Cardiovascular Physiology — Heart Valves, Valvular Defects, & Congenital Heart Defects

Heart Sounds

Normal Heart Sounds

“lub” — first heart sound

“dub” — second heart sound

Causes of First and Second Heart Sounds

Duration and Pitch of the First and Second Heart Sounds

first sound:  0.14 s

second sound:   0.11 s

audible range of frequency (pitch) in first and second heart sound from about 40 Hz to above 500 Hz

larger proportion of sound is down to 3–4 Hz, peaking at about 20 Hz

Third Heart Sound.

weak, rumbling sound at the beginning of the middle third of diastole

Atrial Heart Sound (Fourth Heart Sound).

usually 20 Hz or less

occurs when the atria contract

Valvular Lesions

Rheumatic Valvular Lesions

rheumatic fever

autoimmune disease

initiated by streptococcal toxin

preliminary streptococcal infection by group A hemolytic streptococci

initially cause sore throat, scarlet fever, or middle ear infection

antibodies

large hemorrhagic, fibrinous, bulbous lesions grow along the inflamed edges of the heart valves

mitral valve is most often seriously damaged

aortic valve is second most frequently damaged

Scarring of the Valves.

leaflets become stuck together

free edges of leaflets become solid, scarred masses

stenosis

regurgitation

Other Causes of Valvular Lesions.

congenital stenosis

congenital valvular atresia

Heart Murmurs Caused by Valvular Lesions

Systolic Murmur of Aortic Stenosis

blood pressure in L ventricle rises as high as 300 mm Hg

nozzle effect created during systole

causes severe turbulence of the blood in root of aorta

sound is harsh

in severe stenosis may heard several feet away from patient

“thrill”

Diastolic Murmur of Aortic Regurgitation

blood flows backward from aorta into L ventricle

“blowing” murmur of relatively high pitch with a swishing quality

results from turbulence of blood jetting backward into blood already in low-pressure L ventricle

Systolic Murmur of Mitral Regurgitation

causes a high-frequency “blowing,” swishing sound similar to that of aortic regurgitation

Diastolic Murmur of Mitral Stenosis

pressure in L atrium seldom rises above 30 mm Hg

abnormal sounds are usually weak and of very low frequency

Abnormal Circulatory Dynamics in Valvular Heart Disease

Circulation in Aortic Stenosis & Aortic Regurgitation

net stroke volume output of heart is reduced

compensations:

Hypertrophy of the Left Ventricle

Increase in Blood Volume

results from

(1) an initial slight decrease in arterial pressure, plus

(2) peripheral circulatory reflexes that the decrease in pressure induces increase in blood volume tends to increase venous return

Eventual Failure of Left Ventricle & Development of Pulmonary Edema

considerable degrees of aortic stenosis or aortic regurgitation often occur before patient knows there is serious heart disease

beyond a critical stage in these aortic valve lesions, the L ventricle finally cannot keep up with work demand

L atrial pressure rises progressively

at mean LA pressures above 25 to 40 mm Hg, serious edema appears in the lungs

Dynamics of Mitral Stenosis & Mitral Regurgitation

either of these conditions reduces net movement of blood from the LA into LV

Pulmonary Edema in Mitral Valvular Disease

eventually results in development of serious pulmonary edema

lethal edema does not occur until mean LA pressure rises above 25 mm Hg

Enlarged Left Atrium & Atrial Fibrillation

predisposes to development of excitatory signal circus movements

in mitral stenosis, atrial fibrillation usually occurs

Compensation in Early Mitral Valvular Disease

blood volume increases

increases venous return

after compensation, cardiac output may fall only minimally

as the LA pressure rises, blood begins to dam in lungs,

incipient edema of lungs causes pulmonary arteriolar constriction

increase in systolic pulmonary arterial pressure and also RV pressure

hypertrophy of right side of the heart

Circulatory Dynamics During Exercise in Patients with Valvular Lesions

severe symptoms often develop during heavy exercise

exercise can cause acute LV failure followed by acute pulmonary edema

the patient’s cardiac reserve diminishes in proportion to the severity of the valvular dysfunction

Abnormal Circulatory Dynamics in Congenital Heart Defects

three major types of congenital anomalies of the heart and vessels:

(1) stenosis

congenital aortic valve stenosis

coarctation of the aorta

(2) left-to-right shunt

(3) right-to-left shunt

Patent Ductus Arteriosus—A Left-to-Right Shunt

Closure of the Ductus Arteriosus After Birth

in about 1 of every 5500 babies, ductus does not close

Dynamics of the Circulation with a Persistent Patent Ductus.

Recirculation Through the Lungs

in older child with PDA, one-half to two-thirds of the aortic blood flows backward through the ductus into PA

these do not show cyanosis until later in life, when the heart fails or the lungs become congested.

Diminished Cardiac and Respiratory Reserve

with even moderately strenuous exercise, person is likely to become weak and may even faint from momentary heart failure.

high pressures in the pulmonary vessels often lead to pulmonary congestion and pulmonary edema

most patients with uncorrected PDA die from heart disease between ages 20 and 40 years

Heart Sounds: Machinery Murmur

Surgical Treatment

Tetralogy of Fallot—A Right-to-Left Shunt

most common cause of “blue baby”

four abnormalities of the heart occur simultaneously:

1. aorta originates from the right ventricle or it overrides a hole in the septum, receiving blood from both ventricles

2. PA is stenosed, so low amounts of blood pass from RV to lungs

3. blood from LV flows either through VSD into RV and then into Ao or directly into Ao that overrides this hole

4. enlarged RV

Abnormal Circulatory Dynamics

shunting of blood past the lungs without its becoming oxygenated.

diagnosis of tetralogy of Fallot is usually based on

(1) baby’s skin is cyanotic (blue)

(2) measurement of high systolic pressure in the RV

(3) enlarged RV

(4) abnormal blood flow through interventricular septal hole and into overriding aorta

Surgical Treatment

average life expectancy increases from only 3 to 4 years to 50 or more years.

Causes of Congenital Anomalies

viral infection in the mother during the first trimester of pregnancy

particularly prone to develop when expectant mother contracts German measles

some congenital defects are hereditary

Hypertrophy in Valvular and Congenital Heart Disease

increased strength of contraction of the heart muscle

increased metabolic rate of the muscle

heart sounds