Phys 23

Front 1

lub/first heart sound

Back 1

AV valves at beginning of systole

Front 2

dub/second heart sound

Back 2

closure of semilunar valves at end of systole

Front 3

what causes the 1st and 2nd heart sounds

Back 3

vibration of taut valves immediately after closure along with vibration of adjacent walls of heart and major vessels around heart

Front 4

duration of 1st and 2nd heart sounds

Back 4

0.14s and 0.11 s

Front 5

why is the 2nd heart sound have a shorter duration

Back 5

semilunar valves are more taut and vibrate for a shorter time

Front 6

pitch of first 2 heart sounds

Back 6

lowest human detectible of 40 cycles/s to 500 cycles/s (goes down to 3 or 4 cycles/s)

Front 7

why does 2nd heart sound have higher frequency

Back 7

tautness and greater elastic coefficient

Front 8

3rd heart sound

Back 8

wek rumble heard at beginning of middle third of diastole

Front 9

reason for 3rd heart sound

Back 9

oscillation of blood back anf forth btwn walls of verntricles (unproven)

Front 10

4th heart sound

Back 10

occurs when atria contract; caused by in-rush of blood into ventricles; almost never heard via stethoscope - less than 20 cycles/s

Front 11

aortic valve ausculation area

Back 11

right chest next to sternum under 2nd rib

Front 12

how often is the 3rd heart sound recorded by phonocardiogram

Back 12

1/3 to 1/2 of all people

Front 13

how often is the 4th heart sound recorded by phonocardiogram

Back 13

1/4 all people

Front 14

rheumatic fever

Back 14

autoimmune disease in which heart valves are likely to be damaged or destroyed

Front 15

What is rheumatic fever generally initiated by

Back 15

streptococcal toxin (group A hemolytic streptococci infection)

Front 16

what is the degree of heart valve damage correlated with in rheumatic fever

Back 16

concentration and persistence of antibodies

Front 17

Why are mitral than aortic valve more vulnerable

Back 17

more trauma during contraction

Front 18

stenosis

Back 18

valves adherant to one another so that blood can not flow through it normally

Front 19

regurgitation

Back 19

valve can not close

Front 20

systolic murmur of aortic stenosis

Back 20

high velocity through valve creates turbulence in root of aotra, which causes intense vibration and a loud murmur

Front 21

diastolic murmur of aortic reguritation

Back 21

backwards flow of blood causes a 'blowing' murmur of high pitch with a swishing quality

Front 22

systolic murmur of mitral regurgitation

Back 22

backwards flow through mitral valve; created blowing/swishing sound; transmitted most strongly into L atrium

Front 23

diastolic murmur of mitral stenosis

Back 23

weak and of very low frequency

Front 24

compensations to reduced net stroke volume (in aortic stensosis or regurgitation)

Back 24

hypertrophy of L ventricle, increase in blood volume

Front 25

what occurs when L ventricle can not keep up with work load

Back 25

pulmonary edema; serious edema at L atrial Ps of 25-40 mmHg

Front 26

high L atrial P in mitral valve disease (stenosis or regurgitation) causes

Back 26

enlargement of L atrium; predisposed patient to atrial fibrilation (circus movements)

Front 27

what occurs as L atrial Ps rise in mitral valvular disease

Back 27

pulmonary arteriolar constriction, daming of blood back to pulmonary artery, causes hypertrophy of R side of heart

Front 28

exercise in patients with aortic valvular lesions

Back 28

acute L ventricular failure followed by acute pulmonary edema

Front 29

exercise in patients with mitral disease

Back 29

damming of blood in lungs can cause serious/lethal pulmonary edema in as little as 10 minutes

Front 30

3 major types of congenital abnormalities in vessels

Back 30

1) stenosis 2) left-to-right shunt 3) right-to-left shunt

Front 31

how often does the ductus arteriosus not close

Back 31

1 out of 5500 babies

Front 32

how much blood goes through the patent ductus arteriosis of an older child

Back 32

1/2 to 2/3; blood is often better oxygenated in early life due to the number of times it passes through lungs

Front 33

major effect of patient with patent ductus arteriosus

Back 33

decreased cardiac and respiratory reserve

Front 34

when does a patent ductus arteriosus become lethal if not corrected

Back 34

btwn 20-40

Front 35

murmur of patent ductus arteriosus by age

Back 35

neonate: none or insignificant; 1-3 yrs: harsh, blowing murmur in pulmonary area of chest - called machinery murmur

Front 36

Tetralogy of Fallot (right-to-left shunt)

Back 36

1) aorta originates from R ventricle 2) pulmonary artery stenosed 3) L ventricular blood goes to R ventricle then aorta 4) R ventricle highly muscular

Front 37

diagnosis of tetralogy of fallot

Back 37

1) cyanotic 2) high systolic R ventricular pressure 3) radiological silhouette of heart 4) angiograms

Front 38

life expectancy of corrected tetralogy of fallot vs uncorrected

Back 38

50 yrs or more vs 3-4 yrs

Front 39

most comon cause of congenital heart defects

Back 39

viral infection of mother during 1st trimester (ex German measles)

Front 40

methods of extracorporeal circulation

Back 40

1) bubble oxygen through blood and remove bubbles 2) dripping blood over surface of plastic sheets with O2 3) pass blood over rotating discs 4) pass blood btwn thin membranes or tubes

Front 41

2 theries of how heart hypertrophies

Back 41

1) strength of contraction 2) increased metabolic rate