Heart Murmur, Sounds, and Congenital Flashcards
(45 cards)
1
Q
Compare the following for fetal circulation vs neonatal
- organization of system and pulmonary circuit
- presence of intracardiac shunts
- pulmonary vascular resistance and cardiac output
- location of gas exchange
A
Fetal circulation:
- parallel circulation
- intracardiac shunts
- high pulm vasc resistance, low CO
- gas exchange in placenta
Neonatal circulation:
- series
- NO shunts
- low pulm vasc resistance, high CO
- gas exchange in lungs
2
Q
in fetal ciruclation, where does blood leaving the pulmonary trunk go?
A
Pulmonary artery USUALLY post birth delivers blood to lungs. In fetal circulation, there is high resistance in lungs, so blood flows down ductus arteriosus in R–> L fashion to the aorta to supply the lower part of body
(90% crosses PDA and goes to descending aorta, rest goes to lungs)
3
Q
In fetal vasculature, which pressures are similar and why
A
- LV and RV pressures (65-70)
- pulmonary and systemic arterial pressures (70/30)
- equal because output to both sides is connected by the giant ductus arteriosus
- RA and LA pressures (3-5)
- wide foramen ovale
4
Q
What are the important changes when baby takes first breath
A
- lungs fill up with oxygen, alveoli expand
- oxygen = potent vasodilator
- blood vessels DILATE rapidly
- exception: ductus arteriosus CONSTRICTS (receptors constrict when exposed to high levels of oxygen), functionally closes in 2 days
- thats why you see patent ductus arteriosus in places with low oxygen i.e. colorado
- resistance in lung beds drop dramatically, now blood goes there since lower resistance
5
Q
7 important postnatal changes
A
- foramen ovale closes due to increased LA flow and pressure
-
PDA closes
- O2, ventilation, decreased PGE
- ductus venosus closes passively
-
circulation in series
- no more mixing
-
systemic saturation increases from 60% to >95%
- within minutes of birth
- systemic vascular resistance increases
- placenta removed from circulation
- pulmonary vascular resistance decreases
- pulm blood floow increases
6
Q
6 explanations for post natal pulmonary vasculature low resistance
A
- oxygen mediated changes
- prostacyclin = vasodilator = endothelial derived factors of arachidonic acid –> PGI2 –> cAMP
- NO –> Increases cGMP –> dilation
- mechanical changes
- increased total cross sectional area of vasc bed with growth
- remodeling of vasc smooth muscle
7
Q
equation for flow
what is pulmonary artery pressure determined by?
A
Pressure = Flow x Resistance
(P = QR)
(Q = P/R)
PA pressure determined by:
- pulmonary arteriolar resistance
- right ventricular output (flow)
8
Q
Fick Equation
to determine Pulmonary flow
A
function of consumption over content
Qpulm= O2 consumption (VO2) / pulm venous (PVO2) - pulm artery (PAO2) oxygen content
normal pulmonary flow = 2.5-3.5 L/min/M2
9
Q
explain whey you somtimes hear a diastolic mumur (in addition to a holosytolic murmur) in ventricular septal defect. What is the cause for both murmurs?
A
- mumur is due to turbulence
- big hole equalizes the pressures in the ventricles, so the mumrmur is not coming from L to R
- most of the turbulence is coming across the outflow tract from the RV
- fixed normal sized outflow tract, but more bloodflow through it –> turbulence occurs in the pulmonary artery
- mumur you hear is pulmonary blood flow
- fif you put all the blood in the lungs, it has to go back through pulmonary veins, needs to cross normal sized mitral valve, it will create a noise during diastole (filling)
10
Q
Source of mumur in a small VSD vs Large VSD
A
small = resitrctive, pressure limiting
-noise comes from fast jet of pressure from small hole –> systolic murmur
large = unrestrictive, RV pressure = LV pressure
- smaller shunt due to equalization of pressures
- systolic mumur: pulmonic artery
- diastolic murmur: mitral valve when filling LV
11
Q
3 locations for VSD and most common
A
supracristal
perimembranous (thinnest portion of septum, right near tricuspid)
muscular
12
Q
how do you manipulate PVR and systemic vascular resistance in a large ventricular defect?
A
- you want to minimize the blood that gets to the lungs and increase blood to systemic circuit (since pulmonary has lower resistance than systemic)
- lowering SVR:
- vasodilating agents: ace inhibitors
- raising PVR:
- pulmonary artery band (constrict main artery)
- note: lowering PVR (as with O2) is harmful-raising PVR will cause pHTN in long run
- diuretics help remove excess lung water and reduce preload
13
Q
review the locations for cardiac auscultation. What are the landmarks?
