Carotid Artery Palpation
External pressure on carotid artery may
slow HR
 Due to direct stimulation of barorecptor in
carotid artery
 Still appropriate site to measure HR during
ex.
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Cortical Input
Impulses from cerebral cortex pass via
small afferent nerves through CVC in
medulla
 Allows emotional state to influence CV
response
 Impulses cause HR to rise rapidly prior to
ex. (anticipatory HR)
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Probably due to increase in sympathetic
discharge and a decrease in vagal tone
Magnitude of increase is greatest in short
sprint events and lower in longer events
Represents a 74% increase of HR during a
60 yd sprint
Large portion of HR adjustment to exercise
reflects the cortical input that occurs during
initial stages of activity
Receptors in joints and muscles (muscle
afferents) probably provide a large amount of
input to increase HR during initial stages as
well
Heart as a pump
increase HR  increase in SV;
limitations
Once HR reaches a certain level,
strength of contraction decreases,
may be due to overuse of
substrates in cardiac muscle
Period of diastole is so short,
cannot fill adequately
with artificial stimulation: peak ability to
pump blood is 100-150 bpm
 with sympathetic stimulation: increase HR
and strength of contraction peak ability:
170-220 bpm
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Cardiac Contractility
ΔP/ Δt: rate of change of ventricular
pressure with respect to time
 way to assess the strength of the
contraction of the heart
 as ventricular pressure increases at its
most rapid rate, the ΔP/ Δt also peaks
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usually, rate of rise of ventricular pressure
correlates well with strength of ventricular
contraction…….. two factors that influence
ΔP/ Δt which are not related to cardiac
contractility are:
1. Increased input pressure to the left
ventricle (EDV, preload)
2. Pressure in the aorta, afterload
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Influence of Potassium and
Calcium ions
Excess potassium in extracellular fluids
causes heart to become dilated, flaccid,
and slows HR
 large quantities can block the cardiac
impulse from the atria to the ventricles via
AV bundle
 elevations of 2-3X normal can weaken
heart enough to lead to death
high extracellular potassium
concentrations can cause a decrease in
the resting membrane potential in
cardiac muscle fibers
 lower resting membrane potential 
decrease in AP potential  weaker
contraction
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Excess calcium causes opposite effect
 heart goes into spastic contraction
 due to direct influence of calcium ions in
exciting the cardiac contractile process
 deficiency in calcium will cause flaccidity,
similar to excess potassium
 changes due to calcium are rare, blood
levels are tightly controlled
Temperature
increased T will increase HR,
sometimes as much as 2X
 decreased T will cause decreased HR,
as low as few bpm when body
temperature is 60-70 F, near death
 moderate T increase can enhance the
contractile strength of the heart
 prolonged elevation in T can cause an
exhaustion of the metabolic systems of
the heart, causing weakness
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Blood Transport
arteries carry oxygenated blood (except
pulmonary artery)
 can withstand high pressures
 composed of connective tissue and
smooth muscle
 from aorta (elastic as well as muscular),
through arteries, arterioles, metarterioles,
and finally, capillaries
 arterioles: smooth muscle; can constrict
and dilate dependent on peripheral blood
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capillaries are microscopic blood
vessels which contain ~5% of the total
blood volume
– single layer of endothelial cells, may abut
the membranes of surrounding cells
– density may be 2-3,000/ mm2
– capillary density is higher in cardiac muscle
– precapillary spinchter controls the mouth of
the capillary, local control of BF in the
capillaries of specific tissues
– ~1.5 seconds to pass a blood cell through
an average capillary (effective way to
exchange)
Blood pressure
surge of blood enters the aorta every time
the L ventricle contracts
 portion is stored in aorta, arteries and
arterioles cannot handle the rapid run off
of blood equal to ejection
 causes a pressure wave through the
arterial system (pulse)
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Mean arterial pressure (MAP): average
pressure in the arterial system during the
cardiac cycle
– spend more time in diastole, it is a little less
than the average of systole and diastole
Veins
blood flows from capillaries into venules to
veins
 blood from lower body enters heart via
inferior vena cava
 blood from the head and shoulders
empties into the superior vena cava
 when blood enters venules, the impetus
for flow is minimal (low pressure)
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blood returns via
1. Flap-like valves (one-way) at short intervals
in the veins
2. Valves are easily compressed by neighboring
muscles
couple the one-way valves with the
compression, milking action returns blood
 65% of blood volume is in the veins at rest
 veins are considered capacitance vessels
and reservoirs for blood