INTRODUCTION — LOGIC OF THE NORMAL HEARTBEAT

1. Orderly sequence of contraction

Normal sequence

1. Atrial systole → atria contract
2. Ventricular systole → ventricles contract
3. Diastole → all four chambers relaxed

Why this order matters

• Atrial contraction tops up ventricular filling
• Ventricular contraction then ejects blood efficiently
• Diastole allows coronary perfusion + filling

2. Why the heart beats rhythmically (core logic)

• The heartbeat does not start randomly
• It originates from a specialized conduction system
• Electrical impulses spread in a fixed pathway
• Mechanical contraction follows electrical activation

3. Components of the cardiac conduction system

In order of impulse flow:

1. Sinoatrial (SA) node
2. Internodal atrial pathways
3. Atrioventricular (AV) node
4. Bundle of His
5. Right & left bundle branches
6. Purkinje system
7. Ventricular myocardium

4. Why SA node is the pacemaker

• Many cardiac cells can discharge spontaneously
• But:
• SA node fires fastest
• Its depolarization reaches others before they fire
• Therefore:
• SA node suppresses all other pacemakers
• This is called overdrive suppression

👉 Result:

SA node sets heart rate

5. Electrical activity → ECG

• Each cardiac cell type has a distinct action potential
• The sum of all electrical activity recorded on the body surface = ECG
• ECG reflects:
• Timing
• Sequence
• Spread of depolarization and repolarization

ORIGIN & SPREAD OF CARDIAC EXCITATION

ANATOMIC CONSIDERATIONS

6. Location of key structures

SA node

• Junction of:
• Superior vena cava
• Right atrium

AV node

• Right posterior interatrial septum

7. Atrial conduction pathways (why atria conduct fast)

Three specialized tracts containing Purkinje-type fibers:

1. Anterior tract
2. Middle tract → Tract of Wenckebach
3. Posterior tract → Tract of Thorel

• Conduction also occurs via atrial myocytes
• But conduction is faster in these bundles

Bachmann bundle

• Branch of anterior internodal tract
• Connects right atrium → left atrium
• Explains synchronous atrial contraction

8. AV node → His → bundle branches

• AV node continues as bundle of His
• At top of interventricular septum:
• Gives off left bundle branch
• Continues as right bundle branch

Left bundle branch divides into:

• Anterior fascicle
• Posterior fascicle
• These run subendocardially
• Join Purkinje system
• Purkinje fibers distribute excitation to entire ventricular myocardium

9. Histology of the conduction system (logic of speed)

General principle

• Conduction system = modified cardiac muscle

Purkinje fibers

• Large cells
• Few mitochondria
• Few striations
• Specialized for rapid conduction, not contraction

SA & AV nodal cells

• Smaller
• Sparsely striated
• High internal resistance
• Therefore:
• Slow conduction
• Important for AV nodal delay

10. Electrical insulation between atria & ventricles

• Fibrous ring separates atrial and ventricular muscle
• Prevents random spread of impulses
• Only normal conducting bridge:
• Bundle of His

👉 Prevents atrial impulses from directly stimulating ventricles

11. Embryologic basis of autonomic control

Development

• SA node → right-sided embryologic origin
• AV node → left-sided origin

Adult autonomic pattern

• Right vagus → mainly SA node
• Left vagus → mainly AV node
• Same sidedness for sympathetic supply

Sympathetic fibers

• Originate mainly from stellate ganglion
• Noradrenergic
• Epicardial

Parasympathetic fibers

• Vagal
• Endocardial

12. Reciprocal autonomic inhibition

• Acetylcholine:
• Inhibits norepinephrine release presynaptically
• Neuropeptide Y (from sympathetic endings):
• Inhibits acetylcholine release

👉 Explains fine autonomic balance

PROPERTIES OF CARDIAC MUSCLE

13. Resting membrane potential

• Myocardial fibers: ~ −90 mV
• Cells connected by gap junctions
• Act electrically like a functional syncytium

14. Ventricular action potential phases (logic)

Cardiac Action Potentials — Logic Framework

Big picture logic

• Working myocardium (atria/ventricles) → built for forceful contraction
• Pacemaker tissue (SA/AV node) → built for automatic rhythm generation
• Therefore:
• Muscle cells need a plateau
• Nodal cells need spontaneous depolarisation

A. Ventricular (Cardiac Muscle) Action Potential

(Phases 0–4 present)

Purpose

• Strong, synchronized contraction
• Prevent tetany → allow filling time

Phase 4 — Resting potential (~ −90 mV)

Why stable?

• High K⁺ permeability

Channels

• IK₁ (inward rectifier K⁺ channels)(or limits outward flow) → open

Logic

• K⁺ leak out slowly→ keeps membrane very negative
• Cell is electrically quiet until stimulated

Phase 0 — Rapid depolarisation

Trigger

• Incoming impulse from conduction system

Channels

• Fast voltage-gated Na⁺ channels OPEN
• Massive Na⁺ influx

Logic

• Sudden positive shift → sharp upstroke
• Defines conduction velocity (fast)

Phase 1 — Initial repolarisation

Why brief dip?

