Anatomy & Physiology II · In-depth topic guides

Cardiac Electrophysiology and the Cardiac Cycle

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This topic covers the electrical and mechanical events that drive the heartbeat: from the spontaneous generation of action potentials in autorhythmic cells, through conduction along the intrinsic conduction system, to the coordinated contraction and relaxation captured in the cardiac cycle and its pressure-volume loop. Understanding these fundamentals is essential for interpreting clinical tools like the electrocardiogram (ECG) and for recognizing pathologies such as arrhythmias, heart murmurs, and heart failure.

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4.1 Autorhythmicity and the Intrinsic Conduction System

Cardiac muscle possesses the unique property of autorhythmicity — the ability to generate its own action potentials without nervous input. This is due to specialized, non-contractile pacemaker cells that spontaneously depolarize. The nervous system modulates heart rate but does not initiate the heartbeat.

The intrinsic conduction system is a hierarchy of autorhythmic cells that ensures coordinated, unidirectional depolarization from atria to ventricles:

Sinoatrial (SA) node — Located in the upper right atrial wall near the superior vena cava. The SA node fires at the fastest intrinsic rate (approximately 100 beats per minute), making it the natural pacemaker of the heart. It initiates each cardiac impulse.

Atrioventricular (AV) node — Located in the inferior interatrial septum, just above the tricuspid valve. The AV node fires intrinsically at about 40–60 bpm. Its key role is to introduce a physiological delay (~0.1 seconds) that allows the atria to finish contracting and emptying into the ventricles before ventricular contraction begins.

Bundle of His (atrioventricular bundle) — Travels from the AV node through the interventricular septum. It is the only electrical bridge between the atria and ventricles; the fibrous skeleton insulates the rest.

Right and left bundle branches — The bundle of His divides into two branches that descend along the interventricular septum toward the apex.

Purkinje fibers — Terminal branches that penetrate the ventricular myocardium from the apex upward. They have an intrinsic firing rate of about 20–40 bpm and conduct the impulse rapidly (up to 4 m/s) to ensure near-simultaneous ventricular contraction from apex to base.

Structure	Location	Intrinsic Firing Rate	Function
SA node	Upper right atrial wall	~100 bpm	Primary pacemaker; initiates impulse
AV node	Inferior interatrial septum	~40–60 bpm	Delays impulse (~0.1 s); protects ventricles
Bundle of His	Interventricular septum	~40–60 bpm	Only electrical bridge between atria and ventricles
Bundle branches	Interventricular septum	~40–60 bpm	Distribute impulse to left and right ventricles
Purkinje fibers	Ventricular walls (apex → base)	~20–40 bpm	Rapid conduction for coordinated ventricular contraction

The hierarchy ensures that the fastest-discharging cells (SA node) normally set the pace. Slower intrinsic pacemakers are latent or ectopic pacemakers — they take over only if higher pacemakers fail (as in complete heart block).

4.2 Pacemaker Cell Action Potential

Pacemaker cells (SA node, AV node) do not have a stable resting membrane potential. Instead, they exhibit slow, spontaneous depolarization called the pacemaker potential or prepotential. The key phases are:

Phase 4 — Spontaneous depolarization (pacemaker potential): After repolarization, the membrane potential drifts upward from about −60 mV toward threshold (≈ −40 mV). This is driven primarily by opening of funny channels (If channels) that conduct a mixed Na⁺/K⁺ inward current. As these channels open at hyperpolarized potentials (below −50 mV), Na⁺ influx slowly depolarizes the cell. Transient (T-type) Ca²⁺ channels also open late in phase 4, further depolarizing the membrane.

Phase 0 — Depolarization (rising phase): Once threshold is reached (~ −40 mV), long-lasting (L-type) Ca²⁺ channels open. Calcium influx produces the relatively slow, calcium-dependent upstroke. This differs from contractile myocytes, where Na⁺ channels drive phase 0.

Phase 3 — Repolarization: L-type Ca²⁺ channels inactivate and voltage-gated K⁺ channels open. K⁺ efflux repolarizes the membrane back to approximately −60 mV, at which point the K⁺ channels close and the If channels open again, restarting the cycle.

Key distinction: pacemaker cells lack a plateau phase (phase 2) and rely on Ca²⁺ (not Na⁺) for the upstroke.

