Heart Sounds and Murmurs Flashcards
(20 cards)
What is the Physiological Splitting of S2?
- A2: Closure of the aortic valve
- P2: Closure of the pulmonary valve
Normally, during inspiration, there is a physiological split because the pulmonary valve closes slightly later than the aortic valve due to increased venous return to the right heart, delaying right ventricular (RV) systole.
When this split is abnormal, it can tell us a lot about underlying cardiac pathology.
Let’s break this down for each condition you listed:
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- Physiological Splitting
- Normal: During inspiration, S2 splits into A2 and P2 because:
- Increased venous return → prolonged RV systole → delayed pulmonary valve closure.
- Decreased return to the left heart → slightly earlier aortic valve closure.
- During expiration: A2 and P2 are close together (may sound like a single sound).
What is a Wide Splitting S2?
Right Bundle Branch Block (RBBB)
* Type of split: Wide splitting (delayed P2)
* Mechanism:
* Conduction through the right bundle is delayed → delayed right ventricular contraction → delayed pulmonary valve closure.
* Effect: Split widens during inspiration and remains wide during expiration.
* Key point: The right ventricle is always contracting later.
Pulmonary Stenosis
* Type of split: Wide splitting (delayed P2)
* Mechanism:
* Obstruction at the pulmonary valve → prolonged RV systole → delayed pulmonary valve closure.
* Effect: Split widens during inspiration and expiration.
* Key point: The pulmonary valve takes longer to close due to obstruction.
What is a Fixed Split S2?
Atrial Septal Defect (ASD)
* Type of split: Fixed splitting (consistent split, no variation with respiration)
* Mechanism:
* Constant left-to-right shunt → chronically increased right heart volume → prolonged RV systole all the time.
* Effect: The split is “fixed”—the pulmonary valve is always delayed regardless of the breathing cycle.
* Key point: Left-to-right shunt keeps right heart volume consistently high.
What is Paradoxal Splitting of S2?
Left Bundle Branch Block (LBBB)
* Type of split: Paradoxical splitting (reversed split)
* Mechanism:
* Delayed left ventricular contraction → delayed aortic valve closure.
* Effect:
* On expiration, A2 is late, may occur after P2 → split sounds reversed.
* On inspiration, P2 is delayed and comes closer to A2 → split may narrow or disappear.
* Key point: Split is more pronounced on expiration and “paradoxically” narrows on inspiration.
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Aortic Stenosis
* Type of split: Paradoxical splitting
* Mechanism:
* Aortic valve takes longer to close due to obstruction → delayed A2.
* Effect:
* Similar to LBBB: Split is wider on expiration and narrows on inspiration.
* Key point: Prolonged left ventricular systole delays aortic valve closure.
What is the mechanism of Blood flow in heart during inspiration and expiration?
🔹 Key Concept: What Happens During Inspiration vs. Expiration
✔️ During Inspiration:
* Intrathoracic pressure decreases (the chest cavity expands like a vacuum).
* This does two major things:
1. More venous blood returns to the right side of the heart.
2. Less blood returns to the left side (because blood pools in the lungs temporarily due to the expanded chest).
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✔️ Effects of Inspiration on the Heart:
* Right side:
* More blood → right ventricle takes longer to pump → delayed pulmonary valve closure (P2).
* Left side:
* Less blood → left ventricle empties faster → earlier aortic valve closure (A2).
🔑 RESULT:
* The split between A2 and P2 widens during inspiration.
* This is why we hear the “physiological split” of S2 best on inspiration.
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✔️ During Expiration:
* Intrathoracic pressure increases (chest cavity relaxes).
* Venous return decreases to the right heart → less blood → right ventricle finishes faster → pulmonary valve closes sooner.
* Left side fills more → left ventricle takes a little longer → but aortic valve closure is still usually first.
🔑 RESULT:
* The split between A2 and P2 narrows (or may disappear) during expiration.
