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Cardiogenic Shock
1
Nathan Peterson, DVM, DACVECC and James W. Barr DVM, DACVECC 2
1 VCA West Los Angeles Animal Hospital, Los Angeles, CA, USA
2 BluePearl Veterinary Partners, Tampa, FL, USA

Pathophysiology Since stroke volume is one of two determinants of
cardiac output (cardiac output = heart rate × stroke vol-
Cardiogenic shock occurs when oxygen delivery is insuf- ume), a decrease in inotropy will reduce cardiac output
ficient to maintain normal aerobic cellular metabolism in a direct fashion unless compensation occurs by
as a result of cardiac dysfunction in the presence of ade- increasing heart rate. Perceived ventricular dysfunction
quate intravascular volume. In other words, cardiogenic also occurs when there is a sudden change in valvular
shock occurs when cardiac output is decreased despite integrity resulting in an acute increase in regurgitant
adequate blood volume. Importantly, cardiogenic shock fraction and decrease in cardiac output. If this occurs, a
does not imply congestive heart failure (CHF) although large portion of the ventricular load is directed back-
CHF can be present in cardiogenic shock patients. wards through the atrioventricular valve rather than the
Cardiogenic shock occurs in two settings. Forward semilunar valves of the aorta or main pulmonary artery.
failure results from the heart’s inability to adequately Although this occurrence is uncommon in the general
pump blood forward from either the left or right ventri- population, animals that have existing degenerative val-
cle into either the aorta or main pulmonary artery vular disease are at an increased risk of suffering rupture
respectively. Backward failure, on the other hand, results of one or more of the chordae tendinae.
from inadequate ventricular filling of the heart during Bradycardia is an uncommon cause of forward failure
diastole with a subsequent reduction in stroke volume and cardiogenic shock but can occur with third‐degree
and cardiac output. Common conditions resulting in atrioventricular block. This condition results in dimin-
forward failure of the heart include rupture of one or ished cardiac output as a result of drastic reduction in
more chordae tendinae or acute‐onset severe pulmonary heart rate (the other main determinant of cardiac out-
hypertension. Causes of backward failure include parox- put). Regardless of the inciting cause of forward failure,
ysmal ventricular tachycardia or pericardial tamponade. the end‐result is an increase in the end‐diastolic ventric-
Cardiogenic shock is somewhat different from other ular volume with subsequent increases in atrial volumes
forms of shock due to the greater potential impact on the and pressures. Cardiogenic shock from forward failure
myocardium. When cardiac dysfunction underlies the states is often exacerbated by development of pulmonary
development of shock, coronary perfusion is often edema and hypoxemia.
impaired as a result of increased right‐sided pressures or Backward failure results from diseases that cause
decreased aortic root pressure. Because of the potential decreased ventricular volume at end‐diastole. Since the
for decreased coronary perfusion and subsequent volume of blood pumped out of the heart is dependent
ischemic myocardial injury, it is imperative that cardio- on the volume of blood present at the beginning of the
genic shock is recognized early and treated aggressively. cardiac cycle, it follows that any decrease in this volume
When ventricular function or efficiency is acutely will result in diminished cardiac output. The Frank
diminished, cardiac output declines rapidly. If ventricu- Starling law of the heart states that the greater the vol-
lar dysfunction is a result of systolic myocardial failure ume of the ventricle at end‐diastole, the more forceful
(as seen with dilated cardiomyopathy), the force of the corresponding contraction has to be to meet the
ventricular contractions (inotropy) is not sufficient to demand for greater output, effectively tying preload
eject a normal volume of blood from the ventricles. (end‐diastolic volume) to cardiac output.

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