Chapter 17 The Cardiovascular system: The Heart
Objectives:
1. Describe the size and shape of the heart, and indicate its location and orientation in the
thorax.
2. Name the coverings of the heart.
3. Describe the structure and function of each of the three layers of the heart wall.
4. Describe the structural and functional properties of cardiac muscle, and explain how it
differs from skeletal muscle.
5. Briefly describe the events of cardiac muscle cell contraction.
6. Name the components of the conduction system of the heart, and trace the conduction
pathway.
7. Draw a diagram of a normal electrocardiogram tracing; name the individual waves and
intervals, and indicate what each represents. Name some abnormalities that can be
detected on an ECG tracing.
8. Describe the timing and events of the cardiac cycle.
9. Name and explain the effects of the various factors involved in regulating stroke volume
and heart rate.
10. Explain the role of the autonomic nervous system in regulating cardiac output.
11. Describe fetal heart formation, and indicate how the fetal heart differs from the adult
heart.
Location: in mediastinum (medial cavity of thorax) along w/ esophagus, trachea, great vessels and
nerves. Apex points into left lung. See figure 17.1
Pericardium: protective sac around heart. Double layered
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Fibrous: protects, anchors, and prevents overfilling
Serous: produces fluid that fills pericardial cavity for lubrication
Layers of Heart See figure 17.2
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Epicardium: also called the visceral/serous pericardium; outer layer of heart, infiltrated with fat.
Myocardium: made of cardiac muscle. Makes up the fibrous skeleton of the heart
Endocardium: simple squamous epithelium, lines chambers, covers valves.
Microscopic Anatomy See figure 17.11
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Intercalated discs and gap junctions for cell-cell communication
Cylindrical cells, striated w/ single nucleus
Branching fibers
Mechanism and events of contraction
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Means of stimulation: autorhythmicity, self excitable cells
Organ vs. motor unit contraction
Length of absolute refractory period: 250 ms. Prevents tetanic contractions.
Electrical events in contractile cells See figure 17.12
1. Na+ channels open very briefly and gates close quickly for initial depolarization
2. Ca2+ gates (slow Ca2+ channels) open to allow Ca2+ in from ECF to help open channels in SR.
3. Ca2+ prolongs depolarization (plateau). As long as Ca2+ enters cells, they continue to contract.
4. Tension develops during plateau and peaks just after. Contractile phase and action potential are
longer in cardiac muscle to help eject blood from heart.
5. After 200 ms, Ca2+ gates close and K+ open for repolarization.
Energy requirements
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More mitochondria carry out aerobic respiration, uses glucose, fatty acids, lactic acid.
GREATEST THREAT TO CARDIAC MUSCLE: LACK OF O2 NOT FUEL!!!!
Ischemia: lack of blood supply and O2 starvation causes pH to drop (too many H+ ) that impairs ATP
production to pump Ca2+ in ECF. Gap junctions close, cells are electrically isolated, and action
potentials cannot connect to cells beyond ischemic areas.
Intrinsic conduction system: independent but coordinated activity of heart. See figure 17.13
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Noncontractile cardiac cells have an unstable resting potential that continuously depolarizes toward
threshold.
Gradually reduced membrane permeability to K + and Na+ make membrane hypopolarized. Fast
Ca2+ gates open and action potential occurs. Cells then initiate and distribute impulses through
heart.
Sequence of Excitation See figure 17.14
1. SA (sinoatrial) Node: in upper right atrial wall. Typically generates 75 impulses/min. It is the
heart’s pacemaker w/sinus rhythm.
2. Internodal tracts: depolarization wave spreads across and through via internodal tracts (through
gap junctions) to AV node above tricuspid valve. Impulse is delayed 0.1 s @ AV node to allow atria to
respond before ventricles contract.
3. AV bundle (Bundle of His): in inferior interatrial septum, then into right and left branches through
interventricular septum.
4. Purkinje fibers: found in ventricular walls. Signals begin in apex and travels upward.
Arrhythmia: defects in intrinsic conduction system.
Fibrillation: rapid and irregular or out of phase contractions. Shocking is used to stop everything and
allow SA node to start again.
Ectopic focus:
 Abnormal pacemaker may appear if SA node is defective.
