Ganong's Review of Medical Physiology, 23rd Edition

512
SECTION VI
Cardiovascular Physiology

The strength of the pulse is determined by the pulse pressure
and bears little relation to the mean pressure. The pulse is weak
(“thready”) in shock. It is strong when stroke volume is large;
for example, during exercise or after the administration of his-
tamine. When the pulse pressure is high, the pulse waves may
be large enough to be felt or even heard by the individual (pal-
pitation, “pounding heart”). When the aortic valve is incompe-
tent (aortic insufficiency), the pulse is particularly strong, and
the force of systolic ejection may be sufficient to make the head
nod with each heartbeat. The pulse in aortic insufficiency is
called a
collapsing, Corrigan,
or
water-hammer pulse.
The
dicrotic notch,
a small oscillation on the falling phase
of the pulse wave caused by vibrations set up when the aortic
valve snaps shut (Figure 31–3), is visible if the pressure wave
is recorded but is not palpable at the wrist. The pulmonary
artery pressure curve also has a dicrotic notch produced by
the closure of the pulmonary valves.

ATRIAL PRESSURE CHANGES

& THE JUGULAR PULSE

Atrial pressure rises during atrial systole and continues to rise
during isovolumetric ventricular contraction when the AV
valves bulge into the atria. When the AV valves are pulled down
by the contracting ventricular muscle, pressure falls rapidly and
then rises as blood flows into the atria until the AV valves open
early in diastole. The return of the AV valves to their relaxed po-
sition also contributes to this pressure rise by reducing atrial ca-
pacity. The atrial pressure changes are transmitted to the great
veins, producing three characteristic waves in the record of jug-
ular pressure (Figure 31–3). The
a wave
is due to atrial systole.
As noted above, some blood regurgitates into the great veins
when the atria contract. In addition, venous inflow stops, and the
resultant rise in venous pressure contributes to the a wave. The
c
wave
is the transmitted manifestation of the rise in atrial pres-

sure produced by the bulging of the tricuspid valve into the atria

during isovolumetric ventricular contraction. The

v wave

mir-

rors the rise in atrial pressure before the tricuspid valve opens

during diastole. The jugular pulse waves are superimposed on

the respiratory fluctuations in venous pressure. Venous pressure

falls during inspiration as a result of the increased negative intra-

thoracic pressure and rises again during expiration.

HEART SOUNDS

Two sounds are normally heard through a stethoscope during

each cardiac cycle. The first is a low, slightly prolonged “lub”

(first sound),

caused by vibrations set up by the sudden clo-

sure of the AV valves at the start of ventricular systole (Figure

31–3). The second is a shorter, high-pitched “dup”

(second

sound),

caused by vibrations associated with closure of the

aortic and pulmonary valves just after the end of ventricular

systole. A soft, low-pitched

third sound

is heard about one

third of the way through diastole in many normal young indi-

viduals. It coincides with the period of rapid ventricular filling

and is probably due to vibrations set up by the inrush of blood.

A

fourth sound

can sometimes be heard immediately before

the first sound when atrial pressure is high or the ventricle is

stiff in conditions such as ventricular hypertrophy. It is due to

ventricular filling and is rarely heard in normal adults.

The first sound has a duration of about 0.15 s and a fre-

quency of 25 to 45 Hz. It is soft when the heart rate is low,

because the ventricles are well filled with blood and the leaflets

of the AV valves float together before systole. The second sound

lasts about 0.12 s, with a frequency of 50 Hz. It is loud and

sharp when the diastolic pressure in the aorta or pulmonary

artery is elevated, causing the respective valves to shut briskly at

the end of systole. The interval between aortic and pulmonary

valve closure during inspiration is frequently long enough for

the second sound to be reduplicated (physiologic splitting of

the second sound). Splitting also occurs in various diseases.

The third sound, when present, has a duration of 0.1 s.

MURMURS

Murmurs,

or

bruits,

are abnormal sounds heard in various

parts of the vascular system. The two terms are used inter-

changeably, though “murmur” is more commonly used to de-

note noise heard over the heart than over blood vessels. As

discussed in detail in Chapter 32, blood flow is laminar, non-

turbulent, and silent up to a critical velocity; above this veloc-

ity and beyond an obstruction, blood flow is turbulent and

creates sounds. Blood flow speeds up when an artery or a heart

valve is narrowed.

Examples of vascular sounds outside the heart are the bruit

heard over a large, highly vascular goiter, the bruit heard over

a carotid artery when its lumen is narrowed and distorted by

atherosclerosis, and the murmurs heard over an aneurysmal

dilation of one of the large arteries, an arteriovenous (A-V)

fistula, or a patent ductus arteriosus.

TABLE 31–1
Variation in length of action potential
and associated phenomena with cardiac rate.
a

Heart

Rate

75/min

Heart

Rate

200/min

Skeletal

Muscle

Duration, each cardiac cycle 0.80 0.30 ...

Duration of systole 0.27 0.16 ...

Duration of action potential 0.25 0.15 0.007

Duration of absolute refractory

period

0.20 0.13 0.004

Duration of relative refractory

period

0.05 0.02 0.003

Duration of diastole 0.53 0.14 ...

a
All values are in seconds.
Courtesy of AC Barger and GS Richardson
.