Page 106 - Cardiac Nursing

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82 PA R T I / Anatomy and Physiology
which had maximal cardiac function occurring at an sarcomere between actin and myosin filaments. In the intact heart, a change
length where there was optimal overlap of actin and myosin. 179 in contractility is defined as an alteration in cardiac performance
that is independent of preload and afterload. An increase in con-
tractility results in greater magnitude and velocity of shortening
Afterload
and augmented stroke volume. Contractility, which reflects the
In muscle fiber experiments, preload is the tension in the muscle availability of calcium to the myofilament and sensitivity of the
before contraction and afterload is the additional tension that myofilament to calcium, can be increased by an increase in circu-
must develop in the muscle during contraction before shortening lating epinephrine and norepinephrine released from cardiac sym-
occurs. 173,180 At the level of the ventricle, afterload is defined as pathetic nerves, and by a decrease in the interval between beats
ventricular wall tension during the shortening phase of contrac- (increasing heart rate), a phenomenon known as the Bowditch
tion and reflects the sum of the forces against which the ventricle treppe (staircase) effect. 185,186 There is also an important relation-
must act to eject blood. However, given the heterogeneous direc- ship between heart rate and -adrenergic stimulation and my-
tion of myocardial fibers and the torsion or twisting of the ventri- ocardial contractility, with the effects of -adrenergic stimulation
cle during systole, a single measure of ventricular wall tension is expressed only when there is a concomitant increase in heart rate
inadequate to define afterload. In the intact system in vivo, after- (positive force–frequency relation). 187 The positive force–frequency
load is defined as the pressure in the aorta during systole. 181 The relation is considered the fourth intrinsic factor influencing my-
aortic blood pressure is essentially equal to left ventricular pressure ocardial contractility, along with length-dependent activation, basal
during the ejection phase of systole; thus, these values are inter- force frequency effect, and direct positive inotropic effect of my-
changeable. The key factors that affect aortic blood pressure dur- ocardial -adrenergic receptor stimulation. 182 Clinically, loss of the
ing ejection are arterial compliance, arterial resistance, and the re- force–frequency relationship during heart block and downregula-
flection of pulse waves from the periphery. tion of -adrenergic stimulation during heart failure contributes to
As described by the force–velocity relation, for any given pre- impaired cardiac function. 185,186 In patients with diastolic dysfunc-
load there is an inverse relation between afterload and muscle tion, the positive force–frequency relation is maintained, whereas
shortening, and thus stroke volume. 182 Although this relationship the positive force–relaxation relation is impaired, resulting in de-
is observed in the isolated muscle fiber, it is not clinically appar- creased stroke volume with increasing heart rate. 188
ent in people with normal cardiac function. 168 However, in indi-
viduals with a chronically depressed inotropic state (e.g., heart
failure, cardiomyopathy), a steady state with altered ventricular EXTRINSIC CONTROL:
dimensions (hypertrophy, dilatation) and maximal use of the PERICARDIAL LIMITATION
length–tension relation occurs. Therefore, in these people in
the face of an increase in afterload, the reserve provided by the Under normal resting conditions, the pericardium has little or no
length–tension relationship is exhausted and stroke volume de- effect on cardiac filling; however, during acute increases in cardiac
creases acutely. 183,184 These findings help to explain the use of volume, the pericardium affects ventricular interaction and plays
afterload-reducing agents in patients with heart failure. a role in the compensatory increase or decrease in stroke volume
In clinical practice, systemic vascular resistance, which is often between the two ventricles. 189 Additionally, in the face of in-
considered the indicator of afterload, is used interchangeably with creased filling pressures, the pericardium restricts cardiac filling,
afterload. This conceptualization is incorrect because afterload can which is important in preventing excessive dilation during acute
change independently of vascular resistance. For example, in a pa- increases in cardiac volume. 190 Under conditions of acute failure,
tient who has experienced a severe hemorrhage, despite the fact the pericardium augments ventricular interaction with decreased
that the systemic vascular resistance is increased (often to ex- stroke volume. 191,192 In chronic cardiac dilation, however, there is
treme), afterload is actually decreased. Recalling the original defi- growth of new pericardial tissue or slippage of the collagen fibers,
nition of afterload as the additional tension that develops in the and the pericardium actually enlarges in size and mass. As a result
muscle during contraction before shortening occurs helps to clar- of this pericardial distortion or remodeling, there is limited in-
ify this area of confusion. The tension or stress that develops in crease in pericardial constraint in chronic cardiac dilation. 193,194
the ventricular wall according to the Laplace relation is: After pericardiectomy there is an increase in the maximal car-
diac output, O 2 consumption, and left ventricular end-diastolic
PR
T segment length. 195 The increase in cardiac output is caused by an
2h
increase in stroke volume, which is caused by an increase in end-
where T is average circumferential wall stress (force/cross-sectional diastolic volume and myocardial fiber length, as described by the
area), P is intraventricular pressure, R is the radius of curvature of Frank–Starling law of the heart. 196 However, the effects of peri-
the wall, and h is wall thickness. In hemorrhage, the radius of the cardiectomy on stroke volume and cardiac output are apparent
ventricle is decreased, and if the compensatory actions of in- only during exercise. 195,197
creased heart rate and systemic vasoconstriction are inadequate to Cases in which the pericardium has been opened and reap-
maintain pressure, the intraventricular pressure also decreases. proximated, pericardial constraint increases because of develop-
Thus, despite an increase in systemic vascular resistance, ventric- ment of adhesions between the pericardium and the heart. 198 The
ular afterload decreases. increased constraint is manifested as an increase in intraventricu-
lar pressure for any given volume, which reflects an increase in
Contractility juxtacardiac pressure. 199 Consideration of the increased juxtacar-
diac pressure is important in the interpretation of hemodynamic
Contractility refers to the intrinsic properties of cardiac myocytes data (increased pressure for any given volume) in postcardiac sur-
that reflect the activation, formation, and cycling of crossbridges gery patients who have had pericardial reapproximation.