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Phys Ch 23
Heart Valves and Heart Sounds; Valvular and Congenital Heart Defects
 Normal heart sounds – “lub, dub” with “lub” as closure of AV valves and “dub” being closure of semilunar valves
 Cause of sounds is vibration of taut valves immediately after closure, along with vibration of adjacent walls of
heart and major vessels around heart
o In generating first heart sound, contraction of ventricles first causes sudden backflow of blood against
AV valves, causing them to close and bulge toward atria until the chordae tendineae abruptly stop the
back bulging
o Elastic tautness of chordae tendineae and valves cause back-surging blood to bounce forward again into
each respective ventricle, causing blood and ventricular walls, as well as taut valves, to vibrate and
causes vibrating turbulence in blood
o Vibrations travel through adjacent tissues to chest wall, where they can be heard as sound
o Second heart sound results from sudden closure of semilunar valves at end of systole – when semilunar
valves close, they bulge backward toward ventricles and elastic stretch recoils blood back into the
arteries, which causes a short period of reverberation of blood back and forth between walls of arteries
and semilunar valves, as well as between these valves and ventricular walls
o Vibrations occurring in arterial walls then transmitted mainly along arteries – when vibrations of vessels
or ventricles come into contact with “sounding board”, such as the chest wall, they create sound that
can be heard
 Duration of each heart sound is slightly more than 0.1 sec. – first heart sound is 0.14 sec and second is 0.11 sec –
second sound is shorter because semilunar valves are more taut than AV valves, so they vibrate for a shorter
time than AV valves
 Frequencies of first heart sounds are largely below the audible range, so major portions of the heart sounds can
be recorded electronically in phonocardiograms even though they cannot be heard via stethoscope
 Second heart sound normally has higher frequency because of more tautness in semilunar valves and greater
elastic coefficient of taut arterial walls that provide principal vibrating chambers for second sound
 Third heart sound – occasionally weak rumbling – heard at beginning of middle third of diastole – thought to
(not proven ) be oscillation of blood back and forth between walls of ventricles initiated by inrushing blood from
atria – doesn’t occur until middle third of diastole because ventricles not filled sufficiently to create even the
small amount of elastic tension necessary for reverberation – usually so low, it cannot be heard, but shows up
on phonocardiogram
 Atrial heart sound – fourth heart sound – sometimes recorded in phonocardiogram, but almost never heard
because of its weakness and very low frequency (20 Hz or less) – occurs when atria contract, and presumably,
caused by inrush of blood into ventricles, which initiates vibrations similar to those of third heart sound
 Heart sounds for aortic area hear just to patient’s right of sternum between 1st and 2nd rib below clavicle –
pulmonic area best heart just to patient’s left of sternum between 1st and 2nd rib below clavicle – tricuspid area
heard just to patient’s left of sternum right below the last fully attached rib – mitral area heard just to patient’s
left of tricuspid area where costal cartilage becomes bone
 Phonocardiogram records heart sounds into wave format (look much like a seismometer)
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Greatest number of valvular lesions result from rheumatic fever, an autoimmune disease in which heart valves
likely to be damaged or destroyed – usually initiated by streptococcal toxin
o Preliminary strep infection by group A hemolytic streptococci, causing strep throat, scarlet fever, or
middle ear infection
o Strep bacteria release several proteins against which the person’s reticuloendothelial system produces
antibodies – these Ig’s react with other protein tissues of the body with these proteins, causing severe
immunologic damage – can last as long as these antibodies persist in blood for up to a year or more
o Degree of heart valve damage directly correlated with concentration and persistence of Ig’s – large
hemorrhagic, fibrinous, bulbous lesions grow along inflamed edges of heart valves
o Mitral valve is one most often seriously damaged because it receives more trauma during valvular action
than any other valves – aortic valve is 2nd most frequently damaged
Scarring of valves – lesions such as those incurred from rheumatic fever frequently occur on adjacent valve
leaflets simultaneously so edges of leaflets become stuck together – however long healing takes, lesions become
scar tissue, permanently fusing portions of adjacent valve leaflets – free edges of leaflets, normally filmy and
free-flapping, often become solid, scarred masses
o Stenosed – adjective describing valve in which leaflets adhere to one another so blood cannot flow
through it normally
o When valve edges are so destroyed by scar tissue that they cannot close as ventricles contract,
regurgitation (backflow) or blood occurs when valve should be closed
o Stenosis and regurgitation usually coincide
