Page 111 - Cardiac Nursing

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C HAPTER 3 / Regulation of Cardiac Output and Blood Pressure 87
Normal
flow C
■ Figure 3-14 (Right) The Krogh model divides the cir-t t 1
culation between two circuits, one compliant (C 1 ) and the
other noncompliant (C 2 ). (Left) The relation between the
t
t
change in organ venous volume and blood flow through a
compliant organ (C 1 ) and a noncompliant organ (C 2 ). The V C 2
volume of blood available to the heart is determined by the Venous volume
distribution of blood flow between such circuits. For exam-
ple, in hyperthermia there is increased blood volume in the
compliant vascular beds of the skin, and the amount of C 1
blood available to the heart is decreased. (From Rowell, C 2
L. B. [1986]. Human circulation: Regulation during physical
stress [p. 60]. New York: Oxford University Press.)
Organ blood flow
the diaphragm descends and intrathoracic pressure decreases and
intra-abdominal pressure increases. These pressure changes create VALSALVA MANEUVER
a gradient for blood flow from the point where the vena cava en-
ters the thoracic cavity to the right atrium and thereby increases ve- Extreme changes in intrathoracic pressure (Valsalva maneuver)
nous return to the heart. During expiration, the diaphragm relaxes also have potentially serious consequences for patients with car-
and intrathoracic pressure increases, whereas intra-abdominal pres- diovascular disease. The Valsalva maneuver, which is a deep breath
sure decreases. The increased intrathoracic pressure impedes tho- followed by straining to expire against a closed glottis, causes an
racic venous flow; however, there is an increase in blood flow from abnormal increase in intrathoracic pressure. The hemodynamic
the lower extremities. During mechanical ventilation, the relation response to the sudden increase in intrathoracic pressure associ-
between the respiratory cycle and venous return is reversed. 250 ated with the Valsalva maneuver can be subdivided into four
These ventilatory-induced changes in preload have been exploited phases 252–254 (Fig. 3-15). During the initial phase (phase 1: strain
to aid in determining if a patient will respond to a fluid bolus with phase), which is produced by forcefully exhaling against a closed
a clinically significant increase in stroke volume (see Chapter 21). glottis, there is a transient increase in arterial systolic and diastolic
As described by the Krogh model (Fig. 3-14), the relative dis- pressures due to aortic compression caused by increased intratho-
tribution of the cardiac output to compliant vascular beds racic pressure, and a marked decrease in venous return subsequent
(splanchnic—liver, gastrointestinal tract, pancreas, and the skin) to compression of the vena cava and a decrease in pulse pressure
and the remaining noncompliant vascular beds affects cardiac fill- and heart rate. During the remainder of the strain phase (phase 2),
ing pressures. 70,231,251 For example, the administration of an - there is a progressive decrease in blood pressure and cardiac out-
adrenergic agent to a patient who is vasodilated will cause vaso- put due to a decrease in venous return and left ventricular filling
constriction of vessels leading into compliant vascular beds (e.g., and stroke volume subsequent to compression of the vena cava.
splanchnic), which results in a passive collapse of the vascular bed The decrease in cardiac output and arterial pulse pressure, which
with translocation of blood into the central circulation and a sub-
sequent increase in blood return to the heart. However, a decrease
in blood flow to the splanchnic region is not risk-free; as decreased
gastrointestinal tract perfusion and ischemic bowel can occur if the 200
Heart rate
vasoconstrictor-induced decrease in flow is too great. Conversely,
MABP
the Krogh model is also useful for understanding the potentially Exp pressure
negative consequences of recreational hyperthermia (i.e., hot tub 150
or sauna) on coronary blood flow and cardiac output in a person
with coronary artery disease. With hyperthermia, the highly com-
pliant cutaneous vascular bed dilates, with up to 60% of the car- 100
diac output directed to the skin to facilitate heat dissipation. 67,73
Generally, the redistribution of blood volume does not compro-
mise oxygen delivery to vital organs. However, in individuals with b c
compromised coronary circulation, there is a potential for a de- 50
crease in blood volume available to the heart and a subsequent de-
crease in cardiac output and coronary artery perfusion. The effects
of environmental thermal stress plus exercise can also precipitate 0
problems. In this case, the ability to increase cardiac output is lim- a d e
ited by the decrease in central venous pressure and stroke volume, ■ Figure 3-15 The normal hemodynamic response to a Valsalva
which is caused by vasodilation of the cutaneous vascular bed and maneuver. Phase 1: a–b, phase 2: b–c, phase 3: c–d, and phase 4: d–e.
the subsequent large increase in venous volume. This finding has MABP, mean arterial blood pressure; Exp pressure, expiratory pressure.
important implications for exercise programs that are a part of car- (From Freeman, R. [1997]. Noninvasive evaluation of heart rate vari-
diac rehabilitation and highlights the need for control of ambient ability. In P. A. Low [Ed.], Clinical autonomic disorders [2nd ed., p. 302].
temperature to maximize the benefits of exercise. 70,99 Philadelphia: Lippincott-Raven.)