ECG, Cardiac Cycle and Heart Sounds

 

Cardiac Muscle Tissue and the Cardiac Conduction System: A Friendly Guide for UG Students

Think of the heart as a smart, self-beating muscle with its own wiring. In this post, we’ll first look at the “muscle” (histology and mechanics), then the “wires” (conduction system), how the electricity translates into the ECG and a coordinated pump, and finally, about the cardiac cycle.

Histology of Cardiac Muscle: Built for Teamwork and Endurance

• Size and shape
  • Shorter than skeletal fibers (≈50–100 µm long, ≈14 µm wide), branched, with 1 (sometimes 2) central nuclei.
• Intercalated discs
  • Desmosomes: rivets that keep cells attached during forceful beats.
  • Gap junctions: electrical tunnels that let ions flow cell-to-cell so entire atria or ventricles can contract as a unit (functional syncytium).
• Mitochondria and energy
  • Larger and more numerous than in skeletal muscle (≈25% of cell volume vs ≈2% in skeletal). This reflects heavy reliance on aerobic metabolism.
• Myofilament layout
  • Same actin–myosin sarcomeres, bands, and Z discs as skeletal muscle.
• T-tubules and SR
  • T-tubules: wider but fewer; located at Z discs (not at A–I junction like skeletal muscle).
  • Sarcoplasmic reticulum is smaller → smaller intracellular Ca2+ reserve. Cardiac cells rely more on extracellular Ca2+ influx.

Why this matters: The heart must beat together (gap junctions), never tire (many mitochondria), and be calcium‑dependent but carefully regulated (smaller SR, critical Ca2+ influx).

Autorhythmic (Pacemaker) Fibers: The Heart’s Built‑in Clock and Cables

Only ≈1% of cardiac cells become autorhythmic. They:

1. Set the pace (pacemaker function).
2. Provide the conduction pathways that coordinate contraction.

Key pathway (top to bottom, then back up):

• SA node (right atrial wall near Superior Vena Cava)
  • Cells lack a stable resting potential; they slowly depolarize (pacemaker potential) until threshold fires an action potential (AP).
  • Intrinsic rate ≈ 100/min; parasympathetic acetylcholine usually slows this to ≈ 75/min at rest.
• AV node (low interatrial septum)
  • Brief delay (≈0.1 s) lets atria finish pushing blood into ventricles.
• AV bundle (Bundle of His)
  • Only electrical bridge across the fibrous skeleton between atria and ventricles.
• Right and left bundle branches
  • Run down the interventricular septum toward the apex.
• Purkinje fibers
  • Rapidly spread AP from apex upward through ventricular myocardium → efficient “bottom‑up” ejection toward semilunar valves.

Clinical pearl: Problems anywhere along this path can cause arrhythmias or AV blocks. The SA node is the natural pacemaker because it fires fastest; its impulses capture slower sites.

Contractile Fibers: From Electrical Spike to Muscle Squeeze

Once the SA node triggers the system, the AP enters the working myocardium (atrial and ventricular contractile fibers). Their AP has three hallmark phases:

• Depolarization (fast Na+ influx)
  • Resting potential ≈ −90 mV. A threshold stimulus opens voltage‑gated fast Na+ channels → rapid upstroke. Channels inactivate within milliseconds.
• Plateau (Ca2+ in, K+ out)
  • Voltage‑gated “slow” Ca2+ channels open; Ca2+ enters from extracellular fluid and triggers additional Ca2+ release from SR (calcium‑induced calcium release).
  • Simultaneous K+ efflux through some K+ channels balances the Ca2+ influx → maintained depolarization near 0 mV for ≈0.25 s.
  • Raised cytosolic Ca2+ binds troponin → actin–myosin cross‑bridge cycling → contraction.
• Repolarization (more K+ out, Ca2+ channels close)
  • Additional K+ channels open; Ca2+ channels close → membrane returns to −90 mV.

Two crucial functional consequences:

• Long refractory period (> contraction time) prevents tetanus. The heart must alternate contract–relax to fill and eject; sustained tetanus would stop flow.
• Inotropy is Ca2+‑dependent. Agents that increase Ca2+ entry (e.g., epinephrine) increase contractile force.

ATP Supply: The Heart Loves Oxygen

• Predominantly aerobic metabolism in abundant mitochondria.
  • Fuels at rest: ≈60% fatty acids, ≈35% glucose; also uses lactate, amino acids, ketones.
  • During exercise: lactate contribution rises.
• Creatine phosphate provides a small ATP buffer; elevated serum creatine kinase (CK) indicates myocardial injury.

The ECG: Seeing the Heart’s Electricity on Paper

The electrocardiogram (ECG/EKG) records summed electrical activity via skin electrodes (standard 12‑lead).

• Waves
  • P wave: atrial depolarization.
  • QRS complex: rapid ventricular depolarization; masks atrial repolarization.
  • T wave: ventricular repolarization (slower, hence broader).
• Intervals and segments
  • P–Q (PR) interval: start of atrial depolarization to start of ventricular depolarization; prolonged in AV nodal conduction delays/scar.
  • S–T segment: ventricular plateau (steady depolarization); elevated in acute MI, depressed in ischemia.
  • Q–T interval: start of ventricular depolarization to end of repolarization; prolonged in ischemia, drug effects, channelopathies.

Stress testing and Holter monitoring help reveal transient ischemia or intermittent arrhythmias not seen at rest.