4.3 Contractile Cardiomyocyte Action Potential

Contractile (working) cardiomyocytes have a stable resting membrane potential of about −90 mV and exhibit a prolonged action potential with five distinct phases:

Phase 4 — Resting membrane potential: The cell sits at −90 mV, maintained by the Na⁺/K⁺-ATPase pump and high resting K⁺ permeability (IK1 channels).

Phase 0 — Rapid depolarization: When a threshold of ~ −70 mV is reached, voltage-gated Na⁺ channels open. Fast Na⁺ influx causes a rapid, steep depolarization to about +20 mV. This is analogous to the neuronal upstroke.

Phase 1 — Initial repolarization: Na⁺ channels inactivate and a transient outward K⁺ current (Ito) produces a small notch of repolarization.

Phase 2 — Plateau: L-type Ca²⁺ channels open, and Ca²⁺ influx balances K⁺ efflux, sustaining depolarization for 200–300 ms. This prolonged plateau prevents tetany and allows time for Ca²⁺-induced Ca²⁺ release and contraction. It is the hallmark of the cardiac action potential.

Phase 3 — Repolarization: L-type Ca²⁺ channels inactivate while multiple K⁺ channels (IKr, IKs, IK1) open fully. Net K⁺ efflux restores the membrane potential to −90 mV.

Feature	Pacemaker Cells	Contractile Cardiomyocytes
Resting potential	None (unstable, −60 mV most negative)	Stable at −90 mV
Phase 0 ion	Ca²⁺ (L-type channels)	Na⁺ (voltage-gated channels)
Phase 0 speed	Slow	Fast
Plateau (Phase 2)	Absent	Present (200–300 ms, Ca²⁺ + K⁺ balance)
Pacemaker potential (Phase 4)	Present (If channels)	Absent
Threshold	~ −40 mV	~ −70 mV

4.4 The Electrocardiogram (ECG/EKG)

The electrocardiogram (ECG) records the summed electrical activity of the heart as detected by surface electrodes. It does not measure mechanical contraction directly; rather, electrical depolarization precedes and triggers contraction.

Key waves and intervals:

P wave — Represents atrial depolarization. The atria contract (atrial systole) about 0.1 seconds after the P wave begins.

QRS complex — Represents ventricular depolarization. This large, sharp waveform masks atrial repolarization, which occurs simultaneously. The QRS heralds ventricular contraction. A normal QRS duration is < 0.12 seconds.

T wave — Represents ventricular repolarization. It is broader and lower-amplitude than the QRS because repolarization is a slower, less synchronous process than depolarization.

PR interval — Measured from the start of the P wave to the start of the QRS complex, normally 0.12–0.20 seconds. It reflects the time from SA node firing to ventricular depolarization, including the AV node delay.

QT interval — Measured from the start of the QRS to the end of the T wave; reflects total ventricular depolarization and repolarization. Prolonged QT can predispose to dangerous arrhythmias.

ST segment — The isoelectric period between QRS and T wave when the ventricles are fully depolarized and in the plateau phase. ST elevation is a hallmark of myocardial infarction.

Atrial repolarization is usually not visible because it coincides with, and is obscured by, the much larger QRS complex.

4.5 The Cardiac Cycle: Mechanical Events

The cardiac cycle encompasses all events from the beginning of one heartbeat to the beginning of the next. For a heart rate of 75 bpm, one cycle lasts approximately 0.8 seconds.

4.5.1 Atrial Systole (Active Ventricular Filling)

The atria contract, pushing the remaining 20–30% of blood into the ventricles (most ventricular filling — ~70–80% — occurs passively during the preceding diastole).
This completes end-diastolic volume (EDV) — typically ~120–130 mL in a resting adult.
The P wave precedes atrial systole.

4.5.2 Ventricular Systole

Isovolumetric Contraction:

Ventricular contraction begins; ventricular pressure rises rapidly.
When ventricular pressure exceeds atrial pressure, the AV valves (mitral and tricuspid) snap shut. This closure produces the first heart sound (S1, "lub").
For a brief moment, both AV and semilunar valves are closed — volume remains constant while pressure rises steeply.
This phase ends when ventricular pressure exceeds aortic/pulmonary artery pressure.

