Heart Sounds & Murmurs (Ninja Nerd)

- beginning of ventricular systole
- closure of the MV d/t increased pressure in LV & LV begins to attempt to push blood into the aorta
- closure of the TV as RV pressure increases
--> sound caused by closure of the TV & MV (but at the same time, PV & AV are opening)

- onset of ventricular diastole
- during diastole, blood will attempt to "recoil" back, so preceding valve closure required for continued forward blood flow
- AoV closes faster than PV d/t increased pressure naturally in the aorta, S2 may be represented in 2 parts: A2 and P2
---> sound of S2 = closure of AoV and PV

- extra heart sound, occurring immediately after S2 (bc occurs during filling)
- occurs with LV dilation, LV rapidly fills and blood "bounces" of ventricle walls during filling/diastole, a sound of "turbulence"
- rapid ventricular filling (primarily r/t LV) d/t ventricular dilation, which causes turbulent blood flow/filling of the ventricle
- causes: systolic HF, dilated CMP, young athletes (physiologic ventricular dilation to increase SV/CO during activity)

- rigid, hypertrophic ventricles (primarily LV) --> decreased ventricular filling --> increased work/pressure on atria --> late atrial contraction (S4)
- occurs late after S2/just before S1 (late diastole, just prior to systole)
- causes: diastolic HF, any causes of LV hypertrophy (Ao stenosis & chronic HTN)

- S2 = AoV and PV closure.
- Physiologically, AoV closes before PV as increased aortic pressure (vs PA pressure) aids in rapid AoV closure, although this distincation is not generally auscultated.

Although AoV generally physiologically closes before PV d/t greater pressure in the aorta compared to the PA, it is not usually heard. Split S2 = two distinct sounds for AoV & PV closure/late closure of PV

PHYSIOLOGIC: split not present on expiration but present on inspiration; physiologic decrease in intrathoracic pressure during insp --> increased R venous return --> more blood to be moved by RV/increased RV work --> increased transit time through PV = delayed PV closure = split (+ physiologic early AoV closure as higher pressures in aorta cause earlier closure); CAUSE: respirophasic changes
WIDE: split present on exp and more profound on insp; at baseline/expiration R heart already overloaded then, physiologic increased venous return during insp causes further delay to PV closure = increase R venous return in strained R heart; CAUSES: RBBB, pulm HTN
FIXED: equally split S2 during exp & insp; during exp, L heart pressure > R, when ASD present that change in pressure causes shunting of blood L --> R, causing increased volume to be ejected by RV PLUS heart must deal with physiologic increased venous return caused by decreased intrathoracic pressure of inspiration; increased volume/workload on RV/increased transit time through PV during exp and insp; CAUSE: (primarily) ASD
PARADOXICAL: P2 occurs prior to A2, split/time is decreased during insp; delay in LV ejection; CAUSES: LBBB, increased pressure in the aorta/increased LV work (aortic stenosis, HCM, systemic HTN)

- AORTIC: systolic murmur (aortic stenosis)
- PULMONIC: pulmonic valve diseases
- ERB'S POINT: diastolic murmur (aortic regurg (valvular), HCM)
- TRICUSPID: holosystolic murmur (VSD)
- MITRAL: holosystolic (MR), systolic (MV prolapse), diastolic (mitral stenosis)

- aortic: R 2 IC space, parasternal
- pulmonic: L 2nd IC space, parasternal
- Erb's point: L 3rd IC space, parasternal
- tricuspid: L 4th IC space, parasternal
- mitral: L 5th IC space, midclavicular

- systolic: heard between S1 and S2
- diastolic: heard between S2 and S1 (heard during diastole)
- continuous:

SYSTOLIC
- crescendo-decrescendo: murmur becomes loud then quiet, typically caused by aortic stenosis (initial ejection "click" d/t bowing of the AoV with initial contraction, followed by c-d; found in RUSB radiating to carotids) and HCM (LV outflow obstruction, sound not caused by valve, no "click"; heard ~Erb's point)
- holosystolic/pansystolic (no change in intensity during stystole): MV prolapse (ejection "click" then holosystolic murmur; heard at apex; may also have MVR murmur), MVR (true holosystolic (heart entire time between S1 & S2) as blood flows back into RA; heard at apex, may rad. to axilla), VSD (holosystolic murmur, L 4th ICS)
DIASTOLIC
- decrescendo: aortic regurg (flow from aorta back into LV; heard at Erb's point) and mitral stenosis (strained from from LA to LV, valves "buckle"/"clicking" = "opening snap" then decrescendo murmur; heard at apex)
CONTINUOUS
- PDA (crescendo from S1, decrescendo after S2; "machine-like murmur"; blood shunting from aorta to PA during systole and diastole since aortic pressures > pulmonic in both systole and diastole; heart in L infraclavicular area)

- L sided murmurs indicate pathologies more likely to require tx and R less common
- R sided murmurs generally same quality of murmur/sound but different location (e.g. aortic stenosis vs pulmonic stenosis, MVR vs TVR)