. Therefore, the goals of this chapter are to maker cells within the sinoatrial (SA) node and the
highlight the classification schemes for heart failure, dis- heart’s conduction system. Therefore, perturbed
cuss normal cardiovascular physiology along with the systolic or diastolic function produced by alterations
mechanisms that contribute to the maladaptive hemody- in myocardial function, valvular integrity, pericardial
namic and neurohormonal alterations precipitating confinement, volume loading, increased resistance to
heart failure, and outline how understanding of these ejection or electrical instability may all produce cardiac
mechanisms leads to targeted medical therapy. dysfunction with subsequent development of heart
failure (Box 18.1).

Components of the Circulatory System Origin of Ventricular Contraction

The circulatory system is composed of the heart and its The electrical impulse that produces ventricular systole
associated arteries, capillaries, and veins. Appropriate begins within the SA node and propagates along the
function of the circulatory system further requires all of specialized conduction system and cell walls to produce
the constituents of normal circulating blood. The heart, atrial and ventricular myocyte depolarization. Calcium
blood vessels, and blood carry essential substances to influx through the L‐type calcium channels within the
metabolizing tissues and effectively remove unneeded sarcolemma along the T‐tubules contributes to a larger
by‐products of metabolism. Additional functions of the calcium release from the sarcoplasmic reticulum (so‐
circulatory system include regulation of body tempera- called calcium‐induced calcium release). The rise in
ture, humoral communication, and appropriate adjust- cytosolic calcium enhances binding to troponin‐C and
ments of blood delivery depending on the underlying enables configurational changes in the actin and myo-
physiologic condition. sin molecules so that cross‐bridge cycling (and hence
myocardial contraction during systole) can occur.
Diastole (myocardial relaxation) occurs as calcium
Determinants of Normal Cardiac influx through the L‐type calcium channel and release
Function from the sarcoplasmic reticulum terminate, and cal-
cium is resequestered by the sarco(endo)plasmic retic-
Mechanical function of the heart requires coordinated ulum calcium ATPase (SERCA) into the sarcoplasmic
filling of the cardiac chambers (diastolic function) reticulum. The fall in cytosolic calcium concentration
followed by an effective contraction (systolic function) during diastole results in inhibition of the interaction of

Clinical Small Animal Internal Medicine Volume I, First Edition. Edited by David S. Bruyette.
© 2020 John Wiley & Sons, Inc. Published 2020 by John Wiley & Sons, Inc.
Companion website: www.wiley.com/go/bruyette/clinical