Ventricular Ejection:

The semilunar valves (aortic and pulmonic) are forced open.
Blood is ejected rapidly at first (rapid ejection), then more slowly (reduced ejection).
The volume of blood ejected is the stroke volume (SV) — typically ~70 mL at rest.
The blood remaining in each ventricle after ejection is the end-systolic volume (ESV) — typically ~50–60 mL.
EDV − ESV = Stroke Volume.
The T wave occurs late in ventricular systole, signaling the start of ventricular repolarization.

4.5.3 Ventricular Diastole

Isovolumetric Relaxation:

Ventricular muscle relaxes; ventricular pressure drops rapidly.
When ventricular pressure falls below aortic/pulmonary pressure, the semilunar valves snap shut. This closure produces the second heart sound (S2, "dub").
For a brief moment, all four valves are closed again as the ventricle relaxes without changing volume.

Passive Ventricular Filling:

When ventricular pressure drops below atrial pressure, the AV valves open.
Blood flows passively from the atria into the ventricles (~70–80% of ventricular filling occurs here).
This phase is sometimes called rapid filling followed by diastasis (slow filling).

4.6 The Pressure-Volume Loop

The pressure-volume (PV) loop plots left ventricular pressure against left ventricular volume over a single cardiac cycle. The loop proceeds counterclockwise:

Ventricular filling (diastole): Volume increases from ESV (~50 mL) toward EDV (~120 mL) at low, near-constant pressure. This is the bottom edge of the loop moving rightward. The AV valves are open.

Isovolumetric contraction: Pressure rises vertically from the EDV point with no change in volume (both valve sets closed). This is the right vertical edge moving upward.

Ejection: The semilunar valve opens. Volume decreases from EDV to ESV while pressure initially rises further, then falls. This forms the top and left edges of the loop. Stroke volume is the width of the loop: EDV − ESV.

Isovolumetric relaxation: Pressure drops vertically from the ESV point with no volume change. This is the left vertical edge descending.

Key derived values:

Stroke volume (SV) = EDV − ESV (width of the loop)
Ejection fraction (EF) = (SV / EDV) × 100%. Normally ≥ 55%. A reduced EF (< 40–50%) suggests systolic heart failure.

End-systolic pressure-volume relationship (ESPVR): The upper-left boundary, reflecting ventricular contractility (inotropy).
End-diastolic pressure-volume relationship (EDPVR): The bottom boundary, reflecting ventricular compliance.

Increased preload (greater EDV) widens the loop (Frank-Starling mechanism). Increased afterload (higher aortic pressure) narrows the loop and reduces SV. Increased contractility shifts ESPVR upward and leftward, increasing SV.

4.7 Heart Sounds

Heart sounds arise from turbulent blood flow associated with valve closure:

S1 ("lub") — Closure of the AV valves (mitral and tricuspid) at the start of ventricular systole. Best heard at the apex (mitral area, 5th intercostal space, midclavicular line). Coincides with the QRS complex.

S2 ("dub") — Closure of the semilunar valves (aortic and pulmonic) at the start of ventricular diastole. Splitting of S2 (A2 before P2) can be normal during inspiration. Coincides with the end of the T wave.

S3 — An early diastolic sound heard shortly after S2, caused by rapid passive ventricular filling. It can be normal in children and young adults (physiologic S3) but in older adults often indicates volume overload or systolic heart failure (pathologic S3 or "ventricular gallop").

S4 — A late diastolic sound heard just before S1, caused by atrial contraction pushing blood into a stiff, non-compliant ventricle. It always indicates pathology, such as left ventricular hypertrophy, hypertrophic cardiomyopathy, or diastolic dysfunction ("atrial gallop").

4.8 Heart Murmurs

A heart murmur is an abnormal sound produced by turbulent blood flow. Murmurs can be either innocent/physiologic (common in children, pregnancy, high-output states) or pathologic.

Valvular causes of murmurs:

Stenosis — Valve fails to open fully, causing turbulent flow through a narrowed orifice. Heard as a crescendo-decrescendo (diamond-shaped) murmur.

Regurgitation (insufficiency) — Valve fails to close properly, allowing backward flow. Heard as a holosystolic (pansystolic) or decrescendo murmur.

Timing is critical for diagnosis:

Systolic murmurs: Occur between S1 and S2. Examples: aortic stenosis, mitral regurgitation, ventricular septal defect.
Diastolic murmurs: Occur between S2 and S1. Examples: aortic regurgitation, mitral stenosis.
Continuous murmurs: Span systole and diastole. Example: patent ductus arteriosus.

