11 03 2014 Heart Sounds Flashcards
(36 cards)
Where are the 3 pathways of getting blood back to the RA?
- Coronary Sinus
- Superior Vena Cava
- Inferior vena Cava
What would cause a prominent increase in the A-wave in a Jugular Venous Pulsation fluctuations?
Tricuspid Stenosis
Right Ventricular Hypertrophy
- anything that would make the atria have to squeeze harder
What would cause a prominent increase in the v-wave in a Jugular Venous Pulsation (JVP) graph?
V-wave : diastolic filling (muscle is relaxed)
Tricuspid Regurgitation
What would cause a prominent y-wave in a Jugular venous pulsation (JVP) schematic?
Y : passive filling of RV (tricuspid opens)
Constrictive Percarditis
What are the 3 factors that affect the intensity of the S1 sound
- Distance (PR interval) between opening of valves and ventricle contraction
- mobility of leaflets
- rate of rise in the ventricular pressure.
Pathological effects that will INCREASE the intensity of S1 sound?
- shortened PR interverval
- leaflets are far apart and slammed shut - Mitral stenosis
- Tachycardia/ high cardiac outputs (exercise or anemia)
Pathological effects that will DECREASE the intensity of S1 sound?
- prolonged PR interval
- gives more time for leaflets to come back towards each other = smaller distance - Mitral regurgitation
- Severe mitral stenosis
- Stiff ventricle: systematic hypertension
Where is S1 best heard?
At the apex of the heart
What is the reasoning behind the physiological splitting of the S2 ; where does it occur; where is it best heard?
- occurs during inspiration
- Increase in negative pressure
- Delays Pulmonic Valve closure
(b/c of delay in back pressures from pulmonic artery)
- early Aortic valve closure
(less venous return from pulmonic vein to LA = less blood going to LV = less filling time = early aortic closure)
Best heard over the pulmonic valve area (2nd left intercostal space)
Explain pathophysiology of a cause that would INCREASE INTENSITY of S2?
Hypertension (systemic or pulmonary)
- velocity of blood in aorta/ pulmonary artery is augments = hits against valve harder
Explain pathophysiology of a douse that would DECREASE INTENSITY of S2?
Aortic or Pulmonic valve stenosis because the leaflets are fixed in position
what are the 3 ways S2 abnormally splits
- widening
- fixed splitting
- Paradoxical splitting
Widening splitting
Separation of A2 and P2 in expiration and EVEN MORE SO in Inspiration
usually caused by RBBB or pulmonic valve stenosis
Fixed splitting
abnormal widening that is constant throughout respiratory cycle
caused by Atrial-septal defect – delay in P2 closure due to chronic volume overload in Rt. heart
Pardoxical splitting
Audible separation between A2 and P2 during EXPIRATION and 1 sound during inspiration
LBBB and severe aortic stenosis
A2 is delayed so much that during inspiration it comes after P2.
LBBB: delay in contraction of A1
Severe aortic stenosis: ventricular ejection is prolongued
What are early extra-systolic sounds?
- name
- what causes sound?
- Characteristic of sound?
- what causes these heart sounds?
- Ejection click
- -opening of aortic or pulmonic valves (after S1)
- sharp- High pitched
heard best over respective valves
- sharp- High pitched
4a. Stenosis: valve reaches elastic limit and velocity with which it opens descends abruptly = click
4b. Dilation of great vessel
tensing of aortic or pulmonic root as blood rushes in.
Aortic ejection click
opening of aortic valve
heard best over aortic area and a base and apex of heart. Does not vary with inspiration
Pulmonic ejection click
opening of pulmonic valve
best heard at base of heart.
intensity decreases with inspiration (due to backflow)
A mid- to- late extra systolic sound is due to what?
Where is this extra systolic sound heard the loudest?
- Ejection click
- systolic prolapse of mitral or tricuspid valve during ventricular contraction
Over perspective mitral or tricuspid valve area
What are the two types of early diastolic Sounds?
- Opening snap
- S3
What causes an opening snap?
What does it sound like? best heard where?
Does it vary with respiration?
Mitral or tricuspid stenosis – early diastolic sound
sharp, high pitched sound; mitral stenosis is best heard between apex and left sternal border.
Does not vary with inspiration; can get confused with widening split (3 heart sounds)
HOwever, the more advanced the stenosis, the shorter then interval
What causes S3 sound?
What does it sound like? best heard where?
when can these sounds be normal?
Overloaded ventricle – tension on chordae tendinae. AKA a VENTRICULAR GALLOP
Dull, low pitched sound
Left-sided : loudest over apex in left lateral decubitus
Right sided: loudest over lower-left sternal borer (tricuspid is)
normal in children.
Sign of congestive heart failure in adult population
What causes S4 sound?
When does it usually appear– as in timing? What does it sound like? best heard where?
Aka as Arterial Gallop
- due to a stifff heart – usually occurs Late Diastole – contraction of atria to try to get blood into stiff LV.
Dull, low pitched sound heard best at the apex in the left lateral decubitus position
What is Quadruple Rhythm?
Timing of beats?
Both S3 and S4 are heard
heard as mid-diastolic low-pitched sound often louder than S1 and S2