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🔥 Common Misunderstanding:
You said:
“In inspiration, blood returns to the heart. In expiration, blood goes out of the heart.”
Actually:
* Blood is always going in and out.
* What changes is how much blood is returning to the right heart with each breath.
What matters:
* Inspiration: Increases right heart filling → delays P2.
* Expiration: Less right heart filling → P2 is not delayed → S2 sounds closer together.
Why is the Split in S2 smaller during Expiration compared to Inspiration?
💡 The key is that inspiration affects the right and left sides of the heart in opposite ways.
It’s not that the left ventricle isn’t affected — it is. But the effect is different because of the way the lungs and thoracic pressures interact.
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👉 Why Doesn’t the Left Ventricle Get More Blood During Inspiration?
Here’s the step-by-step physiology:
When you inhale:
1. Intrathoracic pressure decreases.
→ This pulls more blood from the body into the right atrium and right ventricle.
✅ Right side filling increases.
2. BUT — at the same time:
* The lungs expand and become a temporary “blood reservoir.”
* Pulmonary vessels expand and “hold on” to more blood temporarily.
→ This decreases the amount of blood returning to the left atrium.
✅ Left side filling decreases.
✅ Why Does This Happen?
The pulmonary circulation is the key middle player.
* Blood from the right ventricle goes through the lungs to reach the left atrium.
* When you inspire:
* More blood enters the lungs → but this blood takes a few heartbeats to transit through the lungs.
* Meanwhile, the expanded pulmonary vessels temporarily trap more blood.
→ So the left atrium momentarily gets less blood.
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🎯 Important Point:
* Right heart sees immediate increase in preload.
* Left heart sees a momentary decrease in preload.
* Both sides are affected — but in opposite directions.
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💬 Simple Takeaway:
* Inspiration → More blood to the right heart, less to the left heart.
* Expiration → Normalizes the flow on both sides.
✅ Why Does This Happen?
The pulmonary circulation is the key middle player.
* Blood from the right ventricle goes through the lungs to reach the left atrium.
* When you inspire:
* More blood enters the lungs → but this blood takes a few heartbeats to transit through the lungs.
* Meanwhile, the expanded pulmonary vessels temporarily trap more blood.
→ So the left atrium momentarily gets less blood.
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🎯 Important Point:
* Right heart sees immediate increase in preload.
* Left heart sees a momentary decrease in preload.
* Both sides are affected — but in opposite directions.
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💬 Simple Takeaway:
* Inspiration → More blood to the right heart, less to the left heart.
* Expiration → Normalizes the flow on both sides.
Here’s the core idea:
When you breathe in (inspiration):
* Intrathoracic pressure drops → this acts like a vacuum that sucks more blood into the right side of the heart → more venous return to the right atrium → right ventricle fills more → takes longer to pump → delayed pulmonary valve closure (delayed P2).
BUT AT THE SAME TIME:
* The lungs expand.
* The blood vessels in the lungs (the pulmonary capillaries) stretch and temporarily hold more blood.
* This temporarily traps blood in the lungs.
* So less blood returns to the left atrium and left ventricle during that phase → the left ventricle fills less → it contracts faster → earlier aortic valve closure (earlier A2).
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🔥 So, in short:
Inspiration:
* 🫀 Right heart → more blood → P2 delayed
* ❤️ Left heart → less blood → A2 happens earlier
This is why the split between A2 and P2 widens on inspiration.
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✅ The lung vessel dilation isn’t primarily for oxygen exchange in this case.
It’s more about:
* The physical expansion of the lungs
* The pulmonary vessels stretching and holding more blood temporarily
* Causing a temporary reduction in the blood flowing back to the left heart.
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🔄 Expiration:
When you breathe out:
* Thoracic pressure increases → less blood to the right heart → RV empties faster → pulmonary valve closes sooner.
* Pulmonary vessels are less expanded → blood more easily flows to the left atrium → more filling of the left heart → LV takes slightly longer to contract.