• Na⁺ channels inactivate
• Transient outward K⁺ current

Channels

• Ito (transient K⁺ efflux)

Logic

• Small repolarisation before plateau starts

Phase 2 — Plateau (key cardiac feature)

Why plateau exists

• Balance between inward Ca²⁺ and outward K⁺

Channels

• L-type Ca²⁺ channels OPEN → Ca²⁺ influx
• Delayed rectifier K⁺ channels partially open

Logic

• Ca²⁺ entry:
• Maintains depolarisation
• Triggers Ca-induced Ca release → contraction
• Plateau = long refractory period

📌 Exam lock

• Plateau prevents tetanic contraction

Phase 3 — Repolarisation

What changes

• Ca²⁺ channels close
• K⁺ efflux dominates

Channels

• IKr, IKs (delayed rectifier K⁺ channels)

Logic

• Return to resting membrane potential

15. ECG logic

• ECG = summed extracellular electrical activity
• Shape reflects:
• Contributions from different regions
• Different timings of depolarization

PACEMAKER POTENTIALS

16. Why pacemaker cells fire automatically

• After each action potential:
• Membrane does not stay flat
• It slowly depolarizes again
• This slow depolarization = prepotential / pacemaker potential

17. Ionic basis of pacemaker potential

(SA node / AV node — phases 0, 3, 4 only)

Purpose

• Automatic rhythm generation
• Not force production

Phase 4 — Pacemaker potential (unstable!)

Key difference

• No true resting potential

Channels

• If (funny current / HCN channels) → Na⁺ influx
• ↓ K⁺ efflux
• T-type Ca²⁺ channels open late

Logic

• Slow, spontaneous depolarisation
• Determines heart rate

📌 Autonomic control

• Sympathetic → ↑ If slope → ↑ HR
• Parasympathetic → ↓ If slope → ↓ HR

Phase 0 — Slow depolarisation

Why slow?

• No fast Na⁺ channels

Channels

• L-type Ca²⁺ channels OPEN

Logic

• Ca²⁺-mediated upstroke → slower conduction
• AV node delay is physiological

Phase 3 — Repolarisation

Channels

• K⁺ channels OPEN

Logic

• Repolarisation → cycle repeats automatically

Core Comparison Table (Exam Gold)

One-line Memory Logic

• Muscle cells contract → need Ca²⁺ plateau
• Nodes fire rhythm → need funny Na⁺ drift
• Fast Na⁺ = speed
• Ca²⁺ = timing

18. Nodal vs myocardial action potentials

19. Latent pacemakers

• Present in:
• AV node
• Bundle branches
• Purkinje system
• Normally suppressed by SA node
• Take over when:
• SA node fails
• Conduction blocked

20. Effect of vagal stimulation

Mechanism

• Acetylcholine → M2 receptors
• βγ subunit opens IKACh
• ↑ K⁺ conductance

Effects

• Membrane hyperpolarization
• ↓ slope of pacemaker potential
• ↓ cAMP → ↓ Ca²⁺ channel opening

👉 Result:

↓ firing rate

Strong stimulation → temporary arrest

21. Effect of sympathetic stimulation

Mechanism

• Norepinephrine → β1 receptors
• ↑ cAMP

Effects

• Faster Ih depolarization
• ↑ ICa via L-type channels
• Faster phase 0 in nodal cells

👉 Result:

↑ heart rate

22. Other modifiers of pacemaker rate

• Temperature ↑ → ↑ firing rate (fever tachycardia)
• Digitalis:
• Depresses nodal tissue
• Vagal-like effect
• Especially on AV node

SPREAD OF CARDIAC EXCITATION

23. Atrial depolarization

• Starts at SA node
• Spreads radially through atria
• Completed in ~0.1 s

24. AV nodal delay (why it exists)

• AV node conducts slowly
• Delay ≈ 0.1 s

Why important

• Allows:
• Complete atrial emptying
• Proper ventricular filling

Modifiers

• Sympathetic → shortens delay
• Vagal → lengthens delay

25. Importance of Na⁺ current for conduction

• Loss of INa in phase 0:
• Marked conduction slowing
• Explains why:
• AV node (Ca²⁺-based) conducts slowly

26. Ventricular depolarization sequence

Time: 0.08–0.1 s

Order:

1. Left side of interventricular septum
2. Rightward across mid septum
3. Down septum to apex
4. Up ventricular walls
5. Endocardium → epicardium

Last areas to depolarize:

• Posterobasal LV
• Pulmonary conus
• Upper septum

CLINICAL BOX — DIGITALIS (LOGIC)

27. Source & basic action

• Derived from foxglove plant
• Inhibits Na⁺/K⁺ ATPase

28. Mechanical effect

• ↓ Na⁺ extrusion
• ↑ intracellular Na⁺
• ↓ Ca²⁺ extrusion
• ↑ intracellular Ca²⁺
• ↑ Ca²⁺ release during contraction

👉 Result:

Stronger contraction (positive inotropy)

29. Electrical effect

• ↓ AV nodal conduction velocity
• ↓ number of impulses reaching ventricles

30. Therapeutic uses

Systolic heart failure

• ↑ contractility
• ↑ cardiac output
• ↓ ventricular filling pressure

Atrial fibrillation / flutter

• Slows AV conduction
• Provides rate control

31. Modern perspective

• Use reduced due to:
• Narrow therapeutic window
• Availability of safer alternatives
• Still important with:
• Careful dosing
• Proper understanding of toxicity