Heart Murmurs
o Systolic murmur of aortic stenosis – blood is ejected from left ventricle through small fibrous opening of
aortic valve – because of resistance to ejection, blood pressure in left ventricle can reach 300 mm Hg
while pressure in aorta is normal, thus nozzle effect created during systole, with blood jetting at
tremendous velocity through small opening of valve
 Severe turbulence of blood in root of aorta caused by above – turbulent blood impinging against
aortic walls causes intense vibration, and a loud murmur occurs during systole and transmitted
throughout superior thoracic aorta and into large arteries of neck
 Sounds as harsh, possibly loud, sound vibrations that can be felt with hand on upper chest and
lower neck, called “thrill”
o Diastolic murmur of aortic regurgitation – no abnormal sound hear during systole, but during diastole,
blood flows backward from high-pressure aorta into left ventricle, causing “blowing” murmur of
relatively high pitch with swishing quality heard maximally over left ventricle – results from turbulence
of blood jetting backward into blood already in low-pressure diastolic left ventricle
o Systolic murmur of mitral regurgitation – blood flows backward through mitral valve into left atrium
during systole – causes high-frequency “blowing”, swishing sound similar to that of aortic regurgitation
but occurring during systole rather than diastole – transmitted most strongly into left atrium
 Left atrium is so deep within chest, it is difficult to hear sound directly over atrium – as a result,
sound transmitted to chest wall mainly through left ventricle to apex of heart
o Diastolic murmur of mitral stenosis – blood passes with difficulty through stenosed mitral valve from left
atrium into left ventricle, and because pressure in left atrium seldom rises above 30 mm Hg, a large
pressure differential forcing blood from left atrium into left ventricle does not develop
 Sounds usually very weak and very low frequency, so most of the sound spectrum is below
hearing threshold
 During early part of diastole, left ventricle with stenotic mitral valve has so little blood in it and
its walls are so flabby that blood does not reverberate back and forth between walls of ventricle,
so no murmur may be heard during first third of diastole
 After partial filling, ventricle has stretched enough for blood to reverberate and low rumbling
murmur begins
Abnormal circulatory dynamics in valvular heart disease
o Dynamics of circulation in aortic stenosis and aortic regurgitation
 Aortic stenosis – left ventricle fails to empty adequately
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Aortic regurgitation – blood flows backward into ventricle from aorta after ventricle has just
pumped blood into aorta
 In both cases, net stroke volume output of heart is reduced
 Left ventricular musculature hypertrophies because of increased ventricular workload
 in regurgitation, left ventricular chamber enlarges to hold all regurgitant blood from aorta
 when aortic valve seriously stenosed, hypertrophied muscle allows left ventricle to develop as
much as 400 mm Hg intraventricular pressure at systolic peak
 in severe aortic regurgitation, sometimes hypertrophied muscle allows left ventricle to pump
stroke volume output as great as 250 mL, although as much as ¾ of this blood returns to
ventricle during diastole
 increased blood volume occurs because initial slight decrease in arterial pressure and peripheral
circulatory reflexes occur that the decrease in pressure induces
 both causes diminish renal output of urine, causing blood volume to increase and mean
arterial pressure to return to normal
 red cell mass eventually increases because of slight degree of tissue hypoxia
 increase in blood volume increases venous return to heart, causing left ventricle to
pump with extra power required to overcome abnormal pumping dynamics
 during early stages, ability of left ventricle to adapt to increasing loads prevents significant
abnormalities in circulatory function during rest, so considerable degrees often occur before
person knows that he or she has a serious heart disease
 beyond a critical stage in aortic valve lesions, left ventricle finally cannot keep up with the work
demand, so it dilates and cardiac output begins to fall – blood simultaneously dams up in left
atrium and in lungs behind failing left ventricle – left atrial pressure rises progressively, and
serious edema appears in the lungs
dynamics of mitral stenosis and mitral regurgitation
 reduces net movement of blood from left atrium into left ventricle
 buildup of blood in left atrium causes progressive increase in left atrial pressure, and eventually
results in development of serious pulmonary edema
 Ordinarily, lethal edema does not occur until mean left atrial pressure rises above 25 mm Hg
and sometimes as high as 40 mm Hg, because lung lymphatic vessels enlarge manyfold and can
rapidly carry fluid away from lung tissues
 High left atrial pressure causes progressive enlargement of left atrium, which increases distance
cardiac electrical excitatory impulse must travel in atrial wall – pathway may eventually become
so long that it predisposes to development of excitatory signal circus movements, causing atrial