Murmurs are graded on a I–VI scale (I = barely audible, VI = audible with stethoscope off the chest).

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The same idea, in plain words

Explain it like I’m 10

ELI-10: Autorhythmicity and the Conduction System

Think of the heart's pacemaker cells like a line of dominoes, but with a twist — the first domino can stand itself back up and fall again all by itself without anyone pushing it. The SA node is the lead domino that starts every wave; it falls ~100 times a minute, faster than any other domino. The AV node is like a speed bump — it slows the wave down just enough to let the top chambers finish squeezing before the bottom ones start. Then the signal races down a divided highway (the bundle branches) to the very bottom of the heart, where the Purkinje fibers spread it back upward like water spraying from a garden hose at the bottom of a wall, so every bit of the ventricles squeezes at almost the same time.

ELI-10: Pacemaker Action Potential

Imagine a leaky bucket with a pump. Water (positive charge) keeps leaking in through small holes (the funny channels, which let sodium sneak in), so the bucket slowly fills by itself. Once the water level reaches the rim (threshold), a floodgate (L-type calcium channels) swings open all at once, letting in a big rush of water — that's the action potential! Then a drain (potassium channels) opens at the bottom to let everything out, the bucket empties, and the leaking starts all over again. The bucket fills and empties by itself forever — no one needs to turn on the faucet.

ELI-10: Contractile Cardiomyocyte Action Potential

If the pacemaker action potential is a quick splash in a bucket, the working heart cell's action potential is a swimming pool with a diving board. First, sodium rushes in like a diver cannonballing into the pool (phase 0 — fast splash). Then calcium holds the gate open so the pool stays filled for a long time (phase 2 — the long float, the plateau). This long float is the heart's built-in rest period — it keeps the heart from twitching uncontrollably. Finally, potassium drains the pool (phase 3), and everything goes quiet until the next signal.

ELI-10: The ECG

Picture the ECG as a stadium wave done by heart cells. The P wave is when the fans in the top section (atria) stand up and sit down. Next comes the big wave — the QRS complex — when the entire lower bowl (ventricles) leaps to their feet. The T wave is when those lower-section fans all sit back down. The flat lines between waves are moments when everybody is either all standing or all sitting. A doctor reading an ECG is like a referee watching to see whether every section is doing the wave in the right order and at the right time.

ELI-10: The Cardiac Cycle

Think of the cardiac cycle as a four-step water pump: (1) The top tank (atria) squeezes the last bit of water into the bottom tank (ventricles) — that's atrial systole. (2) The bottom tank's exit door slams shut and pressure builds without any water leaving — isovolumetric contraction, like pushing against a locked door. (3) The exit door finally flies open and water shoots out to the pipes — ejection. (4) The bottom tank relaxes, the exit door snaps shut, and water from the top tank starts flowing in passively — filling. Then the cycle repeats, with the pump resetting itself ~70 times every minute of your life.

ELI-10: The Pressure-Volume Loop

Draw a rectangle, then tip it on its side. Start at the bottom right — the heart is filling (volume goes up, pressure stays low). Then shoot straight up — the heart clenches but both doors are shut, so pressure skyrockets while volume can't change. Then move left across the top — blood sprays out, volume goes down. Then plunge straight down — the heart relaxes, doors snap shut, pressure crashes. The width of your sideways rectangle is how much blood got pumped out in one beat (stroke volume). A wider rectangle means a stronger pump.

ELI-10: Heart Sounds

"Lub-dub." The "lub" is the sound of the doors between the top and bottom chambers slamming shut — the AV valves. The "dub" is the sound of the exit doors to the big arteries snapping closed — the semilunar valves. An extra sound before S1 (S4) is the top chamber straining to push blood into a stiff bottom chamber — like trying to blow up a balloon that won't stretch. An extra sound after S2 (S3) is blood sloshing into an already-overfilled bottom chamber — like water splashing into a bucket that's already half full.

ELI-10: Murmurs

Normal blood flow is silent, like water flowing smoothly through a garden hose. A murmur is what you hear when you pinch the hose — the water gets turbulent and noisy. A narrow valve (stenosis) is like a kinked hose. A leaky valve (regurgitation) is like a hose with a hole that sprays backward. Both make a whooshing sound the doctor can hear with a stethoscope, and the timing of the whoosh — between "lub" and "dub" (systolic) or between "dub" and the next "lub" (diastolic) — tells the doctor which valve is misbehaving.