This makes A2 and P2 closer together during expiration.
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🎯 Super Simple Final Summary:
* Inspiration:
→ More blood into the right heart
→ Less blood into the left heart
→ A2 happens earlier, P2 happens later → WIDER SPLIT
* Expiration:
→ Normal blood flow to both sides
→ A2 and P2 close together → NARROWER SPLIT
What is a murmur?
- Heart murmurs are produced by turbulent flow (Reynolds no. >2000) across an
abnormal valve, septal defect or outflow obstruction or by increased volume or
velocity of flow through a normal valve. - Murmurs may occur in a healthy heart. These ‘Innocent murmurs” occur when
stroke volume is increased e.g., during pregnancy, in athletes with resting
bradycardia or children with fever and anemia.
What are the heart sounds S1 and S2?
💡 Heart Sounds: The Basics
We have two key heart sounds:
* S1 (“lub”) → AV valves close (mitral & tricuspid)
* S2 (“dub”) → Semilunar valves close (aortic & pulmonary)
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🔄 Timing of Valve Events in the Cardiac Cycle
✅ Systole (After S1)
* AV valves are CLOSED → So blood can’t go backward into the atria.
* Semilunar valves are OPEN → Blood is being ejected into the aorta and pulmonary artery.
✅ Diastole (After S2)
* Semilunar valves are CLOSED → To prevent blood from flowing back into ventricles.
* AV valves are OPEN → To allow blood to flow from atria into ventricles.
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🎯 So Why Do We Hear Murmurs When We Do?
🔹 If the valve is supposed to be OPEN → you hear a murmur if it’s NARROW (Stenosis)
* Aortic/Pulmonary Stenosis → Systolic Murmur
Semilunar valves should be wide open during systole → if they’re narrowed → turbulent flow → systolic murmur.
* Mitral/Tricuspid Stenosis → Diastolic Murmur
AV valves should be wide open during diastole → if they’re narrowed → turbulent flow → diastolic murmur.
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🔹 If the valve is supposed to be CLOSED → you hear a murmur if it’s LEAKY (Regurgitation)
* Mitral/Tricuspid Regurgitation → Systolic Murmur
AV valves should be closed during systole → if they leak → blood flows backward → systolic murmur.
* Aortic/Pulmonary Regurgitation → Diastolic Murmur
Semilunar valves should be closed during diastole → if they leak → blood flows backward → diastolic murmur.
S1:
- AV valves close (mitral/tricuspid) → Start of systole
S2:
- Semilunar valves close (aortic/pulmonary) → Start of diastole
What are the different heart sounds?
🎧 Heart Murmurs by Valve Problem
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🔹 1. Aortic Valve
✅ Aortic Stenosis (AS)
* Type: Systolic ejection murmur (crescendo-decrescendo)
* Timing: Mid-systole
* Sound: Harsh, crescendo-decrescendo
* Best heard: Right upper sternal border (2nd intercostal space)
* Radiates to: Carotids
* Key clue: Pulsus parvus et tardus (slow, weak pulse)
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✅ Aortic Regurgitation (AR)
* Type: Diastolic murmur
* Timing: Early diastole
* Sound: Blowing, decrescendo
* Best heard: Left sternal border (3rd intercostal space)
* Key clue: Wide pulse pressure, bounding pulses, may have an Austin Flint murmur (functional mitral stenosis)
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🔹 2. Pulmonary Valve
✅ Pulmonary Stenosis (PS)
* Type: Systolic ejection murmur (crescendo-decrescendo)
* Timing: Mid-systole
* Sound: Harsh
* Best heard: Left upper sternal border (2nd intercostal space)
* Radiates to: Neck/left shoulder
* Key clue: Can have widened S2 split
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✅ Pulmonary Regurgitation (PR)
* Type: Diastolic murmur
* Timing: Early diastole
* Sound: Blowing, decrescendo
* Best heard: Left upper sternal border
* Key clue: In pulmonary hypertension → called Graham Steell murmur
