Initiation and Coordination of Heart Action

Spec Mapping — OCR H420 Module 3.1.2 — Transport in animals, content statements covering the myogenic nature of cardiac muscle, the conduction pathway (sinoatrial node, atrioventricular node, Bundle of His, Purkinje fibres), the role of the AVN delay in coordinating atrial and ventricular contraction, and the interpretation of an electrocardiogram (P wave, QRS complex, T wave) (refer to the official OCR H420 specification document for exact wording). This lesson supplies the electrical control system that drives the mechanical events of Lesson 8.

Unlike skeletal muscle, cardiac muscle does not need a nerve impulse to make it contract — it is myogenic, meaning that the signal to contract originates within the muscle tissue itself. A single intrinsic pacemaker coordinates the activity of the whole heart and ensures that the four chambers contract in the correct order. This lesson examines the conducting system of the heart (SAN, AVN, Bundle of His and Purkyne tissue), how nervous and hormonal input modify the heart rate, and how all this activity can be monitored non-invasively using an electrocardiogram (ECG).

The discovery that cardiac muscle is myogenic dates to the late 19th century, when Walter Gaskell in Cambridge showed that an isolated heart continues to beat in saline solution. Willem Einthoven (1903) invented the string galvanometer and recorded the first practical electrocardiogram in humans, naming the deflections P, Q, R, S, T — letters chosen specifically to allow expansion if more waves were discovered. He won the 1924 Nobel Prize for the work. Modern ECG remains the front-line investigation for chest pain, palpitations and unexplained collapse worldwide.

Key Definitions:

• Myogenic — able to initiate contraction without any external (nervous) signal.
• Pacemaker — the tissue that sets the rhythm of heart contraction; in mammals this is the sinoatrial node (SAN).
• Electrocardiogram (ECG) — a recording of the electrical activity of the heart, made by electrodes placed on the skin.

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The Conducting System

A special group of modified cardiac muscle fibres carries electrical signals rapidly through the heart, ensuring coordinated contraction. The key components are:

1. Sinoatrial node (SAN)
2. Atrioventricular node (AVN)
3. Bundle of His
4. Purkyne tissue (Purkinje fibres)

flowchart TB
    SAN[SAN in right atrium wall] -->|Wave of depolarisation across atria| ATR[Atria contract]
    ATR --> AVN[AVN at base of atria]
    AVN -->|Delay about 0.1 s| BH[Bundle of His in septum]
    BH --> PK[Purkyne fibres in ventricle walls]
    PK --> VENT[Ventricles contract from apex upwards]

Ventricles contract from apex upwards (toward semilunar valves)

Step 1: The SAN

The sinoatrial node is a small patch of modified cardiac muscle in the wall of the right atrium, near the entry of the superior vena cava. It spontaneously generates a wave of depolarisation about 75 times per minute at rest. This is the intrinsic heart rate, and why the SAN is called the pacemaker.

Step 2: Atrial Contraction

The wave of depolarisation spreads across the walls of both atria, causing atrial systole. Because atrial muscle cells are electrically coupled by intercalated discs containing gap junctions, the wave travels rapidly through the atrial syncytium.

Step 3: The AVN

The wave cannot cross directly into the ventricles because the base of the atria is separated from the ventricles by a non-conducting fibrous ring (the annulus fibrosus). Instead, it is funnelled through the atrioventricular node (AVN), located at the base of the right atrium near the septum. The AVN introduces a delay of about 0.1 s, which is essential to allow the atria to finish contracting and to empty completely into the ventricles before the ventricles themselves start to contract.

Step 4: The Bundle of His

From the AVN, the signal passes down the Bundle of His, a strand of specialised conducting fibres in the interventricular septum. It divides into left and right bundle branches that run towards the apex (tip) of the heart.

Step 5: Purkyne Fibres and Ventricular Contraction

At the apex, the bundle branches spread out into a network of Purkyne fibres (Purkinje fibres) that penetrate the walls of the ventricles. These conduct the wave rapidly through the ventricular muscle, triggering contraction from the apex upwards — effectively squeezing blood towards the semilunar valves at the top, like squeezing toothpaste out of a tube. This is why ventricular contraction is so efficient at ejecting blood.