Check yourself

12 review questions from the chapter. Try each one, then open the answer.

If the SA node is damaged and stops firing, which structure would most likely become the primary pacemaker of the heart?
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Purkinje fibers, firing at ~20–40 bpm B. AV node, firing at ~40–60 bpm C. Bundle of His, firing at ~80 bpm D. Left bundle branch, firing at ~60–80 bpm Answer: B. AV node, firing at ~40–60 bpm Why It's the Answer: The intrinsic conduction system follows a firing-rate hierarchy. When the fastest pacemaker (SA node, ~100 bpm) fails, the next-fastest structure — the AV node at ~40–60 bpm — takes over. The Purkinje fibers (A) fire too slowly (~20–40 bpm) and would only become dominant if both SA and AV nodes failed. The bundle of His (C) does not have an intrinsic rate of 80 bpm; it fires at ~40–60 bpm like the AV node. The left bundle branch (D) fires at ~20–40 bpm, similar to Purkinje fibers, not 60–80 bpm. ELI-10: The SA node is the fastest drummer in the band. If the drummer stops, the next-fastest musician — the AV node — picks up the beat, but at a slower tempo. If that one stops too, slower and slower backups keep the music going.
In the SA node, the spontaneous depolarization of phase 4 (pacemaker potential) is primarily driven by which ion channel?
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Voltage-gated Na⁺ channels B. L-type Ca²⁺ channels C. Funny channels (If channels) D. Delayed rectifier K⁺ channels Answer: C. Funny channels (If channels) Why It's the Answer: The funny channels (If) open at hyperpolarized membrane potentials (below −50 mV) and carry a mixed Na⁺/K⁺ inward current that slowly depolarizes the pacemaker cell during phase 4. Voltage-gated Na⁺ channels (A) drive phase 0 in contractile myocytes, not pacemaker cells. L-type Ca²⁺ channels (B) drive phase 0 (the upstroke) in pacemaker cells, not the pacemaker potential itself. Delayed rectifier K⁺ channels (D) are responsible for repolarization (phase 3), not depolarization. ELI-10: The funny channels are like a slow drip from a leaky faucet — they let a tiny bit of positive charge trickle in until the cell finally reaches its trigger point and fires. They open when the cell is most negative, which is the opposite of most other channels — hence "funny."
Which phase of the contractile cardiomyocyte action potential is most directly responsible for preventing tetanic (sustained) contraction of the heart?
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Phase 0 — rapid Na⁺ influx depolarization B. Phase 1 — initial K⁺ efflux repolarization C. Phase 2 — Ca²⁺/K⁺ plateau D. Phase 3 — K⁺ efflux repolarization Answer: C. Phase 2 — Ca²⁺/K⁺ plateau Why It's the Answer: The plateau phase (phase 2) lasts 200–300 ms and keeps the cardiac cell depolarized and refractory during most of the mechanical contraction. This prolonged absolute refractory period prevents a second action potential from being initiated while the cell is still contracting, making summation and tetanus impossible — a critical safety feature. Phase 0 (A) is the rapid upstroke that initiates the action potential. Phase 1 (B) is a brief repolarization notch. Phase 3 (D) restores resting potential but the plateau is what extends the refractory period. ELI-10: The plateau is the heart's built-in "cool-down" timer. Just like you can't start a new round of a video game until the current round is over, the heart cell can't fire again until the plateau finishes. This keeps your heart from clenching up and never letting go — which would stop blood flow.
The QRS complex on an ECG corresponds to which mechanical event?
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Atrial contraction B. Ventricular repolarization C. Ventricular depolarization, preceding ventricular contraction D. Ventricular relaxation and passive filling Answer: C. Ventricular depolarization, preceding ventricular contraction Why It's the Answer: The QRS complex represents the spread of depolarization through the ventricular myocardium. Electrical depolarization triggers mechanical contraction via excitation-contraction coupling, so the QRS complex immediately precedes ventricular systole. Atrial contraction (A) follows the P wave, not the QRS. Ventricular repolarization (B) is represented by the T wave. Ventricular relaxation and filling (D) occur during diastole, well after the QRS. ELI-10: The QRS is the "Ready, set..." before the ventricles "Go!" It's the big electrical shout that tells the lower chambers to squeeze, and the squeezing starts right after the shout finishes.
A 72-year-old man's ECG shows a PR interval of 0.28 seconds (normal: 0.12–0.20 s). Which component of the intrinsic conduction system is most likely responsible for this finding?