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🔹 3. Mitral Valve
✅ Mitral Regurgitation (MR)
* Type: Holosystolic murmur
* Timing: Entire systole
* Sound: Blowing, constant
* Best heard: Apex
* Radiates to: Left axilla
* Key clue: Loud, constant throughout systole
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✅ Mitral Stenosis (MS)
* Type: Diastolic rumbling murmur
* Timing: Mid-to-late diastole, following an opening snap
* Sound: Low-pitched rumble
* Best heard: Apex, left lateral decubitus
* Key clue: Opening snap after S2, pre-systolic accentuation if sinus rhythm
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🔹 4. Tricuspid Valve
✅ Tricuspid Regurgitation (TR)
* Type: Holosystolic murmur
* Timing: Entire systole
* Sound: Blowing
* Best heard: Lower left sternal border
* Key clue: Louder with inspiration (Carvallo’s sign)
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✅ Tricuspid Stenosis (TS)
* Type: Diastolic rumbling murmur
* Timing: Mid-to-late diastole, may have an opening snap
* Sound: Low-pitched rumble
* Best heard: Lower left sternal border
* Key clue: Louder with inspiration
“SAD” = Systolic Aortic and Pulmonary Stenosis, AV valve regurgitation
“Diastolic = Semilunar regurgitation and AV valve stenosis”
Blowing Murmurs vs. Holosystolic Murmurs: Key Differences?
✅ Blowing Murmurs:
* Typically associated with regurgitation.
* Common in:
* Aortic regurgitation (AR)
* Pulmonary regurgitation (PR)
* Timing:
* Often early diastolic (for semilunar valves)
* Sound:
* High-pitched, blowing, decrescendo
* Why?
* Blood is leaking back through a semilunar valve when it should be closed.
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✅ Holosystolic Murmurs:
* Specifically associated with AV valve regurgitation.
* Common in:
* Mitral regurgitation (MR)
* Tricuspid regurgitation (TR)
* Timing:
* Throughout systole (from S1 to S2)
* Sound:
* Blowing, but specifically constant throughout systole.
* Why?
* Blood is leaking back through an AV valve throughout the entire time the ventricle is contracting → no change in murmur intensity → it’s uniform (holosystolic).
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🚨 Key Distinction:
* Both can be described as “blowing” because that’s the quality of the sound (high-pitched, smooth turbulence).
* But “holosystolic” describes timing → the murmur is heard uniformly across all of systole.
💥 Summary:
✔️ All holosystolic murmurs are typically blowing in quality.
✔️ But not all blowing murmurs are holosystolic.
* For example, aortic regurgitation has a blowing murmur that is diastolic, not holosystolic.
AV Valve vs. Semilunar Valve Murmurs?
🔹 AV Valve Stenosis → Diastolic Murmur
* Why?
AV valves (mitral and tricuspid) are supposed to be open during diastole to allow blood to flow from the atria to the ventricles.
* If stenotic:
The narrowed valve creates turbulence when blood is trying to flow through during diastole.
* Example:
* Mitral stenosis → diastolic, low-pitched, rumbling murmur
* Tricuspid stenosis → diastolic, low-pitched, rumbling murmur
* Often associated with:
Opening snap + pre-systolic accentuation if sinus rhythm is present.
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🔹 Semilunar Valve Stenosis → Systolic Murmur
* Why?
Semilunar valves (aortic and pulmonary) are supposed to be open during systole to allow blood ejection from ventricles.
* If stenotic:
The narrowed valve creates turbulence when blood is being ejected during systole.
* Example:
* Aortic stenosis → systolic, crescendo-decrescendo murmur
* Pulmonary stenosis → systolic, crescendo-decrescendo murmur
* Often associated with:
Ejection clicks, radiating murmurs (e.g., to carotids in aortic stenosis)
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🔑 Quick Mnemonic:
“Stenosis = Turbulence when the valve is supposed to be open.”