Exam Tip: Always emphasise the delay at the AVN and the apex-to-base direction of ventricular contraction. These two features ensure the correct sequence and efficient emptying, and are worth marks in exam answers.

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Myogenic Heart Muscle

"Myogenic" means generated by the muscle itself. If the heart is removed and kept in a suitable saline solution, it will continue to beat — because the SAN does not require any nerve impulse to trigger it. In contrast, skeletal muscle is neurogenic: it only contracts when stimulated by a motor neuron.

Although the heartbeat is myogenic, the rate at which the SAN fires can be modified by:

• Autonomic nervous system — parasympathetic fibres (vagus nerve, via acetylcholine) slow the SAN; sympathetic fibres (via noradrenaline) speed it up.
• Hormones — adrenaline binds to receptors on SAN cells and increases heart rate (and stroke volume).
• Temperature — higher temperatures generally increase heart rate.
• Ion levels — especially K⁺ and Ca²⁺, which affect the membrane potentials of pacemaker cells.

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The Electrocardiogram (ECG)

An ECG is produced by placing electrodes on the skin over the heart and chest. These detect the minute voltage changes on the body surface that result from depolarisation and repolarisation of cardiac muscle. A standard ECG trace contains three components in each cycle, labelled with letters:

• P wave — depolarisation of the atria → atrial contraction.
• QRS complex — depolarisation of the ventricles → ventricular contraction. It is the largest deflection because ventricular muscle is so massive. Atrial repolarisation occurs at the same time but is hidden by the QRS complex.
• T wave — repolarisation of the ventricles → ventricular relaxation.

Between these waves are important intervals:

• P–R interval — the delay at the AVN; the time between atrial and ventricular activity.
• S–T segment — the plateau of ventricular contraction.
• R–R interval — the time between successive beats, from which heart rate is calculated.

P Atrial depolarisation

PR interval

QRS Ventricular depolarisation

T Ventricular repolarisation

Next cycle...

The trace is sometimes summarised in a flowchart form:

flowchart LR
    P[P wave: atrial depolarisation] --> QRS[QRS complex: ventricular depolarisation] --> T[T wave: ventricular repolarisation]

Detailed components of the ECG

Component	Duration	Underlying event
P wave	~80 ms	Atrial depolarisation; small because atrial muscle is thin
PR interval	120–200 ms	Time from P onset to QRS onset; reflects AVN delay
QRS complex	80–120 ms	Ventricular depolarisation; large because ventricular muscle is thick; atrial repolarisation is hidden here
ST segment	~80 ms	Plateau of ventricular action potential (Ca²⁺-driven)
T wave	~160 ms	Ventricular repolarisation
R-R interval	600–1000 ms at rest	Time between successive beats; heart rate = 60 / R-R(s)

Calculating Heart Rate from an ECG

At a standard paper speed of 25 mm/s, each small square (1 mm) represents 0.04 s. To estimate heart rate:

$\text{Heart rate (bpm)} = \frac{60}{\text{R-R interval in seconds}}$Heart rate (bpm)=R-R interval in seconds60​

For example, if the R-R interval is 0.8 s, heart rate = 60 / 0.8 = 75 bpm.

Abnormal ECG Patterns

• Tachycardia — resting heart rate above 100 bpm; short R-R intervals, often with normal waveforms.
• Bradycardia — resting heart rate below 60 bpm; long R-R intervals.
• Atrial fibrillation — chaotic atrial activity; P waves absent or irregular; ventricular rhythm often irregular ("irregularly irregular pulse"). Loss of synchronised atrial kick → ~20% reduced stroke volume.
• Ventricular fibrillation — chaotic, high-frequency waveforms; no coordinated QRS; medical emergency requiring defibrillation within minutes.
• Ectopic beat — an extra heartbeat originating outside the SAN; gives a premature QRS with no preceding P wave.
• Heart block — failure of conduction between atria and ventricles. First-degree = prolonged PR interval (>200 ms); second-degree = some P waves are not followed by QRS (Mobitz I or II); third-degree (complete) heart block = atria and ventricles dissociated, ventricular escape rhythm at ~40 bpm.

Effects on heart rate of nervous, hormonal and ionic input