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SA node — decreased firing rate B. AV node — prolonged conduction delay C. Bundle of His — conduction block D. Purkinje fibers — slowed conduction velocity Answer: B. AV node — prolonged conduction delay Why It's the Answer: The PR interval primarily reflects the time from SA node firing to ventricular depolarization, and the bulk of this delay (~0.1 seconds normally) occurs at the AV node. A prolonged PR interval indicates first-degree AV block — a delay at the AV node. The SA node (A) affects heart rate, not the PR interval. A bundle branch block (C) widens the QRS complex, not the PR interval. Purkinje fiber dysfunction (D) would also widen the QRS rather than prolong the PR interval. ELI-10: The PR interval is like measuring how long it takes a message to travel from the boss's office (SA node) through the mailroom (AV node) to the factory floor (ventricles). A longer PR interval means the mailroom is moving too slowly — the message gets through, but it's taking too long.
During isovolumetric contraction, which of the following is true?
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The semilunar valves are open and the AV valves are closed B. Both the AV valves and semilunar valves are closed C. Blood is being ejected into the aorta D. The ventricles are filling with blood from the atria Answer: B. Both the AV valves and semilunar valves are closed Why It's the Answer: In isovolumetric contraction, ventricular pressure has risen above atrial pressure (closing the AV valves, producing S1) but has not yet exceeded aortic/pulmonary artery pressure (so the semilunar valves remain closed). With all four valves shut, ventricular volume cannot change — pressure rises at constant volume. Option A describes the ejection phase. Option C also describes ejection. Option D describes diastolic filling, when the AV valves are open and the semilunar valves are closed. ELI-10: Imagine squeezing a sealed water bottle with both hands — the pressure inside goes up, but no water can escape because the cap is still on. That's exactly what happens during isovolumetric contraction: the ventricle squeezes, both doors are shut, and pressure builds until the exit door finally pops open.
In a left ventricular pressure-volume loop, an increase in afterload (e.g., elevated aortic pressure) would cause which of the following changes?
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Increased EDV and a wider loop B. Decreased ESV and increased stroke volume C. Increased ESV and decreased stroke volume D. Decreased peak systolic pressure and increased EDV Answer: C. Increased ESV and decreased stroke volume Why It's the Answer: Afterload is the pressure the ventricle must overcome to eject blood. Higher aortic pressure means the ventricle must generate more pressure before the semilunar valve opens, so ejection starts later and ends earlier, leaving more blood behind — ESV increases. Since EDV stays roughly the same, stroke volume (EDV − ESV) decreases, narrowing the loop. Option A describes increased preload (Frank-Starling). Option B is the opposite of what increased afterload does. Option D is incorrect — peak systolic pressure would increase (not decrease) with higher afterload. ELI-10: Afterload is like adding a heavier weight to the end of a water pump's output hose. The pump has to work harder to push open the valve, so it pushes out less water each cycle and more water stays behind in the pump chamber.
A physician auscultates an S3 gallop in a 68-year-old patient with shortness of breath and bilateral leg edema. This finding most likely indicates:
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Aortic stenosis with a narrowed valve orifice B. Normal variant in an elderly patient C. Volume overload and possible systolic heart failure D. Atrial contraction against a stiff, non-compliant ventricle Answer: C. Volume overload and possible systolic heart failure Why It's the Answer: An S3 in an older adult is pathologic and reflects rapid passive ventricular filling into a dilated, volume-overloaded ventricle — a hallmark of systolic heart failure with reduced ejection fraction. The clinical presentation of dyspnea and edema supports this diagnosis. Aortic stenosis (A) produces a systolic ejection murmur, not an S3. S3 is not a normal variant (B) in elderly patients — it can be normal in children and young adults but always raises concern after age 35–40. Option D describes S4, which is an atrial gallop associated with a stiff, non-compliant ventricle (diastolic dysfunction), not the early diastolic sound of S3. ELI-10: An S3 in an older person is like hearing a big splash when you pour water into a bucket that's already too full — the ventricle is stretched and floppy, and incoming blood sloshes around loudly instead of flowing in quietly.
All of the following occur during ventricular systole EXCEPT:
