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Heart Physiology, Cardiac Cycle, Heart Sounds & Murmurs

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1. Heart Physiology Overview

• Pulmonary circulation: Right heart → lungs → oxygenation
• Systemic circulation: Left heart → body → oxygen delivery

Initiation of the Heartbeat

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2. The Cardiac Cycle — Seven Phases

Phase A — Atrial Systole

• ECG event: P wave (atrial depolarization)
• Mechanism: Left atrium contracts → left atrial pressure rises → blood is actively pushed through the open mitral valve into the left ventricle
• Valve status: Mitral valve open; aortic valve closed
• Volume: Ventricular volume increases slightly (~final 20–30 mL of filling = "atrial kick")
• Venous pulse: a wave (atrial contraction reflected back to jugular veins)
• Heart sound: S4 — not heard in normal adults; heard if ventricular compliance is reduced (e.g., hypertrophy)
• Clinical note: At end of atrial systole, the ventricle reaches end-diastolic volume (EDV) ≈ 120–130 mL

Phase B — Isovolumetric Ventricular Contraction (IVC)

• ECG event: QRS complex (ventricular depolarization)
• Mechanism: Ventricles begin contracting → ventricular pressure rises rapidly → mitral valve snaps closed when LV pressure exceeds LA pressure
• Valve status: All valves CLOSED — no blood leaves or enters; volume is constant (hence "isovolumetric")
• Pressure: LV pressure rises steeply but has not yet exceeded aortic pressure (~80 mmHg)
• Heart sound: S1 ("lub") — caused by closure and vibration of mitral + tricuspid valves
• Duration: Very short (~0.05 s)

Phase C — Rapid Ventricular Ejection

• ECG event: ST segment
• Mechanism: LV pressure exceeds aortic pressure (~80 mmHg) → aortic valve opens → blood is rapidly ejected into aorta
• Valve status: Aortic valve open; mitral valve closed
• Volume: Ventricular volume falls rapidly (ejects ~70% of stroke volume here)
• Pressure: Both LV and aortic pressure rise to maximum (~120 mmHg)
• Venous pulse: c wave (tricuspid valve bulging into right atrium)

Phase D — Reduced Ventricular Ejection

• ECG event: T wave begins (ventricular repolarization)
• Mechanism: Ventricles continue ejecting but rate slows; ventricular pressure begins to fall; aortic pressure also slowly falls as blood runs off into the arterial tree
• Volume: Ventricular volume reaches minimum = end-systolic volume (ESV) ≈ 50–60 mL
• Stroke volume = EDV − ESV ≈ 70 mL

Phase E — Isovolumetric Ventricular Relaxation (IVR)

• ECG event: After T wave
• Mechanism: Ventricles relax → LV pressure falls rapidly below aortic pressure → aortic valve closes
• Valve status: All valves CLOSED again
• Volume: Constant (no flow)
• Heart sound: S2 ("dub") — caused by closure and vibration of aortic + pulmonary valves
• Dicrotic notch: Brief backflow of blood against the closed aortic valve creates a small notch on the aortic pressure tracing

Phase F — Rapid Ventricular Filling

• Mechanism: LV pressure falls below left atrial pressure → mitral valve opens → blood flows passively and rapidly from atrium into ventricle
• Volume: LV volume rises steeply
• Venous pulse: v wave (blood accumulated in atrium during ventricular systole now empties)
• Heart sound: S3 — a low-frequency "gallop" sound at the beginning of rapid filling; normal in children/young adults; pathological in adults over 40 (indicates reduced ventricular compliance or heart failure)

Phase G — Reduced Ventricular Filling (Diastasis)

• Mechanism: Filling slows as pressure gradients equalize; ventricle passively fills at a much slower rate
• Volume: Gradual further increase until the next atrial systole
• This phase shortens significantly at high heart rates

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Summary Table (Costanzo Physiology, Table 4.5)

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3. Heart Sounds in Detail

S1 — First Heart Sound ("lub")

• Timing: Beginning of systole (phase B)
• Cause: Closure of the mitral + tricuspid valves. Sudden backflow of blood against the closing AV valves causes them to bulge toward the atria, the chordae tendineae snap taut, and blood reverberates within the ventricle — generating vibrations that travel through the chest wall.
• Characteristics: Low pitch, longer (~0.14 s), heard best at the apex (mitral area)
• Components: M1 (mitral) precedes T1 (tricuspid) by a few milliseconds; normally heard as a single sound

S2 — Second Heart Sound ("dub")

• Timing: Beginning of diastole (phase E)
• Cause: Closure of the aortic + pulmonary valves. Blood rebounds back toward the ventricles, striking the closed semilunar valves and reverberating in the arterial walls.
• Characteristics: Higher pitch, shorter (~0.11 s) — semilunar valves are tauter than AV valves and produce shorter vibration
• Physiological splitting: During inspiration, increased venous return fills the RV → pulmonic valve (P2) closes slightly later than aortic valve (A2). This physiological split of S2 on inspiration is normal.
• Fixed splitting: In ASD (atrial septal defect), splitting doesn't vary with respiration
• Paradoxical splitting: In aortic stenosis or LBBB, A2 is delayed — the split is heard on expiration

S3 — Third Heart Sound

• Timing: Early diastole, during rapid ventricular filling (phase F)
• Cause: Vibrations from rapid, turbulent filling of a ventricle that suddenly decelerates when it reaches its elastic limit
• Normal in: Children, young adults, pregnant women
• Pathological in: Adults >40 years → indicates heart failure (ventricular dysfunction/increased preload) or mitral regurgitation
• Quality: Low-pitched, soft, heard best with the bell of the stethoscope at the apex
• Rhythm: Produces a "gallop" — "lub-dub-dub" (Ken-tuc-ky)

