Cardiology Flashcards
sound pattern of increasing intensity caused by increased blood velocity
crescendo
site farthest from the location of greatest intensity at which the sound is still heard; usually transmitted in the direction of blood flow
radiation
heart and stomach are to the right and the liver to the left
situs inversus
forms most of the anterior surface of the heart
right ventricle
location of the apical pulse
5th L ICS at the midclavicular line
AV valves
tricuspid (R) & mitral (L)
number of cusps of the semilunar valves
3
produces S1 heart sound
closure of the mitral & tricuspid valves at the beginning of systole
produces S2 heart sound
closure of the pulmonic & aortic valves
A2 is produced by the aortic (occurs first)
P2 is produced by the pulmonic
sound heard when atria contract to eject any remaining blood
S4
sound produced by ventricular filling
S3
refers to two distinct components to diastolic sounds
split S2 (A2 then P2)
atrial depolarization on ECG
P wave
time from initial stimulation of atria to initial stimulation of ventricles (0.12-0.20 sec)
PR interval
spread of the stimulus through the ventricles
QRS complex (<0.10 sec)
ventricular repolarization on ECG
T wave
When does the ductus arteriosus close?
typically 24-48 hrs after birth
yellowish tumor on upper & lower eyelids
xanthelasma
if apical pulse is more vigorous than expected it should be characterized as
heave or lift
apical pulse that is more forceful & widely distributed, fills systole or is displaced laterally & downward may indicate
increased CO or left ventricular hypertrophy
cause of lift along left sternal border
right ventricular hypertrophy
fine, palpable, rushing vibration over the base of the heart and in the area of the R or L 2nd ICS
thrill
indicates turbulence
What pulse is synchronous with S1
carotid
intensity of sound increases with handgrip
mitral regurgitation
murmur increases in intensity with inspiration & decreases during expiration
right-sided
valsalva increases the intensity of this murmur
hypertrophic
location for auscultation of the aortic valve
R 2nd ICS
The pulmonic is at the same level but on the left
location for auscultation of tricuspid
L 4th ICS
When is split S2 heard?
inspiration
Which heart sound suggests pathology & needs additional investigation?
S4
mid-to-late nonejection systolic clicks
mitral prolapse
rhythm sounds like TEN-nes-see
S4 (atrial gallop)
rhythm sounds like Ken-TUCK-y
S3 (ventricular gallop)
produces an opening “snap”
valvular stenosis
causes a pericardial friction rub
inflammation of the pericardial sac
best position to auscultate for s3 or S4
left lateral
Grading of Heart murmurs
I: barely audible in quiet room II: quiet but clearly audible III: Moderately loud IV: loud, associated with thrill V: very loud with palpable thrill VI: Very loud & audible without stethoscope contact with skin
low diastolic rumble with no radiation
palpable thrill at apex in late diastole
opening snap
decreased arterial pulse amplitude
mitral stenosis
mid-systolic ejection murmur
crescendo-decrescendo
palpable S4
aortic stenosis
murmur fills systole diamond-shaped palpable thrill in systole brisk arterial pulse prominent JVP
subaortic stenosis
systolic murmur heard over pulmonic area & radiating into neck
almost always congenital cause
pulmonic stenosis
diastolic rumble in early and late diastole
decreased arterial pulse amplitude
prominent JVP
caused by rheumatic heart disease, congenital defect
tricuspid valve stenosis
holosystolic high-pitched blowing sound that obliterates S2
radiates to base or left axilla
caused by rheumatic fever, MI, myxoma, rupture of chordae
mitral regurgitation
late systolic murmur preceded by midsystolic clicks
mitral valve prolapse
early diastolic, high pitch
sounds vary with blood pressure
caused by rheumatic heart disease, endocarditis, Marfan, syphilis
aortic regurgitation
holosystolic murmur over right ventricle
blowing
congenital defects, bacterial endocarditis (esp in IV drug users), pulmonary HTN
tricuspid regurgitation
characterized by exaggerated decrease in the amplitude of pulsation during inspiration and increased amplitude in expiration
Can be caused by pericardial effusion, constrictive pericarditis, emphysema, asthma
pulsus paradoxus
Pulse amplitude descriptions
4 = bounding 3 = full, increased 2 = expected 1 = diminished, barely palpable 0 = absent, not palpable
pain from muscle ischemia
claudication
intact system capillary refill time
< 2 sec
normal pulse pressure range
30-40 mm Hg
when would bp in the legs be measured?
if suspect coarctation of the aorta or if diastolic > 90 mm Hg
redness, thickening or tenderness along a superficial vein
thrombophlebitis
complaint of pain when flex the knee with one hand and dorsiflex the foot with the other
+ Homan sign
may indicate venous thrombosis
very deep pit that lasts 2-5 min after compression, coupled with gross distortion of the dependent extremity
4+ pitting edema
Why is HTN a common process of aging?
blood vessels lose elasticity
is essential HTN symptomatic?
typically no
ascites & peripheral edema
evidence of Rt heart failure
stenosis in the descending aortic arch near the origin of the left subclavian artery and ligamentum arteriosum
coarctation of the aorta
sleeping on more than one pillow to breathe
orthopnea
outward movement of the sternal/parasternal area
lift
outward movement of prolonged duration, increased amplitude
heave
inward movement of the chest wall
retraction
outward chest movement
thrust
low-pitched murmurs are heard best with the
bell
observe to evaluate arterial & venous insufficiency
skin color, skin texture, skin temperature, hair distribution
