Refractory period of cardiac
muscle
cardiac muscle has refractory period,
preventing restimulation
 during this interval, a normal cardiac
impulse cannot re-excite an already
excited area of the heart
 ventricles: 0.25-0.30 sec
 another, relative refractory period of 0.05
sec, muscle is more difficult to excite, but
can be stimulated

atria: ~0.15 sec
 relative refractory: 0.03 sec
 rhythmical rate of atria can be faster than
that of ventricles

Cardiac Cycle
beginning of heart beat to beginning of the
next
 R to R or P to P wave is often how one is
measured

Systole and Diastole
relaxation phase: heart fills with blood,
diastole
 work phase: heart pumps blood, systole
 cardiac cycle curve

Diastole
first third: rapid filling
 middle third: small amount of filling
 last third: atria contract, ~25% of blood
flows into ventricles

Systole
Isovolumic or isovolumetric contraction
occurs at onset of ventricular contraction
 ventricles need to develop sufficient
pressure to open semilunar valves against
the aorta and pulmonary artery
 ventricles contract isometrically, volume
does not change

Ejection next
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pressure in L vent. >80 mm Hg and R vent. >
8 mm Hg, valves open
first third: rapid ejection, 70% of blood is
ejected
next two-thirds: final 30% is ejected, slow
ejection
isovolumic relaxation
sudden onset, rapid drop in pressure, no
change in volume
intraventricular pressure drops to diastolic
level
End Diastolic Volume (EDV)
volume in ventricles after the period of
filling
 usually ~110-120 ml of blood/ventricle

Stroke Volume (SV)
volume ejected during systole
 ~70 ml

End Systolic Volume (ESV)

volume in ventricles after systole, ~40-50
ml
Ejection Fraction (EF)
fraction of EDV that is ejected
 usually ~ 60%
 when contraction force is strong, ESV can
fall to 10-20 ml
 EDV can be as high as 150-180 ml of
blood
 increase EDV and decrease ESV, SV can
double resting SV

Volume Pressure curves for
Systole and Diastole
Phase I: filling phase ESV to EDV
increase vol. ~70 ml pressure rises ~5
mm Hg (diastolic)
 Phase II: isovolumic contraction,
increase pressure (~80 mm Hg), not
volume

Phase III: ejection period
 Phase IV: isovolumic relaxation ventricle
pressure decreases to diastolic levels

Preload: degree of tension on the
heart muscle when it begins
contraction

Volume of blood in the ventricle at the
end of diastole (EDV)
Afterload: load against which the
muscle exerts its contractile force

Pressure in artery leading from the
ventricles
Regulation of the heart’s pumping
@ rest, Q is usually 4-6 l/min
 Q is reliant upon rate of blood flow into
heart (venous return)
 Frank-Starling Mechanism: increase in
venous return (EDV) increases the amount
of blood pumped into the aorta

F-S: Heart pumps what heart gets

Due to increased return: increased stretch of the
heart  increase force of the contraction
(optimal length for force)
 Increase in force is also seen in skeletal muscle
 Stretch R atrial wall can increase heart rate by
10-20% increasing Q (less than from F-S
mechanism)
 High pressure in the arteries does not increase
Q
Ventricular Function Curves
As arterial pressure increases, work output
of stroke volume increases until it reaches
the limit of the heart
As arterial pressure increases (EDV) EF
also increases
Extrinsic Regulation of the Heart
Rate
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Neural influences can be superimposed on
inherent rhythmicity of heart
Originate in CVC in medulla
Transmitted via autonomic NS via
sympathetic and parasympathetic
Ventricles: sympathetic
Atria: both
Sympathetic Innervation
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Can increase Q by 100%
Causes release of epi and norepi,
speeding rate of SA depolarization
Result: tachycardia
Also increases the force of contraction
Inhibition of sympathetic NS can decrease
HR and pumping
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Mechanism the continuously
discharges, maintains HR ~30% higher
than if there were no stimulation
If depress sympathetic stimulation, HR
and force of contraction decrease,
decreasing Q ~30%
Adrenal glands are also active and can
release epi with general sympathetic
activation
Parasympathetic innervation
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Can slow HR to almost zero
Ach released, decreasing the rate of sinus
discharge: bradycardia
Cell bodies are in cardioinhibitory center of
medulla
With strong stimulus, heart can stop
beating for few seconds, start again, at a
rate of 20-30 bpm
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Strong parasympathetic stimulation will
decrease the force of contraction by 2030%
Decrease is not great in its extent, most
fibers are in atria, few in ventricles
Large decrease in HR combined with
small decrease in contractility: decrease
ventricular pumping 50%
Training Effect
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Exercise favors vagal dominance
Increase in parasympathetic activity, may
also have a decrease in sympathetic
activity
Training may also reduce intrinsic firing
rate of SA node
Peripheral input
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Peripheral receptors in blood vessels,
joints, muscles
Input to ventrolateral medulla
Modify vagal or sympathetic outflow
Baroreceptors in aortic arch and carotid
sinus (alterations in BP)
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Increase BP: reflex slowing of HR and
dilation of peripheral vasculature
Decrease BP to normal levels
This feedback is overridden during
exercise
But, still may act to prevent abnormally
high BP during ex.