🎯 Summary:
* ✔️ AV valve stenosis (mitral, tricuspid) → Diastolic murmur
* ✔️ Semilunar valve stenosis (aortic, pulmonary) → Systolic crescendo-decrescendo murmur
Causes of Systolic Murmurs?
✅ 1. Semilunar Valve Stenosis
* Examples:
* Aortic Stenosis
* Pulmonary Stenosis
* Sound:
Classic crescendo-decrescendo (ejection-type murmur)
* Why?
The semilunar valves should be wide open in systole → if they are narrowed → turbulence → systolic murmur.
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✅ 2. AV Valve Regurgitation
* Examples:
* Mitral Regurgitation
* Tricuspid Regurgitation
* Sound:
Holosystolic (uniform throughout systole), typically blowing in quality.
* Why?
AV valves should be closed in systole → if they leak → blood regurgitates backward → systolic murmur.
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✅ 3. Ventricular Septal Defect (VSD)
* Sound:
Holosystolic murmur, similar to mitral regurgitation.
* Why?
There’s a left-to-right shunt from high-pressure left ventricle to low-pressure right ventricle → occurs throughout systole → systolic murmur.
✅ Key Takeaway:
* ✔️ Semilunar valve stenosis → systolic crescendo-decrescendo murmur.
* ✔️ AV valve regurgitation → systolic holosystolic murmur.
* ✔️ VSD → systolic holosystolic murmur.
* ✔️ High flow (like anemia) → can also cause innocent systolic murmurs.
🔊 Heart Murmurs: Full Summary for Each Valve Problem:
🫀 Aortic Valve
* Aortic Stenosis:
This is a systolic murmur. It has a crescendo-decrescendo (diamond-shaped) sound that peaks mid-systole. It is typically harsh and heard best at the right upper sternal border, and it often radiates to the carotids. It happens because the aortic valve is narrowed, making it harder for blood to leave the left ventricle during systole.
* Aortic Regurgitation:
This is a diastolic murmur. It is a blowing, decrescendo sound heard best along the left sternal border. It occurs because the aortic valve is leaky and allows blood to flow backward into the left ventricle during diastole. It often comes with a widened pulse pressure and bounding pulses.
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🫀 Pulmonary Valve
* Pulmonary Stenosis:
This is a systolic murmur with a crescendo-decrescendo pattern. It is best heard at the left upper sternal border and may radiate to the left shoulder or neck. It occurs because the pulmonary valve is narrowed, making it harder for blood to leave the right ventricle during systole.
* Pulmonary Regurgitation:
This is a diastolic murmur. It is a blowing, decrescendo sound heard best at the left upper sternal border. It happens because the pulmonary valve is leaky, allowing blood to flow backward into the right ventricle during diastole. In pulmonary hypertension, this can produce the high-pitched Graham Steell murmur.
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🫀 Mitral Valve
* Mitral Regurgitation:
This is a holosystolic murmur. It is blowing and heard best at the apex, often radiating to the left axilla. It happens throughout systole because the mitral valve is leaking, allowing blood to flow backward into the left atrium the whole time the ventricle is contracting.
* Mitral Stenosis:
This is a diastolic murmur. It has a low-pitched, rumbling sound heard best at the apex, especially in the left lateral decubitus position. It usually follows an opening snap after S2 and often gets louder just before systole (called pre-systolic accentuation) if the patient is in sinus rhythm. It happens because the mitral valve is narrowed, restricting blood flow from the left atrium to the left ventricle during diastole.
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🫀 Tricuspid Valve
* Tricuspid Regurgitation:
This is a holosystolic murmur. It is blowing and heard best at the lower left sternal border. It gets louder with inspiration (Carvallo’s sign) because right-sided murmurs increase with venous return during inspiration. It happens because the tricuspid valve is leaking, allowing blood to flow backward into the right atrium throughout systole.