 May appear even when SA node is functioning (too much nicotine or caffeine)
 Leads to extrasystole (premature contraction) and PVC’s (premature ventricular contractions)
result.
Heart block: damage to AV node, interferes with the ability of the ventricles to receive pacing impulses.
In total heart block, the ventricles beat at their intrinsic rate, which is too slow to maintain adequate
circulation. In partial heart block, only some of the atrial impulses reach the ventricles.
Pacemakers are used to recouple the atria to the ventricles. The programmable devices speed up in
response to increased physical activity like a normal heart.
Electrocardiography: deflection waves caused by electrical activity of cardiac muscle. See figure
17.16, 17.17, 17.18
1. P wave: lasts 0.08 s. SA node thru internodal tracts to atria (0.1 s later atria contract)
2. QRS complex: lasts 0.08 s. Ventricular depolarization just before ventricular contraction.
3. T wave: 0.16 s. Ventricular repolarization, lasts longer since repolarization is slower. Atrial
repolarization is lost in the QRS complex.
4. P-Q interval: 0.16 s. From beginning of atrial excitation to beginning of ventricular excitation.
5. ST segment: entire ventricular myocardium is depolarized.
6. QT interval: 0.38 s. Beginning of ventricular depolarization to end of repolarization.
Heart sounds: associated with closing of heart valves. The first sound occurs as the AV valves close,
when ventricular pressure rises above atrial pressure (the beginning of ventricular systole). The second
heart sound is heard as the semilunar (SL) valves close, at the beginning of ventricular relaxation. See
figure 17.19
Cardiac cycle: systole = contraction, diastole = relaxation See figure 17.20
1. Ventricular filling: mid to late diastole – 70% filling occurs here.
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AV valves open since pressure is higher in atria than in ventricles
P wave occurs; atrial contraction begins
Semilunar valves are closed
At the end the AV valves begin drifting closed
At end diastolic volume in ventricles
Finally, atria relax and QRS wave occurs
2. Ventricular systole:
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Ventricular pressure increases due to ventricular contraction beginning
AV valves are closed and produce the first heart sound
Isovolumetric contraction phase begins (no blood leaves the heart)
Semilunar valves are forced open
The ventricular ejection phase begins and blood leaves the ventricles
3. Isovolumetric relaxation:
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Early diastole, ventricles relax
T wave occurs
End systolic volume is left in heart
Ventricular pressure drops
Semilunar valves close and produce the second heart sound
Atria are filling and pressure is increasing.
Length of cardiac cycle
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About 0.8s
Atrial systole = 0.1s
Ventricular systole = 0.3s
0.4s is quiescent period or total relaxation
Cardiac output (CO): See Figure 17.23
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The amount of blood pumped out by each ventricle in one minute. HR x SV = CO (heart rate
times stroke volume equals cardiac output.
Stroke volume:
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The volume of blood pumped out by a ventricle with each beat. It equals about 70 ml/beat.
So, 75 bpm x 70 ml/beat = average adult CO (5.25 L/min or the entire blood supply pumped every
minute)
CO increases with either an increase in HR or SV or both.
Cardiac reserve:
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How much more blood we can pump with exertion.
In nontrained individuals it is 4-5x CO (or 20-25 L/min)
In athletes it is 7x CO (or 35 L/min)
Regulation of stroke volume:
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SV = EDV – ESV
EDV or end diastolic volume is how much blood is in the ventricle after it is filled by the atrium and
is approx. 120 ml.
ESV or end systolic volume is how much blood is left in the ventricle after it contracts and the
blood leaves the heart and is approx. 50 ml.
So SV ends up about 70 ml. How do you change that?
Preload: See figure 17.21
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a measure of the degree of stretch of the heart muscle.
Frank-Starling law of the heart says that the greater the stretch of cardiac muscle cells, the greater
the force of contraction.
The EDV increases this stretch and EDV increases with slow heart rate (more time to fill ventricles)
or exercise (speeds up venous return).
Stroke volume may double due to these factors
Contractility: See figure 17.22
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Slow calcium channels and greater calcium from SR allows more complete ejection of blood and a
lower ESV.
