Chapter 9: Cardiac Muscle; The Heart
As A Pump and Function of the Heart Valves
Guyton and Hall, Textbook of Medical Physiology, 12th edition
Physiology of Cardiac Muscle
•
Physiologic Anatomy
a.
b.
c.
d.
Muscle fibers arranged in a latticework
Striated and Involuntary
Actin and myosin, typical myofibrils
Sliding filament mechanism
Fig. 9.1 Structure of the heart
and blood flow through
it.
Physiology (cont.)
•
Cardiac Muscle as a Synctium-cardiac muscle fibers
are made up of many individual cells connected in
series and in parallel (intercalated discs)
Fig. 9.2 Synctium
Physiology (cont.)
a. Composed of two synctiums: atrial and ventricular
b. Disks allow the action potential to travel easily from
cell to cell
•
Action Potentials in Cardiac Muscle
a. What causes the long action potential and plateau?
b. The AP is caused by the opening of two channel types
1. The same fast Na+ channels as in skeletal muscle
2. Slow Ca++ channels (slower to open and close)
3. Longer period of depolarization leads to plateau
Fig. 9.3 Rhythmic AP+s from Purkinje fibers and a ventricular muscle.
Physiology (cont.)
c. Permeability for K+ decreases about 5-fold
d. Prevents an early return to depolarized state
•
Velocity of Signal Conduction
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Refractory Period of Cardiac Muscle
a. Refractory to restimulation during the AP
b. Ventricle; 0.25-0.30 sec. which is the duration
of the plateau
c. There is an additional relative refractory period
Fig. 9.4 Force of ventricular heart muscle contraction, showing the duration of the refractory period
and relative refractory period, plus the effect of premature contraction. Note that there is no
summation as occurs in skeletal muscle.
Physiology (cont.)
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Excitation-Contraction Coupling
Fig. 9.5
•
Excitation-Contraction Coupling (cont.)
a. Calcium enters from extracellular fluid
b. Triggers calcium release from SR
c. At the end of the plateau, calcium flow stops and
calcium is reabsorbed by the SR
Cardiac Cycle
•
Cardiac Cycle-events from the beginning of one
heartbeat to the beginning of the next
a. Cycle is initiated by the spontaneous generation
of an AP by the sinus node
b. Delay of 0.1 sec from the atria to the ventricle
which allows the atria to contract before the ventricles
•
Diastole-relaxation
•
Systole-contraction
Fig. 9.6 Events of the cardiac cycle
Cardiac Cycle (cont.)
•
Effect of Heart Rate on the Duration of the CycleAs heart rate increases, the duration of the cycle
decreases
•
Relationship of the ECG to the Cycle-electrical
voltages generated by the heart
a. P wave-spread of depolarization through the atria
followed by atrial contraction
b. QRS waves-electrical depolarization of the ventricles
c. T wave-repolarization of the ventricles
Cardiac Cycle (cont.)
•
Function of the Atria as a Primer Pump-about 80%
of the blood flows directly through the atria to the
ventricles; atrial contraction adds another 20% so
it functions as a primer pump
•
Pressure Changes in the Atria-in Figure 9.6 there
are three minor pressure elevations
a. a wave-caused by atrial contraction
b. c wave-occurs when the ventricles begin to contract
c. v wave-occurs at the end of ventricular contraction
Cardiac Cycle (cont.)
•
Function of the Ventricles as Pumps-period of
of rapid filling; lasts about the first third of diastole;
a small amount fills during the second third and the
atrial contraction fills the last third
Emptying of the Ventricles During Systole
•
Period of Isovolumic Contraction
a. Ventricular pressure rises as contraction begins
b. Initially the pressure is not sufficient to open the
semilunar valves
c. Therefore, contraction is occurring but no
emptying
•
Period of Ejection
a. Pressure >80 mm Hg pushes the semilunar valves
open
b. Period of rapid ejection-first third (70%)
c. Period of slow ejection-second 2/3 (30%)
•
Period of Isovolumic Relaxation
a. At the end of systole, ventricles relax quickly
b. Blood in the arteries push back and close the
semilunar valves
c. Ventricles continue to relax but volume does
not change
•
End Diastolic Volume-during diastole, volume of
the ventricles increases to about 110-120 ml
•
Stroke Volume Output-as ventricles empty during
systole, the volume decreases about 70 ml
•
End Systolic Volume-remaining volume in the
ventricle (40-50 ml)
•
Ejection Fraction-fraction of the end diastolic that
is ejected (60%)
Function of the Valves
•
Atrioventricular Valves (tricuspid and mitral)
a. Prevent backflow from the ventricles to the atria
b. Close and open passively
Fig. 9.7
Valves (cont.)
