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C HAPTER 3 / Regulation of Cardiac Output and Blood Pressure 89
■ Figure 3-17 Summary of how the arterial baroreflex restores
blood pressure back toward normal during arterial hypotension. Cor-
rection is by relatively slow (5 to 15 seconds) vasoconstriction. In- ■ Figure 3-18 Summary of how the arterial baroreflex restores
creased heart rate has little or no effect if cardiac filling pressure is low blood pressure back toward normal after sudden hypertension. Cor-
and cardiac output cannot be increased, for reasons illustrated in the rection is rapid and achieved by immediate vagal activation and re-
small graph next to “cardiac output” (central venous pressure vs. car- duced heart rate and cardiac output. Release of tonic vasoconstriction
diac output). When normal (N) cardiac output increases, central ve- is slow and has a minimal effect because only skeletal muscle has sig-
nous pressure falls. When both cardiac output and central venous nificant tonic vasoconstriction to be withdrawn in resting humans.
pressure are low during hemorrhage (H), cardiac output cannot rise (From Rowell, L. B. [1993]. Human cardiovascular control [p. 58.].
much without collapsing central veins as central venous pressure goes New York: Oxford University Press.)
to 0. (From Rowell, L. B. [1993]. Human cardiovascular control
[p. 57]. New York: Oxford University Press.)
Arterial Baroreceptor Response to The rapid baroreflex response is extremely important in the
Increased Arterial Pressure protection of the cerebral vessels 272 . An impaired baroreflex re-
An acute increase in blood pressure results in increased stimula- sponse can be observed in patients after a stroke, where over 70%
tion of the sinoaortic baroreceptors. The increased baroreceptor- of these individuals exhibit increased blood pressure. 273 There is
firing rate increases sinus and vagal afferent input into the nucleus also a decrease in baroreflex-mediated buffering with aging, 162,274
tractus solitarius of the medulla (see Figs. 3-1 and 3-3). In which may place older individuals at increased risk for the nega-
response to the increased baroreceptor input, the following occur tive effects of blood pressure perturbations. Of clinical impor-
(Fig. 3-18): tance, older individuals may have an altered response to vasoactive
medications, such as greater blood pressure response to any given
1. A rapid (within one beat) decrease in heart rate, secondary to a 162,275–277
does of nitroprusside.
sudden increase in vagal tone.
2. A secondary decrease in stroke volume due to the negative in-
otropic effects of the increased vagal tone (minor effect). REFE R E NC ES
3. A sympathetic nervous system-mediated decrease in vascular
1.Scher, A. (1989). Cardiovascular control. In H. Patton, A. Fuchs, B.
tone (minor effect).
Hille, et al. (Eds.), Textbook of physiology. Circulation, respiration, body
The net result or this response is a decrease in heart rate, with a fluids, metabolism, and endocrinology (pp. 972–990). Philadelphia: WB
Saunders.
subsequent decrease in cardiac output and blood pressure. The 2.McMahon, N. C., Drinkhill, M. J., Myers, D. S., et al. (2000). Reflex
most important point is that the response, which occurs within responses from the main pulmonary artery and bifurcation in anaes-
one beat, is mediated by a vagally induced decrease in heart rate thetised dogs. Experimental Physiology, 85, 411–420.
and cardiac output. 271 Passive vasodilation due to a decrease in 3. Minisi, A. J. (1998). Vagal cardiopulmonary reflexes after total cardiac
deafferentation. Circulation, 98, 2615–2620.
sympathetic tone occurs only in the skeletal muscles, and thus 4. Hainsworth, R. (1995). Cardiovascular reflexes from ventricular and
does not contribute greatly to the sudden lowering of arterial coronary receptors. Advances in Experimental Medicine and Biology, 381,
blood pressure. 70 157–174.