Linking Conduction to Contraction Timing (Big‑Picture Physiology)

• SA node fires → P wave → atrial systole tops up ventricles.
• AV nodal delay → ventricles fill before they contract.
• QRS complex → ventricular systole begins at the apex and proceeds upward, pushing blood toward semilunar valves.
• T wave → repolarization → ventricular diastole and filling.

This orderly sequence is guaranteed by the conduction system and the insulating fibrous skeleton. Disrupt the sequence, and pump efficiency drops.

High‑Yield Exam Nuggets

• Intercalated discs = desmosomes + gap junctions; basis of syncytial behavior.
• SA node intrinsic rate ≈ 100/min; resting ≈ 75/min due to vagal tone.
• AV node delay ≈ 0.1 s; essential for ventricular filling.
• Contractile AP plateau depends on L‑type Ca2+ channels; long refractory period prevents tetanus.
• Energy: highly aerobic; CK rise suggests myocardial infarction.
• ECG changes: ST elevation (acute MI), ST depression (ischemia), prolonged PR (AV block), prolonged QT (repolarization abnormalities).

Quick Self‑Check

• Why can’t the heart develop tetanus like skeletal muscle?
• What two junction types are found in intercalated discs, and what do they do?
• Which structure electrically insulates atria from ventricles, and why is that important?
• How do epinephrine and calcium handling affect contractile force?

Grasp these structure–function links, and the rest of cardiovascular physiology becomes far easier to reason through—on both exams and the wards.

The Cardiac Cycle: From Electrical Spark to Heart Sounds

Think of one heartbeat as a well‑choreographed dance between electricity, pressure, valves, and flowing blood. That entire sequence is the cardiac cycle. At a heart rate of 75 beats/min, one cycle takes about 0.8 s and includes systole and diastole of both atria and ventricles.

Ground rules

• Blood moves from higher pressure to lower pressure.
• When a chamber contracts, its pressure rises; when it relaxes, pressure falls.
• Valve opening/closure is purely pressure driven—no muscles pull valves open.

Below, times and pressures refer to the left heart (systemic side). The same pattern occurs on the right but with lower pressures.

1) Atrial systole (~0.1 s)

Electrical event

• SA node depolarization → P wave on ECG.

Mechanical events

• Atria contract, topping up relaxed ventricles through open AV valves.
• Adds ~25 mL to each ventricle, bringing end‑diastolic volume (EDV) to ~130 mL.
• The end of atrial systole = end of ventricular diastole.

Key definition

• EDV: volume in each ventricle at the end of filling (~130 mL at rest).

2) Ventricular systole (~0.3 s)

Electrical event

• QRS complex marks ventricular depolarization.

Mechanical events

• Isovolumetric contraction (~0.05 s): Ventricular pressure rises, AV valves snap shut; SL valves still closed. Volume unchanged; pressure climbs.
• Ejection phase (~0.25 s): When LV pressure exceeds aortic pressure (~80 mmHg), aortic valve opens.
  • LV pressure peaks ~120 mmHg.
  • Stroke volume (SV) ejected into aorta ≈ 70 mL.
  • End‑systolic volume (ESV) left behind ≈ 60 mL.

Core formula

• Stroke volume:

SV=EDV−ESV=130mL−60mL≈70mL

Tip: The right ventricle ejects the same volume into the pulmonary trunk but at lower pressures (opens near ~20 mmHg; peaks ~25–30 mmHg).

3) Relaxation period (~0.4 s)

Electrical event

• T wave marks ventricular repolarization.

Mechanical events

• Isovolumetric relaxation: As ventricular pressure falls below aortic/pulmonary trunk pressure, SL valves close (aortic closure near ~100 mmHg) producing the dicrotic notch/wave. All valves closed; volume unchanged.
• Ventricular filling: When ventricular pressure drops below atrial pressure, AV valves open.
  • Rapid passive filling occurs first.
  • By the end of this period, ventricles are ~three‑quarters full; the next P wave initiates a new cycle and atrial systole adds the final “top‑up.”

High‑yield note

• With faster heart rates, the relaxation period (diastole) shortens the most—this can reduce filling time.

Heart sounds: what you hear and why

• S1 (“lubb”): Closure of AV valves just after ventricular systole begins; louder/longer.
• S2 (“dupp”): Closure of SL valves at the start of ventricular diastole; shorter/softer.
• S3: Turbulence during rapid ventricular filling (usually inaudible; can be normal in children/athletes).
• S4: Turbulence during atrial systole against a stiff ventricle (usually inaudible; often pathologic in adults).

Clinical listening tip: S1 and S2 are best heard at surface points downstream from valves because blood flow carries the sound away from the actual valve cusps.

Putting it all together: a quick mental movie

• P wave → atria squeeze → EDV ≈ 130 mL.
• QRS → AV valves shut (S1) → isovolumetric contraction → SL valves open → ejection → ESV ≈ 60 mL.
• T wave → SL valves shut (S2) → isovolumetric relaxation → AV valves open → rapid filling → next P wave.

Exam checkpoints

• Define EDV, ESV, and SV and state typical values at rest.
• Name the two “iso” phases and which valves are closed in each.
• State the pressures that open the aortic and pulmonary valves.
• Explain why diastole shortens more than systole during tachycardia.

Master this sequence and you can confidently interpret ECG–pressure–volume relationships and heart sounds in clinical scenarios.