A
A-P-T-M “apartment”
14
Q
Systolic murmurs:
- when they occur
- during which heart sounds
- 6 reasons you hear it
A
- occur when heart contracts/squeezes
- between S1-S2
- 6 conditions:
- aortic stenosis
- pulmonic stenosis
- mitral regurgitation
- tricuspid regurgitation
- VSD
- hypertrophic cardiomyopthy (blood has to flow around thick septum during contraction)
15
Q
Diastolic murmurs
- when they occur
- during which heart sounds
- 4 conditions causing it
A
- when the heart relaxes/fills
- between S2-S1 (longer period than S1-S2)
- 4 conditions:
- mitral stenosis
- tricuspid stenosis
- aortic regurgitation
- pulmonic regurgitation
16
Q
Aortic stenosis-Murmur
- type of murmur
- what happens to murmur as degree of AS worsens
- what happens to S2?
- radiates where?
- pulsus parvus et tardus”
A
- systolic murmur: crescendo-decrescendo
- as AS worsens, murmur peaks later
- S2 gets quiet (stiff valve can’t slam shut)
- often radiates to carotids
- pulsus parvus et tardus - delayed carotid upstroke
17
Q
aortic regurgitation: type of murmur
A
- decrescendo (blowing) diastolic murmur after S2
18
Q
Mitral regurgitation: type of murmur
-where is it best heard?
A
- holosystolic murmur heard best at apex (5th intercostal space, mid-clavicular line)
- between S1-S2
19
Q
Mitral stenosis
- type of murmur
- heart sounds
A
- diastolic rumble (murmur) from S2-S1
- hear an extra heart sound after S2-opening snap sort of like an S3
- occurs because stiff mitral valve leafletts have to open in diastole, after opening and hearing snap, then you get that holostytolic murmur
- dont see an S3 or S4 (indication of rapid filling) becuase here we have a stiff and stenotic valve-hard to fill rapidly
20
Q
Triscuspid and pulmonic disease are valve lesions that sound like left-sided counterparts. The murmur is louder with (inspiration/expiration) because _____. What’s this called?
A
- Inspiration
- when take in breath, increased venous return to right side of heart
- dilates veins in lungs, but drops venous return to L side fo heart
- taking breath of air is sucking air to lungs, will pull more blood past right side of heart but will take some away from L side
- Carvallo’s sign
21
Q
What are clues for the following tricuspid/pulmonic diseases?
- Pulmonic stenosis (2)
- Tricuspid stenosis (2)
- Pulmonic regurg (2)
- Tricuspid regurg (2)
A
- Pulmonic stenosis
- children (congenital)
- carcinoid
- Tricuspid stenosis
- rheumatic heart disease-immigrants, pregnancy
- carcinoid
- Pulmonic regurg
- pulm HTN
- repaird tetralogy of fallot
- Tricuspid regurg
- IV drug users
- pulm HTN (high pressure pushes blood backwards)
22
Q
What are the 3 causes of holosystolic murmurs?
A
- VSD
- mitral valve prolapse (Mitral regurg)
- Tricuspid regurgitation
23
Q
Continuous, “machine-like” murmur
A
PDA (such a small connector of atria to L pulmonary artery
24
Q
Describe the changes that occur with inspiration
-In general, which murmurs increase with inspiration, and which increase with exhalation?
A
- breathe in –> diaphgram moves down –>veins compress in abdomen, veins in thorax dilate and accept blood –> blood moves from abdomen to thorax into heart
- inspiration –> increased venous return to right side of heart
- decreased left heart blood flow (pooling in lungs)
- less flow in mitral stenosis (softer)
- less flow in mitral regurg (softer)
- right sided murmurs INCREASE with inspiration (tricuspid regurg, pulmonic stenosis)
- left sided murmurs INCREASE with exhalation
25
manuevers to increase preload/venous return
* squatting (kink femoral arteries --\> blood in legs forced back to heart) EXCPETION is with TOF: when they squat, they increase their afterload which helps them feel better, because less blood from RV--\> LV via VSD and more blood to lungs
* leg raise (blood falls back toward heart)
26
2 manueveres to decrease preload/venous return
* Valsalva (increase intra thoracic pressure --\> thoracic vein compression --\> decreased venous return)
* Standing (blood falls towards feet, away from heart)
27
Most murmurs INCREASE with preload with the exception of these two:
- **mitral valve prolapse** (mitral valve regurg: when there's more preload, the valve leaflets tighten and dont billow as much up into LA
- Hypertrophic cardiomyopathy: when theres more preload on left side of heart, it pushes the thick septum out of the way from outflow track and decreases murmur [note this is opposite of aortic stenosis, whose murmur INCREASES with INCREASED preload
28
What is one manuever to increase afterload?
What is one manuever to decrease afterload?
Increase: Hand grip - tightly grip fingers, constrict hand arterioles, increase afterload
Decrease: Amyl nitrate (vasodilator)
29
* What is a backward/diastolic murmur
* Is it louder or softer with more afterload?