fibrillation, further reducing pumping effectiveness of heart and causing further cardiac debility
 Blood volume increases principally because of diminished excretion of water and salt by kidneys
– increased blood volume increases venous return to heart, thereby helping overcome the
effect of the cardiac debility – after compensation, cardiac output may fall only minimally until
late stages of mitral valve disease even though left atrial pressure is rising
 As left atrial pressure rises, blood begins to dam up in lungs, eventually all the way back to
pulmonary artery – Incipient edema of lungs causes pulmonary arteriolar constriction –
together, these increase systolic pulmonary arterial pressure and right ventricular pressure,
sometimes as high as 60 mm Hg, causing hypertrophy of right side of heart, which partially
compensates for increased workload
Circulatory dynamics during exercise in patients with valvular lesions
 During exercise, large quantities of venous blood returned to heart from peripheral circulation,
so all dynamic abnormalities become more exacerbated
 Severe symptoms often develop during heavy exercise, even in the mildest of cases of heart
disease
 For example, in patients with aortic valvular lesions, exercise can cause acute left
ventricular failure followed by acute pulmonary edema
 In patients with mitral disease, exercise can cause so much damming of blood in lungs
that serious or even lethal pulmonary edema may ensue in as little as 10 minutes
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Patient’s cardiac reserve diminishes in proportion to severity of valvular dysfunction – cardiac
output does not increase as much as it should during exercise, and therefore muscles fatigue
rapidly because of too little increase in muscle blood flow
Abnormal circulatory dynamics in congenital heart defects
o Congenital anomaly – heart or associated blood vessels malformed during fetal life
o Three major types of congenital anomalies
 Stenosis of channel of blood flow at some point in heart or closely allied major blood vessel
 Left-to-right shunt – allows blood to flow backward from left side of heart or aorta to right side
of heart or pulmonary artery
 Right-to-left shunt – allows blood to flow directly from right side of heart into left side of heart,
failing to flow through lungs
o congenital stenosis causes same results as those caused by lesions
o coarctation of aorta – congenital stenosis, often occurring near level of diaphragm – causes arterial
pressure in upper part of body (above level of coarctation) to be much greater than pressure in lower
body because of great resistance to blood flow through coarctation to lower body – part of blood must
go around coarctation through small collateral arteries
o Left-to-right shunt – during fetal life, lungs are collapsed and elastic compression of lungs that keeps
alveoli collapsed keeps most of lung blood vessels collapsed as well, and therefore, resistance to blood
flow through lungs is so great that pulmonary arterial pressure is high in fetus
 Because of low resistance to blood flow from aorta through large vessels of placenta, pressure
in aorta of fetus is lower than normal – lower than pulmonary artery – causes almost all
pulmonary arterial blood to flow through ductus arteriosus, which connects pulmonary artery
with aorta
 As soon as baby born and begins to breathe, lungs inflate, filling alveoli with air and decreasing
resistance to blood flow through pulmonary vascular tree, allowing pulmonary arterial pressure
to fall
 Aortic pressure rises because of sudden cessation of blood flow from aorta through placenta
 As a result of pulmonary arterial pressure falling and aortic pressure rising, forward blood flow
through ductus arteriosus ceases suddenly at birth and blood begins to flow backward through
ductus from aorta into pulmonary artery
 Backward blood flow causes ductus arteriosus to become occluded within a few hours to a few
days, so blood flow through ductus does not persist – believe to close because oxygen
concentration of aortic blood is about twice as high as that of blood flowing from pulmonary
artery into ductus during fetal life – oxygen presumably constricts muscle in ductus wall
 1 in 5500 babies – ductus does not close, causing patent ductus arteriosus
 During early months, does not cause severely abnormal function, but as child grows, differential
between high pressure in aorta and lower pressure in pulmonary artery progressively increases,
with corresponding increase in backward flow of blood from aorta into pulmonary artery
 High aortic blood pressure causes diameter of partially open ductus to increase with time,
making the condition even worse
 In older child, ½-2/3 of aortic blood flows backward through ductus into pulmonary artery, then
through lungs, and back into left ventricle and aorta, passing through lungs and left side of heart
two or more times for every one time it passes through systemic circulation
 Patients do not show cyanosis until later in life, when heart fails or lungs become congested –
young patients may even be better for increased times through pulmonary circuit
 Major effects are decreased cardiac and respiratory reserve – left ventricle pumping 2 or more