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Isovolumetric contraction with rising ventricular pressure B. Closure of the AV valves producing S1 C. Opening of the semilunar valves for ejection D. Passive ventricular filling from the atria Answer: D. Passive ventricular filling from the atria Why It's the Answer: Passive ventricular filling occurs during ventricular diastole, when the ventricles are relaxed and the AV valves are open. During ventricular systole, the ventricles are contracting — the AV valves are shut (producing S1, option B), pressure rises isovolumetrically (option A), then the semilunar valves open for ejection (option C). No filling can occur through closed AV valves during systole. ELI-10: Ventricular systole is "push time" — the ventricles are squeezing blood out. Filling the tank is "relax time" — that's diastole. You can't fill a tank while you're squeezing it; those are two different parts of the cycle.
The second heart sound (S2) is produced by closure of which valves, and when does this occur in the cardiac cycle?
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Mitral and tricuspid valves — beginning of ventricular systole B. Aortic and pulmonic valves — beginning of ventricular diastole C. Aortic and pulmonic valves — beginning of ventricular systole D. Mitral and tricuspid valves — beginning of atrial systole Answer: B. Aortic and pulmonic valves — beginning of ventricular diastole Why It's the Answer: S2 ("dub") results from closure of the aortic and pulmonic semilunar valves at the start of ventricular diastole, when ventricular pressure drops below aortic/pulmonary artery pressure. Option A describes S1, which is AV valve closure at the start of systole. Option C is wrong both in valve identity (S2 = semilunar, not AV) and timing (closing at start of diastole, not systole). Option D is wrong — AV valve closure produces S1, not S2, and this occurs at the start of ventricular systole, not atrial systole. ELI-10: "Dub" (S2) is the sound of the exit doors slamming shut as soon as the ventricles stop pushing. The "lub" (S1) happened earlier when the entrance doors closed as the ventricles started pushing.
A researcher records left ventricular pressure and volume simultaneously. At a specific moment, pressure is 80 mmHg, volume is 130 mL, and the AV valves are open while the semilunar valves are closed. Which phase of the cardiac cycle is being recorded?
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Isovolumetric contraction B. Ventricular ejection C. Late ventricular diastole during atrial systole D. Isovolumetric relaxation Answer: C. Late ventricular diastole during atrial systole Why It's the Answer: A volume of 130 mL is consistent with EDV (near-maximal ventricular filling). The AV valves being open with semilunar valves closed confirms this is a filling phase (diastole), not ejection or isovolumetric contraction. The relatively high volume suggests this is late diastole, specifically during atrial contraction which tops off ventricular volume. Isovolumetric contraction (A) has both valve sets closed. Ventricular ejection (B) has the semilunar valves open and volume decreasing. Isovolumetric relaxation (D) also has all valves closed and volume at ESV (~50–60 mL), not 130 mL. ELI-10: At 130 mL, the ventricle is like a water balloon that's been filled almost to capacity. Both entrance doors (AV valves) are open letting the last bit in, and the exit doors are still shut — that's the final fill-up just before the big squeeze.
A 55-year-old woman is found to have a holosystolic murmur heard best at the cardiac apex that radiates to the axilla. The murmur begins with S1 and continues through S2. Which valvular abnormality best explains this finding?
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Aortic stenosis — systolic ejection murmur B. Mitral regurgitation — holosystolic murmur C. Aortic regurgitation — early diastolic murmur D. Mitral stenosis — mid-diastolic murmur Answer: B. Mitral regurgitation — holosystolic murmur Why It's the Answer: A holosystolic (pansystolic) murmur that begins with S1 and continues throughout systole to S2 is characteristic of mitral regurgitation — blood flows backward from the left ventricle into the left atrium throughout systole because the mitral valve fails to close properly. The murmur is heard best at the apex and radiates to the axilla (classic for mitral valve pathology). Aortic stenosis (A) produces a crescendo-decrescendo systolic ejection murmur, not holosystolic. Aortic regurgitation (C) is a diastolic murmur. Mitral stenosis (D) produces a diastolic murmur. ELI-10: A holosystolic murmur is like a hose with a hole that sprays water the entire time you're squeezing — from the moment the trigger is pulled (S1) until you let go (S2). Mitral regurgitation means the one-way door between the left atrium and left ventricle is broken and leaks backward during the entire squeeze phase.