* what are the 3 examples
* diastolic murmur--all the bloow flowing in the wrong direction
* louder with more afterload (more force pushing blood backward)
* AR, MR, VSD
30
* What is a forward/systolic murmur?
* Is it louder or softer with more afterload
* 2 examples
* heart during systole, murmur heard when blood flowing in the right direction
* softer with more aftelroad
* less presusre difference moving blood forward (will be harder for blood to flow across those valves when there is more afterload, murmur will get softer
* MS, A
31
* most murmurs are LOUDER with preload, except these 2
* Backward murmurs are louder with afterload (3)
* Murmurs softer with afterload(3)
* most murmurs are LOUDER with more preload, except: **HCM **and **MVP**
* Backward murmurs are louder with more afterload: **AR, MR, VSD**
* Murmurs softer with more afterload:** AS, MS, HCM, MVP**
32
CLUES TO DIAGNOSIS:
* young female, otherwise healthy
* healthy, young athlete, syncope
* immigrant or pregnant
* IV drug abuser
* Marfan, turner coarctation of aorta
* Marfan
* young female, otherwise healthy = MVP
* healthy, young athlete, syncope = HCM
* immigrant or pregnant = MITRAL STENOSIS
* IV drug abuser = TRICUSPID REGURG
* Marfan, Turner; coarctation of aorta = biscupid AV, early stenosis, aortic regurgitation
* Marfan = MVP
33
list the murmurs for each condition, when they occur, and what type of murmur
* AS/HCM
* MR/VSD
* AR
* MS
* PDA
see figure
34
S1
S2
which sided valves open first and close last
S1: mitral and tricuspid valves CLOSE
S2: aortic and pulmonic valves CLOSE
RIGHT sided valves open first and close last
35
What is physiologic S2 splitting?
when take in breath, slightly increase VR to RV --\> takes RV longer to pump out all the blood, slightly delays the pulmonic closure
Sum up: S2 has more splitting during inspiration than during exhalation
36
Persisitent S2 splitting
- what is it?
- what 2 conditions are associated with it?
* splitting increases with inspiration like normal, but then doesn't go away even during exhalation
* implies delayed conduction through RV: delays PV closure even during exhalation
* **RBBB**-delayed contraction of RV
* **Pulmonary HTN-** consisitently harder for RV to empty all its blood due to the blockage
peRsistent splitting = Right sided delay
\*note how the splitting in S2 for expiration and inspiration are still different in size
37
* What is fixed S2 splitting?
* how is it different than persistent S2 splitting?
* What condition is associated with it?
* splitting of AV and PV closure (S2) during exhalation and inspirtation
* different than persistent: doesn't change in size, the degree and timing of separation is identical with exhalation and inhalation
* atrial septal defect: flow across ASD created increased venous return during exhalation and inhalation
38
What is paradoxical S2 splitting and what can cause it
when you have an increased split of S2 during exhalation, and during inspiration, heart sounds come together to form a single S2
during exhalation, something is delaying closure of **aortic valve**
or delayed conduction through LV delays AV closure
* Electrical causes --\> delayed activation
* LBBB
* RV Pacing
* Mechanical causes --\> delayed LV outflow
* LV systolic failure
* aortic stenosis
* Hypertrophic cardiomyopathy
ParadoxicaL = Left sided delay
39
Loud P2
* Pulmonic component of S2
* gets louder with pulmonary hypertension
* if you can hear it at apex, you know its loud (usually not heard at apex)
40
S3 and S4 (general description of what they are)
* both are made during diastolic filling of ventricle (they come after S2....)
* S3 --\> early filling sound
* S4 --\> late filling sound
THE NUMBER GIVES YOU THE ANSWER
41
What does S3 usually indicate and why
* indicates person in heart failure
* high LA pressure --\> rapid early filling of LV --\> S3
* associated with increased LA pressure and Increased LVEDP
* "pushers" --\> push blood into LV
* **very specific sign of high left atrial pressure**
* exceptions: young patients, pregnant women = "suckers" due to vigorous LV relaxation, lowering pressure rapidly, sucking blood out of LA
42
Is S3 louder or softer with exhalation
louder with exhalation (pushes heart closer to chest wall)
"ken tucky"
43
S4
what does it indicate and why?
* late filling sound
* indicates a stiff left ventricle
* long standing HTN
* HCM
* diastolic HF
* rapid late filling of LV due to atrial kick -slams blood into stiff wall, this sound requires the atrial kick
* cannot occur in A fib
"tene see"
44
When do you hear an ejection click or a non-ejection click?
SYSTOLIC CLICKS
* Ejection click:
* early in systole
* before carotid pulse
* bicuspid aortic valve
* Non-ejection click:
* late in systolie
* AFTER carotid pulse
* mitral valve prolapse
45
Why do you hear a non-ejection click with MVP?
What does the murmur look like?
- cause click when leaflets snap into the LA, then you get a small amount of mitral regurgitation
- get a click then a murmur