* Tricuspid Stenosis:
This is a diastolic murmur. It is a low-pitched, rumbling sound heard best at the lower left sternal border and also gets louder with inspiration. It happens because the tricuspid valve is narrowed, restricting blood flow from the right atrium to the right ventricle during diastole.
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🫀 Key Patterns to Remember:
* Systolic Murmurs:
* Semilunar valve stenosis (aortic, pulmonary) → crescendo-decrescendo
* AV valve regurgitation (mitral, tricuspid) → holosystolic, blowing
* Ventricular septal defect → holosystolic, blowing
* Diastolic Murmurs:
* Semilunar valve regurgitation (aortic, pulmonary) → early diastolic, blowing, decrescendo
* AV valve stenosis (mitral, tricuspid) → low-pitched, rumbling, often with an opening snap
What is Patent Ductus Arteriosus (PDA) murmur?
What is it?
The ductus arteriosus is a normal fetal blood vessel that connects the pulmonary artery to the aorta to bypass the fetal lungs. After birth, it should close within 10-18 hours.
* Why does it stay open?
* Prematurity
* Perinatal distress
* Hypoxia
But most cases occur even without these risk factors.
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🔊 Murmur Characteristics:
* Type:
Continuous “machinery-like” murmur (it occurs during both systole and diastole).
* Why continuous?
There’s always a pressure gradient from the aorta (higher pressure) to the pulmonary artery (lower pressure), so blood continuously flows through the ductus in both systole and diastole.
* Where heard best?
Left upper chest (left infraclavicular area).
* Extra clue:
The murmur is often louder during systole (accentuated then), but it is still present throughout the cardiac cycle.
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🚨 Clinical Tip:
* PDA often presents with bounding pulses and widened pulse pressure (because of the runoff of blood into the pulmonary circulation during diastole).
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🔑 Key Takeaway:
* PDA = Continuous, machinery murmur, loudest at left upper chest, often louder in systole.
What Causes a Bounding Pulse?
A bounding pulse typically happens when there is:
* Increased stroke volume (the heart is pumping a large amount of blood per beat)
* Decreased diastolic pressure (blood is rapidly leaving the arteries during diastole)
This creates a wide pulse pressure (the difference between systolic and diastolic pressures is large).
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🫀 Classic Causes of Bounding Pulses:
1. Patent Ductus Arteriosus (PDA)
2. Aortic Regurgitation
3. High-output states (fever, anemia, hyperthyroidism, pregnancy)
4. Arteriovenous fistulas
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📌 Why in PDA?
In PDA, blood is continuously shunting from the high-pressure aorta to the low-pressure pulmonary artery → this lowers diastolic pressure because blood is running off into the lungs → results in a wide pulse pressure and bounding pulse.
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🚨 What it feels like:
* Strong, rapid upstroke
* Feels like the pulse “hits your fingers hard”
* Rapid collapse or fall-off after the peak
Why Aortic Regurgitation Causes a Bounding Pulse?
✅ In AR, you’re actually pumping out more blood, not less.
Here’s why:
* In aortic regurgitation, when the heart pumps during systole, it ejects a normal stroke volume into the aorta.
* But during diastole, some of that blood leaks backward into the left ventricle.
* So in the next heartbeat, the left ventricle has to pump out:
* The normal blood returning from the lungs plus
* The extra blood that just leaked back in.
👉 This causes the left ventricle to pump a larger stroke volume than normal.
It’s actually a kind of volume overload.
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✅ Resulting Hemodynamic Changes:
1. Increased Systolic Pressure:
The heart is ejecting a huge amount of blood → systolic pressure goes up.
2. Decreased Diastolic Pressure:
Blood is leaking out of the aorta rapidly during diastole → diastolic pressure falls.
3. Wide Pulse Pressure:
Big difference between high systolic and low diastolic pressures → this is the classic setup for a bounding pulse.