Contractility increases with an increase in sympathetic stimulation by epinephrine and an increase
in calcium permeability of membrane
Decreased contractility comes from acidosis (too many H+), increased K+, and calcium channel
blockers
Afterload See figure 17.21b
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Pressure from blood on pulmonary and aortic semilunar valves may affect the amount of pressure
that must be produced by the ventricles to eject blood.
This is not a major determinant on stroke volume, but may have some effect on patients with
hypertension because more blood remains within the heart.
The result of afterload is an increased ESV and decreased SV
Autonomic Nervous System Regulation
1. Extrinsic innervation of heart: ANS modifies heart beat. Sympathetic division increases rate and
force with NE. Parasympathetic division decreases rate with vagus nerve. (Intrinsic rate of heart is
actually 25 bpm faster when vagus nerve is cut). See figure 17.15
2. Cardiac centers in the medulla:
1. Cardioacceleratory center: works with sympathetic division to increase HR and force
2. Cardioinhibitory center: works with parasympathetic division to decrease HR and force
Both centers act on the SA and AV nodes to regulate heart rate.
3. Norepinephrine: binds to beta-adrenergic receptors, threshold of cardiac muscle cells is reached
more quickly and relaxation is accelerated, the pacemaker fires more rapidly and the heart beats faster.
NE also allows enhanced Ca2+ entry into contractile cells for greater contractility. This lowers ESV, and
even though heart rate is faster, SV doesn’t drop (like it would if only rate increased and decreased time
for filling and decreased EDV).
4. ACh: the NT of the vagus nerve hyperpolarizes membranes of SA and AV node effector cells by
opening K+ channels. Under resting conditions, both sympathetic and parasympathetic send signals, but
the dominant signal is inhibitory. Vagal tone (through the vagus nerve) slows the heart rate to less than
what it would be without it. If vagal tone is too great, the heart will experience vagal escape, where heart
seems to ignore the stimulus to slow and returns to a normal rate.
5. Baroreceptors/Bainbridge reflex: sensory input generated by baroreceptors that respond to
changes in systemic blood pressure result in the Bainbridge reflex. Increased venous return and blood
congestion in atria stretch atrial walls. This in turn stimulates SA node and baroreceptors that trigger a
reflex that increases sympathetic stimulation of the heart.
6. Chemical Regulation
a. hormones: epinephrine: enhances heart rate and contractility (like NE). Thyroxine, in large
quantities, causes a slower but more sustained increase in heart rate.
b. ions: Hypocalcemia (low calcium) depresses the heart. Hypercalcemia (high calcium) prolongs
the plateau phase of the action potential to dramatically increase heart irritability, which can lead to
spastic heart contractions that permit the heart little rest. Hypernatremia (high sodium) inhibits transport
of calcium into cardiac cells, thus blocking heart contraction. Hyperkalemia (high potassium) interferes
with depolarization by lowering resting potential and may lead to heart block and cardiac arrest.
Hypokalemia causes a feeble and arrhythmic heart beat.
Tachycardia: abnormally fast HR due to increased body temperature, stress, drugs, heart disease
Bradycardia: slower than 60 bpm; due to decreased body temperature, drugs, parasympathetic
stimulation, or endurance-type athletic training.
Congestive heart failure: CO of heart is so low that blood circulation is inadequate to meet tissue
needs. It is usually a worsening condition; weakening of myocardium (due to atherosclerosis), high blood
pressure, multiple MI’s. The coronary arteries are susceptible to atherosclerosis because the blood
entering them is the most oxygenated and nutrient-rich (full of fat!). The coronary arteries also branch
very quickly and often, and in the bifurcations the plaques build up.
Dilated cardiomyopathy: ventricles stretch and become flabby, myocardium deteriorates; see:
http://www.americanheart.org/presenter.jhtml?identifier=4468
Left side failure: pulmonary congestion. Blood vessels in lungs become engorged, pressure increases,
fluid leaks, edema results.
Right side failure: peripheral congestion. Blood stagnates in body organs. Tissues cannot rid
themselves of wastes, and don’t receive nutrients and oxygen. Edema is most noticeable in extremities.
Heart Murmur: blood flowing back into atria during ventricular systole due to leaky atrioventricular
valves (bicuspid and tricuspid). Semilunar valves rarely have murmurs. Can result in atrial congestion.