Heart Sounds and Heart Murmurs

Normal Heart Sounds (S1 and S2)

S1:
- Represents the closure of the mitral and tricuspid valves.
- Occurs when ventricular pressure rises, preventing backflow from the ventricles into the atria.
- After closure, the aortic and pulmonary valves should open, allowing blood to flow out of the ventricles.
S2:
- Represents the closure of the aortic and pulmonary valves.
- Occurs during diastole, preventing backflow of blood from the aorta and pulmonary artery into the ventricles.
- S2 has two components due to pressure differences:
  - A2: Closure of the aortic valve. Occurs slightly earlier because of higher pressure in the aorta.
  - P2: Closure of the pulmonary valve.

Extra Heart Sounds (S3 and S4)

S3:
- Occurs due to rapid ventricular filling, often associated with dilated ventricles.
- Blood rapidly fills the ventricle and bounces off the ventricular walls, creating turbulence of blood flow, and this turbulence triggers a murmur.
- Causes include:
  - Systolic Heart Failure (CHF).
  - Dilated Cardiomyopathy.
  - Physiologic in young, healthy athletes (due to increased stroke volume).
- Occurs early in diastole: after S2, when the mitral and tricuspid valves open.
S4:
- Occurs due to a rigid left ventricle that decreases ventricular filling.
- The atria must contract forcefully to push blood into the stiff ventricle, generating the S4 sound.
- Late atrial contraction is required to overcome the high pressure.
- Causes include:
  - Diastolic Heart Failure.
  - Left Ventricular Hypertrophy, which can be caused by:
    - Aortic Stenosis.
    - Chronic Hypertension.
- Occurs later in diastole: after S2 and after S3 (if present), just before S1 of the next cycle.

Splitting of S2

Splitting refers to the audible separation of the A2 and P2 components of S2. This can be normal (physiological splitting) or abnormal.
Physiological Splitting:
- Normal phenomenon due to respiratory changes.
- During expiration, A2 and P2 are close together and hard to differentiate.
- During inspiration:
  - Intrathoracic pressure drops, increasing venous return to the right ventricle.
  - Increased filling of the right ventricle prolongs the time it takes to eject blood, delaying the closure of the pulmonary valve (P2).
  - A2 remains unchanged, but the separation between A2 and P2 increases.
Wide Splitting:
- The split between A2 and P2 is easily heard during both expiration and inspiration.
- Caused by conditions that delay right ventricular emptying, such as:
  - Right Bundle Branch Block: Delays right ventricular contraction.
  - Pulmonary Hypertension: Increases the afterload on the right ventricle.
- Increased venous return during inspiration further extends the split.
Fixed Splitting:
- The split between A2 and P2 is always the same, regardless of inspiration or expiration.
- Most commonly caused by an Atrial Septal Defect (ASD).
- ASD allows continuous shunting of blood between the atria, equalizing pressures and volumes in the right heart.
- The right heart venous return becomes fixed during both inspiration and expiration because the blood coming from the left heart to the right heart during expiration (left atrial pressures are higher) and because of inspiration dropping the intrathoracic pressure. but overall, the venous return to the right heart is constant.
Paradoxical Splitting:
- P2 occurs before A2 (reversed order).
- The split is wider during expiration and less wide during inspiration.
- Caused by conditions that delay left ventricular emptying, such as:
  - Left Bundle Branch Block: Delays left ventricular depolarization and contraction.
  - Aortic Stenosis.
  - Hypertrophic Obstructive Cardiomyopathy.
  - Systemic Hypertension.
- During expiration, more blood flow comes to the left heart, which will make it harder to get blood out delaying the actual process even more, leading to a wider split.
- During inspiration, right side venous return increases, so it will take a little bit longer to get blood out of it because it's going to have to deal with more blood. This will cause P2 to come closer to A2.

Heart Murmurs

Auscultation Areas:
- Aortic Area: Right second intercostal space; may indicate aortic stenosis.
- Pulmonic Area: Left second intercostal space; may indicate pulmonic valve diseases.
- Erb's Point: Left third intercostal space; sound for aortic regurgitation and HCM.
- Tricuspid Area: Left fourth intercostal space; may indicate a VSD.
- Mitral Area (Apex): Left fifth intercostal space, midclavicular line; may indicate mitral valve disease (stenosis, regurgitation, prolapse).
Timing:
- Systolic: Occurs between S1 and S2.
- Diastolic: Occurs between S2 and S1.
- Continuous: Occurs throughout systole and diastole.
Systolic Murmurs:
- Crescendo-Decrescendo Murmurs:
  - Aortic Stenosis: Louder initially and decreases in intensity. May have an ejection click. Heard at the right upper sternal border, radiating to the carotids.
  - Hypertrophic Cardiomyopathy: Similar sound to aortic stenosis. Heard best at Erb's point, with no radiation to the carotids and no ejection click.
- Holosystolic (or Pansystolic) Murmurs:
  - Mitral Regurgitation: Heard throughout systole. No click. Heard best at the apex, radiating to the axilla.
  - Ventricular Septal Defect (VSD): Also holosystolic. Heard best at the left fourth intercostal space. Louder with smaller holes.
  - Mitral Valve Prolapse: Usually pretty consistent through the systolic process. Hear a click right before the mumur takes place.
Diastolic Murmurs:
- Decrescendo Murmurs:
  - Aortic Regurgitation: The murmur decreases in intensity throughout diastole. Heard best at Erb's point. Involves blood jetting backwards during diastole.
  - Mitral Stenosis: Follows an opening snap (OS) at the apex. Decrescendo murmur. Super difficult to get blood from heart to ventricle.
Continuous Murmurs:
- Patent Ductus Arteriosus (PDA): Machine-like murmur heard throughout systole and diastole. Located around the left infraclavicular area. Aorta pressures are generally higher and blood will keep shunting from the aorta into the pulmonary artery during both systole and diastole.

Maneuvers to Determine Murmur Type

Helpful in differentiating and confirming the origin and severity of murmurs.
Inspiration:
- Increases the intensity of right-sided murmurs due to increased right-side venous return.
- Decreases the intensity of left-sided murmurs.
Expiration:
- Increases left-side venous return which increases the intensity of left-sided murmurs.
- Decreases the intensity of right-sided murmurs.
Leaning Forward:
- Brings the aortic valve closer to the chest wall, increasing the intensity of aortic murmurs.
Lateral Decubitus Position (Lying on Left Side):
- Brings the mitral valve closer to the chest wall, increasing the intensity of mitral murmurs.
Increasing Venous Return (Squatting, Leg Raise):
- Increases the intensity of most murmurs except:
  - Hypertrophic Cardiomyopathy (HCM): Decreases intensity.
  - Mitral Valve Prolapse: Delays the click and shortens the murmur.
Decreasing Venous Return (Valsalva, Standing):
- Decreases the intensity of most murmurs except:
  - Hypertrophic Cardiomyopathy (HCM): Increases intensity.
  - Mitral Valve Prolapse: Advances the click and lengthens the murmur.
Increasing Afterload (Hand Grips):
- Increases the intensity of aortic and mitral regurgitation murmurs.
- Decreases the intensity of aortic stenosis, mitral valve prolapse, and HCM murmurs.
Decreasing Afterload (Amlodipine):
- Decreases the intensity of aortic and mitral regurgitation murmurs.
- Increases the intensity of aortic stenosis, mitral valve prolapse, and HCM murmurs.