times more than the normal cardiac output, and maximum it can pump after hypertrophy of
heart has occurred is 4-7 times normal
 During exercise, net blood flow through remainder of body can never increase to levels
required for strenuous activity – person becomes weak and may faint from momentary
heart failure
 High pressures in pulmonary vessels caused by excess flow through lungs often lead to
pulmonary congestion and pulmonary edema
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Most patients with uncorrected patent ductus die from heart disease between ages 20-40 years
old
 As baby grows, harsh blowing murmur begins to be heard in pulmonary artery area – much
more intense during systole when aortic pressure is high and much less intense during diastole –
this waxing and waning with each heartbeat called machinery murmur
 Surgical treatment is extremely simple – ligate or sever and close the two ends of the ductus
arteriosus
o Right-to-left shunt – Tetralogy of Fallot
 Most common cause of blue baby
 Most blood bypasses lungs, so aortic blood mainly unoxygenated venous blood
 Four abnormalities occur simultaneously
 Aorta originates from right ventricle rather than left or overrides hole in the septum,
receiving blood from both ventricles
 Pulmonary artery stenosed, so much lower than normal amounts of blood pass from
right ventricle into lungs – most blood passes directly into aorta
 Blood from left ventricle flows either through ventricular septal hole into right ventricle
and then into aorta or directly into aorta that overrides this hole
 Because of larger quantities of blood right side is now pumping, its musculature is highly
developed, causing an enlarged right ventricle
 Major physiological difficulty is shunting of blood past lungs without becoming oxygenated – as
much as 75% of venous blood returning to heart passes directly from right ventricle into aorta
without becoming oxygenated
 Diagnosis of tetralogy of Fallot based on
 Baby’s skin is cyanotic
 Measurement of high systolic pressure in right ventricle, recorded through catheter
 Characteristic changes in radiological silhouette of heart, showing enlarged ventricle
 Angiograms (x-rays) showing abnormal blood flow through interventricular septal hole
and into overriding aorta, but much less flow through stenosed pulmonary artery
 Can usually be treated successfully by surgery – open pulmonary stenosis, close septal defect,
and reconstruct flow pathway into aorta – treatment increases average life expectancy from 3-4
years to 50+ years
Causes of congenital anomalies
o Congenital anomalies occur about 8:1000 live births
o One of most common causes is viral infection in mother during first trimester of pregnancy when fetal
heart is formed – defects particularly prone to develop when mother has German measles
o Some congenital defects hereditary because same defect has occurred in identical twins as well as
succeeding generations
 Children of patients surgically treated for heart disease have about 10x greater chance of having
congenital heart disease than other children do
o Heart defects frequently associated with other congenital defects of baby’s body
Use of extracorporeal circulation during cardiac surgery
o Many types of heart-lung machines developed to take the place of the heart and lungs during heart
surgery – called extracorporeal circulation
 consists primarily of pump and oxygenating device – almost any type of pump that does not
cause hemolysis of blood is suitable
o methods for oxygenating blood include
 bubbling oxygen through blood and removing bubbles from blood before passing it back into
patient
 dripping blood downward over surfaces of plastic sheets in presence of oxygen
 passing blood over surfaces of rotating discs
 passing blood between thin membranes or through thin tubes permeable to oxygen and carbon
dioxide
hypertrophy of heart in valvular and congenital heart disease
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hypertrophy of cardiac muscle is one of most important mechanisms by which heart adapts to increased
workloads, whether loads cause by increased pressure against which heart muscle must contract or by
increased cardiac output that must be pumped
o degree of hypertrophy is predictable by multiplying ventricular output by pressure against which
ventricle must work, with emphasis on pressure
detrimental effects of late stages of cardiac hypertrophy
o extreme degrees of hypertrophy can lead to heart failure because
 coronary vasculature typically does not increase to same extent as mass of cardiac muscle
increase
 fibrosis often develops in muscle, especially in subendocardial muscle where coronary blood
flow is poor, with fibrous tissue replacing degenerating muscle fibers
o because of disproportionate increase in muscle mass relative to coronary blood flow, relative ischemia
may develop as cardiac muscle hypertrophies and coronary blood flow insufficiency may ensue
o angina pain frequently accompanies cardiac hypertrophy
o enlargement of heart also associated with greater risk for developing arrhythmias, which can lead to
further impairment of cardiac function and sudden death because of fibrillation