8

Low Cardiac Output:

Pathophysiology and Treatment

Low cardiac output is often the rnost critical physiologic abnorrnality in the
cardiac surgery patient. The basic thrust of the surgeon should be to prevent
low cardiac output by proper preoperative preparation, excellent anesthesia,
precise surgery, rneticulous rnyocardial preservation, and proper postopera-
tive care. However, low cardiac output may exist in spite of proper periopera-
tive care. The deterrninants of low cardiac output rnust be understood and
the syndrorne properly treated to achieve a successful outcorne of surgery.
Recent advances have occurred in the understanding of the rnechanisrns of
low cardiac output and in the pharrnacologic and rnechanical rneans of irn-
proving cardiac output. This chapter reviews the determinants of cardiac
output and rnyocardial perforrnance and the rneans by which they can be
therapeutically rnanipulated, discusses the indications for institution of rne-
chanical circulatory support using the intraaortic balloon, and presents the
techniques of intraaortic balloon insertion.

Determinants of Cardiac Output

Cardiac output is the product of the stroke volurne of the heart and the heart
rate. Sorne irnprovernent in cardiac output can be achieved by increasing
heart rate alone. 2 However, in the presence of heart rates in the physiologic
range, substantial irnprovernent in cardiac output is achieved by increasing
stroke volurne.
The stroke volurne, or volurne of blood ejected each beat, is determined by
three factors: (1) preload of the ventricle, (2) afterload of the ventricle, and (3)
rnyocardial contractility. The preload of the ventricle is the diastolic volurne,
which is a function of the end-diastolic pressure and the compliance of the
rnyocardiurn. It is difficult to rneasure diastolic volurne or cornpliance in clini-
cal situations, so the filling pressure of the ventricle, or atrial pressure, is
used as the indicator of preload.
Afterload is irnpedance to left ventricular ernptying. The rnajor determi-
nants of irnpedance are arterial cornpliance and arteriolar resistance. Systemic
vascular resistance is an accurate indicator of afterload. Mean arterial blood
pressure can be an accurate reflection of afterload.
Myocardial contractility is the velocity, force, and extent of rnyocardial fiber
shortening. Both preload and afterload affect rnyocardial contractility, rnaking
it difficult to deterrnine accurately the contractile state of the intact hurnan
77

B. J. Harlan et al., Manual of Cardiac Surgery

© Springer-Verlag New York, Inc. 1995
78 Chapter 8. Low Cardiac Output: Pathophysiology and Treatment

heart, even with the sophisticated equipment of the cardiac catheterization

laboratory .
The most accurate methods of assessing myocardial contractility involve
intraventricular pressure measurements in association with ventriculogra-
phy.21,3O,33 Such methods are obviously impractical in the clinical setting, re-
quiring that the diagnosis of depressed myocardial contractility be made by
exclusion of other factors that may cause low cardiac output. Such factors
include hypovolemia, cardiac tamponade, excessive afterload, and possible
valve prosthesis malfunction.
Preload, afterload, and myocardial contractility can all be manipulated to
attain the maximum stroke volume and best level of cardiac output. Such
manipulations must be performed with knowledge of their effect on myocar-
dial oxygen supply/demand balance.

Manipulation of Preload
Preload can be increased by volume infusion or venoconstriction and de-
creased by diuresis, venodilatation, or increased stroke volume. The proper
left ventricular filling pressure postoperatively is determined by the preopera-
tive state of the ventricle, the operation, and other factors. Some ventricles
are stiff or noncompliant and require high filling pressures in order to attain a
satisfactory diastolic volume, such as the markedly hypertrophied ventricle
associated with aortic stenosis. The preoperative atrial and ventricular end-
diastolic pressures can indicate what pressure might be required in the post-
operative period in such a ventricle. In most hearts, however, filling pres-
sures should not exceed 15 mm Hg in either the right or left ventricle unless
preoperative evidence of decreased myocardial compliance is present. Filling
pressures over 15 mm Hg in hearts with normal compliance do not result in
improved cardiac output. 18
Hypovolemia is deficient preload and is a frequent cause of decreased
cardiac output following cardiac surgery. Hypovolemia is diagnosed by ab-
normally low atrial pressures and may by corroborated by absence of pulmo-
nary venous engorgement on chest x-ray. It is treated by volume replacement
and is usually the most easily treated cause of low cardiac output.

Manipulation of Afterload
Afterload reduction can improve cardiac output and myocardial performance
in the postoperative period. 1,6,19,22,42 Systemic vascular resistance is often ele-
vated following cardiopulmonary bypass. 28,34 Vasodilators reduce systemic
vascular resistance and improve cardiac output. Benzing and co-workers5
studied the effects of nitroprusside immediately after open heart surgery in
11 children who had a cardiac index below 2.0 Llmin/m2. Left atrial pressure
was maintained around 15 em H 20. During infusion of nitroprusside, sys-
temic vascular resistance decreased 54%, mean arterial pressure decreased
19%, and cardiac index increased 77%. Bixler and colleagues6 found improved
cardiac output following nitroprusside infusion in adult patients with postop-
erative left ventricular failure.
Drugs that improve myocardial contractility, such as dopamine, may be
combined with nitroprusside for further improvement in myocardial perfor-
mance. 27 When nitroprusside and dopamine are administered together for
treatment of severe chronic congestive heart failure, the increase in cardiac
output can be significantly greater than with either agent alone. 40