Ganong's Review of Medical Physiology, 23rd Edition

562
SECTION VI
Cardiovascular Physiology

to brief periods of straining (forced expiration against a closed
glottis: the
Valsalva maneuver
). Valsalva maneuvers occur
regularly during coughing, defecation, and heavy lifting. The
blood pressure rises at the onset of straining (Figure 33–8) be-
cause the increase in intrathoracic pressure is added to the
pressure of the blood in the aorta. It then falls because the high
intrathoracic pressure compresses the veins, decreasing venous
return and cardiac output. The decreases in arterial pressure
and pulse pressure inhibit the baroreceptors, causing tachycar-
dia and a rise in peripheral resistance. When the glottis is
opened and the intrathoracic pressure returns to normal, car-
diac output is restored but the peripheral vessels are constrict-
ed. The blood pressure therefore rises above normal, and this
stimulates the baroreceptors, causing bradycardia and a drop
in pressure to normal levels.
In sympathectomized patients, heart rate changes still
occur because the baroreceptors and the vagi are intact. How-
ever, in patients with autonomic insufficiency, a syndrome in
which autonomic function is widely disrupted, the heart rate
changes are absent. For reasons that are still obscure, patients
with primary hyperaldosteronism also fail to show the heart
rate changes and the blood pressure rise when the intratho-
racic pressure returns to normal. Their response to the Val-
salva maneuver returns to normal after removal of the
aldosterone-secreting tumor.

PERIPHERAL CHEMORECEPTOR REFLEX

Peripheral arterial chemoreceptors
in the
carotid and aortic
bodies
(Figure 33–2) have very high rates of blood flow. These
receptors are primarily activated by a reduction in partial pres-
sure of oxygen (PaO
2
), but they also respond to an increase in
the partial pressure of carbon dioxide (PaCO
2
) and pH.
Chemoreceptors exert their main effects on respiration; how-
ever, their activation also leads to vasoconstriction. Heart rate
changes are variable and depend on various factors, including

changes in respiration. A direct effect of chemoreceptor activa-

tion is to increase vagal nerve activity. However, hypoxia also

produces hyperpnea and increased catecholamine secretion

from the adrenal medulla, both of which produce tachycardia

and an increase in cardiac output. Hemorrhage that produces

hypotension leads to chemoreceptor stimulation due to de-

creased blood flow to the chemoreceptors and consequent

stagnant anoxia of these organs. Chemoreceptor discharge

may also contribute to the production of

Mayer waves.

These

should not be confused with

Traube–Hering waves,

which are

fluctuations in blood pressure synchronized with respiration.

The Mayer waves are slow, regular oscillations in arterial pres-

sure that occur at the rate of about one per 20–40 s during hy-

potension. Under these conditions, hypoxia stimulates the

chemoreceptors. The stimulation raises the blood pressure,

which improves the blood flow in the receptor organs and

eliminates the stimulus to the chemoreceptors, so that the pres-

sure falls and a new cycle is initiated.

DIRECT EFFECTS ON THE RVLM

When intracranial pressure is increased, the blood supply to

RVLM neurons is compromised, and the local hypoxia and

hypercapnia increase their discharge. The resultant rise in sys-

temic arterial pressure

(Cushing reflex)

tends to restore the

blood flow to the medulla and over a considerable range, the

blood pressure rise is proportional to the increase in intracra-

nial pressure. The rise in blood pressure causes a reflex de-

crease in heart rate via the arterial baroreceptors. This is why

bradycardia rather than tachycardia is characteristically seen

in patients with increased intracranial pressure.

A rise in arterial P

CO 2

stimulates the RVLM, but the direct

peripheral effect of hypercapnia is vasodilation. Therefore, the

peripheral and central actions tend to cancel each other out.

Moderate hyperventilation, which significantly lowers the

CO

2

tension of the blood, causes cutaneous and cerebral

FIGURE 33–8
Diagram of the response to straining (the Valsalva maneuver) in a normal man, recorded with a needle in the brachial
artery.
Blood pressure rises at the onset of straining because increased intrathoracic pressure is added to the pressure of the blood in the aorta. It
then falls because the high intrathoracic pressure compresses veins, decreasing venous return and cardiac output.
(Courtesy of M Mcllroy.)

Esophageal

pressure

(cm H 2 O)

Arterial

pressure

(mm Hg)

+ 40

0

200

0

− 40

Start Stop 10 s