S4 — Fourth Heart Sound

• Timing: Late diastole, just before S1, during atrial systole (phase A)
• Cause: Vibrations when atria contract forcefully against a stiff (non-compliant) ventricle
• Always pathological in adults — heard in:
  • Left ventricular hypertrophy (hypertension, aortic stenosis)
  • Hypertrophic cardiomyopathy
  • Acute MI (stiff, ischemic ventricle)
• Quality: Low-pitched; heard with bell at the apex
• Rhythm: "Ten-nes-see" — "dub-lub-dub"

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4. Cardiac Murmurs — Mechanism and Classification

General Mechanisms of Murmur Production:

1. Forward flow through a stenotic (narrowed) valve — high-velocity jet through a small orifice creates turbulence (e.g., aortic stenosis, mitral stenosis)
2. Backward flow (regurgitation) through an incompetent valve — blood jets retrograde creating turbulence (e.g., mitral regurgitation, aortic regurgitation)
3. Abnormal communications — blood flows between chambers/vessels at different pressures (e.g., VSD, PDA)
4. High flow states — increased cardiac output can produce "innocent" flow murmurs even through normal valves (anemia, fever, pregnancy, hyperthyroidism)

Murmur Grading (Levine Scale, I–VI):

Phonocardiograms of Valvular Murmurs:

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Individual Murmur Descriptions

🔴 Aortic Stenosis — Systolic Ejection Murmur

• Timing: Systolic (between S1 and S2)
• Mechanism: Blood is forced through a narrow, fibrotic/calcified aortic valve orifice. LV pressure may reach 300 mmHg. A nozzle effect creates a high-velocity jet into the aortic root → severe turbulence → loud vibration of the aortic walls.
• Character: Harsh, crescendo-decrescendo (diamond-shaped), systolic ejection murmur
• Radiation: Upper sternal border → carotid arteries
• Associated signs: Thrill at the upper chest/neck; soft/absent A2; slow-rising carotid pulse (pulsus parvus et tardus)
• Best heard: Right upper sternal border (aortic area), 2nd right intercostal space

🔴 Mitral Regurgitation — Systolic Murmur

• Timing: Systolic (holosystolic — throughout systole)
• Mechanism: Incompetent mitral valve fails to close properly → blood jets backward from high-pressure LV into low-pressure LA during systole → turbulent, high-frequency "blowing" sound
• Character: High-pitched, blowing, holosystolic
• Radiation: To the axilla
• Best heard: Apex of the heart
• Functional MR: In dilated cardiomyopathy, papillary muscle displacement pulls leaflets apart

🔵 Aortic Regurgitation — Diastolic Murmur

• Timing: Diastolic (immediately after S2, during IVR and filling)
• Mechanism: Incompetent aortic valve allows blood to flow backward from high-pressure aorta into the LV during diastole → turbulent jet into low-pressure ventricle → "blowing" sound
• Character: High-pitched, blowing, decrescendo, "soft and swishing"
• Best heard: Left sternal border (3rd/4th intercostal space), with patient leaning forward
• Duration: Starts immediately after A2; length correlates with severity

🔵 Mitral Stenosis — Diastolic Murmur

• Timing: Diastolic (mid-to-late diastole, during ventricular filling)
• Mechanism: Fibrotic/fused mitral valve leaflets restrict flow from LA into LV during diastole. Because LA pressure rarely exceeds 30 mmHg, the pressure differential is small → weak, low-frequency rumble. The ventricle is so empty and flabby that blood does not reverberate well.
• Character: Low-pitched, rumbling, presystolic accentuation (if sinus rhythm — atrial kick amplifies flow just before S1)
• Opening snap: High-pitched early diastolic sound immediately after S2 (stiff leaflets opening under LA pressure)
• Best heard: Apex, with patient in left lateral decubitus position

🟡 Patent Ductus Arteriosus (PDA) — Continuous "Machinery" Murmur

• Timing: Continuous — throughout systole and diastole (both phases)
• Mechanism: The ductus arteriosus connects the aorta to the pulmonary artery. Aortic pressure exceeds pulmonary artery pressure in both systole and diastole → continuous left-to-right shunt → turbulent flow in the pulmonary artery throughout the entire cardiac cycle
• Character: "Machinery murmur" — waxes during systole (higher aortic pressure) and wanes during diastole (lower pressure)
• Best heard: Left upper sternal border/infraclavicular area

Right Heart Murmurs

• Pulmonic stenosis: Systolic ejection murmur, best at left upper sternal border
• Tricuspid regurgitation: Holosystolic, left lower sternal border; increases with inspiration (Carvallo's sign) — more venous return to RV during inspiration increases regurgitant flow

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5. Key Clinical Points — Differentiating Murmurs

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6. Integration: ECG-Cardiac Cycle-Heart Sounds

ECG:     P    Q R S      T
         |     |          |
Sounds:  S4   S1          S2    S3
         |     |          |     |
Events:  Atrial  IVC  Ejection  IVR  Filling
         systole
Valves:        MV   AoV opens  AoV MV
               closes          closes opens

• P wave → atrial depolarization → atrial systole → (S4 if present)
• QRS → ventricular depolarization → ventricular contraction → S1 (MV/TV closure)
• ST segment → rapid ejection phase
• T wave → ventricular repolarization → ventricular relaxation begins
• After T → S2 (AoV/PV closure) → diastole begins
• Early diastole → S3 (if present, during rapid filling)

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