• Function of the Papillary Muscles-attach to the AV
valves by the chordae tendineae; prevent the valves
from bulging back into the atria
• Aortic and Pulmonary Artery Valves
a. Because of smaller openings the velocity of flow is
greater than with the AV valves
b. Subject to greater mechanical abrasion than AVs
c. No chordae tendineae
•
Relationship of Heart Sounds to Heart Beating
a. First sound is closure of the AV valves
b. Second sound is closure of the SL valves
c. Lub-Dub
•
Work Output of the Heart
a. Stroke work output-amount of energy the heart
converts to work during each heartbeat
b. Minute work output-total amount of energy
converted to work in one minute
c. Volume-pressure work and kinetic energy of
blood flow
Graphic Analysis of Ventricular Pumping
Fig. 9.8 Relationship between left ventricular volume and intraventricular pressure during diastole and systole.
Heavy red lines indicate the volume pressure diagram (EW-external work).
Volume-Pressure Diagram During the Cardiac Cycle
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Phase I: Period of Filling
•
Phase II: Period of Isovolumic Contraction
•
Phase III: Period of Ejection
•
Phase IV: Period of Isovolumic Relaxation
Fig. 9.9
•
Preload-the degree of tension on cardiac muscle
when it begins to contract; usually is the enddiastolic pressure when the ventricle has filled
•
Afterload-pressure in the aorta leading from the
ventricle;
Energy Requirements
•
Oxygen Utilization By the Heart
a. 70-90% from the oxidative metabolism of fatty acids
b. 10-30% from lactate and glucose
•
Efficiency of Cardiac Contracton
a. Most of the chemical energy is converted to heat
b. 20-25% max. efficiency of the normal heart
c. As low as 5-10% in heart failure
Regulation of Heart Pumping
•
Intrinsic Regulation of Heart Pumping—Frank-Starling
Mechanism-intrinsic ability of the heart to adapt to
increasing volumes of inflowing blood
a. Within physiologic limits, the heart pumps all the
blood that returns to it by way of the veins
b. Muscle stretches and brought to optimal degree of
overlap for contraction
c. Stretch of the right atrial muscle increases the heart
rate by 10-20%
Ventricular Function Curves :
Another Way of Expressing the Frank-Starling Mechanism
9.10 Left and right ventricular function curves
Fig. 9.11 Normal right and left ventricular output
Control by the ANS
•
Excitation by the Sympathetic Nerves
a. Stimulation can increase heart rate from 70 bpm
to 180-200 bpm
b. Increases the force of contraction two-fold
c. Increases the volume pumped and the ejection
pressure
d. Inhibition decreases the heart rate and strength
of contraction
ANS Control (cont.)
•
Parasympathetic (Vagal) Stimulation
a. Strong stimulation will stop the heart for a few
seconds; then 20-40 bpm
b. Decrease the strength of contraction 20-30%
c. Distributed mainly to the atria
Fig. 9.12 Cardiac sympathetic and parasympathetic nerves
Fig. 9.13 Effect on the cardiac output curve of different degrees
of sympathetic and parasympathetic stimulation
Effects of Potassium and Calcium Ions on Heart Function
•
Potassium Ions
a. Excess causes the heart to become flaccid and
dilated and slows heart rate
b. Excess can block conduction through the AV bundle
c. Contraction becomes progressively weaker
•
Calcium Ions
a. Excess causes the heart to go to spastic contractions
b. Deficiency causes flaccidity
c. Regulated within a narrow range so seldom
important clinically
Effect of Temperature on Heart Function
•
Effects of Temperature
a. Increase body temperature increases heart rate
b. Decrease body temp. decreases heart rate
c. Contractile strength enhanced by moderate
increases in temperature
d. Prolonged elevation eventually causes weakness