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🔊 Why the Pulse Feels Bounding:
* The pulse rapidly rises because the heart is ejecting a large volume forcefully.
* The pulse falls quickly because blood is rapidly leaking backward into the ventricle during diastole → arterial pressure drops quickly → this rapid rise and fall creates the characteristic “water-hammer” or bounding pulse.
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✅ Key Signs of Bounding Pulse in Aortic Regurgitation:
* Wide pulse pressure (e.g. 160/50 mmHg)
* Water-hammer pulse (also called Corrigan pulse) → rapidly rising and falling pulse
* Head bobbing (de Musset’s sign), nail bed pulsations (Quincke’s sign), and other high-pulse-pressure signs can also be seen.
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🔥 Bottom Line:
Even though blood is leaking back in aortic regurgitation, the heart compensates by pumping out more blood with each beat, which actually creates a higher stroke volume and a more forceful pulse.
The combination of high systolic pressure and low diastolic pressure is what gives you the bounding, water-hammer pulse.
Where causes the turbulence for Aortic Stenosis?
- Root of the Aorta
Difference between Ejection Click and Opening Snap?
👉 Actually, an ejection click is not typically associated with mitral stenosis.
Let me explain the key differences and the right associations:
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🔔 What is an Ejection Click?
* An ejection click is an early systolic, high-pitched sound that occurs shortly after S1.
* It is caused by the sudden opening of abnormal semilunar valves (aortic or pulmonary).
* Common causes:
* Bicuspid aortic valve
* Aortic stenosis (when the valve is still mobile)
* Pulmonary stenosis
* It’s best heard just after S1, during systole.
🔥 Key: Ejection clicks are linked to semilunar valves.
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🫀 What Happens in Mitral Stenosis?
In mitral stenosis, you don’t get an ejection click.
Instead, you hear an Opening Snap (OS).
➤ Opening Snap:
* A sharp, high-pitched sound that occurs just after S2 during early diastole.
* It happens when the stiff, stenotic mitral valve snaps open under high left atrial pressure.
* Best heard at the apex or lower left sternal border.
➤ Why no ejection click here?
* Because the mitral valve is not a semilunar valve and it doesn’t “snap open” during systole — it opens during diastole.
* Ejection clicks only happen with aortic or pulmonary valve abnormalities.
🗣️ Easy Mnemonic: * Ejection Click = Outflow problem (aortic/pulmonary) * Opening Snap = Inflow problem (mitral/tricuspid)
What does S1 and S2 represent?
🫀 Heart Sounds and the Cardiac Cycle
✅ S1 → Start of Systole
* What happens?
* Closure of mitral and tricuspid valves (the AV valves).
* Ventricles start contracting.
* On ECG: Just after the QRS complex starts.
✅ S2 → Start of Diastole
* What happens?
* Closure of aortic and pulmonary valves (the semilunar valves).
* Ventricles relax → filling begins.
* On ECG: Just after the T wave ends.
🗣️ Quick Mnemonic:
* “S1 is Shut the AV valves → Systole starts.”
* “S2 is Shut the semilunar valves → Diastole starts.”
What is S3 and S4?
🫀 S3 – Ventricular Gallop
* When: Early diastole (right after S2)
* Cause: Rapid filling of a dilated or overly compliant ventricle.
* Who has it?
* Normal in: Children, young adults, athletes
* Pathological in: Heart failure, volume overload (mitral regurgitation, dilated cardiomyopathy)
* Mnemonic: “Slosh-ing-in” (Kentucky rhythm)
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🫀 S4 – Atrial Gallop
* When: Late diastole (just before S1)
* Cause: Atrial contraction into a stiff, non-compliant ventricle.
* Who has it?
* Always pathological: Seen in left ventricular hypertrophy (hypertension, aortic stenosis, hypertrophic cardiomyopathy)
* Absent in: Atrial fibrillation (atria aren’t contracting)
* Mnemonic: “A-stiff-wall” (Tennessee rhythm)
